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Comment by Dr. Krishna Kumari Challa on April 13, 2024 at 1:40pm

Scientists uncover a missing link between poor diet and higher cancer risk

A research team has unearthed new findings that may help explain the connection between cancer risk and poor diet, as well as common diseases like diabetes, which arise from poor diet. The insights gained from this study hold promise for advancing cancer prevention strategies aimed at promoting healthy aging.

Cancer is caused by the interaction between our genes and factors in our environment, such as diet, exercise, and pollution. How such environmental factors increase cancer risk is not yet very clear, but it is vital to understand the connection if we are to take preventive measures that help us stay healthy longer.

A chemical linked to diabetes, obesity, and poor diet can heighten cancer risk

The research team first studied patients who are at a high risk of developing breast or ovarian cancers because they inherit a faulty copy of the cancer gene—BRCA2—from their parents. They demonstrated that cells from such patients were particularly sensitive to the effects of methylglyoxal, which is a chemical produced when our cells break down glucose to create energy.

The study showed that this chemical can cause faults in our DNA that are early warning signs of cancer development.

The team's research also suggested that people who do not inherit a faulty copy of BRCA2 but could experience higher-than-normal levels of methylglyoxal—such as patients with diabetes or pre-diabetes, which are connected with obesity or poor diet—can accumulate similar warning signs indicating a higher risk of developing cancer.

This research suggests that patients with high methylglyoxal levels may have higher cancer risk. Methylglyoxal can be easily detected by a blood test for HbA1C, which could potentially be used as a marker. Furthermore, high methylglyoxal levels can usually be controlled with medicines and a good diet, creating avenues for proactive measures against the initiation of cancer.

Interestingly, the research team's work also revised a longstanding theory about certain cancer-preventing genes. This theory—called the Knudson's 'two-hit' paradigm—was first formulated in 1971, and it was proposed that these genes must be inactivated permanently in our cells before cancer can arise.

The NUS team has now found that methylglyoxal can temporarily inactivate such cancer-preventing genes, suggesting that repeated episodes of poor diet or uncontrolled diabetes can 'add up' over time to increase cancer risk. This new knowledge is likely to be influential in changing the direction of future research in this area.

Li Ren Kong et al, A glycolytic metabolite bypasses "two-hit" tumor suppression by BRCA2, Cell (2024). DOI: 10.1016/j.cell.2024.03.006

Comment by Dr. Krishna Kumari Challa on April 13, 2024 at 12:17pm

Scientists wanted to know how this inflammatory process was damaging the brain. They Researchers were particularly interested in molecular aggregates, called cofilactin rods (CARs), that appear after a stroke. CARs form when two proteins, called cofilin and actin, that normally maintain neurites, break loose, forming messy clumps.

CARs are known to form in response to a chemical called superoxide, which immune cells release when the brain is inflamed.

To get a closer look at this process, the researchers stimulated inflammation in a part of the mouse brain that controls movement. They expected that neurons would die and the mice would have trouble moving.

The mice did struggle to move, but when the researchers looked at their brain tissue under a microscope, they were surprised to see that only the neurites had withered away, leaving the neurons isolated like stars in the night sky. The loss of these connections was enough to rob the mice of some of their motor coordination.

The scientists then tried reducing the amount of either superoxide or cofilin, and treated the brain with the same inflammatory substance. Under these conditions, fewer CARs formed, and the neurites survived. The mice also retained their coordination.

They had discovered a new pathway: inflammation caused immune cells to release superoxide, pulling cofilin and actin out of neurites and making CARs. Neurites died, and the disconnected brain malfunctioned.

Many neurological diseases involve inflammation, including multiple sclerosis, traumatic brain injury, and amyotrophic lateral sclerosis (ALS).

Now that scientists understand it better, they can design therapies to interrupt this inflammatory pathway. Stroke patients, for example, could be treated early on with anti-inflammatory agents to shield neurites from damage and preserve cognition.

Gökhan Uruk et al, Cofilactin rod formation mediates inflammation-induced neurite degeneration, Cell Reports (2024). DOI: 10.1016/j.celrep.2024.113914

Part 2

Comment by Dr. Krishna Kumari Challa on April 13, 2024 at 12:15pm

How the inflamed brain becomes disconnected after a stroke

Whether reeling from a sudden stroke or buckling under the sustained assault of Alzheimer's, the brain becomes inflamed, leading to cognitive problems and even death.

Scientists have known for many years that severe inflammation can kill the brain's neurons. Now, researchers  have discovered that even subtle inflammation damages the brain.

Instead of killing neurons outright, however, relatively mild inflammation only destroys the arm-like projections, called neurites, that wire neurons together. These connections are vital for everything the brain does, including learning and memory.

The findings, published last month in Cell Reports, describe in detail a new degenerative pathway that scientists can now try to disrupt. This could help stem the damage from common neurological diseases.

There are several exciting drugs now entering clinical use that interrupt these inflammatory processes, and now we know to look at their effects on neurites.

Not too far off, this could have a big impact on helping patients.

Inflammation is the body's first line of defense when something goes wrong. It rushes blood to an injured area, bathing it with immune cells that release chemicals to kill pathogens.

The strategy works well against bacteria, but it's brutal on the brain's delicate neural networks.

Part 1

Comment by Dr. Krishna Kumari Challa on April 12, 2024 at 12:32pm

Tiny AI-trained robots demonstrate soccer skills

Comment by Dr. Krishna Kumari Challa on April 12, 2024 at 11:08am

Don't depend on old Biology text books and theories for knowledge. Why Biology, all science is changing rapidly and progressing with rocket speed.

