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Role of Stem Cells in Chronic Lung Diseases Revealed – Technology Networks

By Stem Cell Medical Center

A novel population of lung stem cells plays an important role in regulating the pulmonary microvasculature the network of tiny blood vessels where oxygen and carbon dioxide exchange takes place.

The stem cells, called mesenchymal progenitor cells (MPCs), likely contribute to the pathobiology of chronic lung diseases, said Susan Majka, Ph.D., associate professor of Medicine.

Understanding the normal function and disease-associated dysfunction of MPCs could lead to earlier diagnosis and improved treatment for diseases such as pulmonary fibrosis, emphysema and pulmonary hypertension. The findings were reported this month in the Journal of Clinical Investigation.

Chronic lung diseases are marked by changes in lung tissue structure that include remodeling and loss of microvessels. The loss of microvessels impairs gas exchange, causing shortness of breath.

The vascular remodeling had been attributed to the endothelial cells that line blood vessels or the smooth muscle cells that surround them, Majka said. But endothelial and smooth muscle cells are terminally differentiated they are not likely to become other types of cells and Majka believed that unidentified stem cells, which can produce multiple types of mature cells with varied functions, were more likely to underlie tissue remodeling.

She and her colleagues had isolated vascular stem cells from mouse and human lungs and characterized them as MPCs that are located next to the microvasculature in the adult tissue. Now, they have used novel advanced lineage mapping tools to track the cells, under normal conditions and when signaling pathways associated with adult lung diseases are activated (Wnt signaling) or reduced (BMPR2 signaling).

When these cells are abnormal, animals develop vasculopathy a loss of structure in the microvessels and subsequently the lung. They lose the surfaces for gas exchange, Majka said.

The investigators also followed the cells after lung injury experimentally induced fibrosis (scarring). They discovered that the MPCs, which are abnormally activated after injury, formed an adaptive vascular structure that had never been previously characterized.

It appears to be a form of vascular mimicry, tubular structures that will circulate blood but are not normal blood vessels, Majka said. Its a new form of angiogenesis that could get blood into the middle of fibrotic areas, but our studies ended early after the injury, during peak fibrosis, and we dont know yet if its helping repair the injury or is actually detrimental.

Majka and her colleagues also used human lung tissues obtained from transplant or other surgeries to isolate MPCs. They compared human and mouse MPCs from normal and diseased lung tissue and showed that the cells have similar characteristics and gene expression profiles, defining the work as relevant to human disease.

Its very exciting to discover something new like this cell type that is so important in maintaining microvascular and lung tissue structure and that has potential implications in disease and repair, Majka said.

Understanding the MPCs, and other cell populations in the lung, is important for efforts to use stem cells to repair injured lung tissues, or to build lung tissue grafts.

Its critical to understand how different cells in the lung microenvironment regulate each other, and we really dont know that yet, Majka said.

By studying gene expression patterns in MPCs from normal and diseased or injured lungs, Majka and her colleagues have discovered new targets that may point to biomarkers for earlier detection of pulmonary diseases and that may guide the development of interventions that promote repair.

With pulmonary vascular diseases, by the time a patient has symptoms, theres already major damage to the microvasculature, Majka said. Using new biomarkers to detect the disease before symptoms arise would allow for earlier treatment, which could be effective at decreasing progression or even reversing the disease process.

In addition, MPCs are present in many adult tissues, including skin, kidney and uterus, suggesting that the findings may improve understanding of the microvascular basis of disease pathophysiology in these tissues.

This article has been republished frommaterialsprovided by Vanderbilt University Medical Center. Note: material may have been edited for length and content. For further information, please contact the cited source.

Reference:

Gaskill, C. F., Carrier, E. J., Kropski, J. A., Bloodworth, N. C., Menon, S., Foronjy, R. F., . . . Majka, S. M. (2017). Disruption of lineage specification in adult pulmonary mesenchymal progenitor cells promotes microvascular dysfunction. Journal of Clinical Investigation. doi:10.1172/jci88629

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Role of Stem Cells in Chronic Lung Diseases Revealed - Technology Networks

Adaptimmune Therapeutics (ADAP) Begins Study to Evaluate … – StreetInsider.com

By Uncategorized

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Adaptimmune Therapeutics plc (Nasdaq: ADAP), a leader in T-cell therapy to treat cancer, today announced that it has initiated its study of NY-ESO SPEAR Tcells targeting NY-ESO in combination with KEYTRUDA (pembrolizumab), an anti-PD-1 inhibitor marketed by Merck & Co., Inc., Kenilworth, NJ, USA (known as MSD outside the US and Canada), in patients with multiple myeloma. This study is now open for enrollment.

