Yearly Archives: 2017


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Access Denied: Stem Cell Therapy Shows Some Promise in Refractory Angina, but Patients Can’t Get It – TCTMD

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NEW ORLEANS, LADespite new data showing that stem cell therapy has the potential to improve exercise time and reduce mortality in patients with refractory angina, researchers said at the Society for Cardiovascular Angiography and Interventions (SCAI) 2017 Scientific Sessions last week that the option is all but dead due to withdrawal of financial support, resulting in patients being denied access to a promising treatment.

Presenting a summation of all the data that have been collected over the last decade on the use of autologous CD34+ cells to treat patients with class III or IV angina despite optimal medical therapy, Thomas Povsic, MD, PhD (Duke Clinical Research Institute, Chapel Hill, NC), said this group of patients is in dire need of new treatment options, and maintained that it is imperative to explore methods to bring this therapy to patients.

He and colleagues conducted a meta-analysis from the only three trials of CD34+ therapy in refractory angina patients: a phase I study (n = 24); ACT-34 CMI and its 24-month extension study (n = 168); and the RENEW study (n = 112). All three were randomized, double-blind, placebo-controlled trials. However, RENEW was terminated early by the sponsor due to financial reasons.

Taken together, the trials showed that among the 187 patients who received the therapy, total exercise time improved by 90.5 seconds at 12 months compared with an improvement of just 39.5 seconds in those who received a placebo.

Additionally, patients who received CD34+ treatment had more than a fourfold lower rate of mortality by 24 months (2.6% vs 11.8%; P = 0.003) and fewer instances of MACE (29.8% vs 40.0%; P = 0.08).

A Cloudy Future

Povsic said the CD34+ trials are extremely expensive to run, resulting in the only sponsor, Baxter Healthcare, divesting itself of all further research in this area.

I personally believe that this therapy has more data associated with it for efficacy and safety than any other cell therapy thats been investigated in the cardiovascular disease space, he observed. The passage of the 21st Century Cures Act may hold some hope for the future, Povsic added, since it allows for a therapy that fulfills a specific medical need to undergo expedited approval.

Its challenging because this patient population has no options, Povsics co-author Timothy Henry, MD (Cedars-Sinai Heart Institute, Los Angeles, CA), said in a press briefing prior to the presentation. This is by far the strongest data for any therapy for refractory angina. Its also the . . . strongest data for cell therapy, and its a shame that its not available to patients.

Henry added that hes hopeful the data from the meta-analysis may be well received by the US Food and Drug Administration.

Povsic noted that although other companies have expressed interest in the therapy, its future is cloudy. Referencing the termination of RENEW for financial reasons, he added that it shows the ramifications that early cessation of a clinical trial can have, because its truly a disservice to the patients that were enrolled in the trial, the investigators that invested time, and the fact that this therapy . . . seemed so close to the finish line, but [now] the path forward is unclear.

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Access Denied: Stem Cell Therapy Shows Some Promise in Refractory Angina, but Patients Can't Get It - TCTMD

Caution urged in using PRP or stem cells to treat young athletes’ injuries – Medical Xpress

By Stem Cell Treatment

May 19, 2017

Physicians, parents and coaches should be cautious when considering treating injured young athletes with platelet rich plasma (PRP), stem cells or other types of regenerative medicine, says a nationally recognized sports medicine clinician and researcher at the University of Miami Miller School of Medicine and UHealth Sports Medicine Institute.

"While regenerative medicine appears to have promise in many areas of medicine, little is known about the safety or effectiveness of these treatments for bone, cartilage, ligament or muscle tissue injuries in children and adolescents," said Thomas Best, M.D., Ph.D., professor of orthopedics, family medicine, biomedical engineering and kinesiology, and team physician for University of Miami athletics and the Miami Marlins. "Everyone wants a young athlete to get back to sports as quickly as possible, but it is important to look first at treatments that have been shown to be effective, before considering unproven options."

Best was the lead author of a new collaborative study, "Not Missing the Future: A Call to Action for Investigating the Role of Regenerative Medicine Therapies in Pediatric/Adolescent Sports Injuries," published May 15 in the American College of Sports Medicine's Current Sports Medicine Reports.

"Evidence from laboratory and veterinary research suggests that mesenchymal stem cells (MSC) may provide an alternative treatment option for conditions that affect muscle, tendons, ligaments, and cartilage," said the authors. "This evidence, however, is based largely on studies in adults and it remains unknown whether these results will be duplicated in our younger populations."

