A landmark international study that pooled brain scans and memory tests from thousands of adults has shed new light on how structural brain changes are tied to memory decline as people age. The findings - based on more than 10,000 MRI scans and over 13,000 memory assessments from 3,700 cognitively healthy adults across 13 studies - show that the connection between shrinking brain tissue and declining memory is nonlinear, stronger in older adults, and not solely driven by known Alzheimer's-associated genes like APOE ε4. This suggests that brain aging is more complex than previously thought, and that memory vulnerability reflects broad structural changes across multiple regions, not just isolated pathology. Published in Nature Communications, the study, "Vulnerability to memory decline in aging revealed by a mega-analysis of structural brain change," found that structural brain change associated with memory decline is widespread, rather than confined to a single region. While the hippocampus showed the strongest association between volume loss and declining memory performance, many other cortical and subcortical regions also demonstrated significant relationships. This suggests that cognitive decline in aging reflects a distributed macrostructural brain vulnerability, rather than deterioration in a few specific brain regions. Importantly, the relationship between regional brain atrophy and memory decline was not only variable across individuals but also highly nonlinear. Individuals with above-average rates of structural loss experienced disproportionately greater declines in memory, suggesting that once brain shrinkage reaches higher levels, cognitive consequences accelerate rather than progress evenly. This nonlinear pattern was consistent across multiple brain regions, reinforcing the conclusion that memory decline in cognitively healthy aging is linked to global and network-level structural changes, with the hippocampus playing a particularly sensitive role but not acting alone. By integrating data across dozens of research cohorts, we now have the most detailed picture yet of how structural changes in the brain unfold with age and how they relate to memory." Alvaro Pascual-Leone, MD, PhD, senior scientist at the Hinda and Arthur Marcus Institute for Aging Research and medical director at the Deanna and Sidney Wolk Center for Memory Health These results suggest that memory decline in aging is not just about one region or one gene - it reflects a broad biological vulnerability in brain structure that accumulates over decades. Hebrew SeniorLife Hinda and Arthur Marcus Institute for Aging Research Vulnerability to memory decline in aging revealed by a mega-analysis of structural brain change. In our latest interview, News-Medical speaks with Rosanna Zhang from ACROBiosystems about utilizing organoids for disease modeling in the field of neuroscience research. GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún Discover how AI, flow chemistry, and NMR come together in the PiPAC project to revolutionize scalable and autonomous API production. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

is perhaps the most common question patients with inflammatory bowel disease ask their doctors. There have been few large studies of dietary interventions for IBD, a group of disorders that includes ulcerative colitis and Crohn's disease. Now, new research by Stanford Medicine investigators and their colleagues provides one potential answer. Their national, randomized controlled clinical trial found that a short-term, calorie-restrictive diet significantly improved both physical symptoms and biological indicators of mild-to-moderate Crohn's disease. The findings will be published Jan. 13 in Nature Medicine. While dietary interventions are difficult to study - participants' reports of what they're eating aren't always accurate, and the placebo effect can't be avoided because participants know which diet they're on - the findings were notable, demonstrating significant declines in objective markers of inflammation in biologic samples alongside improvements in clinical symptoms. The study may help physicians guide patients in finding a diet that alleviates symptoms. This study will give physicians evidence to support recommendations in an area that patients are very curious about." A chronic condition affecting about a million Americans, Crohn's disease causes inflammation in the digestive tract, leading to symptoms of diarrhea, cramping, abdominal pain and weight loss. Steroids are the only approved therapeutic for mild Crohn's, but their use is limited due to significant side effects, particularly with long-term use. The study compared the symptoms and biological indicators of patients with mild-to-moderate Crohn's disease as they either followed a fasting mimicking diet or ate their normal diet for three consecutive months. Participants in the fasting mimicking group severely limited their calories for five consecutive days per month, eating between about 700 and 1,100 calories a day, Sinha said. Plant-based meals were provided during the fasting period. "We were very pleasantly surprised that the majority of patients seemed to benefit from this diet," Sinha said. "We noticed that even after just one FMD cycle, there were clinical benefits." The improvement was likely a result of natural symptom fluctuations in Crohn's disease and because patients continued to follow their standard care regimens, such as taking medications. Some participants in the fasting mimicking group experienced fatigue and headache, Sinha