NBC-5 News anchor Rob Stafford will return to the air Monday, after months of grueling treatment for a rare blood disorder that gave him a harrowing look at "my own mortality."

"I thought we'd get this thing nipped in the bud," said Stafford, 58, who took a leave of absence in March after being diagnosed to be in the early stages of amyloidosis.

Instead, Stafford said, he spent much of the last six months too sick to eat, drink or walk while learning that the road back to health from serious illness is a process.

"You learn that everybody reacts to these drugs differently and there is no guarantee of any outcome," he said.

Amyloidosis occurs when abnormal protein called amyloid is produced in bone marrow and can be deposited in tissues and organs. There are more than 40 types of the disorder that affect the heart, kidneys, liver, spleen, nervous system and digestive tract. Stafford's type known as light chain amyloidosis is rare, according to Dr. Ronald Go, Stafford's hematologist at the Mayo Clinic in Rochester, Minn.

Doctors had planned to remove or "harvest" stem cells from Stafford's own bone marrow and freeze millions of healthy ones. After wiping out the unhealthy cells using chemotherapy, Stafford was to have the healthy stem cells transplanted back into his bone marrow, where they were to reproduce themselves, Go said in March.

Zbigniew Bzdak/Chicago Tribune

Rob Stafford, shown Aug. 24, 2017, is planning to return to the anchor desk at NBC-5 News on Aug. 28 after months battling amyloidosis.

Rob Stafford, shown Aug. 24, 2017, is planning to return to the anchor desk at NBC-5 News on Aug. 28 after months battling amyloidosis. (Zbigniew Bzdak/Chicago Tribune)

But Stafford ran into several complications immediately after the transplant process began that forced him to remain hospitalized for most of March.

"There were times in the hospital when I thought he might not make it," said his wife, Lisa Stafford, who would jog around the Rochester area to alleviate her stress.

"On the runs, I would stop at every church to pray and light a candle."

Stafford returned to his home in Hinsdale in early April, too weak sometimes to walk across the room, drink a milkshake or even stay awake for the news, he said.

In June, test results showed the bone marrow transplant did not work as they had planned, and Stafford would need a new course of action to fight the disease, he said.

It was a terrifying place to be, Stafford said.

"You think, 'What if nothing works?'" he said. "I have clearly thought about my own mortality."

Doctors at Rush University Medical Center started Stafford on a new regimen of weekly chemotherapy, which dramatically improved his health. While he has not yet reached the low amyloid measurements that define remission, doctors are optimistic about his recovery and have cleared Stafford to return to work, he said.

Stafford will return to the 10 p.m. news. Dick Johnson and Patrick Fazio will share anchoring duties with Allison Rosati at 5 p.m. and 6 p.m. until Stafford is ready to return to those newscasts, said Frank Whittaker, station manager and vice president of news for NBC Chicago.

"We are eagerly looking forward to Rob's return on Monday night," Whittaker said in an email. "He has inspired all of us with his courage and determination over the past six months. It will be great to have him back in our newsroom."

Stafford said he remains grateful for the support he and Lisa felt from viewers, who sent him a steady stream of Facebook messages, cards and personal stories.

"It's like running a marathon, and there are all these people along the side cheering you on," Stafford said. "It helps you get through it."

vortiz@chicagotribune.com

Follow this link:
After treatment for serious illness, NBC-5 anchor Rob Stafford returning to air - Chicago Tribune

I didnt want it to affect my job as a BBC correspondent covering religious affairs. But in 2015 I went numb down one side of my body for several weeks. A scan showed multiple lesions, and a specialist confirmed I had relapsing-remitting MS. It felt like a life sentence. My family wasnt surprised wed long known it was a possibility. No tears were shed; my parents are of the stiff-upper-lip generation.

The next drug failed to stop another relapse. I wanted to keep reporting for as long as possible, but last September I finally stepped down frommy job, and my bosses helped me find other options involving less travel and with more predictable hours.

My MS seemed to be moving from relapsing-remitting to secondary progressive, as my body became less able to repair the brain damage caused by each relapse. So, after months of research, I decided to take a risk and have an autologous hematopoietic stem cell transplant (HSCT) a chemotherapy treatment that wipes out then regrows your immune system at a private clinic in Mexico.

HSCT has long been used to treat blood cancers, but its use in autoimmune diseases like MS is still undergoing trials. It destroys the malfunctioning cells thought to be responsible for damaging the myelin sheath, while stem cells harvested from your bone marrow are given back to shorten your time without a working immune system.

HSCT holds the most promise for people having regular MS attacks and its now offered to some MS patients at a few NHS hospitals in England under tight criteria. I didnt qualify, but I met several others who had been helped by it.

Read the original here:
'I approached my 50th birthday unable to balance or speak' - Telegraph.co.uk

Let our news meet your inbox.

From clot-busting drugs to bypass surgery, cardiologists have many options for treating the 700,000-plus Americans who suffer a heart attack each year. But treatment options remain limited for the 5.7 million or so Americans who suffer from heart failure, an often debilitating condition in which damage to the heart (often resulting from a heart attack) compromises its ability to pump blood.

Severe heart damage can pretty much incapacitate people, says Dr. Timothy Henry, director of cardiology at the Cedars-Sinai Medical Center in Los Angeles. You cant climb a flight of stairs, youre fatigued all the time, and youre at risk of sudden cardiac arrest.

Medication is available to treat heart failure, but its no panacea. And some heart failure patients undergo heart transplantation, but it remains an iffy proposition even 50 years after the first human heart was transplanted in 1967.

But soon, there may be another option.

A patch for the heart

Researchers are developing a new technology that would restore normal cardiac function by covering scarred areas with patches made of beating heart cells. The tiny patches would be grown in the lab from patients own cells and then surgically implanted.

The patches are now being tested in mice and pigs at Duke University, the University of Wisconsin and Stanford University. Researchers predict they could be tried in humans within five years with widespread clinical use possibly coming within a decade.

The hope is that patients will be again to live more or less normally again without having to undergo heart transplantation which has some serious downsides. Since donor hearts are in short supply, many patients experiencing heart failure die before one becomes available. And to prevent rejection of the new heart by the immune system, patients who do receive a new heart typically must take high doses of immunosuppressive drugs.

Heart transplants also require bypass machines which entails some risk and complications, says Dr. Timothy Kamp, co-director of the University of Wisconsins Stem Cell and Regenerative Medicine Center and one of the researchers leading the effort to create heart patches. Putting a patch on doesnt require any form of bypass, because the heart can continue to pump as it is.

To create heart patches, doctors first take blood cells and then use genetic engineering techniques to reprogram them into so-called pluripotent stem cells. These jack-of-all-trade cells, in turn, are used to create the various types of cells that make up heart muscle. These include cardiomonocytes, the cells responsible for muscle contraction; fibroblasts, the cells that give heart tissue its structure; and endothelial cells, the cells that line blood vessels.

These cells are then grown over a tiny scaffold that organizes and aligns them in a way that they become functional heart tissue. Since the patches would be made from the patients own blood cells, there would be no chance of rejection by the patients immune system.

Once the patch tissue matures, MRI scans of the scarred region of the patients heart would be used to create a digital template for the new patch, tailoring it to just the right size and shape. A 3D printer would then be used to fabricate the extracellular matrix, the pattern of proteins that surround heart muscle cells.

The fully formed patch would be stitched into place during open-heart surgery, with blood vessel grafts added to link the patch with the patients vascular system.

In some cases, a single patch would be enough. For patients with multiple areas of scarring, multiple patches could be used.

Inserting patches will be delicate business, in part because scarring can render heart walls thin and susceptible to rupture. Researchers anticipate that heart surgeons will look at each case individually and decide whether it makes more sense to cut out the scarred area and cover the defect with a patch or simply affix the patch over the scarred area and hope that, over time, the scars will go away.

