Stem Cells Archives - Amazing Health Advances

Cells ‘Vomit’ Waste to Promote Healing, Mouse Study Reveals

The AHA! Team — Wed, 03 Sep 2025 05:36:33 +0000

Washington University in St. Louis via Newswise – Newly discovered purging process in gastric cells hints at how injury recovery can go wrong – The researchers dubbed the new purging process “cathartocytosis,” combining Greek root words meaning cellular cleansing. When injured, cells have well-regulated responses to promote healing. These include a long-studied self-destruction process that cleans up dead and damaged cells as well as a more recently identified phenomenon that helps older cells revert to what appears to be a younger state to help grow back healthy tissue. Now, a new study in mice led by researchers at Washington University School of Medicine in St. Louis and the Baylor College of Medicine reveals a previously unknown cellular purging process that may help injured cells revert to a stem cell-like state more rapidly. The investigators dubbed this newly discovered response cathartocytosis, taking from Greek root words that mean cellular cleansing. Published online in the journal Cell Reports, the study used a mouse model of stomach injury to provide new insights into how cells heal, or fail to heal, in response to damage, such as from an infection or inflammatory disease. “After an injury, the cell’s job is to repair that injury. But the cell’s mature cellular machinery for doing its normal job gets in the way,” said first author Jeffrey W. Brown, MD, PhD, an assistant professor of medicine in the Division of Gastroenterology at WashU Medicine. “So, this cellular cleanse is a quick way of getting rid of that machinery so it can rapidly become a small, primitive cell capable of proliferating and repairing the injury. We identified this process in the GI tract, but we suspect it is relevant in other tissues as well.” Jettisoning of waste Brown likened the process to a “vomiting” or jettisoning of waste that essentially adds a shortcut, helping the cell declutter and focus on regrowing healthy tissues faster than it would be able to if it could only perform a gradual, controlled degradation of waste. As with many shortcuts, this one has potential downsides: According to the investigators, cathartocytosis is fast but messy, which may help shed light on how injury responses can go wrong, especially in the setting of chronic injury. For example, ongoing cathartocytosis in response to an infection is a sign of chronic inflammation and recurring cell damage that is a breeding ground for cancer. In fact, the festering mess of ejected cellular waste that results from all that cathartocytosis may also be a way to identify or track cancer, according to the researchers. A novel cellular process The researchers identified cathartocytosis within an important regenerative injury response called paligenosis, which was first described in 2018 by the current study’s senior author, Jason C. Mills, MD, PhD. Now at the Baylor College of Medicine, Mills began this work while he was a faculty member in the Division of Gastroenterology at WashU Medicine and Brown was a postdoctoral researcher in his lab. In paligenosis, injured cells shift away from their normal roles and undergo a reprogramming process to an immature state, behaving like rapidly dividing stem cells, as happens during development. Originally, the researchers assumed the decluttering of cellular machinery in preparation for this reprogramming happens entirely inside cellular compartments called lysosomes, where waste is digested in a slow and contained process. From the start, though, the researchers noticed debris outside the cells. They initially dismissed this as unimportant, but the more external waste they saw in their early studies, the more Brown began to suspect that something deliberate was going on. He utilized a model of mouse stomach injury that triggered the reprogramming of mature cells to a stem cell state all at once, making it obvious that the “vomiting” response — now happening in all the stomach cells simultaneously — was a feature of paligenosis, not a bug. In other words, the vomiting process was not just an accidental spill here and there but a newly identified, standard way cells behaved in response to injury. Although they discovered cathartocytosis happening during paligenosis, the researchers said cells could potentially use cathartocytosis to jettison waste in other, more worrisome situations, like giving mature cells that ability to start to act like cancer cells. The downside to downsizing While the newly discovered cathartocytosis process may help injured cells proceed through paligenosis and regenerate healthy tissue more rapidly, the tradeoff comes in the form of additional waste products that could fuel inflammatory states, making chronic injuries harder to resolve and correlating with increased risk of cancer development. “In these gastric cells, paligenosis — reversion to a stem cell state for healing — is a risky process, especially now that we’ve identified the potentially inflammatory downsizing of cathartocytosis within it,” Mills said. “These cells in the stomach are long-lived, and aging cells acquire mutations. If many older mutated cells revert to stem cell states in an effort to repair an injury — and injuries also often fuel inflammation, such as during an infection — there’s an increased risk of acquiring, perpetuating and expanding harmful mutations that lead to cancer as those stem cells multiply.” More research is needed, but the authors suspect that cathartocytosis could play a role in perpetuating injury and inflammation in Helicobacter pylori infections in the gut. H. pylori is a type of bacteria known to infect and damage the stomach, causing ulcers and increasing the risk of stomach cancer. The findings also could point to new treatment strategies for stomach cancer and perhaps other GI cancers. Brown and WashU Medicine collaborator Koushik K. Das, MD, an associate professor of medicine, have developed an antibody that binds to parts of the cellular waste ejected during cathartocytosis, providing a way to detect when this process may be happening, especially in large quantities. In this way, cathartocytosis might be used as a marker of precancerous states that could allow for early detection and treatment. “If we have a better understanding of this process, we could develop ways to help encourage the healing response and perhaps, in the context of chronic injury, block the damaged cells undergoing chronic cathartocytosis from contributing to cancer formation,” Brown said. Brown JW, Lin X, Nicolazzi GA, Liu X, Nguyen T, Radyk MD, Burclaff J, Mills JC. Cathartocytosis: jettisoning of cellular material during reprogramming of differentiated cells. Cell Reports. Online July 20, 2025. DOI: 10.1016/j.celrep.2025.116070. To read the original article click here.

