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Comment by Dr. Krishna Kumari Challa on January 29, 2023 at 3:11pm

Robot clears foreign body from stomach

Comment by Dr. Krishna Kumari Challa on January 28, 2023 at 11:06am

Harvesting energy from moving trains

Researchers  want to harness the energy created by moving trains and transform that energy into usable electricity. And they are conducting various experiments to do the same. 

After several years of design review,  researchers created a new kind of tie that replaces the conventional wooden variety and is equipped to generate power. Their high-tech tie, placed underneath the rail, is topped with a heavy metal bar mounted on a spring. As the wheels of the train pass over the rail, the train’s weight pushes down on that bar, triggering a series of gears. Those gears rotate a generator, creating electricity, which can then be stored in a battery.

As trains passed over the rail, researchers got a clearer picture of how much power it might produce and how that power might be put into use. For every wheel of the train that goes by, they are harvesting 15 to 20 watts of power.

 A long train with maybe 200 railcars, that’s 800 wheels, makes 1.6 kilowatts. Once that energy is stored,  they are able to use it to make the tracks more intelligent by embedding sensors in them.

Deploying their energy harvesting system could mean greater expansion of the vital sensor systems that keep railways safe.

Yu Pan et al, A half-wave electromagnetic energy-harvesting tie towards safe and intelligent rail transportation, Applied Energy (2022). DOI: 10.1016/j.apenergy.2022.118844

Comment by Dr. Krishna Kumari Challa on January 28, 2023 at 8:59am

One of the causes of aggressive liver cancer discovered: A 'molecular staple' that helps repair broken DNA

Error-correcting mechanisms are very important for cells, because with all the cellular activity constantly going on, malfunctions arise all the time. But when it comes to killing cancer cells, it is in the cells' best interest to induce errors. Radiotherapy and chemotherapy can cause cellular defects by breaking the DNA of the cells. However, some tumor cells have an exceptionally efficient DNA repair machinery that allows them to evade cancer treatment. Researchers have now revealed the workings of one of these extraordinary repair systems: a molecular staple that has been shown in action for the first time using a new nanotechnology technique.

A few years ago, scientists discovered that about half of patients with hepatocellular carcinoma (the most common type of liver cancer) produce an RNA molecule called NIHCOLE, which is found mainly in the most aggressive tumors and is associated with a poor prognosis.

NIHCOLE is not a protein synthesized by a gene, but an RNA molecule. It is part of what biologists dubbed junk DNA two decades ago when the human genome was being sequenced. At the time, they mistakenly believed that this DNA was useless.

Cancer researchers concluded that NIHCOLE is very effective at helping repair broken DNA, which is why radiotherapy is less effective in tumors where it is present. By eliminating NIHCOLE, cancer cells treated with radiotherapy die more easily. However, the molecular mechanism by which NIHCOLE facilitates the repair of DNA breaks was not known. The paper just published in Cell Reports explains this: NIHCOLE forms a bridge that binds the broken DNA fragments together. It interacts simultaneously with proteins that recognize the two ends of a fragmented DNA, as if stapling them together. Only a small piece of NIHCOLE is required for it to act as a molecular staple.

Understanding this mechanism may help in the development of strategies to combat liver cancers with the worst prognosis. 

Sara De Bragança et al, APLF and long non-coding RNA NIHCOLE promote stable DNA synapsis in non-homologous end joining, Cell Reports (2022). DOI: 10.1016/j.celrep.2022.111917

Comment by Dr. Krishna Kumari Challa on January 27, 2023 at 11:49am

Liquid-metal robots can melt and re-form

Researchers have created a material that can move, soften and re-harden under the influence of magnetic fields. To demonstrate the material’s promise, researchers showed how it could be manipulated to pass through barriers, extract an object from an artificial stomach, and move a tiny light bulb into place and then melt into the solder required to make it work.

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How much greenhouse gas do tropical soils emit?

Nitrogen changes form as it cycles between air, soil, and life. Soils, for example, emit nitrogen either as inert dinitrogen (N2), which dominates our atmosphere, or as nitric oxide (NO) or nitrous oxide (N2O), the greenhouse gases that warm it.

