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Comment by Dr. Krishna Kumari Challa on November 13, 2023 at 11:39am

Semantic hearing: Future of intelligent hearables

Comment by Dr. Krishna Kumari Challa on November 12, 2023 at 9:11am

 They began synthesizing and testing derivatives with slight changes to the region that binds to ergosterol and cholesterol, while also boosting the kinetics of the ergosterol-removing process to maintain efficacy.

 The researchers tested the most promising derivatives – first with in vitro assays, quickly assessing the efficacy in killing fungi; then moving to cell cultures and eventually live mice, assessing toxicity.

The researchers tested this molecule against over 500 different clinically relevant pathogen species in four different locations. And this molecule completely surprised us by either mimicking or surpassing the efficacy of current clinically available antifungal drugs.

The researchers tested AM-2-19 in human blood and kidney cells to screen for toxicity. They also tested AM-2-19 in mouse models of three common, stubborn fungal infections and saw high efficacy.

Maji, A. et al. Tuning sterol extraction kinetics yields a renal-sparing polyene antifungal. Nature https://doi.org/10.1038/s41586-023-06710-4 (2023).

Part 2

Comment by Dr. Krishna Kumari Challa on November 12, 2023 at 9:07am

New antifungal molecule kills fungi without toxicity in human cells, mice

A new antifungal molecule, devised by tweaking the structure of prominent antifungal drug Amphotericin B, has the potential to harness the drug’s power against fungal infections while doing away with its toxicity, researchers  reported in the journal Nature.

Amphotericin B, a naturally occurring small molecule produced by bacteria, is a drug used as a last resort to treat fungal infections. While AmB excels at killing fungi, it is reserved as a last line of defense because it also is toxic to the human patient – particularly the kidneys.

This work is a demonstration that, by going deep into the fundamental science, you can take a billion-year head start from nature and turn it into something that hopefully is going to have a big impact on human health.

These researchers spent years exploring AmB in hopes of making a derivative that can kill fungi without harm to humans. In previous studies, they developed and leveraged a building block-based approach to molecular synthesis and teamed up with a group specializing in molecular imaging tools called solid-state nuclear magnetic resonance. They  uncovered the mechanism of the drug: AmB kills fungi by acting like a sponge to extract ergosterol from fungal cells.

The researchers also found that that AmB similarly kills human kidney cells by extracting cholesterol, the most common sterol in people. The researchers also resolved the atomic-level structure of AmB sponges when bound to both ergosterol and to cholesterol.

Using this structural information along with functional and computational studies, they achieved a significant breakthrough in understanding how AmB functions as a potent fungicidal drug. This provided the insights to modify AmB and tune its binding properties, reducing its interaction with cholesterol and thereby reducing the toxicity.

Part 1

Comment by Dr. Krishna Kumari Challa on November 12, 2023 at 8:47am

How animals get their stripes and spots

Nature has no shortage of patterns, from spots on leopards to stripes on zebras and hexagons on boxfish. But a full explanation for how these patterns form has remained elusive.

Now engineers  have shown that the same physical process that helps remove dirt from laundry could play a role in how tropical fish get their colorful stripes and spots. Their findings were published Nov. 8 in the journal Science Advances.

Biologists have previously shown that many animals evolved to have coat patterns to camouflage themselves or attract mates. While genes encode pattern information like the color of a leopard’s spots, genetics alone do not explain where exactly the spots will develop, for example.

In 1952, before biologists discovered the double helix structure of DNA, Alan Turing, the mathematician who invented modern computing, proposed a bold theory of how animals got their patterns.

Turing hypothesized that as tissues develop, they produce chemical agents. These agents diffuse through tissue in a process similar to adding milk to coffee. Some of the agents react with each other, forming spots. Others inhibit the spread and reaction of the agents, forming space between spots. Turing’s theory suggested that instead of complex genetic processes, this simple reaction-diffusion model could be enough to explain the basics of biological pattern formation.

Surely Turing’s mechanism can produce patterns, but diffusion doesn’t yield sharp patterns.

Where particles  form sharply defined stripes,  the process known as diffusiophoresis plays a role in nature’s pattern formation.

Diffusiophoresis happens when a molecule moves through liquid in response to changes, such as differences in concentrations, and accelerates the movement of other types of molecules in the same environment. While it may seem like an obscure concept to non-scientists, it’s actually how laundry gets clean.

One recent study showed that rinsing soap-soaked clothes in clean water removes the dirt faster than rinsing soap-soaked clothes in soapy water. This is because when soap diffuses out of the fabric into water with lower soap concentration, the movement of soap molecules draws out the dirt. When the clothes are put in soapy water, the lack of a difference in soap concentration causes the dirt to stay in place.

