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Category: biotech/medical – Page 46

A novel intervention to potentially improve the outcome of children with malnutrition

Researchers at Baylor College of Medicine and Texas Children’s Hospital have uncovered an intervention that could potentially improve outcomes for children with malnutrition, a condition that contributes to nearly half of all deaths among children younger than 5. The study appears in the Proceedings of the National Academy of Sciences.

“One poorly understood consequence of malnutrition is intestinal barrier erosion, which allows bacteria to escape the gut and cause invasive infections, including sepsis, which are leading causes of mortality in malnourished children,” said study lead and co-corresponding author Dr. Geoffrey Preidis, associate professor of pediatrics—gastroenterology, hepatology and nutrition and member of the USDA/ARS Children’s Nutrition Research Center at Baylor and Texas Children’s.

The intestinal barrier is a dynamic system maintained through coordinated functions of the mucus layer, the junctions between epithelial cells lining the gut and immune cells. In addition, gut microbes and products of their metabolism also play a role in regulating intestinal barrier function, but how this occurs is not well understood.

CRISPR roadblocks: Scientists identify genes blocking gene therapy success

Like a delivery driver navigating crowded city streets, a gene-therapy-toting lipid nanoparticle faces a gauntlet of potential detours on its journey toward a cell’s nucleus. First, there’s entering the cell’s plasma membrane; then navigating around organelles like the Golgi apparatus, mitochondria and endoplasmic reticulum—all destinations that can errantly absorb the particle’s payload, rendering it ineffective at best or harmful at worst. And that’s all before the particle even enters the nucleus and successfully makes a genetic change.

Anthropic Reportedly in Talks to Acquire Peer Decart for $6 Billion, Bolstering Compute Ahead of IPO

AI startup Anthropic is reportedly in talks to acquire peer Decart AI for approximately $6 billion (about NT$190 billion). If finalized, the deal would mark the largest acquisition in Anthropic’s history, coming at a time when the company is preparing for its highly anticipated IPO. Bloomberg first reported the deal on August 13, noting that the agreement has not yet been finalized and negotiations could still fall through.

Anthropic has been moving at a rapid pace on both fundraising and listing preparations this year. In February, it completed a $30 billion Series G round at a post-money valuation of $380 billion. Less than three months later, in May, it closed a $65 billion Series H round, pushing its post-money valuation to $965 billion — nearly $1 trillion. In early June, Anthropic confidentially filed its S-1 registration statement with the U.S. Securities and Exchange Commission (SEC), paving the way for a future public listing. If this acquisition goes through, it would occur during a period when the company’s valuation and IPO preparations are both accelerating simultaneously.

Market sources indicate that Anthropic, which has historically made very few large acquisitions, has been investing heavily in compute capacity to develop new products and serve customers. According to sources, Decart’s software enables chips to operate more efficiently, thereby reducing the cost of training AI models. This technology would help Anthropic’s existing infrastructure handle greater demand. Upon completion of the deal, Decart’s team would join Anthropic’s inference and performance division. According to Forbes, FierceBiotech, and other media tallies, Anthropic has completed at least four acquisitions this year, including compiler startup Stainless and biotech startup Coefficient Bio (in a roughly $400 million stock deal), but all were far smaller than the Decart transaction — $6 billion would be more than ten times the size of any previously known deal.

Distinguishing true progression from treatment effects in glioblastoma: a practical, evidencegraded imaging framework for the multidisciplinary team NeuroOncology

Distinguishing true progression (TP) from treatment effects—pseudoprogression (PsP) and radiation necrosis (RN)—after chemoradiation for glioblastoma (GBM) is a consequential, unresolved decision that conventional MRI cannot reliably make in 30–40% of cases, and that is rarely made by any single specialty alone.

We synthesized and graded evidence from RANO 2.0, advanced MRI (perfusion, diffusion, and spectroscopy), amino acid PET (per PET RANO 1.0), and radiomics, based on a literature search of PubMed/MEDLINE, Embase, and Cochrane (2010–2025).

In selected cohorts, combined MRI plus amino acid PET reports areas under the curve of 0.90–0.95 versus 0.65–0.72 for conventional MRI alone; however, these figures come from cohorts spanning the full range of post-treatment enhancement—including easily classified cases—rather than the ambiguous subset in which advanced imaging is actually used, and therefore likely overstate real-world accuracy. We organize the evidence around clinical modifiers of pretest probability—MGMT methylation, interval since chemoradiation, neurologic trajectory, antiangiogenic or immunotherapy exposure, reirradiation, and lesion location—that determine how heavily each imaging tier should be weighted. For amino acid PET, we address U.S. access, including recently published prospective and multicenter diagnostic-accuracy data for 18 F-fluciclovine.

New brain map connects mice and primates to strengthen medical research

Most neuroscience research still runs on mice, even though much of what applies to mice does not hold up in humans. Marmosets have emerged as a bridge between species. However, comparing the brains of mice and marmosets runs into a chicken-and-egg problem. Scientists need to know which part of one brain matches the respective region of the other, but almost every brain map draws those areas differently.

For a new study published in Communications Biology, Cold Spring Harbor Laboratory Professor Partha Mitra and colleagues built the first cross-species map to systematically link mouse and marmoset brain regions.

“It’s the kind of problem that nobody wants to address, because it’s hard,” Mitra says. Comparing genomes across species is relatively straightforward. DNA aligns letter by letter. But brain circuits vary even within one species. Compounding the problem, research teams have built different brain atlases that divide the same mouse brain differently.