said, but no serious side effects were reported. Sinha was inspired to study the fasting mimicking diet in patients with Crohn's disease after earlier research indicated the diet could reduce levels of C-reactive protein, a common marker of systemic inflammation in patients who had high baseline C-reactive protein levels. "The effects seen on inflammatory markers made this an appealing diet to study in Crohn's disease since many patients with this disease also have elevated inflammatory markers," he said. Along with tracking participants' clinical response and remission, the researchers also explored changes in biological specimens, such as shifts in common markers of inflammation in both stool and blood. "Our goal in collecting these and other biospecimens was to dig deeper into why there's this differential response," Sinha said. "Can we find mechanisms to explain the findings and signatures that might help predict patients who will respond to the diet?" Some inflammation-promoting lipid mediators derived from fatty acids also declined in fasting mimicking group participants. "There's still a lot more to be done to understand the biology behind how this and other diets work in patients with Crohn's disease," Sinha said. The study's first authors are Stanford Medicine's Chiraag Kulkarni, MD, an instructor in gastroenterology and hepatology, and assistant clinical research coordinator Touran Fardeen. In our latest interview, News-Medical speaks with Rosanna Zhang from ACROBiosystems about utilizing organoids for disease modeling in the field of neuroscience research. GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún Discover how AI, flow chemistry, and NMR come together in the PiPAC project to revolutionize scalable and autonomous API production. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. Please check the box above to proceed. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

Associate Professor of Medicine, Department of Hematology/Oncology, Harvard Medical School; Director, Central Nervous System Metastasis Center, Massachusetts General Hospital, Boston, Massachusetts Disclosure: Priscilla K. Brastianos, MD, has disclosed the following relevant financial relationships: In the past 24 months, serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AtavistikBio; Eli Lilly; Medscape; MPM; Kazia Therapeutics; Genentech-Roche; CraniUS; Selectin (with Equity); Exelixis; InCephaloReceived research grant or clinical trial support (to institution) from: Pfizer; Kazia Therapeutics; GSK; Genentech-Roche; Bristol Myers Squibb; Merck; Eli Lilly; AstraZeneca; Kinnate; MiratiReceived honoraria from: Medscape and International Academy for Advanced Oncology Disclosure: Priscilla K. Brastianos, MD, has disclosed the following relevant financial relationships: In the past 24 months, serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AtavistikBio; Eli Lilly; Medscape; MPM; Kazia Therapeutics; Genentech-Roche; CraniUS; Selectin (with Equity); Exelixis; InCephaloReceived research grant or clinical trial support (to institution) from: Pfizer; Kazia Therapeutics; GSK; Genentech-Roche; Bristol Myers Squibb; Merck; Eli Lilly; AstraZeneca; Kinnate; MiratiReceived honoraria from: Medscape and International Academy for Advanced Oncology I'm a physician-scientist at Mass General Hospital and Harvard Medical School, and I'm director of the brain metastasis center at Mass General Hospital. Thank you for the opportunity to share a brief update on advances in the management of brain metastases in metastatic breast cancer. In the next few minutes, I'll touch on three areas: one, how our understanding of the biology of brain metastases has evolved; two, the newer systemic agents with meaningful intracranial activity; and three, how our therapeutic approach, especially around radiation, has shifted as a result. Our view of brain metastases in the past decade or so has really changed dramatically. In a paper we had published in Cancer Discovery a few years ago, where we sequenced matched primaries and brain metastases, we demonstrated what's called branched evolution, meaning the primary tumor and the brain metastasis shared a common ancestor but then diverged over time. Brain metastases often have distinct genomic profiles and unique pathway activation patterns. Furthermore, interestingly, ER, PR, and HER2 subtype switching is not uncommon when comparing brain metastases to primary breast cancers. That's all very important because it may open the door to better targeted therapies and to designing trials specifically for this patient population. We're also learning more about what helps these metastases grow once they arrive in the brain. Tumor cells just don't land there and passively sit. That may potentially give us a second layer of potential targets, not just in the cancer cells themselves, but in the ecosystem that surrounds them. More research is needed in this area, of course. Let's now talk more about systemic therapies that have shown intracranial activity. Against that biological backdrop that we just talked about, the major clinical advance has been the development of systemic therapies with meaningful intracranial activity, particularly in HER2-positive and triple-negative breast cancer. We see durable control, even in patients with active, previously treated brain lesions. Sacituzumab govitecan for HER2-negative disease has demonstrated encouraging clinical benefit in patients with brain metastases as well. A recent phase 0 surgical study confirmed CNS penetration at therapeutic levels, and early signals