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The Value of Saving Umbilical Cord Blood

The AHA! Team — Wed, 06 Nov 2024 06:06:28 +0000

Duke Health – Jessica M. Sun, MD, a pediatric hematologist/oncologist at Duke Children’s, explains why you might want to save your child’s umbilical cord blood. What is umbilical cord blood? Umbilical cord blood is a baby’s blood left in the placenta (also called the afterbirth) after the baby is born and the umbilical cord is cut. Historically, umbilical cord blood was discarded with the placenta as medical waste. Over the past few decades, cord blood has been shown to contain stem cells and early precursor cells that can be used for life-saving stem cell transplantation for children and adults in need of a stem cell transplant. Cord blood is more tolerant of a new host and can be used without full matching, providing increased access to transplantation for patients who cannot find a matched donor. How is umbilical cord blood used in medicine? Hematopoietic stem cell transplantation can be an effective therapy for children and adults with certain cancers, immune deficiencies, bone marrow failure syndromes, and some genetic diseases including inborn errors of metabolism and hemoglobinopathies. Traditionally, stem cells used for transplantation were obtained from bone marrow or blood. More recently, cord blood has become an alternative source of stem cells for transplantation. A major limitation to stem cell transplantation therapy is the ability to find a suitable donor. Only 20 to 25% of patients in need of a transplant have relative who is a “match” and can serve as their donor. Of those without a related donor, only 10 to 50% of patients (depending on their race and ethnicity) will find a matched unrelated bone marrow donor through the National Marrow Donor Program and other donor registries. Cord blood transplantation does not require as strict matching as bone marrow, so many people who cannot find a matched bone marrow donor can find a suitable cord blood donor. It is estimated that more than 4,000 cord blood transplants are being performed each year around the world. Cord blood and cells derived from birthing tissues are also being studied as a source of stem cells for other purposes, including regenerative therapies for tissues damaged by injury or disease. Duke researchers are currently studying whether an infusion of cord blood can help a child with cerebral palsy, children born with hydrocephalus, and babies with birth asphyxia. We are also studying whether a cell manufactured from cord blood can help repair the lining of nerve cells in the brains of children with leukodystrophies and adults with primary progressive multiple sclerosis. However, these applications remain unproven and are currently the subject of ongoing research. How is umbilical cord blood collected and stored? Umbilical cord blood can be collected without risk to the mother or infant donor. Cord blood can be collected from the placenta, either during the third stage of labor or within 10 to 15 minutes after delivery of the placenta, by sterilely puncturing one of the umbilical veins with a needle and allowing the cord blood to drain into a sterile bag containing an anticoagulant to prevent clotting. After collection from the placenta, some of the red blood cells are usually removed and the volume of the cord blood collection is reduced. For long-term storage, cells undergo specialized freezing procedures and are stored in special freezers under liquid nitrogen. Maximal storage time, or expiration date, is unknown, but cells are likely to remain usable for decades. Cord blood units from public banks have been successfully transplanted after 18 years in storage. What are the options for cord blood storage? There are two main types of cord blood banks, public and private. In general, public banks are nonprofit entities supported by federal or private funding. After the mother consents, public banks collect cord blood from healthy full-term pregnancies at no cost to the donor’s family. In giving consent, the infant’s mother acknowledges that the donation is voluntary and gives up all rights to the cord blood for the public good. The mother also agrees to allow her medical records and the baby’s newborn records to be reviewed, gives a detailed family medical history, and allows a sample of her own blood to be taken for infectious disease testing. Units passing screening tests designed to eliminate risks of transmitting genetic or infectious diseases are typed, placed in the search registry, and are available to any suitable patient in need of transplantation. Units that do not meet criteria for public banking may be discarded or used for research purposes. Private cord blood banks are generally for-profit companies that store “directed donations” intended for future use by the child or a family member. Using a kit provided by the bank, the cord blood is collected by the physician, midwife, or nurse delivering the baby and shipped back to the company’s banking facility. The parents of the infant are charged an initial fee for collection and processing of the cord blood and then an annual fee for storage. Varying degrees of testing is performed on the units, and minimal standards are used to determine whether a unit is eligible for processing and banking. The majority of private collections are undertaken as an investment in the unknown potential for cord blood to be used to treat serious illnesses in the future. Most obstetricians and pediatricians feel that routine cord blood storage in healthy babies is unnecessary. In this regard, it is important to note that a child’s own cord blood would not be used for transplantation of a child with leukemia or other cancers, in part due to concern for contamination with cancerous cells, and it would not be used to treat a genetic condition because the cord blood would contain the same genetic problem. Currently, directed donation of umbilical cord blood for another family member is recommended when a first-degree relative has a high risk pediatric cancer that can be treated with transplantation therapy, a hemoglobinopathy or other transfusion-dependent blood disorder, a congenital immune deficiency, or an inborn error of metabolism. How can I donate my child’s umbilical cord blood? It is always a good idea to discuss options for cord blood banking with your obstetric provider or pediatrician. To privately store your baby’s cord blood for possible future use by the child or a family member, you may contact one of the many private cord blood banks to arrange collection, shipment, and payment. Additional information about cord blood banking, including a list of private banks, can be found through the Parent’s Guide to Cord Blood Foundation. To donate your baby’s cord blood for public use, first check whether the hospital at which you plan to deliver works with a cord blood bank to collect cord blood for public donation. In North Carolina, public collections are available at Duke, UNC, Womack Army Medical Center, and Rex Hospitals. If your hospital does not participate in public cord blood banking, there are a few public cord blood banks, including the Carolinas Cord Blood Bank at Duke, that offer a free kit program so that public donations may be collected at other hospitals. Interested parents should contact the bank (919-668-2071) at least six weeks before the baby’s due date to learn more about the program. Currently, public donations are limited to mothers who have a healthy pregnancy, are 18 years or older, and are pregnant with a single baby. More information about public cord blood donation is available through the National Marrow Donor Program. To read the original article click here.