Comment by Dr. Krishna Kumari Challa on January 27, 2023 at 11:41am

E. coli: Lab discovers evidence of multicellularity in single cell organism

Researchers have uncovered something new in one of the most studied organisms on Earth, and their discoveries could impact the treatment and prevention of devastating bacterial diseases.

Escherichia coli, or E. coli, gets a bad rap, and for good reason. This diverse group of bacteria that live in our intestines are mostly harmless and play an important role in sustaining a healthy digestive system. But some E. coli are among the most virulent disease-causing micro-organisms.

Pathogenic E. coli takes a deadly, costly toll on humanity, costing billions of dollars to treat and killing millions of people worldwide each year. It's responsible for diarrheal diseases, peritonitis, colitis, respiratory illness and pneumonia, and other illnesses, and is the main cause in 80% of urinary tract infections, which are the most common bacterial infection.

Consequently, researchers have been keen to learn everything they can about E. coli for the past century or so. They have probed it from every angle, synthesized it, scrutinized it to the extent that, many people believe, there isn't much else to learn.

But some researchers have taken a closer look at E. coli and their research is yielding novel insights, and raising new questions, about this prevalent unicellular organism. For one thing, it appears that E. coli may not always be unicellular. The research team explained it all in their study, "Evidence of a possible multicellular life cycle in Escherichia coli," published in the journal iScience.

In nature, bacteria live in communities called biofilms, which are clusters of microbes encased in a self-made, self-sustaining slime matrix, and attached to many kinds of wet surfaces. They're everywhere around us and inside of us. Common, everyday examples of biofilms include dental plaque and pond scum. They can grow on plant and animal tissue, like the inside of our digestive tract, and cause serious infections. On top of that, the bacteria living inside a biofilm's protective matrix are less likely to be affected by antibiotics. Biofilms are clinically important, particularly in relation to infection.

Approximately 80% of all bacterial infections have a biofilm component. "And almost any bacteria that's ever been studied can make them."

Researchers now 

discovered something new—a multicellular self-assembly process in E. coli. Researchers observed unattached, single-celled organisms combining into four-cell rosettes, a natural multicellular formation thought to be uncommon in bacteria.

Rosettes are rather significant in higher organisms, like mammals, because they initiate developmental processes like embryogenesis.

They observed E. coli rosettes grow into constant-width chains, which continue growing for 10 generations before attaching to a surface and creating a biofilm. They saw and recorded the bacterial processes that had never been seen or recorded before.

Devina Puri et al, Evidence of a possible multicellular life cycle in Escherichia coli, iScience (2022). DOI: 10.1016/j.isci.2022.105795

Comment by Dr. Krishna Kumari Challa on January 27, 2023 at 11:18am

New spray fights infections and antibiotic resistance

Antibiotic resistance as one of the top ten threats to global health. There is therefore a great need for new solutions to tackle resistant bacteria and reduce the use of antibiotics. A group of researchers at Chalmers University of Technology in Sweden are now presenting a new spray that can kill even antibiotic-resistant bacteria, and that can be used for wound care and directly on implants and other medical devices.

This innovation  can have a dual impact in the fight against antibiotic resistance. The material has been shown to be effective against many different types of bacteria, including those that are resistant to antibiotics, such as Methicillin-resistant Staphylococcus aureus (MRSA), while also having the potential to prevent infections and thus reduce the need for antibiotics.

The material consists of small hydrogel particles equipped with a type of peptide that effectively kills and binds bacteria. Attaching the peptides to the particles provides a protective environment and increases the stability of the peptides. This allows them to work together with body fluids such as blood, which otherwise inactivates the peptides, making them difficult to use in health care. In previous studies, the researchers showed how the peptides can be used for  wound care materials such as wound dressings.

They have now published two new studies in which the bactericidal material is used in the form of a wound spray and as a coating on medical devices that are introduced into our bodies. This new step in the research means that the innovation can be used in more ways and be of even greater benefit in health care.

