Stem Cell Therapy Los Angeles – Darrow Stem Cell Institute

Darrow Stem Cell Institute

Marc Darrow, MD., JD. is the medical director and founder of the Darrow Stem Cell Institute in Los Angeles, California. With over 23 years experience in regenerative medicine techniques and the treatment of thousands of patients, Dr. Darrow is considered a leading pioneer in the non-surgical treatment of degenerative Musculoskeletal Disordersandsports related injuries.He is one of the busiest Regenerative Medicine doctors in the world.

Dr. Darrow has co-authored and continues to co-author leading edge medical research including the use of bone marrow derived stem cell therapy for shoulder, hip, knee and spinal disorders. He also comments and writes on research surrounding the treatment of chronic tendon injury, ankle and foot pain, elbow, hand and finger pain.

ABOUT US THE DARROW STEM CELL INSTITUTE

Over the years Dr. Darrow has made it his mission to help get people out of pain and to do so without surgery. To achieve this goal, Dr. Darrow and the staff of the Stem Cell institute guide patients through a hands on approach to healing. This includes reliance of physical examination over MRI and a realistic healing program designed around Bone Marrow Derived Stem Cells instead of surgery.

From Dr. Darrows book: A firm believer in regenerative medicine, I have been using these therapies since 1997, when I was doing my physical medicine residency at UCLA. My Los Angeles clinic, the Darrow Stem Cell Institute, has long been recognized for utilizing advanced, nonsurgical options for musculoskeletal pain, and degenerative joint disease, with Stem Cell Therapy and PRP having become a very exciting option in the past several years. In fact, I have been told by others in my field that no one does anywhere near as much regenerative medicine with Stem Cell Therapy and PRP as I do. A question I am asked by most patients is why these treatments have never been offered to them by other doctors. Part of the answer to this question is supplied in the research shown throughout this book. In this book, I will share with you the latest medical information on the use of Stem Cell Therapy and PRP for osteoarthritis and soft tissue damage, and I will also present the research supporting their use in the clinical setting for pain in most areas of the musculoskeletal system of the body.

Non-surgical treatment of degenerative disc disease

My MRI says I need back surgery. Can I avoid it?

Stem cell therapy for spinal stenosis

Four case studies of low back pain treated with stem cell therapy

Research: Some spinal surgeries and MRIs are unjustified and wasteful

Treatment of Hip Osteoarthritis with Platelet-Rich Plasma Injections

You need a hip replacement and spinal surgery. What are your non-surgical options?

PRP treatments for hip bursitis and Greater trochanteric pain syndrome

Stem cell therapy for a bone on bone hip waiting for hip replacement

Can stem cell therapy help you play golf again? Golf, stem cells and the knee replacement alternatives

Platelet Rich Plasma Injections for knee osteoarthritis

Weight loss can be a knee replacement alternative treatment

Research on stem cell therapy bone marrow derived treatments for knee osteoarthritis

Knee pain, back pain, and hip pain after knee replacement

Meniscus

Stem Cell Therapy Alternative For Meniscus Surgery

Platelet Rich Plasma (PRP) Therapy for Partial Meniscus Tears

Stem cell therapy and PRP for Whiplash associated disorders

Cervical Spine and Neck Pain

Shoulder Labrum Repair and biceps tenodesis

Shoulder Impingement Subacromial shoulder pain non-surgical options

Alternatives to shoulder replacement

PRP and Stem Cell Therapy for Slap Tears

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Stem Cell Therapy Los Angeles - Darrow Stem Cell Institute

Stem Cell Transplants: A Lifesaving Treatment for Cancer …

If you have leukemia or lymphoma, you may need a stem cell transplant. These cells help replace cells damaged by the cancer. They also let your body recover faster from intense chemotherapy and radiation treatments.

For some, it may be the best -- or only -- approach.

They grow inside your marrow, the soft tissue of your bones. Theyre also in your blood, as well as blood from umbilical cords.

As they mature, blood stem cells change into threetypes of cells your body needs:

There are two types of transplants. Your doctor will decide which is best for you.

In an autologous (AUTO) transplant, doctors take healthy stem cells from your bone marrow or blood. Theyre frozen and carefully stored. Since they're outside your body, they arent harmed during the chemotherapy or radiation treatments youll need to get rid of your cancer cells.

