Comment

Comment by Dr. Krishna Kumari Challa on August 25, 2024 at 12:25pm

How insulin, zinc and pH can block harmful protein clumps linked to type 2 diabetes

An estimated 462 million people around the world suffer from type 2 diabetes, a chronic disease in which the body has problems using sugar as a fuel, leading to a buildup of sugar in the blood and chronic health issues.

New research shows how zinc, pH levels and insulin work together to inhibit the buildup of protein clumps that contribute to this disease. The work, which points toward promising avenues for innovative treatments, was published in Communications Biology.

The research focuses on the intricate dance between insulin and the hormone amylin, or human islet amyloid polypeptide (hiAPP). Amylin is a naturally occurring peptide hormone that plays a role in regulating glycemia and energy balance. But human amylin can form amyloid fibers, which can destroy insulin-producing cells in the pancreas.

Amylin is produced in the pancreas alongside insulin and has a tendency to clump into aggregates called amyloid. They're like the plaques that form in the brain with Alzheimer's or Parkinson's disease.

For individuals with type 2 diabetes, amylin tends to cluster into harmful amyloid plaques, devastating the islet cells responsible for hormone production. However, insulin emerges as a potential hero, showing capabilities to hinder amylin's aggregation.

This study unravels the nuances of their interaction, alongside the roles of zinc and pH levels, bringing scientists closer to decoding the cellular intricacies of diabetes.

The results promise not just groundbreaking insights into this biomedical mystery, but also practical solutions. The research will help drug development aimed at neutralizing amylin's toxicity.

This could potentially revolutionize treatment approaches, offering hope to those battling this pervasive illness.

Samuel D. McCalpin et al, Zinc and pH modulate the ability of insulin to inhibit aggregation of islet amyloid polypeptide, Communications Biology (2024). DOI: 10.1038/s42003-024-06388-y

**

Comment by Dr. Krishna Kumari Challa on August 25, 2024 at 12:09pm

Mosquitoes sense infrared from body heat to help track humans down, study shows

While a mosquito bite is often no more than a temporary bother, in many parts of the world it can be scary. One mosquito species, Aedes aegypti, spreads the viruses that cause over 100,000,000 cases of dengue, yellow fever, Zika and other diseases every year. Another, Anopheles gambiae, spreads the parasite that causes malaria. The World Health Organization estimates that malaria alone causes more than 400,000 deaths every year. Indeed, their capacity to transmit disease has earned mosquitoes the title of deadliest animal.

Male mosquitoes are harmless, but females need blood for egg development. It's no surprise that there's over 100 years of rigorous research on how they find their hosts. Over that time, scientists have discovered there is no one single cue that these insects rely on. Instead, they integrate information from many different senses across various distances.

A team of researchers  has added another sense to the mosquito's documented repertoire: infrared detection. Infrared radiation from a source roughly the temperature of human skin doubled the insects' overall host-seeking behavior when combined with CO₂ and human odor.

The mosquitoes overwhelmingly navigated toward this infrared source while host seeking. The researchers also discovered where this infrared detector is located and how it works on a morphological and biochemical level. The results are detailed in the journal Nature.

Craig Montell, Thermal infrared directs host-seeking behaviour in Aedes aegypti mosquitoes, Nature (2024). DOI: 10.1038/s41586-024-07848-5. www.nature.com/articles/s41586-024-07848-5

Comment by Dr. Krishna Kumari Challa on August 25, 2024 at 12:04pm

Inherited NUMTs are mostly benign, probably because they arise early in development and the harmful ones are weeded out.
But if a piece of mitochondrial DNA inserts itself within a gene or regulatory region, it could have important consequences on that person's health or lifespan. Neurons may be particularly susceptible to damage caused by NUMTs because when a neuron is damaged, the brain does not usually make a new brain cell to take its place.
The researchers' analysis showed that nuclear mitochondrial DNA insertion happens in the human brain—mostly in the prefrontal cortex—and likely several times over during a person's lifespan.
They also found that people with more NUMTs in their prefrontal cortex died earlier than individuals with fewer NUMTs. "This suggests for the first time that NUMTs may have functional consequences and possibly influence lifespan.
"NUMT accumulation can be added to the list of genome instability mechanisms that may contribute to aging, functional decline, and lifespan.
Stress accelerates NUMTogenesis
What causes NUMTs in the brain, and why do some regions accumulate more than others?

