10th Annual Regenerative Medicine Essentials Course and World Stem Cell Summit Return to Live with Virtual Option in 2023 – Newswise

10th Annual Regenerative Medicine Essentials Course and World Stem Cell Summit Return to Live with Virtual Option in 2023  Newswise

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10th Annual Regenerative Medicine Essentials Course and World Stem Cell Summit Return to Live with Virtual Option in 2023 - Newswise

Discover Inspiring Animal Research Topics – Studyclerk.com

Why Choose Animal Research Topics For Writing Purposes?

Contrary to popular belief, animal research topics are not only used by veterinarians. They are also pursued by students majoring in Healthcare, Sound Engineering, and even subjects like Fashion Studies and Chemistry. Of course, it may require writing an excellent custom research paper because the trick here is to tailor things to what you need. The most challenging, however, is to choose your topic correctly and avoid being vague about what you must explore. Even if you would like to explore environmental issues, using animal research topics will be essential. You need to provide an explanation of your reasoning and the negative effects of human interaction with flora and fauna.

While there may be no universal topic that will reflect all sides of animal-related research, consider those subjects that you know well. It must inspire you and be an area where you feel comfortable. If you love marine life and can provide personal research examples, it would be good to choose something that will suit a reflection journal. Alternatively, consider animal topics for research papers that can be supported by reliable sources and statistical information.

Start with an outline or a list of arguments that you would like to explore. Once done, continue with the wording for your topic that introduces the problem and offers a solution. You may also pose a research question about a problem or make a claim that will be supported by what you include in your paper. Always refer to your grading rubric and choose your research paper type accordingly. For example, your nursing research paper may talk about the use of animals for rehabilitation purposes, while a legal student may talk about animal rights in various countries. It all should be approached through the lens of what you learn as a primary subject!

As you might already know, animal physiology studies anything related to the physical processes, changes in behaviors, breeding patterns, and more. As you think about choosing the animal physiology branch, always narrow things down if possible.

This aspect of animal research essay writing may not be everyones cup of tea, which is why it is necessary to explore the facts and provide information that represents both sides of the debate. Stay sensitive and avoid being too graphic unless it is necessary. Below are some ideas to consider:

The subject of animal rights is popular among students coming from all academic disciplines. Since you can approach it via the philosophical, legal, or medical lens, think about how to reflect your primary skills. It will make your research of animal right topics sound more confident.

In the majority of cases, you may refer to your veterinary branch first and proceed from there or take a look at the variety of veterinary research topics that we have presented below. Remember to quote every citation and idea that has been taken from other sources to avoid plagiarism.

Even though this subject seems to be discussed everywhere these days, finding good animals topics to write about that deal with animal testing is not easy. Think about what are the underlying reasons for testing and what forces scientists to use it as a method. It will help you come up with ideas and better exploration strategies.

Warning: writing about animal cruelty subject is not for everyone, which is why you must be aware that the facts and statistics you may find will be shocking. It should be explored only if you are ready to embrace this disturbing subject. At the same time, you can explore milder animal cruelty cases like using pets as influencers on social media or the use of donkeys at the beaches to entertain tourists. There is always something to think about!

When you would like to take a general approach to animals research, it is good to come up with a research question as a part of your thesis statement or main argumentation. See these animals research paper examples:

Without a doubt, it is easy to get stuck with a multitude of topics and ideas. If you are planning to write about animal rights but do not know how to include certain animal physiology principles, it is safer to consider timely help with research paper. Our skilled team of specialists in this field will provide you with relevant sources and will help you polish things to perfection when you need assistance or do not know how to continue.

The same relates to checking your existing draft and citations in terms of plagiarism and originality. Writing about animals is never easy, which is why we know how you feel and also realize what your college professors expect to see. Take a look at our research topics about animals, trust us with your concerns and we shall help you achieve success!

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Discover Inspiring Animal Research Topics - Studyclerk.com

Sex Hormones and Their Receptors Regulate Liver Energy Homeostasis

The liver is one of the most essential organs involved in the regulation of energy homeostasis. Hepatic steatosis, a major manifestation of metabolic syndrome, is associated with imbalance between lipid formation and breakdown, glucose production and catabolism, and cholesterol synthesis and secretion. Epidemiological studies show sex difference in the prevalence in fatty liver disease and suggest that sex hormones may play vital roles in regulating hepatic steatosis. In this review, we summarize current literature and discuss the role of estrogens and androgens and the mechanisms through which estrogen receptors and androgen receptors regulate lipid and glucose metabolism in the liver. In females, estradiol regulates liver metabolism via estrogen receptors by decreasing lipogenesis, gluconeogenesis, and fatty acid uptake, while enhancing lipolysis, cholesterol secretion, and glucose catabolism. In males, testosterone works via androgen receptors to increase insulin receptor expression and glycogen synthesis, decrease glucose uptake and lipogenesis, and promote cholesterol storage in the liver. These recent integrated concepts suggest that sex hormone receptors could be potential promising targets for the prevention of hepatic steatosis.

Obesity rapidly becomes a worldwide epidemic disease with increased risk of cardiovascular diseases, type 2 diabetes mellitus, and metabolic syndrome [1]. Metabolic syndrome is characterized by increased visceral adiposity, hyperlipidemia, insulin resistance, and hypertension [2]. The liver is the largest visceral organ for maintaining homeostasis in glucose, lipid, and protein. Hepatic steatosis is characterized by massive fat accumulation in the liver and thus is strongly related to several features of metabolic syndrome, including hyperlipidemia and insulin resistance [3]. Indeed, reduction or loss of insulin action in the liver leads to abnormally increased hepatic gluconeogenesis, glucose production, and lipogenesis, as well as decreased insulin clearance, hepatic glucose uptake, and lipolysis, consequently resulting in dyslipidemia [4].

Age and sex are physiologic factors that have strong association with the prevalence and features of metabolic syndrome. The state of estrogen deficiency as seen in postmenopausal women and the state of androgen deficiency as seen in aging men predispose older population to the metabolic syndrome and associated diabetes and cardiovascular diseases, indicating that sex hormones play important roles in regulating energy metabolism [5, 6]. Nonalcoholic fatty liver disease (NAFLD) disproportionally affects people with obesity, diabetes with insulin resistance, and dyslipidemia [79]. The prevalence of NAFLD varies among ethnicities, with the highest prevalence in Hispanics, correlated with the high prevalence of obesity and insulin resistance in this ethnic group, compared to whites and blacks [10]. Similar to the incidence of metabolic syndrome, the frequency of NAFLD varies between genders, with greater prevalence in men than in women among whites (42% in white men versus 24% in white women) but not in other ethnicities [10]. This is consistent with another epidemiology study showing that the rate of NAFLD is a little higher in men than in women with all ethnicities combined [7]. Interestingly, NAFLD is twice as common in postmenopausal women as in premenopausal women whose estrogen levels are higher than postmenopausal women [7, 11], which suggests the protective role of estrogens in NAFLD [12, 13].

In general, androgens are considered as hormones of the male sex due to their masculinizing effects and their roles in regulating male sexual behavior, whereas estrogens are considered as hormones of the female sex due to their roles in regulating female reproductive physiology and behaviors, although all sex hormones are present in both males and females, albeit at different levels between these two sexes. The most important biologically relevant forms of estrogens and androgens in humans are estradiol (E2) and testosterone, respectively. Understanding of how estrogens and androgens regulate energy metabolism via their receptors may shed light on potential pharmaceutical applications. In the present review, we discuss the roles of estrogens and androgens in regulating liver glucose and lipid homeostasis in rodents and humans. We also deliberate the distinct, important effects of estrogen receptors (ERs) and androgen receptors (ARs) on the regulation of liver metabolism.

In both males and females, E2 is derived from the aromatization of testosterone. In premenopausal women, E2 is mainly synthesized from cholesterol in the ovaries, with E2 concentration being approximately 5 times higher than that in men, while in postmenopausal women E2 is primarily converted from testosterone by aromatase in peripheral tissues, such as adipose tissue, adrenal glands, bones, vascular endothelium, and smooth muscle [14], with E2 concentration being similar compared with men (http://www.hemingways.org/GIDinfo/hrt_ref.htm).

Estrogens act on ERs, including classic nuclear receptors ER- and ER-, and membrane-bound receptors, including G protein-coupled ER (GPER, also known as GPR 30) and membrane-associated ER- and ER- variants [15]. All these nuclear and membrane ER subtypes are expressed in the livers of male and female humans and rodents, but at a lower level compared with reproductive organs such as uterus, prostate, testis, ovary, and breast [1618]. ER- is less abundant in liver cells than ER- [19, 20] and GPER (unpublished observation).

One study by Lax et al. determines levels of ERs in male and female rat livers and reports that the levels of nuclear ERs are not sex dependent but are age dependent, as levels of ERs are similar between male and female rats and vary with the course of life in a comparable manner in males and females [21]. Specifically, levels of ERs in the liver of both male and female rats are the highest during the perinatal period, decline till the onset of puberty, and increase to reach postpubertal peak. Additionally, levels of ERs are maintained as a stable level across the estrous cycles of female rats [21]. Consistently, Eisenfeld group has reported that ER concentration in the rat liver increases evidently at puberty [22]. Ovariectomy (OVX), a procedure that removes ovaries and thus majority of endogenous estrogens, is a suitable preclinical model to study postmenopausal diseases. Liver ER- expression does not change following OVX; however, it significantly increases by E2 treatment at a superphysiological level in rats with OVX, higher than sham-operated rats with intact ovaries and normal levels of endogenous estrogens [23]. These studies indicate that ER- expression in the liver is similar between gonad intact males and females and remains stable in postmenopausal females but could increase following hormone replacement therapy or during puberty. There is no available literature showing changes of expression of ER- and GPER during menstrual period or postmenopausal stage, and these questions remain unknown.

Males also express ERs in the liver, and aromatase metabolizes androgens to generate E2 and other estrogen metabolites locally in many target tissues. A growing body of evidence suggests that estrogens also have important metabolic functions in males. The aromatization of testosterone to E2 is beneficial for preventing intra-abdominal adiposity in men, demonstrated by a clinical study showing increased intra-abdominal fat in men by reduced estrogens due to aromatase inhibition [24]. The effects of estrogens on male and female reproductive organs have been extensively studied, but the beneficial effects of estrogens in nonclassical endocrine targets including the liver are less appreciated. We will discuss how hepatic estrogen signaling via ERs regulates metabolism in male and female animal and human models.

Upon estrogen binding, classic estrogen nuclear receptors ER- and ER- form homo- or heterodimers and bind to estrogen response element (ERE) in target gene promoters or to other transcription factors, such as activator protein-1 (AP-1) and stimulating protein-1 [25], to induce expression of target genes. The genomic action following E2-ER binding varies as the level of sex hormone changes. Specifically, the transcriptional activity of ER- alters during the 4-day estrous cycle, demonstrated by using ERE-luciferase reporter mice which have luciferase reporter controlled by activated ERs. The peak of the transcriptional activity of ER- in the liver occurs in proestrus [26], indicating dynamics of ER- transcriptional activity that is possibly modulated by different concentration of estrogens [27]. These findings suggest that liver ER- could recognize the changes in circulating E2 levels and response to reproductive cues during transition of different stages of the estrous cycles and select appropriate genetic programs to adapt the hepatic metabolism to the energy requirements of each stage. Thus, the hepatic ER- could serve as a peripheral coordinator of energy homeostasis. ER- also exists in the form of membrane-associated receptor. There are many lines of evidence showing that the full length ER- and truncated ER- may exert actions via nongenomic signaling which is faster than the classic genomic signaling. Such nongenomic signaling usually involves activation of intracellular second messenger systems, such as protein kinase A (PKA), protein kinase C, and mitogen-activated protein kinase (MAPK)/extracellular signal-regulated protein kinase (ERK) [2830]. GPER is structurally unrelated to ER- and ER- and is a seven-transmembrane domain G protein-coupled receptor located at the cell membrane and endoplasmic reticulum membrane. GPER is reported to rapidly activate different nongenomic estrogen signaling pathways, including PKA, MAPK/ERK, and phosphoinositide 3-kinase (PI3K) [31] (Figure 1).

Females, as compared with males, tend to store more energy in subcutaneous fat instead of in visceral fat. The liver is a key visceral organ for controlling energy storage, as the liver has high capacity for lipid transport, de novo lipogenesis, lipid oxidation, and lipolysis. Liver steatosis, as seen in the nonalcoholic fatty liver disease (NAFLD), is due to the excess of triglyceride (TG) accumulation within the hepatocytes. Incidence of hepatic steatosis is frequently associated with low levels of high density lipoprotein cholesterol (HDL-C) and high levels of low density lipoprotein cholesterol (LDL-C) in the circulation. Epidemiological studies have showed higher plasma level of LDL-C and lower plasma level of HDL-C in men and postmenopausal women compared with premenopausal women, suggesting that lower circulating estrogen levels may promote fat deposition in the liver [32]. Further evidence is supported by using OVX mouse model combined with pair-feeding between sham operation and OVX groups. Removal of the ovaries and thus the majority of endogenous estrogens in female mice results in increased fat proportion in the liver even when they are pair-fed with the same amount of calories as females with intact ovaries, which indicates the direct role of estrogens in inhibiting lipogenesis in the liver, rather than the secondary effects to OVX induced overfeeding [33]. In another E2-deficient aromatase knockout (ArKO) mouse model, spontaneous obesity and hepatic steatosis result from impaired fatty acid -oxidation and elevated fatty acid synthase (FAS) in the liver in both female and male mice [34]. These findings are further supported by previous studies demonstrating that E2 inhibits lipogenic gene expression and lipid uptake in the liver by decreasing lipoprotein lipase activity, as well as promoting lipolysis by increasing expression of hormone-sensitive lipase and adipose TG lipase in the liver [35, 36].

ER- is the predominant ER subtype presented in both male and female hepatocytes [19, 20]. Estrogen signaling is important in both males and females in the regulation of lipogenesis, demonstrated by using animal models and human studies. Specifically, estrogens regulate the activity and expression of lipogenic genes to directly inhibit lipogenesis in several animal species [37, 38]. Liver enzymes may also be regulated by circulating estrogen levels. One study of genome-wide analyses demonstrated that the subtle oscillations of estrogens occurring during the estrous cycle are sufficient to influence liver gene expression, and that ERs are involved in the pulsatile synthesis of fatty acids and cholesterol in the liver [27]. Thus this study demonstrated the importance of the maintenance of estrogen oscillation to limit fat deposition in the hepatic tissues in females [27]. Additionally, treatment of the specific ER- agonist PPT decreases weight, fat mass, and TG in the liver in both wild-type mice and obese ob/ob mice [39, 40]. Thus, the metabolically protective effect of estrogen may be attributed to estrogen signaling via ER- [41].

This is further demonstrated by investigation of estrogen and estrogen signaling using knockout or transgenic animal models. Male and female ER- knockout mice exhibit hepatic steatosis by increasing gene expression of lipogenic transcription factors such as sterol regulatory element binding protein 1c (SREBP-1c) and decreasing lipid transport genes [42, 43]. Mice with liver-specific ER- knockout [44, 45] or liver-specific GPER knockout [46] show increases in fat accumulation in the liver and develop disturbed insulin signaling under high-fat diet (HFD) feeding. Thus, hepatic steatosis has been observed in both of the above genetic models, one with liver-specific ER- knockout with functional GPER and the other with liver-specific GPER knockout with functional ER-. Thus, although it is widely recognized that estrogens regulate liver lipid metabolism and reduce triglyceride accumulation in the liver mainly via ER- [47, 48], both ER- and GPER are required to be present in the liver to maintain lipid homeostasis. Estrogen is produced in males by aromatization of testosterone. Male but not female mice in which the aromatase gene has been deleted (ArKO) develop hepatic steatosis that can be normalized by estrogen treatment [49]. Thus, E2 treatment reduces fatty acid synthesis and lipid accumulation and prevented NAFLD in castrated male rats [50].

Hepatic TG and diacylglyceride increase in the livers of ER- knockout male mice under HFD feeding, explained by dysregulation of insulin-stimulated ACC phosphorylation and DGAT1/2 protein levels [44]. Interestingly, a recent study using specific plasma membrane ER- knockout has demonstrated that it is the membrane-localized ER-, but not nuclear ER-, that is responsible for protection from hyperlipidemia by decreasing expressions of many hepatic genes involved in lipid synthesis, at least in female mice with OVX [51]. Although ER- is antilipogenic in the liver, the role of ER- in the liver is not consistent in the literature. ER- deficient mice have higher body weight but lower liver weight due to increased insulin sensitivity and decreased TG accumulation in the liver [52], indicating that ER- might be lipogenic and diabetogenic in the liver. Opposite finding has been reported where, different from treatment of E2 or ER- agonists that decrease hepatic PPAR expression, treatment of ER- agonist 8-VE2 comparably elevates PPAR expression to the same mRNA level as non-drug treated group in the liver of HFD-fed female rats with OVX [53]. Interestingly, all treatments of E2, ER- agonist, or ER- agonist are capable of reducing TG accumulation in the liver of HFD-fed rats with OVX [53]. Thus, the mechanism for reduced hepatic lipid accumulation in both suppressed ER- signaling as seen in ER- knockout mice [52] and activated ER- signaling as seen in ER- agonist-treated rats [53] is awaiting further elucidation. Hepatic steatosis is also found in GPER deficient female mice fed with HFD rather than male mice [46]. Although both 6-month-old female and male GPER KO mice display increased body weight, only female mice had glucose intolerance, while male mice developed glucose intolerance at the age of 18 months [54]. Furthermore, GPER agonist G-1 decreases fatty acid synthesis and TG accumulation in both human and rodent pancreatic cells [55], but the effect of G-1 treatment on lipid metabolism in the liver is not clear. Both liver GPER and membrane-associated ER- are critical for liver lipid metabolism. However, it is possible that GPER has greater impacts on male lipid regulation [54], whereas membrane-associated ER- variant [51] may have greater impacts on female lipid regulation, as female livers have markedly higher expression of all three membrane-associated ER- variants compared with male livers [56].

Hepatic glucose homeostasis is determined by glucose uptake and glucose production. The major glucose transporter (GLUT) in the liver is GLUT2 that bidirectionally transports glucose across liver cell plasma membrane, efflux of glucose formed from gluconeogenesis or glycogenolysis out of liver cells, and uptake of circulating glucose into liver cells. Hepatic GLUT2 is upregulated by glucose, FAS, and insulin [57]. Since estrogen treatment has been shown to increase insulin synthesis and release [58], estrogens might indirectly increase GLUT2 expression in the liver, which has not been demonstrated yet. A recent study demonstrates that it is estriol, instead of E2, that downregulates GLUT2 in pregnant women during late stages of pregnancy whose peak postprandial glucose levels are much lower than glucose levels of healthy nonpregnant women [59]. Estrogens are also important in hepatic insulin clearance. Several lines of evidence show that intravenous conjugated estrogen treatment or low dose of oral contraceptive does not significantly alter insulin sensitivity but slightly increases hepatic insulin clearance in postmenopausal women [60, 61]. Estrogens reduce gluconeogenesis and increase glycogen synthesis and storage in the liver, lowering circulating glucose level [43, 62]. Additional observations using rodents with OVX that lacks majority of endogenous estrogens support the notion that estrogens lower glucose levels [63, 64]. A recent study reports increased glucagon signaling due to increased amount of glucagon receptor that accounts for enhanced glucose production, accompanied with increased gluconeogenic enzymes in rats with OVX [65]. Interestingly, such changes cannot be prevented by E2 replacement, which indicates that disrupted liver glucose homeostasis following OVX is not merely caused by deficiency of endogenous E2 [65] but could be caused by deficiency of other ovarian hormones such as progesterone. Although classic nuclear progesterone receptor has not been found in the liver [22, 66], progestins can either bind to membrane-bound progesterone receptors [67] or bind to ARs [22] in human liver and carry metabolic effects. On the other hand, estrogens are also found to facilitate epinephrines action via 2-adrenergic receptor in regulating glycogenolysis and gluconeogenesis in the rat liver to increase circulating glucose level [68].

Estrogen signaling is important in both males and females in the regulation of glucose homeostasis, improving glucose tolerance and insulin sensitivity, demonstrated by using animal models and human studies [6971]. Additionally, although estrogens do not affect hepatic glucose metabolism in vivo, estrogens increase insulin receptor to enhance glucose metabolism in vitro [72, 73].

ER- deficient mice exhibit significantly impaired glucose tolerance and hepatic insulin resistance, while ER- deficient mice exhibit normal glucose tolerance, suggesting that ER- instead of ER- plays an important role in the regulation of hepatic glucose homeostasis [43]. The importance of ER- in the regulation of hepatic glucose tolerance is further supported by inadequate suppression of hepatic glucose production during hyperinsulinemic clamp study in ER- deficient mice [74]. Although impaired glucose tolerance is seen in GPER1 knockout mice, GLUT2 and glucokinase are not affected [1], and glucose production in liver has not been measured yet. Hepatic PPAR expression rises markedly following OVX in HFD-fed rats [53]. The rats treated with E2 or ER- agonist have reduced PPAR expression in the liver, whereas the rats treated with ER- agonist maintain a similarly high mRNA level of PPAR as non-drug treated HFD-fed rats with OVX. The sustained hepatic PPAR gene expression correlates with increased glucose uptake into the liver of rats with OVX [53].

Dyslipidemia is determined by decreased HDL but increased LDL and TG in the blood. The liver is the principal organ for cholesterol de novo biosynthesis, which is catalyzed by the rate limiting enzyme 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGR). The SREBP-1c is the master regulator of cholesterol by stimulating transcription of LDL and HMGR [75]. Postmenopausal women have elevated LDL and VLDL and lower HDL [76].

A previous in vitro study points out that HMGR promoter is induced by estrogen treatment in the breast cancer cell line MCF-7 but not in any hepatic cell line [77], indicating differential regulation of HMGR by estrogens among different tissues. Estrogen treatment does not increase cholesterol synthesis in liver cells in vitro. In an in vivo study using castrated male rats, DHT, but not E2, treatment increases phosphorylation of HMGR to decrease cholesterol synthesis in the liver [50]. Thus, at least in castrated male rats, androgen action is associated with downregulation of cholesterol biosynthesis in the liver.

