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With the aid of physics and a minuscule magnet, researchers have discovered a new structure of telomeric DNA. Telomeres are sometimes seen as the key to living longer. They protect genes from damage but get a bit shorter each time a cell divides. If they become too short, the cell dies. The new discovery will help us understand aging and disease.

Physics is not the first scientific discipline that springs to mind at the mention of DNA. But John van Noort from the Leiden Institute of Physics (LION) is one of the scientists who found the new DNA structure. A biophysicist, he uses methods from physics for biological experiments. This also caught the attention of biologists from Nanyan Technological University in Singapore. They asked him to help study the DNA structure of . They have published the results in Nature.

Biotech start-up Pretzel Therapeutics launched Monday with $72.5 million in Series A financing to develop novel, mitochondria-based therapies for rare genetic disorders and diseases of aging.

Pretzel plans to target mitochondrial diseases, a highly heterogenous group of conditions caused by DNA mutations in the mitochondria or the nucleus. These disorders are very rare, afflicting around one in 5,000 people.

Pretzel CEO Jay Parrish told BioSpace the fundingshould enable us to get close to the clinic if not into the clinic with one or more programs.”

Summary: Determining the structure of vitronectin, a protein implicated in age-related macular degeneration and some neurodegenerative disorders, and using pressure to alter the protein shape may help in the development of new treatments for AMD.

Source: Sanford Burnham Prebys.

Research led by Sanford Burnham Prebys professor Francesca Marassi, Ph.D., is helping to reveal the molecular secrets of macular degeneration, which causes almost 90% of all age-related vision loss.

Senescent macrophages are in fact also found to express senescence-related markers p16(Ink4a) and β-galactosidase (β-gal), and promote inflammation in diseased tissues [25, 26]. Our previous work has indicated increased cellular senescence in dystrophic muscles of mdx/utr(−/−) mice [3], however, whether or not macrophages in particular develop cellular senescence and promote senescence associated phenotypes was still unknown. To this end, here we further examined mdx/utr(−/−) mice and solved these puzzles.

Immune cells in the skeletal muscle are activated during muscle injury and promote the process of muscle regeneration by coordinating with muscle stem cells. However, studies with severely diseased muscles further demonstrate that immune cells can become dominantly activated and is inductive of increased fatty infiltration and fibrosis formation, while at the same time potently repress the proliferation and function of muscle stem cells [27]. Our current results in severely dystrophic muscle reveal a similar situation of interaction between macrophages and MPCs, showing that the function of MPCs is repressed by the senescent macrophages. As senescent cells accumulate in the aged or diseased tissues, it can exert profound effects on the growth and function of normal cells by releasing SASPs [9, 10].

O.o!!!


According to recent research, the protein CHIP can control the insulin receptor more effectively while acting alone than when in a paired state. In cellular stress situations, CHIP often appears as a homodimer – an association of two identical proteins – and mainly functions to destroy misfolded and defective proteins. CHIP thus cleanses the cell. In order to do this, CHIP works with helper proteins to bind a chain of the small protein ubiquitin to misfolded proteins.

As a result, the cell detects and gets rid of defective proteins. Furthermore, CHIP controls insulin receptor signal transduction. CHIP binds to the receptor and degrades it, preventing the activation of life-extending gene products.

Researchers from the University of Cologne have now shown via tests using human cells and the nematode Caenorhabditis elegans that CHIP can also label itself with ubiquitin, preventing the formation of its dimer. The CHIP monomer regulates insulin signaling more effectively than the CHIP dimer. The research was conducted by the University of Cologne’s Cluster of Excellence for Cellular Stress Responses in Aging-Associated Diseases (CECAD) and was recently published in the journal Molecular Cell.

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Article originally published on LINKtoLEADERS under the Portuguese title “Sem saber ler nem escrever!”

In the 80s, “with no knowledge, only intuition”, I discovered the world of computing. I believed computers could do everything, as if it were an electronic God. But when I asked the TIMEX Sinclair 1000 to draw the planet Saturn — I am fascinated by this planet, maybe because it has rings —, I only glimpse a strange message on the black and white TV:

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