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Genetic Variant linked to Increased Risk of Leukemia in Hispanic/Latino Children

The AHA! Team — Fri, 17 May 2024 08:07:50 +0000

Keck School of Medicine of USC via News-Medical – Acute lymphoblastic leukemia (ALL), the most common childhood cancer, disproportionately affects children of Hispanic/Latino origin in the United States. They are 30-40% more likely to get ALL than non-Hispanic white children, but the exact genetic basis and cause of that increased risk are unknown. (ALL) disproportionately affects children of Hispanic/Latino origin in the United States Now, a study from the Keck School of Medicine of USC has revealed a key genetic variant contributing towards the increased risk, as well as details about the biological basis of ALL. The team used genetic fine-mapping analysis, a statistical method that allows researchers to disentangle the separate effects of genetic variants in a region of the genome. They identified a variant found at a relatively high frequency in people of Hispanic/Latino origin that increases ALL risk by around 1.4 times. The study, funded in part by the National Institutes of Health, was just published in the journal Cell Genomics. “Combined with the fact that around 30% of Hispanic/Latino people in the United States carry this gene variant, but it’s basically absent in people of predominantly European ancestry, we think it’s an important contributor to the increased ALL risk among this group,” said the study’s lead author, Adam de Smith, PhD, an assistant professor of population and public health sciences and a member of the USC Norris Comprehensive Cancer Center at the Keck School of Medicine, as well as a scholar of the Leukemia & Lymphoma Society. The researchers also performed tests to better understand how the variant, located on the IKZF1 gene, which underlies B-cell development, relates to ALL through its influence on the development of B-cells, a type of white blood cell known to be disrupted by the disease. “Together, the analyses in our study provide the statistical, biological and evolutionary insights behind this increased risk, and may ultimately aid scientists working to develop screening tools and therapies for ALL.” -Charleston Chiang, PhD, associate professor of population and public health sciences and associate director of the Center of Genetic Epidemiology at the Keck School of Medicine and study’s co-senior author The genetic basis of leukemia risk To pinpoint the genetic basis of the elevated ALL risk Hispanic/Latino children face, the researchers analyzed genetic data from the California Cancer Records Linkage Project. Their dataset included 1,878 Hispanic/Latino children in California with ALL and 8,411 without the condition; 1,162 non-Hispanic white children with ALL and 57,341 without; and 318 East Asian children with ALL and 5,017 without. The research team focused on the IKZF1 gene, known to relate to ALL but never before linked with ethnic risk disparities. Using genetic fine-mapping analysis, they independently analyzed each position along the gene-;known as a single nucleotide polymorphism (SNP)-;to determine whether having a certain variant increased ALL risk. They found three independent SNPs linked to higher ALL incidence, one of which was present in about 30% of people of Hispanic/Latino origin in the U.S. and less than 1% of people of primarily European origin. Although overall risk for the disease is low across all racial/ethnic groups, children with that gene variant, located at SNP rs76880433, were 1.44 times as likely to develop ALL as children without the variant. The genetic ancestry of most Hispanics/Latinos can be traced to Europe, Africa, and Indigenous America. Further investigation revealed that the risk variant was specifically linked with Indigenous American ancestry and may have become more common in this group because it conferred a selective advantage at some point in human history. Next, the Keck School of Medicine team partnered with co-senior author Vijay Sankaran, MD, PhD, an associate professor of pediatrics at Harvard Medical School and attending physician at the Dana-Farber/Boston Children’s Cancer and Blood Disorders Center, to conduct a series of experiments to better understand how the genetic variant at IKZF1 increases risk for ALL. One experiment analyzed chromatin accessibility, a test which indicates how fully a given gene can be expressed. The researchers found that the risk variant reduced chromatin accessibility, preventing IKZF1 proteins from being fully expressed. Sankaran and his team also conducted experiments with stem cells, finding that “knocking out” the IKZF1 gene caused B-cell development to stall in its early stages. “Looking at all of this together, we think that the risk variant is reducing IKZF1 expression,” de Smith said. “By doing so, it’s keeping B-cells in a more immature state, which would increase ALL risk by giving the cells more chance to develop mutations that could eventually lead to overt leukemia.” Leukemia screening and treatment The new insights about IKZF1 bring researchers one step closer to developing effective screening tools to predict who may develop ALL, but more research is needed. In addition, the findings provide important clues about potential ways to treat the disease, for instance by progressing B-cell development after it stalls. “We also need to understand whether this variant is associated with different patient outcomes, such as the risk of relapse or chances of survival, and why that might be,” de Smith said. He and his colleagues also hope to explore whether the newly identified risk variant helps explain the even higher risk of ALL among Hispanic/Latino adolescents and young adults, who are more than twice as likely to get the disease than people who are non-Hispanic white. About this research In addition to de Smith, Chiang and Sankaran, the study’s other authors are Soyoung Jeon, Jalen Langie, Tsz-Fung Chan, Steven Gazal, Nicholas Mancuso and Joseph Wiemels from the Center for Genetic Epidemiology and the USC Norris Comprehensive Cancer Center, Keck School of Medicine of USC; Lara Wahlster, Susan Black, Liam Cato, Soumyaa Mazumder and Fulong Yu from Boston Children’s Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute; Linda Kachuri from the Stanford University School of Medicine; Nathan Nakatsuka from the New York Genome Center; Guangze Xia from the Guangzhou National Laboratory, Guangzhoi, China; Wenjian Yang and Jun Yang from St. Jude Children’s Research Hospital, Memphis; Celeste Eng, Donglei Hu, Esteban Gonzalez Burchard and Elad Ziv from the Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco; Catherine Metayer from the School of Public Health, University of California, Berkeley; and Xiaomei Ma from the Yale School of Public Health. This work was supported by the National Institutes of Health [R01CA262263, R01CA155461, R00CA246076, R35GM142783, R01DK103794, R01CA265726]; the New York Stem Cell Foundation; and the Dana-Farber Cancer Institute Presidential Priorities Initiative. Source: Keck School of Medicine of USC Journal reference: de Smith, A. J., et al. (2024) A noncoding regulatory variant in IKZF1 increases acute lymphoblastic leukemia risk in Hispanic/Latino children. Cell Genomics. doi.org/10.1016/j.xgen.2024.100526. To read the original article click here.