This is Adaptimmunes third clinical trial to initiate within the past month. The Company recently announced the initiation of clinical studies with its wholly-owned SPEAR T-cells targeting AFP in hepatocellular carcinoma, as well as its wholly-owned SPEAR T-cells targeting MAGE-A4 in seven malignant solid tumors.

We are excited to initiate this study as we have already seen encouraging data in a previous singleagent study of NYESO SPEAR T-cells in patients with advanced myeloma in the context of stem cell transplantation, said Rafael Amado, Adaptimmunes Chief Medical Officer. KEYTRUDA has also shown preliminary evidence of activity in multiple myeloma in combination, and there is preclinical evidence to support the view that the combination of NY-ESO SPEAR T-cells and anti-PD-1 therapy may lead to meaningful antitumor activity.

This is an open-label, randomized pilot study designed to evaluate the safety and anti-tumor activity of Adaptimmunes NY-ESO therapeutic candidate alone or in combination with KEYTRUDA in patients who are HLA-A*02 positive and have relapsed and refractory multiple myeloma expressing NY-ESO-1 and/or LAGE1a. The study will enroll up to 20 patients. The primary objective of the study is to evaluate the safety and tolerability of NY-ESO SPEAR T-cell therapy alone or in combination with KEYTRUDA. Additional objectives include antitumor activity, persistence of genetically modified cells in the body, and evaluation of the phenotype and functionality of genetically modified cells isolated from peripheral blood or tumor post infusion.

Adaptimmune is developing the NY-ESO SPEAR T-cell program under a strategic collaboration agreement with GSK.

Clinical Trial Collaboration Agreement for use of KEYTRUDA

Adaptimmune has a clinical trial collaboration agreement with Merck & Co., Inc., Kenilworth, NJ, USA for the use of KEYTRUDA in this study. The agreement is between Adaptimmune and Merck & Co., Inc., Kenilworth, NJ, USA, through a subsidiary. Under the agreement, the trial will be sponsored by Adaptimmune. The agreement also includes provision for potential expansion to include Phase III registration studies in the same indication. Additional details were not disclosed.

KEYTRUDA is a registered trademark of Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc., Kenilworth, NJ, USA.

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Adaptimmune Therapeutics (ADAP) Begins Study to Evaluate ... - StreetInsider.com

Old drug points to promising new direction for treatment of autism – Medical News Today

By Uncategorized

A small trial involving 10 boys with autism spectrum disorder showed promising results from treatment with a drug called suramin, which was originally developed 100 years ago to treat African sleeping sickness, a parasitic disease. Boys who received a single dose of the drug showed measurable, though not permanent, improvements in autism spectrum disorder symptoms.

A report on the trial - led by the University of California-San Diego (UCSD) - is published in the Annals of Clinical and Translational Neurology.

Autism spectrum disorder (ASD), or autism, is a developmental disability with a cluster of behavioral symptoms that typically surface in childhood and generally affect social interaction and communication.

ASD is considered a complex, wide-spectrum disorder because the many symptoms can vary in combination and intensity. For this reason, no two people with ASD will have exactly the same symptoms.

Some of the behavioral symptoms of ASD include:

According to the Centers for Disease Control and Prevention (CDC), ASD affects around 1 in 68 children in the United States and occurs in all socioeconomic, racial, and ethnic groups. However, it is about 4.5 times more common in boys than in girls.

There is no single cause of ASD, but it is thought that a combination of genetic and environmental factors is involved, ranging from pollutants to viral infections and pregnancy complications.

Robert K. Naviaux, a professor of medicine, pediatrics, and pathology at UCSD School of Medicine and first author of the new study, believes that the idea of an abnormal "cell danger response" may offer a unifying theory for the development of ASD.

The cell danger response is a normal signal sent out by all cells when they suffer injury or stress. Its purpose, says Prof. Naviaux, "is to help protect the cell and jump-start the healing process." The signal causes the cell to stiffen its cell walls, stop talking to other cells, and withdraw until the threat subsides.

However, Prof. Naviaux explains that the cell danger response "can get stuck" and stop the completion of the cell's healing cycle. The cell persists in the threat response state, which can "permanently alter the way the cell responds to the world."

