Unethical Stem Cell Therapy for Autism In India? – Discover Magazine (blog)

I just read a concerning paper about an experimental stem cell treatment for children with autism.

The authors are Himanshu Bansal and colleagues of India. The senior author, Prasad S Koka, is the Editor-in-Chief of the Journal of Stem Cells where the paper appeared, which raises questions about whether the manuscript received a thorough peer review. Koka is actually an author on all five of the research papers published in that issue of the journal. But thats a minor issue compared to the content of the paper.

Bansal et al. describe a procedure in which they extracted fluid from the bone marrow of each child. This fluid (bone marrow aspirate) was treated in the laboratory to purify the stem cells within, and then injected into the childs spinal canal. The whole operation took place under general anaesthesia. 10 autistic children aged 4-12 were treated.

I found this pretty shocking. An invasive procedure involving general anaesthesia should only be performed if its medically justified especially in children as young as 4! Bansal et al. provide no scientific explanation for why they thought this treatment was suitable for these patients. They vaguely name immunological and neural dysregulation believed to underlie autism as the target of the cells.

For what its worth, the results showed a slight improvement in autism symptoms after the treatment. However, there was no control group, so placebo effects are likely, and were told that the patients were also given speech therapy, occupational therapy and psychological intervention which might account for the benefits.

So who gave the green light to this project? Well, remarkably, Bansal et al.s paper contains no information about which ethics committee reviewed and approved the study. I dont know about the laws in India, but in the UK or the USA, conducting even the most benign research without the proper ethical approval is serious misconduct. Most journals absolutely wont publish medical research without an ethics statement.

The paper also contains no mention of conflicts of interest another thing that most medical journals require. I believe that financial conflicts of interest are likely to exist in this case because Bansal gives his affiliations as Mother Cell, his own private venture, and RegennMed, who sell various stem cell treatments.

Overall, to say that this paper is ethically questionable is an understatement, and it would have been rejected by any real journal.

This isnt Dr Himanshu Bansals first foray into the amazing world of dodgy stem-cells. He briefly made headlines around the globe last year when he announced his ReAnima project to bring a brain dead woman back to life (with stem cells). Indian authorities eventually blocked his resurrection attempt. Theres some more interesting dirt on Bansal on this forum.

This is also not the worlds first stem cells for autism trial. For example, Duke University launched a $40 million trial in 2014. The treatment in that trial was a blood infusion, so it was pretty non-invasive: no bone marrow, spinal needles, or general anaesthesia. However, critics argue that its pure speculation to think that stem cells would help in autism. Then again, the same could be said about a great many stem cell therapies.

Bansal H, Verma P, Agrawal A, Leon J, Sundell IB, Koka PS. (2016). A Short Study Report on Bone Marrow Aspirate Concentrate Cell Therapy in Ten South Asian Indian Patients with Autism Journal of Stem Cells, 11 (1)

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Unethical Stem Cell Therapy for Autism In India? - Discover Magazine (blog)

Hitachi Chemical Agrees $75M Deal for Caladrius Cell Therapy Manufacturer, PCT – Genetic Engineering & Biotechnology News

Caladrius Biosciences is selling the 80.1% stake it retains in its PCT subsidiary to Hitachi Chemical, which already owns the other 19.9% of the cell therapy manufacturing and development services business. Hitachi Chemical has agreed to pay Caladrius $75 million in cash to acquire PCT outright and potentially another $5 million on the achievement by PCT of certain revenue-based milestones. The transaction is expected to close in May, subject to customary closing conditions and the approval of Caladrius shareholders. If ratified, PCT will continue to provide development and manufacturing services to Caladrius for the latters cell therapeutics programs for a period of 7 years after closing.

PCT has more than 130 employees and operates cGMP compliant facilities in the NY/NJ region and in California. The firms Center for Innovation and Engineering offers process and analytical development, engineering solutions, and consulting services. PCT president, Robert A. Preti, Ph.D., said all PCT customers, including Caladrius, will benefit from integration of the firm into Hitachis global engine. Hitachi Chemical intends to deploy the capital and engineering expertise needed to leverage PCTs own engineering and cell therapy development and manufacturing expertise, thereby accelerating the creation of a global commercial manufacturing enterprise.

Caladrius said it will use funds from the PCT sale to support Phase II development of its lead type 1 diabetes (T1D) candidate CLBS03 to eliminate its $5.5 million in debt and to identify new pipeline candidates. Hitachi Chemicals purchase of our remaining interest in PCT unlocks the value of this asset for our Company both by transforming Caladrius into a well-capitalized pure play therapeutics development company and by eliminating our need to contribute the tens of millions of dollars of future capital investment in PCT needed for it to fully realize its cell therapy commercial manufacturing growth goals, said David J. Mazzo, Ph.D., Caladrius CEO. The transaction provides considerable nondilutive capital to fund the execution of our ongoing Phase II trial while also allowing us to exploit compelling therapeutic prospects.

Hitachi took its initial 19.1% stake in PCT in March 2016 as part of a licensing deal and collaboration for PCTs cell therapy manufacturing technology in Japan and parts of Asia.

Cell therapeutics firm Caladrius is exploiting its T-regulatory cell, CD34, and tumor cell/dendritic cell technologies to develop a pipeline of cell therapy candidates for autoimmune and cardiology indications. Lead candidate CLBS03 is an autologous T-regulatory cell therapy in Phase II development for treating recent-onset T1D. The study is partnered with Sanford Research. CLBS03 has been granted Fast Track and Orphan Drug Designation for the T1D indication by the FDA and Advanced Therapeutic Medicinal Product classification by the EMA. In February, Caladrius won up to $12.2 million in funding from the California Institute for Regenerative Medicine (CIRM) to support the CLBS03 development program.

The firms second pipeline product, CLBS12, is a CD34 cell therapy, which Caladrius says it plans to partner for the indication of critical limb ischemia, in Japan, under the countrys regenerative medicine law.

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Hitachi Chemical Agrees $75M Deal for Caladrius Cell Therapy Manufacturer, PCT - Genetic Engineering & Biotechnology News

3 Women Blinded After Stem Cell Therapy – Newser

Newser

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