Stem Cell Clinic

3 Women Blinded After Stem Cell Therapy – Newser

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3 Women Blinded After Stem Cell Therapy Newser CORRECTS FROM MD ANDERSON HOSPITAL TO MD ANDERSON CANCER CENTER -Senior Clinical Cell Therapy Specialist Megan Raggio prepares stem cells from bone marrow before they are transplanted into sportscaster... (AP Photo/David J. Phillip). Stem Cell Therapy Blinds Three Patients at Florida ClinicMedscape Cutting-edge stem cell therapy proves safe, but will it ever be effective?Science Magazine 3 Women Blinded By Unproven Stem Cell TreatmentsNPR CNN -New Vision -The New England Journal of Medicine -The New England Journal of Medicine all 131 news articles »

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3 Women Blinded After Stem Cell Therapy - Newser

Immune cell may turn heart inflammation into heart failure – Medical News Today

Heart inflammation, or myocarditis, is a disorder usually caused by an infection reaching the heart. Although the condition is rare, it can sometimes lead to dilated cardiomyopathy - a leading cause of heart failure in younger adults. New research helps to explain why this happens in some cases and not others, by examining an immune cell that appears to cause heart failure in mice.

Myocarditis occurs when an infection has reached the heart. During an infection, the body's immune system produces disease-fighting cells - but in heart inflammation, these cells enter the heart and can damage its muscle.

The condition is not often diagnosed; it rarely causes severe symptoms and detecting it requires a heart biopsy - a rather invasive procedure of moderate risk.

In some cases, myocarditis progresses into inflammatory dilated cardiomyopathy (DCMi) - a disorder in which the heart's muscle dilates, weakens, and can no longer properly pump blood. In the United States, DCMi is one of the leading causes of heart failure among younger adults, with a prevalence of between 300 and 400 patients per million U.S. adults.

New research, led by Dr. Daniela Cihakova from the Johns Hopkins University School of Medicine in Baltimore, MD - set out to understand why in some cases the heart heals from the inflammation, while in others it progresses into DCMi.

As the authors of the new paper mention, previous studies have pointed to the role of eosinophils - a specific type of immune cell - in the development of heart disease. As Dr. Cihakova explains, the new research "provide[s] more details about how these immune system cells may lead to deterioration of heart muscle function in mice in a way that lets us draw some parallels to human disease processes."

The findings were published in The Journal of Experimental Medicine.

Dr. Cihakova and colleagues genetically modified a group of mice to have a deficiency of eosinophils. They then induced myocarditis in this group, using a technique called experimental autoimmune myocarditis. In this procedure, mice receive a peptide from their heart muscle cells, which makes the body's immune system attack the heart.

The researchers also induced myocarditis in another group of normal mice, with a healthy level of eosinophils. After 21 days, the scientists measured the inflammation in the hearts of both groups of mice.

They also analyzed the hearts for fibrosis or scar tissue - both signs of dying heart muscles in mammals. Scar tissue is also present in cases of DCMi.

The scientists found similarly acute inflammation in both groups.

However, when the scientists examined the groups for signs of heart failure, they found drastic differences between the eosinophil-deficient group and the normal group.

The mice with normal levels of eosinophils went on to develop heart failure, whereas the mice with eosinophil deficiency displayed no signs of heart malfunction.

The team also found scar tissue in both groups to a similar degree. However, the normal mice had DCMi, while the eosinophil-deficient ones were not affected.

To see if they could replicate their findings, the team designed an additional experiment in which they genetically modified mice to have an excess of an eosinophil-producing protein called IL5.

The IL5-excessive mice developed more inflammation and more scar tissue in the heart's upper chambers (or atria) compared with normal mice.

Mice with excessive IL5 protein also had more heart-infiltrating cells. As much as 60 percent of these cells were eosinophils in the IL5-excessive mice, compared with only 3 percent in the normal mice.

Additionally, the researchers examined the mice's hearts 45 days after the experiment and found severe DCMi in the mice with too much IL5 protein.