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Hyaluranic Acid, a Naturally Occurring Compound, Awakens Stem Cells to Repair Damaged Muscle

AHA Publisher — Fri, 12 Aug 2022 07:00:51 +0000

Ottawa Hospital via Newswise – A new study published in the journal Science reveals a unique form of cell communication that controls muscle repair. In damaged muscle, stem cells must work together with immune cells to complete the repair process, yet how these cells coordinate to ensure the efficient removal of dead tissue before making new muscle fibers has remained unknown. The scientists have now shown that a natural substance called hyaluronic acid, which is used in cosmetics and injections for osteoarthritis, is the key molecule that manages this fundamental interaction. “When muscles get damaged, it is important for immune cells to quickly enter the tissue and remove the damage before stem cells begin repair,” said Dr. Jeffrey Dilworth, senior scientist at The Ottawa Hospital and professor at the University of Ottawa and senior author on the study. “Our study shows that muscle stem cells are primed to start repair right away, but the immune cells maintain the stem cells in a resting state while they finish the cleanup job. After about 40 hours, once the cleanup job is finished, an internal alarm goes off in the muscle stem cells that allows them to wake up and start repair.” Dr. Dilworth and his team identified hyaluronic acid as the key ingredient in this internal alarm clock that tells muscle stem cells when to wake up. When muscle damage occurs, stem cells start producing and coating themselves with hyaluronic acid. Once the coating gets thick enough, it blocks the sleep signal from the immune cells and causes the muscle stem cells to wake up. Using mouse and human tissues, Dr. Dilworth and his team also discovered how muscle stem cells control the production of hyaluronic acid using epigenetic marks on the Has2 gene. “Interestingly, aging is associated with chronic inflammation, muscle weakness and a reduced ability of muscle stem cells to wake up and repair damage,” said lead author Dr. Kiran Nakka, a research associate with Dr. Dilworth who conducted this research as part of his postdoctoral studies. “If we could find a way to enhance hyaluronic acid production in the muscle stem cells of older people it might help with muscle repair.” The authors note that the regenerative effect of hyaluronic acid seems to depend on it being produced by the muscle stem cells. The team is currently examining if drugs that modify the epigenetics of muscle stem cells could be used to increase their production of hyaluronic acid. To read the original article click here.