Another challenge will be making sure the patches contract and relax in synchrony with the hearts onto which theyre grafted. We think this will happen because cells of the same type like to seek each other out and connect over time, Kamp says. We anticipate that if the patch couples with the native heart tissue, the electrical signals which pass through the heart muscle like a wave and tell it to contract, will drive the new patch to contract at the same rate.

How much would it cost to patch a damaged heart? Researchers put the price tag at about $100,000. Thats far less than the $500,000 or so it costs give a patient a heart transplant. And regardless of the cost, researchers are upbeat about the possibility of having a new way to treat heart failure.

Using these patches to repair the damaged muscle is likely to be very effective, says Henry. Were not quite there yet itll be a few years before you see the first clinical trials. But this technology may really provide a whole new avenue of hope for people with these conditions who badly need new treatment options.

FOLLOW NBC MACH ON TWITTER, FACEBOOK, AND INSTAGRAM.

Let our news meet your inbox.

Original post:
'Beating Heart' Patch Offers New Hope for Desperately Ill Patients - NBCNews.com

The St. Louis-based Washington University School of Medicine is a new clinical study site for Asterias Biotherapeuturics SCiStar clinical trial of AST-OPC1 stem cells in patients with severe cervical spinal cord injuries.

Here are seven takeaways:

1. Patients participating in the trial are categorized into:

AIS-A patients: those who have lost all motor and sensory functions below their injury sites.

AIS-B patients: those who have lost all motor function but have minimal sensory function below their injury site.

2. The stem cells are administered 21 to 42 days post injury and patients are followed by neurological exams and imaging procedures to asses the progress and safety of the trial.

3. W. Zachary Ray, MD, a neurological and orthopedic surgery associate professor at Washington School of Medicine, will lead the site's investigation.

4. Asterias Biotherapeuturics receive FDA clearance to progress its clinical study after phase one of the trial showed five patients with neurologically complete thoracic spinal cord injuries improved motor function after being administered 2 million AST-OPC1 cells.

5. The California Institute for Regenerative Medicine granted Asterias Biotherapeuturics $14.3 million in funding for the clinical trial and other product development activities for AST-OPC1.

6. There are now nine centers across the U.S. participating in the clinical trial.

7. Asterias Biotherapeuturics is a biotechnology company focuses on developing regenerative medicine.

More articles on practice management: Study: Obesity alone shouldn't determine TJR candidates Michelson 20MM Foundation, Center for Intellectual Property Understanding to increase intellectual property awareness: 5 things to know Titan Medical partners with French hospital: 6 highlights

See the article here:
Washington University School of Medicine new spinal cord injury clinical trial site: 7 takeaways - Becker's Orthopedic & Spine

For Immune System Stem Cell Studies, Mice Aren't Enough Science 2.0 Stem cell therapy is all the rage, with suspect companies sprouting up like supplement stores, claiming to be a benefit for this and that. Often all they have are mouse studies and FDA disclaimers on ... The authors found that two varieties of ... and more »

Read the original post:
For Immune System Stem Cell Studies, Mice Aren't Enough - Science 2.0

Soon we will be closing the pool, putting away the patio furniture, and getting jackets out of the closet. As summer comes to an end, our skin is usually in need of some tender loving care and it is a good time to think about repairing your summer skin damage.

Nicole Norris MD Medical Spa, in Peru, Illinois, provides medical-grade professional cosmetic treatments for the skin. We asked them to give their opinion on the top 3 procedures they do to reverse sun damage. Dr. NicoleNorris says Microneedling, Laser Photofacial and Chemical peels are by far the most effective ways to reverse damage from thermal energy safely and effectively.

We all know that UVA and UVB radiation from the sun is stronger in the summer, although it affects our skin all year long. This radiation produces free radicals in our skin and slows our skins ability to repair itself. When damage persists and the skin cannot keep up with the repair backlog, wrinkles, poor texture and skin laxity are formed. Microneedling, also referred to as collagen induction therapy, utilizes a device with multiple small needles which penetrate the skin, stimulating the skin to repair itself. Through these new open channels in the skin, products can also be introduced into the dermis without any barrier. Dr. Norris comments, At our office, we like to put hyaluronic acid, a building block of collagen, into the skin while the microneedling channels are still open. We are also seeing great results with a new product on the market that stimulates brand new skin stem cells. When we are born, a certain number of skin stem cells are activated that we use our whole lives to repair injured skin. These old stem cells get tired out, so activating new ones is really at the forefront of skin rejuvenation . Microneedling is done with topical numbing medicine making it very tolerable. There is some initial redness after the procedure but special make-up can be applied, if necessary, to cover it. Results are gradually seen over time as it takes our bodies about 3 to 6 months to make new collagen. The degree of skin damage determines how many treatments are needed.

When it heats up outside, we are not only exposed to UVA and UVB radiation that directly contributes to older looking skin, but also to heat. Heat stimulates our pigment cells which produce pigment or melanin. These pigment deposits create our tan, but also freckles, and worse yet, age spots. A laser treatment called Photofacial or Intense Pulse Light (IPL) is the most effective way to destroy pigment that has accumulated in the skin. The treatment is quick and feels like a few warm rubber band snaps. There is no downtime. In 7-14 days, you begin to see the pigment slough off. Depending how deep the pigment is deposited, determines how many IPL treatments you will need.

Medical-grade chemical peels are performed to treat unwanted pigment deposits in the skin as well as lines, skin texture and skin laxity. A combination of acids are applied to the skin for a brief period of time in multiple layers. The acids stimulate the skin to repair itself. A medium to deep chemical peel stimulates skin cell turnover which is important in treating aging skin. When we are 20 years old, our skin cell turnover to repair damaged skin is 10 days. Every 10 years, the time it takes to produce new skin goes up by 10 days. This is the physiologic reason that we gradually look older. Chemical peels decrease our time for new skin production resulting in reversal of facial aging states Tamara Smith, RN at Nicole Norris MD Medical Spa. Chemical peels are usually done in a series and are customized to each patient. If done correctly, chemical peels are not painful and you may experience a few days of mild flaking after the procedure.

I think many patients are fearful of these medical-grade skin rejuvenation procedures because of what they see on reality television and what they read on the internet. I encourage anyone interested in improving their appearance, repairing their summer sun damage, or deciding to not age gracefully to try these procedures under the supervision of a qualified physician, advises Dr. Norris. At Nicole Norris MD Medical Spa, they are offering a Flight of Medical Spa Procedures Package. This is a great way to rejuvenate your summer skin while sampling some new procedures. The flight includes 1 Microneedling procedure, 1 IPL Photofacial, and 1 Chemical Peel and is being offered for $300 off through September 30, 2017. Call 815-780-8264 for your appointment today. Mention Medical Spa Flight when you call. Procedures are typically done 3-4 weeks apart.

Originally posted here:
Three Medical Spa Procedures to Reverse Your Summer Skin Damage - LaSalle News Tribune

- Meeting medical and beauty standards, the mask focuses on skincare and rejuvenation with advanced technologies

GUANGZHOU, China, Aug. 23, 2017 /PRNewswire/ -- French traditional medicine manufacturer Santinov has developed and launched its CICABEL mask using stem cells as the main material, through its strong technological power and years of research. The mask focuses on daily skincare based on advanced technologies, and meets medical standards, aiming to become a premium beauty product.

Based on 130 years of French brand heritage

In 1887, the great-grandfather of M.D. Jean-Pierre, the owner of the CICABEL brand, founded medical institutions and laboratories for skin wound healing. In 2007, M.D. Jean-Pierre founded a laboratory specializing in the research on facial skin based on more than 130 years of experience in skin rejuvenation and wound healing, and officially created the CICABEL brand. The CICABEL mask is the first mask product under the brand, and is one of the few beauty products on the market that feature bio-medical technologies.

