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Comment by Dr. Krishna Kumari Challa on November 18, 2024 at 9:18am

Their analysis of mangrove wood revealed that the dead trees showed greater signs of salinity stress compared to living trees.

This stress indicates that the roots of the trees were struggling to cope with increased salt levels, which was a key factor in their eventual death.
The researchers found that sea levels around the Maldives rose at an accelerated rate of over 30mm per year between 2017 to 2020. Towards the end of this period, an unusually intense climate phenomenon known as the Indian Ocean Dipole occurred. This caused warmer sea surface temperatures and an increase in sea level in the Western Indian Ocean.

Although mangroves naturally build up their own sediment, allowing them to adapt to gradually rising seas, this rate of sea level rise was too fast for the mangroves to keep pace.

As tidal movements are more limited in the basin areas where many mangrove forests grow, the rising sea level meant that seawater effectively flooded the forests. This lack of tidal movement and flooding prevented the mangroves from building the sediment they needed to stay above water. They eventually lost their resilience and died off by drowning.
As the mangroves' build-up of sediment slowed down due to the pace of the rising sea level, the soil salinity increased beyond what even these salt-tolerant trees could handle. Essentially, the mangroves were drowning.

The extreme magnitude of dieback seen in the Maldives is a vivid illustration of how climate change may push natural systems past their limits, with cascading consequences for both nature and people.

Carruthers, L. et al. Sea-level rise and extreme Indian Ocean Dipole explain mangrove dieback in the Maldives, Scientific Reports (2024). DOI: 10.1038/s41598-024-73776-z

Part 2

Comment by Dr. Krishna Kumari Challa on November 18, 2024 at 9:15am

'Drowning' and 'dying' mangrove forests in Maldives signal global coastal threat, say researchers

Researchers have found evidence that mangrove forests—which protect tropical and subtropical coastlines—are drowning in the Maldives.

Their findings, published 12 November in Scientific Reports,

The research team, led by Northumbria University, warn that the findings have implications not only for the Maldives, but also for other island nations and coastal ecosystems around the world.

In 2020, more than a quarter of the Maldivian islands containing mangrove forests saw their trees experiencing a gradual deterioration before dying, a condition known as dieback.

In 2020, more than a quarter of the Maldivian islands containing mangrove forests saw their trees experiencing a gradual deterioration before dying, a condition known as dieback.
Satellite imagery of both inhabited and uninhabited islands revealed the severity of this issue, showing that some islands lost over half of their mangrove cover.

Mangroves play an essential role in protecting coastal regions by acting as natural barriers against storms, erosion and flooding. As biodiversity hotspots, they are vital nurseries for marine species such as crabs, prawns and fish making them crucial for food security and livelihoods in many coastal communities. They also provide valuable resources such as construction materials for housing.

Researchers combined evidence from sea level, climate data and remote sensing with field observations of sediment geochemistry and dendrology to investigate the mangrove dieback.

Part 1

Comment by Dr. Krishna Kumari Challa on November 18, 2024 at 9:07am

DNA packaging directly affects how fast DNA is copied in cells, scientists discover

Researchers have found that the way DNA is packaged in cells can directly impact how fast DNA itself is copied during cell division. They discovered that DNA packaging sends signals through an unusual pathway, affecting the cell's ability to divide and grow.

This opens up new doors to study how the copying of the DNA and its packaging are linked. These findings, published in Molecular Cell, may help scientists to find therapies and medicines for diseases such as cancer in the future.

Every day, our cells divide. Each time they need to copy both their DNA and the structure in which the DNA is packed. This packaging, called chromatin, acts as a guide. It tells the cell how, where and when to 'read' and use the information in the DNA. It is important that both the DNA and its chromatin are copied accurately to ensure young and healthy cells. Problems with this process are often seen in diseases like cancer.

