Latest news with #stemcells
South China Morning Post
2 days ago
- Health
- South China Morning Post
China-Singapore team's nanovaccine suppresses cancer recurrence and spread in animal tests
A joint China-Singapore research team is using nanoparticle technology to create a cancer vaccine that has produced promising results in animal tests – reducing the regrowth and spread of tumours up to seven times more effectively than existing treatments. The nanovaccine attacks not only regular cancerous cells but also cancer stem cells (CSCs), which can lie dormant within tumours during treatment, only awakening when conditions are more favourable to the disease. The bioinspired approach developed by the researchers, led by Yang Yanlian from the National Centre for Nanoscience and Technology and Chen Xiaoyuan from the National University of Singapore, has potential for personalised cancer vaccines. The researchers detailed their findings in a paper published last month by the peer-reviewed Nature Nanotechnology. Post-surgical recurrence and metastasis of cancers are mainly driven by CSCs, which are highly resistant to conventional therapies. Some studies have even suggested that traditional treatments like radiotherapy may inadvertently promote their spread. The body's normal stem cells work continuously, whether generating blood or helping to renew the gut's lining every three to five days. But their unique self-renewal and unlimited proliferation qualities are also harboured by CSCs within tumours.
Yahoo
4 days ago
- Health
- Yahoo
New pocket-size model of ALS 'breathes and flows like human tissue'
When you buy through links on our articles, Future and its syndication partners may earn a commission. Scientists invented a pocket-sized model of the most common form of amyotrophic lateral sclerosis (ALS). The "disease-on-a-chip," made using stem cells, could pave the way for new treatments for the progressive condition, the researchers say. In ALS, the brain and spinal-cord cells that control voluntary muscle movements — known as motor neurons — break down and die. As a result, the brain can no longer send signals to the muscles, leading to symptoms of muscle weakness and paralysis, as well as trouble speaking, swallowing and breathing. In a study published July 3 in the journal Cell Stem Cell, scientists unveiled a new model of sporadic ALS, which accounts for up to 95% of ALS cases and occurs spontaneously without a clear genetic cause or known family history. The platform mimics the early stages of the disease and does so more accurately than previous lab models could. To build the model, researchers collected blood cells from young-onset ALS patients, all under age 45, and healthy male donors, whose cells were used to build a "healthy" chip, for comparison. The blood cells were reprogrammed into induced pluripotent stem cells (iPSCs), which can be turned into any type of cell in the body. The stem cells were then turned into spinal motor neurons, which normally enable movement and degenerate in ALS. A second set of iPSCs was turned into cells similar to the blood-brain barrier (BBB), which helps prevent harmful germs and toxins from entering the brain. The spinal neurons were seeded into one channel within the chip, while the BBB cells were placed in another channel. Separated by a porous membrane, the two chambers were then perfused with nutrient-rich fluid to mimic continuous blood flow. The resulting "spinal-cord chip" maintained both sets of cells for up to about a month and helped the neurons mature beyond what models without flowing fluids allowed. Related: Scientists invent 1st 'vagina-on-a-chip' The basic chip was developed by the biotech company Emulate and then customized for use in the ALS model by researchers at Cedars-Sinai in Los Angeles, California. Earlier models of ALS also used iPSC-derived neurons and structures mimicking those found in the brain, but they lacked dynamic flow, making it hard to capture specific aspects of the disease. "Our previous models were static, like a dish of cells sitting still, and couldn't differentiate between ALS and healthy cells," said study co-author Clive Svendsen, executive director of the Board of Governors Regenerative Medicine Institute at Cedars-Sinai. "We recreated an in vitro [lab dish] environment that breathes and flows like human tissue, which allowed us to detect early differences in ALS neurons." Other experts agree. "Unlike most lab models that lack vascular features and dynamic flow, this chip improves neuron health and maturation," said Dr. Kimberly Idoko, a board-certified neurologist and medical director at Everwell Neuro, who was not involved in the study. "It captures early disease signals in ALS that are often hard to detect," Idoko told Live Science in an email. With their ALS and healthy chips in hand, the researchers analyzed the activity of more than 10,000 genes across all the cells. One of the most striking findings was abnormal glutamate signaling in the neurons within the ALS chip. Glutamate is a major excitatory chemical messenger, meaning it makes neurons more likely to fire and send on a message to additional neurons; its counterpart, GABA, is inhibitory. The team saw increased activity in glutamate receptor genes and decreased activity in GABA receptor genes in the motor neurons, compared