The effect at the molecular level is to disrupt the chemistry of cell equilibrium and cause chronic disease. Prof. Naviaux says that "when this happens during early child development, it causes autism and many other chronic childhood disorders."

Cells activate the cell danger response by releasing a small molecule from their energy-making compartments, or mitochondria. The release of this molecule is what acts as the danger signal, and it keeps being released as long as the cell danger response is active.

Suramin blocks the ability of the small molecule to release the danger signal. The effect, says Prof. Naviaux, is to signal that "the cellular war is over, the danger has passed and cells can return to 'peacetime' jobs like normal neurodevelopment, growth, and healing."

The drug was originally developed in 1916 by the German firm Frederich Bayer and Co. for treating diseases caused by trypanosome parasites, such as those that cause African sleeping sickness and river blindness.

For their small study - which took the form of a randomized, double-blind, placebo-controlled phase I/II clinical trial involving 10 boys, all aged between 5 and 14, who were diagnosed with ASD - the team tested the effect of a single dose of suramin on symptoms of ASD.

The aim of the trial was to find out whether the cell danger response theory might explain the development of ASD and to assess the safety of suramin, which is not approved for the treatment of ASD. An earlier trial that tested the drug on mice had found that a single dose "temporarily reversed" symptoms of ASD.

The boys were randomly assigned to receive either a single intravenous transfusion of suramin, or a placebo.

The results showed that all five boys who received the active drug showed measurable improvements in ASD symptoms not seen in the placebo group. The improvements were specifically in speech and language, social communication and play, coping skills, calm and focus, and repetitive behavior.

The researchers used a battery of standardized tests and interviews to measure the improvements. When these involved parent observations, the team only counted a change as an improvement if it persisted for at least a week. This was to rule out any fluctuations in day-to-day behavior that may have occurred anyway.

Prof. Naviaux says that there were four non-verbal children in the trial: two aged 6 and two aged 14, with one of each age having been assigned to the drug group and the placebo group.

"The 6-year-old and the 14-year-old who received suramin said the first sentences of their lives about one week after the single suramin infusion," he notes. "This did not happen in any of the children given the placebo."

The team reports that while the children were on suramin, there was a dramatic improvement in the benefits they derived from the speech therapy, occupational therapy, and other programs that they were taking part in.

However, the effects of the drug waned over time. The measured improvements peaked and then gradually dwindled after a few weeks.

The team is not dispirited by this. They say that the findings are sufficient to show that it is worth testing different doses of suramin in larger, more diverse groups of people with ASD, over longer periods. This could help to establish how long improvements last, and also whether side effects other than the mild skin rash observed in the small trial might emerge.

Andrew W. Zimmerman, a clinical professor of pediatrics and neurology at UMass Memorial Medical Center, was not involved in the trial but is also researching in a similar field. He says that the results of the trial are "encouraging for the field of autism," both in terms of the promising changes in the children and also because it supports the cell danger response theory. He comments:

"As the authors point out, many genetic variants have been found in ASD, but few have led to specific treatments. The CDR [cell danger response] includes a number of metabolic pathways that may be affected by a number of genetic mutations or by environmental factors that have effects epigenetically - beyond the genes themselves."

Prof. Naviaux and colleagues point out that suramin is not approved for the treatment of autism. They strongly urge against using it in unauthorized settings. The drug must undergo years of rigorous testing through clinical trials to identify any rare side effects and establish safe doses.

Learn how a new biochemical method accurately diagnosed autism in children.

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Old drug points to promising new direction for treatment of autism - Medical News Today

Therapy Focus – Not Quite The Hammer For Sickle Cell Disease – Seeking Alpha

By Uncategorized

When it comes to serious diseases with virtually no treatments the US FDA has shown flexibility in approving new therapies, even if these have questionable efficacy. This could play out again when the agency decides on Emmaus' Endari for sickle cell disease by July 7, especially as the project now has an adcom's blessing.

The case of Endari is curious for several reasons, not least the fact that it has a cheaply available active ingredient and a data package flattered by statistical changes; its maker until recently looked like being taken over by the struggling Generex (OTCPK:GNBT) (OTCPK:GNBTD). Still, given how barren the industry's sickle cell disease pipeline is, patients might welcome any advance, however speculative (see table below).

As such, the US adcom's 10-3 vote in support of Endari's risk/benefit profile is understandable. This came despite questions at the meeting about a high rate of dropouts, missing data in the project's pivotal GLUSCC09-01 study, and doubts about the relevance of the primary endpoint - reduction of sickle cell crises over 48 weeks.

