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Comment by Dr. Krishna Kumari Challa on June 3, 2023 at 11:10am

Reducing noise by ionizing air

Scientists show that a thin layer of plasma, created by ionizing air, could be promising as an active sound absorber, with applications in noise control and room acoustics.

Did you know that wires can be used to ionize air to make a loudspeaker? Simply put, it’s possible to generate sound by creating an electric field in a set of parallel wires, aka a plasma transducer, strong enough to ionize the air particles. The charged ions are then accelerated along the magnetic field lines, pushing the residual non-ionized air in a way to produce sound.

If a loudspeaker can generate sound, it can also absorb it.

While this plasma loudspeaker concept is not new,  scientists went ahead and built a demonstration of the plasma transducer, with the aim to study noise reduction. They came up with a new concept, what they call the active “plasmacoustic metalayer” that can be controlled to cancel out noise. Their results are published in Nature Communications.

Not only is the plasma efficient at high frequencies, but it is also versatile since it can be tuned to work at low frequencies as well. Indeed, the scientists show that the dynamics of thin layers of air plasma can be controlled to interact with sound over deep-subwavelength distances, to actively respond to noise and cancel it out over a broad bandwidth. The fact that their device is active is key, since passive noise reduction technologies are limited in the band of frequencies that can be controlled.

The plasma absorber is also more compact that most conventional solutions. Exploiting the unique physics of plasmacoustic metalayers, the scientists experimentally demonstrate perfect sound absorption: 100% of the incoming sound intensity is absorbed by the metalayer and nothing is reflected back.

Stanislav Sergeev, Romain Fleury, Hervé Lissek. Ultrabroadband sound control with deep-subwavelength plasmacoustic metalayers. Nature Communications, 2023; 14 (1) DOI: 10.1038/s41467-023-38522-5

Comment by Dr. Krishna Kumari Challa on June 3, 2023 at 9:27am

Scientists reveal new details of cellular process that prevents spread of cancer

Researchers have for the first time characterized a unique molecular mechanism of the early stages of programmed cell death or apoptosis, a process which plays a crucial role in prevention of cancer.

 It is the most recent in a series of research collaborations by this team, investigating the cellular proteins responsible for apoptosis.

Apoptosis is essential for human life, and its disruption can cause cancerous cells to grow and not respond to cancer treatment. In healthy cells, it is regulated by two proteins with opposing roles known as Bax and Bcl-2.

The soluble Bax protein is responsible for the clearance of old or diseased cells, and when activated, it perforates the cell mitochondrial membrane to form pores that trigger programmed cell death. This can be offset by Bcl-2, which is embedded within the mitochondrial membrane, where it acts to prevent untimely cell death by capturing and sequestering Bax proteins.

In cancerous cells, the survival protein Bcl-2 is overproduced, leading to uninhibited cell proliferation.

Using neutron reflectometry on SURF and OFFSPEC, they were able to study in real time the way that the protein interacts with lipids present in the mitochondrial membrane, during the initial stages of apoptosis. By employing deuterium-isotope labeling, they determined for the first time that when Bax creates pores, it extracts lipids from the mitochondrial membrane to form lipid-Bax clusters on the mitochondrial surface.

By using time-resolved neutron reflectometry in combination with surface infrared spectroscopy in the ISIS biolab, they were able to see that this pore creation occurred in two stages. Initial fast adsorption of Bax onto the mitochondrial membrane surface was followed by a slower formation of membrane-destroying pores and Bax-lipid clusters, which occurred simultaneously. This slower perforation process occurred on timescales of several hours, comparable to cell death in vivo.

This is the first time that scientists have found direct evidence of the involvement of mitochondrial lipids during membrane perturbing in cell death initiated by Bax proteins.

This mechanism by which Bax initiates cell death is previously unseen. Once we know more about the interplay between Bax and Bcl-2 and how it relates to this mechanism, we'll have a more complete picture of a process that is fundamental to human life.

Luke Clifton et al, Creation of distinctive Bax-lipid complexes at mitochondrial membrane surfaces drives pore formation to initiate apoptosis, Science Advances (2023). DOI: 10.1126/sciadv.adg7940. www.science.org/doi/10.1126/sciadv.adg7940

Comment by Dr. Krishna Kumari Challa on June 2, 2023 at 12:17pm

 

DNA: a novel, green, natural flame retardant and suppressant for cotton

DNA could be considered an intrinsically intumescent flame retardant as it contains the three main components that are usually present in an intumescent formulation, namely: the phosphate groups, able to produce phosphoric acid, the deoxyribose units acting as a carbon source and blowing agents (upon heating a (poly)saccharide dehydrates forming char and releasing water) and the nitrogen-containing bases (guanine, adenine, thymine, and cytosine) that may release ammonia. The flammability tests in horizontal configuration have clearly shown that after two applications of a methane flame for 3 s, the DNA-treated cotton fabrics do not burn at all. Furthermore, when exposed to an irradiative heat flux of 35 kW m⁻², no ignition has been observed. Finally, an LOI value of 28% has been achieved for the treated fabrics as opposed to 18% of the untreated fabric.