to the healthy chip. "We were intrigued to find this increase in glutamate activity," Svendsen said. "Although there was no visible neuron death, we hypothesize this hyperexcitability could trigger degeneration at later stages." RELATED STORIES —Body parts grown in the lab —Scientists developing new 'heart-on-a-chip' —Could mini space-grown organs be our 'cancer moonshot'? This finding aligns with long-standing theories about ALS, which suggest that boosted glutamate signalling contributes to nerve damage. It also corresponds with the mechanism of the ALS drug riluzole, which blocks glutamate. The new chip adds to the evidence for this mechanism and could help reveal how it manifests in the earliest stages, before symptoms would be evident in a patient, Svendsen suggested. While Idoko praised the model, she noted it lacks glial cells — additional nervous-system cells involved in ALS — and doesn't capture the late-stage degeneration seen in ALS. "However, a model like this could conceivably be useful for early drug screening, to study how a drug might cross a barrier similar to the blood-brain barrier, in preparation for animal or human studies," she said. The team is now working toward maintaining the cells in the model for up to 100 days. They also would like to incorporate other cell types, like muscle cells, to fully mimic ALS progression. As motor neurons die off in the disease, muscle cells also waste away. "Our goal is now to build models where more neurons die, so we can better map disease pathways and test treatments in a human-like setting," Svendsen said. For now, the chip offers a window into ALS's earliest molecular changes and a tool to figure out how to detect and slow the disease before irreversible damage occurs. Solve the daily Crossword
Medscape
14-07-2025
- Health
- Medscape
Stem Cell Therapy for Parkinson's Disease Reality Check
This transcript has been edited for clarity. Indu Subramanian, MD: Hello, everyone. Welcome to Medscape. I'm so excited to have Prof Roger Barker here, who is a professor of clinical neuroscience and honorary consultant in neurology at the University of Cambridge in England. I am Indu Subramanian. I work at UCLA, and I'm excited to speak about the very hot topic of stem cells, and specifically today, about stem cells and Parkinson's. We may end up talking about stem cells in general as a focus, so keep watching and you'll learn a lot. Prof Barker, I know that you are an amazing fount of knowledge in this space. Perhaps we can start with you describing a minute or two of your background and the history of stem cells. Fetal Dopamine Cells Roger A. Barker, MBBS, PhD: I started on cell-based therapies to repair disease of the brain many years ago — probably best to leave it at that rather than be too specific, otherwise it gives away my age. I'm essentially a neurologist here in Cambridge. I see patients half the week and the other half of the time I do research. My original work was with Steve Dunnett here in Cambridge, and we were looking at how we could better repair the brain in Parkinson's. Particularly, the premise is, as you know in Parkinson's, you critically lose this population of dopamine cells. You have half a million on each side of your midbrain. When you lose half of those, you get the first features. In theory, if you could transplant back a quarter of a million healthy dopamine cells of the type that are lost in Parkinson's, you should be able to put that bit of the brain back to normal. It's not a cure, but you should be able to repair that. This has been a topic people have looked at since the 1980s, and I came into it and did my PhD in the early 1990s to look at this. Those early studies showed that you could put dopamine cells into the brain. They weren't stem cells; they were fetal dopamine cells. In some cases they survived, and in some cases they had very marked clinical benefits to the patients. Best-case scenario, patients could go 20 years off medication with normal dopamine levels in their brain and looked normal, for all intents and purposes. It was a minority, and it was ethically a big problem because fetal tissue was being used. In different parts of the world, that receives different types of concerns. There was also a problem with logistics. We recently published a trial called TransEuro, which used human fetal dopamine cells to treat Parkinson's. We found that there were major problems with getting sufficient tissue. With the 21 transplants we did, we had another 86 that were canceled because we didn't have sufficient tissue. Regardless of the benefits from using fetal dopamine cells, logistically it's not possible. It's ethically very contentious. That work laid the foundation for the recent stem cell work because it showed that it could be done. When it worked well, it worked very well. It was just rather inconsistent. Pluripotent Stem Cells Subramanian: That brings us to the nonfetal type of stem cells. What are those exactly and why are we using them? Barker: The main problems with the fetal tissue were, as I say, with logistics and ethics. It was very difficult to get sufficient amounts of them because you needed tissue from at least three or four fetuses to transplant one side of the brain, so the numbers needed were quite high. Each person had their own individual product, so what we