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Comment by Dr. Krishna Kumari Challa on December 13, 2024 at 10:06am

As wildfires intensify, prolonged exposure to pollution linked to premature death

Researchers have found evidence that living in areas prone to wildfire smoke may negatively impact an individual's life expectancy.

In many parts of the contiguous United States, wildfires are rapidly growing more intense, endangering the humans and wildlife that live in the region. Even once fires are doused, serious health risks remain because of the many adverse effects caused by wildfire smoke and the airborne pollution that the blaze releases into the atmosphere.

Now, scientists  have found that not only is wildfire smoke linked to a shortened lifespan, it also greatly diminishes the positive health impacts of local greenspaces, like forests or parks.

When considering the environment's effect on human life expectancy, we have to account for all kinds of factors. Forests, for example, provide essential ecosystem services to mitigate the impact of wildfire smoke because they can purify the air.

Generally, greenspaces benefit human health by helping to regulate the local ecosystem and climate through capturing carbon dioxide, oxygen production and air filtration as well as by providing open spaces to foster social and community connection. It's why higher levels of greenspaces are usually correlated with higher life expectancies. But because these lush areas can essentially act as fuel for wildfires, their presence is also tightly correlated with higher wildfire smoke emissions.

 Due to its high toxicity, human exposure to this smoke has been known to cause respiratory issues, cardiovascular disease, and an increase in the risk of dementia and hospitalization.

The research was presented this week at the annual meeting of the American Geophysical Union (AGU 2024).

Their findings concluded that for every additional day of smoke exposure, a person's life expectancy could be expected to decrease by about 0.02 years—or about one week.

Conversely, living in a green neighborhood can be beneficial, as even a 1% increase in these spaces can lead to a slight life expectancy increase. While wildfire smoke can negate the benefits of greenspace, the team's results suggest that sociodemographic factors such as income, population density, age and race also significantly impact future life expectancies.

Impacts of Wildfire Smoke PM2.5, Greenspace and Terrain Ruggedness on Life Expectancy in the Contiguous United States. agu.confex.com/agu/agu24/meeti … pp.cgi/Paper/1620628

Comment by Dr. Krishna Kumari Challa on December 13, 2024 at 9:20am

Neanderthal-human interbreeding lasted 7,000 years, new study reveals

A new analysis of DNA from ancient modern humans (Homo sapiens) in Europe and Asia has determined, more precisely than ever, the time period during which Neanderthals interbred with modern humans, starting about 50,500 years ago and lasting about 7,000 years—until Neanderthals began to disappear.

That interbreeding left Eurasians with many genes inherited from our Neanderthal ancestors, which in total make up between 1% and 2% of our genomes today.

The genome-based estimate is consistent with archaeological evidence that modern humans and Neanderthals lived side-by-side in Eurasia for between 6,000 and 7,000 years.

The analysis, which involved present-day human genomes as well as 58 ancient genomes sequenced from DNA found in modern human bones from around Eurasia, found an average date for Neanderthal-Homo sapiens interbreeding of about 47,000 years ago. Previous estimates for the time of interbreeding ranged from 54,000 to 41,000 years ago.

The new dates also imply that the initial migration of modern humans from Africa into Eurasia was basically over by 43,500 years ago.

The longer duration of gene flow may help explain, for example, why East Asians have about 20% more Neanderthal genes than Europeans and West Asians. If modern humans moved eastward about 47,000 years ago, as archaeological sites suggest, they would already have had intermixed Neanderthal genes.

The period of mixing was quite complex and may have taken a long time. Different groups could have separated during the 6,000- to 7,000-year period and some groups may have continued mixing for a longer period of time. But a single shared period of gene flow fits the data best.

 Leonardo N. M. Iasi et al, Neandertal ancestry through time: Insights from genomes of ancient and present-day humans, Science (2024). DOI: 10.1126/science.adq3010. www.science.org/doi/10.1126/science.adq3010

Arev Sümer, Earliest modern human genomes constrain timing of Neanderthal admixture, Nature (2024). DOI: 10.1038/s41586-024-08420-x. www.nature.com/articles/s41586-024-08420-x

Comment by Dr. Krishna Kumari Challa on December 12, 2024 at 11:46am

Car height, not just speed, matters when pedestrians are hit

Watch out for tall, fast-moving cars. The height of a vehicle, not only its speed, determines its potential danger to a pedestrian, new research shows.

Multiple factors—in this case speed and vehicle height—converge to create negative outcomes on the road.