Bold breakthrough, aiming to create revolutionary skin aesthetics

In terms of ingredients, the CICABEL mask selects purified elements that can provide energy for skin stem cells, to protect and activate the cells and promote the proliferation of skin epidermal cells and the anagenesis of skin fibrosis. This improves facial skin's self-healing and rejuvenation speed, achieving the goal of deep skincare.

Future mask innovator goes global

Facial rejuvenation is becoming the main theme of skincare, which provides a huge development space for CICABEL's proprietary technologies and drives the brand to go global. The brand is expected to set off an upsurge in the high-tech medical skincare sector.

CONTACT: 400-639-1958, rel="nofollow">hantao@1958difo.com

Photo - https://photos.prnasia.com/prnh/20170823/1923965-3-a Photo -https://photos.prnasia.com/prnh/20170823/1923965-3-b

SOURCE CICABEL

Go here to read the rest:
French CICABEL Mask Launched, Changing Traditional Mask Products - Markets Insider

TROY The second annual Buckeye Be The Match will build on its opening year by adding bikes to the event while raising awareness for bloodborne cancers this Saturday.

The Buckeye Be The Match will begin at 8 a.m. Aug. 26, at Treasure Island Park. New this year is a 15-mile and 50-mile bike route in addition to the 5K and 1K Fun Run in the park.

The event added the 15-mile family bike ride north to Piqua and back to Treasure Island as well as a more challenging 50-mile ride throughout the county to expand the use of the nearby bike paths to include cyclists of all levels. Bikers may begin to ride as early as 7:30 a.m. Saturday.

Online registration ends on Thursday, but registration in person will continue through 8 a.m. Saturday at the park. Opening events kick off at 9 a.m. All proceeds benefit the Be The Match organization, which helps build a national registry to find potential donors through a simple cheek swab.

The funding goes to Be The Match, which is dedicated to finding the bone marrow matches or stem cell matches for those with blood born cancers. It is very vital, said city council member Tom Kendall. If you dont want to run or be part of the bike ride, you do have the opportunity to save a life also. They will be taking swabs of those who would like to be put on the registry to be a potential donor for a person in need.

Kendall said Rum River Blend will provide entertainment as well as family-friendly activities through noon. There also will be a ceremony featuring the Be The Hero award, which nominates someone who has helped a survivor during their treatment and will be given out at the event.

Kendalls daughter, Lisa, was diagnosed at 28 with acute myeloid leukemia in 2011. She received a stem cell transplant that saved her life. Shes been a coordinator of the event and advocate for the Be The Match organization since it moved to Troy last year from Columbus.

Kendall said previous the Buckeye Be The Match raised more than $11,000 last year, exceeding its goal of $10,000.

For more information, visit http://www.bethematchfoundation.org.

Event to raise funds and awareness for bone marrow registry

Follow Melanie Yingst on Twitter @Troydailynews

The rest is here:
Buckeye Be The Match set for Saturday - Piqua Daily Call

It sounds like science fiction: with a light zap of electricity, a tiny stamp-like device transforms your skin cells into reservoirs of blood vessels or brain cells, ready to heal you from within.

Recently, a team of medical mavericks at the Ohio State University introduced a device that does just that. The technology, dubbed tissue nanotransfection (TNT), is set to blow up the field of organ regeneration.

When zapped with a light electrical jolt, the device shoots extra bits of DNA code from its nanotube arrays directly into tiny pores in the skin. There, the DNA triggers the cells to shed their identity and reprograms them into other cell types that can be harvested to repair damaged organs.

Remarkably, the effect spreads with time. The rebooted cells release tiny membrane bubbles onto their neighboring skin cells, coaxing them to undergo transformation. Like zombies, but for good.

So far, the device has already been used to generate neurons to protect the brains of mice with experimental stroke. The team also successfully healed the legs of injured mice by turning the skin cells on their hind limbs into a forest of blood vessels.

While still a ways from human use, scientists believe future iterations of the technology could perform a myriad of medical wonders: repairing damaged organs, relieving brain degeneration, or even restoring aged tissue back to a youthful state.

By using our novel nanochip technology, injured or compromised organs can be replaced. We have shown that skin is a fertile land where we can grow the elements of any organ that is declining, says lead author Dr. Chandan Sen, who published the result in Nature Nanotechnology.

In my lab, we have ongoing research trying to understand the mechanism and do even better, adds Dr. L. James Lee, who co-led the study with Sen. So, this is the beginning, more to come.

The Ohio teams research builds on an age-old idea in regenerative medicine: that even aged bodies have the ability to produce and integrate healthy, youthful cellsgiven the right set of cues.

While some controversy remains on whether replacement cells survive in an injured body, scientistsand some rather dubious clinicsare readily exploring the potential of cell-based therapies.

All cells harbor the same set of DNA; whether they turn into heart cells, neurons, or back into stem cells depend on which genes are activated. The gatekeeper of gene expression is a set of specialized proteins. Scientists can stick the DNA code for these proteins into cells, where they hijack its DNA machinery with orders to produce the protein switchesand the cell transforms into another cell type.

The actual process works like this: scientists harvest mature cells from patients, reprogram them into stem cells inside a Petri dish, inject those cells back into the patients and wait for them to develop into the needed cell types.

Its a cumbersome process packed with landmines. Researchers often use viruses to deliver the genetic payload into cells. In some animal studies, this has led to unwanted mutations and cancer. Its also unclear whether the reprogrammed stem cells survive inside the patients. Whether they actually turn into healthy tissue is even more up for debate.

The Ohio teams device tackles many of these problems head on.

Eschewing the need for viruses, the team manufactured a stamp-sized device out of silicon that serves as a reservoir and injector for DNA. Microetched onto each device are arrays of nanochannels that connect to microscopic dents. Scientists can load DNA material into these tiny holding spots, where they sit stably until a ten-millisecond zap shoots them into the recipients tissue.

We based TNT on a bulk transfection, which is often used in the lab to deliver genes into cells, the authors explain. Like its bulk counterpart, the electrical zap opens up tiny, transient pores on the cell membrane, which allows the DNA instructions to get it.

The problem with bulk transfection is that not all genes get into each cell. Some cells may get more than they bargained for and take up more than one copy, which increases the chance of random mutations.

We found that TNT is extremely focused, with each cell receiving ample DNA, the authors say.

The device also skips an intermediary step in cell conversion: rather than turning cells back into stem cells, the team pushed mouse skin cells directly into other mature cell types using different sets of previously-discovered protein factors.

In one early experiment, the team successfully generated neurons from skin cells that seem indistinguishable from their natural counterparts: they shot off electrical pulses and had similar gene expression profiles.

Surprisingly, the team found that even non-zapped cells in the skins deeper layers transformed. Further testing found that the newly reprogrammed neurons released tiny fatty bubbles that contained the molecular instructions for transformation.

When the team harvested these bubbles and injected them into mice subjected to experimental stroke, the bubbles triggered the brain to generate new neurons and repair itself.

We dont know if the bubbles are somehow transforming other brain cell types into neurons, but they do seem to be loaded with molecules that protect the brain, the researchers say.

In an ultimate test of the devices healing potential, the researchers placed it onto the injured hind leg of a handful of mice. Three days prior, their leg arteries had been experimentally severed, whichwhen left untreatedleads to tissue decay.

The team loaded the device with factors that convert skin cells into blood vessel cells. Within a week of conversion, the team watched as new blood vessels sprouted and grew beyond the local treatment area. In the end, TNT-zapped mice had fewer signs of tissue injury and higher leg muscle metabolism compared to non-treated controls.

This is difficult to imagine, but it is achievable, successfully working about 98 percent of the time, says Sen.

A major draw of the device is that its one-touch-and-go.

There are no expensive cell isolation procedures and no finicky lab manipulations. The conversion happens right on the skin, essentially transforming patients bodies into their own prolific bioreactors.

