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Category: biotech/medical – Page 1,053

National Institutes of Health researchers have developed and released an innovative software tool to assemble truly complete (i.e., gapless) genome sequences from a variety of species.

This software, called Verkko, which means “network” in Finnish, makes the process of assembling complete genome sequences more affordable and accessible. A description of the new software was published today in Nature Biotechnology.

Verkko grew from assembling the first gapless human genome sequence, which was finished last year by the Telomere-to-Telomere (T2T) consortium, a collaborative project funded by the National Human Genome Research Institute (NHGRI), part of NIH.

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It acted with rudimentary intelligence, learning, evolving and communicating with itself to grow more powerful.

A new model by a team of researchers led by Penn State and inspired by Crichton’s novel describes how biological or technical systems form complex structures equipped with signal-processing capabilities that allow the systems to respond to stimulus and perform functional tasks without external guidance.

“Basically, these little nanobots become self-organized and self-aware,” said Igor Aronson, Huck Chair Professor of Biomedical Engineering, Chemistry, and Mathematics at Penn State, explaining the plot of Crichton’s book. The novel inspired Aronson to study the emergence of collective motion among interacting, self-propelled agents. The research was recently published in Nature Communications.

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Year 2020 face_with_colon_three

Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are two fatal and incurable neurodegenerative diseases linked by a shared genetic cause – a heterozygous hexanucleotide (GGGGCC) repeat expansion in a single allele of the C9orf72 gene. The goal of this work is to develop novel CRISPR based therapeutic gene editing technologies and test whether gene editing can reverse the cellular pathology caused by this repeat expansion in patient derived cells. The results of these studies will advance our use of CRISPR technologies for therapeutic editing in FTD/ALS, inform our understanding of the regulation of C9orf72 gene, and will be applicable to many other repeat expansion and single gene disorders.

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For years, researchers have searched for the working principles of self-assembly that can build a cell (complex biological organism) as well as a crystal (far simpler inorganic material) in the same way.

Now, a team of scientists in Turkey has demonstrated the fundamental principles of a universal self-assembly process acting on a range of materials starting from a few atoms-large quantum dots up to nearly 100 trillion atoms-large human cells. Their method is highlighted in Nature Physics.

“To initiate self-assembly, either you force the system to deliver a specific outcome, or you use its inner dynamics to your advantage for universal outcomes. We followed the second approach,” says Dr. Serim Ilday of Bilkent University-UNAM, who lead the study.

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Three years into the pandemic, the immune systems of the vast majority of humans have learnt to recognize SARS-CoV-2 through vaccination, infection or, in many cases, both. But just how quickly do these types of immunity fade?

New evidence suggests that ‘hybrid’ immunity, the result of both vaccination and a bout of COVID-19, can provide partial protection against reinfection for at least eight months1. It also offers greater than 95% protection against severe disease or hospitalization for between six months and a year after an infection or vaccination, according to estimates from a meta-analysis2. Immunity acquired by booster vaccination alone seems to fade somewhat faster.

But the durability of immunity is much more complex than the numbers suggest. How long the immune system can fend off SARS-CoV-2 infection depends not only on how much immunity wanes over time but also on how well immune cells recognize their target. “And that has more to do with the virus and how much it mutates,” says Deepta Bhattacharya, an immunologist at the University of Arizona College of Medicine in Tucson. If a new variant finds ways to escape the existing immune response, then even a recent infection might not guarantee protection.

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As technology will progress robots will become cheaper.in future healthcare robots can be available at v less cost.then we can gift these robots to our bedridden friends and relatives.

A nurse-assisting robot named Moxi has been working with clinical staff on the neurology unit at Texas Health Presbyterian Hospital Dallas. During the month-long trial, Moxi helped with fetch-and-gather tasks such as delivering admissions kits, lab specimens and picking up and dropping off linen bags. Texas Health Dallas is the first hospital in the country to deploy Moxi. The robot was designed to provide clinical staff more time to focus on patient care.