After your treatment ends, your thawed stem cells are returned to your bloodstream through an IV. Theyll find their way back to your bone marrow.

Once there, they can help your body make healthy blood cells again.

In an allogeneic (ALLO)transplant, you get healthy stem cells from a donor.

Its important that the donors bone marrow closely matches yours. If it doesnt, your body may reject their cells. Your donor might be a family member. You can also get stem cells from someone you dont know.

Before an ALLO transplant, youll get chemotherapy, radiation, or both. This wipes out your own stem cells and gets your body ready for the new ones soon after your treatment is done.

If your doctor cant find a donor,theymay use cells from donated umbilical cord blood. After a baby is born, blood rich in stem cells remains in the discarded cord and placenta. It can be frozen and stored in a cord blood bankuntil its stem cells are needed.

Cord blood is tested before its banked. This lets doctors quickly check to see if theres a match for you. Plus, the pairing doesnt have to be as perfect as it would be from a donor.

If youre being treated with your own stem cells, you may have high-dose chemotherapy first. This can cause side effects. What and how severe they are depend on the dose. You might have:

That doesnt sound great, but advances in cancer treatment can make them easier to live with.

When you get stem cells from a donor or cord blood, theres a risk of something called graft-versus.-host disease. Its when your body fights to get rid of the new cells, or the cells launch an attack against you. It could happen right after the transplant or not until a year later.

Thanks to strides in the matching process in the past decade or so, your odds of having more problems from the treatment are much lower than they used to be.Youll also get medicine after your transplant that can workto keep those problems at bay.

Still, if youre older, it can be harder for you to manage side effects. Also, its more likely youhave another health condition like high blood pressure or diabetes. Your doctor may want you to have a reduced-intensity, or mini, stem cell transplant.

Youll start out with a lower dose of chemo and radiation before you get the stem cells. Its less taxing on your body, and new cells can still grow and fight your cancer.

They sound like special cells that fight cancer. They arent. Theyre cells that advance cancer.

Experts used to think all cancer cells were the same. Now, theres reason to believe that special, fast-growing cancer stem cells keep your disease alive by reproducing.

If thats true, in the next few years, the focus of treatments could shift from trying to shrink tumors to trying to kill this type of cell.

WebMD Medical Reference Reviewed by Kumar Shital, DO on July 17, 2020

SOURCES:

MD Anderson Cancer Center: Stem Cell Transplantation.

National Cancer Institute: Stem Cell Transplant.

Linda Burns, MD, vice president and medical director of health services research, National Marrow Donor Program/Be The Match, Minneapolis, MN.

Jack Jacoub, MD, medical oncologist and director of thoracic oncology at MemorialCare Cancer Institute at Orange Coast Memorial Medical Center, Fountain Valley, CA.

American Society of Clinical Oncology: What Is a Stem Cell Transplant?

American Cancer Society: Stem Cell Transplant for Multiple Myeloma.

City of Hope: Breakthroughs: Mini Stem Cell Transplant: What Is It and How Does It Treat Cancer?

National Cord Blood Program: Cord Blood Q&A.

Stanford Medicine Ludwig Center for Cancer Stem Cell Research and Medicine: The Stem Cell Theory of Cancer.

Cleveland Clinic: Graft vs Host Disease: An Overview in Bone Marrow Transplant.

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Stem Cell Transplants: A Lifesaving Treatment for Cancer ...

Smart Stem Cells Made From Fat Have the Power to Heal – Freethink

New smart stem cells show a promising power to heal.

Researchers have reprogrammed human fat cells into adaptive smart stem cells that can lie dormant in the body until they are needed to heal various tissues. They demonstrated the cells' effectiveness at healing damaged tissue in a mouse study.

To create the smart stem cells, the team from UNSW Sydney exposed human fat cells to a compound mixture. After about three and a half weeks, the cells lost their original identity and began acting like stem cells, or iMS (induced multipotent stem cells).

"The stem cells acted like chameleons. They followed local cues to blend into the tissue that required healing."

"The stem cells we've developed can adapt to their surroundings and repair a range of damaged tissues," said UNSW hematologist John Pimanda, and co-author of the study, which they published in Science Advances.

"To my knowledge, no one has made an adaptive human multipotent stem cell before. This is uncharted territory."

