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Artificial kinetochores take the pressure off aging chromosomes during meiosis

For sexual reproduction to yield healthy offspring, newly generated oocytes—immature egg cells—must receive the correct amount of DNA after cell division. This process of segregating chromosomes becomes more prone to failure as we age. Now, RIKEN researchers have identified a strategy that could help to prevent such errors and restore healthy production of oocytes.

Oocytes are produced by a cell-division process known as meiosis, during which every chromosome is duplicated. These replicates form X-shaped structures in which the chromosomes are joined via structures called centromeres, where a protein called cohesin locks chromosome copies together.

As division proceeds, protein fibers called microtubules spread from opposite poles of the dividing cell, attaching to each chromosome. These microtubules eventually pull the two apart, so that each newly formed cell receives one copy of each chromosome.

Abstract: Glioblastoma remains profoundly resistant to current immunotherapeutic strategies

Here, Fanghui Lu & team report OLIG2, a master transcription factor in glioblastoma stem cells, enables immune evasion by suppressing CXCL10. And, targeting OLIG2 overcomes immunotherapy resistance and improves survival.


1Department of Cancer Center, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.

2Department of Neurosurgery, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

3School of Basic Medical Sciences, Chongqing Medical University, Chongqing, China.

Robust Mouse Rejuvenation: Breaking the Ceiling of Longevity Research

For decades, the field of biogerontology has largely focused on a single strategy: manipulating metabolism to slow down the rate at which we age. While approaches like caloric restriction have produced fascinating results in short-lived organisms like worms and flies, they have shown clear limits in mammals. Slowing the accumulation of damage does not remove the damage that is already there. It merely delays (not prevents) the onset of disease, particularly when applied late in life.

Your gut microbes can be anti-aging—scientists are uncovering how to keep your microbiome youthful

People have long given up on the search for the Fountain of Youth, a mythical spring that could reverse aging. But for some scientists, the hunt has not ended—it’s just moved to a different place. These modern-day Ponce de Leóns are investigating whether gut microbes hold the secret to aging well.

The gut microbiome refers to the vast collection of microscopic organisms—bacteria, fungi, and viruses—that largely inhabit the colon. These microbes aid in digestion and produce molecules that affect your physiology and psychology. The composition of the microbiome is influenced by a combination of factors, including genetics, diet, the environment, medications, and age.

I’m a microbiology professor and author of “Pleased to Meet Me: Genes, Germs and the Curious Forces That Make Us Who We Are,” which describes how the gut microbiome contributes to physical and mental health. The discovery that the gut microbiome changes with age has ignited studies to determine whether the Fountain of Youth might be right under your nose, down inside your gut.

New strategy to fight chronic kidney inflammation

Mayo Clinic researchers have identified a drug-and-supplement combination therapy that is capable of reducing the harmful effects of senescent cells – also known as “zombie cells” – in diabetic kidney disease.

In eBioMedicine, a publication of The Lancet, the team reported that the combination of the cancer drug dasatanib and a naturally occurring substance known as quercetin decreased inflammation and boosted protective factors in the kidney.

Diabetic kidney disease affects more than 12 million people in the U.S. and is the leading cause of kidney failure. While newer treatments can delay loss of kidney function, there is currently no cure.

Abstract: Presenting a cutting-edge discovery on the mechanisms by which immune cells influence health and disease at the later stages of cerebral ischemic stroke

Here, Chuan Qin & team use complementary models in experimental ischemic stroke, showing early post-stroke stages in which microglia recruit B cells into ischemic lesions through MIF/CD74/CXCR4, while later stage post-stroke effects involve interferon signaling in B cells that drives neuroinflammation and brain injury:

The image shows B lymphocytes (Green) in mouse dura tissue colocalizing with CD31+ blood vessels (Red).


1Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases;

2Key Laboratory of Vascular Aging, Ministry of Education, Tongji Hospital of Tongji Medical College; and.

3Hubei Key Laboratory of Neural Injury and Functional Reconstruction, Huazhong University of Science and Technology, Wuhan, Hubei, China.

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