Edvin Blomstrand et al, Cross-linked lyotropic liquid crystal particles functionalized with antimicrobial peptides, International Journal of Pharmaceutics (2022). DOI: 10.1016/j.ijpharm.2022.122215

Annija Stepulane et al, Multifunctional Surface Modification of PDMS for Antibacterial Contact Killing and Drug-Delivery of Polar, Nonpolar, and Amphiphilic Drugs, ACS Applied Bio Materials (2022). DOI: 10.1021/acsabm.2c00705

Comment by Dr. Krishna Kumari Challa on January 27, 2023 at 10:08am

Experimental vaccine for deadly Marbug virus guards against infection with just a single dose

An experimental vaccine for Marburg virus—a deadly cousin of the infectious agent that causes Ebola—can protect large animals from severe infections for up to a year with a single shot, scientists have found in a new study.

Developed by the National Institute of Allergy and Infectious Diseases, along with collaborators at other institutions, the vaccine produces durable protection, a factor that underlines its promise for clinical translation and pandemic preparedness. So far its safety profile suggests that investigators may be on the brink of a vaccine that, in the not-too-distant future, may help control a Marburg virus outbreak.

The pathogen is extraordinarily virulent, one of the most lethal in the world—an infectious agent so dangerous that it's on lists of viruses with potential to be exploited in devastating acts of bioterrorism. It causes a severe infection that once was known as Marburg hemorrhagic fever, but now is widely referred to as Marburg virus disease. The pathogen belongs to the Filovirdae family, the same viral family as Ebolavirus.

As with Ebolavirus, it's posited that the Marburg infectious agent jumped the species barrier from bats to people and nonhuman primates. While bats live without harm from the pathogen, scientists at the World Health Organization estimate human mortality at 90%.

The authors of the research paper report that in nonhuman primates
 a single shot of the vaccine generated protective immunity within seven days of vaccination. Additionally—and perhaps more important—the investigational vaccine protected nonhuman primates when they were challenged with exposure to the lethal Marburg virus.

 Ruth Hunegnaw et al, A single-shot ChAd3-MARV vaccine confers rapid and durable protection against Marburg virus in nonhuman primates, Science Translational Medicine (2022). DOI: 10.1126/scitranslmed.abq6364

Comment by Dr. Krishna Kumari Challa on January 26, 2023 at 12:18pm

Drug pollution: What happens to drugs after they leave your body?

Swallowing a pill only seems to make it disappear. In reality, the drug eventually leaves your body and flows into waterways, where it can undergo further chemical transformations. And these downstream products aren't dead in thewater.

Many pharmaceuticals, for example, are designated as contaminants of emerging concern, or CECs, because they alter hormone levels or otherwise harm wildlife. Some downstream products formed during drug breakdown are even more harmful than their parent molecule. It's critical, then, to chart out the chemical course of drugs to assess risk, but this is a daunting task because it depends on myriad hard-to-predict reaction patterns that are difficult to observe.

In a new study published in Water Resources Research, researchers devise a new method to chart these reaction possibilities. The newly proposed method is based on a multimodel global sensitivity analysis. This balances model fit and mathematical complexity: It generates a well-fitting model by simplifying it.

The researchers estimated how the arthritis drug diclofenac breaks down upon entering groundwater. First, using existing chemical transformation data, they built a comprehensive model of breakdown that included the gamut of possible chemical reactions. However, the estimates from this model were highly uncertain.

To adjust the model to better fit their data, the researchers quantified the relative importance of each possible chemical process and removed the least relevant ones.

This led to three simplified yet plausible models of drug breakdown. They ranked these models on the basis of their fit with the data and showed that a simplified model outperformed the most complex one.

The method yielded a flexible and accurate model. The team says their new method is especially useful when data are limited. Applying it to other drugs, they say, could reveal the full toll that pharmaceutical pollution takes on the planet.

More information: Laura Ceresa et al, On Multi‐Model Assessment of Complex Degradation Paths: The Fate of Diclofenac and Its Transformation Products, Water Resources Research (2023). DOI: 10.1029/2022WR033183

Comment by Dr. Krishna Kumari Challa on January 26, 2023 at 12:12pm

Scientists discover evolutionary secret behind different animal life cycles

Why do some animals become larvae before growing into adults while some embryos directly  develop into miniature version of the adult?

