https://stemaid.com/Stemaid™ : Pluripotent Stem Cells : news2024-03-18T19:11:47-07:00e107https://e107.org/e107e107https://stemaid.com//e107_media/343825e64d/images/2017-06/screenshot_stemaid.com_2017_06_05_15_49_28.pngadmin - noreply@nospam.comhttps://stemaid.com/news/pluripotent-stem-cells-as-a-treatment-for-liver-failure.htmlPluripotent Stem Cells as a Treatment for Liver Failure2021-10-13T08:00:00-06:00admincameron@nospam.comIntroductionChronic liver disease is a condition where the liver becomes damaged and unable to function properly. It can lead to cirrhosis, cancer, and even death. There are several types of chronic liver diseases, including liver cirrhosis, viral hepatitis, alcoholic liver disease, nonalcoholic fatty liver disease, primary biliary cholangitis, biliary cirrhosis and hepatocellular carcinoma (liver cancer). Acute-on-chronic liver failure ranks globally as the 4th leading cause of death.Up until now, patients with end-stage liver disease typically had one therapeutic strategy for this condition - liver transplant surgery. Transplantation in patients is considered to be a high-risk procedure and the complications after liver transplantation can seriously affect quality of life. Alternative treatment is an integral part of medical regenerative therapy. Regenerative medicine in the form of stem cell-based therapies holds promise as an effective treatment of liver diseases and alternative to liver transplantation. Previous studies and clinical trials using mesenchymal stem cells have already showed some promising results. Pluripotent stem cell therapy is the next frontier as leading cell-based therapy for all forms of liver damage, from acute liver failure to end-stage liver disease. What are the types of liver disease?Liver disease is a condition where the liver does not function properly. It may cause serious problems such as cirrhosis, scarring or cancer.There are many different types of liver disease, viral hepatitis, alcoholic liver disease, nonalcoholic fatty liver disease, primary biliary cholangitis, biliary cirrhosis and hepatocellular carcinoma (liver cancer). Hepatitis is an inflammation of the liver caused by viruses, bacteria, toxins, drugs, alcohol, or autoimmune diseases. Fatty liver disease is a type of liver disease that occurs when fat builds up in the liver.What causes cirrhosis?Cirrhosis of the liver is often caused by long term exposure to a toxins. It leads to scarring of the liver tissue and eventually liver failure. Liver cirrhosis patients show end-stage liver disease scores. Chronic disease like liver cirrhosis is often coupled with chronic hepatitis, inflammation and autoimmune diseases. The immune cells are often involved in disease progression in acute-on-chronic liver failure patients. Improvement in liver function is always proceeded by positive changes in immune responses. Anti-inflammatory effects and a immunomodulatory therapeutic tool is needed. Pluripotency is indicated. What challenges do patients with liver cirrhosis experience? Cirrhosis is a condition where the liver becomes damaged and scarred. It causes the liver to become enlarged and hard. The liver is responsible for filtering toxins out of the blood. If the liver does not function properly, these toxins build up in the body and patients experience fatigue, abdominal discomfort and pain. Systemic metabolic problems arise. What are Pluripotent Stem Cells?Pluripotent embryonic stem cells (PESCs) are undifferentiated cells that have the ability to self-renew and repair indefinitely and can therefore be used for regenerative medicine. They release potent paracrine factors that signal repair in all 220+ types of the human body, including hepatic tissue. They release repair transcription factors, like angiocrine factors, that instigate cellular reprogramming of hepatic cells. The Case StudyPurpose:The purpose of this study was to assess the therapeutic efficacy of the Stemaid™ protocol as a cell-based therapy for cirrhosis (alcoholic cirrhosis) and other chronic liver diseases. Liver function blood tests were taken pre-treatment, during treatment and 18-months post-treatment, in order to assess the beneficial effects of Pluripotent stem cells in the treatment of liver cirrhosis. Background:Acute and long-term therapeutic effects of pluripotent embryonic stem cells (ESC) in patients with liver diseases have been observed at the Stemaid Institute clinical practice since 2012. Pluripotency is comprehensive in its signaling profile and has paracrine effects that are capable of signaling repair in all 220+ tissue types of the body, including liver tissue. Repair of cirrhotic livers and overall liver regeneration is considered possible