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“These neurons are playing an outsized role in hyperglycemia and type 2 diabetes,” said UW Medicine endocrinologist Dr. Michael Schwartz, corresponding author of the paper.

To determine if these neurons contribute to elevated blood sugar in diabetic mice, researchers employed a widely used viral genetics approach to make AgRP neurons express tetanus toxin, which prevents the neurons from communicating with other neurons.

Unexpectedly, this intervention normalized high blood sugar for months, despite having no effect on body weight or food consumption.

Conventional wisdom is that diabetes, particularly type 2 diabetes, stems from a combination of genetic predisposition and lifestyle factors, including obesity, lack of physical activity and poor diet. This mix of factors leads to insulin resistance or insufficient insulin production.

Until now, scientists have traditionally thought the brain doesn’t play a role in type 2 diabetes, according to Schwartz.

The paper challenges this and is a “departure from the conventional wisdom of what causes diabetes,” he said.

The new findings align with studies published by the same scientists showing that injection of a peptide called FGF1 directly into the brain also causes diabetes remission in mice. This effect was subsequently shown to involve sustained inhibition of AgRP neurons.

Ribonucleic acid, also called RNA, is a molecule present in all living cells. It plays a critical role in transmitting genetic instructions from DNA and creating proteins. With the power to execute a plethora of functions, the little RNA “messenger” has led to important innovations across therapeutics, diagnostics, and vaccines, and made us rethink our understanding of life itself.

A team of researchers from Boston University’s Biological Design Center and the Department of Biomedical Engineering recently made significant steps forward in the development of the next generation of computational RNA tools. They recently published a study in Nature Communications describing a generative AI technique for designing different types of RNA molecules with improved function.

Much like a that can be used to compose entirely new texts, the model can compose new RNA sequences tailored for specific tasks in the cell or in a diagnostic assay. Their research has shown that it’s possible to predict and generate RNA sequences that have specific functions across a broad array of potential applications.

One of the reasons why this has never happened before is that spiders themselves are difficult organisms to work with within the laboratory. They are a diverse group, have a complex genome structure, and their cannibalistic nature means that they have to be reared individually, otherwise their cage neighbors would be gobbled up. Despite this, new developments in Parasteatoda tepidariorum have allowed this species to become a research model.

The research team looked into spider silk as the target. Spider silk is an incredibly strong and scientifically interesting substance, as it is five times stronger than a steel cable of the same weight, tear-resistant, while also being biodegradable, lightweight, and elastic.

To genetically modify this arachnophobe’s nightmare, the scientists developed an injection solution. This had a gene-editing system that also included a red fluorescent protein gene sequence. This solution was then injected into oocytes inside unfertilized female spiders, when these spiders mated with males, it resulted in the genetically modified offspring.

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In Biology 101, we learn that RNA is a single, ribbon-like strand of base pairs that is copied from our DNA and then read like a recipe to build a protein. But there’s more to the story. Some RNA strands fold into complex shapes that allow them to drive cellular processes like gene regulation and protein synthesis, or catalyze biochemical reactions.

We know that these active molecules, called non-coding RNAs, are present in all life forms, yet we’re just starting to understand their many roles—and how they can be harnessed for applications in environmental science, agriculture, and medicine.

To study—and potentially modify—the functions of non-coding RNAs, we need to determine their structure. Scientists from Lawrence Berkeley National Laboratory (Berkeley Lab) and the Hebrew University of Jerusalem have developed a streamlined process that predicts the structure of an RNA molecule down to the atomic level.

A new study combining satellite imagery with genetic analysis reveals that climate and land use changes are driving increased vegetation growth in Europe’s mountain regions, ultimately leading to a decline in the genetic diversity of medicinal plants such as Greek mountain tea. Mountain regions a.

A method is developed for expressing large dystrophins to enhance muscle function in mouse models of muscular dystrophy, with potential clinical benefits for numerous disorders caused by mutations in large genes that exceed the adeno-associated virus capacity.

One of the most terrifying things about Dune is the fact that it rather accurately predicted what the next front of warfare will look like: genetic warfare. In twenty twenty five, gene manipulation is the biggest threat in the theatre of war, because one gene-altering weapon can render an enemy force infertile at best, and terribly mutated at worst. But that’s not something that happens to the products of breeding programmes in the Dune-verse, at least on a physical level. In this video, we will take a look at every breeding programme in Frank Herbert’s creation, and talk about their horrifying histories in detail.

Developmental time (or time to maturity) strongly correlates with an animal’s maximum lifespan, with late-maturing individuals often living longer. However, the genetic mechanisms underlying this phenomenon remain largely unknown. This may be because most previously identified longevity genes regulate growth rate rather than developmental time. To address this gap, we genetically manipulated prothoracicotropic hormone (PTTH), the primary regulator of developmental timing in Drosophila, to explore the genetic link between developmental time and longevity. Loss of PTTH delays developmental timing without altering the growth rate. Intriguingly, PTTH mutants exhibit extended lifespan despite their larger body size. This lifespan extension depends on ecdysone signaling, as feeding 20-hydroxyecdysone to PTTH mutants reverses the effect. Mechanistically, loss of PTTH blunts age-dependent chronic inflammation, specifically in fly hepatocytes (oenocytes). Developmental transcriptomics reveal that NF-κB signaling activates during larva-to-adult transition, with PTTH inducing this signaling via ecdysone. Notably, time-restricted and oenocyte-specific silencing of Relish (an NF-κB homolog) at early 3rd instar larval stages significantly prolongs adult lifespan while delaying pupariation. Our study establishes an aging model that uncouples developmental time from growth rate, highlighting NF-κB signaling as a key developmental program in linking developmental time to adult lifespan.