In a new paper, scientists prove that the timing of activation of essential genes involved in embryogenesis—the transformation of a fertilized egg into an organism—correlates with the presence or absence of a larval stage and with whether the larva feeds from their surroundings or relies on nourishment the mother deposited in the egg.

It's impressive to see how evolution shaped the way animal embryos 'tell the time' to activate important groups of genes earlier or later in development. Suppose a larval stage is no longer essential for your survival. In that case, it might be evolutionarily advantageous to, for example, activate the genes to form the trunk earlier and develop straight into an adult instead.

This new study used state-of-the-art approaches to decode the genetic information, activity, and regulation in three species of marine invertebrate worms called annelids. They combined these with public datasets from other species in a large-scale study involving more than 600 datasets of more than 60 species separated by more than 500 million years of evolution.

Only by combining experimental datasets generated in the lab and systematic computational analyses were we able to unravel this new undiscovered biology.

José Martín-Durán, Annelid functional genomics reveal the origins of bilaterian life cycles, Nature (2023). DOI: 10.1038/s41586-022-05636-7. www.nature.com/articles/s41586-022-05636-7

Comment by Dr. Krishna Kumari Challa on January 26, 2023 at 11:42am

Cancer cells may shrink or super-size to survive

Cancer cells can shrink or super-size themselves to survive drug treatment or other challenges within their environment, researchers have discovered.

Scientists combined biochemical profiling technologies with mathematical analyses to reveal how genetic changes lead to differences in the size of cancer cells—and how these changes could be exploited by new treatments.

The researchers think smaller cells could be more vulnerable to DNA-damaging agents like chemotherapy combined with targeted drugs, while larger cancer cells might respond better to immunotherapy. The study combines innovative high-powered image analysis with examination of DNA and proteins to study size control in millions of skin cancer cells.

The skin cancer melanoma is driven by two different genetic mutations—60% of cases are caused by a BRAF gene mutation, while 20% to 30% of cases are caused by an NRAS mutation. The researchers set out to investigate the differences in size and shape of skin cancer cells harboring the two mutations, by using mathematical algorithms to analyze huge amounts of data on DNA and proteins. The major difference was cell size.

BRAF-mutant cancer cells were very small whereas NRAS-mutant cancer cells were much bigger. Drug resistant NRAS cells were even bigger. Smaller cells appear to be able to tolerate higher levels of DNA damage, as they are very concentrated with proteins that repair DNA—like PARP, BRCA1, or ATM1 proteins. The researchers think that this could make them more vulnerable to drugs like PARP inhibitors—drugs blocking proteins responsible for repairing DNA damage—especially when combined with DNA-damaging agents such as chemotherapy.

In contrast, the larger NRAS-mutant cancer cells contained damage to their DNA instead of repairing it, accumulating mutations and enlarging. These larger cells were not as reliant on DNA repair machinery, so using chemotherapy and PARP inhibitors against them might not be as effective. Scientists think larger cells could be more responsive to immunotherapy—because their larger number of mutations could make them look more alien to the body.

They are already exploring this theory with further studies. The researchers think BRAF and NRAS mutations may be driving the differences in cell size by regulating levels of a protein known as CCND1—which is involved in cell division, growth and maintaining the cytoskeleton—and its interactions with other proteins.

While the study focused on skin cancer cells, researchers suspect that this size-shifting ability and its impact on treatment response is common to multiple cancer types. They have already identified similar mechanisms in breast cancer and are now investigating whether the findings could apply to head and neck cancers.

The discovery provides new insight into how the size of cancer cells affects the overall disease, allowing for better predictions of how people with cancer will respond to different treatments simply by analyzing cell size.

Existing drugs could even be used to force cancer cells into a desired size prior to treatments like immunotherapy or radiotherapy, which could improve their effectiveness.

Ian Jones et al, Characterization of proteome-size scaling by integrative omics reveals mechanisms of proliferation control in cancer, Science Advances (2023). DOI: 10.1126/sciadv.add0636. www.science.org/doi/10.1126/sciadv.add0636

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