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Category: biotech/medical – Page 2271

A number of therapies that directly target the aging processes are currently in human trials and could change medicine significantly in the next decade if the results are positive.

What is aging?

Aging is basically the accumulation of damage and errors caused by a collection of varied processes that harm the functions of the body through the accumulation of waste, imperfect repair, the deregulation of cellular processes, the dysfunction of the immune system, chronic inflammation, and other disorders.

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There is increasing evidence that the microbiome contributes to esophageal disease. Diet, especially fiber and fat intake, is a known potent modifier of the colonic microbiome, but its impact on the esophageal microbiome is not well described. We hypothesized that dietary fiber and fat intake would be associated with a distinct esophageal microbiome.

We collected esophageal samples from 47 ambulatory patients scheduled to undergo endoscopy who completed a validated food frequency questionnaire quantifying dietary fiber and fat intake. Using 16S high-throughput sequencing, we determined composition of the esophageal microbiome and predicted functional capacity of microbiota based on fiber and fat intake.

Among all samples, the most abundant phyla were Firmicutes (54.0%), Proteobacteria (19.0%), Bacteroidetes (17.0%), Actinobacteria (5.2%), and Fusobacteria (4.3%). Increasing fiber intake was significantly associated with increasing relative abundance of Firmicutes (p = 0.04) and decreasing relative abundance of Gram-negative bacteria overall (p = 0.03). Low fiber intake was associated with increased relative abundance of several Gram-negative bacteria, including Prevotella, Neisseria, and Eikenella. Several predicted metabolic pathways differed between highest and lowest quartile of fiber intake. Fat intake was associated with altered relative abundance of few taxa, with no alterations at the phylum level and no changes in microbiome functional composition.

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You probably learned two things about mitochondria in high school biology. First, they’re the powerhouses of the cell. Second, you can only inherit them from your mother. But a new study seems to cloud that second point.

A team of researchers from the United States, China, and Taiwan identified three unrelated families with members whose mitochondria contained DNA from both parents. While this discovery could reignite debate about the nature of inheriting mitochondrial DNA, the researchers hope it will open up new ways to treat disease.

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In order to advance innovation and keep pace with the rapidly evolving healthcare industry, the US Food and Drug Administration (FDA) is modernizing the approval process most medical device manufacturers undergo when bringing new products to market.

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D esigner therapies are treatments tailored to a specific disease, and nowhere is the need greater for new therapies than in a group of nervous system disorders, known as “neurodegenerative diseases.”

Many of these diseases are common and well-known, such as Alzheimer’s or Parkinson’s disease. However, some are very rare, genetic disorders that are the consequence of a defective gene. In all these diseases, a mutant protein that misfolds causes the degeneration and death of neurons. One effective therapeutic strategy is to prevent the rogue protein from ever being made.

Spinocerebellar ataxia type 7 (SCA7) is one such disease in which nerves in different parts of the brain, including the eye, degenerate, which leads to blindness and difficulty walking, speaking, and balancing. SCA7 is dominantly inherited — which means that you just need one bad copy of the mutation to cause disease. The disease occurs when a short section of DNA that encodes ataxin-7 gene is erroneously repeated — like a word in a book printed two or three times. In this case, three chemical units of the DNA sequence — C-A-G — are repeated over and over.

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New research suggests that exposure to childhood adversity is associated with reduced cognitive control and alterations in key brain networks. The findings, which appear in the journal Social Cognitive and Affective Neuroscience, could help explain the link between childhood adversity and depression.

“My work focuses on how we can use objective biomarkers to aid in clinical decision making,” said study author Scott A. Langenecker of the University of Utah.

“One challenging clinical decision point is what to do when individuals have recovered from a depressive episode. Do we continue treatment? Do we exercise regular check-ins? Or do we just wait and see?”

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