Perhaps most egregious of all was that Endari failed according to the trial's planned analysis, yielding a non-significant p value of 0.063 versus the control comparator, maltodextrin. It was only when Emmaus amended the statistical method that it claimed success with a 0.005 p value (Upcoming events - Panel woes for Puma and statistical uncertainties for Emmaus, May 12, 2017).

A low bar

Still, if Endari is approvable, competitors might celebrate the fact that the bar in sickle cell disease has been set so low.

Perhaps the most important near-term challenge will come from Glycomimetics' (NASDAQ:GLYC) rivipansel, a pan-selectin antagonist, given that this was licensed to Pfizer, which is now in charge of a phase III trial called Reset.

Sickle cell disease is an autosomal recessive disorder caused by a simple mutation in the gene coding for hemoglobin, which affects hemoglobin's ability to carry oxygen and causes it to polymerize. These hemoglobin polymers distort red blood cells' shape and increase their rigidity, leading to anemia, occluded blood flow and pain crises during severe episodes.

Sickle cell disease is curable with stem cell transplantation, but most patients do not have a matched donor to serve as the graft source. Two groups, Gamida Cell and Bellicum (NASDAQ:BLCM), are working on expanded grafts that might be used by non-matched or partially matched patients.

Clearly, this is complex, but unlike stem cells few small-molecule or antibody approaches will treat the disease's underlying cause. The aim with rivipansel, for instance, is to reduce adhesion of red blood cells, thus making it harder for them to aggregate.

Also acting via anti-adhesive properties is Modus Therapeutics' Sevuparin, a phase II asset that has been licensed to Ergomed. Endari is similarly a symptom-targeting agent, aiming to reduce oxidative damage to cells, while Eliquis is being studied for its anticoagulant effects.

In terms of potential cures the spotlight is on Bluebird's (NASDAQ:BLUE) gene therapy Lentiglobin, which aims to correct the disease's underlying genetic defect. Both this and Global Blood Therapeutics' GBT440, which inhibits hemoglobin polymerization, have had rollercoaster developments, and updates will be presented at December's Ash meeting.

It is also worth noting that data generated by Selexys' crizanlizumab, an antibody targeting cell adhesion, were good enough to secure a buyout by Novartis (NYSE:NVS) (Ash delivers early for Selexys, November 21, 2016).

Will it sell?

All that said, in the near term Emmaus faces a more fundamental threat: it is by no means certain that Endari is a viable business proposition.

Its active ingredient is a pharmaceutical-grade form of L-glutamine, which is available over the counter; it is also available on prescription as Nutrestore for short bowel syndrome. Approval for sickle cell disease would lock out competitors on the basis of data exclusivity, but getting insurance coverage could be tricky, especially in a price-conscious political environment.

Then there is the mystery of Emmaus' proposed takeover by the troubled oral insulin company Generex. This was to have involved Generex buying a 51% stake at a $441m valuation, under a letter of intent signed in January, but the deal was quietly terminated on May 16.

Among the unusual aspects of this transaction was the $500,000 cash advanced to Generex by its chief executive and a senior vice-president to cover the up-front fee under the letter of intent. Generex then raised $3m, and paid $3.5m to Emmaus in March, but scrapped the deal citing delays in its plan to eliminate warrants and preferred stock and carry out a reverse split.

Generex says it is now due a $4m refund. It seems that the group will not, after all, become a player in sickle cell disease.

Editor's Note: This article covers one or more stocks trading at less than $1 per share and/or with less than a $100 million market cap. Please be aware of the risks associated with these stocks.

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Therapy Focus - Not Quite The Hammer For Sickle Cell Disease - Seeking Alpha

New baldness cause accidentally discovered by scientists could lead to hair loss treatment – The Independent

By Stem Cell Treatment

A new cause of baldness has been accidentally discovered by scientists in the US in a breakthrough that could help develop a way to regrow hair.

The researchers were investigating the role played by anti-inflammatory immune cells called Tregs in skin health generally.

They found a way to temporarily remove the Tregs from the skin of laboratory mice, who had been shaved to allow the effects to be observed.

But the scientists then noticed something unexpected the hairfailed to grow back.

Previously it was thought that stem cells cause hairs to regrow after they fall out, but the team discoveredthat this only happens if Tregs are present.

