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Comment by Dr. Krishna Kumari Challa on August 24, 2024 at 10:08am

Faulty gene makes the brain too big—or too small

A gene called ZNRF3, known to be involved in cancer, also messes with the mind. The human brain relies on two copies of this gene to build a correctly sized brain. If one of the copies is defective, the brain will be either too small or too large—known as mirror effect—leading to various neurological symptoms.

Scientists tested the faulty versions of the gene in the lab and found a correlation between patients' brain size and the location of the mutations in the gene. After a long diagnostic odyssey, they were finally able to establish a definitive cause for the disease of these patients. Their study is published in the American Journal of Human Genetics.

The gene ZNRF3 produces two copies of a protein that prevents the brain from making too many or too few brain cells. It also does the same in many other organs, so that mutations in its DNA sequence can lead to uncontrolled cell proliferation and are therefore associated with a variety of tumors, such as colon or adrenal cancer.

One of their analyses revealed that there is a small region of the ZNRF3 gene, called RING, where many mutations found in cancers are located compared to the rest of the gene. In fact, most of the patients with abnormally large brains have their mutations in the RING region. This means that they may have an increased risk of developing tumors during their lifetime.

Further analyses showed that almost all the mutations that lead to abnormal development are located in two distinct regions of the gene: one in the RING region, and the other in a smaller region that is important for interacting with another gene called RSPO. It turned out that almost all the defects in the RING region were from the patients with an abnormally large brain, while the defect in the RSPO-interacting region came from the patient with an abnormally small brain.

However, one patient had a fault in the RING region but had an abnormally small brain. We traced his family history and found that his mother used drugs heavily during her pregnancy, which could explain his abnormally small—instead of large—brain. Apparently, environmental influences can override genetic defects in this condition.

The gene ZNRF3 orchestrates the perfect balance of biochemical signals, particularly in the Wnt signaling pathway, needed to produce the right number of brain cells. This gene works in concert with the gene RSPO, which also interacts with the Wnt signaling.

These results showed that the right brain size depends on a balanced Wnt signaling, which, once tipped toward too much or too little, can cause the brain to become too large or too small.

 Paranchai Boonsawat et al, Deleterious ZNRF3 germline variants cause neurodevelopmental disorders with mirror brain phenotypes via domain-specific effects on Wnt/β-catenin signaling, The American Journal of Human Genetics (2024). DOI: 10.1016/j.ajhg.2024.07.016

Comment by Dr. Krishna Kumari Challa on August 24, 2024 at 9:58am

In female flies fed NPs, heart size (diastolic diameter) increased, and diastolic intervals increased in females fed both MPs and NPs. Meanwhile, heart sizes of male flies fed both sizes of plastic exhibited significant changes to diastolic and systolic diameters.

Furthermore, the researchers write, "Unlike females, male flies also see changes to Systolic Interval (SI) Time and fractional shortening. Total SI time is reduced by 40% in flies exposed to MPs while female flies see no change. Finally, males exposed to NPs experience an 11% reduction in fractional shortening. This phenomenon is unique to males, as females see no change to fractional shortening following dietary exposure to either plastic size."
The researchers note that they had initially hypothesized that the changes they recorded might have resulted from MPs and NPs actually creating a physical barrier to normal heart development. They also believe that "molecular interactions between the plastics and the heart itself" are responsible for the sexually dimorphic changes they observed, especially the differences in male and female heart sizes.

However, they acknowledge, "The true mechanism behind these observed changes is unknown, and so further research is needed to identify if exposure to MPs and NPs interacts with any mammalian conserved genes which may lead to cardiac dysfunction."
They also suggest that further research could include a variety of ingestible plastic shapes, and that further research should also focus on pinpointing the specific molecular changes causing the observed functional disorders.

 Alyssa M. Hohman et al, The heart of plastic: utilizing the Drosophila model to investigate the effects of micro/nanoplastics on heart function, Frontiers in Toxicology (2024). DOI: 10.3389/ftox.2024.1438061

Part 2

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Comment by Dr. Krishna Kumari Challa on August 24, 2024 at 9:56am

Micro- and nanoplastics ingested by Drosophila cause changes in heart size and function

Plastics are ubiquitous in products we use every day, and recent studies have begun to reveal the effects of micro- and nanoplastics (MPs and NPs) on the health of humans and animals.

