Lifeboat Foundation: Safeguarding Humanity
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Category: biotech/medical – Page 933

It was once thought that inflammation and immune responses in the brain were limited; that is was a so-called immune privileged organ. But there is increasing evidence to the contrary. New research has shown that immune cells called mucosal-associated invariant T cells (MAITs) can serve critical roles in the brain that reduce the levels of damaging reactive oxygen species, which prevents neuroinflammation, and protects learning and memory. The findings have been reported in Nature Immunology.

In this study, researchers genetically engineered mice so MAITs would no longer be produced. These mice were compared to a normal group and mice and while cognitive function was the same in both groups to start with, difference appeared as the mice approached middle age. The MAIT-deficient mice had difficulty forming new memories.

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But even junk has hidden treasures. Studies found variations in these unsequenced regions were intricately involved in human health, from aging to conditions like cancer and developmental disorders like autism. In 2022, a landmark study finally resolved the genomic unknown, completely sequencing the remaining eight percent of undeciphered DNA remaining.

Now, scientists are discovering that some genetic sequences encode proteins that lack any obvious ancestors, what geneticists call orphan genes. Some of these orphan genes, the researchers surmise, arose spontaneously as we evolved, unlike others that we inherited from our primate ancestors. In a paper published Tuesday in the journal Cell Reports, researchers in Ireland and Greece found around 155 of these smaller versions of DNA sequences called open reading frames (or ORF) make microproteins potentially important to a healthy cell’s growth or connected to an assortment of ailments like muscular dystrophy and retinitis pigmentosa, a rare genetic disease affecting the eyes.

“This is, I think, the first study looking at the specific evolutionary origins of these small ORFs and their microproteins,” Nikolaos Vakirlis, a scientist at the Biomedical Sciences Research Center “Alexander Fleming” in Greece and first author of the paper, tells Inverse. It’s an origin, he says, that’s been mired in much question and mystery.

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Researchers at the Netherlands Institute for Neuroscience have discovered that the energy management of inhibitory brain cells is different than that of excitatory cells in our brain. Why is that the case and what is the link with multiple sclerosis?

Brain cells are connected to each other by , the parts of the neuron that transmit electrical signals. To do this efficiently, axons are wrapped in myelin, a lipid-rich material which increases the speed at which electrical pulses are conducted. The importance of myelin becomes apparent in diseases such as multiple sclerosis (MS), where myelin is broken down, which has detrimental effects on .

As a result of myelin loss, the conduction of is disrupted, which also means that the energy costs of this process become much higher.

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Investigators from the Smidt Heart Institute at Cedars-Sinai have identified how biological pacemaker cells—cells that control your heartbeat—can “fight back” against therapies to biologically correct abnormal heartbeat rates. The research also uncovered a new way to boost the effectiveness of RNA therapies by controlling this “fighting back” activity.

This novel concept, published today in the peer-reviewed journal Cell Reports Medicine, is an important step in the evolution and creation of biological pacemakers—which aim to one day replace traditional, electronic pacemakers.

“We are all born with a specialized group of heart that set the pace for our heartbeats,” said Eugenio Cingolani, MD, senior author of the study and director of the Cardiogenetics Program in the Smidt Heart Institute at Cedars-Sinai. “But in some people, this natural is too slow, leading to the need for an electronic pacemaker.”

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In what could be the first direct link between AI and the human brain, interventional neurologist Thomas Oxley reveals the world’s first minimally invasive digital spinal cord. He shares the exciting story behind the ongoing development of this unique wireless device that can interpret signals from the brain for patients with paralysis without the need for open brain surgery or direct contact with brain tissue. Endovascular neurologist Thomas Oxley’s 2016 research demonstrated the potential for a neural recording device to be engineered onto a stent and implanted into a blood vessel in the brain, without the need for open brain surgery.

This research has progressively attracted investment, with completion of a Series A fundraiser in 2017. His company’s technology, the Stentrode, currently under FDA review, is planned for a first in human trial. Patients with tetraplegia due to spinal cord injury, stroke and ALS will be recruited into a trial of direct brain control over a suite of assistive technologies. This talk was given at a TEDx event using the TED conference format but independently organized by a local community.

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Throughout our lives, our skin goes through a lot. We get sunburns, we skin our knees, we bleed, we scar and we do it again. Our skin is our largest organ and, in many ways, serves as our protector. Beyond acting as a protective barrier between us and our environment, our skin regulates our body temperature, provides immune protection against harmful microbes and blocks out harmful sunlight in ways that benefit the whole body. And when skin is injured, blood brings healing substances to the site to promote healing as the body awaits new, replacement skin cells.

Regardless of scrapes and scratches, skin cells are constantly renewing themselves throughout our lives — a process reliant on skin stem cells. These skin stem cells turn over slowly, keeping our skin healthy and young. But as we age, these skin stem cells either numerically or functionally deplete, our skin thins and we are consequentially at higher risk for developing ulcers. The older the skin, the harder it is to heal these ulcers, meaning they can become chronic, open wounds that impact lifestyle and invite infection.

But what if we could activate a skin stem cell to be more responsive to injury? To get an 80-year-old’s skin to function like a 30-year-old’s skin? Could we reverse skin stem cell age-related deterioration and improve their turnover? What if we could do so in a way that healed wounds regeneratively, without any scarring? With these questions in mind, a collaborative team of researchers from the Mass General Brigham, Boston Children’s Hospital, and four additional Harvard institutions set off to study these powerful cells.

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