of intracranial activity are encouraging and continuing to mature. Importantly, we are trying to move away from whole-brain radiation when possible. Historically, when a patient developed brain metastases, the reflex was often whole-brain radiation therapy. Although it can be effective for controlling diffuse intracranial disease, unfortunately, whole-brain radiation does come with neurocognitive toxicity, particularly memory and executive function decline. We are trying to move away from routine whole-brain radiation when feasible in many patients. We're increasingly using techniques such as stereotactic radiosurgery, or SRS, which is precise focal radiation with less cognitive impact; systemic therapies with brain activity, as mentioned earlier; and more nuanced sequencing of local and systemic therapies to maximize intracranial control while still preserving cognition. This shift is driven both by better radiation techniques and by the availability of systemic agents that can control brain metastases without exposing the entire brain to radiation. First, it means we're moving away from that nihilistic view of brain metastases. Second, because we know brain metastases can be molecularly distinct, it does raise the possibility that molecular profiling of brain metastasis tissue, if it has already been resected or biopsied as part of routine clinical care, may provide additional insights into tumor evolution and potential therapeutic targets. At this stage, it does remain investigational; whether acting on those alterations identified specifically in the brain will translate into improved survival outcomes, we don't yet know. This is an active area of research with ongoing clinical trials. Third, we're starting to think more strategically about sequencing treatment and combinations, so, how to integrate these systemic agents with surgery, stereotactic radiosurgery, and, when needed, whole-brain radiation therapy to maximize intracranial control while preserving cognition and quality of life. There is still a large amount of work to do, but compared to even 5 or 10 years ago, the landscape for breast cancer brain metastases looks so different and much more hopeful.

Wearable health devices, such as smartwatches, have become commonplace, enabling the continuous monitoring of physiological signals at the skin's surface. A joint research group, led by Tokyo City University and the University of Tokyo, in collaboration with RIKEN and Canon Medical Systems Co., has unveiled a living sensor display: an engineered skin graft that fluoresces in response to specific biomarkers, such as inflammation. Reported in Nature Communications, the system leverages the body's natural skin regeneration to support long-term biomarker monitoring, providing a visual readout without blood sampling after implantation and enabling intuitive assessment by observation. The monitoring of internal biomarkers-proteins that indicate inflammation, stress, or disease-typically relies on blood sampling or externally attached sensors that operate only for limited durations. "Conventional approaches are often invasive or provide only snapshots in time," Distinguished Professor Hiroyuki Fujita of Tokyo City University (Professor Emeritus, The University of Tokyo). "Our goal was to explore a biologically integrated system that enables continuous sensing and intuitive interpretation, even at home." By genetically engineering these cells to respond to inflammatory signaling-more specifically, the activation of the NF-κB pathway-the team generated skin tissue that expresses enhanced green fluorescent protein (EGFP) in response to inflammation-related signals. Upon the induction of inflammation, the grafted area emitted green fluorescence, translating internal molecular signals to an external optical signal. Unlike conventional devices that require power sources or periodic replacement, this system is biologically maintained by the body itself. This study demonstrates a proof of concept for long-term, biologically integrated sensing without batteries, wiring, or active user operation. Although this work focused on inflammatory signaling, the underlying strategy is adaptable. By modifying the molecular targets, similar engineered skin constructs could be designed to respond to other physiological or metabolic cues. The researchers note that such technology could have applications beyond human healthcare, including those in animal research and veterinary medicine, where visual indicators of health status may aid the early detection of disease in animals unable to communicate symptoms. Although still at an early preclinical stage, this work offers a biologically grounded approach for interfacing living tissues with sensing functions, blurring the boundary between biological systems and engineered devices. Living sensor display implanted on skin for long-term biomarker monitoring. In our latest interview, News-Medical speaks with Rosanna Zhang from ACROBiosystems about utilizing organoids for disease modeling in the field of neuroscience research. GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún Discover how AI, flow chemistry, and NMR come together in the PiPAC project to revolutionize scalable and autonomous API production. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