The copying of chromatin has a direct effect on the mechanisms that copy DNA itself. If there is a problem with DNA packaging, the cell quickly senses this issue. But instead of triggering a typical stress response, the cell responds by slowing down its cycle of growth and division, without stopping it completely. The slower cycle still allows the cell to divide, but the new cells often struggle to continue to grow, preventing them from dividing again.

So, these mechanisms, which copy DNA and its packaging, are closely connected to cell growth. This discovery paves the way for new studies on these pathways and how DNA packaging can control cell growth. In the future, this knowledge could help to find new treatments for diseases like cancer.

 Acute multi-level response to defective de novo chromatin assembly in S-phase, Molecular Cell (2024). DOI: 10.1016/j.molcel.2024.10.023. www.cell.com/molecular-cell/fu … 1097-2765(24)00863-3

Comment by Dr. Krishna Kumari Challa on November 18, 2024 at 8:36am

In the second study, researchers turned their attention to triple-negative breast cancer, the most aggressive type of breast cancer there is. The disease is responsible for around one in eight breast cancer diagnoses and amounts to roughly 200,000 new cases each year worldwide.

Usually, excessive DNA damage triggers cell death. However, TNBC has a propensity to accumulate DNA damage without consequence, making it resilient to conventional treatments. The study helps partly explain why: the metabolic enzyme IMPDH2 relocates to the nucleus of TNBC cells to assist in DNA repair processes.

IMPDH2 acts like a mechanic in the cell's nucleus, controlling the DNA damage response that would otherwise kill the cancer cell.
By experimentally manipulating IMPDH2 levels, the team found they could tip the balance. Increasing IMPDH2 within the nucleus overwhelmed the cancer cells' repair machinery, causing cells to self-destruct.

It's like overloading a sinking ship with more water—eventually, it sinks faster. Their approach effectively forces TNBC cells to succumb to the very DNA damage they are typically resilient to.
The study can also lead to new ways of monitoring cancer. The research on IMPDH2 also studied its interaction with PARP1, a protein already targeted by existing cancer drugs. IMPDH2 could serve as a biomarker to predict which tumors will respond to PARP1 inhibitors.
Both studies contribute to an emerging field of therapies targeting cancer by exploiting its metabolic vulnerabilities.

Nuclear localization of MTHFD2 is required for correct mitosis progression, Nature Communications (2024). DOI: 10.1038/s41467-024-51847-z

Nuclear IMPDH2 controls the DNA damage response by modulating PARP1 activity, Nature Communications (2024). DOI: 10.1038/s41467-024-53877-z

Part 2

Comment by Dr. Krishna Kumari Challa on November 18, 2024 at 8:33am

'Moonlighting' enzymes may lead to new cancer therapies

Researchers at the Center for Genomic Regulation (CRG) reveal that metabolic enzymes known for their roles in energy production and nucleotide synthesis are taking on unexpected "second jobs" within the nucleus, orchestrating critical functions like cell division and DNA repair.

The discovery, reported in two separate research papers in Nature Communications, not only challenges longstanding biological paradigms in cellular biology but also opens new avenues for cancer therapies, particularly against aggressive tumors like triple-negative breast cancer (TNBC).

For decades, biology textbooks have neatly compartmentalized cellular functions. Mitochondria are the powerhouses of the cell, the cytoplasm is a bustling factory floor for protein synthesis, and the nucleus a custodian of genetic information. However, scientists have now discovered that the boundaries between these cellular compartments are less defined than previously thought.

Metabolic enzymes are moonlighting outside of their traditional neighborhood. There's an overlap in the skillset, but they're doing entirely different jobs for entirely different purposes. Surprisingly, their secondary roles in the nucleus are just as critical as their primary metabolic functions.

In one of the studies, researchers  focused on the metabolic enzyme MTHFD2. Traditionally, MTHFD2 is found in the mitochondria, where it plays a key role in synthesizing the building blocks of life and contributing to cell growth. Others research  work reveals that MTHFD2 also moonlights within the nucleus, where it plays a pivotal role in ensuring proper cell division.