One of the scientists, Professor Michael Rosenblum, an immunologist and dermatologist at University of California San Francisco, said: Our hair follicles are constantly recycling. When a hair falls out, the whole hair follicle has to grow back.

This has been thought to be an entirely stem cell-dependent process, but it turns out Tregs are essential.

If you knock out this one immune cell type, hair just doesn't grow.

Its as if the skin stem cells and Tregs have co-evolved, so that the Tregs not only guard the stem cells against inflammation but also take part in their regenerative work.

The stem cells rely on the Tregs completely to know when it's time to start regenerating.

The researcher believe that defects in Tregs could be responsible for the immune disease, alopecia areata, which causes hair to fall out in patches and possibly also play a part in other kinds of baldness.

The same stem cells that regrow hair are also involved in healing damage to the skin, so Tregs may also be involved in this process.

Tregs role as previously understood was mainly to regulate the immune system, helping it tell what to attack and what to leave alone.

When they malfunction it can lead to allergies to peanuts and other harmless substances or cause the immune system to attack the body.

Professor Rosenblum and colleagues had previously showed that Tregs help the immune systems of baby mice learn which skin microbes are not harmful and also that they secrete molecules that help heal wounds.

They were investigating these effects further when they noticed that patches of shaved hair on the lab mice were not regrowing.

We thought, Hmm, now thats interesting, Professor Rosenblum said. We realised we had to delve into this further.

Using sophisticated imaging techniques, the researchers were able to show that Tregs gathered around follicle stem cells at the start of the process to regrow a hair.

When Tregs were removed from the skin, this prevented the regrowth of hair but only if this was done within three days of the hair being shaved. After this time, the hair would regrow normally despite the absence of Tregs.

The cause of alopecia is poorly understood, but previous studies have showed genes associated with the condition are mostly related to Tregs. Boosting Treg function has been found to help.

Professor Rosenblum suggested further research into Tregs role could lead to improved treatments for hair loss generally and better understanding of their role in wound healing.

We think of immune cells as coming into a tissue to fight infection, while stem cells are there to regenerate the tissue after it's damaged, he said.

But what we found here is that stem cells and immune cells have to work together to make regeneration possible.

The research was described in the journal Cell.

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New baldness cause accidentally discovered by scientists could lead to hair loss treatment - The Independent

Stem Cell Research in Hair Loss – Financial Tribune

By Stell Cell Research

Researchers at Royan Institute have taken a step towards stem cell treatment of hair loss through laboratory studies on rats. Dermal papillas are small ridges at the surface of the skin, and in the scalp, which provide oxygen and nutrients to hair follicles so that healthy new hair may grow. Epithelial stem cells(EpSCs) in thehairfollicle helpin normal hairfollicle growth cycle.Any damage to these cells is the main cause of hair loss. Researchers at the institute Irans leading center for stem cell research conducted experiments in which they cultivated dermal papilla and epithelial stem cellsextracted from the human scalp in laboratory conditions, Mehr News Agency reported. In the research, around 15 laboratory rats were divided into three groups: one received dermal papilla, the second simultaneously received both dermal papilla and epithelial stem cells, and the third (control group) did not receive any cells. Results published in the institutes Cell Journal showed that hair growth occurred in the two groups receiving cells, but in the group receiving both kinds of cells, the hair growth was more tangible and visible to the naked eye. It was also revealed that transplantation of stem cells effective on hair growth can cause hair growth in hairless rats. With further research and better understanding of hair growth mechanism in humans, researchers may find effective ways to treat hair loss, the institute said.

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Stem Cell Research in Hair Loss - Financial Tribune

Why Tooth Banking Might Just Be The Next Wave In Stem Cell Research – UPROXX

By Stell Cell Research

Shutterstock

Uproxx knows that science, technology, engineering, and math (STEM) disciplines are driving the future of this planet forward. Every day, we see new ideas, fresh innovations, and bold trailblazers in these fields. Follow us this month as we highlight how STEM is shaping the culture of NOW.

Placentas, umbilical cords pretty much anything that comes out of a womans body is awesome in science speak. Stem cells are the master cells of the body, just waiting to help you out when you get sick. Theyre your own personal repair kit, but, like anything, time kind of screws them up. They become damaged or mutated thanks to environmental factors and the aging process and one day, they lose their incredible healing abilities altogether.