with the help of pluripotent signaling factors, such as DNA repair factors, growth factors, neurotrophic factors, angiocrine factors and immunomodulatory properties. Cells in liver cirrhosis are considered to be reprogrammable back to their healthy phenotype with pluripotent stem cell treatments. Liver injuries and post-treatment improved liver function can be measured via blood liver profiles in patients with a diseased liver. This case report is of one Stemaid patient with hepatic failure due to chronic liver cirrhosis.Methods:The participant aged 62 received 12 intravenous injection treatments of single dose 20 million ESC (Stemaid™ standard line #331) in 50 mL DPBS over a period of 2 weeks. His liver enzymes and bilirubin levels were measured before treatment, one week into the treatment, on the last day of the treatment and 18 months post-treatment. The patient didn't change his current diet during treatment and kept taking his prescribed medications. He received 5 Ascorbic Acid intravenous infusion therapies during treatment.Administration route: Intravenous Injections. Results:Day 1Day 6Day 12>18 monthsNormal RangeAST16613074550-40 U/LALT958551330-38 U/LALP18919613517133-135 U/LBilirubin Total12.78.354.022.10-1.2 mg/dLBilirubin Conjugated8.34.092.910.70-0.5 mg/dLBilirubin Non Conjugated4.404.261.111.400-0.8 mg/dLESR394540230-15 mm/hrDiscussion:The patient had a history of heart failure and had a by-pass surgery 8 years prior to the current treatment. His gallbladder was removed 4 years prior to treatment.The patient had to stop alcohol intake 3 months prior to treatment due to his condition. He wasn't accepted as a candidate for liver transplant due to his history of alcoholism. Icterus, the jaundiced tone of his skin, started to fade at the end of the first week and his energy and appetite improved. The patient reported continuing improvement after returning home and resumed work shortly after, including a flight to Brazil which his doctors initially recommended he cancels. Long term function in patient was reported 2 years later. Total bilirubin levels have been at approximately 2.0 mg/dL for 2 years post-treatment.ConclusionStem cell based therapies around the world use many different types of stem cells. The adult stem cell based therapy options are mesenchymal stem cells, hematopoietic stem cells, fat-derived and bone marrow-derived stem cells. Previous studies, clinical trials and systematic review and meta-analysis sources show positive results with adult stem cell-based therapy. However, out of all the cell-based therapies, pluripotent cells have the most wide tissue reach and most potent cellular reprograming potency of all types of cells. Hepatic progenitor cells are quiescent or degenerated in a cirrhotic liver. Exposure to Yamanaka and other pluripotent factors reprograms damaged phenotype to a more healthy youthful state. Daily pulsing dose of pluripotent factors over a period of 2-week and 4-week intervals creates a restorative microenvironment and causes cellular changes towards health. Therapy for Liver disease is vastly accelerated by pluripotent cell type activity and potency. The quality of life of patients with liver diseases improves drastically with these therapeutic effects. We hope to see a future pilot study and clinical studies investigating the changes in inflammatory markers and epigenetic markers in the treatment of liver diseases with pluripotent stem cells.2021-10-13T08:00:00-06:00https://stemaid.com/news/how-does-pluripotent-stem-cell-therapy-differ-from-other-stem-cell-therapies.htmlHow Does Pluripotent Stem Cell Therapy Differ From Other Stem Cell Therapies?2021-01-05T16:56:33-07:00admincameron@nospam.comMany clinics worldwide provide stem cell therapy, but what are the actual differences between the stem cells available?There are many answers to this question but all experts would agree on the following important facts about stem cell therapy in the world:Availability of Stem CellsHarvesting mesenchymal stem cells (MSC) requires expert staff and expensive technical equipment. Whether they come from the patient’s own tissues or from an umbilical cord source, their source availability and expansion are limited. The cord blood of one new-born, for example, contains an average of 1.8 million MSC. These stem cells can be cultured and expanded 20 to 50 times until they lose their stem cell nature and differentiate into one of the eight types of cells they can become. The risk of contamination for these cells is high also. For every 200 million MSC, a new source must be found and evaluated for pathogens before culture. All these steps and inconsistencies in the success of isolation add to the cost of