Young athletes are vulnerable to a wide range of injuries, including overuse of arm, shoulder and leg muscles, ligaments and joints in sports like baseball, tennis, soccer and golf, said Best, who is past president of the American College of Sports Medicine (ACSM). "Unregulated clinics may sound attractive to parents and youngsters seeking aggressive regenerative therapy," Best said. "But far more scientific research is necessary to determine if those treatments are helpful in overcoming sports injuries and, more importantly, without serious short- or long-term side effects."

The new ACSM study grew from an August 2016 meeting of sport medicine clinicians, researchers, and a bioethicist who felt that a call to action was urgently needed to understand the current evidence, risks and rewards, and future directions of research and clinical practice for regenerative medicine therapies in youth sports. The meeting was supported by the National Youth Sports Health and Safety Institute, a partnership between the American College of Sports Medicine and SanfordHealth, a Midwest HMO.

The collaborative study included a seven-point call to action:

1. Exercise caution in treating youth with cell-based therapies as research continues.

2. Improve regulatory oversight of these emerging therapies.

3. Expand governmental and private research funding.

4. Create a system of patient registries to gather treatment and outcomes data.

5. Develop a multiyear policy and outreach agenda to increase public awareness.

6. Build a multidisciplinary consortium to gather data and promote systematic regulation.

7. Develop and pursue a clear collective impact agenda to address the "hype" surrounding regenerative medicine.

Reflecting on the evidence, the study's authors wrote, "Despite the media attention and perceived benefits of these therapies, there are still limited data as to efficacy and long-term safety. The involvement of clinicians, scientists and ethicists is essential in ourquest for the truth."

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Caution urged in using PRP or stem cells to treat young athletes' injuries - Medical Xpress

PIO doctor to open application of stem cell research in Nitte … – Times of India

By Stell Cell Research

MANGALURU: UK-based orthopaedic surgeon, Dr Anand A Shetty will start a clinical application of stem cell research in the city along with Nitte University. This will help in curing cancer and other related ailments.

Dr Shetty, who hails from Asode near Koteshwara in Udupi district, was honoured with the 'Outstanding Clinical Excellence' award by the UK's House of Lords this year. Dr Shetty is winner of a host of awards including the prestigious Hunterian Surgical Medal and Hunterian Professorship for 2017 awarded by the Royal College of Surgeons of England for his research on stem cells in particular cartilage repair. Only four Indians have received this award so far.

A knee surgeon and director of stem cell research at Canterbury Christ Church University, Dr Shetty's main interest lies in stem cell research, cartilage transplant, accelerated bone healing, and robotics in minimally invasive surgery.

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PIO doctor to open application of stem cell research in Nitte ... - Times of India

Cancer therapy may work in unexpected way, study finds – Science Daily

By Stem Cell Medical Center

Antibodies to the proteins PD-1 and PD-L1 have been shown to fight cancer by unleashing the body's T cells, a type of immune cell. Now, researchers at the Stanford University School of Medicine have shown that the therapy also fights cancer in a completely different way, by prompting immune cells called macrophages to engulf and devour cancer cells.

The finding may have important implications for improving and expanding the use of this cancer treatment, the researchers said.

A study describing the work, which was done in mice, published online May 17 in Nature. The senior author is Irving Weissman, MD, professor of pathology and of developmental biology. The lead author is graduate student Sydney Gordon.

PD-1 is a cell receptor that plays an important role in protecting the body from an overactive immune system. T cells, which are immune cells that learn to detect and destroy damaged or diseased cells, can at times mistakenly attack healthy cells, producing autoimmune disorders like lupus or multiple sclerosis. PD-1 is what's called an "immune checkpoint," a protein receptor that tamps down highly active T cells so that they are less likely to attack healthy tissue.

How cancer hijacks PD-1

About 10 years ago, researchers discovered that cancer cells learn to use this immune safeguard for their own purposes. Tumor cells crank up the production of PD-L1 proteins, which are detected by the PD-1 receptor, inhibiting T cells from attacking the tumors. In effect, the proteins are a "don't kill me" signal to the immune system, the Stanford researchers said. Cancer patients are now being treated with antibodies that block the PD-1 receptor or latch onto its binding partner, PD-L1, to turn off this "don't kill me" signal and enable the T cells' attack.

