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Category: health

Study suggests protein made in the liver is a key factor in men’s bone health

New research suggests the liver plays a previously unrecognized role in bone health, but only in males. A McGill University-led study published in Matrix Biology found that a protein made in the liver helps regulate bone growth in male mice, but not in females. The findings may help explain why men with liver disease are more likely to experience bone loss.

The protein, known as plasma fibronectin, is naturally present in blood at higher levels in men than in women, declines when the liver is damaged and builds up in bone to modulate bone formation. This suggests men rely more heavily on the protein to maintain bone strength than do women.

“About 60% of osteoporosis cases in men are secondary to other underlying health conditions,” said senior author Mari Tuulia Kaartinen, Associate Professor in McGill’s Faculty of Dental Medicine and Oral Health Sciences. “Our findings suggest this protein may be one of the biological links connecting liver disease to bone loss.”

Got milk? how T cells shape lactation and beyond

Lactation supports babies’ immune health and reduces the risk of breast cancer for the mother.

TrendsInImmunology.

Lactation is increasingly recognized as an immune-regulated process. Immune cells shape mammary gland development, coordinate tissue remodeling, and aid in milk production with lasting consequences for maternal health. Here, we summarize recent advances on the roles and dynamics of T cells in the mammary gland during lactation and beyond.

Jumping DNA Sequences Drive Early Tumor Growth

New research reveals that LINE-1 retrotransposons don’t just nudge genes, they also trigger massive structural upheavals early in cancer development.

Read about the findings.

Where there’s a bountiful host, there are parasites ready to take advantage of the resources. This holds true even at microscopic levels. Lying within human DNA are repetitive elements called LINE-1 (L1) retrotransposons that promote their own propagation at the cost of the host organism’s health.1 These genetic parasites create copies of themselves that then get inserted at new locations within the genome. Until recently, scientists thought that the activity of L1s mostly resulted in local alterations to genes.

Now, in a new study published in Science, researchers have demonstrated that L1s can trigger dramatic structural changes in DNA, resulting in cancer-causing mutations.2 These findings, which shed light on the intricate relationship between cancer evolution and the genome, could lead to improved diagnostic and therapeutic strategies for different cancers.

“Cancer genomes are more influenced by these jumping fragments of DNA parasites than we previously thought,” said José Tubio, a molecular biologist at the University of Santiago de Compostela, in a statement.

Clinically informed AI outperforms foundation models in spinal cord disease prediction

Cervical spondylotic myelopathy (CSM) refers to spinal cord compression from arthritis in the neck and is the leading cause of spinal cord dysfunction in older adults. CSM is a chronic, progressive condition that can cause neck pain, muscle weakness, difficulty walking and other debilitating symptoms. While the diagnosis is sometimes clear, often the diagnosis can take years because symptoms aren’t recognized until the later stages, and by then, treatment options are limited.

A multidisciplinary team of surgeon-scientists, computer scientists and researchers at WashU developed an artificial intelligence (AI)-based approach that could help clinicians screen for and diagnose CSM up to 30 months earlier, opening new opportunities for earlier treatment. The findings are published in npj Digital Medicine.

Salim Yakdan, MD, a postdoctoral research fellow in the Taylor Family Department of Neurosurgery at WashU Medicine, and Ben Warner, a doctoral student in computer science and engineering at the McKelvey School of Engineering, co-first authors on the research, used seven different AI models to analyze large datasets containing electronic health record data of more than 2 million people with and without CSM. The models examined patterns of health-care interactions, such as tests and diagnoses, recorded in electronic health records to spot patients whose medical histories resemble those already diagnosed with CSM, helping to flag individuals who may be at higher risk.

Sleep loss induces cholesterol-associated myelin dysfunction

The increasing prevalence of sleep deprivation poses a public health challenge in modern society. Manifestations of reduced alertness, such as slowed reaction times and increased errors, are well-documented behavioral indicators of sleep loss (SL). Yet, the biological consequences of sleep deprivation and their role in behavioral impairment remain elusive. Our study reveals significant effects of sleep deprivation on myelin integrity. As a result, we identify increased conduction delays in nerve signal propagation, hindered interhemispheric synchronization, and impaired cognitive and motor performance associated with SL. By profiling oligodendrocyte transcriptome and lipidome, we observe SL-induced endoplasmic reticulum stress and lipid metabolism dysregulation, particularly affecting cholesterol homeostasis.

Genetic defect that weakens esophageal lining identified!

But the molecular factors responsible for the onset of Barrett’s esophagus remain poorly understood.