The movement of molecules during diffusiophoresis, as researchers observed in their simulations, always follows a clear trajectory and gives rise to patterns with sharp outlines. To see if it may play a role in giving animals their vivid patterns, researchers ran a simulation of the purple and black hexagonal pattern seen on the ornate boxfish skin using only the Turing equations. The computer produced a picture of blurry purple dots with a faint black outline. Then the team modified the equations to incorporate diffusiophoresis. The result turned out to be much more similar to the bright and sharp bi-color hexagonal pattern seen on the fish.

The research team’s theory suggests that when chemical agents diffuse through tissue as Turing described, they also drag pigment-producing cells with them through diffusiophoresis—just like soap pulls dirt out of laundry. These pigment cells form spots and stripes with a much sharper outline.

 Benjamin Alessio et al, Diffusiophoresis-Enhanced Turing Patterns, Science Advances (2023). DOI: 10.1126/sciadv.adj2457. www.science.org/doi/10.1126/sciadv.adj2457

Comment by Dr. Krishna Kumari Challa on November 11, 2023 at 9:53am

World's First Entire Eye Transplant

A team of surgeons in New York has performed the world's first transplant of an entire eye in a procedure widely hailed as a medical breakthrough, although it isn't yet known whether the man will ever see through the donated eye. The groundbreaking surgery involved removing part of the face and the whole left eye – including its blood supply and optic nerve – of a donor and grafting them onto a lineworker from Arkansas who survived a 7,200-volt electric shock in June 2021.

Aaron James, 46, suffered extensive injuries including the loss of his left eye, his dominant left arm above the elbow, his nose and lips, front teeth, left cheek area and chin.
He was referred to NYU Langone Health, a leading medical center for facial transplants, which carried out the procedure on May 27.

Transplanting an entire eye has long been a holy grail of medical science, and though researchers have had some success in animals – where they have restored partial vision – it's never before been performed in a living person.
The transplanted left eye appears very healthy, said retinal ophthalmologist.
It has a good blood supply, is maintaining its pressure, and is generating an electrical signal, though James is not yet able to see. But the doctors have a lot of hope.
The doctors used bone marrow-derived adult stem cells to promote nerve repair.
Source: News Agencies

Comment by Dr. Krishna Kumari Challa on November 11, 2023 at 9:29am

Why do massive stars make up such a high proportion of runaway stars? There are two competing theories that attempt to explain runaway stars, and both involve massive stars. One is the dynamical ejection scenario (DES), and the other is the binary supernova scenario (BSS).

OB stars often form in binary pairs. In the BSS, one star explodes as a supernova, and the explosion kicks the other star. If the situation is right, the surviving star is given enough energy in the right direction that it can escape from its bond with its partner, which is now a neutron star or a black hole. It can also escape the gravitational pull of the Milky Way. If that happens, it begins its long journey into intergalactic space.

In the DES, there's no dramatic supernova explosion. Instead, a star in a compact, densely packed region experiences gravitational interactions with other stars. Encounters between binary and single stars can produce runaways, and so can encounters between two binary pairs. The OB associations where O-type and B-type stars tend to form are the types of dense environments that can trigger runaway stars. Since most of these stars are massive, most of the runaway stars are, too.

Scientists have been wondering about the two scenarios and debating them for decades. Both scenarios can produce stars with enough velocity to escape the galaxy. In studying their sample of 175 runaway stars, the researchers found that their data favors one explanation over the other.

The higher percentages and higher velocities found for O-type compared to Be-type runaways underline that the dynamical ejection scenario is more likely than the binary supernova scenario.

The percentages of spectral types represented in runaway stars help explain their conclusion. 25% of the O-type stars in their sample are runaways versus 5% of the Be-type. Other studies have come up with different numbers, but as the researchers point out, there is agreement in the sense that the percentage of runaway O stars is significantly higher than for B or Be stars.

Previous research shows that O-type runaway stars have higher velocities than B and Be-type stars. Previous research also shows that dynamical ejection often results in faster, more massive runaways than the binary supernova scenario. 

M. Carretero-Castrillo et al, Galactic runaway O and Be stars found using Gaia DR3, Astronomy & Astrophysics (2023). DOI: 10.1051/0004-6361/202346613. On arXiv: DOI: 10.48550/arxiv.2311.01827

Part 2

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Comment by Dr. Krishna Kumari Challa on November 11, 2023 at 9:26am

Astronomers find dozens of massive stars fleeing the Milky Way

The Milky Way can't hold onto all of its stars. Some of them get ejected into intergalactic space and spend their lives on an uncertain journey. A team of astronomers took a closer look at the most massive of these runaway stars to see what they could find out how they get ejected.