Estrogens also decrease LDL level and increase HDL to promote cholesterol secretion into bile in postmenopausal women [78]. Total cholesterol and LDL are elevated in ArKO mice with E2 deficiency [79]. Increased hepatic HMGR activity and subsequently increased levels of cholesterol and LDL are seen in rats with OVX with reduced level of endogenous estrogens [65]. Estrogen replacement in both ArKO mice and rats with OVX normalizes the levels of LDL and cholesterol. The above mentioned cell, animal, and human studies collectively indicate important roles of estrogens in reducing LDL and increasing HDL.

ER- is able to protect the liver from hypercholesterolemia [47, 48]. To support this, lack of ER- (whole body) is associated with increased expression of genes involved in lipid biosynthesis and lipid metabolism [43]. A male patient without functional ER- has been reported with dyslipidemia [80], supporting the importance of ER- in regulating cholesterol homeostasis. Consistently, the expressions of ER- (and AR) and phosphorylated HMGR are significantly reduced in the human liver samples from male severe steatotic NAFLD patients compared with the liver samples from subnormal men [50].

Aromatase deficient mice without endogenous estrogen production exhibit obesity [79] and dyslipidemia [81] and mice with liver-specific ER- knockout accumulate liver triglycerides and diacylglycerides [42, 43]. In contrast, ER- agonist PPT increases the expression of genes involved in lipid oxidation and metabolism [82]. Additionally, ER- deficient mice and ER- and ER- double knockout mice display increased body fat and serum cholesterol level, but these changes are not found in ER- deficient mice [83].

In GPER KO mice, LDL levels increase approximately by 200%, but HDL levels do not show any significant differences from WT, which indicates that GPER mainly regulates the LDL metabolism instead of HDL [54]. A recent study shows that human individuals with hypofunctional P16L genetic variant of GPER have increased plasma LDL [84, 85]. In contrast, GPER activation upregulates LDL receptor expression in the liver via downregulation of proprotein convertase subtilisin kexin type 9 to enhance LDL metabolism [85]. Interestingly, animals with estrogen deficiency do not increase cholesterol synthesis; instead they decrease cholesterol catabolism by reducing activity of 7-hydroxylase, the enzyme that catalyzes the initial step in cholesterol catabolism and bile acid synthesis in calcium supplementation-induced hypercholesterolemia [86]. This study further demonstrates that estrogen treatment protects against increase in circulating level of cholesterol by activating of GPER [86].

The major circulating androgens include dehydroepiandrosterone, androstenedione, testosterone, and dihydrotestosterone (DHT), in descending order of circulating concentrations. Only testosterone and DHT bind to the AR whereas the rest are considered as proandrogens. Within target cells, testosterone can be converted to active androgen DHT via 5-reductase or converted to E2 by aromatase.

ARs are expressed in the liver of male and female humans and rodents, and AR expression in the liver is sex dependent. In adult rats, basal AR expression in the liver of male rats is about 20 times higher than that in the liver of female rats [87]. AR expression is also age dependent in the liver of either sex, which is very low, almost undetectable, before puberty, increases in postpubertal life, and gradually declines during aging, reaching an almost nondetectable level after about 2224 months of age in rats [88]. The sex- and age-dependent AR expression in the liver is programed by a regulatory element in the AR gene promoter [89].

There are isoforms of ARs which are AR-A with N-terminal truncated that resulted from proteolysis and AR-B with full length [90, 91]; among these two AR isoforms, the AR-B with full length is more potent than AR-A [92]. It is not clear, however, which isoform of AR is dominant in the liver. Androgens, like estrogens, work on both nuclear and nonnuclear receptors. The genomic effect of androgens is achieved through activation of nuclear receptor, followed by binding to specific DNA known as androgen response element (ARE) motifs in its target gene [93]. AR can recruit other transcription factors such as AP-1, nuclear factor-B, sex-determining region Y, and the E26 transformation-specific family of transcription factors and bind to DNA regions other than ARE, to participate in transcription activation of many other genes [94]. The nonnuclear receptor of androgens function is independent of DNA interaction and is more rapid by interacting with cytoplasmic signal transduction pathways, including PKA and MAPK/ERK [95] (Figure 1). The AR knockout animals are well developed, but the membrane-only AR knockout animals are not established yet, and that is why the exact role of membrane AR in liver metabolism is unclear.

Many studies have shown that androgens and androgen signaling suppress the development of hepatic steatosis [96, 97]. One population-based cross-sectional study has reported a close association between low serum testosterone level and hepatic steatosis in men [98]. Mice with 5-reductase knockout do not covert testosterone to DHT. These mice upregulate expression for the genes involved in lipid storage and downregulate genes for fatty acid oxidation and accumulate lipid in their livers when they are fed with HFD [99]. An inhibitor of 5-reductase induces liver steatosis in male obese Zucker rats [100]. Therefore, normal level of active androgen is critical to prevent liver steatosis.

Besides androgen level, ARs are also critical in maintaining lipid metabolism in the liver. Testicular feminized (Tfm) mice with nonfunctional AR and very low serum testosterone levels greatly increase HFD feeding-induced hepatic lipid deposition compared with control male mice with functional AR and normal circulating levels of testosterone. Replacement of testosterone reduces lipid deposition in the liver of Tfm mice to a similar level to control males [101]. Moreover, Kelly et al. [101] found that the expressions of key regulatory enzymes for fatty acid synthesis, including acetyl-CoA carboxylase (ACC) and FAS, are elevated in placebo-treated Tfm mice comparing with placebo-treated wild-type littermates and Tfm mice receiving testosterone treatment, indicating that the action of androgens on lipid deposition is independent of AR and at least partially via affecting key regulatory lipogenic enzymes to protect against hepatic steatosis [101]. Male but not female hepatic ArKO mice fed with a normal chow diet developed liver steatosis at 10 months with reduced fatty acid oxidation and increased de novo fatty acid synthesis [102]. Thus, males with either functional AR or normal circulating testosterone level would maintain normal level of fatty acid synthesis and avoid increased lipid deposition in the liver.

Although many studies have shown that androgens protect against NAFLD [50, 103], other studies have reported an opposite finding that androgens promote NAFLD development and progression [104, 105]. The inconsistencies might be due to different animal models employed and different treatments utilized in various studies. The findings reported by Mnzker et al. indicate that the testosterone/DHT ratio is more important for NAFLD development and progression than concentrations of testosterone and/or DHT [106]. In contrast, the role of AR in hepatic steatosis is less controversial. The total AR knockout mice develop liver steatosis and insulin resistance in both male and female mice [107]. Hepatic AR knockout mice with HFD feeding also show hepatic steatosis and insulin resistance, via upregulation of hepatic expression of SREBP-1c, ACC, and PPAR to increase lipid synthesis and downregulation of PPAR to decrease fatty acid oxidation; interestingly, such effects are evident in males but absent in females [102, 108]. Thus, hepatic AR plays more critical roles in maintaining liver lipid metabolism in males than in females.

Testosterone is either converted to E2 binding to ERs or converted to DHT binding to ARs. From the above studies, ARs are vital in regulating liver lipid homeostasis in both males and females [107], although hepatic ARs have greater impact in males than in females [102, 108]. In order to test the role of androgen-AR signaling in female metabolic process, Kanaya et al. replace DHT in female mice with OVX and find that those mice accumulate greater amount of fat in the liver and develop other symptoms and signs of metabolic dysfunction when these mice are fed with either a standard chow diet or HFD [109]. Therefore, androgen action has great impact on lipid metabolism in female livers.

Women have lower basal levels of androgens compared with males, and increased androgen level can affect metabolism in women. The role of androgens in females is not well established, but many lines of evidence indicate that hyperandrogenism in women with polycystic ovary syndrome (PCOS) increases risk of developing NAFLD. NAFLD is frequently present in PCOS women with excessive production of androgens by the ovaries and thus elevated circulating level of androgens, suggesting that abnormally high level of androgens in women may contribute to increased fat storage in the liver. It is noteworthy that the risk for NAFLD in women with PCOS is independent of obesity or insulin resistance but is triggered directly by the hepatotoxic, destructive effect in the liver, indicated by elevated level of alanine aminotransferase [110]. To summarize, normal level and signaling of androgens prevent hepatic lipid accumulation in males, while androgen deficiency in males is associated with fatty liver. Abnormally high level of androgens increases lipid deposition in the liver in females. Androgens therefore have differential effects in men and women.

Testosterone levels are lower in diabetic men than nondiabetic men [111]. Androgen deprivation therapy for prostate cancer patients lowers their circulating testosterone level and increases their risk of diabetes [112, 113] and not only increases circulating level of glucose but also diminishes pancreatic cell function [114]. Testosterone treatment markedly reduces circulating levels of glucose and TG in men [115].

GLUT2 directionally transports glucose across liver cell plasma membrane to maintain glucose homeostasis, as mentioned above in Section 2.3. Upregulation of GLUT2 plays a more critical role in regulating glucose export out of, rather than regulating glucose import into, the liver. It has been reported that blood glucose level, along with the mRNA and protein levels of GLUT2 in the liver, significantly increases following castration in male rats with deficiency of endogenous androgens [116]. Supplementation of testosterone or a combination of testosterone with E2 normalizes GLUT2 mRNA and protein levels in the livers of castrated rats, whereas treatment of E2 alone does not have any effect [116]. These findings suggest that testosterone maintains glucose homeostasis by regulating hepatic glucose output, and testosterone deprivation due to castration increases hepatic glucose output, induces hyperglycemia, and develops symptoms seen in type 2 diabetes and metabolic syndrome. Testosterone replacement restores GLUT2 mRNA and protein levels suggesting that testosterone may have a direct effect on GLUT2 transcription and translation of mRNA. Although the presence of ARE has not been identified in the promoter region of GLUT2, AR could function as a ligand-activated transcription factor by itself [117] or bind to some other coactivators [118, 119] to increase GLUT2 expression.

In contrast, estrogens have little effect on hepatic GLUT4 and insulin receptor in male rats, but estrogens increase level of insulin receptor in HepG2, a liver cancer cell line [72]. Interestingly, insulin receptor mRNA level as well as insulin sensitivity is increased in a human liver cell line when being treated with testosterone [73]. Similarly, replacement of testosterone in castrated male mice also increases insulin receptor mRNA and protein levels in the liver and normalizes castration-induced glucose metabolic impairment [120]. Treatment of testosterone induces glycogen synthesis in both intact and castrated male rats [108, 121].

High testosterone level is associated with a low risk of diabetes in men, whereas it is associated with a high risk of diabetes in women [111, 122124]. Excess androgen in women with PCOS impairs hepatic glucose metabolism by decreasing insulin-stimulated glucose uptake and glycogen synthesis and predisposes women with PCOS to insulin resistance [125, 126]. Metformin, the most commonly used first-line drug to treat diabetes, is found to be effective to treat NAFLD and also suppresses the serum androgen concentration in PCOS patients [127, 128]. Increased androgen activity in postmenopausal women correlates with impaired glucose tolerance [129, 130].

To summarize, testosterone in males favors hepatic glucose metabolism, whereas testosterone in females impairs it. Thus, androgens in males and females differentially regulate glucose homeostasis.

Old men have increased risks of developing dyslipidemia with increased serum cholesterol and LDL levels, and decreased HDL level, and testosterone replacement reverses such dyslipidemia [108]. Hepatic scavenger receptor class B member 1 (SR-1B) is important in regulating cholesterol uptake from circulating HDL. DHT treatment in castrated obese mice increases SR-1B compared with vehicle-treated castrated mice. At the same time, LDL secretion is decreased by DHT treatment. Cholesterol 7-hydroxylase, a key enzyme in bile formation and cholesterol removal, is also decreased after DHT treatment. All these above results provide a comprehensive explanation for how chronic androgen replacement can decrease serum levels of cholesterol and LDL via enhancing liver cholesterol uptake and via suppressing cholesterol removal, which in turn increases liver cholesterol accumulation [120]. A clinical study, however, shows that a single dose of testosterone treatment increases the serum cholesterol level after two days by increasing the expression of HMGR, the rate limiting enzyme for cholesterol de novo biosynthesis in the liver, but 15 days after the testosterone administration the cholesterol levels in the volunteers were back to baseline levels [131]. The mechanisms for the androgen induced upregulation of HMGCR transcription as well as the physiological consequences have not been investigated and need to be further elucidated.

The metabolic syndrome and its related diseases, such as obesity and diabetes, increase the health problems worldwide. The liver is the largest organ in the body that regulates lipid, glucose, and cholesterol homeostasis. Hepatic steatosis is one of the major manifestations of metabolic syndrome. Several lines of epidemiological data have suggested that sex hormones are associated in fatty different types of receptors. Estrogens seem to play protective roles against hepatic fat accumulation via suppressing lipogenesis and gluconeogenesis and promoting lipolysis and glycogen storage. Interestingly, estrogens increase both cholesterol synthesis and secretion. ER- and its membrane form are more important in regulating energy homeostasis than ER-. GPER and its roles in energy homeostasis are currently under intensive investigation; however, there is less evidence about the role of GPER in the liver compared with classic nuclear estrogen receptors. Since the GPER specific agonist and antagonist have been developed, further studies should apply these new chemicals to examine the role of GPER in liver energy homeostasis, yet the underlying molecular mechanisms are still unclear and longing for further investigation.

We review and discuss the roles played by estrogens, androgens, and their receptors in regulating liver energy homeostasis (Figure 2). The action mechanisms of estrogens are complicated in the body, as they work through multiple different subtypes of estrogen receptors. Estrogens promote liver glucose storage via increasing glucose transporters and glycogen synthesis and suppress liver glucose production via decreasing gluconeogenesis. Estrogens also actively participate in maintaining lipid and cholesterol balance and play protective roles against hepatic lipid accumulation, via suppressing lipogenesis, lipid uptake, and cholesterol synthesis and promoting lipolysis and cholesterol removal. Interestingly, estrogens increase both cholesterol synthesis and secretion. Classic nuclear ER- and its membrane form are more important in regulating energy homeostasis than ER-. GPER and its roles in energy homeostasis are currently under intensive investigation; however, there is less evidence about the roles of GPER in the liver compared with classic nuclear ERs. Since the GPER specific agonist and antagonist have been developed, further studies should apply these new chemical compounds to examine the role of GPER in liver energy homeostasis.

Androgens and nuclear AR have been shown to increase insulin receptor, decrease lipogenesis, and promote cholesterol storage in the liver. The membrane AR, however, is not well studied, which is also a potential research area to explore. It must be emphasized that the integration of nongenomic effects via membrane receptor signaling and genomic effects via nuclear receptor signaling of sex hormones is critical to produce the final sex hormone cellular outcomes.

Further investigation about differential androgen action in males and females is needed. Androgen deficiency, or excessive androgens as seen in women with PCOS, the most common endocrine disorder and cause of infertility among women of reproductive age, is closely associated with disturbed lipid and glucose metabolism in the liver.

The authors declare that there is no conflict of interests regarding the publication of this paper.

The authors thank funding from the Sigma Xi (G2012161930 and G20141015719335 to Minqian Shen), National Institutes of Health (R15 DK090823 to Haifei Shi), and Madalene and George Shetler Diabetes Research Award (to Haifei Shi). They also thank the Department of Biology at Miami University for providing Graduate Assistantship to Minqian Shen.

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Sex Hormones and Their Receptors Regulate Liver Energy Homeostasis