Measurements of the vehicles involved were used to examine the moderating effect of hood height.

The report involved an analysis of 202 crashes involving people ages 16 and older in cities across the United States. The accidents occurred between 2015 and 2022.

In general, higher vehicle front ends increased the likelihood of both moderate and serious pedestrian injuries, data showed. At 27 mph, the average speed of the crashes, a median-height car had a 60% chance of causing moderate injuries to a pedestrian and a 30% chance of causing serious injuries.

Risks rose along with hood height, however: A median-height pickup—with a front end 13 inches higher than that of a median car—had an 83% chance of causing moderate injuries and a 62% chance of causing serious injuries.

This tracks with earlier IIHS research that found that vehicles with taller front ends are more likely to kill people when they hit them. Compared to smaller cars, large vehicles  such as sports utility vehicles or SUVs, are more likely to harm internal organs.

The increased risk and severity of injury from these vehicles is related to their tendency to inflict more severe injuries higher on the body: to the head, torso, and hip," the study authors explained.

In addition to impact, car size influences how well a driver can see pedestrians.

"Taller vehicles may be more likely to be involved in certain pedestrian crash configurations than shorter ones, potentially due to limitations in driver visibility," the authors said.

In cases where the pedestrian is at the vehicle's front corner, obstructed driver sight lines could make a collision more likely and may reduce pre-impact braking behavior, leading to greater injuries.

What's more, the findings reinforce the importance of redesigning vehicles and roadways to reduce speed in congested areas, the study authors said.

It will take a combination of actions from different corners of the transportation world to improve pedestrian safety.

Monfort, Samuel S., Mueller, Becky C. A modern injury risk curve for pedestrian injury in the United States: the combined effects of impact speed and vehicle front-end height. Insurance Institute for Highway Safety. www.iihs.org/topics/bibliography/ref/2322

Comment by Dr. Krishna Kumari Challa on December 12, 2024 at 11:40am

Tumors grow larger in female fruit flies than males. Here's what that could mean for humans

A study by  researchers has uncovered new insights into how biological sex differences can influence tumor growth. The findings, published in Science Advances, could lead to a better understanding of cancer development and potentially boost efforts to identify a method to stop tumors in their tracks.

The study found that tumors in female fruit flies grew 2.5 times larger than tumors in male fruit flies over the same time period.

Fruit flies are an often used biological research model due to their genetic similarity to humans. In this study, researchers found that the female fruit flies had a stronger innate immune response to the tumors than the males. This response accelerated the growth of tumors by triggering a signaling pathway between cells.

The question now is, do we see this same difference in humans?

Genetically, many of these signaling pathways are well preserved between mammals and insects so this finding is highly relevant to our knowledge of cancer development.

The study found that once a tumor formed, female fruit flies' immune cells (hemocytes) produced more of an inflammatory response signal than their male counterparts. This signal protein, called Eiger, is comparable to a similar protein in mammals, which also regulates immune system and inflammatory responses.

While inflammation is often effective at combating outside invaders, too much inflammation can create an environment that allows tumors to thrive. "We found that in female fruit flies, their stronger immune response caused a downstream cascade of events, culminating in the release of insulin-like peptides which allowed the tumors to accelerate their growth.

The next step is to determine if the bias in tumor growth is regulated by hormones or sex chromosomes, work that may shed further light on why and how tumors grow.

 Xianfeng Wang et al, Sex-dimorphic tumor growth is regulated by tumor microenvironmental and systemic signals, Science Advances (2024). DOI: 10.1126/sciadv.ads4229

Comment by Dr. Krishna Kumari Challa on December 12, 2024 at 11:35am

substituted the gene encoding a piece of tetanus toxin for the gene fragment encoding a component that normally gets displayed in this giant treelike protein's foliage. Now it's this fragment—a harmless chunk of a highly toxic bacterial protein—that's waving in the breeze."

Would the mice's immune systems "see" it and develop a specific antibody response to it?
And it did!
The mice swabbed with bioengineered S. epidermidis, but not the others, developed extremely high levels of antibodies targeting tetanus toxin. When the researchers then injected the mice with lethal doses of tetanus toxin, the mice given natural S. epidermidis all succumbed; the mice that received the modified version remained symptom-free.

A similar experiment, in which the researchers snapped in the gene for diphtheria toxin instead of the one for tetanus toxin into the Aap "cassette player," likewise induced massive antibody concentrations targeting the diphtheria toxin.