these MSC. This is probably why patients sometimes have to pay up to $10,000 for a single treatment. In contrast, a single line of pluripotent stem cells is harvested once, and can be expanded millions of times over many years, treating thousands of patients with only one original blastocyst.Quality of SignalsYet, the true challenge is the quality of the information that these stem cells carry. By nature, mesenchymal stem cells are much more aged and already differentiated to signal repair in only eight tissue types. They are effective for bones and muscle (umbilical) and skin (adipose) but do not have the regenerative reach to all 220+ tissue types of cells that our body needs for a comprehensive tune-up. If the MSC are harvested from the patient’s adipose tissues, they have the same age as the patient and will not add youth to the recipient’s metabolism. If the MSC come from umbilical cord blood, they will be younger than stem cells from adipose tissue but still very limited in the signals that they send - their mission to communicate mainly with bones, skin, and muscles. This is where Embryonic Stem Cells shine — in their youthfulness and in their secretory reach for whole body repair and rejuvenation. The signals sent by pluripotent embryonic stem cells to the recipient’s cells are not limited to any tissue. The genes of pluripotency that are known to restore youth in all tissues will release their unique miRNAs and help the surrounding cells to restore their young metabolism.It is important to know also that each batch of MSC will release different signals since they are coming from a different source, a different placenta or a different cord blood sample. It has been reported that these MSC batches are not all equally immunosuppressive or equally potent, which means that the results observed after their application are not reproducible. Instead, by using the same line of pluripotent stem cells, coming from the same source for years, the results are much more reproducible and the treatment more predictable and reliable.Pulse Treatment vs One Single Injection?The number and pace of applications is another important point to understand about stem cell medicine. A one-time injection helps somewhat, but research is more and more clear that it is the regular pulsating doses of pluripotent signaling that make the most significant difference - day after day, week after week, sequential applications over a period of time. Depending on the level of cell degradation to reverse in the patient, the number of applications will vary. Mild conditions may be reversed after only 12 applications. For more advanced conditions like dementia or MS and ALS, 24 applications are recommended along with side treatments that will help restore the metabolism.2021-01-05T16:56:33-07:00https://stemaid.com/news/how-pluripotent-stem-cells-reduce-covid19-mortality.htmlHow Pluripotent Stem Cells Reduce Covid19 Mortality2020-03-30T09:50:47-07:00admincameron@nospam.comA growing number of scientists 1 2 postulate that hyper-inflammation is driving the severity of the COVID-19 disease. Members of the Institute of Immunology of Hefei in China showed that the immune response to the virus infection is such that a high level of Cytokines and inflammatory cells are produced. Inflammatory monocytes and aberrant Th1 cells enter the pulmonary circulation and cause immune damage to the lung, functional disability and quick mortality.
Approaches like using corticosteroids or Janus Kinase inhibitors which are usually considered in case of hyper-inflammation are inadvisable for patients with COVID-19 as they would lead to broad immunosuppression and therefore leave the viral load free to multiply.
The key to help patients with hyper inflammation in their lungs while fighting an aggressive viral infection like in COVID-19 is to provide an efficient immune regulation where the inflammatory response is reduced while killer cells are still produced in an appropriate amount - this is what pluripotent stem cells provide.
Based on our studies, but also on published data 3, we can state that pluripotent stem cells have an immune regulatory effect when exposed to hyper inflammation. They not only suppress the proliferation of CD4+ cells but they also suppress the secretion of various cytokines such as IL-2, IL-12, IFN-γ, TNF-α, IL-4, IL-5, IL-1β, and IL-10 which are involved in hyper-inflammation. They will, however, not change the levels of TGF-β or IDO which are involved in regulating the immune cells.
Pluripotent stem cells have also been used successfully in restoring lung function in patients with mild or severe COPD. Noticeable improvement is recorded within one week of daily treatment.