This process only takes less than a second and is non-invasive, and then youre off. The chip does not stay with you, and the reprogramming of the cell starts,says Sen.

Because the converted cells come directly from the patient, theyre in an immune-privileged position, which reduces the chance of rejection.

This means that in the future, if the technology is used to manufacture organs immune suppression is not necessary, says Sen.

While the team plans to test the device in humans as early as next year, Sen acknowledges that theyll likely run into problems.

For one, because the device needs to be in direct contact with tissue, the skin is the only easily-accessible body part to do these conversions. Repairing deeper tissue would require surgery to insert the device into wounded areas. And to many, growing other organ cell types is a pretty creepy thought, especially because the transformation isnt completely localnon-targeted cells are also reprogrammed.

That could be because the body is trying to heal itself, the authors hypothesize. Using the chip on healthy legs didnt sprout new blood vessels, suggesting that the widespread conversion is because of injury, though (for now) there isnt much evidence supporting the idea.

For another, scientists are still working out the specialized factors required to directly convert between cell types. So far, theyve only had limited success.

But Sen and his team are optimistic.

When these things come out for the first time, its basically crossing the chasm from impossible to possible, he says. We have established feasibility.

Image Credit: Researchers demonstrate tissue nanotransfection,courtesy of The Ohio State University Wexner Medical Center.

Read the original:
This Chip Uses Electricity to Reprogram Cells for Healing - Singularity Hub

In 2013, University of Virginia researcher Michael McConnell published research that would forever change how scientists study brain cells.

McConnell and a team of nationwide collaborators discovered a genetic mosaic in the brains neurons, proving that brain cells are not exact replicas of each other, and that each individual neuron contains a slightly different genetic makeup.

McConnell, an assistant professor in the School of Medicines Department of Biochemistry and Molecular Genetics, has been using this new information to investigate how variations in individual neurons impact neuropsychiatric disorders like schizophrenia and epilepsy. With a recent $50,000 grant from the Bow Foundation, McConnell will expand his research to explore the cause of a rare genetic disorder known as GNAO1 so named for the faulty protein-coding gene that is its likely source.

GNAO1 causes seizures, movement disorders and developmental delays. Currently, only 50 people worldwide are known to have the disease. The Bow Foundation seeks to increase awareness so that other probable victims of the disorder can be properly diagnosed and to raise funds for further research and treatment.

UVA Today recently sat down with McConnell to find out more about how GNAO1 fits into his broader research and what his continued work means for all neuropsychiatric disorders.

Q. Can you explain the general goals of your lab?

A. My lab has two general directions. One is brain somatic mosaicism, which is a finding that different neurons in the brain have different genomes from one another. We usually think every cell in a single persons body has the same blueprint for how they develop and what they become. It turns out that blueprint changes a little bit in the neurons from neuron to neuron. So you have slightly different versions of the same blueprint and we want to know what that means.

The second area of our work focuses on a new technology called induced pluripotent stem cells, or iPSCs. The technology permits us to make stem cell from skin cells. We can do this with patients, and use the stem cells to make specific cell types with same genetic mutations that are in the patients. That lets us create and study the persons brain cells in a dish. So now, if that person has a neurological disease, we can in a dish study that persons disease and identify drugs that alter the disease. Its a very personalized medicine approach to that disease.

Q. Does cell-level genomic variety exist in other areas of the body outside the central nervous system?

A. Every cell in your body has mutations of one kind or another, but brain cells are there for your whole life, so the differences have a bigger impact there. A skin cell is gone in a month. An intestinal cell is gone in a week. Any changes in those cells will rarely have an opportunity to cause a problem unless they cause a tumor.

Q. How does your research intersect with the goals of the Bow Foundation?

A. Let me back up to a little bit of history on that. When I got to UVA four years ago, I started talking quite a lot with Howard Goodkin and Mark Beenhakker. Mark is an assistant professor in pharmacology. Howard is a pediatric neurologist and works with children with epilepsy. I had this interest in epilepsy and UVA has a historic and current strength in epilepsy research.

We started talking about how to use iPSCs the technology that we use to study mosaicism to help Howards patients. As we talked about it and I learned more about epilepsy, we quickly realized that there are a substantial number of patients with epilepsy or seizure disorders where we cant do a genetic test to figure out what drug to use on those patients.

Clinical guidance, like Howards expertise, allows him to make a pretty good diagnosis and know what drugs to try first and second and third. But around 30 percent of children that come in with epilepsy never find the drug that works, and theyre in for a lifetime of trial-and-error. We realized that we could use iPSC-derived neurons to test drugs in the dish instead of going through all of the trial-and-error with patients. Thats the bigger project that weve been moving toward.

The Bow Foundation was formed by patient advocates after this rare genetic mutation in GNAO1 was identified. GNAO1 is a subunit of a G protein-coupled receptor; some mutations in this receptor can lead to epilepsy while others lead to movement disorders.

Were still trying to learn about these patients, and the biggest thing the Bow Foundation is doing is trying to address that by creating a patient registry. At the same time, the foundation has provided funds for us to start making and testing iPSCs and launch this approach to personalized medicine for epilepsy.

In the GNAO1 patients, we expect to be able to study their neurons in a dish and understand why they behave differently, why the electrical activity in their brain is different or why they develop differently.

Q. What other more widespread disorders, in addition to schizophrenia and epilepsy, are likely to benefit from your research?

A. Im part of a broader project called the Brain Somatic Mosaicism Network that is conducting research on diseases that span the neuropsychiatric field. Our lab covers schizophrenia, but other nodes within that network are researching autism, bipolar disorder, Tourette syndrome and other psychiatric diseases where the genetic cause is difficult to identify. Thats the underlying theme.

Visit link:
Researcher Seeks to Unravel the Brain's Genetic Tapestry to Tackle Rare Disorder - University of Virginia

Deadly gene mutations removed from human embryos in landmark study, reports The Guardian. Researchers have used a gene-editing technique to repair faults in DNA that can cause an often-fatal heart condition called hypertrophic cardiomyopathy.

This inherited heart condition is caused by a genetic change (mutation) in one or more genes. Babies born with hypertrophic cardiomyopathy have diseased and stiff heart muscles, which can lead to sudden unexpected death in childhood and in young athletes.

In this latest study researchers used a technique called CRISPR-cas9 to target and then remove faulty genes. CRISPR-cas9 acts like a pair of molecular scissors, allowing scientists to cut out certain sections of DNA. The technique has attracted a great deal of excitement in the scientific community since it was released in 2014. But as yet, there have been no practical applications for human health.

The research is at an early stage and cannot legally be used as treatment to help families affected by hypertrophic cardiomyopathy. And none of the modified embryos were implanted in the womb.

While the technique showed a high degree of accuracy, its unclear whether it is safe enough to be developed as a treatment. The sperm used in the study came from just one man with faulty genes, so the study needs to be repeated using cells from other people, to be sure that the findings can be replicated.

Scientists say it is now important for society to start a discussion about the ethical and legal implications of the technology. It is currently against the law to implant genetically altered human embryos to create a pregnancy, although such embryos can be developed for research.

The study was carried out by researchers from Oregon Health and Science University and the Salk Institute for Biological Studies in the US, the Institute for Basic Science and Seoul University in Korea, and BGI-Shenzen and BGI-Quingdao in China. It was funded by Oregon Health and Science University, the Institute for Basic Science, the G. Harold and Leila Y. Mathers Charitable Foundation, the Moxie Foundation and the Leona M. and HarryB. Helmsley Charitable Trust and the Shenzhen Municipal Government of China. The study was published in the peer-reviewed journal Nature.