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Bioprinted Implant May Help Paralyzed People Walk Again

AHA Publisher — Tue, 08 Feb 2022 08:00:51 +0000

Abigail Klein Leichman via Israel21c – Medical science has not yet found a way to restore walking ability in someone paralyzed from a traumatic spinal cord injury. Within a few years, a first-of-its-kind 3D-printed spinal cord tissue implant, made from the patient’s own cells, could make that dream come true. Using technology developed over the course of a decade in Prof. Tal Dvir’s regenerative biotechnology lab at Tel Aviv University, the implant enabled paralyzed lab mice to walk again. A paper published today in Advanced Science provides the remarkable details. “It is like science fiction,” says Dr. Asaf Toker, CEO of Matricelf, the company working to bring Dvir’s groundbreaking technology to market. ISRAEL21c readers may recall that two years ago, Dvir’s lab 3D-printed the world’s first miniature vascularized human heart. Dvir and Alon Sinai cofounded Matricelf that year and it went public in 2021. On January 30, the company signed an exclusive global licensing agreement with Tel Aviv University technology transfer company Ramot to commercialize and utilize the patent for 3D-printing tissues and organs. “With our technology, we can create any tissue we want,” Toker tells ISRAEL21c. “The first one is neural implants for people with a spinal cord injury causing paralysis.” No Rejection Dvir explained that the technique begins with taking a small biopsy of belly fat tissue from the patient. “This tissue, like all tissues in our body, consists of cells together with an extracellular matrix of substances like collagens and sugars,” he explained. “After separating the cells from the extracellular matrix, we used genetic engineering to reprogram the cells, reverting them to a state that resembles embryonic stem cells capable of becoming any type of cell in the body.” The extracellular matrix didn’t go to waste. It formed the basis of a personalized hydrogel that will not trigger an immune response or rejection after implantation – which is the main problem with donor implants. “We then encapsulated the stem cells in the hydrogel and, in a process that mimics the embryonic development of the spinal cord, we turned the cells into 3D implants of neuronal networks containing motor neurons,” said Dvir. The human spinal cord implants were then implanted in mice. Half had only recently been paralyzed (the acute model) and half had been paralyzed for the equivalent of a year in human terms (the chronic model). Up and Walking Again Following the implantation and a rapid rehabilitation process, 100 percent of the mice with acute paralysis and 80% of those with chronic paralysis regained their ability to walk. “This is the first instance in the world in which implanted engineered human tissues have generated recovery in an animal model for long-term chronic paralysis – which is the most relevant model for paralysis treatments in humans,” Dvir said. “Individuals injured at a very young age are destined to sit in a wheelchair for the rest of their lives, bearing all the social, financial, and health-related costs of paralysis” because there has never been an effective treatment, Dvir pointed out. “Our goal is to produce personalized spinal cord implants for every paralyzed person, enabling regeneration of the damaged tissue with no risk of rejection.” Following discussions with the US Food and Drug Administration (FDA), Matricelf plans the first human clinical trial of the spinal cord implant at the end of 2024. “Since we are proposing an advanced technology in regenerative medicine, and since at present there is no alternative for paralyzed patients, we have good reason to expect relatively rapid approval of our technology,” said Dvir. In the meantime, additional efficacy and safety trials will be done on lab rats. Printing Tissues and Organs Toker explains what makes this technology unique. “Tissue engineering requires two ingredients: cells and extracellular matrix as a scaffold for the cells to build the tissue,” he says. “Many companies do tissue engineering using synthetic materials for scaffolds or using cells from a donor. But when you introduce foreign material to the body, the immune system attacks it, and the implant fails unless the patient takes drugs to suppress the immune system.” The Matricelf technology developed by Dvir uses autologous (the patient’s own) cells and extracellular matrix. The immune system recognizes them and doesn’t attack them. “The new licensing agreement with Ramot also enables us to 3D-print tissues and organs,” says Toker. “An organ is built from a variety of tissues and cells. So our bioprinter has several bio-ink cartridges to print different tissues in the same printing, just like in four-color printing where the printer knows where to put each color.” The bio-ink is enclosed inside another fluid to support the organ’s structure. “When you print a hollow organ like a heart, if you don’t use this technology the tissue will collapse,” Toker explains. “To print organs with cavities inside them you need the technology to support it. That is our unique aspect.” The spinal implant was developed by Dvir and lab members Lior Wertheim, Dr. Reuven Edri and Dr. Yona Goldshmit along with Prof. Irit Gat-Viks from the Shmunis School of Biomedicine and Cancer Research, Prof. Yaniv Assaf from the Sagol School of Neuroscience, and Dr. Angela Ruban from the Steyer School of Health Professions, all at Tel Aviv University. Matricelf, based in Ness Ziona, employs 10 people – seven of whom are women, Toker tells ISRAEL21c. It is well-positioned to become a prominent player in the 3D bioprinting market, estimated to be worth about $650 million in 2019 and an expected $1.6 billion in 2024. To read the original article click here.