Researchers at the University of California, Davis, have uncovered new details about how a once-deadly coronavirus disease in cats spreads through the immune system. The findings may help scientists better understand long COVID and other long-lasting inflammatory illnesses in people. While FIP only affects cats, it shares many features with serious coronavirus-related conditions in humans, including severe inflammation that can damage multiple organs, as well as symptoms that can persist or return. What we found is that it actually infects a much broader range of immune cells, including those that are critical for fighting infection." Amir Kol, lead author, associate professor, UC Davis School of Veterinary Medicine The researchers examined lymph node samples from cats with naturally occurring FIP. Lymph nodes are key immune system hubs where white blood cells gather and coordinate responses to disease. The team found viral material inside several types of immune cells - including B lymphocytes, which produce antibodies, and T lymphocytes, which help the immune system recognize and eliminate infected cells. They also found evidence that the virus was actively replicating itself inside these immune cells, rather than simply leaving behind harmless fragments. Studying this directly in humans is difficult, because doctors rarely have access to immune tissues such as lymph nodes. Cats with FIP offer a rare opportunity to study these processes up close. "This is where cats give us a unique opportunity," Kol said. The researchers also found that traces of the virus could remain in immune cells even after antiviral treatment ended and cats appeared healthy. The findings suggest that FIP may serve as a valuable real-world model for understanding how coronaviruses interact with the immune system over time. Insights gained from cats could help guide future research into chronic inflammation and post-viral syndromes in humans, including long COVID. By bridging veterinary and human medicine, the study highlights how naturally occurring diseases in animals can help answer critical questions about human health. Other authors of the study include Aadhavan Balakumar, Patrawin Wanakumjorn, Kazuto Kimura, Ehren McLarty, Katherine Farrell, Terza Brostoff, Jully Pires, Tamar Cohen-Davidyan, Jennifer M. Cassano, Brian Murphy and Krystle Reagan of UC Davis. It was also supported by the Faculty of Veterinary Medicine at Kasetsart University in Thailand. Beyond macrophages: FIPV tropism includes T and B lymphocytes. In our latest interview, News-Medical speaks with Rosanna Zhang from ACROBiosystems about utilizing organoids for disease modeling in the field of neuroscience research. GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

The study shows that a combination of two well-studied classes of drugs - ERBB inhibitors and Aurora kinase inhibitors - is significantly more effective against KRAS-mutated lung adenocarcinomas than existing therapies. The research, currently published in the journal npj Precision Oncology, opens up a new and promising path for patients for whom there are currently only limited treatment options. KRAS mutations occur in around one third of all lung adenocarcinomas and mainly affect smokers. Although targeted drugs such as the KRAS-G12C inhibitor sotorasib are now available, treatment success is often short-lived. Many tumours develop resistance within a few months by activating alternative signalling pathways - a peculiarity that led the research team led by Iris Uras Jodl (Center for Physiology and Pharmacology, MedUni Vienna) to the newly identified therapeutic perspective. It is precisely this dependency that represents a weak point that can be exploited therapeutically," says Iris Uras Jodl, summarizing the core of the findings. Together, these systems ensure the survival of cancer cells - even when KRAS is already blocked by therapy. Based on this discovery, the researchers conducted extensive screening for active substances that can specifically inhibit the alternative signalling pathways. In cell and mouse models, the combination led to increased apoptosis - a regulated cell death - blocked cell division and prevented the activation of signalling pathways through which tumours otherwise develop resistance. Of particular significance is that the combination also proved effective in tumours that had already developed resistance to afatinib or sotorasib. The simultaneous blockade of ERBB and Aurora kinase signals prevented the survival of cancer cells and completely eliminated resistant cell clones. "The combination of active substances we have discovered opens up promising new therapeutic prospects. Since afatinib is already available and Aurora kinase inhibitors are already in clinical trials, the path to application could be relatively short," said Iris Uras Jodl in the run-up to further, more in-depth studies. KRAS mutated lung adenocarcinoma responds to pan-ERBB and Aurora kinase inhibitors. In our latest interview, News-Medical speaks with Rosanna Zhang from ACROBiosystems about utilizing organoids for disease modeling in the field of neuroscience research. GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún Discover how AI, flow chemistry, and NMR come together in the PiPAC project to revolutionize scalable and autonomous API production. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

