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Category: biotech/medical – Page 233

Discovery shows that even neutral molecules take sides when it comes to biochemistry

A new study led by a pair of researchers at the University of Massachusetts Amherst turns long-held conventional wisdom about a certain type of polymer on its head, greatly expanding understanding of how some of biochemistry’s fundamental forces work. The study, released recently in Nature Communications, opens the door for new biomedical research running the gamut from analyzing and identifying proteins and carbohydrates to drug delivery.

The work involves a kind of polymer made up of neutral polyzwitterions. Because they have a neutral electrical charge, polyzwitterions are not expected to respond to an electric field. However, the team found not only that certain neutral polyzwitterions behave as if they were charged, but also that the electric field surrounding polyzwitterions, once thought to be uniform, varies in strength.

“My interest is in the proteins and , which are the building blocks for protein, inside our body’s cells,” says Yeseul Lee, lead author and graduate student in polymer science and engineering at UMass Amherst.

Tiny RNA molecule may hold the key to treating knee osteoarthritis

The number of people suffering from osteoarthritis is expected to top 1 billion by 2050. The biggest risk factor for the prevalent, often painful, chronic joint disease is aging. And like aging, there is currently no way to stop it.

A discovery by scientists at Henry Ford Health + Michigan State University Health Sciences could pave the way for new breakthroughs in detecting and treating the disease. Their findings were recently published in Nature Communications.

“Our hope is that this discovery will one day allow doctors to catch the disease earlier and intervene before significant joint damage occurs,” said Shabana Amanda Ali, Ph.D., a Henry Ford Health assistant scientist and senior author of the paper. “Osteoarthritis is so complex and so heterogeneous that even with decades of research there hasn’t been a single therapeutic.”

Thyroid eye disease (Graves’ orbitopathy): clinical presentation, epidemiology, pathogenesis, and management

Thyroid eye disease (TED; also known as Graves’ orbitopathy), causes swollen extraocular muscles and orbital fat. Mechanistically, TED involves lid retraction, oedema and redness of the eyelids and conjunctiva, proptosis, diplopia, and optic neuropathy. Investigation of TED involves assessment of disease activity (inflammation) and disease severity. TED is predominantly mild in 77% of cases, moderate-to-severe in 22%, and rarely sight-threatening in 1% of patients. While most patients with TED have Graves’ hyperthyroidism, up to 5% are euthyroid or even hypothyroid.

Experimental Drug Tested in Mice Repairs The Eye to Restore Vision

Our eyes could potentially be coaxed into a special repair mode above and beyond our natural self-healing abilities, according to a new study, thanks to the delivery of antibodies that trigger nerve cell regeneration in the retina.

The South Korean research team says the treatment offers hope for restoring lost vision that otherwise can’t be brought back. For now though, it’s only been tested in mice.

Here’s how it works: a compound antibody drug is used to block the prospero homeobox protein 1 (Prox1). This protein isn’t inherently bad, playing an important role in cell regulation, but it appears to stop retinal nerves from regenerating.

NAD depletion in skeletal muscle does not compromise muscle function or accelerate aging

Nicotinamide adenine dinucleotide (NAD) is a ubiquitous electron carrier essential for energy metabolism and post-translational modification of numerous regulatory proteins. Dysregulations of NAD metabolism are widely regarded as detrimental to health, with NAD depletion commonly implicated in aging. However, the extent to which cellular NAD concentration can decline without adverse consequences remains unclear. To investigate this, we generated a mouse model in which nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ biosynthesis was disrupted in adult skeletal muscle. The intervention resulted in an 85% reduction in muscle NAD+ abundance while maintaining tissue integrity and functionality, as demonstrated by preserved muscle morphology, contractility, and exercise tolerance. This absence of functional impairments was further supported by intact mitochondrial respiratory capacity and unaltered muscle transcriptomic and proteomic profiles. Furthermore, lifelong NAD depletion did not accelerate muscle aging or impair whole-body metabolism. Collectively, these findings suggest that NAD depletion does not contribute to age-related decline in skeletal muscle function.

#Aging #Longevity aging and longevity.

NAD depletion in skeletal muscle does not impair tissue integrity and function or accelerate aging, as shown in a mouse model with an 85% decrease in muscle NAD+ levels. Muscle structure, metabolism, and mitochondrial function remain unaffected, suggesting that NAD depletion does not drive age-related muscle decline.

Lactate mediates training of our innate defenses, research shows

The BCG vaccine protects against tuberculosis, but by inducing trained immunity it also protects against many more respiratory infections. International research led by Radboud University Medical Center shows how this process works. Lactate, a product of scaled-up energy production, appears to play a leading role.

The immune system protects people in two ways. Innate immunity protects us from birth against many bacteria and viruses, while adaptive immunity builds protection against individual pathogens after a prior infection. The adaptive immune system is aided by vaccines that protect us against new pathogens without having to go through an infection. In this way, vaccines contribute greatly to our health.

Once-a-Day Pill Slows Loss of Lung Function in Bronchiectasis Patients

Results of a large, global clinical trial spanning five continents with over 1,700 patients with bronchiectasis, published this April in the New England Journal of Medicine, demonstrated benefits of an investigational, once-a-day pill called brensocatib as a therapy for the chronic lung condition.

The clinical trial findings are important, as there are currently no FDA-approved medications for bronchiectasis, a chronic condition with persistent lung airway inflammation and infection. Bronchiectasis can often stem from various injuries to the airways causing the ‘bronchial’ tubes leading to the lungs to become permanently enlarged, and more prone to infection and chronic inflammation.

Engineered enzymes enable precise control of mitochondrial DNA mutation levels in cells

Mitochondrial diseases affect approximately 1 in 5,000 people worldwide, causing debilitating symptoms ranging from muscle weakness to stroke-like episodes. Some of these conditions result from mutations in mitochondrial DNA (mtDNA), the genetic material housed in these organelles. For patients with the common m.3243A>G mutation, which can cause MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) and diabetes mellitus, treatments remain limited.

How ‘jumping genes’ infiltrate DNA during cell division

Viruses are known to use the genetic machinery of the human cells they invade to make copies of themselves. As part of the process, viruses leave behind remnants throughout the genetic material (genomes) of humans. The virus-like insertions, called “transposable elements,” are snippets of genetic material even simpler than viruses that also use host cell machinery to replicate.

Nearly all these inserted elements have been silenced by our cells’ defense mechanisms over time, but a few, nicknamed “jumping genes,” can still move around the human genome like viruses. Just one, called long interspersed nuclear element 1 (LINE-1), can still move by itself.

As an element type that behaves like the retrovirus HIV, the LINE-1 “retrotransposon” is first copied into a molecule of RNA, the genetic material that partners with DNA, and then the RNA LINE-1 copy is converted back into DNA in a new place in the genome.

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