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How to Build Your Own ‘Longevity Gene’

AHA Publisher — Wed, 26 May 2021 07:00:49 +0000

Al Sears, MD – Kane Tanaka is the oldest person on the planet. At 118, she’s defying the “experts” who insist that genes determine your lifespan. This summer, when the Olympic torch travels through her hometown of Shime, Japan, Kane will carry the flame. Imagine that, a 118-year-old torch bearer! Most doctors attribute her longevity to “good genes.” But despite thousands of studies over the past 50 years, no researcher has been able to identify a single gene explaining the longevity of supercentenarians like Kane. As a regular reader, you’ll know that I believe your genes don’t determine how long, or how well, you can live. And it looks like the geneticists are finally coming around to my point of view. As a matter of fact, many of them now agree that genes only account for about 25% of your longevity.1The remaining 75% is determined by your nutrition, activity level, and lifestyle. Despite the realization that non-genetic factors are much more important, Cornell University researchers wanted to give one unique gene a closer look… A “FOX Hunt” for Longevity… The FOX03 gene plays a key role in regulating metabolism, fighting free radicals, and calming inflammation – three major pathways to aging. Researchers wanted to know how it functions. So they flooded mice brain cells with free radicals and watched FOX03 go to work. FOX03 responded by signaling brain stem cells to halt their usual journey to becoming full-fledged neurons. Now the brain needs a constant supply of new cells to keep you sharp as you age. So the obvious question: Why did FOX03 stop the assembly line? Stem cells are extremely vulnerable as they morph into brain cells. By signaling them to suspend their development, FOX03 was conserving the brain’s limited supply.2 That’s pretty impressive. But even more significant is this: There are several ways you can activate your FOX03 gene to make it twice as powerful. In a sense, you can build your own “longevity gene.” Energize FOX03 to Hunt Free Radicals Energizing FOX03 to hunt down free radicals helps preserve the vital telomeres that protect the integrity of your DNA. Here are three ways to do it: Astaxanthin – My regular readers already know that astaxanthin, nature’s most powerful antioxidant, guards your retinas and staves off macular generation. But recent studies show it nearly doubles FOXO3 activity.3,4 I recommend wild-caught food sources such as salmon, shrimp, and crawfish. But you should also supplement with up to 50 mg of astaxanthin daily. I tell my patients to look for a supplement derived from the best natural source. That’s Haematococcus pluvialis algae. Calorie restriction/fasting – There’s growing evidence FOXO3 and various forms of fasting work to accelerate apoptosis, ridding your body of the dysfunctional cells that contribute to inflammation. Calorie restriction lowers the body’s production of insulin-like growth factor 1 [IGF-1], and as IGF-1 declines FOX03 activity ramps up.5 EGCG – Consider it another reason to make green tea part of your health routine. Already highly regarded for its anti-inflammatory and heart-health benefits, there’s growing evidence the green tea extract EGCG activates the FOX03 gene as well. Most of the studies so far are on animals.6But EGCG-activated FOX03 inhibited the growth of human breast cancer cells.7 A cup of green tea contains about 100 mg of EGCG. I recommend you supplement with up to 1,500 mg of the extract daily. 1 Passarino, G., De Rango, F., & Montesanto, A. (2016). Human longevity: Genetics or Lifestyle? It takes two to tango. Immunity & Ageing, 13(1). https://doi.org/10.1186/s12979-016-0066-z 2 Study Reveals How a Longevity Gene Protects Brain Stem Cells From Stress. (2021, February 19). Retrieved April 5, 2021, from WCM Newsroom website: https://news.weill.cornell.edu/news/2021/02/study-reveals-how-a-longevity-gene-protects-brain-stem-cells-from-stress 3 Research: University of Hawaii reports Astaxanthin can activate the FOX03 “Longevity Gene” in mammals. (2017, March 28). Retrieved April 5, 2021, from John A. Burns School of Medicine website: https://jabsom.hawaii.edu/research-university-of-hawaii-reports-ability-of-astaxanthin-to-significantly-activate-fox03-longevity-gene-in-mammals/ 4 Astaxanthin compound found to switch on the FOX03 “Longevity Gene” in mice. (2017, March 28). Retrieved March 26, 2021, from ScienceDaily website: https://www.sciencedaily.com/releases/2017/03/170328092428.htm 5 Komatsu, T., Park, S., Hayashi, H., Mori, R., Yamaza, H., & Shimokawa, I. (2019). Mechanisms of Calorie Restriction: A Review of Genes Required for the Life-Extending and Tumor-Inhibiting Effects of Calorie Restriction. Nutrients, 11(12), 3068. https://doi.org/10.3390/nu11123068 6 Bartholome, A., Kampkötter, A., Tanner, S., Sies, H., & Klotz, L.-O. (2010). Epigallocatechin gallate-induced modulation of FoxO signaling in mammalian cells and C. elegans: FoxO stimulation is masked via PI3K/Akt activation by hydrogen peroxide formed in cell culture. Archives of Biochemistry and Biophysics, 501(1), 58–64. https://doi.org/10.1016/j.abb.2010.05.024 7 Belguise, K., Guo, S., & Sonenshein, G. E. (2007). Activation of FOXO3a by the Green Tea Polyphenol Epigallocatechin-3-Gallate Induces Estrogen Receptor Expression Reversing Invasive Phenotype of Breast Cancer Cells. Cancer Research, 67(12), 5763–5770. https://doi.org/10.1158/0008-5472.can-06-4327 To read the original article click here. For more articles from Al Sears, MD click here.