Next, they injected the experimental iMS cells into healthy mice to see how the cells would respond. The cells remained dormant for some time, but they activated when the mouse was injured. Because of the cells' regenerative ability to act as "smart stem cells," they transformed themselves into whatever tissue was needed to heal the injured mouse --- like bone tissue, heart, or skin.

"The stem cells acted like chameleons," said Avani Yeola, lead author on the study at UNSW Medicine & Health. "They followed local cues to blend into the tissue that required healing."

All cells in a human body contain the same DNA. To differentiate between tissues, like a skin cell versus a bone cell, the cells only use a small portion of their total DNA. The rest of the DNA is shut down naturally by local modifications.

"The idea behind our approach was to reverse these modifications," said Pimanda. "We wanted the cells to have the option of using that part of the DNA if there was a signal from outside the cell."

Tissue-specific stem cells, like those that are restricted to becoming parts of the liver or lung, are limiting. But smart stem cells that can respond to their environment and become any tissue, like multipotent stem cells, will have many uses.

In the future, doctors could take a patient's fat cells, incubate them with the compound, and inject them into the patient to heal heart damage or trauma injuries.

But applications like this could be a long way off. The team needs to do much more research to prove this is safe in humans for different kinds of trauma before it becomes a real therapy.

We'd love to hear from you! If you have a comment about this article or if you have a tip for a future Freethink story, please email us at [emailprotected]

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Smart Stem Cells Made From Fat Have the Power to Heal - Freethink

Are Covid-19 vaccines safe for cancer patients? Here is what cancer experts say – CNN

It's a question that has been on the minds of researchers and oncologists long before the Pfizer and Moderna vaccine rollouts began. Although there is a consensus that the vaccines are safe for most cancer patients, according to the American Cancer Society and others in the medical community, research into whether they will be effective for cancer patients is still a data-free zone. The American Cancer Society recommends that cancer patients talk to their doctors before getting any type of vaccine because all patients and their courses of treatment are different.

There are several factors that may require a cancer patient to delay vaccination, including recent stem cell transplants or other recent use of therapy agents known to reduce vaccine efficacy, according to Dr. Laura Makaroff, the American Cancer Society's Senior Vice President for Prevention and Early Detection.

"As far as safety of the vaccine, every situation for every patient with cancer is a little different. And there's a spectrum of where any one patient might be in their cancer journey," Makaroff told CNN. "The Covid-19 vaccine is definitely safe for people with cancer but it's important that patients have a conversation with their healthcare provider and their cancer care team to determine when is the right time to have the vaccine."

"All the guidance that we're seeing -- the American Cancer society and other leading oncology groups -- is that Covid-19 immunization is recommended for patients in active therapy, but we really understand that there are limited safety and efficacy data on these patients," Makaroff said.

"Despite the lack of safety data specifically in patients with CLL (chronic lymphocytic leukemia), SARS-Cov-2 vaccination is anticipated to be safe."

CLL is characterized by a weakened immune system. The immunocompromization is so severe that CLL patients are advised to avoid live vaccines such as the ones for measles or yellow fever.

"The thing that people don't quite realize is that the impaired immune system in CLL patients -- due to the disease or some of the treatments for the disease -- can actually impact your response to vaccination," Ujjani told CNN.

"We recommend the Covid-19 vaccines for our patients ... but we're not really sure how effective it's going to be," she added. "Patients with blood cancers are typically excluded from the clinical trials evaluating the efficacy of the vaccine."

To remedy the lack of data, Ujjani is launching a research study involving 500 CLL patients across the country -- all of whom are already slated to receive the vaccine from their doctor or pharmacist -- to determine what kind of immune response they will have to the commercially available vaccines.

Advocacy groups for other more prevalent types of cancer are also encouraging cancer patients to get vaccinated as soon as possible. The Lung Cancer Action Network recently asked the US Advisory Committee on Immunization Practices to give lung cancer patients expedited access to the vaccines.

The scientific community agrees that more research is needed to determine the effectiveness of Covid-19 vaccines in cancer patients -- and many doctors are working around the clock to get more trials off the ground.

"We need these data so that we can better inform patients and better prioritize the allocation of the vaccines. If these vulnerable patients form an adequate immune response, we should certainly vaccinate them as early as possible," Dr. Elad Sharon, senior investigator at the National Cancer Institute, told CNN via email.