Based on our understanding of the inflammatory process involved in advanced stages of COVID-19 and based on our knowledge on how pluripotent embryonic stem cells are able to effectively reduce inflammatory storm without lowering the immune capacity, we believe that our pluripotent stem cells could help patients whose lung functions are declining rapidly due to the COVID-19 inflammatory storm.2020-03-30T09:50:47-07:00https://stemaid.com/news/vaccination-with-embryonic-stem-cells-prevents-lung-cancer.htmlVaccination With Embryonic Stem Cells Prevents Lung Cancer2017-07-06T14:54:09-06:00admincameron@nospam.comResearchers in America have discovered that vaccinating mice with embryonic stem cells prevented lung cancer in those animals that had had cancer cells transplanted into them after the vaccination or that had been exposed to cancer-causing chemicals.
The findings suggest that it could be possible to develop embryonic stem cell vaccines that prevent cancers in humans, such as hereditary breast and colon cancer and lung cancer caused by smoking or other environmental factors.
Professor John Eaton told a news briefing at the EORTC-NCI-AACR [1] Symposium on Molecular Targets and Cancer Therapeutics in Prague today (Wednesday 8 November): "We found that the vaccinations were between 80-100% effective in preventing tumour growth in mice that were subsequently challenged with transplanted Lewis lung carcinoma, and it was between 60-90% effective in mice subsequently exposed to carcinogens that cause lung cancer.
"Our results raise the exciting possibility of developing a prophylactic vaccine capable of preventing the appearance of various types of cancers in humans, especially those with hereditary, chronological or environmental predispositions to neoplastic disease."
However, he warned that the work was still in its early stages and that people should not think that, for instance, they could start, or carry on, smoking because a vaccine to prevent lung cancer was just around the corner.
"Cancer has been prevented and even cured in mice hundreds of times. At present, all I can say is that so far it looks good, and that, unless something unexpected happens, this strategy might some day be applied to humans at high risk for development of cancer. The likelihood of this happening is more a question for the US Food and Drug Agency than for us. Given their stringent regulations I consider it quite likely that, by the time this is tried in humans, I will be pushing up daisies."
Prof Eaton is the James Graham Brown Professor of Cancer Biology and Deputy Director of the James Graham Brown Cancer Center, University of Louisville, USA. He and his colleague, Dr Robert Mitchell, tested two different vaccines in the mice. One consisted of embryonic stem cells (ESC) only, obtained from mouse blastocysts (very early, pre-implantation embryos). The other vaccine consisted of the ESCs combined with cultured fibroblast cells producing GM-CSF, a growth factor usually made by white blood cells and blood vessel-lining endothelial cells, which "supercharges" the immune response and appears to enhance the vaccine-induced immunity to cancer.
Prof Eaton explained: "We needed a delivery vehicle for GM-CSF and chose STO fibroblasts because they are often used as a 'feeder layer' to maintain these particular mouse embryonic stem cells in their embryonic state. If we had used only ESCs expressing GM-CSF, they might have differentiated into non-embryonic cells, which, therefore, would not have worked as a vaccine."
He and his team injected mice with ESCs alone or ESCs STO/GM-CSF. In mice that had Lewis lung carcinoma transplanted into them afterwards, ESCs were 80% effective in preventing tumour growth and ESCs STO/GM-CSF were 100% effective. In mice subsequently exposed to a carcinogen that causes lung cancer (3-methylcholanthrene followed by repetitive dosing with butylated hydroxytoluene), ESCs resulted in 60% of mice remaining tumour free after 27 weeks and ESC STO/GM-CSF resulted in 90% remaining tumour free. Importantly, tumours arising in vaccinated mice were, on average, about 80-90% smaller than tumours in unvaccinated mice. All the unvaccinated mice developed tumours. None of the vaccinated mice developed autoimmune disease or a showed a significant decline in adult pluripotent bone marrow stem cells -- both potential adverse responses to the vaccinations.
