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Immune Macrophages Use Their Own ‘Morse Code’

In the language of Morse code, the letter “S” is three short sounds and the letter “O” is three longer sounds. Put them together in the right order and you have a cry for help: S.O.S. Now an NIH-funded team of researchers has cracked a comparable code that specialized immune cells called macrophages use to signal and respond to a threat.

In fact, by “listening in” on thousands of macrophages over time, one by one, the researchers have identified not just a lone distress signal, or “word,” but a vocabulary of six words. Their studies show that macrophages use these six words at different times to launch an appropriate response. What’s more, they have evidence that autoimmune conditions can arise when immune cells misuse certain words in this vocabulary. This bad communication can cause them incorrectly to attack substances produced by the immune system itself as if they were a foreign invaders.

The findings, published recently in the journal Immunity, come from a University of California, Los Angeles (UCLA) team led by Alexander Hoffmann and Adewunmi Adelaja. As an example of this language of immunity, the video above shows in both frames many immune macrophages (blue and red). You may need to watch the video four times to see what’s happening (I did). Each time you run the video, focus on one of the highlighted cells (outlined in white or green), and note how its nuclear signal intensity varies over time. That signal intensity is plotted in the rectangular box at the bottom.

DeepMind creates ‘transformative’ map of human proteins drawn

DeepMind is using its AI prowess to accelerate scientific work.


AI research lab DeepMind has created the most comprehensive map of human proteins to date using artificial intelligence. The company, a subsidiary of Google-parent Alphabet, is releasing the data for free, with some scientists comparing the potential impact of the work to that of the Human Genome Project, an international effort to map every human gene.

Proteins are long, complex molecules that perform numerous tasks in the body, from building tissue to fighting disease. Their purpose is dictated by their structure, which folds like origami into complex and irregular shapes. Understanding how a protein folds helps explain its function, which in turn helps scientists with a range of tasks — from pursuing fundamental research on how the body works, to designing new medicines and treatments.

Dr Spring Behrouz, PhD — Mitophagy, CNS Disorders, And Aging — CEO, Vincere Bio / NeuroInitiative

Mitochondrial Quality Control (Mitophagy), CNS Disorders, and Aging — Dr. Spring Behrouz, Ph.D., CEO, Vincere Biosciences Inc. / CEO, Neuroinitiative LLC.


Dr. Bahareh (Spring) Behrouz, PhD, is the CEO of Vincere Biosciences Inc (https://vincerebio.com/), a biotech company focused on developing novel, small molecule therapeutics targeting mitochondrial pathways and the improvement of mitochondrial quality.

Dr. Behrouz is also the CEO of NeuroInitiative, LLC (https://www.neuroinitiative.com/), a computational biology company she co-founded in 2014, which develops simulations of disease using their patented software platform. A core focus of her research at NeuroInitiative is on the elucidation of complex, converging pathways that contribute to the pathogenesis of Parkinson’s disease (PD), a neuro-degenerative brain disorder which dramatically effects movement, which nearly one million people in the U.S. are living with, and 10 million patients worldwide.

Dr. Behrouz received her graduate training at Michigan State University in the laboratory of Dr. John Goudreau and studied differential susceptibility of dopaminergic neuron sub-types in models of PD. She completed her post-doctoral training in the laboratory of Dr. Matthew Farrer at the Mayo Clinic in Jacksonville, where she primarily focused on in-vivo and primary culture models of LRRK2-mediated pathogenesis and was part of the team that discovered a new pathogenic mutation in VPS35.

Scientists Made a Biohybrid Nose Using Cells From Mosquitoes

💠 Japanese researchers have created a “nose” mosquito that can detect odors from tiny droplets of liquid droplets. The research could lead to the creation of Smell-O-Vision for machines and a means of diagnosing early cancer, they say. Japanese researchers have created a “nose” that can detect different odors at the same time. The team used two bubbles, each filled with oil, broken horizontally, to create a squinted figure-eight. They hope to use it to develop an artificial nose in the future.

Researchers have developed a “bionic nose” that can detect odor molecules. The team hopes to use the device as an inexpensive way to diagnose the early stages of illness. Eventually, the team wants to use their bionic nose for cancer and other health issues. They hope to make the device available to the public soon.

Thanks and Enjoy 🔥 🔥
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🎥 #BioEngineering #Mosquitoes #Cells.

Sources:
https://www.nature.com/articles/nature.2014.14904#:~:text=Th…%20roughly, report%20today%20in%20Science1.
https://www.eurekalert.org/pub_releases/2021-01/uot-hdy011121.php.
https://advances.sciencemag.org/content/7/3/eabd2013

The potential role of ‘junk DNA’ sequence in aging, cancer

An aging/longevity/junk dna link.