"But, if research efforts show that these patients fail to form a protective response to these vaccines, then what we will need to do will be to vaccinate everyone around these patients first, so that our medically vulnerable patients are most protected by the people living with them and caring for them."

Ujjani added, "We're all working really hard to answer this question, but it's hard because we've been working kind of against the clock as the vaccines just became available."

"A lot of our patients have suffered in isolation and fear, and they're not sure they're going to get back to a normal life," Ujjani told CNN. "So every oncologist is interested to see how their patients will respond to the vaccine."

Correction: An earlier version of this story misstated the academic journal that published a study conducted by the European Research Initiative. It was published in the journal Leukemia. It also misnamed the CLL Society by including the words of the acronym.

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Are Covid-19 vaccines safe for cancer patients? Here is what cancer experts say - CNN

The race to treat a rare, fatal syndrome may help others with common disorders like diabetes – Science Magazine

Misfolded proteins (orange) in the endoplasmic reticulum may play a role in Wolfram syndromes many symptoms.

By Mitch LeslieFeb. 11, 2021 , 2:00 PM

Maureen Marshall-Doss says the first sign that her vision was deteriorating came when she misidentified the color of a dress. At a backyard get-together about 20 years ago, the Indianapolis resident pointed out an attractive yellow dress another woman was wearing. You see that as yellow? Shes wearing a pink dress, Marshall-Doss recalls her husband responding.

Today, Marshall-Doss is virtually blind. With help from custom made eyeglasses that magnify objects 500 times, I can see shapes, she says. But she can no longer drive and had to quit the job she loved as a school librarian. Along with her dimming vision, she has type 1 diabetes and has lost her sense of taste and smell.

Marshall-Doss is one of 15,000 to 30,000 people around the world with Wolfram syndrome, a genetic disease. For decades, the condition remained enigmatic, untreatable, and fatal. But in the past few years, insights into its mechanism have begun to pay off, leading to the first clinical trials of drugs that might slow the illness and sparking hopes that gene therapy and the CRISPR DNA-editing tool might rectify the underlying genetic flaws. Here is a rare disease that the basic science is telling us how to treat, says physiologist Barbara Ehrlich of the Yale School of Medicine.

The research could also aid more than the relatively few patients with Wolfram syndrome. Driving the diseases many symptoms is a malfunction of the endoplasmic reticulum (ER), the multichambered organelle that serves as a finishing school for many cellular proteins. Known as ER stress, the same problem helps propel far more common illnesses, including type 2 diabetes, amyotrophic lateral sclerosis (ALS), Parkinsons disease, and Alzheimers disease. Wolfram syndrome is the prototype of an endoplasmic reticulum disorder, says medical geneticist Fumihiko Fumi Urano of Washington University School of Medicine in St. Louis. Because Wolfram syndrome is simpler, says Scott Oakes, a cell biologist and pathologist at the University of Chicago, researchers think it could illuminate the mechanisms of other ER-disrupting diseases, which affect hundreds of millions of people worldwide.

In the late 1930s,four children with diabetes were going blind, and doctors were stumped. Like many other people in the United States struggling through the Great Depression, the siblings ate a paltry diet, subsisting on potatoes, bread, oatmeal, and a little milk. But after examining three of the children, Donald Wolfram, a physician at the Mayo Clinic in Rochester, Minnesota, and an ophthalmologist colleague ruled out malnutrition as the cause of their puzzling condition. Lead poisoning and syphilisthough common enoughwerent to blame, either. When Wolfram and his partner wrote up the cases in 1938, they concluded that the symptoms could be manifestations of an hereditary or acquired cerebral lesion.

The physicians were right that the syndrome eventually named for Wolfram is hereditary. Recessive mutations in the gene for a protein called wolframin are responsible for most cases, with glitches in a second gene causing most of the rest. However, the pair was wrong to think the defect lies only in the brain. Instead, the symptoms stem from widespread cell death. Its definitely a disease that affects the whole body, Marshall-Doss says.

The first sign of the illness, appearing when patients are children, is usually diabetes mellitus, or faulty sugar metabolism, sparked by the demise of insulin-secreting beta cells in the pancreas. Most patients also develop the unrelated condition diabetes insipidus, in which the pituitary gland doesnt dole out enough of a hormone that helps control the bodys fluid balance, causing the kidneys to produce huge amounts of urine.