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Holy Fruit Turns on Healing Stem Cells

AHA Publisher — Tue, 01 Sep 2020 07:00:12 +0000

Al Sears, MD, CNS – New research has found a way to dramatically increase the number of stem cells circulating in the blood using the “holy fruit of the Himalayas,” or seaberry. This bright orange fruit has been used for thousands of years to treat inflammation and infections, boost immunity, and slow the aging process. Modern research explains why it works. In the study, 12 healthy adults had their blood drawn before and after eating either seaberry extract or a placebo. Data on stem cell activity was analyzed following each blood draw.1 Within two hours of eating the berry, researchers found that: Progenitor stem cells capable of cardiovascular maintenance and repair increased 24%. Endothelial stem cells increased by 33%. These multipotent stem cells found in bone marrow, have the ability to develop into multiple specialized cells. Increasing the number of circulating stem cells in your body has been proven to potentially repair: Acute myocardial infarction2 Stroke3 Bone fracture4 Muscle injury5 Spinal cord injury6 Inner ear damage7 Boost Your Stem Cells Easily at Home First take seaberry extract daily. To get the results researchers saw in the study, take 500 mg daily. It’s available as a softgel, powder and juice. Look for certified organic, non-GMO products. Second, try fasting for two days every six months. A study from the University of Southern California shows that this kind of fasting causes stem cells to awake from their normal dormant state and start regenerating. This practice destroyed damaged and older cells, and caused new cells to be born, effectively renewing the immune system.8 Finally, workout intensely. A study in the European Heart Journal showed that vigorous exercise in mice activated 60% of their cardiac stem cells.9 In a human study, researchers proved that strenuous exercise leads to high levels of stem cells in bone, liver and other organs.10 To Your Good Health, Al Sears, MD, CNS 1. Drapeau C, et al. “Rapid and selective mobilization of specific stem cell types after consumption of a polyphenol-rich extract from sea buckthorn berries (Hippophae) in healthy human subjects.” Clin Interv Aging. 2019:14:253-263. 2. Luo Y, et al. “Short-term intermittent administration of CXCR4 antagonist AMD3100 facilitates myocardial repair in experimental myocardial infarction.” Acta Biochim Biophys Sin (Shanghai). 2013;45(7):561-569. 3. Wang L, et al. “Mobilization of endogenous bone marrow derived endothelial progenitor cells and therapeutic potential of parathyroid hormone after ischemic stroke in mice.” PLoS One. 2014;9(2):e87284. 4. Toupadakis CA, et al. “Mobilization of endogenous stem cell populations enhances fracture healing in a murine femoral fracture model.” Cytotherapy. 2013;15(9):1136-1147. 5. Stratos I, et al. “Granulocyte-colony stimulating factor enhances muscle proliferation and strength following skeletal muscle injury in rats.” J Appl Physiol. 2007;103(5):1857-1863. 6. Urdziková L, et al. “Flt3 ligand synergizes with granulocyte-colony-stimulating factor in bone marrow mobilization to improve functional outcome after spinal cord injury in the rat.” Cytotherapy. 2011;13(9):1090-1104. 7. Elbana AM. “Role of endogenous bone marrow stem cells mobilization in repair of damaged inner ear in rats.” Int J Stem Cells. 2015;8(2):146-154. 8. Cheng CW, et al. “Prolonged fasting reduces igf-1/pka to promote hematopoietic-stem-cell-based regeneration and reverse immunosuppression.” Cell Stem Cell. 14(6):810-823. 9. Gariani K, et al. “Eliciting the mitochondrial unfolded protein response by nicotinamide adenine dinucleotide repletion reverses fatty liver disease in mice.” Hepatology. 2016;63(4):1190-1204. 10. Valero MC, et al. “Eccentric Exercise facilitates mesenchymal stem cell appearance in skeletal muscle.” PLOS One. 2012;7(1):e29760. This article has been modified. To read the original article click here. For more articles by Al Sears MD click here.

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Researchers Discover Stem Cells in Optic Nerve That Preserve Vision