The Guardian carried a clear and accurate report of the study. While their reports were mostly accurate, ITV News, Sky News and The Independent over-stated the current stage of research, with Sky News and ITV News saying it could eradicate thousands of inherited conditions and the Independent claiming it opens the possibility for inherited diseases to be wiped out entirely. While this may be possible, we dont know whether other inherited diseases might be as easily targeted as this gene mutation.

Finally, the Daily Mail rolls out the arguably tired clich of the technique leading to designer babies, which seems irrelevant at this point. The CRISPR-cas9 technique is only in its infancy and (ethics aside) its simply not possible to use genetic editing to select desirable characteristics - most of which are not the result of one single, identifiable gene. No reputable scientist would attempt such a procedure.

This was a series of experiments carried out in laboratories, to test the effects of the CRISPR-Cas9 technique on human cells and embryos. This type of scientific research helps us understand more about genes and how they can be changed by technology. It doesnt tell us what the effects would be if this was used as a treatment.

Researchers carried out a series of experiments on human cells, using the CRISPR-cas9 technique first on modified skin cells, then on very early embryos, and then on eggs at the point of fertilisation by sperm. They used genetic sequencing and analysis to assess the effects of these different experiments on cells and how they developed, up to five days. They looked specifically to see what proportion of cells carrying faulty mutations could be repaired, whether the process caused other unwanted mutations, and whether the process repaired all cells in an embryo, or just some of them.

They used skin cells (which were modified into stem cells) and sperm from one man, who carried the MYBPC3 mutation in his genome, and donor eggs from women without the genetic mutation. This is the mutation known to cause hypertrophic cardiomyopathy.

Normally in such cases, roughly half the embryos would have the mutation and half would not, as theres a 50-50 chance of the embryo inheriting the male or female version of the gene.

The CRISPR-cas9 technique can be used to select and delete specific genes from a strand of DNA. When this happens, usually the cut ends of the strand join together, but this causes problems so cant be used in the treatment of humans. The scientists created a genetic template of the healthy version of the gene, which they introduced at the same time as using CRISPR-cas9 to cut the mutated gene. They hoped the DNA would repair itself with a healthy version of the gene.

One important problem with changing genetic material is the development of mosaic embryos, where some of the cells have corrected genetic material and others have the original faulty gene. If that happened, doctors would not be able to tell whether or not an embryo was healthy.

The scientists needed to test all the cells in the embryos produced in the experiment, to see whether all cells had the corrected gene or whether the technique had resulted in a mixture. They also did whole genome sequencing on some embryos, to test for unrelated genetic changes that might have been introduced accidentally during the process.

All embryos in the study were destroyed, in line with legislation about genetic research on embryos.

Researchers found that the technique worked on some of the stem cells and embryos, but worked best when used at the point of fertilisation of the egg. There were important differences between the way the repair worked on the stem cells and the egg.

Only 28% of the stem cells were affected by the CRISPR-cas9 technique. Of these, most repaired themselves by joining the ends together, and only 41% were repaired by using a corrected version of the gene.

67% of the embryos exposed to CRISPR-cas9 had only the correct version of the gene higher than the 50% that would have been expected had the technique not been used. 33% of embryos had the mutated version of the gene, either in some or all their cells.

Importantly, the embryos didnt seem to use the template injected into the zygote to carry out the repair, in the way the stem cells did. They used the female version of the healthy gene to carry out the repair, instead.

Of the embryos created using CRISPR-cas9 at the point of fertilisation, 72% had the correct version of the gene in all their cells, and 28% had the mutated version of the gene in all their cells. No embryos were mosaic a mixture of cells with different genomes.

The researchers found no evidence of mutations induced by the technique, when they examined the cells using a variety of techniques. However, they did find some evidence of gene deletions caused by DNA strands splicing (joining) themselves together without repairing the faulty gene.

The researchers say they have demonstrated how human embryos employ a different DNA damage repair system to adult stem cells, which can be used to repair breaks in DNA made using the CRISPR-cas9 gene-editing technique.

They say that targeted gene correction could potentially rescue a substantial portion of mutant human embryos, and increase the numbers available for transfer for couples using pre-implantation diagnosis during IVF treatment.

However, they caution that despite remarkable targeting efficiency, CRISPR-cas9-treated embryos would not currently be suitable for transfer. Genome editing approaches must be further optimised before clinical application can be considered, they say.

Currently, genetically-inherited conditions like hypertrophic cardiomyopathy cannot be cured, only managed to reduce the risk of sudden cardiac death. For couples where one partner carries the mutated gene, the only option to avoid passing it on to their children is pre-implantation genetic diagnosis. This involves using IVF to create embryos, then testing a cell of the embryo to see whether it carries the healthy or mutated version of the gene. Embryos with healthy versions of the gene are then selected for implantation in the womb.

Problems arise if too few or none of the embryos have the correct version of the gene. The researchers suggest their technique could be used to increase the numbers of suitable embryos. However, the research is still at an early stage and has not yet been shown to be safe or effective enough to be considered as a treatment.

The other major factor is ethics and the law. Some people worry that gene editing could lead to designer babies, where couples use the tool to select attributes like hair colour, or even intelligence. At present, gene editing could not do this. Most of our characteristics, especially something as complex as intelligence, are not the result of one single, identifiable gene, so could not be selected in this way. And its likely that, even if gene editing treatments became legally available, they would be restricted to medical conditions.

Designer babies aside, society needs to consider what is acceptable in terms of editing human genetic material in embryos. Some people think that this type of technique is "playing God" or is ethically unacceptable because it involves discarding embryos that carry faulty genes. Others think that its rational to use the scientific techniques we have developed to eliminate causes of suffering, such as inherited diseases.

This research shows that the questions of how we want to legislate for this type of technique are becoming pressing. While the technology is not there yet, it is advancing fast. This research shows just how close we are getting to making genetic editing of human embryos a reality.

Read more from the original source:
Gene editing used to repair diseased genes in embryos - NHS Choices

Vitamin C may prompt faulty stem cells in bone marrow to die off, rather than multiplying to spur blood cancers.

A new study has found that vitamin C may communicate to faulty stem cells within bone marrow that they should mature and perish in a normal manner rather than multiplying to spur blood cancers. This is the insight gleaned from a study spearheaded by NYU Langone Health Perlmutter Cancer Center researchers. Study details were recently published in Cell.

About the Findings

The authors of the study state specific genetic alterations are known to decrease the ability of an enzyme referred to as tet methylcytosine dioxygenase 2 (TET2) to promote stem cell maturation and death in patients who have specific types of leukemia. They determined vitamin C activates TET2 functionality in mice designed to lack the enzyme. It is possible that vitamin C will prove to be a safe and effective treatment for diseases spurred by leukemia stem cells deficient in TET2. It is likely that vitamin C will be used in combination with other targeted therapies.

Study Details

The researchers used genetically altered mice in which TET2 was turned off. These mice endured abnormal stem cell activity. Such changes were reversed when a genetic trick restored TET2 expression. Providing high doses of vitamin C functioned similarly to restoring TET2 functionality on a genetic level. Vitamin C's promotion of DNA demethylation caused stem cells to mature and limited the advancement of leukemia cancer stem cells from humans that were implanted in mice. Vitamin C treatment affected leukemic stem cells similar to damaged DNA. Vitamin C was used in combination with a PARP inhibitor to produce an enhanced effect on such stem cells, sending them from self-renewal to maturity and subsequent death.

TET2 and Cancer

Alterations in the genetic code that decrease TET2 functionality are found in 10% of those who have acute myeloid leukemia (AML). About one-third of patients with a form of preleukemia known as myelodysplastic syndrome and upwards of half of those with chronic myelomonocytic leukemia have such genetic code mutations. These cancers spur anemia, bleeding and infection risk as abnormal stem cells multiply within bone marrow until they block the production of blood cells. Recent tests show about 2.5% of cancer patients living in the United States might develop TET2 alterations. This includes some patients with solid tumors and lymphomas.