needed was a source of cells where we could manufacture large numbers of the dopamine cells that we needed, we could do it consistently, and ideally we could then freeze it and you could say we've got a standard package of therapy we could give any patient. This was the ambition, but there wasn't much scope for it really until 1998 when human embryonic stem cells were first made by Jamie Thomson. Obviously, in 2006-2007, Shinya Yamanaka and the team in Kyoto made induced pluripotent stem cells and human pluripotent stem cells. Now you have the capacity to make human lines of embryonic and induced pluripotent stem cells. The next trick was, could you turn those into the dopamine cells you needed for Parkinson's? That was really solved by the labs of Lorenz Studer in New York and Malin Parmar in Lund, who both came up with protocols in 2011-2012 to show that you could convert human stem cells into dopamine cells of a midbrain type. That started a whole process of work about taking these therapies to the clinic from that starting point. It was also shown at around the same time by the group in Japan, led by Jun Takahashi, that they could do it as well. They could make human induced pluripotent stem cells into dopamine cells. Just under 15 years ago, we now had all the substrates to make the dopamine cells, which we could then use in clinical trials. Obviously, a large amount of work needed to take place before we could get to the clinical trials, which have recently just published. Subramanian: Can you explain the pluripotent stem cells? How do you make them make dopamine? How does that work? Barker: It's an interesting question because obviously an embryonic stem cell is a stem cell you get from an embryo. We were all at some point an embryonic stem cell. Those cells can turn into any cell in your body. When you do an induced pluripotent stem cell, you get an adult cell, skin cell, or a blood cell, you reprogram it back to a stem cell state, and then you try and flip it into a dopamine cell. The trick is, can you work out what you need to give a stem cell to convince it to become a brain cell and then convince it to become a dopamine cell? Now, I'm not clever enough to do that, but there are various people who are. That, in part, relates to knowing what happens in normal development. One of the challenges that put the field back for a number of years was thinking that human development in terms of dopamine cells was the same as you'd see in a mouse. People could convert mouse stem cells into mouse dopamine cells quite easily, and that was established over 25 years ago. People thought it'd be the same with human, but it proved not to be the case. It was a different developmental program you had to follow. Once that was cracked, then people could add this cocktail of factors, convince your stem cells to become a neural stem cell, and then to become a dopamine stem cell. Then, the idea is when you put in a dopamine stem cell precursor, which is what we do, that will then mature into the dopamine cell that you want once it's put in the brain. Recent Nature Studies Subramanian: Tell us about the most recent trials, because they're very exciting to many people but I think there's still some caution to be had. Tell us what your thoughts are. Barker: It's been very interesting. Obviously, from those original discoveries back in 2011-2012, the next 10 years was spent trying to show that you could make human stem cells into dopamine precursors of the type needed to replace those lost, and it could be done at clinical grade. That involved an enormous amount of work to show you could manufacture these things to a standard necessary to put into a human. You had to show that they were safe so when you transplanted them, they didn't form tumors or they didn't go and make the wrong type of cells. That was done by the team in Japan, it was done by the team in New York, and we've also done it in Europe. More recently, the two teams led by Viviane Tabar and Lorenz Studer in New York, who set up a company called BlueRock, published their data, and the group of Jun Takahashi and his team in Kyoto published theirs. Both of them published papers in Nature . The Japanese study took seven patients and they used two doses of cells, and the group in New York used 12 patients. They grafted some in New York, some in Toronto; five at one dose, seven at a higher dose. Those studies both showed, if you look at them in totality, that it was safe. Of the 19 patients that were grafted, there were no major problems within them. It wasn't that they weren't without side effects, but there was nothing serious that would give one concern. The patients could tolerate the procedure, they could tolerate the immunosuppression, which they had to make as a result of having this therapy. There were no abnormal signals on the scan that would worry you that they were forming tumors or that things were happening in the brain. It was feasible and it was safe. The question is, was it effective? That, I think, is a little more questionable in the sense that these are very early studies. One of the big challenges is knowing what dose of cells to give, because you can only guess how many you need to put in to make the number you want. Those are often made from assumptions you've made in the lab, so in rats or mice, which