Lifeboat Foundation

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.

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.

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.

Continue reading “Moxi the Robot — Texas Health Resources” »

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 molecular genetics 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.

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.

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.

Researchers at NYU College of Dentistry have developed a single score to describe the level of cytokines in saliva, and this score is linked with the severity of clinical gum inflammation, according to a study published in the journal PLOS ONE.

While more research is needed to test the “cytokine score,” it could hold promise for measuring how well a patient responds to treatment for gum disease, predicting gum disease recurrence, or detecting ongoing inflammation related to systemic diseases.

“Periodontal inflammation is not just apparent upon examination, but is reflected in the patient’s saliva,” said Angela Kamer, DMD, MS, Ph.D., associate professor of the Ashman Department of Periodontology & Implant Dentistry at NYU Dentistry and the study’s senior author.

Potentially huge. Effecting blood plasma via a pill. This is of course a mice experiment and they are working to see if the process happens in humans too.

Some wealthy elites prefer young blood plasma transfusions for anti-aging purposes. There are suggestions that the body’s organs are rejuvenated by young blood. However, a recent study from Columbia University in New York suggests that anti-inflammatory drugs can rejuvenate the body and possibly extend the human lifespan by decades, negating the need for blood transfusions to turn back the body’s clock.

According to Emmanuelle Passegué, Ph.D., director of the Columbia Stem Cell Initiative, who has been researching how blood changes with age, “an aging blood system, because it’s a vector for a lot of proteins, cytokines, and cells, has a lot of bad consequences for the organism,”

Antibiotic resistance is a global threat to public health and associated with the overuse of antibiotics. Although non-antibiotic drugs occupy 95% of the drug market, their impact on the emergence and spread of antibiotic resistance remains unclear. Here we demonstrate that antidepressants, one of the most frequently prescribed drugs, can induce antibiotic resistance and persistence. Such effects are associated with increased reactive oxygen species, enhanced stress signature responses, and stimulation of efflux pump expression. Mathematical modeling also supported a role for antidepressants in the occurrence of antibiotic-resistant mutants and persister cells. Considering the high consumption of antidepressants (16,850 kg annually in the United States alone), our findings highlight the need to re-evaluate the antibiotic-like side effects of antidepressants.