Much research on the health effects of MPs and NPs to date has focused on marine life, especially fish. A few early studies have investigated possible toxic effects of plastics on terrestrial species such as birds, earthworms, insects, humans and other mammals, but myriad specifics remain unknown.

A team of researchers from Iowa State University, using fruit flies (Drosophila melanogaster), has now made the first examination of the effects of MP and NP toxicity on the heart. The team's work is published in a Brief Research Report in Frontiers in Toxicology.

Drosophila hearts and vertebrate hearts are similar with respect to functional and genetic changes during development and aging. For this new study, the researchers obtained wild-type Drosophila fly larvae and divided them into a control group and two test groups.
They fed all the flies a diet of cornmeal from the beginning of their development until they reached maturity (pupation). Flies in the two test groups received cornmeal to which the researchers added polystyrene MPs (larger than 100 nm and smaller than 5 mm) or NPs (smaller than 100 nm).

Five days after the flies hatched, the researchers collected approximately 15 flies of each sex from each of the two test groups and the control group. The team anesthetized the flies, dissected their beating hearts, and recorded high-speed video at over 200 frames/second for analysis.

Among the notable results, the analysis indicates that plastic exposure produces different results in males and females. The heart rates of female flies exposed to both MPs and NPs decreased 13%, while their heart periods (time between the beginning of a heartbeat and the beginning of the next heartbeat) increased correspondingly. Male flies did not exhibit this change, but males fed MPs exhibited greater variability than those fed NPs and those in the control group.
Part 1

Comment by Dr. Krishna Kumari Challa on August 22, 2024 at 11:04am

‘Dark Oxygen’ Is Coming from These Ocean Nodules

Comment by Dr. Krishna Kumari Challa on August 22, 2024 at 10:18am

The blue light theory involves melatonin, a hormone that regulates sleep. During the day, we are exposed to bright, natural light that contains a high amount of blue light. This bright, blue light activates certain cells at the back of our eyes, which send signals to our brain that it's time to be alert. But as light decreases at night, our brain starts to produce melatonin, making us feel sleepy.

It's logical to think that artificial light from devices could interfere with the production of melatonin and so affect our sleep. But studies show it would require light levels of about 1,000–2,000 lux (a measure of the intensity of light) to have a significant impact.

Device screens emit only about 80–100 lux. At the other end of the scale, natural sunlight on a sunny day provides about 100,000 lux.

We know that bright light does affect sleep and alertness. However, research indicates the light from devices such as smartphones and laptops is nowhere near bright or blue enough to disrupt sleep.
There are many factors that can affect sleep, and bright, blue screen light likely isn't one of them.

Part 2

Comment by Dr. Krishna Kumari Challa on August 22, 2024 at 10:06am

How much does your phone's blue light really delay your sleep? Relax, it's just 2.7 minutes!

It's one of the most pervasive messages about technology and sleep. We're told bright, blue light from screens prevents us falling asleep easily. We're told to avoid scrolling on our phones before bedtime or while in bed. We're sold glasses to help filter out blue light. We put our phones on "night mode" to minimize exposure to blue light.

But what does the science actually tell us about the impact of bright, blue light and sleep? When a group of sleep experts from Sweden, Australia and Israel compared scientific studies that directly tested this, they   found the overall impact was close to meaningless. Sleep was disrupted, on average, by less than three minutes.

Scientists showed the message that blue light from screens stops you from falling asleep is essentially a myth, albeit a very convincing one.

Instead, they found a more nuanced picture of technology and sleep.

https://www.sciencedirect.com/science/article/pii/S1087079224000376...

Part 1

Comment by Dr. Krishna Kumari Challa on August 22, 2024 at 10:01am

Mother's gut microbiome during pregnancy shapes baby's brain development, mouse study finds

A study in mice has found that the bacteria Bifidobacterium breve in the mother's gut during pregnancy supports healthy brain development in the fetus. The results are published in the journal Molecular Metabolism.

Researchers have compared the development of the fetal brain in mice whose mothers had no bacteria in their gut, to those whose mothers were given Bifidobacterium breve orally during pregnancy, but had no other bacteria in their gut.

Nutrient transport to the brain increased in fetuses of mothers given Bifidobacterium breve, and beneficial changes were also seen in other cell processes relating to growth.

Bifidobacterium breve is a 'good bacteria' that occurs naturally in our gut, and is available as a supplement in probiotic drinks and tablets.