"Using antibodies to PD-1 or PD-L1 is one of the major advances in cancer immunotherapy," said Weissman, who is also the Virginia and D.K. Ludwig Professor for Clinical Investigation in Cancer Research, director of the Stanford Institute for Stem Cell Biology and Regenerative Medicine and director of the Ludwig Center for Cancer Stem Cell Research and Medicine at Stanford. "While most investigators accept the idea that anti-PD-1 and PD-L1 antibodies work by taking the brakes off of the T-cell attack on cancer cells, we have shown that there is a second mechanism that is also involved."

What Weissman and his colleagues discovered is that PD-1 activation also inhibits the anti-cancer activity of other immune cells called macrophages. "Macrophages that infiltrate tumors are induced to create the PD-1 receptor on their surface, and when PD-1 or PD-L1 is blocked with antibodies, it prompts those macrophage cells to attack the cancer," Gordon said.

Similar to anti-CD47 antibody

This mechanism is similar to that of another antibody studied in the Weissman lab: the antibody that blocks the protein CD47. Weissman and his colleagues showed that using anti-CD47 antibodies prompted macrophages to destroy cancer cells. The approach is now the subject of small clinical trials in human patients.

As it stands, it's unclear to what degree macrophages are responsible for the therapeutic success of the anti-PD-1 and anti-PD-L1 antibodies.

The practical implications of the discovery could be important, the researchers said. "This could lead to novel therapies that are aimed at promoting either the T-cell component of the attack on cancer or promoting the macrophage component," Gordon said.

Another implication is that antibodies to PD-1 or PD-L1 may be more potent and broadly effective than previously thought. "In order for T cells to attack cancer when you take the brakes off with antibodies, you need to start with a population of T cells that have learned to recognize specific cancer cells in the first place," Weissman said. "Macrophage cells are part of the innate immune system, which means they should be able to recognize every kind of cancer in every patient."

Story Source:

Materials provided by Stanford University Medical Center. Original written by Christopher Vaughan. Note: Content may be edited for style and length.

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Cancer therapy may work in unexpected way, study finds - Science Daily

Brain fights West Nile Virus in unexpected way – Medical Xpress

By Uncategorized

May 19, 2017 West Nile virus-infected brain neurons. Credit: Brian Daniels

In a turnabout, a biochemical self-destruct trigger found in many other types of cells appears to guard the lives of brain cells during an infection with West Nile virus.

UW Medicine scientists led research showing that this chemical pathway doesn't have to sacrifice brain cells to destroy the viruses and recruit the body's defenses against infection.

The same chemical pathway can preserve the brain's nerve cells, or neurons, by using an alternative approach to summon protection.

The self-destruct trigger, a protein called RIPK3 (pronounced rip-3), is better known for activating a certain type of cell death during infection or damaging events in other parts of the body. The death of infected cells in this manner is a protective mechanism that helps the body eliminate the infection.

During a West Nile virus infection, however, the activation of RIPK3 in brain cells doesn't cause them to die. That's because its signaling within the central nervous system is not the same as in cell types elsewhere in the body. Its brain-specific role implies that there are central nervous system functions for RIPK3 not observed in other tissues.

"There is something special about neurons, perhaps because they are non-renewable and too important to undergo cell death," said Andrew Oberst, assistant professor of immunology at the University of Washington School of Medicine. He is the senior author of a recent Cell paper on how brain cells ward off West Nile virus.

"RIPK3 acts as part of the milieu of signals that support anti-viral inflammation in the brain," said the lead author of the paper, Brian Daniels, a UW Medicine postdoctoral fellow in immunology.

RIPK3 responds to the presence of West Nile virus in the brain by placing an order for chemokines, the researchers observed.

Daniels explained that these chemicals underlie a successful ousting of West Nile virus. Chemokines attract an influx of infection-fighting white blood cells.

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These efforts contribute to the clearance of the virus from the brain, but not by directly stopping replacement virus from reproducing within brain cells. Instead, the brain tissue undergoes a kind of inflammation that restricts the West Nile virus infection.

In a different cell type, such as a fibroblast, the entry of a West Nile virus would result in the cell initiating its own demise.

Their findings, the researchers noted, suggest that additional care might need to be taken in developing and testing drugs against RIPK3 to treat neurodegenerative disorders, brain damage from stroke or injury, and autoimmune diseases of the nervous system such as multiple sclerosis. Too much interference with RIPK3 in the brain could make it prone to certain viral infections.

