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Category: biotech/medical – Page 2340

Proteins are the building blocks of the cell. They do most of the work and are essential for the structure, function and dynamic regulation of the cell and body’s tissues and organs. Proteins rarely work alone, they interact, form protein complexes or bind DNA and RNA to control what a cell does. These complexes are key pieces of many important reactions within the cell, such as energy metabolism or gene regulation. Any change in those interactions, which can for example be caused by a mutation, can make the difference between health and disease. Hence, for understanding how cells operate, or what might go wrong in ill cells, it is essential to know how their building blocks interact.

New technologies allowed scientists during the last decades to understand the genetic information an organism possess, which of this information is actively used and which proteins are made by the cell in different circumstances. Now it is a big challenge to understand how biomolecules such as proteins and RNA messenger molecules combine to form the complexes required for a functional cell. In other words, we know the ten thousands of parts a cell is build off, but we don’t know how they belong together.

In a paper published in Nature Communications, scientists at the Centre for Genomic Regulation (CRG) describe the development of a new method, named “rec-YnH”, which was designed to understand the complexes formed between hundreds of proteins and RNAs at the same time.

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“Previous work mostly focused on what was going on at the microscale of DNA,” says study co-author Michael Shelley, group leader for biophysical modeling at the Flatiron Institute’s Center for Computational Biology in New York City and co-director of the Courant Institute’s Applied Mathematics Laboratory at New York University. “People didn’t really think about what was going on at the larger scale.”

Shelley and colleagues simulated the motions of chromatin, the functional form of DNA inside the nucleus. Chromatin looks like beads on a string, with ball-like clusters of genetic material linked by strands of DNA. The researchers propose that molecular machines along the DNA cause segments of the chromatin to straighten and pull taut. This activity aligns neighboring strands to face the same direction. That alignment, in turn, results in a cascading waltz of genetic material shimmying across the nucleus.

The dancing DNA may play a role in gene expression, replication and remodeling, though the exact effects remain unclear, the researchers reported online October 22 in Proceedings of the National Academy of Sciences.

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A common virus seems to be behind a puzzling condition that’s paralyzing children, but uncertainties remain.

A s the summer of 2014 gave way to fall, Kevin Messacar, a pediatrician at Children’s Hospital Colorado, started seeing a wave of children with inexplicable paralysis. All of them shared the same story. One day, they had a cold. The next, they couldn’t move an arm or a leg. In some children, the paralysis was relatively mild, but others had to be supported with ventilators and feeding tubes after they stopped being able to breathe or swallow on their own.

The condition looked remarkably like polio—the viral disease that is on the verge of being eradicated worldwide. But none of the kids tested positive for poliovirus. Instead, their condition was given a new name: acute flaccid myelitis, or AFM. That year, 120 people, mostly young children, developed the condition across 34 states. The cases peaked in September and then rapidly tailed off.

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Wonderful to see the continuing progress of Mr. Omar Flores, with the support of his lovely wife, actress Mayra Sierra, today on the Venga la Alegria (VLA) show on TV Azteca (http://www.aztecauno.com/vengalaalegria) — The importance of an integrated approach to curing spinal cord injury including family, physical therapists, and the medical team at Regenerage (https://regenerage.clinic/)

Other common names for the drugs include captopril, cilazapril and enalapri.

They work by reducing the activity of the angiotensin-converting enzyme, or ACE for short. By blocking this enzyme, the blood vessels relax and widen and blood pressure is lowered.

An estimated 103 million adults in the US, which is almost half the adult population, have high blood pressure, according to statistics this year from the American Heart Association.

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The cerebellum can’t get no respect. Located inconveniently on the underside of the brain and initially thought to be limited to controlling movement, the cerebellum has long been treated like an afterthought by researchers studying higher brain functions.

But researchers at Washington University School of Medicine in St. Louis say overlooking the cerebellum is a mistake. Their findings, published Oct. 25 in Neuron, suggest that the cerebellum has a hand in every aspect of higher brain functions — not just movement, but attention, thinking, planning and decision-making.

“The biggest surprise to me was the discovery that 80 percent of the cerebellum is devoted to the smart stuff,” said senior author Nico Dosenbach, MD, PhD, an assistant professor of neurology, of occupational therapy and of pediatrics. “Everyone thought the cerebellum was about movement. If your cerebellum is damaged, you can’t move smoothly ­— your hand jerks around when you try to reach for something. Our research strongly suggests that just as the cerebellum serves as a quality check on movement, it also checks your thoughts as well — smoothing them out, correcting them, perfecting things.”

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Drugs that target multiple aging pathways at once significantly extend the healthspan and lifespan of nematodes.

In a paper published in Developmental Cell, scientists from Yale University have demonstrated how targeting multiple pathways related to aging with different drug combinations can slow aging down and extend healthy lifespan in C. elegans [1].

Abstract

There is growing interest in pharmacological interventions directly targeting the aging process. Pharmacological interventions against aging should be efficacious when started in adults and, ideally, repurpose existing drugs. We show that dramatic lifespan extension can be achieved by targeting multiple, evolutionarily conserved aging pathways and mechanisms using drug combinations. Using this approach in C. elegans, we were able to slow aging and significantly extend healthy lifespan. To identify the mechanism of these drug synergies, we applied transcriptomics and lipidomics analysis. We found that drug interactions involved the TGF-b pathway and recruited genes related with IGF signaling. daf-2, daf-7, and sbp-1 interact upstream of changes in lipid metabolism, resulting in increased monounsaturated fatty acid content and this is required for healthy lifespan extension.

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