Obesity or chronic stress can alter the gut microbiome of pregnant women, often resulting in fetal growth abnormalities. The babies of up to 10% of first-time mothers have low birth weight or fetal growth restriction. If a baby hasn't grown properly in the womb, there is an increased risk of conditions like cerebral palsy in infants and anxiety, depression, autism, and schizophrenia in later life.

These results suggest that improving fetal development—specifically fetal brain metabolism—by taking Bifidobacterium breve supplements while pregnant may support the development of a healthy baby.

Previous work by the same team of researchers found that treating pregnant mice with Bifidobacterium breve improves the structure and function of the placenta. This also enables a better supply of glucose and other nutrients to the developing fetus and improves fetal growth.

Although further research is needed to understand how these effects translate to humans, this exciting discovery may pave the way for future clinical studies that explore the critical role of the maternal microbiome in supporting healthy brain development before birth.

Jorge Lopez-Tello et al, Maternal gut Bifidobacterium breve modifies fetal brain metabolism in germ-free mice, Molecular Metabolism (2024). DOI: 10.1016/j.molmet.2024.102004

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Comment by Dr. Krishna Kumari Challa on August 22, 2024 at 9:51am

To initiate the process, hair follicle stem cells (HFSCs), located in the "bulge" of the follicle's upper root sheath, signal to epithelial and mesenchymal cells, sparking growth. This stage takes its time, lasting from two to six years.

The destructive, or catagen, stage that follows is brief but intense, obliterating about 80% of the hair follicle in just a few weeks. The process begins at the follicle base and works its way upwards towards the HFSC niche. The result is a mass of dying and dead cells that need removal to prevent the resulting decay from triggering inflammatory or autoimmune responses.

Normally, this would be the job of phagocytes like macrophages, but few are found in the hair follicle, meaning they must fall to local epithelial cells to keep things tidy.

 Elaine Fuchs, Stem cells tightly regulate dead cell clearance to maintain tissue fitness, Nature (2024). DOI: 10.1038/s41586-024-07855-6. www.nature.com/articles/s41586-024-07855-6

Part 2

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Comment by Dr. Krishna Kumari Challa on August 22, 2024 at 9:49am

Mechanism for removing dead cells identified

Billions of our cells die every day to make way for the growth of new ones. Most of these goners are cleaned up by phagocytes—mobile immune cells that migrate where needed to engulf problematic substances. But some dying or dead cells are consumed by their own neighbors, natural tissue cells with other primary jobs. How these cells sense the dying or dead around them has been largely unknown till now.

Now researchers from The Rockefeller University have shown how a sensor system operates in hair follicles, which have a well-known cycle of birth, decay, and regeneration put into motion by hair follicle stem cells (HFSCs). In a new study published in Nature, they demonstrate that a duo of sensors works in tandem to pick up signals from both dying and living HFSCs, removing debris before tissue damage can occur and ceasing operation before healthy cells are consumed.

The system is seemingly spatially tuned to the presence of corpses, and it only functions when each receptor picks up the signal is attuned to. If one of them disappears, the mechanism stops operating. It's a really beautiful way to keep the area clean without consuming healthy cells.

By diverting their attention towards eating their dying neighbors, HFSCs keep inflammation-generating immune cells away. They also likely benefit from these extra calories, but as soon as the debris is cleared, they must quickly return to their jobs of maintaining the stem cell pool and making the body's hair.

Part 1

Comment by Dr. Krishna Kumari Challa on August 22, 2024 at 9:44am

Study finds 'DNA scavengers' can stop some antibiotic resistance from spreading

For nearly a century, scientists have waged war on antibiotic-resistant microbes. Researchers now found a new way to prevent it—by unleashing "DNA scavengers" in wastewater treatment plants.

They found an enzyme that breaks up strands of antibiotic-resistant DNA floating in wastewater before bacteria can pick them up and take on their antibiotic-resistant properties. 

This could be a powerful, environmentally friendly tool to control the spread of antibiotic resistance in wastewater and help keep antibiotics effective.

But as with any new discovery, there is more work to be done to optimize the technology.

Yang Li et al, Engineered DNA scavenger for mitigating antibiotic resistance proliferation in wastewater treatment, Nature Water (2024). DOI: 10.1038/s44221-024-00289-4

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