Yueh-Ming Loo is a UW research assistant professor of immunology and another key scientist on the study. Like Oberst, she is from the UW Center for Innate Immunity and Immune Disease. She's interested in why certain pathogens like West Nile virus gravitate toward and invade the central nervous system in some people and animals, but not in others.

Not everyone infected with the West Nile virus develops neurological disease. Some don't even realize they were exposed.

How the body controls brain infections when they do occur, especially with the blood-brain barrier restricting access, is also still poorly understood.

Loo explained that the efforts to subdue the virus in the brain can be a delicate balance. An inappropriately zealous immune response to the pathogen can inadvertently cause long-term neurological problems.

The UW Medicine researchers conducted part of their studies in mice to learn more about the role of RIPK3 in fighting brain infections. They found that mice that were genetically deficient in RIPK3 were highly susceptible to having West Nile virus overtake the brain. These mice displayed a fatal defect in their ability to produce a chemokine-generated neuroinflammation.

The mouse studies and related lab work, the researchers noted, provide evidence that RIPK3 coordinates the infiltration of disease-fighting cells into the central nervous system during West Nile virus infection.

Central nervous system infections are a "profound and growing burden to global public health," the researchers noted in discussing the significance of this scientific question.

Explore further: Researchers moving towards ending threat of West Nile virus

More information: Brian P. Daniels et al, RIPK3 Restricts Viral Pathogenesis via Cell Death-Independent Neuroinflammation, Cell (2017). DOI: 10.1016/j.cell.2017.03.011

Journal reference: Cell

Provided by: University of Washington

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In a turnabout, a biochemical self-destruct trigger found in many other types of cells appears to guard the lives of brain cells during an infection with West Nile virus.

A protein called ZFP568 regulates an important fetal growth hormone called insulin-like growth factor 2 (Igf2), according to a mouse study led by researchers at the National Institutes of Health. The study is one of the first ...

Researchers have discovered that protection from the most severe form of malaria is linked with natural variation in human red blood cell genes. A study from the Wellcome Trust Sanger Institute, the Wellcome Trust Centre ...

Now that we know that egg-making stem cells exist in adult rodents and humans and that these cells can be transplanted into mice with premature ovarian failure to produce offspring, the next question is to assess whether ...

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Brain fights West Nile Virus in unexpected way - Medical Xpress

Stem Cell International – Stem Cell Therapy In Toledo, OH …

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The affiliates of the Stem Cell International are devoted to advancing access and quality care in the area of adult stem cell regenerative medicine in order to help people suffering from a variety of inflammatory and degenerative conditions.

Toledo | Stem Cell International | 419-214-1860

**SCI (Stem Cell International) does not claim to cure any disease or condition stated above. Note: We as a company have invested in state of the art equipment designed to uitilize a combination of growth factors (i.e. adult stem/Stromal cells), allowing us to harness your body's NATURAL restorative properties. We have had training from world renowned specialists on reintroducing your own stem/Stromal cells to activate your body's amazing ability to regenerate, promoting wellness through Regenerative Medicine.

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Anti-CD19 CAR-T cell therapy with defined T-cell subsets for ibrutinib-refractory CLL presentation at iwCLL 2017 – Lymphoma Hub

By Uncategorized

During iwCLL, on 15th May 2017, the Additional Therapies for the Relapsed/Refractory CLL Patient session took place and was co-chaired by Michael Keating (MD Anderson Cancer Center) and Jacqueline Barrientos (The Feinstein Institute for Medical Research).

Anti-CD19 CAR-T Cell Therapy With Defined T-Cell Subsets for Ibrutinib-Refractory CLL was a presentation given during this session by David G. Maloney, MD, PhD, from the Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.

Maloney began by explaining that CAR-T cells produced from distinct T-cell subsets differ in potency. NSG mice bearing Raji tumors (0.5x106 tumor cell inoculation; day 0) were treated with human CAR-T cells manufactured from distinct T-cell subsets (on day 7). CAR-T cells produced from CD8+ TCM cells were highly potent (Sommermeyer et al. 2015).

Engineering selected T-cell subsets could enhance potency and allow delivery of the same cell product in all patients, potentially providing more uniform data on dose response and toxicity.

Pre-clinical studies have established that a defined composition of CD8+ TCM derived and CD4+ derived CAR T-cells provides optimal potency.

