“Everyone thinks that [after] spinal injury, all you want to do is be able to walk again. But if you’re a tetraplegic or a quadriplegic, what matters most is working hands,” she said.

Reid received the device, called ARCex, as part of a 60-person clinical trial. She and the other participants completed two months of physical therapy, followed by two months of physical therapy combined with stimulation. The results, published today in Nature Medicine, show that the vast majority of participants benefited. By the end of the four-month trial, 72% experienced some improvement in both strength and function of their hands or arms when the stimulator was turned off. Ninety percent had improvement in at least one of those measures. And 87% reported an improvement in their quality of life.

This isn’t the first study to test whether noninvasive stimulation of the spine can help people who are paralyzed regain function in their upper body, but it’s important because a trial has never been done before in this number of rehabilitation centers or in this number of subjects, says Igor Lavrov, a neuroscientist at the Mayo Clinic in Minnesota, who was not involved in the study. He points out, however, that the therapy seems to work best in people who have some ability to move below the site of their injury.

22q11.2 deletion syndrome (22q) raises schizophrenia risk through skull malformations linked to the Tbx1 gene, affecting cerebellar development. This highlights how non-brain factors like bone defects can influence neurological disorders.

The chromosomal disorder 22q11.2 deletion syndrome (22q) has emerged as one of the strongest risk factors for schizophrenia. Scientists at St. Jude Children’s Research Hospital identified malformed regions of the cerebellum in both laboratory models and patients with 22q, attributing these malformations to improper skull formation.

Additionally, the researchers linked the skull malformation to the loss of a single gene: Tbx1. This research highlights that neurological disorders can arise from sources outside the nervous system, such as defects in skull development. The findings were published in Nature Communications.

Because glucose metabolism is disrupted in several different neurodegenerative disorders, this treatment strategy also shows promise for other brain conditions.

“The beneficial effect on brain metabolism by IDO1 inhibition cuts across different types of pathology,” Andreasson said.

“It is exciting to think that this may be a more general mechanism that could be targeted in other neurodegenerative disorders, like Parkinson’s disease, where you have accumulation of a-synuclein, or ALS, where there is accumulation of tdp-43.”

Introduction: The lips fulfill various critical physiological roles besides being viewed as a fundamental aesthetic feature contributing to the perception of health and beauty. Therefore, any lip injury, abnormality, or congenital malformation, such as cleft lip, needs special attention in order to restore proper lip function and aesthetics. To achieve this goal, a better understanding of the complex lip anatomy, function, and biology is required, which can only be provided by basic research endeavors. However, the current lack of clinically relevant human lip cells and three-dimensional in vitro lip models, capable of replacing ethically questionable animal experimentations, represents a significant limitation in this area of research.

Methods: To address these limitations, we aimed to pioneer the introduction of immortalized healthy lip-and cleft lip-derived keratinocytes. Primary keratinocytes were isolated from patients’ samples and immortalized by introducing the catalytic domain of telomerase, combined with the targeted knockdown of the cell cycle inhibitor gene, p16^INK4A. We then focused on validating the newly established cell lines by comparing their genetic stability and key phenotypic features with their primary keratinocyte counterparts.

Results: The newly established immortalized keratinocyte cell lines demonstrated genetic stability and preserved the main phenotypic characteristics of primary keratinocytes, such as cellular morphology and differentiation capacity. Three-dimensional lip models, generated using these cell lines, proved to be effective and convenient platforms for screening applications, including wound healing and microbial infection of the lip epithelium.

One of the most elusive challenges oncologists encounter is why some patients respond to a particular therapy while others do not. Thus, optimizing a personalized treatment regimen that gives a patient the best odds of success has become a cornerstone of cancer research. The desire to implement more individualized therapies has brought about an increasing the focus on personalized medicine. This promising approach uses specific patient characteristics, including genetic makeup, environment, and lifestyle, to develop an individualized treatment plan.

Working towards improving the speed and accuracy of genetic screening to inform personalized medicine, a team of researchers conducted a comprehensive study. The journal NPJ Precision Oncol recently published the results. The researchers meticulously investigated the gene expression of almost 800 cancer cell lines and their response to treatment. With this thorough process, the researchers identified specific genetic patterns that correlated with drug resistance.

The study identified 36 genes correlating to resistance to multiple anti-cancer drugs. The researchers calculated a score, called UAB36, based on the correlation coefficient of the 36 genes identified. This UAB36 score, a novel predictive tool, accurately forecasted resistance to tamoxifen, an anti-cancer drug used to treat some types of breast cancer and prevent cancer progression in women with ductal carcinoma in situ (DCIS).

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.

“We want to do something to help those who are suffering from tooth loss or absence,” said lead researcher Katsu Takahashi, head of dentistry and oral surgery at Kitano Hospital. “While there has been no treatment to date providing a permanent cure, we feel that people’s expectations for tooth growth are high.”