Prof Eaton said: "We think the results from the carcinogen-initiated cancers are probably the most important, as they are closer to the 'real-life' model of the development of cancer than just implanting cancer cells in an animal. We are studying several different types of carcinogen-induced mouse cancers (skin, colon, breast) to determine whether the preventative effect of vaccination extends beyond our models of lung cancer (although in our state of Kentucky with its high smoking rates, lung cancer alone would be a big victory). We may also vaccinate ageing rodents, the majority of which develop endocrine tumours in old age.
"In terms of human testing, if all goes well, then I think this vaccination might best be tested in women at high (genetic) risk of breast cancer, in people with high (genetic) risk of colon cancer and, perhaps, in smokers.
"Our progress over the next few years will depend, to a large extent, on whether we can attract significant funding. Our work is presently supported by a pilot grant from our cancer centre and a small grant from the Kentucky Lung Cancer Research Program. US federal funding agencies such as the NIH -- notorious for funding predictable research -- have been quite disinterested."2017-07-06T14:54:09-06:00https://stemaid.com/news/study-on-mice-shows-stem-cells-key-to-maintaining-strength-in-old-age.htmlStudy On Mice Shows Stem Cells Key To Maintaining Strength In Old Age2017-06-26T14:58:27-06:00admincameron@nospam.comROCHESTER, N.Y. — The decline and breakdown of our muscles typically begins in our 30s, but fitness junkies may tell you otherwise. Keeping the human body in tip-top shape gets harder as the years pass, but a new study finds that stem cells may hold the key to staying physically strong in old age.
The study, conducted at the University of Rochester, found that the loss of stem cells in muscles leads to muscular decline in older mice, something that also could happen to humans.
“Even an elite trained athlete, who has high absolute muscle strength will still experience a decline with age,” says study author Dr. Joe Chakkalakal, an assistant professor of orthopaedics, in a university press release.
A new study on mice shows that stem cells might hold the key to people maintaining strength despite their muscles’ decline that starts in their 30s.The research gives stem cells a new role in maintaining muscle mass by bringing forth the notion that all adults have a pool of the cells in their muscle tissue that responds to injury or exercise, allowing the muscle to repair itself or grow.
These findings, which are the first to ever suggest that stem cell loss contributes to muscle loss, directly conflict with the current prevailing theory, which says that age-related muscle loss is caused by the loss of motor neurons in the brain.
Chakkalakal and co-author Wenxuan Liu depleted muscle stem cells in mice and noticed that the loss of the cells sped up their muscle decline. Furthermore, they did not find evidence to suggest that motor neurons are linked with muscle loss, according to statement.
“I think we’ve shown a formal demonstration that even for aging sedentary individuals, your stem cells are doing something,” says Chakkalakal. “They do play a role in the normal maintenance of your muscle throughout life.”
Chakkalakal said he hopes to build upon his research and discover a drug which could help individuals maintain the stem cell pools within their muscles.
The study’s findings were published last week in the journal eLife.2017-06-26T14:58:27-06:00https://stemaid.com/news/embryonic-stem-cell-gene-may-help-prevent-atherosclerosis.htmlEmbryonic Stem Cell Gene May Help Prevent Atherosclerosis2016-08-06T11:00:00-06:00admincameron@nospam.comAccording to a publication in the July 2016 issue of The Journal of the American Medical Association Embryonic Stem Cells contain a gene which may help in the prevention of Atherosclerosis.
A gene that helps regulate pluripotency in embryonic stem cells, octamer-binding transcription factor 4 (Oct4), is thought to be permanently silenced in adult somatic cells, but new research shows that it may play an important role in preventing the development of atherosclerotic plaques (Cherepanova OA et al. Nat Med. doi:10.1038/nm.4109 [published online May 16, 2016]).When investigators at the University of Virginia School of Medicine and their colleagues silenced the gene in smooth muscle cells in a mouse model of atherosclerosis, the animals exhibited increased atherosclerotic lesion size and changes in lesion composition indicative of decreased plaque stability.