PeptideMHCtargeted engineered viruslike particles enable selective priming and gene editing of tumorspecific T cells

As well as T cells bearing an engineered TCR55-A50E, which forms catch-bonds with both HIVpol/B∗35 pMHC and Pep20/B∗35 pMHC. We treated TCR55 and TCR55-A50E cells with pMHC-eVLPs pseudotyped with either HIV/B∗35 or Pep20/B∗35 and subsequently assessed T cell activation by CD69 upregulation and eVLP transduction. Consistent with previous reports, we observed increased CD69 upregulation in TCR55 cells by Pep20/B∗35 eVLPs compared to HIV/B∗35 eVLPs, whereas TCR55-A50E cells were similarly activated by both pMHC-eVLPs (Figure S4G). Notably, pMHC-eVLPs presenting HIV/B∗35 were still able to induce CD69 upregulation on TCR55 cells despite reported slip-bond formation (Figure S4G). Interestingly, both HIV/B∗35 and Pep20/B∗35 pMHC-eVLPs were able to efficiently transduce both TCR55 and TCR55-A50E cells (Figure S4H), suggesting that antigen specificity and physiological TCR·pMHC affinity, rather than catch-bond formation, are the primary determinants of pMHC-eVLP-mediated T cell activation and transduction.

Collectively, these findings demonstrate that the pMHC-eVLP platform can be programmed with different antigens and HLA allotypes to enable selective and efficient targeting of tumor-specific T cells via natural TCRs with physiological antigen affinities, and that pMHC-eVLPs induce antigen-specific T cell activation during TCR-mediated entry.

Sleep could help identify people at risk of developing Alzheimer’s disease at an earlier stage

What if certain signs of the disease were to manifest subtly during sleep, long before the first memory problems appear? This is the line of inquiry being explored by a team of researchers at ULiège.

A team of scientists from the University of Liège (GIGA Neurosciences), supported by the Stop Alzheimer’s Foundation, has analyzed the sleep patterns of more than 500 healthy people. Among middle-aged participants, a higher frequency of nocturnal micro-awakenings was found to be associated with a greater genetic risk of developing Alzheimer’s disease, whereas this link was not observed in young adults. This research, published in the journal Sleep, suggests that the study of sleep could, in the long term, contribute to the early identification of vulnerable individuals.

NASA astronaut Mike Fincke leaves agency months after medical emergency in space

Longtime NASA astronaut Mike Fincke is stepping away from his role at the space agency. The news comes months after he experienced a medical emergency aboard the International Space Station, which forced a premature end to the journey for him and three crewmates.

Fincke’s last day at the space agency is Wednesday, NASA said in a news release.

Although he is leaving NASA, Fincke said he remains “deeply committed to the work of exploration.”

Have we already found the fountain of youth? — The Global Story, BBC World Service

Scientists are optimistic that existing drugs that could one day slow or reverse our ageing.

For centuries, people have pursued the dream of eternal youth. It might seem like the stuff of myth or science fiction, but researchers have been making fascinating progress in understanding what happens in our bodies as we age. There’s optimism that we might soon be able to use drugs to slow down or even reverse how we age, extending the number of years we live healthy, productive lives. What’s more, some of us might be taking these drugs already.

On today’s episode, Lucy Hockings speaks to Dr Andrew Steele, author of Ageless: The New Science of Getting Older Without Getting Old to find out whether we might drink from the fountain of youth in our lifetime.

00:00 Intro.
01:07 Questions about anti-ageing.
02:05 Cosmetic and cellular anti-ageing.
03:48 What is biological age?
05:51 What is ageing?
07:55 Is it a humanitarian crisis?
09:23 Lifespan and healthspan.
10:53 Can we slow down our ageing?
12:29 Is there a drug?
14:10 Therapies for ageing.
16:01 When could this happen?
17:10 Anti-ageing advice.
18:45 Outro.

Watch more episodes of The Global Story here 👉🏽 • The Global Story.

You can listen to more episodes of The Global Story here. Making sense of the news with our experts around the world. Insights you can trust, Monday to Friday, from the BBC 👉🏽 https://www.bbc.co.uk/programmes/w13x… credit: Getty —————- This is the official BBC World Service YouTube channel. If you like what we do, you can also find us here: Instagram 👉🏽 / bbcworldservice Twitter 👉🏽 / bbcworldservice Facebook 👉🏽 / bbcworldservice BBC World Service website 👉🏽 https://www.bbc.co.uk/worldserviceradio Thanks for watching and subscribing! #BBCWorldService #WorldService #ageing #youth.

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Discovering a new layer of control for a decades-old leukemia drug

For more than 70 years, the drug 6-thioguanine (6-TG) has been used to treat leukemia. Although its clinical effects have been studied extensively, scientists are still uncovering the molecular mechanisms that determine whether cells succumb to the drug or survive its attack.

Now, researchers at the CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, together with collaborators at the University of Oxford, the Weizmann Institute of Science and the University of Dundee, have identified an unexpected player in this process: the protein NUDT5. Their paper is published in the journal Nature Communications.

The discovery builds directly on a recent breakthrough from the Kubicek and Huber laboratories. In that work, researchers showed that NUDT5 performs a critical cellular function independently of its enzymatic activity. Instead of acting primarily as a catalyst, NUDT5 was found to serve as a molecular scaffold that helps organize cellular metabolism. This unusual behavior has direct consequences for the action of the important cancer drug.

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