Finally, to account for the possibility that it is the IL5 protein and not the eosinophils that drive DCMi development, the team genetically modified eosinophil-deficient mice to have an excess of the protein.

The researchers found no reduction in the heart function of these IL5-excessive, eosinophil-deficient mice, compared with normal mice. This confirms that it is the immune cells, not the protein, that causes DCMi.

In an attempt to understand exactly how eosinophils are responsible for DCMi, the researchers investigated further and managed to isolate a protein called IL4, which is produced by eosinophils.

Using yet another mouse model, Dr. Cihakova and team established that it is indeed the IL4 that facilitates the development of DCMi, and which is triggered by eosinophils.

"The take-home message is that inflammation severity does not necessarily determine long-term disease progression, but specific infiltrating cell types - eosinophils, in this case - do."

Dr. Daniela Cihakova

The study's senior author points out that their study is the first one to investigate the role of eosinophils in the onset of heart inflammation, and in its development from inflammation to DCMi.

Nicola Diny, a Ph.D. student in the Bloomberg School of Public Health and the study's first author, also comments on the findings:

"Our studies show that the presence of eosinophils in the heart makes mice more likely to get DCMi following myocarditis. And if there are a lot of eosinophils, the mice develop even more severe heart failure," Diny says. "It will be important to test if the same is true in patients. That way, we may be able to intervene early and prevent DCMi."

The researchers hope that their study will help to develop IL4-targeting medicines that could one day treat people with myocarditis, thus potentially halting its progression into DCMi.

Learn how marijuana use may temporarily weaken heart muscle.

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Immune cell may turn heart inflammation into heart failure - Medical News Today

Stressed out by politics? It could be making your body age faster, too – Quartz

The globe is like one big biological cell, each part intricately interdependent. This is true not just of our physical world but for our social world, too: Water, natural resources, pollution, economies, and politics are more interconnected than ever, but our emotional lives are also intertwined with these factors.

Primates like us Homo sapiens have mirror neurons, meaning that our brain responds to seeing other peoples actions as though they were happening to us. We feel peoples joy, but also their pain. In this way, emotions are contagious. A smile at a stranger has an effect on their emotional state. Interacting with close ones can bring your nervous system in synchrony with theirs. Mothers pass on feelings of threat or of calmness to their babies, and this is reflected in the babies nervous system stress arousal levels.

What does this say for our microscopic cells reactions to the worlds current state of affairs? We are witnesses and thus we vicariously experience local and global events. Innocent black men are being harmed by armed police at three times the rate than whites. The horror and pain felt by families trapped in Aleppo, Syria. The shock waves echoing around the world as people see the personal impact of the US president Donald Trumps immigration ban. The uncertainties of whether millions will lose health care coverage.

Our cells are listening to it all. And theyre not liking what theyre hearing.

For over a decade, we and other researchers have been studying a system in our cells that controls one of the ways we age: telomeres. These structures act as protective caps at the ends of chromosomes and shield our genes from damagekind of like the plastic tips at the ends of shoelaces. When telomeres are long, the cell can replenish itself indefinitely, but when they shorten too much, the cell dies. The more telomeres shorten as we age, the less cells can go on dividing and replenishing our tissues, and the more vulnerable we are to the vast range of burdensome diseases of aging. And the effects are not saved up just for the elderlyeven young people with short telomeres are more likely to catch the common cold.

But telomeres dont just shrink as the years passtheyre also affected by stress levels. Unlike the more sturdy genes inside the chromosomes, the tips of our DNA are sensitive to their surrounding environment. Under extreme and chronic psychological stress, they shorten more quickly than they should for ones age. Social factors are associated with the length and strength of our telomeres, such as whether we are in a long-term marriage, the quality of our social relationships, the quality of our neighborhoods, and how much education we received. Discrimination, bullying, and exposure to violence also shorten our telomeres. In short, feeling threatened trumps telomeres.