About Cell Death Switch

The results of the study center on the relationship between cytosine and TET2. Cytosine is one of the several letters of nucleic acidthat make up genes' DNA code. Each cell type has thesame genes yet each receives unique instructions to turn on only those required in a specific cellular context. Examples of such epigenetic mechanisms include DNA methylation. This is an attachment of a diminutive molecule to cytosine bases to put a halt to the action of a gene containing them. Gene expression within stem cells is fine-tuned when methyl groups are attached and removed. Stem cellexpressions can then mature and multiplyto form muscle, nerve, bone and other types of cells. The bone marrow holds stem cell pools as adulthood is reached until they can become replacement cells. Inpatients with leukemia, signals that typically tell blood stem cells to mature end up malfunctioning. This allows for endless multiplication and a self-renewing rather than the generation of regular white blood cells required to combat infection.

TET2 empowers an alteration in the molecular structure of methyl groups required for their removal from cytosines. Such demethylation activates genes that direct stem cells to mature and commence a countdown to self-destruction as a component of regular turnover. This functions as a means of combating cancer yet it is disrupted in blood cancer patients who have TET2 mutations.

Continue reading here:
Vitamin C May Help Slay Blood Cancer Stem Cells - Anti Aging News

The ABMDR team at the meeting with Archbishop Hovnan Derderian (center) and the Very Rev. Fr. Dajad Yardemian.

LOS ANGELESOn Sunday, August 20, during Holy Mass at St. Leon Cathedral in Burbank, Archbishop Hovnan Derderian, Primate of the Western Diocese, offered special prayers for patients of the Armenian Bone Marrow Donor Registry (ABMDR). In his sermon, the Archbishop praised the life-saving mission of ABMDR, and called on congregants to continue to support its work.

To raise public awareness of the ABMDR mission and encourage grassroots involvement in the organizations activities, the Western Diocese has observed a special Prayer Day in honor of ABMDR patients for the past several years. The Prayer Day is marked at St. Leon Cathedral as well as Armenian churches across Southern California.

In the course of his sermon on August 20, Archbishop Derderian stated that participating in the work of ABMDR is tantamount to praying and accomplishing a Godly mission. The Archbishop pledged the continuous support of the Diocese and appealed to all parishes to embrace the work of ABMDR, by joining its ranks as potential bone marrow stem cell donors, signing up as volunteers, and attending its public-benefit events such as the upcoming Match for Life, the ABMDRs 18th annual Gala, which will be held on Sunday, August 27, in Los Angeles.

The ABMDR team outside St. Leon Cathedral

Archbishop Derderian, who is one of ABMDRs most avid and longtime supporters, exemplifies the type of leadership that works tirelessly for the well-being of our community, said ABMDR president Dr. Frieda Jordan. We are honored and grateful for the Primates ongoing guidance and support.

Following the church service, numerous parishioners had the opportunity to become more familiar with the activities of ABMDR, as a team of Board members and volunteers from the organization answered questions and handed out information about becoming donors.

Subsequently Archbishop Derderian, along with the Very Rev. Fr. Dajad Yardemian, met with the ABMDR team at the Diocese. The discussion centered on ABMDRs most recent achievements as well as its plans for the immediate future. At the conclusion of the meeting, Archbishop Derderian presented scarves from Holy Echmiadzin to all members of the ABMDR team, as tokens of his appreciation.

Established in 1999, ABMDR, a nonprofit organization, helps Armenians and non-Armenians worldwide survive life-threatening blood-related illnesses by recruiting and matching donors to those requiring bone marrow stem cell transplants. To date, the registry has recruited over 29,000 donors in 42 countries across four continents, identified over 4,190 patients, and facilitated 30 bone marrow transplants. For more information, call (323) 663-3609 or visit abmdr.am.

Read more from the original source:
Archbishop Derderian Leads Prayers for ABMDR Patients at Diocese Churches - Asbarez Armenian News

Dr. Alexandre R. Colas is an assistant professor at SBP. Credit: James Short

Researchers from Sanford Burnham Prebys Medical Discovery Institute (SBP), the Cardiovascular Institute at Stanford University and other institutions were surprised to discover that the four genes in the Id family play a crucial role in heart development, telling undifferentiated stem cells to form heart tubes and eventually muscle. While Id genes have long been known for their activity in neurons and blood cells, this is the first time they've been linked to heart development. These findings give scientists a new tool to create large numbers of cardiac cells to regenerate damaged heart tissue. The study was published in the journal Genes & Development.

"It has always been unclear what intra-cellular mechanism initiates cardiac cell fate from undifferentiated cells," says Alexandre Colas, Ph.D., assistant professor in the Development, Aging and Regeneration Program at SBP and corresponding author on the paper. "These genes are the earliest determinants of cardiac cell fate. This enables us to generate unlimited amounts of bona fide cardiac progenitors for regenerative purposes, disease modeling and drug discovery."

The international team, which included researchers from the International Centre for Genetic Engineering and Biotechnology in Italy, University Pierre and Marie Curie in France and the University of Coimbra in Portugal, combined CRISPR-Cas9 gene editing, high-throughput microRNA screening and other techniques to identify the role Id genes play in heart development.

In particular, CRISPR played a crucial role, allowing them to knock out all four Id genes. Previous studies had knocked out some of these genes, which led to damaged hearts. However, removing all four genes created mouse embryos with no hearts at all. This discovery comes after a decades-long effort to identify the genes responsible for heart development.

"This is a completely unanticipated pathway in making the heart," says co-author Mark Mercola, Ph.D., professor of Medicine at Stanford and adjunct professor at SBP. "People have been working for a hundred years to figure out how the heart is specified during development. Nobody in all that time had ever implicated the Id protein."

Further study showed Id genes enable heart formation by turning down the Tcf3 and Foxa2 proteins, which inhibit the process, and turning up Evx1, Grrp1 and Mesp1, which support the process.

In addition to contributing a new chapter in the understanding of heart development, this study illuminates a powerful technique to screen for protein function in complex phenotypical assays, which was previously co-developed by Colas and Mercola. This technology could have wide-spread impact throughout biology.

"On a technical level, this project succeeded because it combined high-throughput approaches with stem cells to functionally scan the entire proteome for individual proteins involved in making heart tissue," says Mercola. "It shows that we can effectively walk through the genome to find genes that control complex biology, like making heart cells or causing disease."

Understanding this pathway could ultimately jumpstart efforts to use stem cells to generate heart muscle and replace damaged tissue. In addition, because Id proteins are the earliest known mechanism to control cardiac cell fate, this work is an important milestone in understanding cardiovascular developmental biology.

"We've been influenced by the skeletal muscle development field, which found the regulator of myogenic lineage, or myoD," says Colas. "For decades, we have been trying to find the cardiac equivalent. The fact that Id genes are sufficient to direct stem cells to differentiate towards the cardiac lineage, and that you don't have a heart when you ablate them from the genome, suggests the Id family collectively is a candidate for cardioD."

Explore further: Discovery of a key regulatory gene in cardiac valve formation

More information: Thomas J. Cunningham et al, Id genes are essential for early heart formation, Genes & Development (2017). DOI: 10.1101/gad.300400.117

Read the rest here:
Id genes play surprise role in cardiac development - Medical Xpress - Medical Xpress

LOS ANGELES In the fight against cardiovascular disease, a new super-weapon is now even closer to deployment and its capabilities are turning out to be beyond expectations.

One of the most notorious killers facing humanity, cardiovascular disease, is responsible for about about 1 in every 3 deaths in the U.S., according to the American Heart Association. A new study aimed at combating the disease finds that stem cells, the controversial darlings of modern biomedical research, are not only showing promise in treating heart failure, but in rats are actually reversing problems associated with old age.

