Stem Cell Clinic

The Induced Pluripotent Stem Cells Market To Mark Robustness In The Form Of A Robust CAGR – KYT24

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The healthcare industry has been focusing on excessive research and development in the last couple of decades to ensure that the need to address issues related to the availability of drugs and treatments for certain chronic diseases is effectively met. Healthcare researchers and scientists at the Li Ka Shing Faculty of Medicine of the Hong Kong University have successfully demonstrated the utilization of human induced pluripotent stem cells or hiPSCs from the skin cells of the patient for testing therapeutic drugs.

The success of this research suggests that scientists have crossed one more hurdle towards using stem cells in precision medicine for the treatment of patients suffering from sporadic hereditary diseases. iPSCs are the new generation approach towards the prevention and treatment of diseases that takes into account patients on an individual basis considering their genetic makeup, lifestyle, and environment. Along with the capacity to transform into different body cell types and same genetic composition of the donors, hiPSCs have surfaced as a promising cell source to screen and test drugs.

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In the present research, hiPSC was synthesized from patients suffering from a rare form of hereditary cardiomyopathy owing to the mutations in Lamin A/C related cardiomyopathy in their distinct families. The affected individuals suffer from sudden death, stroke, and heart failure at a very young age. As on date, there is no exact treatment available for this condition.

This team in Hong Kong tested a drug named PTC124 to suppress specific genetic mutations in other genetic diseases into the iPSC transformed heart muscle cells. While this technology is being considered as a breakthrough in clinical stem cell research, the team at Hong Kong University is collaborating with drug companies regarding its clinical application.

The unique properties of iPS cells provides extensive potential to several biopharmaceutical applications. iPSCs are also used in toxicology testing, high throughput, disease modeling, and target identification. This type of stem cell has the potential to transform drug discovery by offering physiologically relevant cells for tool discovery, compound identification, and target validation.

A new report by Persistence Market Research (PMR) states that the globalinduced pluripotent stem or iPS cell marketis expected to witness a strong CAGR of 7.0% from 2018 to 2026. In 2017, the market was worth US$ 1,254.0 Mn and is expected to reach US$ 2,299.5 Mn by the end of the forecast period in 2026.

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Customization to be the Key Focus of Market Players

Due to the evolving needs of the research community, the demand for specialized cell lines have increased to a certain point where most vendors offering these products cannot depend solely on sales from catalog products. The quality of the products and lead time can determine the choices while requesting custom solutions at the same time. Companies usually focus on establishing a strong distribution network for enabling products to reach customers from the manufacturing units in a short time period.

Entry of Multiple Small Players to be Witnessed in the Coming Years

Several leading players have their presence in the global market; however, many specialized products and services are provided by small and regional vendors. By targeting their marketing strategies towards research institutes and small biotechnology companies, these new players have swiftly established their presence in the market.

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The Induced Pluripotent Stem Cells Market To Mark Robustness In The Form Of A Robust CAGR - KYT24

Kobe Hospital Trials Transplant to Reverse Blindness A First in the World – JAPAN Forward

Kobe City Eye Hospital in Hyogo Prefecture announced on October 16 that it had performed the worlds first clinical trial transplant to reverse blindness. The transplant was performed in early October on a woman in her 60s from the Kansai region who had lost most of her eyesight.

The roughly two-hour surgery wrapped up as scheduled without the patient experiencing complications. It involved light responding photoreceptor cells that were taken from induced pluripotent stem cells (iPS cells).

The patient in this case suffered from pigmentary retinal degeneration, a rare eye disease. The surgery was successful and the patient is said to be in good condition.

Regeneration of the photoreceptor cells connected to the central nervous system had been a long-awaited dream come true. Although its a small step, I am touched and relieved that we were able to safely step forward, said Yasuo Kurimoto, who performed the operation.

I would be happy if it could provide hope to those waiting to receive the same treatment, the female patient was quoted as saying after the surgery.

