Researchers have found a new and distinct pathway for chronic pain and have mapped how to target it with therapies, offering hope for people with fibromyalgia and chronic pain.
Category: biotech/medical – Page 8
A study led by biomedical scientists at the University of California, Riverside School of Medicine shows how a genetic mutation associated with Crohn’s disease can worsen iron deficiency and anemia—one of the most common complications experienced by patients with inflammatory bowel disease, or IBD.
While IBD—a group of chronic inflammatory disorders that includes Crohn’s disease and ulcerative colitis—primarily affects the intestines, it can have effects beyond the gut. Iron deficient anemia is the most prevalent of these effects, contributing to chronic fatigue and reduced quality of life, particularly during disease flare-ups.
The study, performed on serum samples from IBD patients, reports that patients carrying a loss-of-function mutation in the gene PTPN2 (protein tyrosine phosphatase non-receptor type 2) exhibit significant disruption in blood proteins that regulate iron levels. This mutation is found in 14–16% of the general population and 19–20% of the IBD population. A loss-of-function mutation is a genetic change that reduces or eliminates the normal function of a gene or its product, a protein.
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Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by macroscopic features such as cortical atrophy, narrowing of the gyri, widening of the sulci, and enlargement of the ventricles. At the cellular level, the pathological characteristics include the extracellular aggregation of β-amyloid (Aβ) forming senile plaques, and the intracellular accumulation of hyperphosphorylated tau proteins forming neurofibrillary tangles. AD leads to the progressive decline of cognitive, behavioral, and social abilities, with no effective treatment available currently. The pathophysiology of AD is complex, involving mechanisms such as immune dysregulation and lipid metabolism alterations. Immune cells, such as microglia, can identify and clear pathological aggregates like Aβ early in the disease.
The background
Most biochemistry labs that study DNA isolate it within a water-based solution that allows scientists to manipulate DNA without interacting with other molecules. They also tend to use heat to separate strands, heating the DNA to over 150 degrees Fahrenheit, a temperature a cell would never naturally reach. By contrast, in a living cell DNA lives in a very crowded environment, and special proteins attach to DNA to mechanically unwind the double helix and then pry it apart.
A lung cancer patient at UCLH is the first to receive a novel cancer vaccine designed to prime the immune system to recognise and fight cancer cells.
How 6 small molecules made old human cells act young again. No gene editing, no stem cells. Just science.
Researchers publishing in Aging Cell have used single-cell transcriptomics to discover new insights into how neural stem cells (NSCs) change with aging.
Adults do generate neurons
The adult brain does generate new neurons [1], particularly in the hippocampus, the part of the brain responsible for memory formation [2]. Neurogenesis is limited to very specific niches, however, and does not occur across the entire brain [3]. This is accomplished by NSCs, cells that can differentiate into neural progenitors (NPs), which can themselves differentiate into both neurons and astrocytes and have less ability to proliferate [4]. Astrocytes are helper cells that support neurons’ connections and metabolism [5].
When DNA breaks inside the cell, it can spell disaster, especially if the damage occurs in areas of the genome that are difficult to repair. Now, scientists Irene Chiolo and Chiara Merigliano at the USC Dornsife College of Letters, Arts and Sciences have discovered that a protein called Nup98, long known for helping traffic molecules in and out of the cell’s nucleus, plays another surprising role: guiding the cell’s most delicate repairs and reducing the risk of genetic mistakes that can lead to cancer. Their findings were published in Molecular Cell.
With support from the National Institutes of Health, the National Science Foundation, and the American Cancer Society, the researchers revealed that Nup98 forms droplet-like structures deep inside the nucleus. These “condensates” act as protective bubbles around broken strands of DNA in areas called heterochromatin—zones where the genetic material is so tightly packed that making accurate repairs is especially challenging.
Heterochromatin—a major focus of Chiolo’s research—is filled with repeated DNA sequences, making it easy for the cell to confuse one stretch for another. Nup98’s droplets help lift the damaged section out of that dense zone and create a safer space where it can be repaired accurately, reducing the chance of genetic mix-ups that could lead to cancer.
In this TEDx talk, Dante Muratore shows the transformative potential of brain-computer interfaces. He explains how they can be used to help patients suffering from neurodegenerative diseases, focusing on an artificial retina he and his team are developing to cure blindness in patients with macular degeneration and retinitis pigmentosa. He also describes how brain-computer interfaces will change what it means to be human in the future and challenges us to think deeply about the use we want to make of this technology in society.
Professor of Bioelectronics at Delft University of Technology, where he leads the Smart Brain Interfaces group. His research group explores hardware and system solutions for brain-computer interfaces capable of interacting with the nervous system. The group is working, in collaboration with leading universities in the field, on a microchip to be implanted in the retina to improve the lives of people affected by retinitis pigmentosa and degenerative maculopathy.
This talk was given at a TEDx event using the TED conference format but independently organized by a local community.