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Category: biotech/medical

Advances and Integrations of Computer-Assisted Planning,… : Operative Neurosurgery

ONSNew ONSReview Advances and Integrations of Computer-Assisted Planning, Artificial Intelligence, and Predictive Modeling Tools for Laser Interstitial Thermal Therapy in Neurosurgical Oncology by Warman et al Johns Hopkins Medicine Congress of Neurological Surgeons (CNS) Isaac Yang.

E to surrounding healthy tissue, LiTT offers promising therapeutic outcomes for both newly diagnosed and recurrent tumors. However, challenges such as postprocedural edema, unpredictable heat diffusion near blood vessels and ventricles in real time underscore the need for improved planning and monitoring. Incorporating artificial intelligence (AI) presents a viable solution to many of these obstacles. AI has already demonstrated effectiveness in optimizing surgical trajectories, predicting seizure-free outcomes in epilepsy cases, and generating heat distribution maps to guide real-time ablation. This technology could be similarly deployed in neurosurgical oncology to identify patients most likely to benefit from LiTT, refine trajectory planning, and predict tissue-specific heat responses.

Why chronic pain lasts longer in women: Immune cells offer clues

Chronic pain lasts longer for women than men, and new research suggests differences in hormone-regulated immune cells, called monocytes, may help explain why.

In a new paper in Science Immunology, researchers at Michigan State University found a subset of monocytes release a molecule to switch off pain. These cells are more active in males due to higher levels of sex hormones such as testosterone, the team found.

Females, however, experienced longer-lasting pain and delayed recovery, because their monocytes were less active. Geoffroy Laumet, MSU associate professor of physiology, and Jaewon Sim, a former graduate student in his lab, discovered the same pattern in both mouse models and human patients.

Polyamine metabolism as a regulator of cellular and organismal aging

Polyamines — putrescine, spermidine, and spermine — are ubiquitous cationic molecules that are essential for cellular proliferation and homeostasis. Their intracellular concentrations decline with age, contributing to physiological and cognitive deterioration. Recent studies have revealed that spermidine supplementation extends lifespan and improves cognitive and cardiac function in various model organisms, suggesting that maintaining polyamine balance has anti-aging potential. Polyamine metabolism is tightly regulated through biosynthesis, degradation, and transport; however, age-associated upregulation of spermine oxidase (SMOX) and accumulation of its toxic byproduct acrolein promote oxidative damage and cellular senescence. Suppressing SMOX activity or polyamine degradation attenuates senescence markers and DNA damage, highlighting spermine catabolism as a therapeutic target. Polyamines also modulate epigenetic regulation, including DNA methylation and histone acetylation, thereby influencing gene expression and chromatin structure during aging. Moreover, polyamine-dependent hypusination of eIF5A sustains protein synthesis in senescent cells. These multifaceted actions indicate that polyamine metabolism integrates redox control, translational regulation, epigenetic maintenance and autophagy to determine cellular and organismal longevity. While animal studies demonstrate clear anti-aging effects of spermidine and spermine, human clinical evidence remains limited, with variable outcomes likely due to bioavailability and metabolic conversion. Future strategies combining dietary or probiotic polyamine enhancement, enzyme-targeted inhibitors, and personalized metabolic interventions hold promise for extending healthspan. Collectively, maintaining optimal polyamine homeostasis emerges as a key approach to counteract aging and age-related diseases.

SGLT2 Inhibitors for Nondiabetic Heart Failure: Equipping PCPs for Success

Once diabetes drugs, SGLT2 inhibitors are now key therapies for heart failure—even in patients without diabetes. A new primary-care guide reviews indications, benefits, and practical prescribing tips to help clinicians integrate these agents into routine HF care.

Are PCPs ready to adopt SGLT2 inhibitors beyond diabetes?

While proven to help, primary care clinicians have been slow to use the drugs once considered only for patients with diabetes.

Role of Dopamine in Pain

Dopamine is a member of a class of molecules called the catecholamines, which serve as neurotransmitters and hormones. In the brain, dopamine serves as a neurotransmitter and is released from nerve cells to send signals to other nerves. Outside of the nervous system, it acts as a local chemical messenger in several parts of the body.