In the clinical trial, iPS cells that form the source of photoreceptor cells were generated from a healthy donor. The visual cells were then cultivated into a sheet with a diameter of one millimeter, and transplanted in three slices into the retina of the patients eye.

The aim is for the cells to develop into healthy photoreceptor cells so that the patients eyesight will improve and she will be able to sense light. The team will observe the procedures safety and effectiveness over a one-year period.

So far, two instances in which iPS cells were transplanted to treat eye disorders in regenerative clinical trials have been conducted. However, this was the first time that visual cells were regenerated in order to treat the core of vision.

Pigmentary retinal degeneration is a progressive disease that narrows vision and leads to vision loss and blindness as the photoreceptor cells of the retina gradually die. It is a genetic disorder for which there is no treatment up to now.

With the implementation of photoreceptor cell transplants using iPS cells, the treatment of blindness through regenerative medicine has taken a giant step forward.

Although transplants for patients with untreatable eye diseases have been conducted in the past, this was a groundbreaking procedure because it challenged the regrowth of the core of the vision system.

In the past, clinical study surgeries on regenerative medicine for the eye using iPS cells had included transplanting pigment epithelial cells in order to nourish the retina, as well as transplants of corneal cells that could act as lenses for the eye. However, neither transplants involved cells that generated vision itself.

Photoreceptor cells are considered the source of vision, as they convert light stimuli into electrical signals that produce information about the colors and shapes of objects we see. The information is then transmitted to the brain through the optic nerve. Without properly functioning photoreceptor cells, it would be impossible to see.

Directly connected to the central nervous system, photoreceptor cells, which have limited regenerative ability on their own, rarely recover naturally once the cells are damaged. That is why there is no fundamental treatment for pigmentary retinal degeneration, which loses the photoreceptor cells in the retina.

According to the Japan Ophthalmologists Association, there are an estimated 187,000 people in Japan with vision loss. If iPS cell-based regenerative medicine is realized, those who have lost their sight due to photoreceptor damage will be able to recover from blindness and at least see light again.

However, this time, the teams primary purpose for the surgery was to verify the fundamental safety and effectiveness of the procedure. The transplanted photoreceptor cells only take up a few percent of the area of the retina. Thus, the patients vision will not drastically improve in a short time.

Patients waiting for the procedure will have high expectations, but the safety and effectiveness of the treatment must be carefully examined before it can be put to practical use. There is hope now, but it will take some time before everyone can have access to the procedure.

Located inside the eyeball, photoreceptors are image-forming cells that make up the retina and play a central role in vision. Arranged in thin layers, the cells are capable of absorbing light that reaches the retina and then convert it into an electrical signal that is sent to the brain as information conveying the color or shape that is being viewed.

There are more than 100 million photoreceptors in each eye, but when a failure occurs, the vision is impaired and may lead to blindness if the condition becomes severe.

(Read the related articles in Japanese here and here.)

Author: Juichiro Ito

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Kobe Hospital Trials Transplant to Reverse Blindness A First in the World - JAPAN Forward

COVID-19 can affect the heart – Science Magazine

The family of seven known human coronaviruses are known for their impact on the respiratory tract, not the heart. However, the most recent coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has marked tropism for the heart and can lead to myocarditis (inflammation of the heart), necrosis of its cells, mimicking of a heart attack, arrhythmias, and acute or protracted heart failure (muscle dysfunction). These complications, which at times are the only features of coronavirus disease 2019 (COVID-19) clinical presentation, have occurred even in cases with mild symptoms and in people who did not experience any symptoms. Recent findings of heart involvement in young athletes, including sudden death, have raised concerns about the current limits of our knowledge and potentially high risk and occult prevalence of COVID-19 heart manifestations.