People | Faculty of Engineering and Physical Sciences – University of Leeds

Abas Prades Sonia S.AbasPrades@leeds.ac.uk Research Fellow Abbas Noorhan +44(0)113 343 0084 N.H.Abbas@leeds.ac.uk Research & Teaching Fellow Abiri Jahromi Amir A.AbiriJahromi@leeds.ac.uk Lecturer in Smart Energy Systems Aboelazayem Omar O.Aboelazayem@leeds.ac.uk Research Fellow in Advanced Biofuels Actis Paolo +44(0)113 343 4625 P.Actis@leeds.ac.uk Associate Professor of Bio-nanotechnology Adam-Day Bea B.Adam-Day@leeds.ac.uk Postgraduate Researcher Adams Peter +44(0)113 343 9718 P.G.Adams@leeds.ac.uk Associate Professor Adesanya Elijah E.D.Adesanya@leeds.ac.uk Visiting Research Fellow Adler Isolde +44(0)113 343 6819 I.M.Adler@leeds.ac.uk Associate Professor Adu-Amankwah Samuel +44(0)113 343 2304 S.Adu-Amankwah@leeds.ac.uk Lecturer in Civil Engineering Agboh Wisdom W.C.Agboh@leeds.ac.uk EPSRC Doctoral Prize Fellow Aivaliotis Georgios +44(0)113 343 5162 G.Aivaliotis@leeds.ac.uk Lecturer Al Arefi Salma S.Alarefi@leeds.ac.uk Teaching Fellow Al-Hajjar Mazen +44(0)113 343 9401 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+44(0)113 343 2271 D.A.Bower@leeds.ac.uk Professor Boyle Jordan +44(0)113 343 2140 J.H.Boyle@leeds.ac.uk Lectureship in Engineering Systems Bradley Derek +44(0)113 343 2115 D.Bradley@leeds.ac.uk Research Professor Brady David D.J.Brady@leeds.ac.uk Research Project Manager Bray Edward +44(0)113 343 2077 E.P.Bray@leeds.ac.uk Technician Bray Nicky +44(0)113 343 9934 N.J.Bray@leeds.ac.uk Team Challenge Administrator Brennan Jessica +44(0)113 343 0075 J.M.Brennan@leeds.ac.uk Project Manager Bressloff Neil N.Bressloff@leeds.ac.uk Professor of Biomedical Engineering & Design Brickwood Alan +44(0)113 343 2224 A.L.Brickwood@leeds.ac.uk Formula Car Support Technician Brindley John +44(0)113 343 5134 J.Brindley@leeds.ac.uk Research Professor Brine Alison +44(0)113 343 2262 A.E.Brine@leeds.ac.uk Education Service Officer Briscoe Adam A.B.Briscoe@leeds.ac.uk Visiting Research Fellow Britton Andrew A.Britton@leeds.ac.uk Research Officer Broadbent Matthew +44(0)113 343 2942 M.Broadbent@leeds.ac.uk 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343 1674 V.G.Dimitrova@leeds.ac.uk Professor of Human-Centred Artificial Intelligence Dixon-Hardy Darron +44(0)113 275 1265 D.W.Dixon-Hardy@leeds.ac.uk Senior Lecturer Djemame Karim +44(0)113 343 6590 K.Djemame@leeds.ac.uk Professor Dogar Mehmet +44(0)113 343 5777 M.R.Dogar@leeds.ac.uk Associate Professor Doidge Fleur +44(0)113 343 2508 F.Doidge@leeds.ac.uk School Administration Manager Doorsamy Wesley W.Doorsamy@leeds.ac.uk Lecturer Dorgham Abdel A.Dorgham@leeds.ac.uk Research Fellow Dougan Lorna +44(0)113 343 8958 L.Dougan@leeds.ac.uk Professor of Physics Douglas Ben +44(0)113 343 2378 B.Douglas@leeds.ac.uk Research Technician Douglas Kevin K.M.Douglas@leeds.ac.uk Research Fellow Drewniok Michal M.P.Drewniok@leeds.ac.uk Research Fellow in Transforming Foundation Industries Drummond-Brydson Rik +44(0)113 343 2369 R.M.Drummond-Brydson@leeds.ac.uk Professor Dubey Shival S.Dubey@leeds.ac.uk Research Fellow in Robotics Duff Gerard G.Duff@leeds.ac.uk Lecturer Duke David +44(0)113 343 6800 D.J.Duke@leeds.ac.uk Professor Emeritus of Computer Science Dupont Valerie +44(0)113 343 2503 V.Dupont@leeds.ac.uk Reader Duxbury Toni +44(0)113 343 2490 T.J.Duxbury@leeds.ac.uk Research Support Officer Dyer Martin +44(0)113 343 5442 M.E.Dyer@leeds.ac.uk Professor Dyer Keith +44(0)113 343 9133 K.Dyer@leeds.ac.uk Research Support Technician Edmonds David +44(0)113 343 2386 D.V.Edmonds@leeds.ac.uk Visiting Professor Edwards Jen +44(0)113 343 3085 J.H.Edwards@leeds.ac.uk University Academic Fellow Efford Nick +44(0)113 343 6809 N.D.Efford@leeds.ac.uk Senior Teaching Fellow Eisele Heribert +44(0)113 343 7074 H.Eisele@leeds.ac.uk Reader Eke Paul P.E.Eke@leeds.ac.uk Royal Academy of Engineering [RAEng] Visiting Professor Eleftheriou Pantelis P.Eleftheriou@leeds.ac.uk University Academic Fellow Elgorashi Taisir T.E.H.Elgorashi@leeds.ac.uk Lecturer in Optical Networks Elliott David +44(0)113 343 9453 D.J.S.Elliott@leeds.ac.uk Technician Ellis Martin Noemy +44(0)113 343 3641 N.EllisMartin@leeds.ac.uk Student Education Service Manager (Programme Support) Elmirghani Jaafar +44(0)113 343 2013 J.M.H.Elmirghani@leeds.ac.uk Head of Institute Elumalai Jayaprasath J.Elumalai@leeds.ac.uk Research Fellow Elwes Richard +44(0)113 343 5864 R.H.Elwes@leeds.ac.uk Senior Teaching Fellow Emery Paul +44(0)113 392 4884 P.Emery@leeds.ac.uk Professor (Clinical) Esat Faye +44(0)113 343 4142 F.Esat@leeds.ac.uk Experimental Officer X-ray Diffraction Espejo Conesa Cayetano +44(0)113 343 9962 C.EspejoConesa@leeds.ac.uk SWJTU Teaching Fellow Etchels Lee +44(0)113 343 6360 L.W.Etchels@leeds.ac.uk Research Fellow Eterovic Sebastian S.Eterovic@leeds.ac.uk Research Fellow Evans Stephen +44(0)113 343 3852 S.D.Evans@leeds.ac.uk Professor Evans Craig +44(0)113 343 4557 C.A.Evans@leeds.ac.uk Associate Professor Evans R M L +44(0)113 343 5861 R.M.L.Evans@leeds.ac.uk Associate Professor Evans Barbara +44(0)113 343 1990 B.E.Evans@leeds.ac.uk Professor of Public Health Engineering Eyley Jenny J.Eyley@leeds.ac.uk Lecturer Faber Eleonore +44(0)113 343 5185 E.M.Faber@leeds.ac.uk Associate Professor Fabiyi Samson S.D.Fabiyi@leeds.ac.uk Transnational Teaching Fellow Fairweather Michael M.Fairweather@leeds.ac.uk Professor Falle Samuel +44(0)113 343 5138 S.A.E.G.Falle@leeds.ac.uk Professor Fang Han H.Fang1@leeds.ac.uk Lecturer in Structural Engineering Fedele Francesca F.Fedele@leeds.ac.uk Research Fellow Fernandes Bruno B.Fernandes@leeds.ac.uk Research Fellow in Durability of Circular Concrete Feroleto Samuel S.Feroleto@leeds.ac.uk Summer Intern Field Sarah S.L.Field@leeds.ac.uk Knowledge Exchange Manager Figueredo Luis L.Figueredo@leeds.ac.uk Marie Curie Fellow Finn Robyn R.Finn@leeds.ac.uk Research Support Technician Finn Adrian A.Finn@leeds.ac.uk Visiting Associate Professor Fisher Quentin +44(0)113 343 1920 Q.J.Fisher@leeds.ac.uk Professor Fisher John +44(0)113 343 2128 J.Fisher@leeds.ac.uk Emeritus Professor Fishwick Colin +44(0)113 343 6510 C.W.G.Fishwick@leeds.ac.uk Professor Fitzgerald Steve +44(0)113 343 4331 S.P.Fitzgerald@leeds.ac.uk Associate Professor Fleming Lauren L.T.Fleming@leeds.ac.uk Research Fellow Fletcher Louise +44(0)113 343 2328 L.A.Fletcher@leeds.ac.uk Lecturer in Environmental Engineering Flint Samuel S.E.Flint@leeds.ac.uk Lead Technician (iTF) Fogarty David +44(0)113 343 6491 D.Fogarty@leeds.ac.uk Technician Fordy Allan +44(0)113 343 5115 A.P.Fordy@leeds.ac.uk Professor Forsyth Helen H.L.Forsyth@leeds.ac.uk CPD, Conference and Events Coordinator Forth John +44(0)113 343 2270 J.P.Forth@leeds.ac.uk Prof of Concrete Engineering & Structure Foster Richard +44(0)113 343 5759 R.Foster@leeds.ac.uk Associate Professor Fox Natalie N.Fox@leeds.ac.uk Senior Research Technician Frame Douglas +44(0)113 343 6587 D.S.Frame@leeds.ac.uk PC Service Leader Francis Charlotte +44(0)113 343 5821 C.Francis@leeds.ac.uk Assistant School Education Service Mger Frangi Alex +44(0)113 343 9640 A.Frangi@leeds.ac.uk Diamond Jubilee Chair in Computational Medicine | Royal Academy Freear Steven +44(0)113 343 2076 S.Freear@leeds.ac.uk Professor of Ultrasonics and Embedded Systems Freeman Helen H.M.Freeman@leeds.ac.uk Network Manager Freeman Joshua +44(0)113 343 8195 J.R.Freeman@leeds.ac.uk Associate Professor Frittaion Emanuele E.Frittaion@leeds.ac.uk Research Fellow in Pure Mathematics Gailani Ahmed A.Gailani@leeds.ac.uk Research Fellow in Industrial Decarbonisation Gale William +44(0)113 343 2796 W.F.Gale@leeds.ac.uk Professor Gallagher Justin J.F.Gallagher@leeds.ac.uk Teaching and Research Fellow Galloway Johanna J.M.Galloway@leeds.ac.uk Post-doctoral Research Associate Garcia-Taengua Emilio +44(0)113 343 0698 E.Garcia-Taengua@leeds.ac.uk Associate Professor in Structures Gardner Sarah +44(0)113 343 3881 S.M.Gardner@leeds.ac.uk Student Education Service Officer (Adm) Garrity Stephen +44(0)113 343 5388 S.W.Garrity@leeds.ac.uk Professor George Midhun M.George@leeds.ac.uk Research Fellow Ghadiri Mojtaba +44(0)113 343 2406 M.Ghadiri@leeds.ac.uk Professor Ghalaii Masoud M.Ghalaii@leeds.ac.uk Research Fellow in Quantum Communications Ghanbarzadeh Ali A.Ghanbarzadeh@leeds.ac.uk Lecturer in Functional Surfaces Gilkeson Carl +44(0)113 343 6915 C.A.Gilkeson@leeds.ac.uk Lecturer in Aerospace Engineering Gilkeson Natalie N.Gilkeson@leeds.ac.uk Teaching Fellow Gleeson Helen +44(0)113 343 3863 H.F.Gleeson@leeds.ac.uk Cavendish Professor of Physics Golshani Shokoufeh S.Golshani@leeds.ac.uk Marie Curie Researcher Goncalves Faria Martins Joao +44(0)113 343 4433 J.FariaMartins@leeds.ac.uk Lecturer in Algebra Gonzalez Montoya Francisco F.GonzalezMontoya@leeds.ac.uk Research Associate Gorman Stephen +44(0)113 343 6512 S.A.Gorman@leeds.ac.uk Laboratory Manager Gorrell Ian I.B.Gorrell@leeds.ac.uk Visiting Research Fellow Gouldson Andy +44(0)113 343 9753 A.Gouldson@leeds.ac.uk Dean: Interdisciplinary Res within CS Graham Emma +44(0)113 343 3804 E.J.Graham@leeds.ac.uk School Administration Manager Grant Rowan +44(0)113 343 0923 R.H.Grant@leeds.ac.uk Communications and Engagement Manager for Medical Technologies Grant-Muller Susan +44(0)113 343 6618 S.M.Grant-Muller@its.leeds.ac.uk Chair in Technologies & Informatics Graves Daniel D.Graves@leeds.ac.uk Teaching Fellow Gray Lucy +44(0)113 343 3086 L.V.Gray@leeds.ac.uk Administrative Support Assistant Green Michael +44(0)113 343 2456 fbsmgr@leeds.ac.uk Technician Greenbank Rachel +44(0)113 343 2302 R.J.Greenbank@leeds.ac.uk Education Service Officer Grieve Peter +44(0)113 343 7276 P.W.Grieve@leeds.ac.uk Technician Griffiths Stephen +44(0)113 343 5186 S.D.Griffiths@leeds.ac.uk Lecturer in applied mathematics Grigorova Miryana M.R.Grigorova@leeds.ac.uk Lecturer in Financial and Actuarial Mathematics Gronqvist Marcus +44(0)113 343 0543 M.N.Gronqvist@leeds.ac.uk Senior Teaching Fellow Guarino Maria Vittoria M.Guarino@leeds.ac.uk Research Fellow Guest Robert +44(0)113 343 2184 R.Guest@leeds.ac.uk Technician Guseva Anna A.Guseva@leeds.ac.uk Marie Curie Research Fellow Gusnanto Arief +44(0)113 343 5135 A.Gusnanto@leeds.ac.uk Associate Professor Hainsworth Tim +44(0)113 343 5163 T.J.Hainsworth@leeds.ac.uk Computer Officer Halcrow Malcolm +44(0)113 343 6506 M.A.Halcrow@leeds.ac.uk Professor Hall Richard M Hall +44(0)113 343 2132 R.M.Hall@leeds.ac.uk Professor Hammersley Camille +44(0)113 343 2190 C.Hammersley@leeds.ac.uk Technician Hammond Robert +44(0)113 343 2428 R.B.Hammond@leeds.ac.uk Lecturer Hanson Bruce +44(0)113 343 0475 B.C.Hanson@leeds.ac.uk Professor Harbottle David +44(0)113 343 4154 D.Harbottle@leeds.ac.uk Associate Professor Hardcastle Thomas T.Hardcastle@leeds.ac.uk KTP Associate Hardie Michaele +44(0)113 343 6458 M.J.Hardie@leeds.ac.uk Professor Harding Dawn +44(0)113 343 2229 D.E.Harding@leeds.ac.uk Education Service Officer Harland Derek +44(0)113 343 5152 D.G.Harland@leeds.ac.uk Associate Professor in Geometry Harlen Oliver +44(0)113 343 5189 O.G.Harlen@leeds.ac.uk Reader Harrington John +44(0)113 343 2559 J.P.Harrington@leeds.ac.uk Facility Manager/Senior Experimental Officer Harris Sarah +44(0)113 343 3816 S.A.Harris@leeds.ac.uk Associate Professor Harris Allen +44(0)113 343 3820 A.Harris@leeds.ac.uk Technician Harris Russell +44(0)113 343 2155 R.Harris@leeds.ac.uk Professor Harris Robert R.I.Harris@leeds.ac.uk Technician Harrison Darren +44(0)113 343 3296 D.R.Harrison@leeds.ac.uk Robotics Manufacturing Technician Hartquist Thomas +44(0)113 343 3885 T.W.Hartquist@leeds.ac.uk Professor Hassanpour Ali +44(0)113 343 2405 A.Hassanpour@leeds.ac.uk Associate Professor Hawksworth Louise +44(0)113 343 6465 L.Hawksworth@leeds.ac.uk School Administrator Hayler Anne +44(0)113 343 2228 A.Hayler@leeds.ac.uk School Education Service Manager Haynes David +44(0)113 343 7907 D.I.Haynes@leeds.ac.uk Senior Administration Assistant Hazlehurst Thomas T.Hazlehurst@leeds.ac.uk Research Fellow Head David +44(0)113 343 4693 D.Head@leeds.ac.uk Lecturer Heard Dwayne +44(0)113 343 6471 D.E.Heard@leeds.ac.uk Professor of Atmospheric Chemistry Heath George G.R.Heath@leeds.ac.uk University Academic Fellow Heggs Peter +44(0)113 343 2386 P.J.Heggs@leeds.ac.uk Visiting Professor Heitor Ana A.Heitor@leeds.ac.uk Lecturer in Geotechnical Engineering Herbert Anthony +44(0)113 343 7371 A.Herbert@leeds.ac.uk Lecturer in Medical and Biological Engineering Herbert Megan M.C.Herbert@leeds.ac.uk Project Manager Heyam Alex A.Heyam@leeds.ac.uk Experimental Officer for NMR Hickey B J +44(0)113 343 3836 B.J.Hickey@leeds.ac.uk Professor Higgins Luke L.J.R.Higgins@leeds.ac.uk EPSRC Doctoral Prize Fellow Hilditch Beth +44(0)113 343 5465 B.A.Hilditch@leeds.ac.uk Education Service Officer Hill Peter +44(0)113 343 8983 P.R.Hill@leeds.ac.uk Pre+Post Award Administrator Hine Peter +44(0)113 343 3827 P.J.Hine@leeds.ac.uk Associate Professor Hiwar Waseem W.F.M.Hiwar@leeds.ac.uk Researcher Hoare Melvin +44(0)113 343 3864 M.G.Hoare@leeds.ac.uk Professor Hobson Susan +44(0)113 343 2070 S.Hobson@leeds.ac.uk Secretary to Institute & PA to Pro Dean Hodges Christopher C.S.Hodges@leeds.ac.uk Research Fellow Hodgson Daniel D.R.E.Hodgson@leeds.ac.uk Demonstrator/Module Assistant Hogg David +44(0)113 343 5765 D.C.Hogg@leeds.ac.uk Professor of Artificial Intelligence Holdsworth Nick +44(0)113 343 1940 N.J.Holdsworth@leeds.ac.uk Faculty Accountant Holdsworth Alex A.Holdsworth1@leeds.ac.uk Apprentice Laboratory Technician Holland Andrew A.D.Holland@leeds.ac.uk Research Fellow in Architectural Heritage and VR Modelling Hollerbach Rainer +44(0)113 343 5134 R.Hollerbach@leeds.ac.uk Professor Hollins Andrew +44(0)113 343 2308 A.T.Hollins@leeds.ac.uk School Education Service Manager Holmes Kimberley +44(0)113 343 6553 K.Holmes@leeds.ac.uk Technician Holmes Stephen +44(0)113 343 8460 S.Holmes@leeds.ac.uk Technician Holroyd Tom +44(0)113 343 2330 T.Holroyd@leeds.ac.uk Education Service Officer Holroyd Sadie S.Holroyd@leeds.ac.uk School Administrative Assistant Holt Raymond +44(0)113 343 7936 R.J.Holt@leeds.ac.uk Lecturer Hondow Nicole +44(0)113 343 2056 N.Hondow@leeds.ac.uk Associate Professor Honore Teresa +44(0)113 343 5222 M.Honore@leeds.ac.uk School Office and Projects Manager Houston Kevin +44(0)113 343 5136 K.Houston@leeds.ac.uk Senior Lecturer Houwing-Duistermaat Jeanne +44(0)113 343 9821 J.Duistermaat@leeds.ac.uk Chair in Data Analytics and Statistics Howling Graeme +44(0)113 343 0908 G.Howling@leeds.ac.uk Technology Manager Hoyle Brian +44(0)113 343 2386 B.S.Hoyle@leeds.ac.uk Visiting Professor Hoz de Vila Eduardo Kattia K.HozdeVila@leeds.ac.uk Research Software Engineer Huang Wengui W.Huang@leeds.ac.uk Research Fellow Huang Yanlong +44(0)113 343 3505 Y.L.Huang@leeds.ac.uk University Academic Fellow Huerta Omar O.I.HuertaCardoso@leeds.ac.uk Lecturer Huggan Michael +44(0)113 343 2196 M.Huggan@leeds.ac.uk Technician Hughes David +44(0)113 343 5105 D.W.Hughes@leeds.ac.uk Professor Hunter Ian +44(0)113 343 2055 I.C.Hunter@leeds.ac.uk Emeritus Professor Hunter Timothy +44(0)113 343 2790 T.N.Hunter@leeds.ac.uk Associate Professor (Academic) Hutchings Paul P.Hutchings@leeds.ac.uk Lecturer in Water, Sanitation & Health Iglesias Vallejo Daniela D.P.Iglesias@leeds.ac.uk Research Fellow Ihara Larissa L.M.Ihara@leeds.ac.uk Marie Curie ESR Researcher Ikonic Zoran +44(0)113 343 7320 Z.Ikonic@leeds.ac.uk Reader Ilee John J.D.Ilee@leeds.ac.uk STFC Ernest Rutherford Fellow & University Academic Fellow Indjin Dragan +44(0)113 343 2082 D.Indjin@leeds.ac.uk Reader Ingham Eileen +44(0)113 343 5691 E.Ingham@leeds.ac.uk Chair of Medical Immunology Ingham Trevor T.Ingham@leeds.ac.uk Senior Research Fellow Ingham Nancy N.Ingham@leeds.ac.uk Centre Manager Iqbal Nasser +44(0)113 343 3388 M.N.Iqbal@leeds.ac.uk Management Accountant Irabor Kenneth K.Irabor@leeds.ac.uk Experimental Officer Isaac Dec D.T.Isaac@leeds.ac.uk Apprentice Technician Isaac Graham G.H.Isaac@leeds.ac.uk Professor Issoglio Elena +44(0)113 343 4660 E.Issoglio@leeds.ac.uk Lecturer (Academic) Iuorio Ornella +44(0)113 343 2294 O.Iuorio@leeds.ac.uk Professor of Architecture & Structures Jackson Andrew +44(0)113 343 6480 A.E.Jackson@leeds.ac.uk Research/Teaching Fellow James Alexander (Sandy) A.James1@leeds.ac.uk Research Fellow Jaramillo Cevallos Pablo P.Jaramillo@leeds.ac.uk Research Fellow Javed Mohammed +44(0)113 343 2396 M.Javed@leeds.ac.uk Technician Jennings Louise +44(0)113 343 2100 L.M.Jennings@leeds.ac.uk Professor of Medical Engineering Jennings David D.Jennings@leeds.ac.uk Lecturer and University Academic Fellow Jha Animesh +44(0)113 343 2342 A.Jha@leeds.ac.uk Professor Ji Lanpeng +44(0)113 343 5891 L.Ji@leeds.ac.uk Lecturer in Actuarial/Financial Maths Jia Xiaodong +44(0)113 343 2801 X.Jia@leeds.ac.uk Lecturer (Academic) Jimack Peter +44(0)113 343 2002 P.K.Jimack@leeds.ac.uk Professor of Scientific Computing Jimenez-Cruz David D.Jimenez-Cruz@leeds.ac.uk Research Fellow Jin Zhongmin Z.Jin@leeds.ac.uk Visiting Professor Jinks Michael M.Jinks@leeds.ac.uk Postdoctoral Research Fellow Johnson Owen +44(0)113 343 5459 O.A.Johnson@leeds.ac.uk Senior Teaching Fellow Johnson Jenny +44(0)113 343 2127 J.E.Johnson@leeds.ac.uk Education Service Officer Johnson Peter +44(0)113 343 6515 P.Johnson@leeds.ac.uk Emertius Professor Johnson Benjamin +44(0)113 343 7127 B.R.G.Johnson@leeds.ac.uk Experimental Officer Johnston Katharine +44(0)113 343 8279 K.G.Johnston@leeds.ac.uk Research Fellow Jones Cliff +44(0)113 343 7311 J.C.Jones@leeds.ac.uk Professor Jones Alison +44(0)113 343 2099 A.C.Jones@leeds.ac.uk Associate Professor of Computational Biomedical Engineering Jones Margaret +44(0)113 343 5101 medsjon@leeds.ac.uk School Administrator Jones Jenny +44(0)113 343 2477 J.M.Jones@leeds.ac.uk Professor Jones Christopher +44(0)113 343 5107 C.A.Jones@maths.leeds.ac.uk Professor Jose Gin +44(0)113 343 2536 G.Jose@leeds.ac.uk Chair in Functional Materials Kaddouh Bilal +44(0)113 343 2201 B.Kaddouh@leeds.ac.uk Lecturer in Aerial Robotics (Assistant Professor) Kailas Lekshmi L.Kailas@leeds.ac.uk Experimental Officer in AFM Kale Girish +44(0)113 343 2805 G.M.Kale@leeds.ac.uk Reader Kamarol Zaman Faizal M.F.KamarolZaman@leeds.ac.uk Marie Curie Early Stage Researcher Kamde Deepak D.K.Kamde@leeds.ac.uk UKRI Research Fellow Kanuganti Sandeep S.R.Kanuganti@leeds.ac.uk Research Fellow Kapur Nik +44(0)113 343 2152 N.Kapur@leeds.ac.uk Professor of Applied Fluid Mechanics Karagila Asaf A.Karagila@leeds.ac.uk University Academic Fellow Karim Mshell +44(0)113 343 2269 M.Karim@leeds.ac.uk Education Service Officer/Reception Kay Robert +44(0)113 343 2139 R.W.Kay@leeds.ac.uk Associate Professor in Advanced Manufacturing Kazlauciunas Algy +44(0)113 343 2939 A.Kazlauciunas@leeds.ac.uk Laboratory Manager Kechidi Smail S.Kechidi@leeds.ac.uk KTP Associate - Cold-Formed Steel Specialist Kee Terence +44(0)113 343 6421 T.P.Kee@leeds.ac.uk Reader Keller Philipp P.Keller1@leeds.ac.uk Marie Curie (ESR) Researcher Kelmanson Mark +44(0)113 343 5150 M.Kelmanson@leeds.ac.uk Professor Kelsall Robert +44(0)113 343 2068 R.W.Kelsall@leeds.ac.uk Professor Kemp Andrew +44(0)113 343 2078 A.H.Kemp@leeds.ac.uk Professor of Communications Kennedy Joanne +44(0)113 343 2514 J.E.Kennedy@leeds.ac.uk