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HPH-15, a compound developed by Kumamoto University, reduces blood glucose and fat accumulation more effectively than metformin, with added benefits like antifibrotic properties and a safer profile. This innovation may revolutionize diabetes treatment.

Scientists at Kumamoto University have unveiled a novel compound, HPH-15, which has dual effects: reducing blood glucose levels and combating fat accumulation. This breakthrough represents a significant advancement in diabetes treatment innovation.

Type 2 diabetes, a condition affecting millions worldwide, is often accompanied by complications such as fatty liver and insulin resistance, posing challenges for current treatment methods. The research team, led by Visiting Associate Professor Hiroshi Tateishi and Professor Eiichi Araki, has identified HPH-15 as a promising alternative to existing medications like metformin.

Researchers at UCLA have developed a new AI model that can expertly analyze 3D medical images of diseases in a fraction of the time it would otherwise take a human clinical specialist.

The deep-learning framework, named SLIViT (SLice Integration by Vision Transformer), analyzes images from different imagery modalities, including retinal scans, ultrasound videos, CTs, MRIs, and others, identifying potential disease-risk biomarkers.

Dr. Eran Halperin, a computational medicine expert and professor at UCLA who led the study, said the model is highly accurate across a wide variety of diseases, outperforming many existing, disease-specific foundation models. It uses a novel pre-training and fine-tuning method that relies on large, accessible public data sets. As a result, Halperin believes that the model can be deployed—at relatively low costs—to identify different disease biomarkers, democratizing expert-level medical imaging analysis.

Summary: SUMO proteins play a key role in activating dormant neural stem cells, vital for brain repair and regeneration. This finding, centered on a process called SUMOylation, reveals how neural stem cells can be “woken up” to aid in brain recovery, offering potential treatments for neurodegenerative diseases.

SUMO proteins regulate neural stem cell reactivation by modifying the Hippo pathway, crucial for cell growth and repair. The study’s insights lay foundational groundwork for developing regenerative therapies to combat conditions like Alzheimer’s and Parkinson’s disease.

Surviving Neanderthal genes in the modern genome tell a story of thousands of years of interactions.

Recent DNA studies have refined the period when Neanderthals and modern humans interbred to a span of about 7,000 years, leaving Eurasians with significant Neanderthal genetic contributions. These findings also help clarify the timeline and routes of ancient human migrations from Africa.

Genetic Insights into Ancient Human-Neanderthal Interactions.

The world’s first human trial of a drug that can regenerate teeth will begin in a few months, less than a year on from news of its success in animals. This paves the way for the medicine to be commercially available as early as 2030.

The trial, which will take place at Kyoto University Hospital from September to August 2025, will treat 30 males aged 30–64 who are missing at least one molar. The intravenous treatment will be tested for its efficacy on human dentition, after it successfully grew new teeth in ferret and mouse models with no significant side effects.

Continue reading “World-first tooth-regrowing drug will be given to humans in September” »

Brain edema can accompany large ischemic strokes and can increase stroke-related morbidity and mortality. The past few decades have seen no advances in pharmacologic treatment of brain edema. These investigators conducted a manufacturer-funded, randomized, placebo-controlled trial of glibenclamide, a sulfonylurea 1–receptor inhibitor that can decrease brain edema. (Glibenclamide is approved to treat type 2 diabetes.) In a previous study, it was associated with fewer deaths from neurologic causes, but its use in patients with stroke is not widespread.

Eligible patients had large ischemic strokes that could be treated within 10 hours of onset. A large hemispheric infarct in at least the middle cerebral artery territory was defined as either an Alberta Stroke Program Early CT Score of 1 to 5 or lesion volumes of 80 mL to 300 mL on computed-tomography perfusion or diffusion-weighted imaging. Glibenclamide (8.6 mg) was given to half the study participants intravenously over 72 hours.

The study was halted early due to underenrollment. Of 535 enrolled patients, 431 were in the intended age range (18–70) and had complete data (mean age, 58; 33% women; median NIH Stroke Scale [NIHSS] score, 19). Treatment began at an average of 9 hours after symptom onset. No favorable shift with glibenclamide occurred on the primary outcome, the 90-day modified Rankin Scale (mRS). Mortality was similar in the two groups (glibenclamide, 32%; placebo, 29%). Hypoglycemia was seen in 6% of glibenclamide recipients and 2% of placebo recipients. Subgroup analysis revealed a signal of potential benefit with glibenclamide in patients with NIHSS scores of 20 or less.

The findings suggest that biochemical and physical effects of exercise could help heal nerves. There’s no doubt that exercise does a body good. Regular activity not only strengthens muscles but can bolster our bones, blood vessels, and immune system.

Now, MIT engineers have found that exercise can also have benefits at the level of individual neurons. They observed that when muscles contract during exercise, they release a soup of biochemical signals called myokines. In the presence of these muscle-generated signals, neurons grew 4X farther compared to neurons that were not exposed to myokines. These cellular-level experiments suggest that exercise can have a significant biochemical effect on nerve growth.

Surprisingly, the researchers also found that neurons respond not only to the biochemical signals of exercise but also to its physical impacts. The team observed that when neurons are repeatedly pulled back and forth, similarly to how muscles contract and expand during exercise, the neurons grow just as much as when they are exposed to a muscle’s myokines.

New research points to a future in which pleasure and pain relief can be independently controlled.

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