To get some clues, the researchers looked at a population of human skin cells that can be cultured and aged in a dish over several months, enabling exceptional longitudinal "lifespan" studies.

These cultured cells gradually accumulated several NUMTs per month, and when the cells' mitochondria were dysfunctional from stress, the cells accumulated NUMTs four to five times more rapidly.

This shows a new way by which stress can affect the biology of our cells.Stress makes mitochondria more likely to release pieces of their DNA and these pieces can then 'infect' the nuclear genome. It's just one way mitochondria shape our health beyond energy production.
Mitochondria are cellular processors and a mighty signaling platform. Now we know mitochondria can even change the nuclear DNA sequence itself.

Somatic nuclear mitochondrial DNA insertions are prevalent in the human brain and accumulate over time in fibroblasts, PLoS Biology (2024). On bioRxiv: DOI: 10.1101/2023.02.03.527065

Part 2

Comment by Dr. Krishna Kumari Challa on August 25, 2024 at 12:00pm

Mitochondria are flinging their DNA into our brain cells, study shows

As direct descendants of ancient bacteria, mitochondria have always been a little alien. Now a study shows that mitochondria are possibly even stranger than we thought.

The study, titled "Somatic nuclear mitochondrial DNA insertions are prevalent in the human brain and accumulate over time in fibroblasts," appears in PLOS Biology.

Mitochondria in our brain cells frequently fling their DNA into the nucleus, the study found, where the DNA becomes integrated into the cells' chromosomes. And these insertions may be causing harm: Among the study's nearly 1,200 participants, those with more mitochondrial DNA insertions in their brain cells were more likely to die earlier than those with fewer insertions.
We used to think that the transfer of DNA from mitochondria to the human genome was a rare occurrence. It's stunning that it appears to be happening several times during a person's lifetime.

Researchers now found lots of these insertions across different brain regions, but not in blood cells, explaining why dozens of earlier studies analyzing blood DNA missed this phenomenon.

Mitochondria live inside all our cells, but unlike other organelles, mitochondria have their own DNA, a small circular strand with about three dozen genes. Mitochondrial DNA is a remnant from the organelle's forebears: ancient bacteria that settled inside our single-celled ancestors about 1.5 billion years ago.

In the past few decades, researchers discovered that mitochondrial DNA has occasionally "jumped" out of the organelle and into human chromosomes.

The mitochondrial DNA behaves similar to a virus in that it makes use of cuts in the genome and pastes itself in, or like jumping genes known as retrotransposons that move around the human genome.

The insertions are called nuclear-mitochondrial segments—NUMTs ("pronounced new-mites")—and have been accumulating in our chromosomes for millions of years.

As a result, all of us are walking around with hundreds of vestigial, mostly benign mitochondrial DNA segments in our chromosomes that we inherited from our ancestors.

Mitochondrial DNA insertions are common in the human brain Research in just the past few years has shown that "NUMTogenesis" is still happening today. "Jumping mitochondrial DNA is not something that only happened in the distant past

It's rare, but a new NUMT becomes integrated into the human genome about once in every 4,000 births. This is one of many ways, conserved from yeast to humans, by which mitochondria talk to nuclear genes.

Part 1

Comment by Dr. Krishna Kumari Challa on August 25, 2024 at 11:54am

Researchers discover gene scissors that switch off with a built-in timer

CRISPR gene scissors, as new tools of molecular biology, have their origin in an ancient bacterial immune system. But once a virus attack has been successfully overcome, the cell has to recover.

Researchers  have discovered a timer integrated into the gene scissors that enables the gene scissors to switch themselves off. The results of the study have been published in the journal Nucleic Acids Research.