Additional experiments revealed that Oct4 controls the movement of smooth muscle cells into the protective fibrous caps inside plaques. Without Oct4 , smooth muscle cell migration is impaired, leading to a reduced number of these cells within lesions and impaired formation of protective fibrous caps. Lack of Oct4 expression also caused an increase in expression of multiple pro-inflammatory genes. Furthermore, overall lesion size expanded as a result of large increases in the amounts of various non-cellular components, including lipids, hemorrhagic products and necrotic tissue.2016-08-06T11:00:00-06:00https://stemaid.com/news/telomere-extension-turns-back-aging-clock-in-cultured-human-cells.htmlTelomere extension turns back aging clock in cultured human cells, study finds2016-01-18T19:45:00-07:00admincameron@nospam.comResearchers delivered a modified RNA that encodes a telomere-extending protein to cultured human cells. Cell proliferation capacity was dramatically increased, yielding large numbers of cells for study.A new procedure can quickly and efficiently increase the length of human telomeres, the protective caps on the ends of chromosomes that are linked to aging and disease, according to scientists at the Stanford University School of Medicine.Treated cells behave as if they are much younger than untreated cells, multiplying with abandon in the laboratory dish rather than stagnating or dying.The procedure, which involves the use of a modified type of RNA, will improve the ability of researchers to generate large numbers of cells for study or drug development, the scientists say. Skin cells with telomeres lengthened by the procedure were able to divide up to 40 more times than untreated cells. The research may point to new ways to treat diseases caused by shortened telomeres.Telomeres are the protective caps on the ends of the strands of DNA called chromosomes, which house our genomes. In young humans, telomeres are about 8,000-10,000 nucleotides long. They shorten with each cell division, however, and when they reach a critical length the cell stops dividing or dies. This internal “clock” makes it difficult to keep most cells growing in a laboratory for more than a few cell doublings.‘Turning back the internal clock’“Now we have found a way to lengthen human telomeres by as much as 1,000 nucleotides, turning back the internal clock in these cells by the equivalent of many years of human life,” said Helen Blau, PhD, professor of microbiology and immunology at Stanford and director of the university’s Baxter Laboratory for Stem Cell Biology. “This greatly increases the number of cells available for studies such as drug testing or disease modeling.”A paper describing the research was published today in the FASEB Journal. Blau, who also holds the Donald E. and Delia B. Baxter Professorship, is the senior author. Postdoctoral scholar John Ramunas, PhD, of Stanford shares lead authorship with Eduard Yakubov, PhD, of the Houston Methodist Research Institute.The researchers used modified messenger RNA to extend the telomeres. RNA carries instructions from genes in the DNA to the cell’s protein-making factories. The RNA used in this experiment contained the coding sequence for TERT, the active component of a naturally occurring enzyme called telomerase. Telomerase is expressed by stem cells, including those that give rise to sperm and egg cells, to ensure that the telomeres of these cells stay in tip-top shape for the next generation. Most other types of cells, however, express very low levels of telomerase.Transient effect an advantageThe newly developed technique has an important advantage over other potential methods: It’s temporary. The modified RNA is designed to reduce the cell's immune response to the treatment and allow the TERT-encoding message to stick around a bit longer than an unmodified message would. But it dissipates and is gone within about 48 hours. After that time, the newly lengthened telomeres begin to progressively shorten again with each cell division.The transient effect is somewhat like tapping the gas pedal in one of a fleet of cars coasting slowly to a stop. The car with the extra surge of energy will go farther than its peers, but it will still come to an eventual halt when its forward momentum is spent. On a biological level, this means the treated cells don’t go on to divide indefinitely, which would make them too dangerous to use as a potential therapy in humans because of the risk of cancer. This new approach paves the way toward preventing or treating diseases of aging.The researchers found that as few as three applications of the modified RNA over a period of a few days could significantly increase the length of the telomeres in cultured human muscle and skin cells. A 1,000-nucleotide addition represents a more than 10 percent increase in the length of the telomeres. These cells divided many more times in the culture dish than did untreated cells: about 28 more times for the skin cells, and about three more times for the muscle cells.