AHA Publisher — Fri, 31 Jul 2020 07:00:03 +0000

University of Maryland School of Medicine via EurekAlert – Researchers at the University of Maryland School of Medicine (UMSOM) have for the first time identified stem cells in the region of the optic nerve, which transmits signals from the eye to the brain. The finding, published this week in the journal Proceedings of the National Academy of Sciences (PNAS), presents a new theory on why the most common form of glaucoma may develop and provides potential new ways to treat a leading cause of blindness in American adults. “We believe these cells, called neural progenitor cells, are present in the optic nerve tissue at birth and remain for decades, helping to nourish the nerve fibers that form the optic nerve,” said study leader Steven Bernstein, MD, PhD, Professor and Vice Chair of the Department of Ophthalmology and Visual Sciences at the University of Maryland School of Medicine. “Without these cells, the fibers may lose their resistance to stress, and begin to deteriorate, causing damage to the optic nerve, which may ultimately lead to glaucoma.” The study was funded by the National Institutes of Health’s National Eye Institute (NEI), and a number of distinguished researchers served as co-authors on the study. More than 3 million Americans have glaucoma, which results from damage to the optic nerve, causing blindness in 120,000 U.S. patients. This nerve damage is usually related to increased pressure in the eye due to a buildup of fluid that does not drain properly. Blind spots can develop in a patient’s visual field that gradually widen over time. “This is the first time that neural progenitor cells have been discovered in the optic nerve. Without these cells, the nerve is unable to repair itself from damage caused by glaucoma or other conditions. This may lead to permanent vision loss and disability,” said Dr. Bernstein. “The presence of neural stem/progenitor cells opens the door to new treatments to repair damage to the optic nerve, which is very exciting news.” To make the research discovery, Dr. Bernstein and his team examined a narrow band of tissue called the optic nerve lamina. Less than 1 millimeter wide, the lamina lies between the light-sensitive retina tissue at the back of the eye and the optic nerve. The long nerve cell fibers extend from the retina through the lamina, into the optic nerve. What the researchers discovered is that the lamina progenitor cells may be responsible for insulating the fibers immediately after they leave the eye, supporting the connections between nerve cells on the pathway to the brain. The stem cells in the lamina niche bathes these neuron extensions with growth factors, as well as aiding in the formation of the insulating sheath. The researchers were able to confirm the presence of these stem cells by using antibodies and genetically modified animals that identified the specific protein markers on neuronal stem cells. “It took 52 trials to successfully grow the lamina progenitor cells in a culture,” said Dr. Bernstein, “so this was a challenging process.” Dr. Bernstein and his collaborators needed to identify the correct mix of growth factors and other cell culture conditions that would be most conducive for the stem cells to grow and replicate. Eventually the research team found the stem cells could be coaxed into differentiating into several different types of neural cells. These include neurons and glial cells, which are known to be important for cell repair and cell replacement in different brain regions. This discovery may prove to be game-changing for the treatment of eye diseases that affect the optic nerve. Dr. Bernstein and his research team plan to use genetically modified mice to see how the depletion of lamina progenitor cells contributes to diseases such as glaucoma and prevents repair. Future research is needed to explore the neural progenitors repair mechanisms. “If we can identify the critical growth factors that these cells secrete, they may be potentially useful as a cocktail to slow the progression of glaucoma and other age-related vision disorders.” Dr. Bernstein added. The work was supported by NEI grant RO1EY015304, and by a National Institutes of Health shared instrument grant 1S10RR26870-1. “This exciting discovery could usher in a sea change in the field of age-related diseases that cause vision loss,” said E. Albert Reece, MD, PhD, MBA, Executive Vice President for Medical Affairs, UM Baltimore, and the John Z. and Akiko K. Bowers Distinguished Professor and Dean, University of Maryland School of Medicine. “New treatment options are desperately needed for the millions of patients whose vision is severely impacted by glaucoma, and I think this research will provide new hope for them.” To read the original article click here.

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Repair Your Gut with This Biomolecule

AHA Publisher — Wed, 22 Jul 2020 07:00:18 +0000

Monash University via EurekAlert– In a world first, Monash University researchers have identified a key biomolecule that enhances the repair of your gut lining by prompting stem cells to regenerate damaged tissue. A strong cellular lining is essential for a healthy gut as it provides a barrier to the billions of microbes and harmful toxins present in our intestinal tract. This barrier is often damaged by infection and inflammation, which causes many painful symptoms. The study, published in Cell Stem Cell and led by Professor Helen Abud and Dr Thierry Jardé from Monash Biomedicine Discovery Institute, investigated the environment that surrounds gut stem cells and used “mini gut” organoid methodology where tiny replicas of gut tissue were grown in a dish. The study defined key cells that reside in close proximity to stem cells in the gut that produce the biomolecule Neuregulin-1 that acts directly on stem cells to kick-start the repair process. “Our really important discovery is that supplementation with additional Neuregulin-1 accelerates repair of the gut lining by activation of key growth pathways,” Professor Abud said. “Our findings open new avenues for the development of Neuregulin 1-based therapies for enhancing intestinal repair and supporting rapid restoration of the critical gut function.” Gastrointestinal disease, such as Crohn’s disease and ulcerative colitis, is a major health issue worldwide and results in severe damage to the epithelial cell layer lining the gut. Under these conditions, the intestine has a limited capacity to repair efficiently to restore its main absorptive function and is associated with symptoms including diarrhoea, dehydration, loss of weight and malnutrition. Developing ways to support intestinal tissue repair will dramatically improve patient recovery. “It was very exciting to observe that Neuregulin 1 can not only drive cells to divide but enhances stem cell properties which supercharges these cells into a repair program,” Dr Jardé said. “This shortens the period of damage. The gut lining is injured during common chemotherapy treatment for cancer and we were also able to show recovery is significantly improved with application of Neuregulin-1 following chemotherapy. To read the original article click here.

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