A recent APA poll showed that around 60% of Americans are stressed out by our political climate. We are now in a period where social culture is darkening with toxic stress. By the very definition of stresssituations that cause loss of control, loss of predictability, and threat to ones sense of self or physical selfthe majority of Americans are under tremendous strain. A recent APA poll showed that around 60% of Americans are stressed out by our political climate. Then there are the post-Brexit shockwaves still rippling through Britain, the fear of far-right rationalists winning elections all over mainland Europe, and the recent impeachment of heads of state in Asia and South America. This only compounds when you consider the precarious conditions in which the roughly 20 million global refugees are currently living. Its hard for our minds to comprehend this scale of human suffering. We are absorbing social and political tumult on top of the usual stressors from work, relationships, and financial strain; ones we were already intimate with, but yet never seem to master.

And its not just your own health youre potentially harming. Telomere science suggests that expectant parents who have severely shortened telomeres can pass them on to their offspring, independent of classic genetics. A parents telomeres might be very short from the wear and tear of decades of chronic stress and poor lifestyle. The next generation could start off with a little less ability for cell replenishment, which means they could be that much closer to developing aging diseases from their first day of life.

The good news is that there are many things we can do to protect our telomeres. These include the usual suspectswhat we eat, how well we sleep, how active we arebut also, more relevant to today, how we respond to stressful situations.

We can only thrive if we do this together. Because of the invisible but pervasive connections between us that science doesnt yet fully understandincluding the mirror-neuron effect and well-documented social-contagion effectsit is truly up to all of us to help control global social stress levels. This goes way beyond political parties to focusing on the fundamental values that most of us share through our common humanity and same basic needs. We can help set the emotional tone for our own lives, relationships, families, and workplaces. Rememberour emotional state is contagious.

Meanwhile, our telomeres are listening. We unknowingly transmit negative emotions inward to our cells, and outward to those around us. Caring for ourselves and our communities better sets positive-feedback cycles between our emotional well-being and our cell renewal.

So think of your telomeres as you react to whatever news pops up todayand every new day as 2017 unfolds.

Elissa and Elizabeth are the co-authors of the New York Times best seller The Telomere Effect: A Revolutionary Approach to Living Younger, Healthier, Longer (Grand Central Publishing). Learn how to write for Quartz Ideas. We welcome your comments at ideas@qz.com.

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Stressed out by politics? It could be making your body age faster, too - Quartz

Cell Medica raises 60M to push cancer therapies into clinic – FierceBiotech

Cell Medica has raised 60 million ($74 million) to expand its clinical pipeline of cancer cellular immunotherapies. The latest fundraising round, which was again backed by heavyweights of the British biotech investment scene, will equip Cell Medica to move new assets into the clinic while wrapping up a phase 2 of its lead candidate.

Touchstone Innovationsthe company formerly known as Imperial Innovationsparticipated in the Series C alongside Neil Woodfords funds and those managed by his former employer, Invesco Perpetual. Those three organizations also drove Cell Medica to a 50 million Series B round late in 2014.

Since then, Cell Medica has begun treating patients with advanced lymphomas associated with the Epstein Barr virus (EBV) with its lead candidate CMD-003also known as baltaleucel-Tin a phase 2 trial, and expanded its technology base through the acquisition of Delenex Therapeutics and collaborations with Baylor College of Medicine and University College London.

The Series C is intended to enable Cell Medica to build on this platform by diversifying its pipeline.

With the strong support of our key shareholders, Cell Medica will implement the next phase of our development programme, bringing a new generation of cell-based immunotherapy products into phase 1 clinical trials as well as completing our phase 2 program for baltaleucel-T, Cell Medica CEO Gregg Sando said in a statement.

Lead candidate CMD-003 is made up of autologous EBV-specific T cells that are extracted from a patients blood before being activated and expanded. Cell Medica thinks the approach can treat advanced lymphomas with minimal side effects.