The study is the first to demonstrate that the nucleus relies on metabolic pathways to maintain the integrity and stability of the human genome. The nucleus isn't just a passive storage space for DNA; it has its own metabolic needs and processes.

Part 1

Comment by Dr. Krishna Kumari Challa on November 18, 2024 at 8:21am

Blood vessel-like coating could make medical devices safer for patients

Researchers have developed a coating that could make medical devices safer for millions of patients, reducing the risks associated with blood clots and dangerous bleeding. The work has been published in Nature Materials.

The new material, designed to mimic the natural behavior of blood vessels, could allow for safer use of blood-contacting devices like catheters, stents, blood-oxygenation machines and dialysis machines—especially in cases where blood clots are a significant concern.

This discovery could be a transformative step in the development of safer medical devices. By designing a coating that mimics the body's natural approach to preventing clots, researchers have created a solution that could dramatically reduce the need for risky blood thinners before and after patients use these devices.

Thrombosis, or clot formation, is a major challenge when blood-contacting devices are used. Unlike natural blood vessels, these devices can trigger clotting by activating specific proteins in the blood. Blood clots can obstruct the device, disrupting treatment, or lead to severe complications such as stroke and heart attack.

Doctors often prescribe high doses of blood thinners to prevent clots on these devices, but this approach increases the risk of dangerous bleeding—a trade-off that many patients and clinicians would rather avoid.

The newly developed coating offers a promising alternative. It's engineered to imitate how blood vessels function—encouraging normal blood flow without triggering clot formation. Imagine the coating as a "soft barrier" on a device that attracts a key blood protein but keeps it from activating the clotting process.

By interacting with this protein in a controlled way, the coating prevents it from sparking a cascade of events that lead to clot formation.

In lab and animal studies, the coating demonstrated significant reductions in clot formation on device surfaces, without the use of blood thinners and without affecting the normal clotting functions elsewhere in the body.

One of the most surprising insights was that controlling the interaction between the coating and specific blood proteins could prevent clotting without disrupting the body's natural balance. This shows us that mimicking the body's own mechanisms, rather than simply repelling blood components, is key to truly biocompatible device design.

The innovation comes as demand for blood-contacting devices continues to rise. 

Additionally, the team is interested in understanding whether this approach could eventually be adapted to address other blood-related complications, such as inflammation or infection, in long-term medical implants.

Antithrombotic coating with sheltered positive charges prevents contact activation by controlling factor XII–biointerface binding, Nature Materials (2024). DOI: 10.1038/s41563-024-02046-0

Comment by Dr. Krishna Kumari Challa on November 17, 2024 at 1:51pm

The first experiments were conducted on board a Convair C-131 Samaritan, and yes, there is absolutely video of the proceedings. A similar experiment involved releasing pigeons inside the C-131 during parabolic flight.

It's fascinating to watch. The narration for the video says the cats' "automatic reflex action is almost completely lost under weightlessness". Almost – but not quite. Although the cats seem disoriented, they are still able to twist and turn their bodies around as they try to figure out where they are going to fall.
Part 2

Comment by Dr. Krishna Kumari Challa on November 17, 2024 at 1:48pm

Scientists Put Cats in Microgravity to See What Would Happen

There is, perhaps, no animal on this planet as lithe as the simple domestic cat. And not least in their bag of acrobatic tricks is one for which they are well-known: the ability to land, safely, on their velvet paws, when subjected to a tumble.

In the 1950s, humans discovered parabolic flight: the ability to simulate zero-G conditions using specially-designed aircraft plummeting along a precise flight trajectory. And with that came a devilish thought. What would happen to a cat's ability to land on its feet if they can't tell the difference between up and down?
So, this is what the bright minds at the US Air Force Aerospace Medical Research Lab decided to find out.