“We were surprised and pleased that modified TERT mRNA worked, because TERT is highly regulated and must bind to another component of telomerase,” said Ramunas. “Previous attempts to deliver mRNA-encoding TERT caused an immune response against telomerase, which could be deleterious. In contrast, our technique is nonimmunogenic. Existing transient methods of extending telomeres act slowly, whereas our method acts over just a few days to reverse telomere shortening that occurs over more than a decade of normal aging. This suggests that a treatment using our method could be brief and infrequent.”Potential uses for therapy“This new approach paves the way toward preventing or treating diseases of aging,” said Blau. “There are also highly debilitating genetic diseases associated with telomere shortening that could benefit from such a potential treatment.”Blau and her colleagues became interested in telomeres when previous work in her lab showed that the muscle stem cells of boys with Duchenne muscular dystrophy had telomeres that were much shorter than those of boys without the disease. This finding not only has implications for understanding how the cells function — or don’t function — in making new muscle, but it also helps explain the limited ability to grow affected cells in the laboratory for study.The researchers are now testing their new technique in other types of cells.“This study is a first step toward the development of telomere extension to improve cell therapies and to possibly treat disorders of accelerated aging in humans,” said John Cooke, MD, PhD. Cooke, a co-author of the study, formerly was a professor of cardiovascular medicine at Stanford. He is now chair of cardiovascular sciences at the Houston Methodist Research Institute.“We’re working to understand more about the differences among cell types, and how we can overcome those differences to allow this approach to be more universally useful,” said Blau, who also is a member of the Stanford Institute for Stem Cell Biology and Regenerative Medicine.“One day it may be possible to target muscle stem cells in a patient with Duchenne muscular dystrophy, for example, to extend their telomeres. There are also implications for treating conditions of aging, such as diabetes and heart disease. This has really opened the doors to consider all types of potential uses of this therapy.”Other Stanford co-authors of the paper are postdoctoral scholars Jennifer Brady, PhD, and Moritz Brandt, MD; senior research scientist Stéphane Corbel, PhD; research associate Colin Holbrook; and Juan Santiago, PhD, professor of mechanical engineering.The work was supported by the National Institutes of Health (grants R01AR063963, U01HL100397 U01HL099997 and AG044815), Germany’s Federal Ministry of Education and Research, Stanford Bio-X and the Baxter Foundation.Ramunas, Yakubov, Cooke and Blau are inventors on patents for the use of modified RNA for telomere extension.Information about Stanford’s Department of Microbiology and Immunology, which also supported the work, is available at [link] Stemaid™ stem cells have been proven to increase telomere length in patients who receive them. For more information, please contact us.2016-01-18T19:45:00-07:00https://stemaid.com/news/age-of-donor-affects-stem-cell-effectiveness-in-repairing-lung-damage-from-pulmonary-fibrosis.htmlAge of Donor Affects Stem Cell Effectiveness in Repairing Lung Damage from Pulmonary Fibrosis2015-12-11T15:34:00-07:00admincameron@nospam.comMiller School of Medicine researchers have found that the age of a donor mouse affects the ability of its mesenchymal stem cells (MSCs) to repair damage to the lungs caused by pulmonary fibrosis.Their laboratory study, published recently in Translational Research, has important implications for clinical stem cell treatments in older patients with damaged and scarred lung tissue caused by smoking or other conditions.