The way the cells work to reverse aging is fascinating, says Dr. Eduardo Marbn,one of the studys primary investigators, in a press release. They secrete tiny vesicles that are chock-full of signaling molecules such as RNA and proteins. The vesicles from young cells appear to contain all the needed instructions to turn back the clock.

Marbn, who serves as director of the Cedars-Sinai Heart Institute, explains this latest study builds on previous lab work and human trials which have shown promise in treating heart failure using cardiac stem cell infusions.

The specific type of stem cells used in the study are known as cardiosphere-derived cells or CDCs. The process to grow these cells was initially developed when Marbn was part of the Johns Hopkins University faculty.

While the latest research involving CDCs indicates possibilities that have previously been in the realm of science fiction, the scientists leading the charge urge restraint in face of the excitement.

This study didnt measure whether receiving the cardiosphere-derived cells extended lifespans, so we have a lot more work to do, says Dr. Lilian Grigorian-Shamagian, the studys first author. We have much to study, including whether CDCs need to come from a young donor to have the same rejuvenating effects and whether the extracellular vesicles are able to reproduce all the rejuvenating effects we detect with CDCs.

Nevertheless, the latest results of stem cell infusions in rats are startling. Not only did rats that received the CDCs experience improved heart function, they also had lengthened heart cell telomeres.

Telomeres, the protective caps at the ends of chromosomes, normally shrink with age. As telomere shrinkage is one of the most studied and least understood phenomenons associated with aging, the effect of CDCs on them is especially fascinating.

LIKE STUDIES? FOLLOW STUDYFINDS.ORG ON FACEBOOK!

Whats more, the researchers said the rats who received the treatment also had their exercise capacity increase by about 20 percent. They also regrew hair faster than rats that didnt receive the cells.

With these thrilling results only the latest in recent stem cell headlines, researchers caution the public that most treatments are still not ready for prime time.

Indeed, a recent Reuters article warned that stem cell therapy still is not approved to treat heart failure in the U.S., yet many unscrupulous clinics are offering questionable services anyway and charging tens of thousands of dollars for it. In some cases, researchers quoted in the article said these labs may not even be injecting stem cells, but rather a useless and dangerous mix of cellular debris.

The article also noted two patients died and another went blind after stem cell injection procedures in Florida clinics.

Still, the legitimate doctors and scientists working to push the frontier of medicine forward are very optimistic about the real possibilities of the therapy. The Cedars-Sinai team said they are also studying the use of stem cells in treating patients with Duchenne muscular dystrophy and patients with heart failure with preserved ejection fraction, a condition that affects more than 50 percent of all heart failure patients.

Their research on CDCs effects on aging was published this month in the European Heart Journal.

See original here:
Study: Cardiac Stem Cell Injections Reverse Effects of Aging - Study Finds

Howard University Hospital's Dr. Ermias Aytenfisu seeks to clear up misconceptions about marrow donation in the minority community.

WASHINGTON, D.C. (August 21, 2017) Elsa Nega is an Ethiopian-Canadian mother of two young children. She loves her children and wants to watch them grow. However, Nega has a rare form of blood cancer, leukemia, and needs a bone marrow transplant to survive.

Black patients like Nega are the least likely to find their suitable blood marrow match, according to Be The Match which is hosting a Stem Cell/Bone Marrow registry event at the Howard University College of Medicine on Wednesday, Aug. 30 between 11 a.m. and 3 p.m. The exact location for the registry drive is the lobby outside of room 1008 in the Numa P. Adams building.

Negas story began in February when she walked into her local ER and was rushed to intensive care. By the next morning Nega was diagnosed with Acute Lymphoblastic Leukemia (ALL) and started on chemo immediately. Unlike 90 percent of patients who go into remission after the first round of chemo, she did not.

Now, after three rounds of chemo, a bone marrow transplant is her only hope of recovery. Negas siblings were not a match and she is reaching out to the Washington region because of its large population of people of Ethiopian descent.

There are a lot of myths associated with marrow donation, said Amanda Holk, community engagement representative with the Be The Match in Washington, D.C. There is so much fear surrounding the process but most donors are back to work the next day.

ErmiasM. Aytenfisu, M.D., stroke medical director at Howard University Hospital said the most common way to donate bone marrow is through a procedure called peripheral stem cell donation. No surgery is involved. Donors receive medication to increase peripheral stem cells before the donation. On the day of donation, blood is removed through a needle on one arm and passed through a machine that separates out the blood-forming cells. Uncommonly marrow donation involves surgical techniques that use a special needle to take out blood forming cells. During the procedure, the patient is anesthetized and feels no pain.

Joining the bone marrow registry at the Howard University College of Medicine event involves a simple as a cheek swab and an application. A persons chance of being a match at that point is only 1 in 500. But, for a patient like Elsa, you could be the only one. Elsa does not have a single match on the registry although there are 30 million people signed up.

For more information, contact Amanda Holk via email AHolk@nmdp.org or 202-875-9987

For the Howard University registry drive, please note that you must be between the ages of 18 and 44 to join the registry since research has shown that the younger the cells, the better the patient outcomes. And the following conditions prevent you from joining:

Hepatitis B or C

HIV

Organ, marrow or stem cell transplant recipient

Stroke or TIA (transient ischemic attack)

Other upcoming local events to support Elsa Nega:

*Empower the community (The Helen Show)

Date: 08/26/2017 (Sat.)

Location: Washington Convention Center

*Ethiopian Day Festival

Date: 09/03/2017 (Sun.)

Location: Downtown Silver Spring

About Howard University Hospital

Over the course of its roughly 155-year history of providing the finest primary, secondary and tertiary health care services, Howard University Hospital (HUH) remains one of the most comprehensive health care facilities in the Washington, D.C. metropolitan area and designated a DC Level 1 Trauma Center. The hospital is the nation's only teaching hospital located on the campus of a historically Black university. For more information, visit huhealthcare.com

More:
Howard University Hosts 'Be The Match' Marrow Registry Drive - Howard Newsroom (press release)

VistaGen Therapeutics has received a notice of allowance for a stem cell production patent, which the firm says could be used in autoimmune disorder and cancer treatments.

The US Patent and Trademark Office (USPTO) issued VistaStem a subsidiary of VistaGen the notice for patent no. 14/359,517, which covers methods for producing hematopoietic precursor stem cells usually found in red blood marrow.

These are stem cells that give rise to all of the blood cells and most of the bone marrow cells in the body, with potential to impact both direct and supportive therapy for autoimmune disorders and cancer, said VistaGen VP Mark McPartland.

With CAR-T cell applications and foundational technology, McPartland said he believed the technology will provide approaches for producing bone marrow stem cells for bone marrow transfusions.

Business opportunities

In December last year, VistaGen signed an exclusive sublicense agreement with stem cell research firm BlueRock Therapeutics, under which the latter paid VistaGen $1.25m (1.06m) upfront for its cardiac stem cell production technologies.

McPartland said he expects this recent notice of allowance to also create potential opportunities for additional regenerative medicine transactions.

IP portfolio growth

VistaGen told us it plans to secure IP protection in multiple domains and international jurisdictions.

We intend to grow our IP portfolio in a manner that emphasises platform protection and maximises opportunities for commercialisation and out-licensing, McPartland said.

View post:
VistaGen's cell production methods receive US patent boost - BioPharma-Reporter.com

There is truth in the old proverb about apple consumption and medical appointments. Insufficient vitamin C can contribute to leukemia. This observed relationship has now been shown to operate through the regulatory role the vitamin plays in the operation of bone marrow stem cells.

These days messages touting a single ingredient as being capable of curing all ills are more likely to peddleturmeric or cannabis, but a few decades ago it was vitamin C that was hailedas preventing everything from theflu to cancer if you took enough. As exaggerated as most of these claims were, it's certainly true that ascorbate, as it is also known, is vital to our health, sometimes in ways that are still unexplained.