is difficult to then translate into the adult human brain. They had to guess how many cells to transplant, which is why there were two doses. If you look at the efficacy and you look at the survival of the cells, which is done using special imaging, using PET imaging, particularly with F-DOPA, which is picked up by dopamine cells, you find that the clinical response in the Japanese study was a bit variable. The response in the New York group, the BlueRock study, was that the higher dose seemed to have more of a clinical response than the lower dose. In the PET imaging, looking at dopamine survival, in the Japanese study, there were little hotspots. There was some evidence that the cells survived, but it was a bit hit-and-miss. In the New York BlueRock study, the signal changes were relatively small. Although there was a clinical response, the imaging was less impressive. The other way, then, to look at it is to ask how much medication did people take. Obviously, if the transplant's working very well, then it's replacing the dopamine and you need less medication. Actually, in both studies, there wasn't a huge reduction in the amount of medication that people took. My conclusion from those trials would be that it was safe, it was feasible, and it was encouraging, but we haven't quite solved the problem. We haven't quite solved the problem of how many cells to give. We certainly haven't restored patients back to normal. There are other things we need to do before we could say that this therapy is ready for a big trial or for primetime in the clinic. Do We Know Where in the Brain to Put Stem Cells? Subramanian: I appreciate that analysis because that's very helpful. I think people are always wanting to jump to conclusions that we're ready for real time, and I think it's still some time away. Just one or two other last thoughts. Where are we putting those cells in the current studies? Barker: It's a very good question. Obviously, at the bottom part of the brain is the substantia nigra at the top of the stem of the brain. They project up to a thing called the striatum, and the striatum has two parts called the caudate and putamen. In Parkinson's, the putamen takes the biggest hit. That's where you lose most of the dopamine and the cells die off in the nigra. The transplant itself is not put in the nigra because we're not convinced the fibers will grow back. We put the cells where the dopamine is lost and where the dopamine is lost the most, so we transplant them directly into the putamen, into the place where we think dopamine will have its maximum effect if these cells survive and innervate. Linked to that is, of course, we're not quite sure how to do that either because there is no device for injecting cells into the brain because no one's done it before. As I say, we don't quite know the dose. We don't quite know how many deposits to put in. The two groups who've published have used slightly different doses, slightly different cannulae to put the cells in the brain, and a slightly different number of tracks. Those may be critical factors. In our own trial, which is yet to finish, we've used slightly different doses, slightly different devices, and slightly different numbers of tracks. I think the other important message to get across is that these trials are not all the same. There are subtle differences between them. They're fundamentally tackling the same problem, but they're not exactly the same. Putting them all together and saying that, together, they show this, is a useful headline, but the detail is actually quite important. Subramanian: Absolutely. The devil is always in the details, isn't it? Thank you so much, Prof Barker. I so enjoyed this conversation. Thank you for joining us today. Barker: Thank you very much.
Yahoo
14-07-2025
- Business
- Yahoo
Adia Nutrition Inc. Celebrates Grand Opening of Adia Med of San Antonio, First Licensed Clinic, Led by Michele DeLeon MD
Winter Park, Florida--(Newsfile Corp. - July 14, 2025) - Adia Nutrition Inc. (OTCQB: ADIA), an emerging leader in regenerative medicine, proudly announces the grand opening of Adia Med of San Antonio, its first licensed clinic under a strategic license agreement, located at 18707 Hardy Oak Blvd, Suite 500, San Antonio, Texas 78258. Headed by esteemed wellness regenerative expert Michele DeLeon MD, this cutting-edge facility marks a significant step in expanding access to innovative regenerative therapies across the United States. Adia Med of San Antonio will offer FDA-registered products, including AdiaVita The Most Trusted Brand (umbilical cord stem cells with 100 million viable cells and 3 trillion exosomes per unit) and AdiaLink (3.5 trillion exosomes per unit). Additionally, Adia Med of San Antonio will collaborate with Adia Med of Winter Park in a groundbreaking clinical study exploring regenerative therapies for autism, further advancing the company's commitment to transformative healthcare solutions. "We are thrilled to launch Adia Med of San Antonio as our first licensed clinic, under the exceptional leadership of Michele DeLeon MD," said Larry Powalisz, CEO of Adia Nutrition Inc. "This vibrant new location, combined with clinical study for autism alongside Adia Med of Winter Park, is a testament to our unwavering commitment to transforming lives through cutting-edge care. San Antonio