“Donor stem cells from younger mice were effective in preventing damage when infused into older mice at the same time as a disease-causing agent,” said Marilyn K. Glassberg, M.D., professor of medicine, surgery and pediatrics, Director of the Interstitial Lung Disease Program, Director of Pulmonary Diseases at the Interdisciplinary Stem Cell Institute, and Vice-Chair of Medicine for Diversity and Innovation. “However, donor MSCs from older mice had virtually no effect.”Because there are no drugs to reverse the damage from pulmonary fibrosis, researchers have studied the potential for autologous MSCs from a patient’s own body as a possible strategy for repairing lung tissue, said Glassberg, who was a senior author of the study, “Therapeutic benefits of young, but not old, adipose-derived mesenchymal stem cells in a chronic mouse model of bleomycin-induced pulmonary fibrosis.”Jun Tashiro, M.D., M.P.H., surgical resident, and Sharon J. Elliot, Ph.D., research associate professor of medicine, were lead authors of the Miller School study, and other co-authors were David J. Gerth, M.D., assistant professor of surgery; Xiaomei Xia, research associate in medicine; Simone Pereira-Simon, research associate in surgery; Rhea Choi, M.Dhttps://stemaid.com/Ph.D. student; Paola Catanuto, Ph.D., senior research associate of surgery; Shahriar Shahzeidi, M.D., clinical assistant professor of pediatrics; and Rahil H. Shah, student assistant. Also contributing to the study were Rebecca L. Toonkel, M.D., of Florida International University; and Fadi El Salem, M.D., of the Icahn School of Medicine at Mount Sinai.“Our study found that the age of the donor animal is important,” said Glassberg. “This would indicate that it’s unlikely that infusions of autologous stem cells from the body of an older patient would be effective in treating pulmonary disease.”A series of laboratory studies in the late 1990s and early 2000s indicated that stem cells could repair lung damage in mice given bleomycin (BLM)-induced pulmonary fibrosis. “These studies used young mice as the model,” said Glassberg. “But data showed that these mice would be able to repair the damage without being given stem cells.”To develop a better representative model for pulmonary fibrosis, Elliot was able to obtain old mice – equivalent to 70 human years – through a grant from the National Institutes of Aging (NIH). When these mice received stem cell infusions from old donor mice, there was no reduction in fibrosis or other signs of improvement. However, when old mice received MSCs from young donor mice, their lung damage did improve. Importantly, when young mice received old donor MSCs their lung repair was altered. Studies are ongoing to determine what old donor cells have or lack compared to young donor cells that render them ineffective.“We plan to continue to develop more representative models of human pulmonary fibrosis,” said Glassberg. “Our goal is not only to develop a preventive model of disease but also to search for a way to offer safe and effective clinical treatments for patients with this deadly disease.”Miller School Departments, Centers and Institutes2015-12-11T15:34:00-07:00https://stemaid.com/news/gordie-howe-comfortable-and-happy-after-second-stem-cell-treatment.htmlGordie Howe ‘comfortable and happy’ after second stem cell treatment2015-06-17T22:05:16-06:00admincameron@nospam.comHall of Fame legend Gordie Howe is “comfortable and happy,” after undergoing his second stem cell treatment at a clinic in Mexico Monday night, said his son, Murray.“Our dad continues to participate in a clinical trial where stem cells are being used in the treatment of a stroke,” Murray Howe said in an email to thn.com. “We’d like to wait until the first phase of that clinical trial is complete before providing any more updates. At this time, our dad is comfortable and happy. That remains our goal. We want to thank everyone for their ongoing support for Mr. Hockey.”Howe is back at the Santa Clarita Clinic in Tijuana, Mexico receiving stem cells in a bid to restore some of the functions to the right side of his body. After suffering a serious stroke last October in which a blood vessel in the area of the brain that controls motor function burst, things looked bleak for the 87-year-old Howe. The family was holding a vigil at his bedside and it looked as though palliative care was the only option.That was until his family took him to Santa Clarita for the first time in December for his first treatment. Since then, Howe has rebounded remarkably and even made a public appearance at a dinner honoring him in Saskatoon in February. This round of stem cell treatments had been planned as a follow-up all along and the family is hoping it will continue to give Howe a reasonable quality of life. While the results of stem cell treatment are not conclusive, the Howe family is unwavering in its opinion that the treatment has saved Gordie’s life.“There’s no doubt in any of our minds that he wouldn’t be here today if they hadn’t treated him,” Mark Howe told thn.com in June. “He had dropped 35 pounds in six weeks and he wasn’t going to live. It’s the first time I’ve seen my dad quit. He didn’t want anything to do with any speech therapy or anything like that and once that goes, you’re kind of toast.”The plan after this round of treatment is for Gordie Howe to go back to Michigan for a short time, then he will move to a nursing home in Ohio that specializes in treating people with dementia.2015-06-17T22:05:16-06:00