CPD Marketing & Development Officer Kent John +44(0)113 343 5103 J.T.Kent@leeds.ac.uk Professor Kersale Evy +44(0)113 343 5149 E.Kersale@leeds.ac.uk Lecturer Khaliq Kishwer K.A.Khaliq@leeds.ac.uk Research Assistant Khan Yasir +44(0)113 343 3854 Y.Khan@leeds.ac.uk Laboratory Technician Khan Amirul +44(0)113 343 2286 A.Khan@leeds.ac.uk Lecturer Khatir Zinedine +44(0)113 343 2220 Z.Khatir@leeds.ac.uk Visiting Research Fellow Khodaparast Sepideh S.Khodaparast@leeds.ac.uk University Academic Fellow Kidd Matthew +44(0)113 343 6542 M.Kidd@leeds.ac.uk Temporary Clerk Kilburn Paul P.Kilburn@leeds.ac.uk IFS ResearchTechnician Kim Yi-Yeoun +44(0)113 343 9407 Y.Y.Kim@leeds.ac.uk Senior Research and Teaching Fellow Kim Jongrae +44(0)113 343 2159 menjkim@leeds.ac.uk Associate Professor King Marco-Felipe +44(0)113 343 1957 M.F.King@leeds.ac.uk Research Fellow King Jenna +44(0)113 343 5746 J.King1@leeds.ac.uk CPD, Conference & Events Coordinator King Sarah S.King@leeds.ac.uk Project Manager King Stuart S.King3@leeds.ac.uk Analytical Technician Kirk Daniel +44(0)113 343 3807 D.R.Kirk@leeds.ac.uk Tutorial Assistant Kisil Vladimir V. +44(0)113 343 5173 V.Kisil@leeds.ac.uk Reader in Applied Analysis Kitayama Shoma S.Kitayama@leeds.ac.uk Research Fellow Knaggs Eve +44(0)113 343 0034 E.Knaggs@leeds.ac.uk Senior Administration Assistant Kokarev Gerasim +44(0)113 343 0599 G.Kokarev@leeds.ac.uk Lecturer Komissarov Serguei +44(0)113 343 5127 S.S.Komissarov@leeds.ac.uk Professor Kortantamer Dicle D.Kortantamer@leeds.ac.uk Lecturer in Project Management Kosarieh Shahriar +44(0)113 343 9741 S.Kosarieh@leeds.ac.uk Lecturer In Mechanical Engineering Krishnan Sreejith S.Krishnan1@leeds.ac.uk Research Fellow in Cementitious Materials Chemistry Kubiak Krzysztof +44(0)113 343 8333 K.Kubiak@leeds.ac.uk Associate Professor Kuffner Dos Anjos Rafael +44(0)113 343 3625 R.KuffnerdosAnjos@leeds.ac.uk Lecturer in Computer Graphics Kulak Alexander A.Kulak@leeds.ac.uk Materials Characterisn Istrmn Speclst Kulikowski Anoushka +44(0)113 343 0554 A.kulikowski@leeds.ac.uk Centre Manager Kumar Satish +44(0)113 343 3722 S.Kumar3@leeds.ac.uk Research Fellow Kumari Pallavi P.Kumari1@leeds.ac.uk Research Fellow in Plant Cell Biophysics Kumi Barimah Eric +44(0)113 343 2540 E.Kumi-Barimah@leeds.ac.uk Experimental Officer Kundu Iman I.Kundu@leeds.ac.uk Research Fellow Kwan Raymond +44(0)113 343 5760 R.S.Kwan@leeds.ac.uk Professor of Scheduling Lai Chun sing C.S.Lai@leeds.ac.uk Visiting Research Fellow Lai Xiaojun +44(0)113 343 2439 X.Lai@leeds.ac.uk Lecturer Lambert Benjamin B.S.Lambert@leeds.ac.uk Lecturer in Pure Mathematics Langfeld Kurt +44(0)113 343 5414 K.Langfeld@leeds.ac.uk Head of School of Mathematics, Professor in Theoretical Physics Lassila Toni +44(0)113 343 3724 T.Lassila@leeds.ac.uk Lecturer Lau Hui +44(0)113 343 3748 H.K.Lau@leeds.ac.uk Teaching Fellow Laughton Tom +44(0)113 343 4480 T.Laughton@leeds.ac.uk Functional Education Service Manager Lawey Ahmed A.Q.Lawey@leeds.ac.uk Lecturer in Communication Networks Lawlor Rob R.S.Lawlor@leeds.ac.uk Lecturer Lawrie Ian I.D.Lawrie@leeds.ac.uk Emeritus Professor Laycock Campbell Jeremy +44(0)113 343 7190 J.Laycock@leeds.ac.uk Resarch & Innovation Development Manager Le Khoa K.Le@leeds.ac.uk Lecturer Lebrero Alejandro A.Lebrero@leeds.ac.uk Research Software Engineer Lecheval Valentin V.Lecheval@leeds.ac.uk Research Fellow Lee Andrew +44(0)113 343 9712 A.Lee@leeds.ac.uk Centre Manager, Bragg Centre for Materials Research Lee Jaemin J.Lee2@leeds.ac.uk University Academic Fellow Leng Joanna +44(0)113 343 3809 J.Leng@leeds.ac.uk Senior Research Software Engineering Fellow Leonardo Diaz Roberto R.LeonardoDiaz@leeds.ac.uk Research Fellow Leonetti Matteo +44(0)113 343 5792 M.Leonetti@leeds.ac.uk Lecturer Lesnic Daniel +44(0)113 343 5181 D.Lesnic@leeds.ac.uk Professor in Applied Mathematics Levesley Martin +44(0)113 343 2110 M.C.Levesley@leeds.ac.uk Professor Lewis Kelly +44(0)113 343 0095 K.Lewis@adm.leeds.ac.uk Human Resources Officer Li Kang K.Li1@leeds.ac.uk Professor of Smart Energy Systems Li Hu +44(0)113 343 7754 H.Li3@leeds.ac.uk Associate Professor Li Zhenhong Z.H.Li@leeds.ac.uk Research Fellow Li Lianhe +44(0)113 343 6887 L.H.Li@leeds.ac.uk Senior Research Fellow/Experimental Officer Li Xiang X.Li11@leeds.ac.uk Research Fellow Lifshitz Ron R.Lifshitz@leeds.ac.uk Visiting Cheney Professor Lima Dos Santos Pedro P.L.LimaDosSantos@leeds.ac.uk Marie Curie Early Stage Researcher Linfield Edmund +44(0)113 343 2015 E.H.Linfield@leeds.ac.uk Professor Linyard Andy +44(0)113 343 5440 A.J.Linyard@leeds.ac.uk Education Service Officer (Admissions) Liu Jian J.Liu9@leeds.ac.uk Lecturer Liu Jason J.H.W.Liu@leeds.ac.uk Research Fellow Liu Ronghui +44(0)113 343 5338 R.Liu@its.leeds.ac.uk Professor Liu Haiyan +44(0)113 343 2930 H.Liu1@leeds.ac.uk University Academic Fellow in Statistical and Machine Learning Liwski Lukasz L.Liwski@leeds.ac.uk Student Education Service Assistant Lloyd Simon +44(0)113 343 2681 S.R.Lloyd@leeds.ac.uk Technician Lockwood Alexander A.P.G.Lockwood@leeds.ac.uk Visiting Researcher: Sludge Centre of Expertise Loganathan Sarathkumar S.Loganathan@leeds.ac.uk Postdoctoral Research Fellow Lopez Garcia Martin +44(0)113 343 8951 M.LopezGarcia@leeds.ac.uk Associate Professor Loveridge Fleur +44(0)113 343 2248 F.A.Loveridge@leeds.ac.uk Associate Professor of Geostructures Lumsden Stuart +44(0)113 343 6691 S.L.Lumsden@leeds.ac.uk Associate Professor Lunn Justin S +44(0)113 343 2320 J.S.Lunn@leeds.ac.uk Associate Professor Lynch Tom +44(0)113 343 1397 T.O.Lynch@leeds.ac.uk Project Manager Lythe Grant +44(0)113 343 5132 G.D.Lythe@leeds.ac.uk Professor of Applied Mathematics M Roufechaei Kamand K.MRoufechaei@leeds.ac.uk Teaching and Thesis supervisor Ma CaiYun +44(0)113 343 7809 C.Y.Ma@leeds.ac.uk Senior Research Fellow Macdonald Geraldine +44(0)113 343 8914 G.Macdonald@leeds.ac.uk Administrative Assistant Macente Alice A.Macente@leeds.ac.uk SEM - XCT Experimental Officer MacIntyre Jay +44(0)113 343 2096 J.M.MacIntyre@leeds.ac.uk Deputy Faculty Finance Manager Macpherson H Dugald +44(0)113 343 5166 H.D.MacPherson@leeds.ac.uk Professor Magee Derek +44(0)113 343 6819 D.R.Magee@leeds.ac.uk Lecturer Mahdi Faiz +44(0)113 343 9965 F.M.Mahdi@leeds.ac.uk Research Fellow Mahmud Tariq +44(0)113 343 2431 T.Mahmud@leeds.ac.uk Associate Professor Mandle Richard R.Mandle@leeds.ac.uk UKRI Future Leaders Fellow and University Academic Fellow Manga Mohamed M.S.Manga@leeds.ac.uk Post-Doctoral Research Fellow Mangan Thomas T.P.Mangan@leeds.ac.uk Research Fellow Mann Richard +44(0)113 343 8988 R.P.Mann@leeds.ac.uk Associate Professor Mansfield Jane +44(0)113 343 8324 J.Mansfield@leeds.ac.uk Student Ed Service Officer (Admissions) Mantova Vincenzo +44(0)113 343 8126 V.L.Mantova@leeds.ac.uk Lecturer Mao Xiaoan +44(0)113 343 4807 X.Mao@leeds.ac.uk Lecturer (Academic) Mardia Kanti +44(0)113 343 5100 K.V.Mardia@leeds.ac.uk Senior Research Professor Marrows Christopher +44(0)113 343 3780 C.H.Marrows@leeds.ac.uk Professor of Condensed Matter Physics Marsden Steve +44(0)113 343 6425 S.P.Marsden@leeds.ac.uk Professor of Organic Chemistry Marsh Daniel +44(0)113 343 9296 D.Marsh@leeds.ac.uk Priestley Chair in Comparative Planetary Atmospheres Marsh Bethany +44(0)113 343 5164 B.R.Marsh@leeds.ac.uk Professor Marsh Alastair A.Marsh@leeds.ac.uk Research Fellow in Alkali-Activated Materials Martin Adrian A.P.Martin@leeds.ac.uk Tutorial Assistant Martin Elaine +44(0)113 343 0889 E.Martin@leeds.ac.uk Professor of Chemical and Process Engineering Martin Paul +44(0)113 343 7787 P.P.Martin@leeds.ac.uk Professor Martin Sue +44(0)113 343 2000 S.Martin@leeds.ac.uk Education Service Officer / Receptionist Mason Lee +44(0)113 343 3735 L.A.Mason@leeds.ac.uk Research & Innovation Development Manager Matamoros Veloza Adriana A.MatamorosVeloza@leeds.ac.uk Research Fellow Mathai Basil B.Mathai@leeds.ac.uk UKRI Research Fellow Mattar Suhaila +44(0)113 343 0800 S.Mattar@leeds.ac.uk Lecturer Matthews Kimberley K.Matthews@leeds.ac.uk CDT Manager (based in Sheffield) Mattsson Johan +44(0)113 343 3815 K.J.L.Mattsson@leeds.ac.uk Associate Professor Matzkin Victor V.F.Matzkin@leeds.ac.uk PhD Student Mayambala Francisca F.J.N.Mayambala@leeds.ac.uk Internship: Equality and Inclusion Project Assistant Mayne Kelly Kaeyo +44(0)113 343 0907 K.Kelly@leeds.ac.uk Communication and Engagement Assistant, Grow MedTech McCaffrey Bill +44(0)113 343 6625 W.D.McCaffrey@leeds.ac.uk Professor McCall Blake B.McCall@leeds.ac.uk Research Fellow McCall Sam +44(0)113 343 8813 S.I.McCall@leeds.ac.uk Senior Marketing Executive McCann Sarah +44(0)113 343 1960 S.McCann@leeds.ac.uk Student Education Service Officer McConnell Claire +44(0)113 343 2380 C.L.McConnell@leeds.ac.uk Senior Education Service Officer McCormack Paul +44(0)113 343 2322 P.J.McCormack@leeds.ac.uk Research Finance Assistant McGonagle Dennis +44(0)113 392 4747 D.G.McGonagle@leeds.ac.uk Professor (Clinical) McGowan Patrick +44(0)113 343 6404 P.C.McGowan@leeds.ac.uk Professor McIntosh Andy Emeritus Professor McKay Alison +44(0)113 343 8175 A.McKay@leeds.ac.uk Professor McKay James +44(0)113 343 2556 J.McKay@leeds.ac.uk CDT Manager Mclaughlan James +44(0)113 343 0956 J.R.McLaughlan@leeds.ac.uk Associate Professor McLean Christopher +44(0)113 343 8573 C.J.McLean@leeds.ac.uk Linux Systems Manager McLernon Des +44(0)113 343 2050 D.C.McLernon@leeds.ac.uk Reader McNeill Erin +44(0)113 343 4065 E.McNeill@leeds.ac.uk Physics Outreach Officer McPhillie Martin +44(0)113 343 6513 M.J.McPhillie@leeds.ac.uk Lecturer in Organic Chemistry Meggs Andrew +44(0)113 343 8845 A.W.S.Meggs@leeds.ac.uk Research Support Officer (Pre Award) Megone Christopher +44(0)113 343 7888 C.B.Megone@leeds.ac.uk Professor Meldrum Fiona +44(0)113 343 6414 F.Meldrum@leeds.ac.uk Professor Meng Qingen Q.Meng@leeds.ac.uk Teaching Fellow Mengoni Marlne +44(0)113 343 5011 M.Mengoni@leeds.ac.uk Associate Professor in Computational Medical Engineering Menzel Robert +44(0)113 343 6407 R.Menzel@leeds.ac.uk Associate Professor Messmer Margit +44(0)113 343 5104 M.Messmer@leeds.ac.uk Principal Teaching Fellow Mhamdi Lotfi +44(0)113 343 6919 L.Mhamdi@leeds.ac.uk Lecturer Micklethwaite Stuart +44(0)113 343 2559 S.L.Micklethwaite@leeds.ac.uk Electron Microscopy Support Technician Mikaitis Mantas M.Mikaitis@leeds.ac.uk Lecturer Mikhailov Alexandre +44(0)113 343 5176 A.V.Mikhailov@leeds.ac.uk Professorial Research Fellow Miles Danielle +44(0)113 343 0921 D.E.Miles@leeds.ac.uk Technology Innovation Manager Milne Steven +44(0)113 343 2539 S.J.Milne@leeds.ac.uk Professor of Materials Chemistry Minton-Taylor Jasper +44(0)113 343 5746 J.Minton-Taylor@leeds.ac.uk CPD, Conference and Events Coordinator Mistry Devesh D.A.Mistry@leeds.ac.uk Leverhulme Trust Early Career Fellow and UAF Mistry Nimesh +44(0)113 343 7459 N.Mistry@leeds.ac.uk Senior Teaching Fellow Mitseas Ioannis +44(0)113 343 5784 I.Mitseas@leeds.ac.uk Lecturer in Structural Engineering Mobilia Mauro +44(0)113 343 1591 M.Mobilia@leeds.ac.uk Professor of Applied Mathematics Mohammed Abdulah A.Mohammed@leeds.ac.uk Chem stores technician Molina-Paris Carmen +44(0)113 343 5151 C.MolinaParis@leeds.ac.uk Professor Molzahn Ben +44(0)113 343 5104 B.Molzahn@leeds.ac.uk Senior Student Education Service Officer Montoya Pachongo Carolina C.MontoyaPachongo@leeds.ac.uk Research Fellow Moodley Kris +44(0)113 343 2329 K.Moodley@leeds.ac.uk Senior Lecturer (Teaching + Scholarship) Moore Thomas +44(0)113 343 3896 T.A.Moore@leeds.ac.uk Assoc Prof in Condensed Matter Physics Moore Rhys +44(0)113 343 8493 R.A.Moore@leeds.ac.uk Senior Technician - Additive Manufacturing / 3D Printing Moorsom Timothy T.Moorsom@leeds.ac.uk Royal Academy of Engineering Fellow Morina Ardian +44(0)113 343 8965 A.Morina@leeds.ac.uk Professor Morris Lindsay +44(0)113 343 2694 L.Morris@leeds.ac.uk Education Service Officer Morris Lisa-Dionne +44(0)113 343 6665 L.D.Morris@leeds.ac.uk Associate Professor of Human Activity & Product Design Developme Morris Kevin +44(0)113 343 9366 K.Morris1@leeds.ac.uk Professor of Radio Frequency Engineering Morrison Ciaran C.M.Morrison@leeds.ac.uk Aviation Simulator Manager Morsy Mohamed M.Morsy@leeds.ac.uk Research Fellow Mortimer Sally +44(0)113 343 2246 S.Mortimer@leeds.ac.uk Senior Education Service Officer Moseley Katy-anne K.A.Moseley@leeds.ac.uk Impact Fellow Motamen Salehi Farnaz F.MotamenSalehi@leeds.ac.uk Teaching Fellow Muhit Imrose I.Muhit@leeds.ac.uk Research Fellow in Masonry Arch Bridges Muller Frans +44(0)113 343 2933 F.L.Muller@leeds.ac.uk Chair in Chemical Process Engineering Muller Haiko +44(0)113 343 5445 H.Muller@leeds.ac.uk Senior Lecturer Mullis Andrew +44(0)113 343 2568 A.M.Mullis@leeds.ac.uk Professor Murphy William +44(0)113 343 5232 W.Murphy@leeds.ac.uk Senior Lecturer Murphy Julie +44(0)113 343 2157 J.F.Murphy@leeds.ac.uk Finance Officer Murphy Graham +44(0)113 343 5187 G.J.Murphy@leeds.ac.uk Senior Teaching Fellow Murray Rachael +44(0)113 343 0893 R.Murray@leeds.ac.uk Marketing and Development Officer Nadin Timothy T.J.Nadin@leeds.ac.uk School Manager Nagaraj Mamatha +44(0)113 343 8475 M.Nagaraj@leeds.ac.uk Lecturer Nahil Mohamad M.A.Nahil@leeds.ac.uk Research/Teaching Fellow Nelson Adam +44(0)113 343 6502 A.S.Nelson@leeds.ac.uk Professor Nelson Andrew +44(0)113 343 6409 A.L.Nelson@leeds.ac.uk Professor Nelson Andrew +44(0)113 343 6409 A.L.Nelson@leeds.ac.uk Professor Neville Anne +44(0)113 343 6812 A.Neville@leeds.ac.uk Professor Newisar May M.Newisar@leeds.ac.uk Research Fellow Nezami Zeinab Z.Nezami@leeds.ac.uk Research Fellow Nguyen Bao +44(0)113 343 0109 B.Nguyen@leeds.ac.uk Associate Professor Ngwana Adama A.Ngwana@leeds.ac.uk Administrative Assistant Nie Luzhen L.Nie@leeds.ac.uk Research Fellow Niesen Jitse +44(0)113 343 5870 J.Niesen@leeds.ac.uk Lecturer Nijhoff Frank +44(0)113 343 5120 F.W.Nijhoff@leeds.ac.uk Professor of Mathematical Physics Nikitas Nikolaos +44(0)113 343 0901 N.Nikitas@leeds.ac.uk Associate Professor in Structural Dynamics and Engineering Nix Michael M.G.Nix@leeds.ac.uk Visiting Senior Research Fellow Nlebedim Valentine V.U.Nlebedim@leeds.ac.uk Teaching Fellow Noakes Catherine +44(0)113 343 2306 C.J.Noakes@leeds.ac.uk Professor of Environmental Engineering for Buildings Noble Lydia L.R.Noble@leeds.ac.uk Student Education Service Assistant Norbertczak Halina +44(0)113 343 5607 H.T.Norbertczak@leeds.ac.uk PDRA Norman Alistair +44(0)113 343 7818 A.W.T.Norman@lubs.leeds.ac.uk Lecturer (Teaching and Scholarship) Normington Chris C.Normington1@leeds.ac.uk Student Education Services Manager O'Reilly Gerard G.A.OReilly@leeds.ac.uk Tutorial Assistant Okoro Shekwaga Cynthia C.K.OkoroShekwaga@leeds.ac.uk BBSRC Discovery Fellow Oliver Richard +44(0)113 343 3832 R.G.Oliver@leeds.ac.uk Technician Onel Lavinia L.Onel@leeds.ac.uk Research Fellow Ong Zhan +44(0)113 343 0051 Z.Y.Ong@leeds.ac.uk Associate Professor Ordyniak Sebastian S.Ordyniak@leeds.ac.uk Lecturer (Algorithms and Complexity) Orlova Ekaterina E.E.Orlova@leeds.ac.uk Research Fellow Oudmaijer Rene +44(0)113 343 3886 R.D.Oudmaijer@leeds.ac.uk Professor Owen Joshua J.J.Owen@leeds.ac.uk Lecturer Ozdemir Servet S.Ozdemir@leeds.ac.uk Post Doctoral Research Associate Pachos Jiannis +44(0)113 343 3817 J.K.Pachos@leeds.ac.uk Professor of Theoretical Physics Paesani Giacomo G.Paesani@leeds.ac.uk Research Fellow (Algorithms and Complexity) Palczewski Jan +44(0)113 343 5180 J.Palczewski@leeds.ac.uk Associate Professor Pallipurath Anuradha A.R.Pallipurath@leeds.ac.uk Royal Society Olga Kennard Fellow Panic Olja O.Panic@leeds.ac.uk Dorothy Hodgkin Fellow Papallas Rafael R.Papallas@leeds.ac.uk Research Fellow Papic Zlatko +44(0)113 343 3882 Z.Papic@leeds.ac.uk Associate Professor in Theoretical Physics Parker Douglas +44(0)113 343 6739 D.J.Parker@leeds.ac.uk Professor of Meteorology (School of Mathematics and School of Ea Parker Shelly +44(0)113 343 2934 M.Parker@leeds.ac.uk School Support Officer Parker Alison +44(0)113 343 5126 A.E.Parker@leeds.ac.uk Associate Professor Partington Jonathan +44(0)113 343 5123 J.R.Partington@leeds.ac.uk Professor Pask Christopher +44(0)113 343 4658 C.M.Pask@leeds.ac.uk Experimental Officer/Sen.Teaching Fellow Paterson Samantha S.Paterson@leeds.ac.uk Research Fellow Peacock David D.C.Peacock@leeds.ac.uk Teaching Fellow Pegler Sam +44(0)113 343 0048 S.Pegler@leeds.ac.uk University Academic Fellow Pensabene Virginia V.Pensabene@leeds.ac.uk Associate Professor Pepper Max M.Pepper@leeds.ac.uk Technician Pessoa de Miranda Marcelo +44(0)113 343 6332 M.Miranda@leeds.ac.uk Lecturer Pessu Frederick Oritseweneye F.O.Pessu@leeds.ac.uk Lecturer in Corrosion engineering Peyman Sally +44(0)113 343 3747 S.Peyman@leeds.ac.uk University Academic Fellow Phillips Luke L.Phillips@leeds.ac.uk Additive Manufacturing/3D Printing Tech Phylaktou Herodotos +44(0)113 343 2505 H.N.Phylaktou@leeds.ac.uk Senior Lecturer Pickering Jonathan +44(0)113 343 5836 J.H.Pickering@leeds.ac.uk Research Fellow Pickering Andrew +44(0)113 343 2131 A.D.Pickering@leeds.ac.uk Robotics Manufacturing Technician Pimm Andrew A.J.Pimm@leeds.ac.uk Research Fellow Pittard Julian +44(0)113 343 3805 J.M.Pittard@leeds.ac.uk Reader in Theoretical Astrophysics Piya Afrina Khan A.K.Piya@leeds.ac.uk Marie Curie ESR Researcher Plane John +44(0)113 343 8044 J.M.C.Plane@leeds.ac.uk Professor of Atmospheric Chemistry Pollock Isobel I.A.Pollock@leeds.ac.uk Visiting Professor Ponjavic Aleks +44(0)113 343 3839 A.Ponjavic@leeds.ac.uk University Academic Fellow Pournaras Evangelos E.Pournaras@leeds.ac.uk Associate Professor Prato Carlo C.Prato@leeds.ac.uk Professor of Transportation Engineering Preston George G.W.Preston@leeds.ac.uk Research Fellow Price Victoria +44(0)113 343 7218 V.Price@leeds.ac.uk Head of Marketing Pryce Gregory G.M.Pryce@leeds.ac.uk Research Fellow Pugazhendi Navaneethakrishnan N.Pugazhendi@leeds.ac.uk Marie Curie ESR Researcher Pugh Samantha +44(0)113 343 2985 S.L.Pugh@leeds.ac.uk Associate Professor in STEM Education Purdy Robert R.Purdy@leeds.ac.uk Lecturer and Admissions Tutor Purnell Philip +44(0)113 343 0370 P.Purnell@leeds.ac.uk Professor of Materials and Structures Qidan Ahmad A.A.Qidan@leeds.ac.uk Postdoctoral Research Fellow Querin Ozz +44(0)113 343 2218 O.M.Querin@leeds.ac.uk Professor of Design Optimisation Rabbani Arash A.Rabbani@leeds.ac.uk Lecturer (Assistant Professor) Raffle-Edwards Shona +44(0)113 343 8598 S.Raffle@leeds.ac.uk Outreach Coordinator Rahman Ali A.Rahman1@leeds.ac.uk SWJTU Joint School staff member Rai Kiran +44(0)113 343 5116 K.K.Rai@leeds.ac.uk Research and Facilities Officer Raihan MM M.M.Raihan@leeds.ac.uk Marie Curie Early Stage Researcher Ramanatha Sachin S.P.H.Ramanatha@leeds.ac.uk Research Fellow Ramasse Quentin Q.M.Ramasse@leeds.ac.uk Chair in Advanced Electron Microscopy Ranathunga Ashani A.S.Ranathunga@leeds.ac.uk Lecturer (Academic) Ranner Thomas +44(0)113 343 4697 T.Ranner@leeds.ac.uk Lecturer Rathjen Michael +44(0)113 343 5109 M.Rathjen@leeds.ac.uk Professor Rathore Rajesh +44(0)113 343 8984 R.S.Rathore@leeds.ac.uk Research Support Officer Ravi Manoj M.Ravi@leeds.ac.uk Lecturer Ravikumar Nishant N.Ravikumar@leeds.ac.uk Lecturer in Computer Science Raxworthy Mike +44(0)113 343 8775 M.J.Raxworthy@leeds.ac.uk