The four common cold human coronavirusesHCoV-229E, HCoV-NL63, HCoV-OC43, and HCoV-HKU1have not been associated with heart abnormalities. There were isolated reports of patients with Middle East respiratory syndrome (MERS; caused by MERS-CoV) with myocarditis and a limited number of case series of cardiac disease in patients with SARS (caused by SARS-CoV) (1). Therefore, a distinct feature of SARS-CoV-2 is its more extensive cardiac involvement, which may also be a consequence of the pandemic and the exposure of tens of millions of people to the virus.

What appears to structurally differentiate SARS-CoV-2 from SARS is a furin polybasic site that, when cleaved, broadens the types of cells (tropism) that the virus can infect (2). The virus targets the angiotensin-converting enzyme 2 (ACE2) receptor throughout the body, facilitating cell entry by way of its spike protein, along with the cooperation of the cellular serine protease transmembrane protease serine 2 (TMPRSS2), heparan sulfate, and other proteases (3). The heart is one of the many organs with high expression of ACE2. Moreover, the affinity of SARS-CoV-2 to ACE2 is significantly greater than that of SARS (4). The tropism to other organs beyond the lungs has been studied from autopsy specimens: SARS-CoV-2 genomic RNA was highest in the lungs, but the heart, kidney, and liver also showed substantial amounts, and copies of the virus were detected in the heart from 16 of 22 patients who died (5). In an autopsy series of 39 patients dying from COVID-19, the virus was not detectable in the myocardium in 38% of patients, whereas 31% had a high viral load above 1000 copies in the heart (6).

Accordingly, SARS-CoV-2 infection can damage the heart both directly and indirectly (see the figure). SARS-CoV-2 exhibited a striking ability to infect cardiomyocytes derived from induced pluripotent stem cells (iPSCs) in vitro, leading to a distinctive pattern of heart muscle cell fragmentation, with complete dissolution of the contractile machinery (7). Some of these findings were verified from patient autopsy specimens. In another iPSC study, SARS-CoV-2 infection led to apoptosis and cessation of beating within 72 hours of exposure (8). Besides directly infecting heart muscle cells, viral entry has been documented in the endothelial cells that line the blood vessels to the heart and multiple vascular beds. A secondary immune response to the infected heart and endothelial cells (endothelitis) is just one dimension of many potential indirect effects. These include dysregulation of the renin-angiotensin-aldosterone system that modulates blood pressure, and activation of a proinflammatory response involving platelets, neutrophils, macrophages, and lymphocytes, with release of cytokines and a prothrombotic state. A propensity for clotting, both in the microvasculature and large vessels, has been reported in multiple autopsy series and in young COVID-19 patients with strokes.

There is a diverse spectrum of cardiovascular manifestations, ranging from limited necrosis of heart cells (causing injury), to myocarditis, to cardiogenic shock (an often fatal inability to pump sufficient blood). Cardiac injury, as reflected by concentrations of troponin (a cardiac musclespecific enzyme) in the blood, is common with COVID-19, occurring in at least one in five hospitalized patients and more than half of those with preexisting heart conditions. Such myocardial injury is a risk factor for in-hospital mortality, and troponin concentration correlates with risk of mortality. Furthermore, patients with higher troponin amounts have markers of increased inflammation [including C-reactive protein, interleukin-6 (IL-6), ferritin, lactate dehydrogenase (LDH), and high neutrophil count] and heart dysfunction (amino-terminal pro-Btype natriuretic peptide) (9).

More worrisome than the pattern of limited injury is myocarditis: diffuse inflammation of the heart, usually representing a variable admixture of injury and the inflammatory response to the injury that can extend throughout the three layers of the human heart to the pericardium (which surrounds the heart). Unlike SARS-associated myocarditis, which did not exhibit lymphocyte infiltration, this immune and inflammatory response is a typical finding at autopsy after SARS-CoV-2 infections. Involvement of myocytes, which orchestrate electrical conduction, can result in conduction block and malignant ventricular arrhythmias, both of which can lead to cardiac arrest.