is just the beginning of an exciting new chapter for Adia Nutrition." "Equipped with state-of-the-art technology and staffed by a highly trained team, Adia Med of San Antonio upholds the rigorous standards of Adia Nutrition's existing clinics, including Adia Med Winter Park. For those interested in licensing Adia Med's name and becoming part of its innovative network, please reach out to ceo@ or call 321-788-0850 for more information. About ADIA Nutrition Inc.:Adia Nutrition Inc. is a publicly traded company (OTCQB: ADIA) dedicated to revolutionizing healthcare and supplementation. With a focus on innovation and quality, the company has established two key divisions: a supplement division providing premium, organic supplements, and a medical division establishing Clinics that specialize in leading-edge stem cell therapies, most significantly Umbilical Cord Stem Cells (UCB-SC) and Autologous Hematopoietic Stem Cell Transplantation (aHSCT) treatments. Through these divisions, Adia Nutrition Inc. is committed to empowering individuals to live their best lives by addressing both nutritional needs and groundbreaking medical treatments. Website: Website: (X): @ADIA_Nutrition Safe Harbor: This Press Release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. These forward-looking statements are based on the current plans and expectations of management and are subject to a few uncertainties and risks that could significantly affect the company's current plans and expectations, as well as future results of operations and financial condition. A more extensive listing of risks and factors that may affect the company's business prospects and cause actual results to differ materially from those described in the forward-looking statements can be found in the reports and other documents filed by the company with the Securities and Exchange Commission and OTC Markets, Inc. OTC Disclosure and News Service. The company undertakes no obligation to publicly update or revise any forward-looking statements, because of new information, future events or otherwise. To view the source version of this press release, please visit
Yahoo
12-07-2025
- Health
- Yahoo
Diabetic Woman No Longer Needs Insulin After Single Dose of Experimental Stem Cells
A Canadian woman with type 1 diabetes spent nearly a decade dependent on her glucose monitor and insulin shots — but after a single dose of manufactured stem cells implanted into her liver, she's now free. In an interview with CTV, 36-year-old Amanda Smith of London, Ontario described how it felt to be part of such a groundbreaking experiment that has allowed her body to once again produce its own insulin. "I remember, like, being scared and excited," Smith said of the study, "and it's history now." Although things are improving for type 1 diabetics, whose pancreases cannot produce their own insulin, the condition still requires ample maintenance and most often results in at least 10 to 12 years being taken off one's life. Diagnosed at 25 with late-onset juvenile diabetes, the woman said that the prognosis for the disease always felt like a "death sentence." "The end is always some sort of complication with diabetes," Smith said. After enrolling in the stem cell study, which is the subject of a new paper in the New England Journal of Medicine, all that changed for the Ontario woman. Smith and 11 other participants on both sides of the border were implanted with special embryonic stem cells, which were altered to grow in the liver and transform into a hormone-producing array of cells that secrete insulin the way a non-diabetic's pancreas does. Of that study cohort, 10 of the 12 stopped needing insulin shots for at least a year — and according to Trevor Reichman, the surgical director of the University Health Network in Toronto's diabetic transplant program and lead author of the paper, the study's "biological replacements" took hold in seconds. "In the liver, they're sensing a patient's blood glucose level, and they're secreting the appropriate hormone," Reichman said of the stem cell implants. "Essentially, it's the same as your native... cells would function." Incredible as these results are, there is a catch: to keep the stem cells working, patients must take immune-suppressing medications so their bodies don't reject the implanted cells — which means they've become more susceptible than most to illness. (Charlbi Dean Kriek, the star of 2022's "Triangle of Sadness," had been on immunosuppressants for a decade following a spleen removal when she died of an infection soon after the film came out.) For Smith, who on August 1 will celebrate her two-year implant-iversary, swapping quality of life for her old insulin shots and the threat of diabetic comas was a no-brainer — even if it means she's more vulnerable to sickness. "Taking a couple of pills three times a day is nothing," she said of her medication regimen. "I take it with breakfast, lunch, and dinner. It's easy." Still, such immunosuppression is no joke. As Reichman told CTV, one of the study cohort patients died, and the culprit may well have been an illness they caught while on said immunosuppressants — which is why the next phase of research will be into stem cell implants that the body won't reject. More on diabetes: RFK Jr. Surprised to Learn He'd Cut a Grant For Youth Diabetes Research