Toxic waste risks spreading and damaging the cell. Now, researchers at Umeå University have revealed the molecular sensors that detect tiny holes in lysosomal membranes so they can be quickly repaired - a process crucial for preventing inflammation, cell death, and diseases such as Alzheimer's. Lysosomes are the cell's recycling stations, handling cellular waste and converting it into building blocks that can be reused. Lysosomal membranes are frequently exposed to stress from pathogens, proteins, and metabolic byproducts. Damage can lead to leakage of toxic contents into the cytoplasm, which in turn may cause inflammation and cell death. Until now, the mechanism by which cells detect these membrane injuries has remained unknown.In a recently published study, professor Yaowen Wu and his research group at the Department of Chemistry at Umeå University, identified the signalling pathway that is activated in response to lysosomal damage. Yaowen Wu, lead author of the study The team used a combination of live-cell imaging, genetic knockout models, advanced microscopy, and functional repair assays to map the sequence of events following controlled lysosomal damage.The results apply to several different types of cells and show the same underlying mechanism. "The discovery provides a new understanding and opens the door to new treatment strategies for diseases where lysosomal damage plays a central role. In future studies, we will investigate links to neurodegeneration, infections, and inflammation," says Yaowen Wu.Dale Corkery, staff scientist and first author, adds:"It is vital that lysosomal contents stay where they belong. If we understand why leaks sometimes go undetected, we can also understand why cells die in neurodegenerative diseases. The ATG8 E3-like ligases sense lysosomal damage and initiate ESCRT-mediated membrane repair. In our latest interview, News-Medical speaks with Rosanna Zhang from ACROBiosystems about utilizing organoids for disease modeling in the field of neuroscience research. GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún Discover how AI, flow chemistry, and NMR come together in the PiPAC project to revolutionize scalable and autonomous API production. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

From saccharin in the 19th century to stevia and monk fruit in the 21st, researchers and the food industry have long sought a sweetener that delivers the taste of sugar without its drawbacks-excess calories, tooth decay, and heightened risk for obesity, insulin resistance, and diabetes. Now, in a study published in Cell Reports Physical Science, Tufts researchers have developed a way to biosynthetically produce an otherwise rare sugar called tagatose, which could very well provide the sweetness and natural taste of table sugar without its potential harms. Tagatose occurs naturally in only very small amounts compared to common sugars like glucose, fructose, or sucrose. It can be found in milk and other dairy products when lactose is broken down by heat or enzymes, such as might be found in the production of yogurt, cheese, and kefir. Since tagatose is typically less than 0.2% of sugars found in natural sources, it is usually manufactured, not extracted, for consumption. "There are established processes to produce tagatose, but they are inefficient and expensive," said Nik Nair, associate professor of chemical and biological engineering at Tufts. "We developed a way to produce tagatose by engineering the bacteria Escherichia coli to work as tiny factories, loaded with the right enzymes to process abundant amounts of glucose into tagatose. This is much more economically feasible than our previous approach, which used less abundant and expensive galactose to make tagatose." The bacteria are engineered to include a newly discovered enzyme from slime mold called galactose-1-phosphate-selective phosphatase (Gal1P), which can help make galactose directly from glucose. The yield of tagatose from glucose generated by the bacteria could reach up to 95%, significantly greater and more cheaply attained than conventional manufacturing in which yields only reach 40 to 77%. Tagatose has been designated "generally recognized as safe" by the FDA, which means it can safely be used in consumer foods. Clinical studies show very low increases in plasma glucose or insulin after ingestion of tagatose. Unlike sucrose, which fuels cavity-causing bacteria in the mouth, tagatose appears to reduce the growth of some of those bacteria, and evidence suggests it has probiotic effects to support healthy oral and gut bacteria. With low calories and low absorption, tagatose is an attractive "bulk sweetener," which means it not only can replace sugar for sweetness, but can also provide a similar bulk texture in cooking that comes with adding the sugar in some quantity, something that high intensity sweetener substitutes can't do. It even browns like table sugar during cooking. That allowed us to reverse a natural biological pathway that metabolizes galactose to glucose and instead generate galactose from glucose supplied as a feedstock. Tagatose and potentially other rare sugars can be synthesized from that point." Nik Nair, associate professor of chemical and biological engineering, Tufts University Reversal of the Leloir pathway to promote galactose and tagatose synthesis from glucose. In our latest interview, News-Medical speaks with Rosanna Zhang from ACROBiosystems about utilizing organoids for disease modeling in the field of neuroscience research. GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún Discover how AI, flow chemistry, and NMR come together in the PiPAC project to revolutionize scalable and autonomous API production. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