The scientists eventually found they could still get life-saving antibody responses in mice after only two or three applications.

They also showed, by colonizing very young mice with S. epidermidis, that the bacteria's prior presence on these mice's skin (as is typical in humans but not mice) didn't interfere with the experimental treatment's ability to spur a potent antibody response. This implies that their species' virtually 100% skin colonization by S. epidermidis should pose no problem to the construct's use in people.
In a change of tactics, the researchers generated the tetanus-toxin fragment in a bioreactor, then chemically stapled it to Aap so it dotted S. epidermidis's surface. To their surprise, this turned out to generate a surprisingly powerful antibody response.
Topical application of this bug generated enough antibodies to protect mice from six times the lethal dose of tetanus toxin.
it works in mice. Now they are trying to experiment with monkeys.
If things go well, they expect to see this vaccination approach enter clinical trials within two or three years.
The researchers think this will work for viruses, bacteria, fungi and one-celled parasites. Most vaccines have ingredients that stimulate an inflammatory response and make you feel a little sick. These bugs don't do that. Scientists expect that you wouldn't experience any inflammation at all.

Discovery and engineering of the antibody response to a prominent skin commensal, Nature (2024). DOI: 10.1038/s41586-024-08489-4 , www.nature.com/articles/s41586-024-08489-4

Skin autonomous antibody production regulates host-microbiota interactions, Nature (2024). DOI: 10.1038/s41586-024-08376-y , www.nature.com/articles/s41586-024-08376-y

Part 4

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Comment by Dr. Krishna Kumari Challa on December 12, 2024 at 10:58am

Step by step, the research team turned S. epidermidis into a living, plug-and-play vaccine that can be applied topically. They learned that the part of S. epidermidis most responsible for tripping off a powerful immune response is a protein called Aap. This great, treelike structure, five times the size of an average protein, protrudes from the bacterial cell wall.

They think it might expose some of its outermost chunks to sentinel cells of the immune system that periodically crawl through the skin, sample hair follicles, snatch samples of whatever is flapping in Aap's "foliage," and spirit them back inside to show to other immune cells responsible for cooking up an appropriate antibody response aiming at that item.
This companion study identifies the sentinel immune cells, called Langerhans cells, that alert the rest of the immune system to the presence of S. epidermidis on the skin.

Aap induces a jump in not only blood-borne antibodies known to immunologists as IgG, but also other antibodies, called IgA, that home in on the mucosal linings of our nostrils and lungs.
Having identified Aap as the antibodies' main target, the scientists looked for a way to put it to work.

Respiratory pathogens responsible for the common cold, flu and COVID-19 tend to get inside our bodies through our nostrils. Normal vaccines can't prevent this. They go to work only once the pathogen gets into the blood. It would be much better to stop it from getting in in the first place.

Part 3

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Discovery and engineering of the antibody response to a prominent skin commensal, Nature (2024). DOI: 10.1038/s41586-024-08489-4 , www.nature.com/articles/s41586-024-08489-4

Skin autonomous antibody production regulates host-microbiota interactions, Nature (2024). DOI: 10.1038/s41586-024-08376-y , www.nature.com/articles/s41586-024-08376-y

Comment by Dr. Krishna Kumari Challa on December 12, 2024 at 10:56am

Researchers conducted experiments to know this. 

The mice's antibody response to S. epidermidis was "a shocker".Those antibodies' levels increased slowly, then some more—and then even more." At six weeks, they'd reached a higher concentration than one would expect from a regular vaccination—and they stayed at those levels.

It's as if the mice had been vaccinated. Their antibody response was just as strong and specific as if it had been reacting to a pathogen.

The same thing appears to be occurring naturally in humans. The researchers got blood from human donors and found that their circulating levels of antibodies directed at S. epidermidis were as high as anything we get routinely vaccinated against.

This is intriguing. Our ferocious immune response to these commensal bacteria loitering on the far side of that all-important anti-microbial barrier we call our skin seems to have no purpose.

It could boil down to a line scrawled by early-20th-century poet Robert Frost: "Good fences make good neighbors." Most people have thought that fence was the skin. But it's far from perfect. Without help from the immune system, it would be breached very quickly.

The best fence is those antibodies. They're the immune system's way of protecting us from the inevitable cuts, scrapes, nicks and scratches we accumulate in our daily existence.

While the antibody response to an infectious pathogen begins only after the pathogen invades the body, the response to S. epidermidis happens preemptively, before there's any problem. That way, the immune system can respond if necessary—say, when there's a skin break and the normally harmless bug climbs in and tries to thumb a ride through our bloodstream.