Sophie C Binder et al, The SAVED domain of the type III CRISPR protease CalpL is a ring nuclease, Nucleic Acids Research (2024). DOI: 10.1093/nar/gkae676

Some bacteria have developed CRISPR gene scissors in response to attacks by so-called phages. This bacterial immune system recognizes the phage genetic material, destroys it and thus protects against viral attacks.

When detecting phages, the type III variants of these immune systems produce messenger substances with cyclic oligoadenylates (cOAs), which the bacteria use to switch on a complex emergency plan. This ensures that a virus can be fought optimally and on a broad front.

**

Comment by Dr. Krishna Kumari Challa on August 25, 2024 at 11:20am

Thyroid hormone fuels the drive to explore by rewiring brain circuits, new study suggests

Thyroid hormone plays a key role in regulating a range of physiologic functions, including metabolism, temperature, heart rate, and growth. It accomplishes this impressive array of activities by interacting with almost every organ system in the body. Yet despite a long history of research on how thyroid hormone influences different organs, its effects on arguably the most crucial organ—the brain—have remained shrouded in mystery.

Now, scientists have gained new insights into thyroid hormone's effects on the brain. The work, conducted in mice and published Aug. 22 in Cell, shows that thyroid hormone changes the wiring of brain circuits in a manner that drives animals to engage in exploratory behaviour. 

By simultaneously changing brain wiring and altering metabolic rate, the researchers concluded that thyroid hormone coordinates the brain and body to produce exploratory behavior when it is most needed—for example, during seasons when animals need to find mates or stockpile resources.

It's well known that thyroid hormone modulates metabolism, and now scientists have shown that it also modulates exploratory behaviours through direct action on the brain.

The findings also help elucidate how low levels of the hormone could lead to depressive states marked by a low desire to explore, while too much could precipitate manic states characterized by an extreme desire for exploration. Thus, the researchers see their work as an important step toward understanding how aberrant levels of thyroid hormone could contribute to certain psychiatric conditions.

Daniel Hochbaum et al, Thyroid hormone remodels cortex to coordinate body-wide metabolism and exploration, Cell (2024). DOI: 10.1016/j.cell.2024.07.041. www.cell.com/cell/fulltext/S0092-8674(24)00835-3

Comment by Dr. Krishna Kumari Challa on August 25, 2024 at 11:15am

What's more, the dendrocolloidal host material itself is relatively inexpensive and easy to fabricate.

 A Primordial DNA Store and Compute Engine, Nature Nanotechnology (2024). DOI: 10.1038/s41565-024-01771-6. www.nature.com/articles/s41565-024-01771-6

Part 2

Comment by Dr. Krishna Kumari Challa on August 25, 2024 at 11:14am

For first time, DNA tech offers both data storage and computing functions

Researchers have demonstrated a technology capable of a suite of data storage and computing functions—repeatedly storing, retrieving, computing, erasing or rewriting data—that uses DNA rather than conventional electronics. Previous DNA data storage and computing technologies could complete some but not all of these tasks.

The paper, titled "A Primordial DNA Store and Compute Engine," appears in the journal Nature Nanotechnology.

In conventional computing technologies, we take for granted that the ways data are stored and the way data are processed are compatible with each other.

But in reality, data storage and data processing are done in separate parts of the computer, and modern computers are a network of complex technologies.

DNA computing has been grappling with the challenge of how to store, retrieve and compute when the data is being stored in the form of nucleic acids.

For electronic computing, the fact that all of a device's components are compatible is one reason those technologies are attractive. But, to date, it's been thought that while DNA data storage may be useful for long-term data storage, it would be difficult or impossible to develop a DNA technology that encompassed the full range of operations found in traditional electronic devices: storing and moving data; the ability to read, erase, rewrite, reload or compute specific data files; and doing all of these things in programmable and repeatable ways.

Now researchers have  demonstrated that these DNA-based technologies are viable, because  they have made one.

The new technology is made possible by recent techniques that have enabled the creation of soft polymer materials that have unique morphologies.

Specifically, the tech developers have created polymer structures that they call dendricolloids—they start at the microscale, but branch off from each other in a hierarchical way to create a network of nanoscale fibers.