Texas Health Resources.
http://www.TexasHealth.org.
1–877-THR-WELL.

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Their findings, published in a Cell Reports paper titled “Palmitoylation and PDE6δ regulate membrane-compartment-specific substrate ubiquitylation and degradation,” have implications for developing new therapies.

Lead author Shafi Kuchay, assistant professor of biochemistry and in the College of Medicine and member of the University of Illinois Cancer Center at UIC, said that most common drugs work by targeting proteins that are located at the membranes of cells. Many of these proteins can cause diseases by being overly active. Unfortunately, most currently available drugs just block the activity of the harmful proteins, and while they are helpful in the short term, resistance to the drugs can develop over time.

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Reconfigurable antennas — those that can tune properties like frequency or radiation beams in real-time, from afar — are integral to future communication network systems, like 6G. But many current reconfigurable antenna designs can fall short: they dysfunction in high or low temperatures, have power limitations, or require regular servicing.

To address these limitations, electrical engineers in the Penn State College of Engineering combined electromagnets with a compliant mechanism, which is the same mechanical engineering concept behind binder clips or a bow and arrow. They published their proof-of-concept reconfigurable compliant mechanism-enabled patch antenna today (February 13, 2023) in the journal Nature Communications.

<em>Nature Communications</em> is a peer-reviewed, open-access, multidisciplinary, scientific journal published by Nature Portfolio. It covers the natural sciences, including physics, biology, chemistry, medicine, and earth sciences. It began publishing in 2010 and has editorial offices in London, Berlin, New York City, and Shanghai.

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Though mitochondrial dysfunction is a known marker of aging and neurodegenerative diseases, the exact mechanism behind it remains unknown. Our study suggests that the decay of SIRT6 levels during aging [18] and in Alzheimer’s disease [18, 23, 46] could be a key mechanism causing the deterioration of mitochondrial functions. The changes induced by the SIRT6 knockout that we observe at the metabolite level support this claim: metabolites related to mitochondrial energy system pathways (in particular, OXPHOS and TCA cycle) are significantly overrepresented among differentially abundant metabolites. In line with the discussed mitochondrial dysfunction in aging, all these metabolites are downregulated in the SIRT6-KO samples. Importantly, the dramatic decline of one of them, NAD+, was also associated with pro-senescence mechanisms in various species [47, 48], as well as with limited neuroprotective activity of sirtuins [49].

Accordingly, the vast majority of differentially expressed mitochondria-related genes were downregulated in our gene expression analysis. As they were strongly enriched with mitochondrial respiratory chain complexes, we measured the mitochondrial membrane potential and mitochondrial content in SIRT6-KO cells because reduced gene expression might indicate the loss of mitochondria. Both measured characteristics were significantly decreased, validating the suggested impairment of mitochondrial oxidative phosphorylation and mitochondrial biogenesis in SIRT6-deficient brains. Interestingly, the average decrease of mtDNA gene expression (~19.7%) in SIRT6-KO was in good agreement with the corresponding reduction of mitochondrial content (21.8%), suggesting impaired mitochondrial biogenesis as a primary cause of the observed transcriptional dysregulation in mitochondria upon SIRT6 knockout.

Concordantly, the impaired membrane potential upon SIRT6-KO can be partially rescued by restoring SIRT3 and SIRT4 levels, which were significantly downregulated in SIRT6-deficient brains. Both of them are localized in mitochondria and impact mitochondrial pathways related to redox homeostasis and cellular metabolism [38] and have important roles in mitochondria metabolism ROS balance and lifespan [50,51,52]. The analysis of our and publicly available gene expression data [39] confirms that SIRT6 transcriptionally regulates SIRT3 and SIRT4. Our analysis further indicates that SIRT6 regulates mitochondrial gene expression through the transcription factor YY1. We have previously shown that SIRT6 and YY1 form a complex that regulates many shared target genes [24]. Our analysis of YY1 ChIP-seq data [53] suggests that SIRT6 and YY1 regulate mitochondrial processes coordinately.

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