The talk then focused on the outline of the phase I/II study of JCAR014 in adult B-cell ALL, NHL, and CLL patients (NCT01865617).

As of 9/1/16, 136 patients had been treated: ALL = 48, NHL = 64, and CLL = 24.

Dose Level

Cells/kg

1

2x105 EGFRt+

2

2x106 EGFRt+

3

2x107 EGFRt+

Lymphodepletion and JCAR014 immunotherapy in high-risk CLL patients:

Treatment

N=24

Lymphodepleting chemotherapy

Cyclophosphamide/fludarabine (Cy/Flu)

21 (87%)

Non-Cy/Flu

3 (13%)

CAR-T cell manufacturing

CD8+ central memory and CD4+

7 (29%)

CD8+ all subsets and CD4+

17 (71%)

CD19 CAR-T cell dose level

DL1 (2x105 EGFRt+ cells/kg)

4 (17%)

DL2 (2x106 EGFRt+ cells/kg)

19 (79%)

DL3 (2x107 EGFRt+ cells/kg)

1 (4%)

Cycles

Single cycle

18 (75%)

Outpatient lymphodepletion and CAR-T cells

18 (75%)

Second cycle for residual disease or relapse

6 (25%)

Maloney then asked can IGH sequencing of the marrow at 4 weeks after JCAR014 identify patients with better outcomes?

Additionally, higher JCAR014 counts in the blood after infusion were associated with better bone marrow response in high-risk CLL. Patients with a higher peak CD3+/EGFRt+ CAR-T cell count in the blood had a reduced hazard of progression or death (HR, 0.56; 95% CI, 0.340.93; P = 0.025).

Maloney concluded that in high-risk CLL patients CD19 CAR-T cells of defined composition (JCAR014) can be administered with an acceptable early toxicity profile. JCAR014 and Cy/Flu lymphodepletion shows a high-level or anti-tumor activity as measured by:

Deep marrow clearance by IGHseq after JCAR014 provides early signs of durable responses with 100% PFS and OS.

Lastly, Maloney presented evidence that ROR1 presents as a novel target for CAR-T cell therapy for CLL, MCL, and solid tumors as it is highly expressed on the surface of malignant B-cells:

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Anti-CD19 CAR-T cell therapy with defined T-cell subsets for ibrutinib-refractory CLL presentation at iwCLL 2017 - Lymphoma Hub

Mouse study looks at safety of stem cell therapy for early menopause – Medical Xpress

By Stem Cell Treatment

May 18, 2017

Now that we know that egg-making stem cells exist in adult rodents and humans and that these cells can be transplanted into mice with premature ovarian failure to produce offspring, the next question is to assess whether the offspring from the egg-making stem cells of a single adult mouse are biologically normal compared to natural births. On May 18 in the journal Molecular Therapy, researchers in China show that female mice with early menopause that receive egg-making stem cells from another mouse are capable of producing healthy pups 2 months later with no observable genetic malfunctions.

"One of our aims is to cure the disease of premature ovarian failure using female germline stem cells," says senior author Ji Wu, a reproductive biologist at Shanghai Jiao Tong University. "Before this treatment can be applied to humans, we need to know the mechanism of female germline stem cell development and safety after transplantation of single mouse female germline stem cells."

Premature ovarian failure, also called early menopause, is the loss of normal ovarian function, and thereby the release of eggs, before the age of 40. The condition is rare, affecting 200,000 women in the United States per year, and is incurable, although it can be treated with hormone supplements. Multiple groups are now looking at whether stimulating tissue regeneration or using stem cell transplants could help.

In the Molecular Therapy study, Wu and her colleagues isolated and characterized female germline stem cells from a single transgenic mouse with cells that show green fluorescence when activated by a blue laser. This allowed the researchers to observe and analyze the development of the transplanted stem cells, which were introduced to the ovaries of other mice using a fine glass needle.

Wu and colleagues found that the transplanted egg-producing stem cells exhibited a homing ability and began to differentiate into early-stage oocytes when they reached the edge of the ovary. The oocytes spent a few weeks maturing and yielded offspring within 2 months. The researchers then demonstrated that the developmental mechanisms of eggs derived from transplanted germline stem cells were similar to that of normal eggs.

"The results are exciting because it's not easy to get offspring from female germline stem cells derived from a single mouse," Wu says.