The good news is, science has finally tapped into the potential of stem cell research and, in doing so, scientists have found a solution for all that wasted power: babies. Yes, babies are disgusting blobs that poop, eat, and slobber their parents to an early grave, but those little devils also just happen to have a whole army of brand new stem cells still in their original packaging. The key is to get them before they sell out. (Im starting to equate body parts with consumerism and its getting creepy so Ill stop now.)

Placenta blood, placenta tissue, and cord blood are three sources of stem cells doctors are urging new parents to consider saving after the mom gives birth. They provide a range of cool benefits from treating certain forms of cancer to helping people heal from spinal cord injuries and they can be cryogenically frozen to help a body out whenever it needs some extra healing power. And yes, some people do eat them. Google it, there are recipes.

But while the placenta party has been raging for a while now, theres a new method of extracting stem cells that can be done all the way up into a persons teen years, and all it takes is a quick trip to the dentist. Tooth banking has become the latest way people are choosing to cryogenically secure their gene sequence.

In 2013, Songtao Shi, a dentist, was researching regenerative dentistry in a lab when Shi witnessed something extraordinary. He discovered that when you get a cavity, the dentin the inner, hard layer of your tooth that protects the nerve and pulp from exposure builds up. Basically, your tooth tries to protect itself by making more organic matter.

This led Shi to conclude that stem cells did, in fact, exist in teeth. A bit more study found that while stem cells in adult molars were able to create more dentin which is great if you want to re-grow lost teeth instead of paying a fortune for an implant baby teeth, or SHED cells (stem cells from human exfoliated deciduous teeth) contained a whole different set of code.

While cord blood and placenta tissue contain Hematopoietic stem cells which have been used for decades to treat over 80 different diseases, SHED cells contain mesenchymal stem cells which differentiate into nerve cells as well as bone, cartilage, muscle, and fat. Cord blood contains mesenchymal stem cells too, but according to Shis research, SHED cells were able to create something unusual, dentin osteogenic material a material thats not quite dentin, not quite bone but full of possibilities like the ability to reconstruct bone.

Extracting dental stem cells is a complicated and sensitive process. First, the soft tissue has to be extracted, then it has to be disinfected (spoiler alert: your mouth is a cesspool of germs). Scientists then drill through the enamel and dentin to get to the pulp of the tooth where all the stem cells like to hide out. They take the pulp out, digest it with an enzyme, and culture the cells.

Its a lot of work, but the payoff is huge. Even tiny bits of dental pulp can carry hundreds of millions of stem cells.

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Why Tooth Banking Might Just Be The Next Wave In Stem Cell Research - UPROXX

Stem Cell Research Experts Meet for Cellular Therapies Conference – KDLT News

By Stell Cell Research

SIOUX FALLS, S.D. Some of the greatest minds in stem cell research came together in Sioux Falls today. One of them is German Doctor Eckhard Alt, for the Cellular Therapies Conference at Sanford Health.

Alt has been working in stem cell research for 15 years focusing on using the healing power of stem cells from the patients own body. He says the cells can be used for common ailments like chronic back pain or knee arthritis and because stem cells are produced naturally, they often work better than traditional medicine.

If you take the early stem cells, which you find in every organ, you dont need to do artificial modification. You just let nature do what the teaching is and the microenvironment that means the side where you inject the cells will tell the new stem cells hey guys, here is heart, here is muscle, here is kidney And they will do the right job, said Dr. Eckhard Alt.

Alt is no stranger to Sanford, in 2015, he was named the leader of the Sanford project, which aims to find a cure for type one diabetes.

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Stem Cell Research Experts Meet for Cellular Therapies Conference - KDLT News

Republicans Want Trump to Fire NIH Director Who Supports Embryonic Stem Cell Research – LifeNews.com

By Embryonic Stem Cells

Republicans in Congress are urging President Donald Trump to oust the director of the National Institutes of Health because of his support for embryonic stem cell research that involves the destruction of human life.

40 Republicans in the House of Representatives wrote president Trump urging him to get rid of NIH director Francis Collins because of his support for the practice, which is opposed by pro-life organizations.

While pro-life advocates strongly support scientific research, they oppose embryonic stem cell research because the only way to obtain embryonic stem cells is to destroy unique human beings just days after conception. On the other hand, ethical adult stem cell research has produced cures or treatments for well over 100 diseases or medical conditions and involves no destruction of human life. Embryonic stem cell research has still yet to treat a single human being successfully.

Here is more from Politico:

Forty House Republicans are urging President Donald Trump to fire the director of the NIH over his support for embryonic and stem cell research that they say conflicts with Trumps pro-life direction.