Image Copyright: Meletios, Image ID: 71,648,629 via shutterstock.com

A number of important neurodegenerative diseases are associated with abnormal function of the dopamine system and some of the main medications used to treat those illnesses work by changing the effects of dopamine. The condition Parkinson’s disease is caused by a loss of dopamine secreting cells in a brain area called the substantia nigra.

Grant supports research into how microglia may spread toxic tau in Alzheimer’s

A paper describing Hopp’s upcoming study published on the CureAlz website, titled, “How Do Microglia Contribute to the Spread of Tau Pathology in Alzheimer’s Disease?”, says that while tau aggregates are a defining feature of Alzheimer’s disease and closely track with brain cell loss, memory problems and cognitive decline, much still isn’t known about how it spreads or what role the brain’s immune system plays in the process.

There is evidence, it says, that toxic forms of tau, which have become “misfolded” or dysfunctional, act like a “bad influence.”

“When they encounter nearby healthy tau proteins, they cause them to misfold as well, triggering a chain reaction that spreads from one brain region to another,” according to the paper. “Microglia … are among the first to encounter these toxic tau ‘seeds.’ Normally, microglia protect the brain by clearing debris and helping repair damage. But growing evidence suggests that microglia may also contribute to tau’s spread by engulfing misfolded tau and inadvertently releasing it, thereby amplifying its harmful effects.”

A researcher with the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases at UT Health San Antonio has received a two-year, $402,500 grant award from the Cure Alzheimer’s Fund to study how microglia, the brain’s resident immune cells, paradoxically might contribute to the spread of toxic forms of tau protein in the disease.

Sarah C. Hopp, PhD, associate professor of pharmacology with the Biggs Institute and the South Texas Alzheimer’s Disease Research Center, along with her lab have been instrumental in uncovering the behavior of microglia. UT Health San Antonio is the academic health center of The University of Texas at San Antonio.

Starting this month, Hopp’s lab will test the hypothesis that microglial uptake of tau is a key mechanism driving its spread through the brain, and that specific molecular pathways determine whether this process protects or harms neurons. The Cure Alzheimer’s Fund, also known as CureAlz, is a nonprofit organization that funds research “with the highest probability of preventing, slowing or reversing Alzheimer’s disease.”

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DeepRare AI helps shorten the rare disease diagnostic journey with evidence-linked predictions

Researchers developed DeepRare, an LLM-driven multi-agent diagnostic system that integrates clinical descriptions, phenotype data, and genomic information to improve rare disease identification. Across thousands of cases, the system showed higher diagnostic recall than existing AI tools and clinicians in benchmark testing, while providing traceable reasoning linked to medical evidence.

By 2050 we could get “10,000 years of technological progress”

Every major AI company has the same safety plan: when AI gets crazy powerful and really dangerous, they’ll use the AI itself to figure out how to make AI safe and beneficial. It sounds circular, almost satirical. But is it actually a bad plan? Today’s guest, Ajeya Cotra, recently placed 3rd out of 413 participants forecasting AI developments and is among the most thoughtful and respected commentators on where the technology is going.

She thinks there’s a meaningful chance we’ll see as much change in the next 23 years as humanity faced in the last 10,000, thanks to the arrival of artificial general intelligence. Ajeya doesn’t reach this conclusion lightly: she’s had a ring-side seat to the growth of all the major AI companies for 10 years — first as a researcher and grantmaker for technical AI safety at Coefficient Giving (formerly known as Open Philanthropy), and now as a member of technical staff at METR.

So host Rob Wiblin asked her: is this plan to use AI to save us from AI a reasonable one?

Ajeya agrees that humanity has repeatedly used technologies that create new problems to help solve those problems. After all:
• Cars enabled carjackings and drive-by shootings, but also faster police pursuits.
• Microbiology enabled bioweapons, but also faster vaccine development.
• The internet allowed lies to disseminate faster, but had exactly the same impact for fact checks.

But she also thinks this will be a much harder case. In her view, the window between AI automating AI research and the arrival of uncontrollably powerful superintelligence could be quite brief — perhaps a year or less. In that narrow window, we’d need to redirect enormous amounts of AI labour away from making AI smarter and towards alignment research, biodefence, cyberdefence, adapting our political structures, and improving our collective decision-making.

The plan might fail just because the idea is flawed at conception: it does sound a bit crazy to use an AI you don’t trust to make sure that same AI benefits humanity.

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