Wu's lab is also working to establish female egg-producing stem cell lines from scarce ovarian tissues derived from follicular aspiratesthe leftover cells gathered when a clinician searches a patient for oocytesthat are produced and discarded in in vitro fertilization centers worldwide. These aspirates can yield stem cells that differentiate into eggs in the lab, with the potential to be transplanted. The study not only provides a new approach to obtain human female germline stem cells for medical treatment, but also opens several avenues to investigate human oogenesis in vitro.

Explore further: Making sperm from stem cells in a dish

More information: Molecular Therapy, Wu et al.: "Tracing and characterizing the development of transplanted female germline stem cells in vivo" http://www.cell.com/molecular-therapy-family/molecular-therapy/fulltext/S1525-0016(17)30180-6 , DOI: 10.1016/j.ymthe.2017.04.019

Journal reference: Molecular Therapy

Provided by: Cell Press

In a turnabout, a biochemical self-destruct trigger found in many other types of cells appears to guard the lives of brain cells during an infection with West Nile virus.

A protein called ZFP568 regulates an important fetal growth hormone called insulin-like growth factor 2 (Igf2), according to a mouse study led by researchers at the National Institutes of Health. The study is one of the first ...

Researchers have discovered that protection from the most severe form of malaria is linked with natural variation in human red blood cell genes. A study from the Wellcome Trust Sanger Institute, the Wellcome Trust Centre ...

Now that we know that egg-making stem cells exist in adult rodents and humans and that these cells can be transplanted into mice with premature ovarian failure to produce offspring, the next question is to assess whether ...

It's a fat-burning secret anyone interested in bone health should know. For the first time, UNC School of Medicine researchers show that exercising burns the fat found within bone marrow and offers evidence that this process ...

A Cedars-Sinai-led team of investigators has successfully repaired severe limb fractures in laboratory animals with an innovative technique that cues bone to regrow its own tissue. If found to be safe and effective in humans, ...

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Mouse study looks at safety of stem cell therapy for early menopause - Medical Xpress

Stem-cell research a step closer to making blood donation redundant – Cosmos

By Stell Cell Research

Illustration showing blood stem and progenitor cells emerging from hemogenic endothelial cells. The left blue cells are emerging hematapoietic stem and progenitor cells. The red cells are red blood cells.

OReilly Science Art

When human embryonic stem cells lit up the worlds headlines in 1998, it seemed the era of spare organs and tissues would soon follow.

One of the hopes was that these blank slate cells would fill the gap in the fraught supplies of blood banks by generating an endless supply of the different blood-cell types.

Almost two decades on this dream is approaching reality, as two papers in Nature suggest.

One team, led by George Daley of Boston Children's Hospital's Stem Cell Program, have trained human pluripotent stem cells (either derived from embryos or induced from skin cells) to do a fair job of replenishing a mouses blood supply.

The other team, led by Shahin Rafii of Cornell University in New York, began with endothelial cells scraped from the lining of mouse blood vessels. After training, these cells did an even better job of replenishing a mouses blood supply.

Both teams relied on genes introduced by viruses to train the cells. While the introduction of these foreign genes raises concerns as to the long-term safety of such cells, the scientists nevertheless achieved what has till now been impossible: repopulating the blood supply of a mouse.

Its great; were part of the way there, says Andrew Elefanty, who has been attempting the same feat without adding foreign genes at the Murdoch Childrens Research Institute in Melbourne.

Elefanty, like his colleagues, found the key to educating stem cells to become blood-cell precursors was to be a keen and patient student of nature.

Whether mice or humans, developing embryos proceed through a precisely choreographed set of stages, cued by specific signals, to form different tissues. In the case of blood cells, the first cue comes at a primitive stage when a tissue called the mesoderm appears. Under further cues, mesoderm cells give rise to what is known as haemogenic endothelium. After several weeks and more cues, these cells give rise to haematopoietic stem cells (HSC) that ultimately reside in the bone marrow. Just one of these cells is powerful enough to replenish the entire blood supply of a mouse.

Repeating this performance in a culture dish starting from stem cells, however, has been difficult. Over the past two decades, researchers have often gone down the wrong path producing yolk blood cells, for instance, that have little ability to regenerate a whole blood supply.

Just last year, Elefanty and colleagues were able to reproduce the first part of the program, training embryonic stem cells to go from the mesoderm stage to haemogenic endothelium using growth factors added to the medium bathing the cells. So far his group has not been able to take the cells the final step of the way.