The Republican House members, in a letter led by Rep. Jim Banks (R-Ind.), question NIH Director Francis Collins support for embryonic cloning and for stem cell research that involves the destruction of human embryos.

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While we deeply respect Dr. Collins Christian faith and commitment to public service, the stances that Dr. Collins has taken in the past regarding embryonic stem cell research and human cloning are not life-affirming and directly conflict with the pro-life direction of your new presidency, the GOP lawmakers wrote. It is because of this troubling paradox that we ask you to re-consider his leadership role at NIH.

Collins has led the NIH since 2009, when he was unanimously confirmed by the Senate.

It has been unclear whether Trump will keep Collins, who came in at the beginning of the Obama administration, at the helm of the biomedical research institution. But Collins has wide support from both Republicans and Democrats.

In fact, several top Republicans former House Energy and Commerce Chairman Fred Upton, Senate HELP Chairman Lamar Alexander and key health care appropriators such as Sen. Roy Blunt and Rep. Tom Cole asked Trump in December to keep Collins.

But the 40 Republicans argue Collins doesnt share in their partys position on embryonic research. They wrote that Collins stance is particularly disturbing considering that NIHs funding for human embryonic stem cell research increased from $146 million in 2012 to $180 million in 2015.

The Obama administration forced Americans to pay for embryonic stem cell research involving the destruction of human life. National Institutes of Health chief Francis Collins approved taxpayer funding of dozens of lines of embryonic stem cells. The cells can only be obtained by destroying unborn children days after conception at which point human embryos are unique human beings.

Obama issued an executive order overturning the limits President Bush put in place on any new embryonic stem cell research funding. Bush directed federal dollars mostly to adult stem cells that are already helping patients now.

The Family Research Council responded to the Obama administrations move by saying that adult stem cells are already helping diabetes patients.

Of course, when it comes to juvenile (type I) diabetes, adult stem cells have already shown success at treating diabetes patients, the pro-life group noted.

It added, Interestingly, none of the human embryonic stem cell lines approved thus far are from the original group of 21 lines that had been receiving NIH funding, only one (H1one of the original five Thomson lines) has been submitted for approval, with only two other lines from Cellartis supposedly to be submitted for review.

This is surprising given that the vast majority of human embryonic stem cell research has been done with those previous lines, thus forcing most embryonic stem cell researchers to start over on experiments with new lines the group continued.

It also shows that this gold rush is just that, an attempt to grab more money built on embryo destruction, not built on science, FRC concluded.

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Republicans Want Trump to Fire NIH Director Who Supports Embryonic Stem Cell Research - LifeNews.com

ESC-Track: A computer workflow for 4-D segmentation, tracking, lineage tracing and dynamic context analysis of ESCs – BioTechniques.com

By Embryonic Stem Cells

ESC-Track: A computer workflow for 4-D segmentation, tracking, lineage tracing and dynamic context analysis of ESCs

Laura Fernndez-de-Manel1, Covadonga Daz-Daz2, Daniel Jimnez-Carretero1, Miguel Torres2, and Mara C. Montoya1

1Cellomics Unit 2Cardiovascular Developmental Program, Cell & Developmental Biology Area, Centro Nacional de Investigaciones Cardiovasculares CNIC, Madrid, Spain

BioTechniques, Vol. 62, No. 5, May 2017, pp. 215222

Abstract

Embryonic stem cells (ESCs) can be established as permanent cell lines, and their potential to differentiate into adult tissues has led to widespread use for studying the mechanisms and dynamics of stem cell differentiation and exploring strategies for tissue repair. Imaging live ESCs during development is now feasible due to advances in optical imaging and engineering of genetically encoded fluorescent reporters; however, a major limitation is the low spatio-temporal resolution of long-term 3-D imaging required for generational and neighboring reconstructions. Here, we present the ESC-Track (ESC-T) workflow, which includes an automated cell and nuclear segmentation and tracking tool for 4-D (3-D + time) confocal image data sets as well as a manual editing tool for visual inspection and error correction. ESC-T automatically identifies cell divisions and membrane contacts for lineage tree and neighborhood reconstruction and computes quantitative features from individual cell entities, enabling analysis of fluorescence signal dynamics and tracking of cell morphology and motion. We use ESC-T to examine Myc intensity fluctuations in the context of mouse ESC (mESC) lineage and neighborhood relationships. ESC-T is a powerful tool for evaluation of the genealogical and microenvironmental cues that maintain ESC fitness.