Part 2

Comment by Dr. Krishna Kumari Challa on December 12, 2024 at 10:48am

Scientists transform ubiquitous skin bacterium into a topical vaccine

Imagine a world in which a vaccine is a cream you rub onto your skin instead of a needle a health care worker pushes into one of your muscles. Even better, it's entirely pain-free and not followed by fever, swelling, redness or a sore arm. No standing in a long line to get it. Plus, it's cheap.

Thanks to Stanford University researchers' domestication of a bacterial species that hangs out on the skin of close to everyone on Earth, that vision could become a reality.

Staphylococcus epidermidis is a generally harmless skin-colonizing bacterial species. These bugs reside on every hair follicle of virtually every person on the planet.

In recent years, researchers have discovered that the immune system mounts a much more aggressive response against S. epidermidis than anyone expected.

In a study published Dec. 11 in Nature, they zeroed in on a key aspect of the immune response—the production of antibodies. These specialized proteins can stick to specific biochemical features of invading microbes, often preventing them from getting inside of cells or traveling unmolested through the bloodstream to places they should not go.

Individual antibodies are extremely picky about what they stick to. Each antibody molecule typically targets a particular biochemical feature belonging to a single microbial species or strain.

But  would the immune system of a mouse, whose skin isn't normally colonized by S. epidermidis, mount an antibody response to that microorganism if it were to turn up there?

Part 1

Comment by Dr. Krishna Kumari Challa on December 12, 2024 at 10:30am

The researchers found that Nsp13 promotes robust human cell death activation; mutating the RHIM in Nsp13 therefore enhanced cell survival.

Nsp13 was found to work in synergy with host RHIM proteins called ZBP1 and RIPK3 to promote cell death activation, which might possibly be contributing to the respiratory damage and disease progression seen in COVID-19. The researchers also found that RNA segments in the Z conformation (Z-RNA) in the virus's genome were driving the Nsp13-mediated cell death activation.

Since bats express host RHIM proteins similar to humans, they can serve as the source for RHIM mimics to mutate and evolve, the study suggests. Interestingly, bats show mild clinical symptoms and tissue damage compared to humans despite harboring viruses with RHIM mimics. To understand this conundrum, the authors tested whether and how Nsp13-RHIM regulates bat cell death.
Nsp13 could also activate cell death in bat cells like in human cells. Researchers found the nature of bat cell death to be preferably non-inflammatory and Nsp13-RHIM independent, possibly just enough to clear the viral replication niche but not cause severe inflammation.
These insights on how cell death is regulated differently in bats and humans provide some clues to why some pathogenic viruses are tolerated in bats but cause more severe diseases in humans.
Understanding fundamental differences in cellular responses to viruses in bats and humans is critical to guide pandemic preparedness for such zoonotic virus infections.

Sanchita Mishra et al, Bat RNA viruses employ viral RHIMs orchestrating species-specific cell death programs linked to Z-RNA sensing and ZBP1-RIPK3 signaling, iScience (2024). DOI: 10.1016/j.isci.2024.111444

Part 2

Comment by Dr. Krishna Kumari Challa on December 12, 2024 at 10:28am

How bat-origin pathogenic viruses manipulate human cell death and inflammation

A study by researchers at the Indian Institute of Science (IISc) offers insights into cell death regulation by viruses like SARS-CoV-2, and how bats and humans respond differently to tricks that such viruses use to manipulate the host's defense.

The paper is published in the journal iScience.

Zoonotic virus infections pose a serious concern to human health. Bats and birds are among the main reservoirs for several pathogenic viruses that show zoonotic transmission potential. When they reach the human host, these viruses can cause either mild or severe disease.

Host cell death after viral infections is a defense strategy to limit viral spread and mount protective immune responses. However, uncontrolled cell death response can drive excessive tissue damage, leading to disease severity. Scientists have strived to pinpoint how zoonotic viruses that originate from bats manipulate the human host to cause excessive cell death and tissue damage.

The study has uncovered how such viruses mimic components of the host's cell death machinery. They zeroed in on protein motifs called RIP homotypic interaction motifs (RHIMs) that regulate host cell death and inflammation.

Several viruses that originate in bats show mimics of these RHIMs. SARS-CoV-2, for example, contains Nsp13—an enzyme protein critical for virus replication—that has an RHIM similar to those found in humans.

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