Associate Professor in Engineering Management and Innovation Rayner Christopher +44(0)113 343 6579 C.M.Rayner@leeds.ac.uk Professor of Organic Chemistry Rayner Christopher +44(0)113 343 6579 C.M.Rayner@leeds.ac.uk Professor of Organic Chemistry Razavi Mohsen +44(0)113 343 9406 M.Razavi@leeds.ac.uk Professor Read Daniel +44(0)113 343 5124 D.J.Read@leeds.ac.uk Professor of Soft Matter Readioff Rosti R.Readioff@leeds.ac.uk Research Fellow Rees Amy +44(0)113 343 1032 A.L.Rees@leeds.ac.uk Research Administrator Rees Simon +44(0)113 343 1638 S.J.Rees@leeds.ac.uk Professor of Building Energy Systems Revill Charlotte C.H.Revill@leeds.ac.uk Research Fellow Rice Hugh H.P.Rice@leeds.ac.uk Postdoctoral research fellow Richards Megan M.K.Richards@leeds.ac.uk Demonstrator/Module Assistant Richards Daniel D.H.Richards@leeds.ac.uk Research Associate Richardson David +44(0)113 343 2101 D.Richardson@leeds.ac.uk Associate Professor of Structural Design Richardson Thomas T.Richardson1@leeds.ac.uk Teaching Assistant Richardson Ian +44(0)113 343 2331 I.G.Richardson@leeds.ac.uk Professor Richardson Robert +44(0)113 343 2156 R.C.Richardson@leeds.ac.uk Professor Richardson-Barlow Clare C.G.Richardson-Barlow@leeds.ac.uk Research Fellow Richter Ralf +44(0)113 343 1969 R.Richter@leeds.ac.uk Associate Professor Ries Michael +44(0)113 343 3859 M.E.Ries@leeds.ac.uk Professor Rigby Andrew A.J.Rigby@leeds.ac.uk Postdoctoral Research Fellow Rimmer Jo +44(0)113 343 6667 J.Rimmer1@leeds.ac.uk Administration Manager Rimmington Emma E.Rimmington@leeds.ac.uk General Support Assistant/ Receptionist Roberts Kevin +44(0)113 343 2408 K.J.Roberts@leeds.ac.uk Professor Robertson Ian +44(0)113 343 7076 I.D.Robertson@leeds.ac.uk Professor Robertson Clare +44(0)113 343 7805 C.Robertson1@leeds.ac.uk Senior Marketing Executive Robinson Amanda +44(0)113 343 2080 A.Robinson@leeds.ac.uk Personal Assistant Robinson Catherine C.L.Robinson1@leeds.ac.uk Research Support Officer (Pre-Award) Robinson Rachel +44(0)113 343 7680 R.A.Robinson@leeds.ac.uk Research Administrator Rooney Gabriel G.G.Rooney@leeds.ac.uk Visiting Research Fellow Roper Richard +44(0)113 343 6445 P.R.Roper@leeds.ac.uk Technician Rosamond Mark +44(0)113 343 7381 M.C.Rosamond@leeds.ac.uk Experimental Officer Ross Andrew +44(0)113 343 1017 A.B.Ross@leeds.ac.uk Associate Professor Rostami Javad J.Rostami@leeds.ac.uk KTP Associate Rucklidge Alastair +44(0)113 343 5161 A.M.Rucklidge@leeds.ac.uk Professor Ruddle Roy +44(0)113 343 1711 R.A.Ruddle@leeds.ac.uk Professor of Computing Rumble Olivia O.J.Rumble@leeds.ac.uk Student Ed Service Officer (Admissions) Ruprecht Daniel +44(0)113 343 2201 D.Ruprecht@leeds.ac.uk Visiting Professor Russo Mirko M.Russo@leeds.ac.uk Research Fellow in Design and Virtual Reality Sabini Luca L.Sabini@leeds.ac.uk Associate Professor in Project Management Sagar Catherine C.Sagar@leeds.ac.uk Research Support Assistant Saha Dipankar D.Saha@leeds.ac.uk Research Fellow Sainati Tristano T.Sainati@leeds.ac.uk Lecturer in project management Saleh Ehab +44(0)113 343 9336 E.Saleh@leeds.ac.uk Lecturer in Manufacturing Processes Salman Naveed N.Salman1@leeds.ac.uk Research Fellow Sanni Olujide O.S.Sanni@leeds.ac.uk Research Fellow/Experimental Officer Santos-Carballal David D.Santos-Carballal@leeds.ac.uk Research Fellow Sarhosis Vasilis +44(0)113 343 9343 V.Sarhosis@leeds.ac.uk Professor of Resilient Structures & Infrastructure Sarrami Foroushani Ali A.Sarrami@leeds.ac.uk Research Fellow Sasaki Satoshi +44(0)113 343 3578 S.Sasaki@leeds.ac.uk Lecturer (Academic) Saul Glyn +44(0)113 343 5528 G.Saul@leeds.ac.uk Faculty Head of Finance Savage Michael +44(0)113 343 3905 M.D.Savage@leeds.ac.uk Emeritus Professor Savy Claire +44(0)113 343 5449 C.Savy@leeds.ac.uk Centre Manager Scarabel Francesca F.Scarabel@leeds.ac.uk Lecturer in Mathematical Biology Schilhan Jonathan J.Schilhan@leeds.ac.uk Senior Research Associate Schneider Judith +44(0)113 343 2126 J.M.Schneider@leeds.ac.uk Administrative Support Officer - iTF Schroeder Sven S.L.M.Schroeder@leeds.ac.uk Centenary Chair-Engineering Applications Scott Andrew +44(0)113 343 2573 A.J.Scott@leeds.ac.uk Senior Lecturer Scott Mark +44(0)113 343 3819 M.Scott@leeds.ac.uk Technician Scott Stephen +44(0)113 343 6492 S.K.Scott@leeds.ac.uk Executive Dean (Interim) Seakins Paul +44(0)113 343 6568 P.W.Seakins@leeds.ac.uk Professor Seakins Paul +44(0)113 343 6568 P.W.Seakins@leeds.ac.uk Professor Selim Gehan +44(0)113 343 3082 G.Selim@leeds.ac.uk Hoffman Wood Professorof Architecture Sergeeva Natalia +44(0)113 343 7553 N.Sergeeva@leeds.ac.uk Lecturer Shafagh Ida I.Shafagh@leeds.ac.uk Research Fellow in Geothermal Energy Exc Shafer Paul +44(0)113 343 4843 P.E.Shafer@leeds.ac.uk Associate Professor Shalashilin Dmitry +44(0)113 343 7610 D.Shalashilin@leeds.ac.uk Professor of Computational Chemistry Shang Shang S.Shang@leeds.ac.uk Visiting Researcher Sharma Krishna K.Sharma1@leeds.ac.uk Research Fellow Sharp Benjamin +44(0)113 343 5487 B.G.Sharp@leeds.ac.uk Lecturer in Mathematical Analysis Shehzad Muhammad M.K.Shehzad@leeds.ac.uk Postdoctoral Research Fellow Shepherd Simon +44(0)113 343 6616 S.P.Shepherd@its.leeds.ac.uk Professor of Transport Modelling Shepley Philippa P.M.Shepley@leeds.ac.uk Experimental Officer Shi Wenyuan W.Shi1@leeds.ac.uk Associate Professor of Electronics and Electrical Engineering Shim Jung-uk +44(0)113 343 3903 J.Shim@leeds.ac.uk Lecturer Shires Andrew +44(0)113 343 5457 A.Shires@leeds.ac.uk Associate Professor Shuttleworth Matthew M.P.Shuttleworth@leeds.ac.uk Research Fellow Simpson Robert +44(0)113 343 2362 R.J.Simpson@leeds.ac.uk Research Technician Skene Calum C.S.Skene@leeds.ac.uk Research Fellow Slade Fiona +44(0)113 343 2202 F.R.Slade@leeds.ac.uk Administrative Support Officer - iFS Sleigh Andrew +44(0)113 343 2398 P.A.Sleigh@leeds.ac.uk Senior Lecturer Smith Ryan R.J.Smith1@leeds.ac.uk Trainee Technician Smith Nigel +44(0)113 343 2301 N.J.Smith@leeds.ac.uk Professor Smith Colin +44(0)113 343 3765 C.C.Smith@leeds.ac.uk Goods Inward Technician Smith Neil N.W.Smith@leeds.ac.uk Technician Smye Stephen S.W.Smye@leeds.ac.uk Professor Soltanahmadi Siavash +44(0)113 343 2107 S.Soltanahmadi@leeds.ac.uk Research Fellow Somjit Nutapong N.Somjit@leeds.ac.uk Associate Professor in Microwave and Wireless Engineering Speight Martin +44(0)113 343 5169 J.M.Speight@leeds.ac.uk Professor of Mathematics Spraggs Rachael +44(0)113 343 3057 R.E.Spraggs@leeds.ac.uk Research and Innovation Development Manager Squires David +44(0)113 343 2183 D.Squires@leeds.ac.uk Estates & Fabrics Officer Staggs John +44(0)113 343 2495 J.E.J.Staggs@leeds.ac.uk Senior Lecturer Steenson Paul +44(0)113 343 2024 D.P.Steenson@leeds.ac.uk Senior Lecturer Steenson Karen +44(0)113 343 2057 K.A.Steenson@leeds.ac.uk ERIS Manager Stell John +44(0)113 343 1076 J.G.Stell@leeds.ac.uk Senior Lecturer Stevens Karen +44(0)113 343 2255 K.Stevens@leeds.ac.uk Lead Technician Stewart Doug +44(0)113 343 2287 D.I.Stewart@leeds.ac.uk Professor Stewart Todd +44(0)113 343 2133 T.D.Stewart@leeds.ac.uk Professor of Mechanical and Medical Engineering Stockdale Andrew A.Stockdale2@leeds.ac.uk Research Support Technician Stone Daniel +44(0)113 343 6508 D.Stone@leeds.ac.uk Associate Professor Straw Philip P.A.Straw@leeds.ac.uk Research Assistant Strohmaier Alexander +44(0)113 343 8884 A.Strohmaier@leeds.ac.uk Chair in Analysis Sturman Rob +44(0)113 343 5139 R.Sturman@leeds.ac.uk Associate Professor Sturman Rob +44(0)113 343 5139 R.Sturman@leeds.ac.uk Associate Professor Subramanian Priya +44(0)113 343 2930 P.Subramanian@leeds.ac.uk Research Fellow Summers Jon +44(0)113 343 2151 J.L.Summers@leeds.ac.uk Senior Lecturer Sutherland Joanne +44(0)113 343 8308 J.Sutherland@leeds.ac.uk SOFI CDT Administrator Sweetman Adam +44(0)113 343 3808 A.M.Sweetman@leeds.ac.uk Royal Society University Research Fellow Szamuk Emil +44(0)113 343 3765 E.Szamuk@leeds.ac.uk Senior Estates and Fabric Technician Szumilo Karol K.Szumilo@leeds.ac.uk Research Fellow Talbot Paula +44(0)113 343 3862 P.Talbot@leeds.ac.uk PA to Head of School Taleb Wassim W.Taleb@leeds.ac.uk Teaching and Research Fellow in Electrochemistry and Corrosion Tang Yuzhou Y.Tang@leeds.ac.uk Research Fellow Tange Rudolf +44(0)113 343 9246 R.H.Tange@leeds.ac.uk Lecturer Tapley Kelvin +44(0)113 343 6732 K.Tapley@leeds.ac.uk Senior Lecturer in Colour Science Tarn Mark +44(0)113 343 5605 M.D.Tarn@leeds.ac.uk Research Fellow Tate James +44(0)113 343 6608 J.E.Tate@its.leeds.ac.uk Associate Professor Taylor Zeike +44(0)113 343 0767 Z.Taylor@leeds.ac.uk Associate Professor Taylor Peter +44(0)113 343 7169 P.G.Taylor@leeds.ac.uk Chair in Sustainable Energy Systems Taylor Paul +44(0)113 343 6529 P.C.Taylor@leeds.ac.uk Professor of Chemical Education Taylor Charles +44(0)113 343 5168 C.C.Taylor@leeds.ac.uk Professor Tedd Christopher C.F.Tedd@leeds.ac.uk Teaching Fellow and Digital Transformation Champion Thomas Briony +44(0)113 343 9694 B.G.Thomas@leeds.ac.uk Associate Professor in Design Science Thomas Jordan J.Thomas@leeds.ac.uk Lead Technician Thompson Peter +44(0)113 343 2471 P.R.Thompson@leeds.ac.uk Technical Officer Thompson Mark M.A.Thompson@leeds.ac.uk Head of School Thompson Harvey +44(0)113 343 2136 H.M.Thompson@leeds.ac.uk Professor of Computational Fluid Dynamics Thomson Neil +44(0)113 343 7289 N.H.Thomson@leeds.ac.uk Reader Thomson Tamaryn-Lee T.L.Thomson@leeds.ac.uk Electronics Engineer in Medical Dev. Thornton Phillip +44(0)113 343 3832 P.Thornton@leeds.ac.uk Electronics Engineer Thornton Paul +44(0)113 343 2935 P.D.Thornton@leeds.ac.uk Lecturer Thorpe Benjamin +44(0)113 343 2785 B.Thorpe@leeds.ac.uk Teaching Fellow in Statistics Thrush Julie +44(0)113 343 7046 J.Thrush@leeds.ac.uk Education Service Officer Tillotson Martin +44(0)113 343 2295 M.R.Tillotson@leeds.ac.uk Chair in Water Management Titarenko Sofya S.Titarenko@leeds.ac.uk Lecturer Tobias Steven +44(0)113 343 5172 S.M.Tobias@leeds.ac.uk Professor Tobias Steven +44(0)113 343 5172 S.M.Tobias@leeds.ac.uk Professor Tomlin Alison +44(0)113 343 2500 A.S.Tomlin@leeds.ac.uk Professor Tomlinson Laura +44(0)113 343 0667 L.E.Tomlinson@leeds.ac.uk Finance Assistant Tomlinson Gordon +44(0)113 343 2035 G.M.Tomlinson@leeds.ac.uk Education Service Officer Toppaladoddi Srikanth S.Toppaladoddi@leeds.ac.uk Lecturer in Applied Mathematics Torres Sebastian +44(0)113 343 5131 S.D.Torres@leeds.ac.uk Student Education Service Officer (Admissions) Trembath Roy +44(0)113 343 2310 R.Trembath@leeds.ac.uk Technician Trigg Mark +44(0)113 343 2265 M.Trigg@leeds.ac.uk Associate Professor of Water Risk Trowsdale Dan +44(0)113 343 8120 D.B.Trowsdale@leeds.ac.uk Excellence and Innovation Fellowship Tsang Yue-Kin +44(0)113 343 9628 Y.Tsang@leeds.ac.uk Research Fellow Turnbull Rory R.P.Turnbull@leeds.ac.uk Research Fellow Turnbull Bruce +44(0)113 343 7438 W.B.Turnbull@leeds.ac.uk Professor of Biomolecular Chemistry Turner Thomas T.D.Turner@leeds.ac.uk Research Fellow Turner Rodney R.J.Turner1@leeds.ac.uk Professor Turner Gavin +44(0)113 343 2348 G.B.Turner@leeds.ac.uk Senior Administration Assistant Turner Amanda A.Turner5@leeds.ac.uk Professor of Statistics Tutesigensi Apollo +44(0)113 343 4678 A.Tutesigensi@leeds.ac.uk Associate Professor Unterhitzenberger Christine C.Unterhitzenberger@leeds.ac.uk Associate Professor in Project Management Valavanis Alexander +44(0)113 343 3224 A.Valavanis@leeds.ac.uk Associate Professor Valdastri Pietro +44(0)113 343 3706 P.Valdastri@leeds.ac.uk Chair in Robotics & Autonomous Systems Valera Sachin S.J.Valera@leeds.ac.uk Visiting Researcher Van de Sande Marie M.VandeSande@leeds.ac.uk Marie Skodowska-Curie Individual Fellow Van Loo Sven S.VanLoo@leeds.ac.uk Lecturer in Astrophysics Varcoe Ben +44(0)113 343 8290 B.Varcoe@leeds.ac.uk Professor Vaughan Matthew M.T.Vaughan@leeds.ac.uk Research Fellow Velenturf Anne A.Velenturf@leeds.ac.uk Research Impact Fellow in Circular Economy Velis Costas +44(0)113 343 2327 C.Velis@leeds.ac.uk Lecturer Vermeeren Mats M.Vermeeren@leeds.ac.uk DFG Research Fellow Vickers Eleanor E.H.Vickers@leeds.ac.uk Tutorial Assistant Virtanen Seppo S.Virtanen@leeds.ac.uk Lecturer in Statistics Voice Alison +44(0)113 343 6647 A.M.Voice@leeds.ac.uk Senior Lecturer Voss Jochen +44(0)113 343 5125 J.Voss@leeds.ac.uk Lecturer Vuskovic Kristina +44(0)113 343 5443 K.Vuskovic@leeds.ac.uk Professor of Algorithms and Combinatorics Wadud Zia +44(0)113 343 7733 Z.Wadud@leeds.ac.uk Associate Professor Walder Carol +44(0)113 343 6494 C.A.Walder@leeds.ac.uk School Administrator Walker Nicole N.Walker@leeds.ac.uk Administration Support Assistant Walker Philip +44(0)113 343 7585 P.Walker@leeds.ac.uk Senior Teaching Fellow Walkley Mark +44(0)113 343 5684 M.A.Walkley@leeds.ac.uk Lecturer Walko Martin M.Walko@leeds.ac.uk Lecturer Walsh Catherine +44(0)113 343 0958 C.Walsh1@leeds.ac.uk Associate Professor; UKRI Future Leader Fellow Walti Christoph +44(0)113 343 2023 C.Walti@leeds.ac.uk Professor Wanatowski Dariusz D.Wan@leeds.ac.uk Professor of Geomechanics Wang Zheng +44(0)113 343 1077 Z.Wang5@leeds.ac.uk Professor of Intelligent Software Technology Wang Yongxing +44(0)113 343 4874 Y.Wang3@leeds.ac.uk Lecturer Wang Judith +44(0)113 343 3259 J.Y.T.Wang@leeds.ac.uk Associate Professor Wang He +44(0)113 343 5767 H.E.Wang@leeds.ac.uk Associate Professor Wang Chun +44(0)113 343 2198 C.Wang@leeds.ac.uk Research Fellow Wang Lin L.Wang2@leeds.ac.uk Visiting Research Fellow Wang Xue +44(0)113 343 2427 X.Z.Wang@leeds.ac.uk Professor Wang Mi +44(0)113 343 2435 M.Wang@leeds.ac.uk Professor Wang Zhaobin Z.Wang4@leeds.ac.uk Visiting Researcher Ward Keeran K.R.Ward@leeds.ac.uk Lecturer Ward Jonathan +44(0)113 343 5157 J.A.Ward@leeds.ac.uk Lecturer Wareing Christopher C.J.Wareing@leeds.ac.uk Research Fellow Warner Katie +44(0)113 343 8104 K.E.Warner@leeds.ac.uk CPD Course and Events Co-ordinator Warren Nicholas N.Warren@leeds.ac.uk Associate Professor Warren James J.P.Warren@leeds.ac.uk Research Fellow Warriner Stuart +44(0)113 343 6437 S.L.Warriner@leeds.ac.uk Senior Lecturer Watson Alan A.A.Watson@leeds.ac.uk Emeritus Professor Webb Michael +44(0)113 343 6423 M.E.Webb@leeds.ac.uk Associate Professor Webster Clair +44(0)113 343 6149 C.Webster@leeds.ac.uk Deputy Faculty Research Manager Wei Lijun L.J.Wei@leeds.ac.uk Research Fellow Wen Dongsheng +44(0)113 343 1299 D.Wen@leeds.ac.uk Chair in Petroleum Engineering Weston Stuart +44(0)113 343 3819 S.Weston@leeds.ac.uk Technician Westwood Aidan +44(0)113 343 2555 A.V.K.Westwood@leeds.ac.uk Lecturer Wetherill Lee +44(0)113 343 2171 L.Wetherill@leeds.ac.uk Technician Whalley Lisa +44(0)113 343 6594 L.K.Whalley@leeds.ac.uk Senior Research Fellow Whitaker Becky +44(0)113 343 0827 R.J.Whitaker@leeds.ac.uk Education Service Functional Manager Whitefoot Hayley +44(0)113 343 9901 H.Whitefoot@leeds.ac.uk Blended Learning Enhancement Officer Whiteley Alison +44(0)113 343 3220 A.J.Whiteley@leeds.ac.uk Manager, CPD Conference & Events Unit Whitley Antonia +44(0)113 343 2411 A.Whitley@leeds.ac.uk School Administration Officer Widrascu Karl K.Widrascu@leeds.ac.uk Analytical Technician Wiese Tony +44(0)113 343 2187 A.M.Wiese@leeds.ac.uk Lead Technician Wijayathunga Nagitha +44(0)113 343 2125 V.N.Wijayathunga@leeds.ac.uk Senior Research Fellow Wilcox Ruth +44(0)113 343 7980 R.K.Wilcox@leeds.ac.uk Professor Wilkins Terry +44(0)113 343 2570 T.A.Wilkins@leeds.ac.uk Professor Wilkins Simon +44(0)113 343 3039 S.A.Wilkins@leeds.ac.uk R&I Development Manager Wilkinson Adam A.J.Wilkinson@leeds.ac.uk Student Education Service Assistant Manager Willans Charlotte +44(0)113 343 5868 C.E.Willans@leeds.ac.uk Associate Professor and Director of Research and Innovation Williams Alan +44(0)113 343 2507 A.Williams@leeds.ac.uk Research Professor Williams Paul +44(0)113 343 2504 P.T.Williams@leeds.ac.uk Professor Williams Jeanine J.Williams4@leeds.ac.uk Experimental Officer: Chromatography and Analysis Williams Gwenllian G.M.Williams@leeds.ac.uk Postdoctoral research fellow Williams Simon S.P.Williams@leeds.ac.uk Research Assistant Williams Sophie +44(0)113 343 2214 S.D.Williams@leeds.ac.uk Professor in Medical Engineering Wills Harriet +44(0)113 343 2494 H.Wills1@leeds.ac.uk CPD Conference and Events Co-ordinator Wilman Marvin +44(0)113 343 9451 M.Wilman@leeds.ac.uk Technician Wilson Samuel +44(0)113 343 5474 S.S.Wilson@leeds.ac.uk Lecturer of Computing Wilson Andrew +44(0)113 343 1409 A.J.Wilson@leeds.ac.uk Professor Wilson Mark +44(0)113 343 2177 M.Wilson@leeds.ac.uk Associate Professor Wilson Sarah +44(0)113 343 0515 S.Wilson3@leeds.ac.uk Marketing Executive Winyard Thomas +44(0)113 343 9628 T.Winyard@leeds.ac.uk Research Fellow Wood Ann +44(0)113 343 2355 A.R.Wood@leeds.ac.uk Education Service Assistant Wood Phillip +44(0)113 343 2188 P.M.Wood@leeds.ac.uk Laboratory Manager Wood Christopher +44(0)113 343 8335 C.D.Wood@leeds.ac.uk Associate Professor Wood David +44(0)113 343 6192 D.J.Wood@leeds.ac.uk Professor Wood John +44(0)113 343 5106 J.C.Wood@leeds.ac.uk Professor Woodhouse Ed +44(0)113 343 2387 E.Woodhouse@leeds.ac.uk Lead Technician Woodin Sarah S.L.Woodin@leeds.ac.uk Senior Research Fellow Woodward Peter P.K.Woodward@leeds.ac.uk Chair in High Speed Rail Engineering Wright Kathleen +44(0)113 343 1755 K.E.Wright@leeds.ac.uk Project Administrator Wright Megan +44(0)113 343 3196 M.H.Wright@leeds.ac.uk University Academic Fellow Wright Nigel +44(0)113 343 0350 N.G.Wright@leeds.ac.uk Visiting Professor Wu Guizhi G.Z.Wu@leeds.ac.uk Experimental Officer Xia Yan Y.Xia@leeds.ac.uk Research Fellow Xie Shane +44(0)113 343 4896 S.Q.Xie@leeds.ac.uk Chair in Robotics+Autonomous Systems Xu Nan N.Xu@leeds.ac.uk EPSRC Research Fellow Xu Bao Hua +44(0)113 343 2423 B.H.Xu@leeds.ac.uk Lecturer Xu Jie +44(0)113 343 5193 J.Xu@leeds.ac.uk Professor Yagmur Ahmet A.Yagmur@leeds.ac.uk Dr. Yamashita Naoto N.Yamashita@leeds.ac.uk Visiting Research Fellow Yang Junfeng +44(0)113 343 2151 J.Yang@leeds.ac.uk Associate Professor Yang Xuebin +44(0)113 343 6162 X.B.Yang@leeds.ac.uk Associate Professor Yang Renyu +44(0)113 343 5236 R.Yang1@leeds.ac.uk Research Fellow Yang Liuquan L.Q.Yang@leeds.ac.uk Lecturer in Surface Engineering Yenigul Beril B.S.Yenigul@leeds.ac.uk Marie Curie (ESR) Researcher Yildirim Kaygun Emine E.YildirimKaygun@leeds.ac.uk Research Fellow Yu Hai-Sui +44(0)113 343 6703 DVC@leeds.ac.uk Deputy Vice-Chancellor Yuan Jiachen J.Yuan@leeds.ac.uk Senior research associate Yuksel Gamze G.Yuksel@leeds.ac.uk Visiting Researcher Yusuf Muhammad M.Yusuf@leeds.ac.uk Research Fellow Yuval Omer O.Yuval@leeds.ac.uk Research assistant Zaidi Syed S.A.Zaidi@leeds.ac.uk Associate professor Zakaria Fiona F.Zakaria@leeds.ac.uk Research Fellow Zakeri Arezoo +44(0)113 343 5254 A.Zakeri@leeds.ac.uk Research Fellow Zhang Zhiqiang Z.Zhang3@leeds.ac.uk Associate Professor Zhang Zhaopeng Z.Zhang1@leeds.ac.uk Research Fellow Zhang Li X +44(0)113 343 2005 L.X.Zhang@leeds.ac.uk Associate Professor Zhang Xinyou X.Zhang5@leeds.ac.uk SWJTU Staff Zhang Li +44(0)113 343 2020 L.Zhang@leeds.ac.uk Senior Lecturer Zhao Hongyuan H.Zhao@leeds.ac.uk Visiting Researcher Zhou Dejian +44(0)113 343 6230 D.Zhou@leeds.ac.uk Professor of Nanochemistry Zhou Chengxu +44(0)113 343 2832 C.X.Zhou@leeds.ac.uk Lecturer in Mobile Robotics