Stem cells provide essential functions during embryonic development and tissue regeneration. Mouse embryonic stem cells (mESCs) are derived from pluripotent cells of the early mouse embryo and can be maintained as stable cell lines with a high self-renewal capacity. They provide a versatile in vitro model for understanding differentiation of human tissues, and their study has led to major advances in cell and developmental biology (1,2). A key challenge in the field is to understand the mechanisms involved in guiding stem cell fate (3-5), which have broad applications in biomedicine, from elucidating the causes of cancer to the use of stem cells in regenerative medicine. Thus, the biological properties of ESCs are a matter of great scientific, commercial, and medical interest.

ESC-Track (ESC-T) is a computational tool for automated segmentation and tracking of single mouse embryonic stem cells (mESCs) from live-cell 4-D confocal image data sets. The ESC-T workflow enables the extraction of parameters related to fluorescence signal localization and dynamics, cellular morphology, and cell motion for individual cells in the context of lineage and neighborhood relationships.

Optical imaging advances have led to the emergence of powerful live imaging tools with individual cell resolution in three-dimensional (3-D) space and in time (3-D + time or 4-D) (6,7). Moreover, a new generation of fluorescent proteins and dyes allows biochemical characterization of signaling pathways in intact living cells (8). Tagging by fluorescent proteins enables positional tracking of any given cell over time, which is easily achieved when the population of tagged cells is distributed among non-expressing cells by virtue of lineage or in experimental mosaics, but it becomes challenging when a fluorescent protein label is widely expressed (9). The ability to track and analyze live cells in time-lapse 4-D microscopy images is a matter of intense research (10,11) since visual inspection and analysis are insufficient to extract meaningful insights, making automated tracking and quantitative analysis of cells an absolute requirement. This is such a challenging task that several competitions have been carried out in order to evaluate cell segmentation and tracking algorithms (12,13). Computational tools are essential for extracting quantitative measurements from stem cell populations growing in 3-D physiological conditions and to translate the measurements into biological knowledge, allowing the study of a range of cell behaviors, such as motility, cell division, death, phagocytosis, etc. Most of these methods have been applied to Drosophila (14-18) and zebrafish (19-21) embryogenesis, or plant morphogenesis (22) studies. Of special relevance to the field of stem cell biology is the ability to integrate the cell behavior analysis with information about lineage (parentprogeny) and contextual (neighborhood) cellular relationships (9,11). In the last decade, several generic processing and tracking packages, such as Icy (23), Cell Profiler (24), tTt (25), qTfy (25), or the Fiji plugin TrackMate (26,27) have been reported. Some complex methods have been developed for specific applications, such as MARS (22), ACME (21), EDGE-4-D (17), and RACE (18) for particle (28), nuclear (16,29) or cellular (17,18,20-22) segmentation, and STARRYNITE (29), U-TRACK (28), ALT (22), EDGE-4-D (17), and TGMM (16) for tracking.

Here, we present a computational workflow that allows the automated segmentation and tracking of individual mESCs from live-cell 4-D confocal image data sets based on the combination of membrane and non-homogeneous nuclear signals, allowing lineage and neighborhood reconstruction. The workflow enables the extraction of parameters for fluorescence signal localization and dynamics, cellular morphological characteristics, and motion-related aspects of individual cells in the context of lineage and neighborhood relationships. ESC-T was used to study Myc dynamics in mESC cultures, and it proved to be a very valuable computational tool for stem cell research as it allowed the evaluation of genealogical and microenvironmental cues during mouse ESC culture in an unprecedented manner.

Automatic cell and nuclei segmentation and cell tracking. The proposed pipeline (Figure 1) uses images obtained from ESCs expressing tdTomato and GFP-MYC signals as described in the Supplementary Material. The pre-processing step consists of median filtering combining both nuclear and membrane signals (mycGFP median minus tdTomato median) (Figure 1, Steps 14) and is followed by application of a 2-D watershed segmentation algorithm, rendering 2-D sets (cell portions) (Figure 1, Step 5). Spatiotemporal (3-D + t) association rules based on the overlap of sets are applied to connect sets in 3-D space and time for automatic segmentation and tracking through the following pipeline:

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ESC-Track: A computer workflow for 4-D segmentation, tracking, lineage tracing and dynamic context analysis of ESCs - BioTechniques.com

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