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In this episode, we explore how a triple-lens supernova observed by the James Webb Space Telescope could help solve the mystery of the Hubble tension, which is the discrepancy between different measurements of the expansion rate of the Universe. We also learn about the details of the supernova and the galaxy cluster that caused the gravitational lensing effect, and how JWST and other telescopes can use this supernova to test various cosmological models and parameters.

Paper Link:
https://arxiv.org/abs/2309.

Chapters:
00:00 Introduction.
01:10 How JWST Discovered a Rare and Triple-Lens Supernova.
04:13 How H0pe Can Measure the Expansion Rate in a New Way.
09:00 How hOpe can test various cosmological models.
11:26 Outro.
12:24 Enjoy.

Best Telescopes for beginners:

Continue reading “James Webb just Found a Supernova That Could Break the Laws of Physics” | >

One proven method for tracking down the genetic origins of diseases is to knock out a single gene in animals and study the consequences this has for the organism. The problem is that for many diseases, the pathology is determined by multiple genes, complicating the task for scientists trying to pinpoint the contribution of any single gene to the condition. To do this, they would have to perform many animal experiments – one for each desired gene modification.

Researchers led by Randall Platt, Professor of Biological Engineering at the Department of Biosystems Science and Engineering at ETH Zurich in Basel, have now developed a method that will greatly simplify and speed up research with laboratory animals: using the CRISPR-Cas gene scissors, they simultaneously make several dozen gene changes in the cells of a single animal, much like a mosaic.

While no more than one gene is altered in each cell, the various cells within an organ are altered in different ways. Individual cells can then be precisely analyzed. This enables researchers to study the ramifications of many different gene changes in a single experiment.

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The researchers compiled an extensive dataset of over 1,200 distinct cell groups, estimating size ranges, mass, and cell counts for each group across 60 tissue systems in three reference humans — an adult man, woman, and child.

“For the first time, we have systematically measured the size and abundance of cells across all major tissues and organs,” said Dr. Hatton. This spans seven orders of magnitude from tiny red blood cells to large muscle fibers.

While many contemporary works focus on molecular profiling, this study adopts a classical cell biology approach, quantifying morphological features of known cell types. The team integrated decades of histological and anatomical research to establish a framework. They discovered a striking near-inverse relationship between cell size and abundance, implying a trade-off between the two variables.

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Though drug developers have achieved some progress in treating Alzheimer’s disease with medicines that reduce amyloid-beta protein, other problems of the disease, including inflammation, continue unchecked. In a new study, scientists at The Picower Institute for Learning and Memory at MIT describe a candidate drug that in human cell cultures and Alzheimer’s mouse models reduced inflammation and improved memory.

The target of the new “A11” molecule is a genetic transcription factor called PU.1. Prior research has shown that amid Alzheimer’s disease, PU.1 becomes an overzealous director of inflammatory gene expression in the brain’s microglia immune cells. A11 suppresses this problematic PU.1 activity, the new research shows, by recruiting other proteins that repress the inflammatory genes PU.1 works to express. But because A11 concentrates mostly in the brain and does not reduce PU.1 levels, it does not appear to disrupt PU.1’s other job, which is to ensure the production of a wide variety of blood cells.

“Inflammation is a major component of Alzheimer’s disease pathology that has been especially hard to treat,” says study senior author Li-Huei Tsai, Picower Professor of Neuroscience at MIT and director of The Picower Institute and MIT’s Aging Brain Initiative. “This preclinical study demonstrates that A11 reduces inflammation in human microglia-like cells, as well as in multiple mouse models of Alzheimer’s disease, and significantly improves cognition in the mice. We believe A11 therefore merits further development and testing.”

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During the month of September, Baylor College of Medicine will be partnering with the Blue Cure Foundation for its annual prostate cancer awareness campaign, Light It Blue. The Blue Cure Foundation is a non-profit organization dedicated to providing information on integrative approaches to prostate cancer prevention and treatment. During the campaign, the foundation works with local organizations to light up their buildings in blue lights in support of prostate cancer.

To help spread awareness and education, Dr. Jennifer Taylor, assistant professor of urology at Baylor, shares prostate cancer risk factors, symptoms and prevention guidelines.

Q: How important is it for an institution like Baylor to help generate awareness for prostate cancer? A: Prostate cancer touches lives every day, and it’s likely that everyone knows somebody who has survived or is suffering from it. It’s so highly prevalent, but there is a very wide spectrum of disease, so it’s important to spread accurate and informative facts about it.

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