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People | Faculty of Engineering and Physical Sciences - University of Leeds

Stainless steel – Wikipedia

Steel alloy resistant to corrosion

Stainless steel is an alloy of iron that is resistant to rusting and corrosion. It contains at least 11% chromium and may contain elements such as carbon, other nonmetals and metals to obtain other desired properties. Stainless steel's resistance to corrosion results from the chromium, which forms a passive film that can protect the material and self-heal in the presence of oxygen.[1]:3

The alloy's properties, such as luster and resistance to corrosion, are useful in many applications. Stainless steel can be rolled into sheets, plates, bars, wire, and tubing. These can be used in cookware, cutlery, surgical instruments, major appliances, vehicles, construction material in large buildings, industrial equipment (e.g., in paper mills, chemical plants, water treatment), and storage tanks and tankers for chemicals and food products.

The biological cleanability of stainless steel is superior to both aluminium and copper, having a biological cleanability comparable to glass.[2] Its cleanability, strength, and corrosion resistance have prompted the use of stainless steel in pharmaceutical and food processing plants.[3]

Different types of stainless steel are labeled with an AISI three-digit number,[4] The ISO 15510 standard lists the chemical compositions of stainless steels of the specifications in existing ISO, ASTM, EN, JIS, and GB standards in a useful interchange table.[5]

Like steel, stainless steels are relatively poor conductors of electricity, with significantly lower electrical conductivities than copper. In particular, the electrical contact resistance (ECR) of stainless steel arises as a result of the dense protective oxide layer and limits its functionality in applications as electrical connectors.[6] Copper alloys and nickel-coated connectors tend to exhibit lower ECR values, and are preferred materials for such applications. Nevertheless, stainless steel connectors are employed in situations where ECR poses a lower design criteria and corrosion resistance is required, for example in high temperatures and oxidizing environments.[7]

As with all other alloys, the melting point of stainless steel is expressed in the form of a range of temperatures, and not a singular temperature.[8] This temperature range goes from 1,400 to 1,530C (2,550 to 2,790F)[9] depending on the specific consistency of the alloy in question.

Martensitic, duplex and ferritic stainless steels are magnetic, while austenitic stainless steel is usually non-magnetic.[10] Ferritic steel owes its magnetism to its body-centered cubic crystal structure, in which iron atoms are arranged in cubes (with one iron atom at each corner) and an additional iron atom in the center. This central iron atom is responsible for ferritic steel's magnetic properties. This arrangement also limits the amount of carbon the steel can absorb to around 0.025%.[11] Grades with low coercive field have been developed for electro-valves used in household appliances and for injection systems in internal combustion engines. Some applications require non-magnetic materials, such as magnetic resonance imaging.[citation needed] Austenitic stainless steels, which are usually non-magnetic, can be made slightly magnetic through work hardening. Sometimes, if austenitic steel is bent or cut, magnetism occurs along the edge of the stainless steel because the crystal structure rearranges itself.[12]

The addition of nitrogen also improves resistance to pitting corrosion and increases mechanical strength.[14] Thus, there are numerous grades of stainless steel with varying chromium and molybdenum contents to suit the environment the alloy must endure.[15] Corrosion resistance can be increased further by the following means:

Galling, sometimes called cold welding, is a form of severe adhesive wear, which can occur when two metal surfaces are in relative motion to each other and under heavy pressure. Austenitic stainless steel fasteners are particularly susceptible to thread galling, though other alloys that self-generate a protective oxide surface film, such as aluminium and titanium, are also susceptible. Under high contact-force sliding, this oxide can be deformed, broken, and removed from parts of the component, exposing the bare reactive metal. When the two surfaces are of the same material, these exposed surfaces can easily fuse. Separation of the two surfaces can result in surface tearing and even complete seizure of metal components or fasteners.[16][17] Galling can be mitigated by the use of dissimilar materials (bronze against stainless steel) or using different stainless steels (martensitic against austenitic). Additionally, threaded joints may be lubricated to provide a film between the two parts and prevent galling. Nitronic 60, made by selective alloying with manganese, silicon, and nitrogen, has demonstrated a reduced tendency to gall.[17]

The invention of stainless steel followed a series of scientific developments, starting in 1798 when chromium was first shown to the French Academy by Louis Vauquelin. In the early 1800s, British scientists James Stoddart, Michael Faraday, and Robert Mallet observed the resistance of chromium-iron alloys ("chromium steels") to oxidizing agents. Robert Bunsen discovered chromium's resistance to strong acids. The corrosion resistance of iron-chromium alloys may have been first recognized in 1821 by Pierre Berthier, who noted their resistance against attack by some acids and suggested their use in cutlery.[19]

In the 1840s, both of Britain's Sheffield steelmakers and then Krupp of Germany were producing chromium steel with the latter employing it for cannons in the 1850s.[20] In 1861, Robert Forester Mushet took out a patent on chromium steel in Britain.[21]

These events led to the first American production of chromium-containing steel by J. Baur of the Chrome Steel Works of Brooklyn for the construction of bridges. A US patent for the product was issued in 1869.[22]:2261[23] This was followed with recognition of the corrosion resistance of chromium alloys by Englishmen John T. Woods and John Clark, who noted ranges of chromium from 530%, with added tungsten and "medium carbon". They pursued the commercial value of the innovation via a British patent for "Weather-Resistant Alloys".[22]:261,11[24][full citation needed]

In the late 1890s, German chemist Hans Goldschmidt developed an aluminothermic (thermite) process for producing carbon-free chromium.[25] Between 1904 and 1911, several researchers, particularly Leon Guillet of France, prepared alloys that would be considered stainless steel today.[25][26]

In 1908, the Essen firm Friedrich Krupp Germaniawerft built the 366-ton sailing yacht Germania featuring a chrome-nickel steel hull, in Germany. In 1911, Philip Monnartz reported on the relationship between chromium content and corrosion resistance.[27] On 17 October 1912, Krupp engineers Benno Strauss and Eduard Maurer patented as Nirosta the austenitic stainless steel[28][29][30][27] known today as 18/8 or AISI Type 304.[31]

Similar developments were taking place in the United States, where Christian Dantsizen of General Electric[31] and Frederick Becket (1875-1942) at Union Carbide were industrializing ferritic stainless steel.[32] In 1912, Elwood Haynes applied for a US patent on a martensitic stainless steel alloy, which was not granted until 1919.[33]

While seeking a corrosion-resistant alloy for gun barrels in 1912, Harry Brearley of the Brown-Firth research laboratory in Sheffield, England, discovered and subsequently industrialized a martensitic stainless steel alloy, today known as AISI Type 420.[31] The discovery was announced two years later in a January 1915 newspaper article in The New York Times.[18]

The metal was later marketed under the "Staybrite" brand by Firth Vickers in England and was used for the new entrance canopy for the Savoy Hotel in London in 1929.[34] Brearley applied for a US patent during 1915 only to find that Haynes had already registered one. Brearley and Haynes pooled their funding and, with a group of investors, formed the American Stainless Steel Corporation, with headquarters in Pittsburgh, Pennsylvania.[22]:360

Brearley initially called his new alloy "rustless steel". The alloy was sold in the US under different brand names like "Allegheny metal" and "Nirosta steel". Even within the metallurgy industry, the name remained unsettled; in 1921, one trade journal called it "unstainable steel".[35] Brearley worked with a local cutlery manufacturer, who gave it the name "stainless steel".[36] As late as 1932, Ford Motor Company continued calling the alloy rustless steel in automobile promotional materials.[37]

In 1929, before the Great Depression, over 25,000 tons of stainless steel were manufactured and sold in the US annually.[38]

Major technological advances in the 1950s and 1960s allowed the production of large tonnages at an affordable cost:

There are five main families, which are primarily classified by their crystalline structure: austenitic, ferritic, martensitic, duplex, and precipitation hardening.

Austenitic stainless steel[43][44] is the largest family of stainless steels, making up about two-thirds of all stainless steel production.[45] They possess an austenitic microstructure, which is a face-centered cubic crystal structure.[46] This microstructure is achieved by alloying steel with sufficient nickel and/or manganese and nitrogen to maintain an austenitic microstructure at all temperatures, ranging from the cryogenic region to the melting point.[46] Thus, austenitic stainless steels are not hardenable by heat treatment since they possess the same microstructure at all temperatures.[46]

Austenitic stainless steels sub-groups, 200 series and 300 series:

Ferritic stainless steels possess a ferrite microstructure like carbon steel, which is a body-centered cubic crystal structure, and contain between 10.5% and 27% chromium with very little or no nickel. This microstructure is present at all temperatures due to the chromium addition, so they are not hardenable by heat treatment. They cannot be strengthened by cold work to the same degree as austenitic stainless steels. They are magnetic. Additions of niobium (Nb), titanium (Ti), and zirconium (Zr) to Type 430 allow good weldability. Due to the near-absence of nickel, they are less expensive than austenitic steels and are present in many products, which include:

Martensitic stainless steels have a body-centered cubic crystal structure, and offer a wide range of properties and are used as stainless engineering steels, stainless tool steels, and creep-resistant steels. They are magnetic, and not as corrosion-resistant as ferritic and austenitic stainless steels due to their low chromium content. They fall into four categories (with some overlap):[53]

Martensitic stainless steels can be heat treated to provide better mechanical properties. The heat treatment typically involves three steps:[55]

Replacing some carbon in martensitic stainless steels by nitrogen is a recent development.[when?] The limited solubility of nitrogen is increased by the pressure electroslag refining (PESR) process, in which melting is carried out under high nitrogen pressure. Steel containing up to 0.4% nitrogen has been achieved, leading to higher hardness and strength and higher corrosion resistance. As PESR is expensive, lower but significant nitrogen contents have been achieved using the standard AOD process.[56][57][58][59][60]

Duplex stainless steels have a mixed microstructure of austenite and ferrite, the ideal ratio being a 50:50 mix, though commercial alloys may have ratios of 40:60. They are characterized by higher chromium (1932%) and molybdenum (up to 5%) and lower nickel contents than austenitic stainless steels. Duplex stainless steels have roughly twice the yield strength of austenitic stainless steel. Their mixed microstructure provides improved resistance to chloride stress corrosion cracking in comparison to austenitic stainless steel Types 304 and 316. Duplex grades are usually divided into three sub-groups based on their corrosion resistance: lean duplex, standard duplex, and super duplex. The properties of duplex stainless steels are achieved with an overall lower alloy content than similar-performing super-austenitic grades, making their use cost-effective for many applications. The pulp and paper industry was one of the first to extensively use duplex stainless steel. Today, the oil and gas industry is the largest user and has pushed for more corrosion resistant grades, leading to the development of super duplex and hyper duplex grades. More recently, the less expensive (and slightly less corrosion-resistant) lean duplex has been developed, chiefly for structural applications in building and construction (concrete reinforcing bars, plates for bridges, coastal works) and in the water industry.

Precipitation hardening stainless steels have corrosion resistance comparable to austenitic varieties, but can be precipitation hardened to even higher strengths than other martensitic grades. There are three types of precipitation hardening stainless steels:[61]

Solution treatment at about 1,040C (1,900F)followed by quenching results in a relatively ductile martensitic structure. Subsequent aging treatment at 475C (887F) precipitates Nb and Cu-rich phases that increase the strength up to above 1000 MPa yield strength. This outstanding strength level is used in high-tech applications such as aerospace (usually after remelting to eliminate non-metallic inclusions, which increases fatigue life). Another major advantage of this steel is that aging, unlike tempering treatments, is carried out at a temperature that can be applied to (nearly) finished parts without distortion and discoloration.

Typical heat treatment involves solution treatment and quenching. At this point, the structure remains austenitic. Martensitic transformation is then obtained either by a cryogenic treatment at 75C (103F) or by severe cold work (over 70% deformation, usually by cold rolling or wire drawing). Aging at 510C (950F) which precipitates the Ni3Al intermetallic phaseis carried out as above on nearly finished parts. Yield stress levels above 1400MPa are then reached.

The structure remains austenitic at all temperatures.

Typical heat treatment involves solution treatment and quenching, followed by aging at 715C (1,319F). Aging forms Ni3Ti precipitates and increases the yield strength to about 650MPa (94ksi) at room temperature. Unlike the above grades, the mechanical properties and creep resistance of this steel remain very good at temperatures up to 700C (1,300F). As a result, A286 is classified as an Fe-based superalloy, used in jet engines, gas turbines, and turbo parts.

There are over 150 grades of stainless steel, of which 15 are most commonly used. There are several systems for grading stainless and other steels, including US SAE steel grades. The Unified Numbering System for Metals and Alloys (UNS) was developed by the ASTM in 1970. The Europeans have developed EN 10088 for the same purpose.[31]

In its early history, stainless steel was sometimes called rustless steel. Both adjectives, stainless and rustless, are duly recognized and accepted as exaggerations: stainless steel is not literally incapable of rusting, but its established name is "stainless steel" nonetheless.

In technical datasets, stainless steel may sometimes be designated as inox (inoxidizable), CRES (corrosion-resistant), or SS or SST (stainless steel). It may also be designated by subclass or grade without further specification, as for example 188, 17-4 PH, 316, 303, or 304.

Unlike carbon steel, stainless steels do not suffer uniform corrosion when exposed to wet environments. Unprotected carbon steel rusts readily when exposed to a combination of air and moisture. The resulting iron oxide surface layer is porous and fragile. In addition, as iron oxide occupies a larger volume than the original steel, this layer expands and tends to flake and fall away, exposing the underlying steel to further attack. In comparison, stainless steels contain sufficient chromium to undergo passivation, spontaneously forming a microscopically thin inert surface film of chromium oxide by reaction with the oxygen in the air and even the small amount of dissolved oxygen in the water. This passive film prevents further corrosion by blocking oxygen diffusion to the steel surface and thus prevents corrosion from spreading into the bulk of the metal.[3] This film is self-repairing, even when scratched or temporarily disturbed by an upset condition in the environment that exceeds the inherent corrosion resistance of that grade.[63][64]

The resistance of this film to corrosion depends upon the chemical composition of the stainless steel, chiefly the chromium content. It is customary to distinguish between four forms of corrosion: uniform, localized (pitting), galvanic, and SCC (stress corrosion cracking). Any of these forms of corrosion can occur when the grade of stainless steel is not suited for the working environment.

The designation "CRES" refers to corrosion-resistant steel.[65]

Uniform corrosion takes place in very aggressive environments, typically where chemicals are produced or heavily used, such as in the pulp and paper industries. The entire surface of the steel is attacked, and the corrosion is expressed as corrosion rate in mm/year (usually less than 0.1mm/year is acceptable for such cases). Corrosion tables provide guidelines.[66]

This is typically the case when stainless steels are exposed to acidic or basic solutions. Whether stainless steel corrodes depends on the kind and concentration of acid or base and the solution temperature. Uniform corrosion is typically easy to avoid because of extensive published corrosion data or easily performed laboratory corrosion testing.