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The human body is essentially made up of trillions of living cells. It ages as its cells age, which happens when those cells eventually stop replicating and dividing. Scientists have long known that genes influence how cells age and how long humans live, but how that works exactly remains unclear. Findings from a new study led by researchers at Washington State University have solved a small piece of that puzzle, bringing scientists one step closer to solving the mystery of aging.

A research team headed by Jiyue Zhu, a professor in the College of Pharmacy and Pharmaceutical Sciences, recently identified a DNA region known as VNTR2-1 that appears to drive the activity of the telomerase gene, which has been shown to prevent aging in certain types of . The study was published in the journal Proceedings of the National Academy of Sciences (PNAS).

The telomerase gene controls the activity of the telomerase enzyme, which helps produce telomeres, the caps at the end of each strand of DNA that protect the chromosomes within our cells. In normal cells, the length of telomeres gets a little bit shorter every time cells duplicate their DNA before they divide. When telomeres get too short, cells can no longer reproduce, causing them to age and die. However, in certain cell types—including reproductive cells and —the activity of the telomerase gene ensures that telomeres are reset to the same length when DNA is copied. This is essentially what restarts the aging clock in new offspring but is also the reason why cells can continue to multiply and form tumors.

Permanent Artificial Hearts Are Closer Than You Think

For decades, scientists have been trying to build a long-lasting replacement for the human heart. Now, an Australian inventor believes he’s cracked one of the hardest problems in medicine.

#Prognosis #Science #BloombergQuicktake.
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Vaccines Are Pushing Pathogens to Evolve

In March 2017, Read and his Penn State colleague David Kennedy published a paper in the Proceedings of the Royal Society B in which they outlined several strategies that vaccine developers could use to ensure that future vaccines don’t get punked by evolutionary forces. One overarching recommendation is that vaccines should induce immune responses against multiple targets. A number of successful, seemingly evolution-proof vaccines already work this way: After people get inoculated with a tetanus shot, for example, their blood contains 100 types of unique antibodies, all of which fight the bacteria in different ways. In such a situation, it becomes much harder for a pathogen to accumulate all the changes needed to survive. It also helps if vaccines target all the known subpopulations of a particular pathogen, not just the most common or dangerous ones. Richard Malley and other researchers at Boston Children’s Hospital are, for instance, trying to develop a universal pneumococcal vaccine that is not serotype-specific.

Vaccines should also bar pathogens from replicating and transmitting inside inoculated hosts. One of the reasons that vaccine resistance is less of a problem than antibiotic resistance, Read and Kennedy posit, is that antibiotics tend to be given after an infection has already taken hold — when the pathogen population inside the host is already large and genetically diverse and might include mutants that can resist the drug’s effects. Most vaccines, on the other hand, are administered before infection and limit replication, which minimizes evolutionary opportunities.

But the most crucial need right now is for vaccine scientists to recognize the relevance of evolutionary biology to their field. Last month, when more than 1000 vaccine scientists gathered in Washington, D.C., at the World Vaccine Congress, the issue of vaccine-induced evolution was not the focus of any scientific sessions. Part of the problem, Read says, is that researchers are afraid: They’re nervous to talk about and call attention to potential evolutionary effects because they fear that doing so might fuel more fear and distrust of vaccines by the public — even though the goal is, of course, to ensure long-term vaccine success. Still, he and Kennedy feel researchers are starting to recognize the need to include evolution in the conversation. “I think the scientific community is becoming increasingly aware that vaccine resistance is a real risk,” Kennedy said.

Preclinical study finds success in reversing age-related memory loss

“What is exciting about this is that although our study was only in mice, the same mechanism should operate in humans – the molecules and structures in the human brain are the same as those in rodents,” says Fawcett. “This suggests that it may be possible to prevent humans from developing memory loss in old age.”


An intriguing new study from researchers in the United Kingdom is proposing an innovative method to treat age-related memory loss. The preclinical research shows memory decline in aging mice can be reversed by manipulating the composition of structures in the brain known as perineuronal nets.

Perineuronal nets (PNNs) are structures in the brain that envelop certain subsets of neurons, helping stabilize synaptic activity. They essentially put the brakes on the neuroplasticity seen in the first few years of life.

Although PNNs are vital to the effective functioning of a mature adult brain, by their very nature they also limit future neural plasticity and adaptability. A new wave of research is beginning to investigate ways to modulate PNNs in adult brains in the hope of treating a variety of diseases from diabetes to post-traumatic stress disorder (PTSD).

Gain-of-Function: Should supercharging viruses be banned? | DW News

Gain-of-function experiments aim to increase the transmissibility and virulence of existing viruses, making them deadlier for humans. The stated purpose is to better understand pathogens and to develop vaccines for possible future pandemics. Critics say this type of research is extremely dangerous and should be banned or regulated. They claim it has not prevented any pandemics to date, and that the COVID-19 outbreak might be the result of an accidental release from a lab that was conducting gain-of-function research.

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#biosafety #GainOfFunction #pandemic