Along with such in-hospital arrythmias, there have been reports of increased out-of-hospital cardiac arrest and sudden death in multiple geographic regions of high COVID-19 spread, such as the 77% increase in Lombardy, Italy, compared with the prior year (10). There have been many reports of myocarditis simulating a heart attack, owing to the cluster of chest pain symptoms, an abnormal electrocardiogram, and increased cardiac-specific enzymes in the blood, even in patients as young as a 16-year-old boy. When there is extensive and diffuse heart muscle damage, heart failure, acute cor pulmonale (right heart failure and possible pulmonary emboli), and cardiogenic shock can occur.

COVID-19associated heart dysfunction can also be attributed to other pathways, including Takotsubo syndrome (also called stress cardiomyopathy), ischemia from endothelitis and related atherosclerotic plaque rupture with thrombosis, and the multisystem inflammatory syndrome of children (MIS-C). The underlying mechanism of stress cardiomyopathy is poorly understood but has markedly increased during the pandemic. MIS-C is thought to be immune-mediated and manifests with a spectrum of cardiovascular features, including vasculitis, coronary artery aneurysms, and cardiogenic shock. This syndrome is not exclusive to children because the same clinical features have been the subject of case reports in adults, such as in a 45-year-old man (11).

Recent series of COVID-19 patients undergoing magnetic resonance imaging (MRI) or echocardiography of the heart have provided some new insights about cardiac involvement (1214). In a cohort of 100 patients recovered from COVID-19, 78 had cardiac abnormalities, including 12 of 18 patients without any symptoms, and 60 had ongoing myocardial inflammation, which is consistent with myocarditis (12). The majority of more than 1200 patients in a large prospective cohort with COVID-19 had echocardiographic abnormalities (13). This raises concerns about whether there is far more prevalent heart involvement than has been anticipated, especially because at least 30 to 40% of SARS-CoV-2 infections occur without symptoms. Such individuals may have underlying cardiac pathology.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has the potential to directly and indirectly induce cardiac damage.

To date, there have been four small series of asymptomatic individuals with bona fide infections who underwent chest computed tomography (CT) scans to determine whether there were lung abnormalities consistent with COVID-19. Indeed, half of the asymptomatic people showed lung CT features that were seen in patients with symptoms. But so far, there have been minimal cardiac imaging studies in people who test positive for SARS-CoV-2 or are seropositive but without symptoms. Furthermore, the time course of resolution or persistence of any organ abnormalities after SARS-CoV-2 infection has not yet been reported. With a high proportion of silent infections despite concurrent evidence of internal organ damage, there is a fundamental and large hole in our knowledge base.

In contrast to people without symptoms, there is a substantial proportion of people who suffer a long-standing, often debilitating illness, called long-COVID. Typical symptoms include fatigue, difficulty in breathing, chest pain, and abnormal heart rhythm. An immunologic basis is likely but has yet to be determined. Nor have such patients undergone systematic cardiovascular assessment for possible myocarditis or other heart abnormalities, such as fibrosis, which could account for some of the enduring symptoms. It would not be surprising in the future for patients to present with cardiomyopathy of unknown etiology and test positive for SARS-CoV-2 antibodies. However, attributing such cardiomyopathy to the virus may be difficult given the high prevalence of infections, and ultimately a biopsy might be necessary to identify virus particles to support causality.

Cardiac involvement in athletes has further elevated the concerns. A 27-year-old professional basketball player, recovered from COVID-19, experienced sudden death during training. Several college athletes have been found to have myocarditis (14), including 4 of 26 (15%) in a prospective study from Ohio State University (15), along with one of major league baseball's top pitchers. Collectively, these young, healthy individuals had mild COVID-19 but were subsequently found to have unsuspected cardiac pathology. This same demographic groupyoung and healthyare the most common to lack symptoms after SARS-CoV-2 infections, which raises the question of how many athletes have occult cardiac disease? Systematic assessment of athletes who test positive for SARS-CoV-2, irrespective of symptoms, with suitable controls through some form of cardiac imaging and arrhythmia screening seems prudent until more is understood.