https://pubs.rsc.org/en/content/articlelanding/2013/ta/c3ta00107e#:...(upon%20heating%20a

Researchers find DNA can work as a flame retardant 

https://phys.org/news/2013-03-dna-flame-retardant-video.html

Comment by Dr. Krishna Kumari Challa on June 2, 2023 at 10:54am

We are exceeding most of Earth’s limits

In 2009, a seminal paper in Nature showed that humanity had crossed three of nine ‘Earth-system boundaries’: the limits of what the planet can support before human activities make it uninhabitable. Now, there’s a reboot of the extraordinarily influential concept that takes into account how changes to climate, ecosystems and other factors disproportionately affect vulnerable communities. We have crossed seven of the eight safe and just boundaries. Only air pollution was inside dangerous limits globally, despite it causing an estimated 4.2 million deaths annually. If our planet got a check-up, “our doctor would say that the Earth is really quite sick right now, and it is sick in terms of many different areas or systems, and this sickness is also affecting the people living on Earth”, says climate-policy researcher and co-author Joyeeta Gupta.

https://apnews.com/article/earth-environment-climate-change-nature-...

Comment by Dr. Krishna Kumari Challa on June 2, 2023 at 10:51am

Brain’s wrinkles help to drive how it works

Our brains’ walnut-like wrinkles have a large effect on brain activity, in much the same way that the shape of a bell determines how it sounds. The discovery challenges the paradigm that brain function emerges from the intricate web of connections between specialized brain-cell populations, called the connectome. Researchers used mathematical models that predict how waves travel across surfaces, and found that the shape of the brain’s outer surface was a better predictor of brainwave data than was the model of the connectome.

Comment by Dr. Krishna Kumari Challa on June 2, 2023 at 9:57am

The researchers experimentally induced DNA damage in human cell lines using a common chemotherapy medication known as etoposide. Etoposide works by breaking DNA strands and blocking an enzyme that helps repair the damage. Surprisingly, inducing DNA damage resulted in reactive oxygen species being generated and accumulating inside the nucleus. The researchers observed that cellular respiratory enzymes, a major source of reactive oxygen species, relocated from the mitochondria to the nucleus in response to DNA damage.

The findings represent a paradigm shift in cellular biology because it suggests the nucleus is metabolically active. Where there's smoke there's fire, and where there's reactive oxygen species there are metabolic enzymes at work. Historically, scientists have thought of the nucleus as a metabolically inert organelle that imports all its needs from the cytoplasm, but this study demonstrates that another type of metabolism exists in cells and is found in the nucleus.

The researchers also used CRISPR-Cas9 to identify all the metabolic genes that were important for cell survival in this scenario. These experiments revealed that cells order the enzyme PRDX1, an antioxidant enzyme also normally found in mitochondria, to travel to the nucleus and scavenge reactive oxygen species present to prevent further damage. PRDX1 was also found to repair the damage by regulating the cellular availability of aspartate, a raw material that is critical for synthesizing nucleotides, the building blocks of DNA.

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The findings can guide future lines of cancer research. Some anti-cancer drugs, such as the etoposide used in this study, kill tumor cells by damaging their DNA and inhibiting the repair process. If enough damage accumulates, the cancer cell initiates a process where it autodestructs.

During their experiments, the researchers found that knocking out metabolic genes critical for cellular respiration—the process that generates energy from oxygen and nutrients—made normal healthy cells become resistant to etoposide. The finding is important because many cancer cells are glycolytic, meaning that even in the presence of oxygen they generate energy without doing cellular respiration. This means etoposide, and other chemotherapies with a similar mechanism, is likely to have a limited effect in treating glycolytic tumors.

The authors of the study call for the exploration of new strategies such as dual treatment combining etoposide with drugs that also boost the generation of reactive oxygen species to overcome drug resistance and kill cancer cells faster. They also hypothesize that combining etoposide with inhibitors of nucleotide synthesis processes could potentiate the effect of the drug by preventing the repair of DNA damage and ensuring cancer cells self-destruct correctly.

"A metabolic map of the DNA damage response identifies PRDX1 in the control of nuclear ROS scavenging and aspartate availability", Molecular Systems Biology (2023). DOI: 10.15252/msb.202211267

Part 2

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Comment by Dr. Krishna Kumari Challa on June 2, 2023 at 9:53am

Study examines how DNA damage is repaired by antioxidant enzymes

A typical human cell is metabolically active, roaring with chemical reactions that convert nutrients into energy and useful products that sustain life. These reactions also create reactive oxygen species, dangerous by-products like hydrogen peroxide which damage the building blocks of DNA in the same way oxygen and water corrode metal and form rust. Similar to how buildings collapse from the cumulative effect of rust, reactive oxygen species threaten a genome's integrity.