Acidic solutions can be put into two general categories: reducing acids, such as hydrochloric acid and dilute sulfuric acid, and oxidizing acids, such as nitric acid and concentrated sulfuric acid. Increasing chromium and molybdenum content provides increased resistance to reducing acids while increasing chromium and silicon content provides increased resistance to oxidizing acids. Sulfuric acid is one of the most-produced industrial chemicals. At room temperature, Type 304 stainless steel is only resistant to 3% acid, while Type 316 is resistant to 3% acid up to 50C (120F) and 20% acid at room temperature. Thus Type 304 SS is rarely used in contact with sulfuric acid. Type 904L and Alloy 20 are resistant to sulfuric acid at even higher concentrations above room temperature.[67][68] Concentrated sulfuric acid possesses oxidizing characteristics like nitric acid, and thus silicon-bearing stainless steels are also useful.[citation needed] Hydrochloric acid damages any kind of stainless steel and should be avoided.[1]:118[69] All types of stainless steel resist attack from phosphoric acid and nitric acid at room temperature. At high concentrations and elevated temperatures, attack will occur, and higher-alloy stainless steels are required.[70][71] In general, organic acids are less corrosive than mineral acids such as hydrochloric and sulfuric acid. As the molecular weight of organic acids increases, their corrosivity decreases. Formic acid has the lowest molecular weight and is a weak acid. Type 304 can be used with formic acid, though it tends to discolor the solution. Type 316 is commonly used for storing and handling acetic acid, a commercially important organic acid.[72]

Type 304 and Type 316 stainless steels are unaffected by weak bases such as ammonium hydroxide, even in high concentrations and at high temperatures. The same grades exposed to stronger bases such as sodium hydroxide at high concentrations and high temperatures will likely experience some etching and cracking.[73] Increasing chromium and nickel contents provide increased resistance.

All grades resist damage from aldehydes and amines, though in the latter case Type 316 is preferable to Type 304; cellulose acetate damages Type 304 unless the temperature is kept low. Fats and fatty acids only affect Type 304 at temperatures above 150C (300F) and Type 316 SS above 260C (500F), while Type 317 SS is unaffected at all temperatures. Type 316L is required for the processing of urea.[1][pageneeded]

Localized corrosion can occur in several ways, e.g. pitting corrosion and crevice corrosion. These localized attacks are most common in the presence of chloride ions. Higher chloride levels require more highly alloyed stainless steels.

Localized corrosion can be difficult to predict because it is dependent on many factors, including:

Pitting corrosion is considered the most common form of localized corrosion. The corrosion resistance of stainless steels to pitting corrosion is often expressed by the PREN, obtained through the formula:

where the terms correspond to the proportion of the contents by mass of chromium, molybdenum, and nitrogen in the steel. For example, if the steel consisted of 15% chromium %Cr would be equal to 15.

The higher the PREN, the higher the pitting corrosion resistance. Thus, increasing chromium, molybdenum, and nitrogen contents provide better resistance to pitting corrosion.

Though the PREN of certain steel may be theoretically sufficient to resist pitting corrosion, crevice corrosion can still occur when the poor design has created confined areas (overlapping plates, washer-plate interfaces, etc.) or when deposits form on the material. In these select areas, the PREN may not be high enough for the service conditions. Good design, fabrication techniques, alloy selection, proper operating conditions based on the concentration of active compounds present in the solution causing corrosion, pH, etc. can prevent such corrosion.[74]

Stress corrosion cracking (SCC) is a sudden cracking and failure of a component without deformation. It may occur when three conditions are met:

The SCC mechanism results from the following sequence of events:

Whereas pitting usually leads to unsightly surfaces and, at worst, to perforation of the stainless sheet, failure by SCC can have severe consequences. It is therefore considered as a special form of corrosion.

As SCC requires several conditions to be met, it can be counteracted with relatively easy measures, including:

Galvanic corrosion[75] (also called "dissimilar-metal corrosion") refers to corrosion damage induced when two dissimilar materials are coupled in a corrosive electrolyte. The most common electrolyte is water, ranging from freshwater to seawater. When a galvanic couple forms, one of the metals in the couple becomes the anode and corrodes faster than it would alone, while the other becomes the cathode and corrodes slower than it would alone. Stainless steel, due to having a more positive electrode potential than for example carbon steel and aluminium, becomes the cathode, accelerating the corrosion of the anodic metal. An example is the corrosion of aluminium rivets fastening stainless steel sheets in contact with water.[76] The relative surface areas of the anode and the cathode are important in determining the rate of corrosion. In the above example, the surface area of the rivets is small compared to that of the stainless steel sheet, resulting in rapid corrosion.[76] However, if stainless steel fasteners are used to assemble aluminium sheets, galvanic corrosion will be much slower because the galvanic current density on the aluminium surface will be many orders of magnitude smaller.[76] A frequent mistake is to assemble stainless steel plates with carbon steel fasteners; whereas using stainless steel to fasten carbon-steel plates is usually acceptable, the reverse is not. Providing electrical insulation between the dissimilar metals, where possible, is effective at preventing this type of corrosion.[76]

At elevated temperatures, all metals react with hot gases. The most common high-temperature gaseous mixture is air, of which oxygen is the most reactive component. To avoid corrosion in air, carbon steel is limited to approximately 480C (900F). Oxidation resistance in stainless steels increases with additions of chromium, silicon, and aluminium. Small additions of cerium and yttrium increase the adhesion of the oxide layer on the surface.[77] The addition of chromium remains the most common method to increase high-temperature corrosion resistance in stainless steels; chromium reacts with oxygen to form a chromium oxide scale, which reduces oxygen diffusion into the material. The minimum 10.5% chromium in stainless steels provides resistance to approximately 700C (1,300F), while 16% chromium provides resistance up to approximately 1,200C (2,200F). Type 304, the most common grade of stainless steel with 18% chromium, is resistant to approximately 870C (1,600F). Other gases, such as sulfur dioxide, hydrogen sulfide, carbon monoxide, chlorine, also attack stainless steel. Resistance to other gases is dependent on the type of gas, the temperature, and the alloying content of the stainless steel.[78][79] With the addition of up to 5% aluminium, ferritic grades Fr-Cr-Al are designed for electrical resistance and oxidation resistance at elevated temperatures. Such alloys include Kanthal, produced in the form of wire or ribbons.[80]

Standard mill finishes can be applied to flat rolled stainless steel directly by the rollers and by mechanical abrasives. Steel is first rolled to size and thickness and then annealed to change the properties of the final material. Any oxidation that forms on the surface (mill scale) is removed by pickling, and a passivation layer is created on the surface. A final finish can then be applied to achieve the desired aesthetic appearance.[81][82]

The following designations are used in the U.S. to describe stainless steel finishes by ASTM A480/A480M-18 (DIN):[83]

A wide range of joining processes are available for stainless steels, though welding is by far the most common.[84][49]

The ease of welding largely depends on the type of stainless steel used. Austenitic stainless steels are the easiest to weld by electric arc, with weld properties similar to those of the base metal (not cold-worked). Martensitic stainless steels can also be welded by electric-arc but, as the heat-affected zone (HAZ) and the fusion zone (FZ) form martensite upon cooling, precautions must be taken to avoid cracking of the weld. Improper welding practices can additionally cause sugaring (oxide scaling) and/or heat tint on the backside of the weld. This can be prevented with the use of back-purging gases, backing plates, and fluxes.[85] Post-weld heat treatment is almost always required while preheating before welding is also necessary in some cases.[49] Electric arc welding of Type 430 ferritic stainless steel results in grain growth in the HAZ, which leads to brittleness. This has largely been overcome with stabilized ferritic grades, where niobium, titanium, and zirconium form precipitates that prevent grain growth.[86][87] Duplex stainless steel welding by electric arc is a common practice but requires careful control of the process parameters. Otherwise, the precipitation of unwanted intermetallic phases occurs, which reduces the toughness of the welds.[88]

Electric arc welding processes include:[84]

MIG, MAG and TIG welding are the most common methods.

Other welding processes include:

Stainless steel may be bonded with adhesives such as silicone, silyl modified polymers, and epoxies. Acrylic and polyurethane adhesives are also used in some situations.[89]

Most of the world's stainless steel production is produced by the following processes:

World stainless steel production figures are published yearly by the International Stainless Steel Forum. Of the EU production figures, Italy, Belgium and Spain were notable, while Canada and Mexico produced none. China, Japan, South Korea, Taiwan, India the US and Indonesia were large producers while Russia reported little production.[45]

European Union

Americas

China

Asia excluding China

Other countries

Breakdown of production by stainless steels families in 2017:

Stainless steel is used in a multitude of fields including architecture, art, chemical engineering, food and beverage manufacture, vehicles, medicine, energy and firearms.

Life cycle cost (LCC) calculations are used to select the design and the materials that will lead to the lowest cost over the whole life of a project, such as a building or a bridge.[90][91]

The formula, in a simple form, is the following:[92][citation needed][93]

where LCC is the overall life cycle cost, AC is the acquisition cost, IC the installation cost, OC the operating and maintenance costs, LP the cost of lost production due to downtime, and RC the replacement materials cost.

In addition, N is the planned life of the project, i the interest rate, and n the year in which a particular OC or LP or RC is taking place. The interest rate (i) is used to convert expenses from different years to their present value (a method widely used by banks and insurance companies) so they can be added and compared fairly. The usage of the sum formula ( {textstyle sum } ) captures the fact that expenses over the lifetime of a project must be cumulated[clarification needed] after they are corrected for interest rate.[citation needed]

Application of LCC in materials selection

Stainless steel used in projects often results in lower LCC values compared to other materials. The higher acquisition cost (AC) of stainless steel components are often offset by improvements in operating and maintenance costs, reduced loss of production (LP) costs, and the higher resale value of stainless steel components.[citation needed]

LCC calculations are usually limited to the project itself. However, there may be other costs that a project stakeholder may wish to consider:[citation needed]

The average carbon footprint of stainless steel (all grades, all countries) is estimated to be 2.90kg of CO2 per kg of stainless steel produced,[94] of which 1.92kg are emissions from raw materials (Cr, Ni, Mo); 0.54kg from electricity and steam, and 0.44kg are direct emissions (i.e., by the stainless steel plant). Note that stainless steel produced in countries that use cleaner sources of electricity (such as France, which uses nuclear energy) will have a lower carbon footprint. Ferritics without Ni will have a lower CO2 footprint than austenitics with 8% Ni or more. Carbon footprint must not be the only sustainability-related factor for deciding the choice of materials:

Stainless steel is 100% recyclable.[95][96][97] An average stainless steel object is composed of about 60% recycled material of which approximately 40% originates from end-of-life products, while the remaining 60% comes from manufacturing processes.[98] What prevents a higher recycling content is the availability of stainless steel scrap, in spite of a very high recycling rate. According to the International Resource Panel's Metal Stocks in Society report, the per capita stock of stainless steel in use in society is 80 to 180kg (180 to 400lb) in more developed countries and 15kg (33lb) in less-developed countries. There is a secondary market that recycles usable scrap for many stainless steel markets. The product is mostly coil, sheet, and blanks. This material is purchased at a less-than-prime price and sold to commercial quality stampers and sheet metal houses. The material may have scratches, pits, and dents but is made to the current specifications.[citation needed]

The stainless steel cycle starts with carbon steel scrap, primary metals, and slag. The next step is the production of hot-rolled and cold-finished steel products in steel mills. Some scrap is produced, which is directly reused in the melting shop. The manufacturing of components is the third step. Some scrap is produced and enters the recycling loop. Assembly of final goods and their use does not generate any material loss. The fourth step is the collection of stainless steel for recycling at the end of life of the goods (such as kitchenware, pulp and paper plants, or automotive parts). This is where it is most difficult to get stainless steel to enter the recycling loop, as shown in the table below:

Stainless steel nanoparticles have been produced in the laboratory.[100][101] These may have applications as additives for high-performance applications. For example, sulfurization, phosphorization, and nitridation treatments to produce nanoscale stainless steel based catalysts could enhance the electrocatalytic performance of stainless steel for water splitting.[102]

There is extensive research indicating some probable increased risk of cancer (particularly lung cancer) from inhaling fumes while welding stainless steel.[103][104][105][106][107][108] Stainless steel welding is suspected of producing carcinogenic fumes from cadmium oxides, nickel, and chromium.[109] According to Cancer Council Australia, "In 2017, all types of welding fumes were classified as a Group 1 carcinogen."[109]

Stainless steel is generally considered to be biologically inert. However, during cooking, small amounts of nickel and chromium leach out of new stainless steel cookware into highly acidic food.[110] Nickel can contribute to cancer risksparticularly lung cancer and nasal cancer.[111][112] However, no connection between stainless steel cookware and cancer has been established.[113]

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Corticobasal syndrome: a practical guide | Practical Neurology

Case vignette 1 (with video)

A 68-year-old woman had a 2-year history of motor symptoms. Her first symptom had been her left hand not doing what it was told to do when drying the dishes. She also developed difficulties getting her words out. On examination, she had pseudobulbar speech and made dysphasic errors, and there was apraxia and hypometria of saccades, particularly leftward (video 1). She showed ideomotor apraxia and features of alien-limb syndrome in the left arm, and intermittent dystonic posturing of the left arm and leg but minimal limb rigidity. Her cognition was preserved.

Schematic of typical saccade abnormalities in CBS, compared with PD and PSP. In this schematic of eye movement recordings, patients were asked to make a leftward saccade of 20 towards a target as quickly as possible. Y axis is displacement amplitude, the X axis is time. Mild undershoot followed by a small secondary saccade is normal. Patients with PD commonly show mild hypometria (undershooting) requiring two or more corrective saccades to reach target. In CBS the degree of saccadic hypometria is often greater than in PD with the key feature being delayed launching of saccades (saccadic apraxia). In PSP the hallmark is early saccadic slowing (especially vertically) with considerable hypometria developing over time. CBS, corticobasal syndrome; PD, Parkinsons disease; PSP, progressive supranuclear palsy. Figure by Bronstein & Anderson (2021), distributed at https://doi.org/10.6084/m9.figshare.14390951 under an open CC-BY 4.0 license.

We diagnosed corticobasal syndrome referred her to physiotherapy and occupational therapy. An MR scan of brain showed only mild involutional changes consistent with age but no perirolandic atrophy.

Her condition progressed over the next 4years. She lost vertical eye movements and her alien limb became very pronounced. Her speech deteriorated to yes and no, although she could still comprehend. She became more rigid with worsening dystonia particularly of neck extension, and her postural reflexes became impaired. We gave an unsuccessful trial of levodopa and sought speech and language involvement; botulinum injections into the neck extensors gave some benefit. She continued to deteriorate and died 6years from symptom onset.

A 79-year-old woman reported decreased coordination, slowed movement and subtle right arm weakness that appeared to follow a fall. Over the next 9 months, her right arm became increasing difficult to use, causing difficulty with tasks such as doing up a bra and cutting food. Her walking felt more uncertain and she had one significant fall. On examination, there was marked right arm rigidity with a grasp reflex, significant bradykinesia and ideomotor apraxia. Eye movements were normal and there were no pyramidal nor cerebellar signs. Our impression was likely corticobasal syndrome. We arranged physiotherapy and occupational therapy, requested brain imaging and gave an empirical trial of levodopa.

Her right arm deficits progressed despite levodopa, which we later stopped. Her right arm became of little use to her, and she held it in a dystonic posture, without pain, though she still felt some agency over it. Her balance deteriorated further with frequent falls. She developed difficulty with speech, stumbling over longer words but her cognition remained unaffected. MR scan of brain showed left perirolandic atrophy consistent with corticobasal syndrome (figure 4). She remained at home with increasing support from physiotherapy and occupational therapy.

In 1968, Rebeiz et al published three cases detailing the clinical and post mortem pathological findings of a hitherto unrecognised disorder of the central nervous system.1 All three had an asymmetric movement disorder characterised by slowed and awkward voluntary movements with additional involuntary movements. Pathological assessment identified frontoparietal atrophy driven by neuronal loss, gliosis and swelling of cell bodies, resulting in resistance to histological staining methods. While the cortex was primarily involved, the substantia nigra was abnormal in all three, and the dentatorubrothalamic system was abnormal in two. They coined the term corticodentatonigral degeneration with neuronal achromasia. Three decades later Gibb et al reported three further patients with similar clinical and histopathological findings. They adopted the shorter name corticobasal degeneration,2 and the next decade saw many further descriptions of this newly named disorder. The clinical phenotype expanded from primarily a movement disorder to include various cognitive and neurobehavioural deficits35 while the underlying pathology of clinically diagnosed cases also expanded to include Alzheimers disease, progressive supranuclear palsy (PSP), Picks disease and Creutzfeldt-Jakob disease.69 Thus, the etymology has slowly transitioned to corticobasal syndrome as a clinical rather than a pathological diagnosis.10 Table 1 shows the current consensus diagnostic criteria for both the clinically defined corticobasal degeneration11 and the pathologically defined corticobasal syndrome.12 13 Figure 1 shows the common clinical phenotypes of corticobasal degeneration and the common pathologies underlying corticobasal syndrome.

Proposed criteria for corticobasal syndrome (the Cambridge criteria, modified Bak and Hodges)12

Unpicking corticobasal syndrome and corticobasal degeneration. From phenotype to underlying pathophysiology. This is a simplified view and includes only the common phenotypes of corticobasal degeneration and common pathological substrates underlying corticobasal syndrome. CBS, corticobasal syndrome; CBD, corticobasal disease; AD, Alzheimers disease; FTLD-TDP43, frontotemporal lobe degeneration TDP43; PSP, progressive supranuclear palsy; FTD Tau, frontotemporal dementia; FBSS, frontal behavioural-spatial syndrome; PPA, primary progressive aphasia.

Corticobasal degeneration is a pathologically established four-repeat tauopathy.14 Its pathological features are cortical and striatal tau-positive neuronal and glial lesions of both white and grey matter, coupled with focal cortical and substantia nigra neuronal loss.14 Importantly, there is not a 1:1 mapping between corticobasal degeneration and corticobasal syndrome, and corticobasal degeneration pathology is associated with various clinical phenotypes (figure 1). There are four suggested broad clinical phenotypes:

Corticobasal syndrome.

Frontal behavioural-spatial syndrome.

Non-fluent/agrammatic variant of primary progressive aphasia.

PSP syndrome.11

Probable corticobasal degeneration criteria require an insidious onset and gradual progression for at least 1year, age at onset >50 years, no similar family history or known tau mutations, and one of the clinical phenotypes outlined above. Features suggesting Parkinsons disease (characteristic tremor, hallucinations, response to levodopa), or multiple system atrophy (prominent autonomic or cerebellar signs) are exclusions. However, the criteria still lack antemortem specificity to separate pathologically proven corticobasal degeneration from its mimics.15

It is difficult to ascertain the true prevalence and incidence of corticobasal syndrome, given the varied use of the term and its interchangeability in early reviews with corticobasal degeneration. Estimates are therefore at best a guide and even then, remain crude. The estimated prevalence of corticobasal degeneration is 4.97.3 cases per 100000 population.16 The annual incidence calculated from the prevalence and life expectancy would be between 0.5 and 1 per 100000 per year, though this is higher than the rate observed in a population based study.17 The typical age of presentation is 50s70s and average lifespan from diagnosis to death is 7 years. There does not appear to be any sex bias.18

A single pathogenic mutation is unlikely to contribute greatly to the pathogenesis of corticobasal syndrome. However, familial clustering can occur with up to 31% have a family history of parkinsonism or dementia19 The most common monogenic mutations associated with familial corticobasal syndrome are in microtubule-associated protein tau (MAPT) resulting in frontotemporal lobar degeneration (FTLD)-tau pathology strongly resembling corticobasal degeneration,20 although genome-wide association studies have identified other single nucleotide polymorphisms.21 More recently corticobasal syndrome has been associated with FTLD with ubiquitin-immunoreactive inclusions (FTLD)22 or TAR DNA-binding protein 43 (TDP-43) leading to frontal temporal lobe degeneration (FTLD-TDP)23 both of which are most often caused by progranulin mutations24 but not always.25 Pathogenic GGGCC expansion with mutations in C9orf72 (chromosome 9 open reading frame 72) and mutations in LRRK2 (previously limited to Parkinsons disease)26 are also associated with corticobasal syndrome.27 Outside of familial monogenic mutations, a casecontrol study suggests single-nucleotide polymorphisms in the H1 haplotype of the MAPT gene may predispose to sporadic corticobasal syndrome.28

Corticobasal syndrome has an insidious onset and is slowly progressive.12 29 Patients with dramatic presentations and/or rapidly progressive disease courses should be considered mimics (see below).

Extrapyramidal motor features are common with no dramatic or sustained response to levodopa therapy.12 29 Rigidity is the most frequent extrapyramidal motor sign, present in 73%100% of cases, mostly presenting as an asymmetric akineticrigid syndrome.13 29 30 Dystonia is much less common than rigidity and tends to affect a single limb, often the upper and usually early in the disease course.12 13 Other extrapyramidal features such as bradykinesia and postural instability may also occur.12 A tremor can develop but is an action or postural jerky movement that subsides with rest, and is quite unlike a resting Parkinsons disease tremor.12 13 29 It can overlap with another common motor featuremyoclonuswhich occurs in roughly 40% of cases.12 13 29 Electrophysiology studies suggest the myoclonus is cortical or subcortical in origin.3133

The alien limb syndrome comprises involuntary limb movements combined with an altered sense of limb belonging or ownership. It usually involves the hand but may uncommonly occur only in the leg, or both arm and leg, and rarely is bilateral.34 35 A detailed account of the underlying neurobiological processes causing alien limb is beyond this review but proposed mechanisms have been suggested.36 The alien limb is easily confused with other neurological signs (table 2). There are three recognised variants: frontal, callosal (together termed anterior) and posterior (figure 2).

Alien limb differential diagnosis

Classification algorithm of the alien limb syndrome. Modified from Hassan and Josephs. 72 CBS, corticobasal syndrome; CJD, Creutzfeldt-Jakob disease.

The posterior variant is the most often encountered type in corticobasal syndrome and usually affects the non-dominant upper limb, with lesions involving the non-dominant parietal lobe.35 It is characterised by a sense that the affected limb does not belong to the person. There are usually other parietal cortical deficits including sensory hemineglect, and astereognosis. The typical motor features are not as intrusive as in the frontal variant but may take the form of levitation and other non-purposeful actions, abnormal posturing and ataxia.