The most intriguing question that arises is why do certain individuals have a propensity for heart involvement after SARS-CoV-2 infection? Once recognized a few months into the pandemic, the expectation was that cardiac involvement would chiefly occur in patients with severe COVID-19. Clearly, it is more common than anticipated, but the true incidence is unknown. It is vital to determine what drives this pathogenesis. Whether it represents an individual's inflammatory response, an autoimmune phenomenon, or some other explanation needs to be clarified. Beyond preventing SARS-CoV-2 infections, the goal of averting cardiovascular involvement is paramount. The marked heterogeneity of COVID-19, ranging from lack of symptoms to fatality, is poorly understood. A newly emerged virus, widely circulating throughout the human population, with a panoply of disease manifestations, all too often occult, has made this especially daunting to unravel.

Acknowledgments: E.J.T. is supported by National Institutes of Health grant UL1 TR001114.

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COVID-19 can affect the heart - Science Magazine

Rethinking the Link between Cannabinoids and Learning – Lab Manager Magazine

Fluorescent image of a mouse brain with the cerebellum highlighted in the shape of a marijuana leaf.

Illustration by Rita Flix, PhD

Cannabinoids have a strong influence on how our brains work and how we behave. Many people are only aware of the recreational aspect of cannabinoids. But in fact these molecules naturally exist in our brains where they participate in various intrinsic processes.

Altered cannabinoid signaling, for instance due to chronic use of marijuana, results in a range of impairments. Similarly, mice lacking cannabinoid receptors exhibit reduced activity levels, as well as deficits in learning and memory.

How do cannabinoids exact their effect on learning? A team led by Megan Carey, a principal investigator at the Champalimaud Centre for the Unknown in Portugal, and Catarina Albergaria, a postdoctoral researcher in the lab, decided to tap into this question by investigating the brain mechanisms involved in a classical learning task called eyeblink conditioning.

In eyeblink conditioning, subjects learn to associate the appearance of a sensory stimulus, for example a flash of light, with a subsequent delivery of an airpuff to the eye. Once learned, the subjectin this case a mousecloses its eyes when the light appears to avoid the airpuff. "It's just like Pavlov's dog and the bell," says Albergaria.

Previous studies had established that this form of learning takes place in a brain structure called the cerebellum, and that it was impaired by altered cannabinoid signaling in both humans and mice. To study the role of cannabinoids in learning, the team used mutant mice lacking cannabinoid receptors, which show impaired eyeblink conditioning.

Why are these mice impaired? When they started, the researchers had an immediate suspect in mind. "Many studies support the idea that cannabinoids mediate neural plasticity, or experience-dependent changes in the connections between neurons," Carey explains. "We therefore first hypothesized that interfering with this process was what was driving the impairments in learning."

But like a good mystery novel, the immediate suspect turned out to be the wrong one. What was the real culprit? "In a study we published two years ago, we found that the more mice ran, the better they learned," Albergaria explains. The team began to suspect that the difference in learning might instead be due to the reduced activity levels of the mutant mice.

"We wondered whether the mutant mice weren't learning as well simply because they weren't active enough," Albergaria recalls. In the journal eLife, the team reports that the altered behavioral state of the mutants fully accounts for their impaired eyeblink conditioning. When the researchers placed the mice on a motorized treadmill that ensured that the mutants walked as much as normal mice, the results were striking: learning was completely restored.

The team also found that other cerebellar behaviors, locomotor coordination and learning, were normal in the cannabinoid mutants. Further, eyeblink conditioning was fully intact in mice that lacked cannabinoid receptors specifically within the cerebellum. "These experiments further supported our hypothesis that disrupted cannabinoid signaling was impairing learning by altering behavioral state, and not through direct effects on neural plasticity in the cerebellum," says Carey.