Mutations in the gene for wolframin disrupt the endoplasmic reticulum and lead to cell death throughout the body, causing a range of symptoms.

DeafnessPatients usually beginto lose their hearingin their teens. Balance andcoordination difficultyThe disease attacks the cerebellum, hampering the ability to control movement. Diabetes mellitusInsulin-producing beta cells die, hindering the bodys use of sugar as energy. Difficulty breathingBy damaging thebrain stem, the diseasecan disrupt respiration. Diabetes insipidusBecause of a faultypituitary gland, the kidneys produce too much urine. Loss of visionAs cells in theoptic nerve die, patientsgradually go blind.

V. Altounian/Science

Ellie White, 19, of Centennial, Colorado, who was diagnosed with Wolfram syndrome 12 years ago, says she hasnt had a full night of sleep since she was 3 years old. She gets up again and again to use the bathroom and monitor her blood sugar.

Yet she and other patients say that as disruptive as those problems are, they are not the diseases most dismaying consequence. The biggest symptom of Wolfram syndrome that affects me the most is my vision, White says. Because neurons in the optic nerve perish, patients usually go blind within 10 years of their first visual symptoms.

Other neurons die as well. As the disease progresses, brain cells expire, and walking, breathing, and swallowing become difficult. Most people with Wolfram syndrome die before age 40, often because they can no longer breathe. At 57, Marshall-Doss is one of the oldest patients; one of her mutated genes may yield a partly functional version of wolframin, triggering a milder form of the disease, Urano says.

Two advanceshave made it possible to begin to tackle those symptoms. The first was Uranos discovery nearly 20 years ago that linked Wolfram syndrome to ER stress. The ER is where about one-third of a cells newly made proteins fold into the correct shapes and undergo fine-tuning. Cells can develop ER stress whenever they are under duress, such as when they dont have enough oxygen or when misfolded proteins begin to pile up inside the organelle.

In test tube experiments, Urano and his colleagues were measuring the activity of genes to pinpoint which ones help alleviate ER stress. One gene that popped up encodes wolframin, which scientists had shown in 1998 was mutated in patients with Wolfram syndrome. Following up on that finding, Urano and his team determined that wolframin takes part in whats known as the unfolded protein response, which is a mechanism for coping with ER stress in which cells take steps including dialing back protein production.

Scientists think wolframin plays a key role in the unfolded protein response, though they havent nailed down exactly how. When wolframin is impaired, cells become vulnerable to ER stress. And if they cant relieve that stress, they often self-destruct, which could explain why so many neurons and beta cells die in the disease.

Defective wolframin may harm cells in other ways. The ER tends the cells supply of calcium, continually releasing and absorbing the ion to control the amount in the cytoplasm. Changes in calcium levels promote certain cellular activities, including the contraction of heart muscle cells and the release of neurotransmitters by neurons. And wolframin affects calcium regulation.

Beta cells genetically engineered to lack functional wolframin brim with calcium, Ehrlich and colleagues reported in July 2020 in theProceedings of the National Academy of Sciences. When exposed to lots of sugar, the altered cells release less insulin and are more likely to die than healthy beta cells, the team found. The cells share that vulnerability with beta cells from patients with Wolfram syndrome. We think that excess calcium is leading to excess cell death, Ehrlich says.

ER malfunctions could hamstring other organelles as well. The ER donates calcium to the mitochondria, the cells power plants, helping them generate energy. In 2018, a team led by molecular biologist Ccile Delettre and molecular and cellular biologist Benjamin Delprat, both of the French biomedical research agency INSERM, discovered that in cells from patients with Wolfram syndrome, mitochondria receive less calcium from the ER and produce less energy. Those underpowered mitochondria could spur the death of optic nerve cells, the researchers speculate.

Fumihiko Urano holds dantrolene, a muscle relaxant drug he helped test as a treatment for Wolfram syndrome.

The link between ER stress and Wolfram syndrome has been crucial for identifying potential treatments because otherwise we would have nothing to target, Urano says. But a second development was also key, he says: the advocacy and support of patient organizations, such as the Snow Foundation and the Ellie White Foundation, headed by its namesakes mother. The foundations have stepped up with money for lab research and clinical trials when other sources, including government agencies, didnt come through.