We have known for a while that people with lower levels of ascorbate (vitamin C) are at increased cancer risk, but we havent fully understood why, said Dr Sean Morrison of Childrens Medical Center Research Institute UT Southwestern. Stem cells clearly played a part, but are so rare in any individual tissue that it is impossible to collect the millions usually used for metabolic analysis. Moreover, most mammals make their own ascorbate, but humans cannot, impeding the use of animal models.

Morrison and his co-authors of a paper published in Nature had to develop new techniques to measure metabolite usage in populations as small as 10,000 stem cells to address the first problem. On applying these techniques the authors discovered each type of blood-forming cell has a distinctive signature to its metabolite consumption. They tackled the second problem using mice that lack ascorbate-producing enzymes.

When given a low vitamin C diet these mice had more, and more active, bone marrow stem cells, increasing blood cell production at the price of higher rates of leukemia. The vitamin C concentration was related to levels of the enzyme Tet2, which regulates blood production. Without enough Tet2, the stem cells behaved like an overheating engine, turning out blood cells at a great rate until they turned cancerous. Something similar is observed when mutations reduce Tet2 production.

The first clinical application of the discovery is for patients with clonal hematopoiesis, a condition that often involves reduced Tet2 production and leukemia. Our results suggest patients with clonal hematopoiesis and a Tet2 mutation should be particularly careful to get 100 percent of their daily vitamin C requirement, Morrison said. These patients... need to maximize the residual Tet2 tumor-suppressor activity to protect themselves from cancer.

Since stem cells are much sparser in the rest of the body than in bone marrow it will be even more challenging to extend the research to other cancers.

The ideal dose of vitamin C remains to be established, although a paper, coincidentally published last week, may indicate benefits beyond current recommendations.

Read the original here:
Vitamin C Can Suppress Leukemia Up To a Point | IFLScience - IFLScience

Home Cancer The power of vitamin C: Can it kill cancer stem cells?

Every three minutes, one person in the United States is diagnosed with blood cancer. Thankfully, there may be a new approach to helping these individuals fight it using vitamin C.

Researchers from Perlmutter Cancer Center at NYU Langone Health recently published a report in the journal Cell indicating that vitamin C may be able to tell faulty cells in bone marrow to mature and die instead of multiplying to cause blood cancers. They explained that specific genetic changes are able to reduce the ability of the enzyme known as TET2 to push stem cells to mature, which die in many people who suffer from leukemia. Experts discovered that vitamin C seemed to activate TET2 in mice that were engineered to be TET2 deficient. In simple terms, TET2 is a tumor suppressor that can prevent certain cells from growing uncontrollably.

Mutations that reduce TET2 function are present in about 10 percent of people with acute myeloid leukemia, 30 percent of patients with a pre-leukemia known as myelodysplastic syndrome, and close to 50 percent of people with chronic myelomonocytic leukemia. Tests indicate that about 2.5 percent of U.S. cancer patients develop TET2 mutations, including some with lymphomas.

The study focused on the relationship between TET2 and cytosine, which is one of four nucleic acid letters that make up the DNA codes in our genes. The attachment of a small molecule, referred to as a methyl group, to cytosine bases can shut down the actions of a gene. As the human body forms, the attachment and removal of methyl groups adjust gene expression in stem cells, which can mature and become muscle, bone, nerve, or other cell types. The bone marrow keeps stem cells in pools, ready to become replacement cells when and if needed. In the case of leukemia, the signals that are supposed to tell a blood stem cell to mature end up malfunctioning, leaving it to multiply instead of developing normal white cells, which are needed to help fight infection.

Medical scientists explain that TET2 allows for a change in methyl groups that are required to be removed from cytosine. This essentially turns on genes and directs stem cells to mature and eventually destroy themselves. Researchers say that this signals an anti-cancer mechanism, something that can help blood cancer patients with TET2 mutations.

The team of researchers genetically engineered mice to manipulate the TET2 gene. Techniques to turn off TET2 in mice lead to abnormal stem cell behavior. The changes were reversed when TET2 was restored. Since previous work indicated that vitamin C could stimulate TET2, the researchers theorized that high doses of vitamin C might reverse the effects of TET2 deficiency. It would be a case of turning up the action on the functional gene. As it turns out, high dose vitamin C treatment did induce stem cells to mature and also suppressed the growth of leukemia cancer cells implanted in mice.

As of now, the NYU team is working on identifying genetic changes that may contribute to the risk of leukemia in specific groups of patients. While this latest study provides some hope for blood cancer patients, the manipulation of TET2 is only a potential new treatment approach until further studies are conducted. Currently approved treatments for blood cancers include stem cell transplantation, chemotherapy, and radiation therapy.

Related: Combining antibiotics and vitamin C helps to combat cancer stem cells

Related Reading:

Mangos show signs of reducing IBS symptoms and potential cancer risk

A simple blood test may soon detect cancer

http://www.cancercenter.com/terms/blood-cancers/https://ghr.nlm.nih.gov/gene/TET2

Read this article:
The power of vitamin C: Can it kill cancer stem cells? - Bel Marra Health

When Alex Shorheardthat he was a match for a stranger in Israel who would likely die without a stem cell transplant, he didn't think twice before saying "yes."

"If I today I help somebody, tomorrow I want somebody to help me too if I [am] sick," said Shor. "I don't think too much about it."

The request came from Ezer Mizion, an Israeli health service with the world's largest Jewish bone marrow registry, countingover 850,000 registrants worldwide. Shor said the representative told him the recipient would be a63-year-old man in Israel.

Shor, 41, had registered his DNA with the registry 10 years ago when he lived in Israel.

Shor and his family emigrated to Winnipeg nearly three years ago. In March, he got word that his stem cells were a match.

Stem cells are immature blood cells that can grow into healthy cells. They can make the difference between life and death for people with various forms of cancer, blood-related illnesses and metabolic disorders.

Shorwas agenetic match for the man based on the human leukocyte antigen (HLA) system, which codes the human immune system. The pair would have had to have 10 of the same HLA markers to be a viable match.

In May, Shorwent to a lab in Winnipeg to draw blood to send off to Israel to ensure hisblood would be compatible with the recipient's. Now, he plans to travel to Israel to donate his stem cells as soon as he hears from the physicians that the patient's condition has improved enough to tolerate the procedure.

Getting Shor's blood to Israel required a cooler, a courier and some creativity.

Vials of Shor's blood were transported to Israel in an ice-packed Thermos.

Dena Bensalmon, Canadian director of Israeli health service Ezer Mizion, put out a call on Facebook for a chaperone that could transport five vials of Shor's blood.

"Sixteen people came forward within about four minutes," she said.

One woman the perfect candidate was travelling from Winnipeg to Toronto, then on to Isreal. They packed the blood in ice in a Coleman thermos for the 12-hour journey.

"I met Dina in Toronto and then I switched the ice packs. They took the blood directly," she said.

Canada'sOneMatchregistry through Canadian Blood Serviceshas about 400,000 registrants.

But"if a person is Jewish, then the chances of them finding their match on a Jewish registry is far greater than them finding their match on a non-Jewish registry," saidBensalmon.

Canadian Blood Services has access to nearly 29 million volunteer donors and more than 720,000 cord blood units from dozens of countries around the world, as all the registries are connected under the umbrella of the World Marrow Donor Association, comprised of millions of people from across the world.

"I find the whole thing almost like watching a circle of life," said Bensalmon.

A volunteer brought vials of Shor's blood to Israel. She kept the thermos in her lap the whole 12-hour trip.

Shor said he just thought of his own father and how he would want someone to help him if he had a life-threatening illness. He encourages everyone to join a stem-cell registry.

"Tomorrow you may save somebody and tomorrow you don't know if you be sick and somebody save you," said Shor.

Read more:
Winnipeg man to donate stem cells to critically ill stranger in Israel - CBC.ca