"There is a growing body of evidence that behavioral state profoundly influences brain function," says Carey. "Our study highlights the need to consider behavioral state as a powerful independent means through which individual genes contribute to complex behaviors."

"We were able to overcome a learning deficit associated with a genetic mutation with a purely behavioral intervention," adds Albergaria, suggesting a potential real-world consequence for these findings.

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Rethinking the Link between Cannabinoids and Learning - Lab Manager Magazine

Cold sore virus can spread to unborn babies harming their brains, docs warn – The Sun

THE cold sore virus can spread to unborn babies and harm their brains, experts have warned.

New research has found that the herpes simplex virus type (HSV-1) can be passed to a fetus during the mother's pregnancy.

1

It may contribute to various developmental disabilities and long-term neurological problems, according to scientists at Wuhan University, China.

HSV-1, commonly known as the cold sore virus, isn't harmful to adults but is already known to be fatal for babies with weaker immune systems.

It can spread quickly to babies' brains and cause multiple organ failure, and ultimately death.

The experts behind the study, published in the open-access journal PLOS Pathogens, wanted to understand more about how HSV-1 can affect unborn babies.

Researchers Pu Chen and Ying Wu said that so far, studies in this area have been hampered by restricted access to fetal human brain tissue.

To address this gap in knowledge, the researchers generated three different cell-based neurodevelopmental disorder models, including a 2D layer of cells and a 3D brain-like structure.

These models are based on human induced pluripotent stem cells (hiPSCs), which are generated by genetically reprogramming specialised adult cells.

Their modelling revealed that HSV-1 infection in these cells resulted in cell death as well as impaired production of new neurons.

It also mimicked the pathological features of neurodevelopmental disorders int he human fetal brain, including abnormalities in the brain structure.

Neonatal herpes is when a newborn or very young babyWhe is infected with the herpes virus.

It's caused by the same strain of herpes that triggers cold sores and genital ulcers in adults.

It can be extremely serious for a young baby, whose immune system won't have fully developed to fight off the virus.

While it's rare, it's important all parents are aware of the dangers.

Newborns can catch herpes in a number of ways.

It can be passed on during birth, if mum has genital herpes for the first time within six weeks of her pregnancy.

After birth, a baby can become infected if a person with a cold sore kisses them.

Or if mum breastfeeds with herpes sores on her breasts.

The warning signs to watch for in your baby are if they:

It's important to get your baby checked over if you suspect they've caught or been exposed to herpes.

It can develop quickly and spread to their brain or other parts of the body, proving fatal.

The 3D model also showed that HSV-1 infection promotes the abnormal spread of non-neuronal cells called microglia, along with by the activation of inflammatory molecules.

According to the authors, the findings open new therapeutic avenues for targeting viral reservoirs relevant to neurodevelopmental disorders.

They added: "This study provides novel evidence that HSV-1 infection impaired human brain development and contributed to the neurodevelopmental disorder pathogen hypothesis".

Studies on neonatal herpes - which is when a newborn baby has been infected with the virus - are more extensive.

It's understood that the younger the baby, the more vulnerable they are to the herpes virus.

While devastating, the condition is rare in the UK.

A baby is at greatest risk of catching the virus in the first four weeks of life, and it can be passed on in one of two main ways:

1. During pregnancy and labour

If mum has genital herpes for the first time in the last six weeks of pregnancy, her baby is at risk.

As a result, you should never kiss a baby if you have, or recently have had, a cold sore.

It's possible for a mum to pass the infection on during vaginal delivery.

2. After birth

The virus can be passed to a baby through a cold sore if someone affected kisses a baby.

It can also be passed via blisters on the breast of a mum, who has HSV-1, and is feeding.

Exclusive

Warning

Call your GP or health visitor straight away if your baby:

The early warning signs your baby is unwell - call 999 if your baby:

To find out more visit theNHS website.

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Cold sore virus can spread to unborn babies harming their brains, docs warn - The Sun