This morphology creates a structure with a high surface area, which allows the techies to deposit DNA among the nanofibrils without sacrificing the data density that makes DNA attractive for data storage in the first place.

You could put a thousand laptops' worth of data into DNA-based storage that's the same size as a pencil eraser.

The ability to distinguish DNA information from the nanofibers it's stored on allows us to perform many of the same functions you can do with electronic devices.

We can copy DNA information directly from the material's surface without harming the DNA. We can also erase targeted pieces of DNA and then rewrite to the same surface, like deleting and rewriting information stored on the hard drive. It essentially allows us to conduct the full range of DNA data storage and computing functions. In addition, they found that when we deposit DNA on the dendricolloid material, the material helps to preserve the DNA.

The researchers have demonstrated that the new data storage and computing technology—which they call a "primordial DNA store and compute engine"—is capable of solving simple sudoku and chess problems. Testing suggests that it could store data securely for thousands of years in commercially available spaces without degrading the information-storing DNA.

Part1

Comment by Dr. Krishna Kumari Challa on August 25, 2024 at 10:59am

When they tested the compound in rats that have a specific type of vasculitis, it decreased the disease severity, which was evident by reduced inflammation and damage in the blood vessels, especially in their kidneys and lungs.
Their findings suggest that CatC inhibition shows promise as a new treatment strategy to reduce neutrophil overactivation and improve conditions in diseases where overactive neutrophils and excessive NET formation play a critical role. This approach differs from current treatments that may have broader immunosuppressive effects.
Current treatments for inflammatory diseases often involve the use of glucocorticoids and immunosuppressive drugs which suppress the immune system's activity as a whole and can lead to secondary immunodeficiency, increasing the risk of opportunistic infections. By specifically targeting the activation of multiple NSPs through CatC inhibition without broadly suppressing the immune system, MOD06051 potentially offers a safer alternative that could reduce the risk of infections and other side effects.

These findings pave the way for further research and clinical trials to evaluate the safety and efficacy of MOD06051 in humans. The team is optimistic that this novel approach holds the promise of providing safer and more effective therapies for patients around the world suffering from a variety of inflammatory diseases, improving their quality of life.

Cathepsin C inhibition reduces neutrophil serine protease activity and improves activated neutrophil-mediated disorders, Nature Communications (2024). DOI: 10.1038/s41467-024-50747-6

Part 2

**

Comment by Dr. Krishna Kumari Challa on August 25, 2024 at 10:57am

A new compound shows great potential for patients with neutrophil-associated inflammation

A newly developed compound that reduces harmful inflammation caused by overactive neutrophils in rats shows great potential as a safer treatment for various inflammatory diseases in humans.

Neutrophils are the most abundant type of white blood cells in the human body, and they play a crucial role in immune response. These immune cells help fight infections by engulfing pathogens and releasing enzymes that kill the invaders.

But although they're essential for fighting infections, neutrophils can also become overactive, leading to various inflammatory diseases. When they are activated by infection, neutrophils can release neutrophil extracellular traps (NETs), web-like structures consisting of DNA and proteins, which trap and kill pathogens as a part of the normal host defense mechanism. However, too much NET formation can significantly damage tissues, thus contributing to inflammation.

A team of researchers  has investigated a recently-developed drug candidate, MOD06051, which reduces harmful inflammation in rat models by targeting neutrophils. The results of their joint research appear in Nature Communications.

They found that MOD06051 works as a selective inhibitor for Cathepsin C (CatC), a key regulator that activates multiple enzymes inside of neutrophils known as neutrophil serine proteases (NSPs). One such NSP is neutrophil elastase, an enzyme involved in killing pathogens but also an essential factor for NET formation.

The scientists found that inhibiting CatC reduces the active form of neutrophil elastase and decreases the ability of neutrophils to form NETs. Excessive NET formation has been linked to several diseases, including vasculitis, lupus, rheumatoid arthritis, and diabetes.

Part 1

• ‹ Previous
• 1
• …
• 192
• 193
• 194
• 195
• 196
• …
• 1111
• Next ›
• Page