Corticobasal syndrome is easily the most common cause of an alien limb (two-thirds of cases).35 By the same token the alien limb syndrome develops in about a half of people with corticobasal syndrome.35 37 While the asymmetry of corticobasal syndrome involves the left and right hemispheres equally, alien limb in this condition usually develops in the non-dominant limb, for unclear reasons.36 In patients presenting with alien limb, the timing of onset during the disease may help to suggest the cause; for example, it can be the presenting symptom of Creutzfeldt-Jakob disease but occurs a median of 1year after disease onset in corticobasal syndrome.35 The associated neurology can also help in the differential diagnosis. Thus, mirror movements develop in 40% of corticobasal syndrome patients with the alien limb but are uncommon in other causes, while intermanual conflict is very uncommon in corticobasal syndrome.36 Myoclonus is usual in patients with Creutzfeldt-Jakob disease but common in corticobasal syndrome, and uncommon in other causes of alien limb.35

There are no proven treatments for alien limb syndrome and management approaches are based on anecdotal experience and the type of alien limb. The frontal variant may respond to sensory tricks (eg, wearing a glove), distracting tasks (eg, holding a ball in the hand), verbal cues that enhance voluntary action and cognitivebehavioural therapy for anxiety reduction. For the posterior variant (common in corticobasal syndrome), treatments used have included clonazepam, botulinum toxin injections into the most active proximal muscles, visualisation strategies (eg, putting the affected hand into a mirror box) and spatial recognition tasks, but these approaches are not always well tolerated or maintained and there is scant information on their long-term benefits.38

Limb apraxia is among the most commonly identified signs that suggests cortical dysfunction in the corticobasal syndrome, occurring in 70%80%.3941 Apraxia is defined as a disorder of higher level motor control, manifesting as impaired skilled and learnt motor acts, despite intact primary sensory and motor pathways39 Apraxia generally affects both sides of the body. Because corticobasal syndrome is usually asymmetrical, finding apraxia on the less affected side (as is common) adds weight to the conclusion that abnormality of movements are not simply due to extrapyramidal features such as rigidity and bradykinesia.40

When screening patients for the presence of apraxia, it can help to test different types of complex movementsthought to correspond to different underlying neurobiological processes that can be disrupted by brain pathology.39 These include:

Performing a gesture, miming the use of tools and copying meaningless gestures. Deficits in these movements, usually referred to as ideomotor apraxia, are common in corticobasal syndrome and can be readily assessed in the clinic.

Performing complex, multistep tasks. Deficits in these processes are often referred to as conceptual, or ideational apraxias, capturing the idea that it is loss of knowledge about objects and their associated actions that underlies the patients difficulties. This is harder to screen for in a routine clinic appointment but may be inferred from the history, or from a formal occupational therapy assessment. Ideational apraxia can be extremely disabling for a persons day-to-day functioning.

Performing repetitive distal limb movements such as tapping the thumb with each finger in turn. Deficits such as clumsy or inaccurate movements, are referred to as limb-kinetic apraxiaa somewhat controversial classification that can be difficult to distinguish from the effects of weakness or bradykinesia.

Other sorts of higher order cortical dysfunction are often termed apraxiasfor example, gait apraxia, constructional apraxia, dressing apraxia, orobuccal apraxia and apraxia of speech (to name a few). When present, these point towards cortical dysfunction signs that can provide evidence for the presence of a corticobasal syndrome.

The traditional oculomotor hallmark of clinically diagnosed corticobasal syndrome is saccade apraxia,42 43 which manifests clinically as difficulty and delay in initiating saccades towards a target, usually with the use of an assisting simultaneous or preceding head movement, and in the laboratory as a substantial increase in saccade latency.44 45 Typically, the saccadic apraxia is greatest towards the side with the greatest limb apraxia.42 43 In contrast to PSP, saccade velocities in patients with corticobasal syndrome are normal46 47 (figure 3). Smooth pursuit can also be moderately impaired but not as severely as in patients with PSP. The neuropathological substrate of saccadic apraxia in corticobasal syndrome awaits further clarification but it remains a distinctly useful clinical diagnostic feature.

The typical language disturbance in corticobasal syndrome is non-fluent variant primary progressive aphasia, with slowed, effortful and/or groping (apraxia of speech) speech and grammatical errors being common.48 However, patients can also develop a logopenic aphasia, characterised by prominent difficulty in word retrieval and sentence repetition.48 The latter is commonly associated with underlying Alzheimers disease pathology, while non-fluent variant primary progressive aphasia, including apraxia of speech, may suggest tau pathology. Therefore, aside from providing evidence of cortical involvement, the pattern of aphasia may help to identify the pathology underlying corticobasal syndrome, but further research is required.

Corticobasal syndrome has a range of neuropsychiatric comorbidities. However, the lack of large scale studies means that while we commonly see features such as depression, apathy, anxiety and agitation (among others) in the clinic, we do not have accurate estimates of their prevalence at different stages of corticobasal syndromeor know whether these features associate with particular underlying pathologies.49 A study of 15 patients with what we would now refer to as corticobasal syndrome found particularly high rates of depression and apathy and also an absence of hallucinations.50 This latter point suggests that the presence of visual hallucinations in a patient with parkinsonism and cognitive deficits should raise concerns they may in fact have an alpha-synucleinopathy such as dementia with Lewy bodies.

We advocate for screening all patients presenting with corticobasal syndrome for neuropsychiatric symptoms, particularly as these features have a major impact on quality of life for patients and their families. Screening can be performed formally (eg, using the neuropsychiatric inventory,51 or by questioning both the patient and an informant for presence of mood disturbance (dysphoria, anhedonia, anxiety), behavioural change (apathy, obsessive or compulsive behaviours, agitation, irritability, impulsivity, loss of empathy) and psychotic features (hallucinations, delusions). Education of caregivers about the possibility of emergence of these complications can be helpful.

Brain imaging has three roles in the assessment of patients with corticobasal syndromeruling out mimics/structural causes (see below), providing support for the clinical diagnosis of a corticobasal syndrome, and providing clues to the underlying pathology.33

Corticobasal syndrome is associated with asymmetrical cortical changes in markers of neuronal loss or dysfunction (grey matter atrophy, hypometabolism or hypoperfusion). This particularly affects frontal-parietal regions encompassing premotor, motor and sensory association cortex, and typically develop contralateral to the more affected side of the body33 52 53 (figure 4). Notably, such perirolandic patterns of change do not appear specific to any underlying pathology but instead associate directly with the clinical features of corticobasal syndrome, consistent with the importance of these regions for processing higher order sensory information and translating this into motor actions. Therefore, finding asymmetrical perirolandic atrophy or hypometabolism on clinical imaging supports a clinical diagnosis of corticobasal syndrome, though its absence does not exclude it. This can be particularly helpful early in the disease course, when the differential may include Parkinsons disease or other parkinsonian syndromes.

Example of an MR scan of a brain in a patient with corticobasal syndrome A. Small arrows show moderate focal asymmetric left perirolandic atrophy on T2-weighted imaging.

Striatal dopamine transporter (DAT) density can be imaged and measured using single-photon emission CT or positron-emission tomography (PET). Most, but not all, patients with corticobasal syndrome have a positive DAT scan.54 One follow-up study suggests that in time all such patients will have a positive result.55 For the clinician, the DAT scans limitation is that it does not differentiate corticobasal syndrome from other parkinsonian disorders.

There has been a recent emphasis on developing measures to identify reliably the underlying pathology in corticobasal syndrome.53 Such measures will be increasingly relevant as protein-specific treatments hopefully emerge over the coming years.33 Ultimately their utility will depend on their ability to distinguish between pathologies at individual rather than at group level.

These strategies can be split into techniques that identify the presence of abnormal protein (such as imaging to detect increased concentrations of brain amyloid protein), and techniques that identify patternseither in neuronal loss/metabolism or brain connectivityclosely associated with the underlying pathology. The use of amyloid PET imaging to identify corticobasal syndrome caused by Alzheimers pathology is the clearest example of the former approach. In turn, researchers are now examining clinical and standard imaging correlates of amyloid positive and negative groups to further refine understanding of how corticobasal syndrome may differ between pathologies.56 Given that there is often an associated underlying tauopathy, emerging tau-based PET techniqueswhich are still troubled by some technical issues such as off-target bindingare also generating strong interest for their potential to identify underlying corticobasal degeneration or progressive supranuclear pathology.33 57

Finally, the distribution of neuronal loss or brain hypometabolism in patients with corticobasal syndrome predicts the underlying pathology, at least at a group level. In particular, corticobasal syndrome caused by Alzheimers pathology often has a posterior pattern of hypometabolism, while corticobasal degeneration may show more subcortical hypometabolism, and PSP pathology shows more frontal hypometabolism.52 58 More complicated techniques assessing brain structural (white matter) or functional connectivity are also showing promise for distinguishing between pathologies but are not yet clinically useful.59

In summary, a corticobasal syndrome diagnosis can be supportedbut not refutedby imaging features, while emerging techniques may direct the neurologist to the underlying pathological cause of a patients syndromeinformation that over time will have practical relevance.

There are currently no proven treatments for corticobasal syndrome. Recent advances in the treatment of tauopathies with immunotherapies and gene expression show promise,60 61 but for the moment we emphasise the importance of making a diagnosis that can explain a puzzling array of problems for a patient and their family. It provides a valid explanation for their symptoms and allows a reframing of priorities from obtaining a diagnosis to coping with the problem. Ideally, treatment should be provided within a multidisciplinary setting with expertise provided by a neurologist, physiotherapist, occupational therapist, speech language therapist, psychiatrist and, ultimately, palliative care services.

Although parkinsonism in corticobasal syndrome does not generally respond well to levodopa, most patients will try it as part of their initial assessments (often when the diagnosis is less clear), and it is reasonable to push the dose up towards at least 1000mg/day before classifying a patient as a non-responder.62 In our experience, other dopaminergic therapies (dopamine agonists, monoamine oxidase inhibitors) also have very limited efficacy in treating motor symptoms of corticobasal syndrome, but a dopamine agonist may be worth considering in those with prominent apathy. Options for treating troublesome myoclonus include levetiracetam and clonazepam. Dystonia can be functionally disabling and at times painful. Anticholinergics, benzodiazepines and amantadine provide modest help at best, and adverse effectsespecially cognitive impairment, hallucinations and confusionoften outweigh any benefit, particularly in older patients, while amantadine can also cause insomnia and leg oedema.63 Botulinum toxin injections can help, depending on the dystonic pattern. Particularly when treating upper limb dystonia, the disabling effects of symptoms must be weighed against the potential limb weakness resulting from injectionsbut as with other interventions a pragmatic trial is certainly reasonable.37 Physiotherapy input is also important in optimising mobility following botulinum toxin injections.

Specific options to consider for the alien limb syndrome are summarised above. Management to mitigate the effects of apraxia is best coordinated by an occupational therapist with knowledge of the condition. Speech therapists can teach patients techniques to overcome some of their language deficits and it is worth seeking their input when speech difficulties are a prominent featurethey can also provide patients with practical advice if swallowing difficulties develop. We often refer patients for physiotherapy aimed at strength and balance training as well as gait assessmentthe addition of gait aids can allow some people to maintain relative physical independence. Although there are no proven treatments for cognitive deficits such as memory and attentional impairment in corticobasal syndrome, many clinicians consider trialling cholinesterase inhibitors if there is a strong suggestion from the history (memory impairment), examination (predominate cortical signs) and cognitive assessment (visuospatial or memory deficits) to suggest an underlying Alzheimers disease pathology.

There are several available pharmacological options for neuropsychiatric manifestations.62 Many mild behavioural issues may be better managed non-pharmacologically (caregiver education, environment changes, etc) but undoubtedly medications can help with more severe disruptions. Seeking psychiatric guidance is useful and building a strong relationship with an interested psychiatrist can help patient management and improve job satisfaction. Selective serotonin reuptake inhibitors are useful for treating common problems such as anxiety, depression and obsessive-compulsive disorder. Apathy, or reduced motivated behaviour, is common, debilitating and difficult to treat. Informing caregivers that it is part of the disease process can help. Agents targeting dopaminergic, cholinergic and serotonergic neuromodulatory networks may help apathy in other degenerative disorders, but there is no good evidence to guide use of these treatments in corticobasal syndrome. Finally, some patients will develop marked behavioural disturbances, including irritability/aggression and psychosis. Management can be difficult but can include atypical antipsychotics, for example, quetiapine or clozapine with appropriate blood count monitoring.

Other practical issues to address include driving safety and checking whether driving licensing agencies need to be informed, the importance of updating a persons will, and establishing an enduring power of attorney early in the disease course, as these can be problematic later if significant cognitive impairment develops. Lastly, putting patients in touch with local charities can greatly help patients and families. If specific charities are not available (eg, the PSP association in the UK and curePSP in the USA) exploring Parkinsons and dementia charities is a reasonable first step.

Conditions that may initially be diagnosed as corticobasal syndrome but turn out to be something else tend to be those with subacute or chronic onset, and those that have some, but not all, symptoms and signs resembling true neurodegenerative corticobasal syndrome. Most of these mimics feature alien limb syndrome with or without myoclonus, and/or one of the rapidly progressive dementias, often with aphasia. Thus, many of the non-neurodegenerative causes of the alien limb syndrome may mimic corticobasal syndrome, including stiff-person syndrome,64 Hashimotos encephalitis,65 66 thalamic cavernoma,67 as well as Creutzfeldt-Jakob disease68 and other rapidly progressive dementias.69 Mimics can usually be distinguished from true corticobasal syndrome by the careful neurological examination to identify peripheral (such as areflexia, proprioceptive loss) or central (eg, pyramidal) nervous system signs, combined with appropriate investigations such as MR scan of brain, electroencephalogram, serum antineuronal and other autoantibody assays, which together may indicate an alternative diagnosis. It is critical to identify these mimics as early as possible as many are treatable or have a better prognosis than true corticobasal syndrome. A careful family history is also important, and clinicians should have a low threshold for genetic testing especially in younger patients with atypical features.

The prognosis for a patient diagnosed with corticobasal syndrome depends mainly on the underlying neuropathology (i.e. cause), the difficulty being that that cause is not easily determined during life. Consequently, there is little available information to assist counselling of the patient and family. In a study of 10 Japanese patients with corticobasal syndrome coming to post mortem (three each with corticobasal degeneration, PSP and Alzheimers disease pathology, and one with atypical tauopathy) median survival was 7 years with a range of 415 years. Survival was similar across pathologies.70 An earlier study of 14 patients with pathologically confirmed corticobasal degeneration reported a median survival time after onset of symptoms of 7.9 years with a considerable range of 2.512.5 years. Survival was shorter in those with early and widespread parkinsonism or frontal lobe syndrome.71 In summary, on present knowledge, average survival in corticobasal syndrome is 78 years but with a considerable range of some 315 years.

Corticobasal syndrome is a disorder of movement, cognition and behaviour, caused by several underlying pathologies including corticobasal degeneration. Clinicians should consider the diagnosis in patients presenting with any combination of extrapyramidal features, apraxia or other parietal signs, aphasia and alien limb phenomena. Neuroimaging showing asymmetrical perirolandic cortical changes supports the diagnosis and advanced neuroimaging may give insight into the underlying pathology. We suggest neuropsychological screening in all patients presenting with corticobasal syndrome. Identifying corticobasal syndrome carries some prognostic significance, management implications and in the future if protein-based treatments arisemay direct further investigations as to underlying pathology.

Corticobasal syndrome is a clinical entity with many different underlying pathologies, including corticobasal degeneration.

Corticobasal degeneration is a pathological diagnosis associated with several clinical syndromes, one of which is corticobasal syndrome.

Corticobasal syndrome has a varied presentation: distinguishing clinical features include asymmetric parkinsonism, myoclonus, alien limb, cortical sensory loss, eye and limb apraxia, and imaging may show asymmetric perirolandic atrophy.

Corticobasal syndrome has several important mimics (eg, Creutzfeldt-Jakob disease, Hashimotos encephalitis), some of which are treatable.

Armstrong MJ, Litvan I, Lang AE, et al. Criteria for the diagnosis of corticobasal degeneration. Neurology 2013;80(5):496503. doi: 10.1212/WNL.0b013e31827f0fd1

Mathew R, Bak TH, Hodges JR. Diagnostic criteria for corticobasal syndrome: a comparative study. J Neurol Neurosurg Psych 2012;83(4):40510. doi: 10.1136/jnnp-2011-300875

Pardini M, Huey ED, Spina S, et al. FDG-PET patterns associated with underlying pathology in corticobasal syndrome. Neurology 2019;92(10):e112135. doi: 10.1212/WNL.0000000000007038

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Automated Cell Culture Systems Market Size to Hit USD 12.43 Billion by 2033; Growing Stem Cell Research & Development and Increasing Prevalence of…

Automated Cell Culture Systems Market Size to Hit USD 12.43 Billion by 2033; Growing Stem Cell Research & Development and Increasing Prevalence of Non-Communicable Diseases to Elevate Market Growth Research Nester  GlobeNewswire

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Automated Cell Culture Systems Market Size to Hit USD 12.43 Billion by 2033; Growing Stem Cell Research & Development and Increasing Prevalence of...

Global Cell Culture Protein Surface Coating Market to Grow at a CAGR of 13.82% During 2022-2031; Market to Expand on the Back of the Technological…

Global Cell Culture Protein Surface Coating Market to Grow at a CAGR of 13.82% During 2022-2031; Market to Expand on the Back of the Technological Breakthrough in Stem Cell Transplantation and Gene Therapy Kenneth Research  GlobeNewswire

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Global Cell Culture Protein Surface Coating Market to Grow at a CAGR of 13.82% During 2022-2031; Market to Expand on the Back of the Technological...

Cornell Prof Explains Relevance of Creating Mouse Embryos from Stem Cells – Cornell University The Cornell Daily Sun

Zack Wise/The New York Times

In August 2022, NIH researchers from the University of Cambridge successfully created a synthetic mouse embryo model using cultured mice stem cells. This project aimed at using stem cells to express specific genes that would lead to the development of these mouse stem cells into embryos.

Stem cells are undifferentiated cells that developed into specialized cells with specific functions.

Prof. John Schimenti, biomedical sciences, explained the processes involved in this project as well as its implications for the future of scientific research.

There are many different types of stem cells and the relevant type for these experiments are called embryonic stem cells. These are totally undifferentiated and in the right context, could make all cells in the body by giving rise to more differentiated cells, Schimenti said.

The stem cells are placed in a culture medium, which optimizes their growth by stimulating cell-to-cell communication. This communication is necessary because cells use signaling during embryonic development.

This system of cell communication as a means of embryonic development is similar to the process of natural embryonic development in mammalian pregnancies such as humans.

During fertilization, the fertilized eggs cells divide into an embryo as it implants into the uterus.

Scientists had applied this knowledge by taking embryonic stem cells extracted in the lab and combining them with these early embryos. They were then placed in the uterus of a mouse subject and the resulting fetus contained cells that were partly, if not entirely, from the stem cells.

While the fetus develops, the mother starts to grow a new organ called the placenta, which supplies the fetus with the necessary nutrients as well as oxygen and glucose. The placenta guides the development of organs, acts as an immunological barrier to protect the fetus against infections, and synthesizes fatty acids and cholesterol, among other critical functions.

However, scientists found it challenging to mimic this natural environment in a petri dish because there was no placenta, which would have normally supplied the right balance of nutrients to the developing embryo.

To direct the development of the synthetic embryo, the researchers in this project started with embryonic stem cells that were completely undifferentiated. They then differentiated some of them into two different cell types by adding the corresponding developed cells.

The first group of differentiated cells would ultimately form the placenta and the other would become the yolk sac, a membranous structure attached to an embryo where the embryos first blood cells are made.

There are three different types of cells present: the unadulterated embryonic stem cells and the two partially differentiated helper tissues. They are mixed together after doing experiments to figure out the right ratios of factors like gas and nutrient levels, Schimenti said.

The project, starting in 2012, culminated in a synthetic embryo with a semi-functioning brain and heart. The organs were semi functioning because while they did work, they were not enough to independently sustain life.

This outcome significantly adds to the understanding of not only stem cells but the science of embryonic development because it allows scientists to experiment with embryonic development in real time. The University provides a unique opportunity to engage more with these concepts through its initiatives for stem cell research such as the Ansary Center for Stem Cell Therapeutics and the later established Cornell Stem Cell Program.

Moving forward with this breakthrough, researchers at the University continue to refine the different aspects of stem cell research by pushing development further and improving the efficiency of the organs being developed.

Despite this scientific breakthrough, there is still more to contribute in the study of the relationship between stem cells and regenerative medicine.

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Cornell Prof Explains Relevance of Creating Mouse Embryos from Stem Cells - Cornell University The Cornell Daily Sun

A $7 million grant to grow stem cell research – Swinburne University of Technology

Swinburne University of Technology has received a share of a $7 million Medical Research Future Fund grant to develop first-of-its-kind Australian research to allow live stem cells to be 3D printed and used in treatments.

The cross-institutional research team will develop novel cartilage-based stem cell therapies that will change the way we care for people living with painful joint disease, such as osteoarthritis, and facial disfigurement.

More than two million Australians live with the painful and degenerative joint disease, osteoarthritis, and one in 2,000 newborns are born with microtia an absent or poorly formed ear which can lead to hearing loss, speech and literacy delays.

This research could actually restore damaged or absent cartilage, transforming how these conditions are treated and vastly improving quality of life for sufferers.

It will use technology to revolutionise the way we think about personalised care, patient involvement and scientific advancements.

Cartilage, like that pictured, is a flexible connective tissue that protects our joints and bones

This ambitious project builds on many years of previous research, including at Swinburne.

In the initial stages, the five-year project will focus on the technologies used to take live stem cell printing from research labs into clinical settings. The team will then proceed to clinical trials to prove the efficacy of the solution.

Led by University of Melbourne Professor Peter Choong, the researchers also hope to simplify processes to bring these treatments into hospitals so that clinicians can treat conditions more quickly, with fewer complications than before.

In addition to Swinburne and the University of Melbourne, the research team also includes experts from La Trobe University, St Vincents Hospital Melbourne, University of Wollongong, University of Sydney, Royal Prince Alfred Hospital, Monash University, RMIT and the University of Toronto.

Swinburne will develop a bioreactor system using its patent-protected materials, which allow stem cells to be expanded to large numbers that can be used to repair and replace damaged or missing cartilage.

Expert in biomedical electromaterials science, Professor Simon Moulton, will lead the Swinburne team.

This grant allows us to continue the work we have already been doing with the other partners over many years in developing innovative cartilage repair strategies, says Professor Moulton.

As a materials engineering researcher in the medical area, we do not always have the opportunity to translate our efforts from fundamental research into a clinical human solution. The $7 million of total grant funding will allow us to continue to develop the stem cell technology towards clinical translation that will provide benefit to a wide range of patients.

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A $7 million grant to grow stem cell research - Swinburne University of Technology