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‘Mob breaker’ TRIM37 prevents abnormal cell division by eliminating extra spindle poles

In 2000, researchers discovered that mutations that inactivate a gene known as TRIM37 cause a developmental disease called Mulibrey nanism. The extremely rare inherited disorder leads to growth delays and abnormalities in several organs, causing afflictions of the heart, muscles, liver, brain and eyes. In addition, Mulibrey nanism patients exhibit high rates of cancer and are infertile.

In 2016, UC San Diego School of Biological Sciences researchers in the labs of Professors Karen Oegema and Arshad Desai began understanding how TRIM37, when operating normally, plays a key role in preventing conditions that lead to Mulibrey nanism. They linked TRIM37 to spindles, which separate chromosomes during , and centrosomes, the spherical organizing structures at each end of spindles.

The image above shows a normal mitotic cell (left) compared to a cell lacking TRIM37 (right), with spindle microtubules (green), centrosomal protein centrobin (magenta) and DNA (white). Normal cells have two spindle poles that ensure proper cell division. Cells lacking TRIM37 frequently have extra spindle poles, containing a cluster of centrobin molecules that disrupt proper cell division. Patients with Mulibrey nanism lack TRIM37 and their cells show similar extra spindle poles.

CERN Scientists Solve Decades-Old Particle Physics Mystery

Researchers from TUM, working at CERN, have made a groundbreaking discovery that reveals how deuterons are formed. Another long-standing question in particle physics has been answered. Scientists working with the ALICE experiment at CERN’s Large Hadron Collider (LHC), led by researchers from the

Genome-wide association study of proteomic aging reveals shared genetic architectures with longevity, early life development, and age-related diseases

There is still relatively little known about the genetic underpinnings of proteomic aging clocks. Here, we describe a genome-wide association study of proteomic aging in the UK Biobank (n=38,865), identifying 27 loci associated with participants’ proteomic age gap (ProtAgeGap). ProtAgeGap exhibits a strong genetic correlation with longevity (rg = −0.83), and in FinnGen a ProtAgeGap polygenic score (PGS) was associated with significantly increased odds of achieving longevity (n=500,348; OR = 1.43). Additional PGS analyses in All of Us (n=117,415), China Kadoorie Biobank (n=100,640), and ABCD Study (n=5,204) demonstrate reproducible associations across biobanks of ProtAgeGap PGS with obesity, cardiometabolic disease, and osteoarthritis in adults, and with developmental timing in children. Finally, colocalization analysis identified FTO as an obesity-related mechanism uniting diverse aging traits. Our results demonstrate a shared genetic architecture across the life course of ProtAgeGap with longevity, early developmental biology, and cardiometabolic and musculoskeletal diseases.

### Competing Interest Statement.

The authors have declared no competing interest.

Cracking the mystery of heat flow in few-atoms thin materials

For much of my career, I have been fascinated by the ways in which materials behave when we reduce their dimensions to the nanoscale. Over and over, I’ve learned that when we shrink a material down to just a few nanometers in thickness, the familiar textbook rules of physics begin to bend, stretch, or sometimes break entirely. Heat transport is one of the areas where this becomes especially intriguing, because heat is carried by phonons—quantized vibrations of the atomic lattice—and phonons are exquisitely sensitive to spatial confinement.

A few years ago, something puzzling emerged in the literature. Molecular dynamics simulations showed that ultrathin silicon films exhibit a distinct minimum in their thermal conductivity at around one to two nanometers thickness, which corresponds to just a few atomic layers. Even more surprisingly, the thermal conductivity starts to increase again if the material is made even thinner, approaching extreme confinement and the 2D limit.

This runs counter to what every traditional model would predict. According to classical theories such as the Boltzmann transport equation or the Fuchs–Sondheimer boundary-scattering framework, reducing thickness should monotonically suppress thermal conductivity because there is simply less room for phonons to travel freely and carry heat around. Yet the simulations done by the team of Alan McGaughey at Carnegie Mellon University in Pittsburgh insisted otherwise, and no established theory could explain why.

Rejuvenating aged haematopoietic stem cells by targeting RhoA

In their nucleus, as they replicate, blood stem cells can accumulate mutations and lose epigenetic marks that used to keep DNA well-arranged, ultimately increasing mechanical tension on the nuclear envelope. This study figured out RhoA is a mechanosensor activated by such tension and conducts a key role in the stem cell ageing process. Researchers subsequently proved its rejuvenating potential: after ex vivo treatment of blood stem cells with the drug Rhosin, a RhoA inhibitor, they observed an improvement in aged-related markers.

As study co-author summarizes: “Overall, our experiments show that Rhosin did rejuvenate blood stem cells, increased the regenerative capacity of the immune system and improved the production of blood cells once transplanted in the bone marrow.”

Ageing is defined as the deterioration of function overtime, and it is one of the main risk factors for numerous chronic diseases. Although ageing is a complex phenomenon affecting the whole organism, it is proved that the solely manifestation of ageing in the haematopoietic system affects the whole organism.

A research team previously revealed the significancy of using blood stem cells to pharmacologically target ageing of the whole body, thereby suggesting rejuvenating strategies that could extend healthspan and lifespan. Now, in a Nature Ageing publication, they propose rejuvenating aged blood stem cells by treating them with the drug Rhosin, a small molecule that inhibits RhoA, a protein that is highly activated in aged haematopoietic stem cells. This study combined in vivo and in vitro assays together with innovative machine learning techniques.

Blood stem cells, or hematopoietic stem cells, are located in the bone marrow, a highly dynamic and specialised tissue within the cavity of long bones. They are responsible for the vital function of continuously producing all types of blood cells: red blood cells (oxygen transporters), megakaryocytes (future platelets) and white blood cells (immune cells, lymphocytes and macrophages). Over time, however, stem cells also do age, they lose their regenerative capacity and generate fewer and lower quality immune cells. This has been linked to immunosenescence, chronic low grade inflammation and certain chronic diseases.

Generative AI tool enhances accuracy in detecting abnormal blood cells

An AI tool that can analyze abnormalities in the shape and form of blood cells, and with greater accuracy and reliability than human experts, could change the way conditions such as leukemia are diagnosed.

Researchers have created a system called CytoDiffusion that uses generative AI – the same type of technology behind image generators such as DALL-E – to study the shape and structure of blood cells.

Unlike many AI models, which are trained to simply recognize patterns, the researchers – led by the University of Cambridge, University College London and Queen Mary University of London – showed that CytoDiffusion could accurately identify a wide range of normal blood cell appearances and spot unusual or rare cells that may indicate disease. Their results are reported in the journal Nature Machine Intelligence.

Too Little and Too Much: Balanced Hippocampal, But Not Medial Prefrontal, Neural Activity Is Required for Intact Novel Object Recognition in Rats

Impaired GABAergic inhibition, so-called neural disinhibition, in the prefrontal cortex and hippocampus has been linked to cognitive deficits. The novel object recognition (NOR) task has been used widely to study cognitive deficits in rodents. However, the contribution of prefrontal cortical and hippocampal GABAergic inhibition to NOR task performance has not been established. Here, we investigated NOR task performance in male Lister hooded rats following regional neural disinhibition or functional inhibition, using intracerebral microinfusion of the GABAA receptor antagonist picrotoxin or agonist muscimol, respectively. Our infusion targets were the medial prefrontal cortex (mPFC), dorsal hippocampus (DH), and ventral hippocampus (VH).

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