Scientists, patients, and their advocates say Urano also deserves much of the credit. Besides treating patients, he heads the international registry of cases and has taken the lead in organizing clinical trials, screening compounds for possible use as treatments, and devising potential therapies. Fumi is clearly the driving force, says Stephanie Snow Gebel, co-founder of the Snow Foundation, who about 10 years ago helped persuade him to forgo a plum job as department chair at a Japanese university and take over the Wolfram program at Washington University.

Patients could soonstart to reap the benefits. In 2016, Urano and colleagues started the worlds first clinical trial for the disease: a phase 1/2 study of dantrolene, an approved muscle relaxant. The molecule was a top performer when they screened 73 potential treatments for their ability to save cells with terminal ER stress. Dantrolene didnt improve vision in the 22 participants, including White, the scientists reported in an October 2020 preprint. But in some patients, beta cells appeared to be working better and releasing more insulin. The drug is safe, but Urano says it will need to be chemically tweaked to target its effects before future trials are warranted.

Researchers are pursuing other possible treatments targeting ER stress or calcium levels. In 2018, U.K. scientists launched a trial that will include 70 patients to evaluate sodium valproate, a therapy for bipolar disorder and epilepsy that, in the lab, prevents cells with faulty wolframin from dying. Last year, another compound that emerged from Uranos screens, the diabetes drug liraglutide, entered a clinical trial. Also last year, an experimental drug developed by Amylyx Pharmaceuticals for Alzheimers disease and ALS received orphan drug designation from the U.S. Food and Drug Administration for Wolfram syndrome because it curbs ER stress. That designation offers tax breaks and other incentives, and it will get trials started sooner, Urano says.

Ehrlich and her team have a candidate of their own that they have begun to test in rodents: the drug ibudilast, which is approved in Japan to treat asthma. The researchers found it reduces calcium levels in beta cells lacking wolframin and boosts their survival and insulin output. New screening projects may reveal still more candidates.

But Urano knows that even if a treatment receives approval, it would be only a Band-Aid for Wolfram syndrome. Hoping to develop a genetic cure, he and colleagues are introducing replacement genes into cells from patients and from mice engineered to replicate the disease. The researchers are endowing the cells with healthy copies of the gene for wolframin or the gene for a protein that reduces ER stress to determine whether they restore cellular function and reduce cell death. At INSERM, Delettre and colleagues are also evaluating whether directing a working gene into optic nerve cells can curtail vision loss in mice with faulty wolframin. The scientists are still gathering data, but early results suggest the treatment can halt the deterioration.

Urano and his collaborators have also turned to the genome editor CRISPR, deploying it to correct the gene defect in patients stem cells and then growing them into beta cells. When the researchers transplanted the revamped cells into mice with diabetes, the animals blood sugar returned to healthy levels, the team reported in April 2020 inScience Translational Medicine.

Stem cell biologist Catherine Verfaillie of KU Leuven is collaborating on the CRISPR research. But she notes that because the faulty wolframin gene affects so many tissues, researchers will have to figure out how to deliver the CRISPR components to most cells in large organs such as the brain and livera prospect she calls pretty daunting. Urano agrees, predicting that CRISPR-based Wolfram therapies might take 10 to 20 years to develop. The alternative approach, gene therapy, could reach clinical trials more quickly, in 3 to 10 years, he says, because researchers have more experience with gene therapy and have created several treatments that have already been approved for other illnesses.

Because it stems from a single genetic glitch, Wolfram syndrome could also help scientists tease out the role of the ER in more complex diseases, including neurological conditions, type 2 diabetes, and cancer. The ER also falters in those diseases, causing cells to die, but the mechanism is harder to discern because they stem from myriad genetic and environmental factors. In Alzheimers disease, for instance, neurons develop ER stress as misfolded proteins accumulate inside and outside the cells.

Besides deepening researchers understanding of other conditions, the research on Wolfram syndrome might even deliver candidate treatments. Everyone would be very excited if we can make advances in targeting ER stress in Wolfram syndrome, Oakes says. It would open up the whole field to doing this in other degenerative diseases.

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The race to treat a rare, fatal syndrome may help others with common disorders like diabetes - Science Magazine