Scientists at The Lundquist Institute for Biomedical Innovation have identified a previously unknown molecular safeguard that protects the heart during pregnancy, shedding new light on the causes of peripartum cardiomyopathy (PPCM), a rare and life-threatening form of pregnancy-related heart failure. In a study published in Nature Communications, Michelle L. Matter, PhD, and her team reveal that the gene PTRH2 plays a critical role in helping the maternal heart adapt to pregnancy-induced stress. This work identifies a previously unrecognized molecular safeguard in the heart. Understanding how the heart normally responds to pregnancy-induced stresses brings us closer to developing targeted treatments for women who develop PPCM." Using advanced mouse models, the researchers showed that loss of PTRH2 leads to severe postpartum heart failure. "During pregnancy, the heart increases in size to account for increased blood flow-but without PTRH2, the heart doesn't return to normal," explained Pooja Choubey, PhD, co-first author and postdoctoral fellow in The Matter Lab. "That kind of enlargement can be extremely dangerous and, in many cases, fatal." "We're opening the door for innovation," Choubey added. Peptidyl-tRNA hydrolase 2 is a negative regulator of peripartum cardiomyopathy with heart failure in female mice. In our latest interview, News-Medical speaks with Rosanna Zhang from ACROBiosystems about utilizing organoids for disease modeling in the field of neuroscience research. GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún Discover how AI, flow chemistry, and NMR come together in the PiPAC project to revolutionize scalable and autonomous API production. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

Researchers at University of California San Diego have identified a previously unrecognized treatment target for triple‑negative breast cancer (TNBC), the most aggressive subtype of breast cancer. Their new study reveals that a protein called PUF60 plays an essential role in helping TNBC cells grow and survive by controlling how key genes are spliced. TNBC is widely recognized as the most difficult breast cancer to treat because it is very aggressive and does not respond to targeted therapies, such as immunotherapy or hormone therapy, that can be used in other subtypes. This study highlights PUF60‑mediated RNA splicing as a promising therapeutic angle for TNBC and potentially other cancers characterized by replication stress. By pinpointing PUF60 as a regulator that cancer cells depend on - but healthy cells do not - the findings suggest a new direction for future drug development. However, further research is needed to explore whether inhibitors targeting PUF60 or its splice‑site interactions can be developed as targeted cancer therapies. The study, published in Cancer Research, was led by Corina Antal, PhD, assistant professor, and Gene Yeo, PhD, professor, both at UC San Diego School of Medicine. Both are also members of UC San Diego Moores Cancer Center. Integrative CRISPR Screening and RNA Analyses Discover an Essential Role for PUF60 Interactions with 3' Splice Sites in Cancer Progression. In our latest interview, News-Medical speaks with Rosanna Zhang from ACROBiosystems about utilizing organoids for disease modeling in the field of neuroscience research. GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún Discover how AI, flow chemistry, and NMR come together in the PiPAC project to revolutionize scalable and autonomous API production. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. Please check the box above to proceed. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

Instead, the team found that, in many cases, two harmful variants can actually restore normal protein function.The research focused on a human enzyme called argininosuccinate lyase (ASL), which plays a critical role in removing toxic ammonia from the body. Variants in ASL that decrease its activity cause one of the urea cycle disorders, a set of rare and potentially life-threatening metabolic diseases.By experimentally measuring the functional impact of several thousand individual variants and variant combinations, PNRI researchers discovered that over 60% of pairs that were individually damaging could, together, bring enzyme activity back to healthy levels. This work shows that genetic variants don't act independently in many important cases. For a defined group of genes, the default assumptions we use to predict disease risk simply don't hold." Michelle Tang, Ph.D., PNRI Staff Scientist and lead author of the study The mechanism was first proposed in 1964 by Francis Crick and Leslie Orgel, but until now had not been tested systematically or shown to be common or predictable at scale.The study was led by scientists in the Dudley Lab at PNRI, in collaboration with clinicians and researchers at Children's National Hospital, St. Jude Children's Research Hospital, George Mason University, and the University of Washington.To make these interactions predictable, the research team developed an AI-based model that accurately forecasted whether two variants would restore protein function. "We've shown that, in many cases, two damaging variants can work together to restore protein function," said Aimée Dudley, Ph.D., PNRI Senior Investigator who led the study. "This kind of genetic interaction is not an isolated exception, but a widespread and underappreciated way that variants can interact, especially in rare disease contexts. For these genes, standard genetic predictions can overestimate disease risk, particularly for people who carry two different variants in the same gene. In our latest interview, News-Medical speaks with Rosanna Zhang from ACROBiosystems about utilizing organoids for disease modeling in the field of neuroscience research. GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.