And an increased all-cause mortality risk…
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Researchers from Osaka Metropolitan University have identified a gene that, when activated by metabolic stress, damages pancreatic β-cells—the cells responsible for insulin production and blood sugar control—pushing them toward dysfunction. The findings highlight a promising new target for early intervention in type 2 diabetes. The study is published in the Journal of Biological Chemistry.
While many factors can contribute to type 2 diabetes, lifestyle, especially diet, plays a major role in its onset. Genetics matter, but poor eating habits can greatly increase the risk of developing what is now often called a “silent epidemic.”
“Type 2 diabetes occurs when pancreatic β-cells, which secrete insulin to regulate blood glucose, become impaired due to prolonged stress caused by poor dietary habits, a condition known as oxidative stress,” said Naoki Harada, an associate professor at Osaka Metropolitan University’s Graduate School of Agriculture and lead author of this study.
In a step toward treating mitochondrial diseases, researchers in the Netherlands have successfully edited harmful mutations in mitochondrial DNA using a genetic tool known as a base editor. The results, published in the open-access journal PLOS Biology, offer new hope for people with rare genetic conditions.
Mitochondria have their own small set of DNA. Mutations in this mitochondrial DNA can lead to a wide range of maternally inherited diseases, cancer, and aging-related conditions. While the development of CRISPR technology has given scientists new ways to correct mutations in nuclear DNA, this system cannot effectively cross the mitochondrial membrane and reach mitochondrial DNA.
In the new study, the researchers used a tool called a base editor—specifically, a DdCBE (double-stranded DNA deaminase toxin A-derived cytosine base editor). This tool allows scientists to change a single letter in the DNA code without cutting it, and it works on mitochondrial DNA.
5k words, 23 minutes reading time
Researchers at VCU Massey Comprehensive Cancer Center and the VCU Institute of Molecular Medicine (VIMM) have discovered a new and potentially revolutionary way to treat glioblastoma (GBM), the most aggressive type of brain cancer, which currently has no curative treatment options.
In a study led by Paul B. Fisher, MPh, Ph.D., FNAI, and Swadesh K. Das, Ph.D., recently published in the Journal for ImmunoTherapy of Cancer, researchers created a new molecule that demonstrates the ability to introduce a combination of treatment outcomes—direct toxicity and immunotoxicity—to kill the tumor while exploiting immunotherapy to potentially prevent the recurrence of GBM. The new molecule, a fusion superkine (FSK), contains dual-acting therapeutic cytokines in a single molecule.
“This is the tip of the iceberg,” said Dr. Fisher, the Thelma Newmeyer Corman Endowed Chair in Cancer Research at Massey, director of the VIMM and professor in the Department of Cellular, Molecular and Genetic Medicine. “We’re optimistic that our first trial in brain cancer, planned for 2026, will show that the IL-24 gene and these therapeutic viruses are effective and safe. And [the FSK] will be the one knocking it out of the ballpark.
In a paper published in the journal Nature Communications, biomedical engineers have shown how two brain regions quickly adapt to shift focus from one planned destination to another.
Stephanie Prince explains her research with a scenario many Atlantans can relate to. Imagine you’re driving to the Atlanta airport to pick up a friend. They call to say they’re in the terminal—but they’re not sure which one. North, maybe? You head in that direction through the maze of roads around the airport.
Then they call back. They’re actually in the South Terminal. So you make a quick mental adjustment and switch your route to arrive at the correct side of the airport.
Using stem cells from patients with ALS (amyotrophic lateral sclerosis), Cedars-Sinai has created a lifelike model of the mysterious and fatal disease that could help identify a cause of the illness as well as effective treatments.
In a study published in the journal Cell Stem Cell, investigators detail how they created “ALS on a chip” and the clues the specialized laboratory chip has already produced about nongenetic causes of the disease, also known as Lou Gehrig’s disease.
The work builds on previous studies where adult cells from ALS patients were reverted into stem cells. The cells were then pushed forward to produce motor neurons, which die in the disease, causing progressive loss of the ability to move, speak, eat and breathe.
Tomato brown rugose fruit virus (ToBRFV) is a soil-borne virus showing a low percentage of ca. 3% soil-mediated infection when the soil contains root debris from a previous 30–50 day growth cycle of ToBRFV-infected tomato plants. We designed stringent conditions of soil-mediated ToBRFV infection by increasing the length of the pre-growth cycle to 90–120 days, adding a ToBRFV inoculum as well as truncating seedling roots, which increased seedling susceptibility to ToBRFV infection. These rigorous conditions were employed to challenge the efficiency of four innovative root-coating technologies in mitigating soil-mediated ToBRFV infection while avoiding any phytotoxic effect. We tested four different formulations, which were prepared with or without the addition of various virus disinfectants. We found that under conditions of 100% soil-mediated ToBRFV infection of uncoated positive control plants, root-coating with formulations based on methylcellulose (MC), polyvinyl alcohol (PVA), silica Pickering emulsion and super-absorbent polymer (SAP) that were prepared with the disinfectant chlorinated-trisodium phosphate (Cl-TSP) showed low percentages of soil-mediated ToBRFV infection of 0%, 4.3%, 5.5% and 0%, respectively. These formulations had no adverse effect on plant growth parameters when compared to negative control plants grown under non ToBRFV inoculation conditions.