Cells are thought to delicately balance their energy needs and avoid damaging DNA by containing metabolic activity outside the nucleus and within the cytoplasm and mitochondria. Antioxidant enzymes are deployed to mop up reactive oxygen species at their source before they reach DNA, a defensive strategy that protects the roughly 3 billion nucleotides from suffering potentially catastrophic mutations. If DNA damage occurs anyway, cells pause momentarily and carry out repairs, synthesizing new building blocks and filling in the gaps.

Despite the central role of cellular metabolism in maintaining genome integrity, there has been no systematic, unbiased study on how metabolic perturbations affect the DNA damage and repair process. This is particularly important for diseases like cancer, characterized by their ability to hijack metabolic processes for unfettered growth.

A research team has now addressed this challenge by carrying out various experiments to identify which metabolic enzymes and processes are essential for a cell's DNA damage response. The findings are published today in the journal Molecular Systems Biology.

Part 1

Comment by Dr. Krishna Kumari Challa on June 2, 2023 at 9:20am

The lead risk variant at the MTHFR–CLCN6 locus has been previously associated with reduced levels of circulating N-terminal pro-BNP43. A recent analysis found that first-trimester levels of N-terminal pro-BNP were unexpectedly lower among female individuals who subsequently developed hypertensive disorders of pregnancy later in pregnancy. These findings suggest that genetic network-driven deficiency in endogenous natriuretic peptide signaling may predispose individuals to hypertensive disorders of pregnancy.

Synthetic natriuretic peptides have been developed, and the authors suggest that natriuretic peptides may represent a future therapeutic target for direct or indirect modulation toward hypertensive disorders of pregnancy prevention and treatment.

 Michael C. Honigberg et al, Polygenic prediction of preeclampsia and gestational hypertension, Nature Medicine (2023). DOI: 10.1038/s41591-023-02374-9

Part 2

Comment by Dr. Krishna Kumari Challa on June 2, 2023 at 9:20am

From genes to gestation, researchers probe predictive markers for pregnancy complications

A new study has identified genetic markers associated with preeclampsia and gestational hypertension in a large cohort study. In the paper, "Polygenic prediction of preeclampsia and gestational hypertension," published in Nature Medicine, the researchers detail how these genetic markers could be used as a predictive risk assessment and offers mechanistic insights into pregnancy disorders.

Preeclampsia and gestational hypertension are common pregnancy complications associated with adverse outcomes, including substantial morbidity and mortality for both mother and child. Current tools for prediction, prevention and treatment are limited.

The team examined the associations of maternal DNA variants in 20,064 preeclampsia cases compared to 703,117 control individuals and gestational hypertension in 11,027 cases compared with 412,788 controls. Polygenic risk scores were tuned to a UK Biobank and then tested against other data sets for validation.

The analysis identified 18 independent loci associated with preeclampsia and gestational hypertension, 12 of which were previously unknown, and an additional two genes were implicated in a follow-up meta-analysis. The genes associated highlight potential roles of natriuretic peptide signaling, angiogenesis, renal glomerular function, trophoblast development and immune dysregulation.

Interestingly, almost none of the associated genes reside on the same chromosome, making them less likely to be inherited together.

Low-dose aspirin starting after week 12 gestation is an evidence-based but underused strategy to reduce risk of preeclampsia. To probe the potential clinical impact of incorporating PRS to guide aspirin allocation, researchers examined aspirin eligibility according to current US Preventive Service Task Force major criteria. Those with polygenic risk scores in the top 10% were shown to increase identification as low-dose aspirin-eligible by 30.4%, offering a potential preemptive intervention.

Part 1

Comment by Dr. Krishna Kumari Challa on June 1, 2023 at 10:16am

Darker skies are disappearing:

Light pollution can have negative consequences for the well-being of many living things—plants, animals and even humans. Between 2011 and 2022 light pollution increased globally by 9.6 percent a year. “This might not sound like much, but it reflects an exponential growth rate,” writes Phil Plait, astronomer and science communicator. 

Why this matters: Light pollution disrupts the migrations of birds, the blossoming of flowers and even the courtship of fireflies. For humans, more light might mean more insomnia or other health impacts. 

What the experts say: To help, you can: Use smarter streetlights that concentrate light downward (which are cheaper, too); turn off your own outdoor lighting at night; use targeted illumination rather than flood lighting; choose lightbulbs and LEDs that shine more red than blue to reduce how much light scatters across the sky. 

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