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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.

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.

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.”

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.

A 58-year-old patient with terminal heart disease became the second patient in the world to receive a historic transplant of a genetically-modified pig heart on September 20. He is recovering and communicating with his loved ones. This is only the second time in the world that a genetically modified pig heart has been transplanted into a living patient. Both historic surgeries were performed by University of Maryland School of Medicine (UMSOM) faculty at the University of Maryland Medical Center (UMMC).

The first historic surgery, performed in January, 2022, was conducted on David Bennett by University of Maryland Medicine surgeons (comprising UMSOM and UMMC), who are recognized as the… More.


After world’s first successful transplant in 2022, also performed at the University of Maryland Medical Center (UMMC), this groundbreaking transplant team per.

“That’s what makes this research unique from a scientific standpoint. The study participant can walk over to the lab, have the blood drawn and within hours their specimen can be transferred to the on-site facility where the process of biomanufacturing the vaccine begins,” says Dr. Block. “That would not be possible with an outside manufacturer.”

A deadly form of reproductive system cancer

Ovarian cancer is the deadliest form of gynecologic cancer. It often is not diagnosed until advanced stages, when it is less treatable. Even with standard surgery and chemotherapy, tumors return in up to 70% of women. The outcome is often poor. 19,000 women in the U.S. are diagnosed with ovarian cancer every year and more than 13,000 die from it, according to the American Cancer Society.

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In the phase 3 GLOW study, ibrutinib plus venetoclax significantly improved progression-free survival and other outcomes in patients with chronic lymphocytic leukemia, across most genomic subgroups.

Patients treated with fixed-duration ibrutinib (Imbruvica) plus venetoclax (Venclexta) achieved higher undetectable minimal residual disease (uMRD), progression-free survival (PFS), and overall survival (OS) rates compared with chlorambucil plus obinutuzumab (Gazyva) across most genomic subgroups of chronic lymphocytic leukemia (CLL).1.

Findings come from the phase 3 GLOW study (NCT03462719) in which data were presented at the 11th Annual Meeting of the Society of Hematologic Oncology (SOHO 2023). Patients treated with ibrutinib and venetoclax achieved a higher uMRD rate at 3 months (54.7%) after the end of treatment compared with patients treated with obinutuzumab and chlorambucil (39.0%), except patients with trisomy-12, IGLL5 mutation, and mutated immunoglobulin heavy-chain variable (mIGHV).