The findings, published in Nature Communications, combined family studies, laboratory experiments and genetically engineered mouse models to identify and understand how genetic defects contribute to disease development.

The team sequenced and analyzed genetic material of 684 people from 302 families where multiple members developed Barrett’s esophagus or esophageal cancer. They discovered that a subset of affected family members carry inherited mutations in a gene called VSIG10L.

“We found that this gene acts like a quality control system for the esophageal lining,” said the lead researcher. “When it’s defective, the cells do not mature properly and the protective barrier in the esophageal lining becomes weak, allowing stomach bile acid to cause tissue changes that enhances the risk of developing Barrett’s esophagus.”

When researchers genetically engineered mice with human-equivalent VSIG10L mutations, they found that the esophageal lining became disrupted structurally and molecularly, according to the author. The study found that when the mice were exposed to bile acid, they developed Barrett’s-like disease over time, effectively replicating the disease’s progression in humans.

These genetically engineered mice also represent the first animal model for Barrett’s esophagus based directly on human genetic predisposition to the disease, the author said.

With VSIG10L shown to be a key gene in maintaining esophageal health, family members can now be screened for genetic variants to identify those at a high-risk of developing Barrett’s esophagus or esophageal cancer. ScienceMission sciencenewshighlights.

Continue reading “Genetic defect that weakens esophageal lining identified!” | >

System isolates single extracellular vesicle surface proteins to map function

Extracellular vesicles (EVs) are tiny biological bubbles that carry nucleic acids and proteins between cells, playing an essential role in tissue repair, neuroprotection and immune health. By isolating the surface proteins of these bubbles, researchers can understand more about their biology and build tools to transform extracellular vesicles into next-generation drugs for cancer, neurological conditions and other diseases.

UC Davis biomedical engineers are using EVs to crack the code of the body’s message system. Their findings are detailed in a paper published in ACS Nano.

“EV-mediated intercellular communication is a very powerful system that controls many physiological and pathophysiological phenomena,” said Aijun Wang, a corresponding author of the new study. Wang is Chancellor’s Fellow and professor of biomedical engineering and surgery. “We know that EVs are therapeutically useful. But how do we define what dictates their functions?”

First evidence of a ‘critical priority’ fungal pathogen becoming more deadly when co-infected with tuberculosis

Cryptococcus neoformans is one of four fungi classified as “critical priority” on the WHO’s Fungal Pathogens Priority List, which was published in October 2022 following decades of research and calls for fungal pathogens to be classified alongside their bacterial and viral counterparts.

The fungus infects people through inhalation of spores or yeast cells in the environment, first colonizing the lungs and can then spread to the brain. In 2020, an estimated 112,000 deaths were associated globally to fungal meningitis caused by C. neoformans.

Increasing evidence shows that co-infection of Mycobacterium tuberculosis, the causative agent of tuberculosis, together with C. neoformans, is a grave public health concern, increasing the risk of death significantly compared to fungal infection alone.

SGLT2 Inhibitors and Cardiorenal Outcomes in T2D With Liver Cirrhosis

Among adults with Type2Diabetes and liver cirrhosis, SGLT2 inhibitor use was associated with lower risks of end-stage kidney disease, cardiovascular events, mortality, and hepatic decompensation compared with DPP4 inhibitors.

Importance Type 2 diabetes (T2D) and liver cirrhosis frequently coexist, creating a high-risk population for adverse outcomes. Patients with both conditions face elevated risks of kidney and cardiovascular complications, yet evidence regarding optimal antidiabetic therapy in this vulnerable population remains limited.

Objective To evaluate the association of sodium-glucose cotransporter–2 inhibitor (SGLT2i) vs dipeptidyl peptidase–4 inhibitor (DPP4i) use with kidney outcomes, cardiovascular events, and hepatic decompensation in patients with concurrent T2D and liver cirrhosis.

Design, Setting, and Participants This nationwide retrospective cohort study utilized data from the Taiwan’s National Health Insurance Database between May 2016 and December 2023. Adults with both T2D and liver cirrhosis who initiated either SGLT2is or DPP4is were included.

The shingles vaccine may reduce your dementia risk—here’s why

Shingles, a viral rash, can be incredibly painful. Vaccination can help prevent the infection, but new research is showing the shingles vaccine may also have another benefit: protection against the development of dementia. With more than 40 percent of Americans estimated to develop dementia at some point in their lives, this discovery could have groundbreaking implications for our health. But what explains the link between the shingles vaccine and reduced dementia risk?

Recent research is part of a growing body of evidence that vaccination against shingles—and potentially other infections—can help prevent and delay the progression of dementia.

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