Parabolic flight is not true microgravity, but a brief experience of its effect. Just as a rapid descent in an elevator can make you feel lighter in your loafers, passengers on an aircraft will experience weightlessness while rapidly descending from a high altitude to a lower one. It's pretty disorienting, earning parabolic flight the nickname 'vomit comet' for good reason.

https://spacemedicineassociation.org/download/history/history_files...

Part 1

Comment by Dr. Krishna Kumari Challa on November 17, 2024 at 1:29pm

The researchers found the incorporation of trans fats through SPT increased lipoprotein secretion from the liver, which then promoted the formation of atherosclerotic plaques.
In the end, they saw mice consuming a high trans fat diet were producing trans fat-derived sphingolipids that promoted the secretion of VLDL from the liver into the bloodstream. This, in turn, accelerated the buildup of atherosclerotic plaques and the development of fatty livers and insulin dysregulation. High cis-fat diet mice, on the other hand, experienced shorter-term, less harmful effects like weight gain.

Jivani M. Gengatharan et al, Altered sphingolipid biosynthetic flux and lipoprotein trafficking contribute to trans-fat-induced atherosclerosis, Cell Metabolism (2024). DOI: 10.1016/j.cmet.2024.10.016

Part 2

Comment by Dr. Krishna Kumari Challa on November 17, 2024 at 1:27pm

Cholesterol may not be the only lipid involved in trans fat-driven cardiovascular disease
Excess cholesterol is known to form artery-clogging plaques that can lead to stroke, arterial disease, heart attack, and more, making it the focus of many heart health campaigns. Fortunately, this attention to cholesterol has prompted the development of cholesterol-lowering drugs called statins and lifestyle interventions like dietary and exercise regimens. But what if there's more to the picture than just cholesterol?
New research from Salk Institute scientists describes how another class of lipids, called sphingolipids, contributes to arterial plaques and atherosclerotic cardiovascular disease (ASCVD). Using a longitudinal study of mice fed high-fat diets—with no additional cholesterol—the team tracked how these fats flow through the body and found the progression of ASCVD induced by high trans fats was fueled by the incorporation of trans fats into ceramides and other sphingolipids. Knowing that sphingolipids promote atherosclerotic plaque formation reveals another side of cardiovascular disease in addition to cholesterol.

The findings, published in Cell Metabolism, open an entirely new avenue of potential drug targets to address these diseases and adverse health events like stroke or heart attacks.

When dietary fats enter the body through the foods we eat, they must be sorted and processed into compounds called lipids, such as triglycerides, phospholipids, cholesterol, or sphingolipids. Lipoproteins—like the familiar HDL, LDL, and VLDL—are used to transport these lipids through the blood.

Sphingolipids have become useful biomarkers for diseases like ASCVD, non-alcoholic fatty liver disease, obesity, diabetes, peripheral neuropathy, and neurodegeneration. However, it is unclear exactly how the incorporation of different dietary fats into sphingolipids leads to the development of ASCVD.

The fate of dietary fat is often determined by the protein that metabolizes it. 

The team suspected that trans fats were being incorporated into sphingolipids by SPT, which, in turn, would promote the excess lipoprotein secretion into the bloodstream that causes ASCVD.

To test their theory, they compared the processing of two different fats, cis fats and trans fats. The difference between these two comes down to the placement of a hydrogen atom; cis fats, found in natural foods like fish or walnuts, have a kink in their structure caused by two side-by-side hydrogen atoms, whereas trans fats, found in processed foods like margarine or anything fried, have a straight-chain structure caused by two opposing hydrogen atoms. Importantly, the kink in cis fats means they cannot be tightly packed—a positive feature for avoiding impenetrable clogs.

The researchers combined mouse model dietary manipulation with metabolic tracing, pharmacological interventions, and physiological analyses to answer their question—what is the link between trans fats, sphingolipids, and ASCVD?

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