Each day I read a large amount of stories that are rewriting the old science textbooks. If you don't get updated, you remain a creature living under the big rock - very ancient, half-blind, half-mute and half-minded!

Science is not wine. It doesn't get better as it ages, it gets stale instead.

Science is like a running river, if you don't move as speedily as it does, you rot like an old log and decay!

(This ‘s my reply to a person who complained that my reports are contradicting Biology text books!)

Comment by Dr. Krishna Kumari Challa on April 12, 2024 at 9:49am

Plant more native trees to reduce landslide risk, control erosion, say researchers

Landslides typically occur under heavy rain. With the potential for increased precipitation due to climate change and a possible return to La Niña reinforcing slopes with native trees and shrubs could be an effective, economical and sustainable solution.

Homeowners, councils and state governments looking to build houses and infrastructure on or near slopes should reconsider cutting down trees or using artificial slope reinforcement to buttress vertical terrain against landslides and slips.

They should plant native trees and shrubs instead, according to scientists. Plants provide a sustainable, natural approach to slope reinforcement, compared to artificial methods, such as steel mesh or sprayed concrete. They also create and maintain crucial habitat.

Jiale Zhu et al, An experimental study on root-reinforced soil strength via a steel root analogue in unsaturated silty soil, Acta Geotechnica (2023). DOI: 10.1007/s11440-023-01918-0

Comment by Dr. Krishna Kumari Challa on April 12, 2024 at 9:25am

In a paper published in Cell in March 2024,  researchers show that the size ratio between UCYN-A (a short DNA sequence of what appeared to be from an unknown nitrogen-fixing cyanobacterium in Pacific Ocean seawater) and their algal hosts is similar across different species of the marine haptophyte algae Braarudosphaera bigelowii.

The researchers use a model to demonstrate that the growth of the host cell and UCYN-A are controlled by the exchange of nutrients. Their metabolisms are linked. This synchronization in growth rates led the researchers to call UCYN-A "organelle-like."

That's exactly what happens with organelles. If you look at the mitochondria and the chloroplast, it's the same thing: they scale with the cell.

But the scientists did not confidently call UCYN-A an organelle until confirming other lines of evidence. In the cover article of the journal Science, published recently, researchers show that UCYN-A imports proteins from its host cells.

That's one of the hallmarks of something moving from an endosymbiont to an organelle. They start throwing away pieces of DNA, and their genomes get smaller and smaller, and they start depending on the mother cell for those gene products—or the protein itself—to be transported into the cell.

These independent lines of evidence leave little doubt that UCYN-A has surpassed the role of a symbiont. And while mitochondria and chloroplasts evolved billions of years ago, the nitroplast appears to have evolved about 100 million years ago, providing scientists with a new, more recent perspective on organellogenesis.

The organelle also provides insight into ocean ecosystems. All organisms need nitrogen in a biologically usable form, and UCYN-A is globally important for its ability to fix nitrogen from the atmosphere. Researchers have found it everywhere from the tropics to the Arctic Ocean, and it fixes a significant amount of nitrogen.

 Tyler H. Coale et al, Nitrogen-fixing organelle in a marine alga, Science (2024). DOI: 10.1126/science.adk1075

Francisco M. Cornejo-Castillo et al, Metabolic trade-offs constrain the cell size ratio in a nitrogen-fixing symbiosis, Cell (2024). DOI: 10.1016/j.cell.2024.02.016

Part 2

Comment by Dr. Krishna Kumari Challa on April 12, 2024 at 9:20am

Scientists discover first nitrogen-fixing organelle

Biology textbooks have to be re-written now. Because  they assert that only bacteria can take nitrogen from the atmosphere and convert it into a form that is usable for life. Plants that fix nitrogen, such as legumes, do so by harbouring symbiotic bacteria in root nodules. But a recent discovery upends that rule.

In two recent papers, an international team of scientists describes the first known nitrogen-fixing organelle within a eukaryotic cell. The organelle is the fourth example in history of primary endosymbiosis—the process by which a prokaryotic cell is engulfed by a eukaryotic cell and evolves beyond symbiosis into an organelle.

It's very rare that organelles arise from these types of things. 

The first time we think it happened, it gave rise to all complex life. Everything more complicated than a bacterial cell owes its existence to that event leading  to the origins of the mitochondria. A billion years ago or so, it happened again with the chloroplast, and that gave us plants.

The third known instance involves a microbe similar to a chloroplast.

The newest discovery is the first example of a nitrogen-fixing organelle, which the researchers are calling a "nitroplast".
Part 1

Comment by Dr. Krishna Kumari Challa on April 11, 2024 at 9:48am

Witness the awe-inspiring spectacle of explosive solar phenomena during the April 8 total eclipse! Expert analysis delves into solar flares, coronal mass ejections, and mesmerizing sunspots

Comment by Dr. Krishna Kumari Challa on April 11, 2024 at 9:15am

AI makes retinal imaging 100 times faster, compared to manual method

Researchers  have applied artificial intelligence (AI) to a technique that produces high-resolution images of cells in the eye. They report that with AI, imaging is 100 times faster and improves image contrast 3.5-fold. The advance, they say, will provide researchers with a better tool to evaluate age-related macular degeneration (AMD) and other retinal diseases.

 Vineeta Das, Furu Zhang, Andrew Bower, et al. Revealing speckle obscured living human retinal cells with artificial intelligence assisted adaptive optics optical coherence tomography, Communications Medicine (2024). DOI: 10.1038/s43856-024-00483-1

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