When astronomers observe a field of stars in the Milky Way, one of the things they measure is the velocity distribution. The overall velocity distribution of the stellar population reflects the rotation of the galaxy. And when a star isn't harmonized with the galaxy's rotation, it catches astronomers' attention.

A team of astronomers working with two catalogues of massive stars found a whole bunch of stars moving differently than the galaxy. They're runaway stars that are on their way out of the galaxy.

Nobody knows how many runaway stars are on their way out of our galaxy, but astronomers keep finding more of them. Some estimates say there are 10 million runaway stars fleeing the Milky Way, but we don't know for sure. It may depend on the mechanism that drives them away, and that's something astrophysicists don't fully understand. A new study aims to shed some light on the runaway star phenomenon by looking specifically at massive stars.

A relevant fraction of massive stars are runaway stars. These stars move with a significant peculiar velocity with respect to their environment.

Massive early-type OB stars are the most luminous stars in the Milky Way. OB stars are not only massive and young, they're extremely hot. They form in loosely organized groups with one another called OB associations. Because they're young and hot, they don't last long. They're important in astronomy because they're so massive and energetic and because many of them explode as supernovae. That's why there are specific catalogues dedicated to them.

Part 1

Comment by Dr. Krishna Kumari Challa on November 11, 2023 at 9:19am

Earth's Moon: Why One Side Always Faces Us

Comment by Dr. Krishna Kumari Challa on November 11, 2023 at 9:05am

Even more exciting is how closely the new study's results in mice appear to be reflected in human cells.

With a blood test, doctors can identify people who are at high-risk of developing type 1 diabetes months in advance of the death of their beta cells.

That may be a perfect timeframe for a treatment based on pharmacological inhibition of Atf6 or induction of LIF and other secreted proteins. If we can get there in time to protect these cells with transient senescence, the onset of diabetes might be prevented.

Hugo Lee et al, Stress-induced β cell early senescence confers protection against type 1 diabetes, Cell Metabolism (2023). DOI: 10.1016/j.cmet.2023.10.014

Part 2

Comment by Dr. Krishna Kumari Challa on November 11, 2023 at 9:03am

Relieving stress in insulin-producing cells protects against type 1 diabetes

Removing a gene that manages stress within insulin-producing beta cells draws helpful attention from the immune system, protecting mice predisposed to type 1 diabetes from developing the disease, a new  study shows.

The study also found that changes discovered in the modified mouse beta cells are also present in human beta cells that manage to survive the widespread beta-cell death that characterizes type 1 diabetes.

This gives the researchers hope that their findings, published in the journal Cell Metabolism, may point to a potential new treatment that could be administered very early in the development of diabetes. 

When we eat, our beta cells produce about 1 million molecules of insulin every minute to help maintain normal blood glucose levels. That is a big and stressful job, especially for a part of these beta cells called the endoplasmic reticulum.

The endoplasmic reticulum is like the cell's warehouse staff. It folds the insulin protein molecules that a beta cell produces, packing them for shipping to other parts of the body. If something goes wrong with the protein folding process, the shipping process backs up or even stops, stressing the endoplasmic reticulum. A stress-response gene called Atf6 perks up when a cell is struggling with unfolded proteins. But if Atf6 can't resolve the protein-folding problem, prolonged stress will eventually kill the cell.

Scientists bred a line of diabetes-predisposed mice without the Atf6 gene in their beta cells. Instead of meeting their typical fate, those mice were protected from diabetes. Analysis of the genes expressed by their beta cells suggested the cells entered a state called senescence far ahead of schedule.

Senescence is a period of the cell's life cycle in which it stops dividing and halts other normal cellular business. Senescing cells can cause problems for neighboring cells by releasing inflammatory messaging molecules that trigger an immune system response.

When researchers removed—knocked-out—the Atf6 gene in the beta cells in the pancreas of their mouse model of type 1 diabetes, and they did not become diabetic. Instead of dying off, these cells unexpectedly appear to go into an early senescence state that initiated a beneficial immune response and helped the cells survive an autoimmune attack.

DNA damage, stress and aging can kick off senescence, which can draw an immune system response that cleans up the senescent cells. If the immune system fails to clear these cells, they accumulate and cause chronic inflammation and disease.

The beta cells without Atf6 exhibit transient senescence and start releasing this group of proteins, including leukemia inhibitory factor, or LIF, that recruits protective immune cells called M2 macrophages.

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