Daleys group followed a similar formula but took the cells the final step by pushing them with seven genes introduced by viruses.

Rafiis group began with endothelial cells derived from the lining of mouse blood vessels, made them stem-cell-like by introducing four genes, and then completed their education them by growing them on a layer of cells derived from umbilical cord.

Both produced cells that, like HSC, were able to repopulate the blood supply of a mouse.

Elefanty notes the blood stem cells produced by the two groups are not perfect at matching the capabilities of what real HSC can do. Given both methods insert foreign genes, he also notes there are safety issues to deal with: These are just the first papers; there are still lots of questions to answer.

The goal, as Daley et al acknowledge, remains the derivation of bona fide transgene-free HSCs for applications in research and therapy.

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Stem-cell research a step closer to making blood donation redundant - Cosmos

Pope Francis to Huntington’s patients: You deserve respect and love – Catholic News Agency

By Stell Cell Research

Vatican City, May 18, 2017 / 08:22 am (CNA/EWTN News).- Pope Francis on Thursday offered a message of hope and love to patients with Huntingtons disease, a rare and incurable genetic brain disorder that causes intense suffering.

According to organizers, it was the first time that a pope - or any world leader - had recognized the plight of those with the disease.

In his speech, Francis said the fears and difficulties of people affected by Huntingtons disease have been surrounded with misunderstandings and barriers (for) far too long.

In many cases the sick and their families have experienced the tragedy of shame, isolation and abandonment. Today, however, we are here because we want to say to ourselves and all the world: HIDDEN NO MORE! he said.

This isnt just a slogan, but a commitment we must foster, he continued.

The strength and conviction with which we pronounce these words derive precisely from what Jesus himself taught us, he said, noting that throughout his ministry, Jesus met many sick people; he took on their suffering; he tore down the walls of stigma and of marginalization that prevented so many of them from feeling respected and loved.

Pope Francis spoke during a conference organized at the Vatican hosting people affected by Huntingtons disease, along with their families and caretakers.

Huntingtons disease is characterized by rapid, uncontrollable muscle movement known as chorea. As the disease progresses, it can lead to loss of control over speech and memory, dementia and death. The gene which causes Huntingtons was discovered nearly 25 years ago, but there is still no cure and relatively limited treatment options.

This is especially true for people living in South America, where prevalence of the disease is almost 1,000 times higher than in the rest of the world and often combined with extreme poverty. Because the disease affects families generationally, they are often caught in a cycle of need.

The meeting with Pope Francis was called HDdennomore (pronounced hidden no more) and put on in special solidarity with South America. Two families from Venezuela, two from Colombia, and one girl from Argentina all affected by the disease in different ways were brought to the Vatican by a humanitarian group to meet the Pope.

Also present at the audience were members of the medical and scientific communities who treat the patients with Huntingtons and perform research on how to prevent the disease or slow its progression.

In total, there were some 1,700 people present from 16 different countries. Seated in the front row were 150 people affected by Huntingtons that each got a personal greeting from Pope Francis, who stayed nearly an hour after the audience concluded in order to greet them all individually.

Jesus never let disease keep him from an encounter with people, but instead taught that every human person is precious and has dignity something no person or illness can erase, the Pope explained.

Brothers and sisters, as you see, you are a large and motivated community, he concluded.

May the life of each of you both those who are directly affected by Huntingtons disease and those who work hard every day to support the sick in their pain and difficulty be a living witness to the hope that Christ has given us, he said, noting that even through suffering there passes a path of abundant good, which we can travel together.

Stressing the value of every human life, the Pope emphasized that no outcome can ever justify the use or destruction of embryos for scientific research even for the commendable cause of trying to help those suffering from incurable diseases.

Some branches of research use human embryos, inevitably causing their destruction. But we know that no ends, even noble in themselves such as a predicted utility for science, for other human beings or for society can justify the destruction of human embryos, he said May 18.

Currently there are several ethical problems surrounding the research on Huntingtons disease, including the use of embryonic stem cells taken from embryos made through in vitro fertilization.

The Pope noted this fact during the audience, encouraging scientists to pursue scientific advancement only through means that do not contribute to the throw-away culture which treats human beings as objects for use.

Originally posted here:
Pope Francis to Huntington's patients: You deserve respect and love - Catholic News Agency

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