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Gene discovery reveals potential for growing new heart arteries

Most people have right-dominant hearts—which to a doctor or a researcher means they have an artery that extends from the right side of their hearts to supply oxygenated blood to the back side. For some people, this artery, called the posterior descending artery, comes from the left side or from both directions. A study has found that the gene CXCL12 is connected to this artery’s formation and that its directional pattern is set very early in human development.

The findings, reported in the journal Cell, represent a step toward developing “medical revascularization,” a long-term goal of Stanford researchers to create a treatment for blocked or limited-flow arteries by growing new ones to compensate.

“For the first time, we have evidence of a gene that regulates the development of one of the most important types of arteries in the human body,” said Kristy Red-Horse, co-senior author of the study and biology professor in the Stanford School of Humanities and Sciences. “And if we know the development pathways of these important arteries, then we can perhaps regrow them by reintroducing these pathways in a diseased heart.”

First-of-Its-Kind Study Identifies How The Brain Could Thwart Alzheimer’s

Training the brain’s immune system to recognize and clear toxic material is rapidly emerging as an promising way to put the brakes on Alzheimer’s disease. Unfortunately researchers haven’t been clear on how this method of protection operates on a cellular level.

An international team of researchers analyzed brain samples taken from people who had died with Alzheimer’s, some of whom had also received approved Alzheimer’s immunotherapy treatments. The therapies encourage cleaning cells called microglia to attack the clumps of amyloid-beta proteins that are thought to be involved in neurodegeneration.

Microglia responses to amyloid beta can lead to inflammation, which in turn risks damage to brain tissues. The researchers wanted to know why immunotherapy turned microglia into ruthless cleaning machines in some cases but not others.

Abstract: Why are so many patients with pancreatic cancer resistant to immunotherapy?

Xueli Bai & team report on the high level of lactate in pancreatic cancer metabolism, which changes tumor immune features by protein lactylation and results in immunotherapy resistance:

The figure shows lactylation labeling of metabolic proteins from paracancerous and tumor tissues.


1Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, School of Medicine and.

2Zhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.

3MOE Joint International Research Laboratory of Pancreatic Diseases, Hangzhou, China.

Abstract: This work was supported in part by the NIH National Cancer Institute grants R01 CA186338

R01 CA203108, R01 CA247234 (to ML), and by the William and Ella Owens Medical Research Foundation (to ML). It was also supported in part by the Department of Medicine, the University of Oklahoma Health Sciences Center.

Address correspondence to: Michael S. Bronze, Department of Medicine, The University of Oklahoma Health Sciences Center, 800 Stanton L. Young Blvd. AAT 6,400, Oklahoma City, Oklahoma, 73,104, USA. Phone: 405.271.5428; Email: [email protected]. Or to: Min Li, Department of Medicine, The University of Oklahoma Health Sciences Center, 975 NE 10th Street, BRC 1262A, Oklahoma City, Oklahoma, 73,104, USA. Phone: 405.271.1796; Email: [email protected].

Hedonic eating is controlled by dopamine neurons that oppose GLP-1R satiety

Hedonic eating is defined as food consumption driven by palatability without physiological need. However, neural control of palatable food intake is poorly understood. We discovered that hedonic eating is controlled by a neural pathway from the peri–locus ceruleus to the ventral tegmental area (VTA). Using photometry-calibrated optogenetics, we found that VTA dopamine (VTADA) neurons encode palatability to bidirectionally regulate hedonic food consumption. VTADA neuron responsiveness was suppressed during food consumption by semaglutide, a glucagon-like peptide receptor 1 (GLP-1R) agonist used as an antiobesity drug. Mice recovered palatable food appetite and VTADA neuron activity during repeated semaglutide treatment, which was reversed by consumption-triggered VTADA neuron inhibition.

Does Methylene Blue Impact Lifespan?

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Shocking Result from DESI Stuns Cosmology

Evolving cosmological constant.


Thanks to Storyblocks for sponsoring this video! Download unlimited stock media at one set price with Storyblocks: https://storyblocks.com/CoolWorlds.

The Standard Model of Cosmology has reigned supreme for decades, confirmed over and over again. But chinks in the armour have been developing, such as the Hubble Tension. Now, however, a new result threatens to completely upend our view of the Universe — we no longer even know how it will end.

Written & presented by Prof. David Kipping.

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Giving up on photosynthesis: How a borrowed bacterial gene allows some marine diatoms to live on a seaweed diet

A group of diatom species belonging to the Nitzschia genus gave up on photosynthesis and now get their carbon straight from their environment, thanks to a bacterial gene picked up by an ancestor. Gregory Jedd of Temasek Life Sciences Laboratory, Singapore, and colleagues report these findings in a study published in the open-access journal PLOS Biology.

Unlike most diatoms, which perform photosynthesis to generate carbon compounds, some members of the genus Nitzschia have no chlorophyll and instead consume carbohydrates from seaweed and decaying plant matter. Previously, it was unclear how exactly they made this major lifestyle transition, so researchers sequenced the genome of one species, Nitzschia sing1, to look for clues.

N. sing1’s showed that the diatom carries a gene for an enzyme that breaks down alginate, a carbon polymer in the cell walls of brown algae—a group that includes kelp and other common seaweeds. The gene originally came from a , and an ancestor of N. sing1 took up the gene and incorporated it into its genome.