Cell Medica developed CMD-003 with Baylor College of Medicine and it has since returned to the same source in search of other pipeline prospects. Last year, Cell Medica struck and then expanded an agreement with Baylor to apply CAR technology to natural killer T cells. In between forming and expanding the Baylor deal, Cell Medica bought Swiss biotech Delenex. The takeover gave Cell Medica a targeting system for the therapies it had recently begun working on with Baylor

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Cell Medica raises 60M to push cancer therapies into clinic - FierceBiotech

In the Coming Decade, Off-the-Shelf Cell Therapy will Become a Reality – Labiotech.eu (blog)

David Sourdive, co-founder of Cellectis, discusses his pioneering work developing off-the-shelf CAR-T for cancer and the future directions of cell therapy.

Last week I had the opportunity to attend the World ADOPT Summit and hear from some of the world leaders in cell therapy. There I met David Sourdive, co-founder and VP of Cellectis, a French company that is leading the development of the first off-the-shelf CAR-T therapy.

CAR-T therapy consists in the infusion of T-cells engineered to better identify and kill cancer cells. The most advanced approaches, which could be approved as soon as by the end of this year, use an autologous approach by engineering cells from the own patient.Cellectis is taking the technology a step further and developing an allogeneic CAR-T therapy that uses cells from healthy donors instead.

The company uses TALEN gene editing to develop off-the-shelf products that could make this miracle cancer therapy faster, cheaper and accessible to a wider patient population. Its first therapy, UCART19, now licensed to Servier and Pfizer, has shown striking results in two babies with leukemia. A second one, UCART123, recently received approval from the FDA to start clinical trials.

With his company positioned at the forefront of innovation in cell therapy, I decided to ask David Sourdive how he thinks new technologies will change the scene.

Cell therapy is now transitioning from the world of grafts, where it has been confined for decades, to the world of products. This happened with antibodies. People used to give their blood and antibodies. Then it became possible to manufacture antibodies from cells in an industrial setting, and then it became a product. I think that were going in that direction with cell therapy.

In the coming decade, off-the-shelf cell therapy will become a reality. That is a revolution and is going to change a lot of things. We will need to establish standards and regulations.Cells usually have not been regarded as products, so its a big leap. We have to discuss with regulators how to define the products.

The immune system is going to start being tweaked like it has never been and we will be able to take advantage of it to address very difficult diseases. For example, solid tumors.We think UCARTs can also target solid tumors. To that end, we work with two pharma partners that have strong capability to tackle these complicated tumors.

We are the first ones to do [allogeneic CAR-Ts] and theres no precedent. We have to invent everything. We have to figure out all the possibilities, all the solutions, and theres no real way to predict how things are going to behave in patients because historically, the one kind of cell nobody has ever used is an allogeneic unmatched situation is T-cells, by definition.

Its very exciting because every week we have to do something for the first time, its challenging.I think this year is the year when we will know better how allogeneic products behave in patients.

We have shown that gene editing can really be transformative in the CAR-T space. With gene editing, you can make the cells overcome the defense mechanisms of tumors. You can, for example, knock out genes such as PD1 so that CAR T-cells become capable of killing PDL1-bearing tumors.

Tumors that succeed in the body are tumors that have found a way to evade the immune system.You need to put additional features to empower the T-cells to do what normal T-cells fail to do. People will realize the transformative power of gene editing. We think it will take over the industry.

I think globally, gene editing is going to be a strong power because we are going to be able to tweak cells like weve never done before.We will be able to program cells to deliver a treatment locally. This is happening. Its not futuristic. Its now.

This is definitely going to be an exciting year, with the first CAR-T therapies approaching market approval and the first results from allogeneic CAR-Ts due soon. Keep tuned for the latest updates!

Images from Tyler Olson /Shutterstock; Cellectis;Fascinadora, ImageFlow /Shutterstock

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In the Coming Decade, Off-the-Shelf Cell Therapy will Become a Reality - Labiotech.eu (blog)