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Category: biotech/medical – Page 1,143

T cells aren’t the first immune forces on the scene, they arrive after being alerted by other immune system warriors that a microbe has invaded or a cancer has silently seeded.

Exactly how T cells obtain the energy they need to build a massive army in the face of infiltrators has been the subject of speculation, theory and decades-long laboratory inquiries.

Now, scientists are taking a deeper dive into the question, and their investigations are shedding new light on an array of dynamic biological activities that help bolster T cell populations. Their research demystifies how T cells can power their growth and proliferation when disease emerges and T cell strength is in greatest need.

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Human microproteins encoded by small ORFs have been found to be functional. By comparing the corresponding sequences across vertebrate genomes, Vakirlis et al. show that a number of these originated “from scratch” from noncoding sequences, including two very recent cases unique to humans. These cases demonstrate the rapid evolution of genetic novelty.

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It will provide a better understanding of how drugs affect men and women differently.

Scientists created male and female cells with the same genetic code from the same person for the first time. This unique set of cells could provide researchers with valuable insights into how sex chromosomes affect various diseases and their role in early development.

CDC/Dr. Laine.

The sex chromosome.

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This impressive achievement could potentially revolutionize how we treat cancer and immunity deficiencies.

Children born with Artemis-SCID face many challenges, from a missing repertoire of T and B cells to reduced resistance against chemotherapy used in bone marrow transplants. Additionally, malfunctioning DNA repair mechanisms increase the risk of developing graft-versus-host disease, where the donor’s immune system attacks host tissues.

That’s why researchers are trying everything to find an antidote for such a rare genetic disease and have now turned to gene therapy to treat Artemis-SCID. Gene therapy eliminates the need for donor cells.

Infant gene therapy – a breakthrough to save Artemis-SCID children

In a recent medical breakthrough, scientists have discovered how to use gene therapy to treat babies born with Severe Combined Immunodeficiency (SCID), or “bubble boy syndrome,” without needing immune-suppressing drugs.

This new innovation has proven to be potentially life-changing for infants suffering from rare diseases, giving them an exponentially improved chance of leading a relatively healthy and normal life.

Continue reading “Gene therapy could save children from a rare genetic disease” | >

A new study develops ‘environment-modulating’ drugs that reinvigorate T-cells to once again destroy cancer cells.

T-cells, typically thought to be anti-cancer, can switch sides and work against us in the right environment (or battlefield!), according to a new study published on December 21 in Nature.

This discovery is unexpected because many extensive studies before this believed that most worn-out T-cells’ properties were “irreversible.” Simply put, they were doomed to being subpar tumor killers.

Meletios Verras/iStock.

In light of this, the study went a step further by proving that altering the local environment around the tumor could “reinvigorate” T-cells to once again destroy cancer cells.

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The deadly brain cancer is no longer a mystery.

Glioblastoma is one of the most dangerous cancer types affecting the human brain and spinal cord. Over 240,000 people lose their lives because of nervous system cancer annually, and in most of these cases, the leading cause of death is glioblastoma.

Its tumors spread fast and induce highly painful seizures and headaches. What’s worse is that there is no known 100 percent effective cure for this disease. US president Joe Biden’s eldest son Beau Biden and late American actor Robert Forster were also among the many victims of glioblastoma.

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The newly-created Longevity Escape Velocity Foundation (LEV) has released details of the first study in its flagship research programme: Robust Mouse Rejuvenation – Study 1.

Longevity. Technology: A highlight of Longevity Summit Dublin 2022 was Dr Aubrey de Grey’s announcement of his new foundation; LEV Foundation exists to proactively identify and address the most challenging obstacles on the path to the widespread availability of genuinely effective treatments to prevent and reverse human age-related disease, and to that end, its flagship research programme is a sequence of large mouse lifespan studies.

Mouse models are significant in aging research for several reasons. Mice and humans share many genetic and physiological similarities, including similar aging-related pathways, and this makes mice a useful model for studying the molecular and cellular processes underlying aging in humans.

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𝐀𝐥𝐳𝐡𝐞𝐢𝐦𝐞𝐫’𝐬 𝐃𝐢𝐬𝐞𝐚𝐬𝐞

One of the main features of Alzheimer’s disease is that the β-amyloid peptide, a molecule found inside neurons that has many diverse functions, begins to fold incorrectly and accumulates. This process, which ends up causing neuronal death, is linked to a series of other cellular alterations, making it difficult to determine whether they are the cause or the consequence. An example is the case of the deregulation of a type of dynorphin.

Dynorphins are the body’s own opioid peptides, which play a key role in many brain pathways. They are located in different areas of the brain, such as the hippocampus, amygdala or hypothalamus, and are involved in memory processes, emotion control, stress and pain, and among other processes. In addition, several studies have shown their involvement in epilepsy, stroke, addictions, depression and schizophrenia.

Now, in a study published in the Computational and Structural Biotechnology Journal, a research group led by Àlex Perálvarez-Marín, researcher in the Department of Biochemistry and Molecular Biology and the UAB Institut de Neurociències, has studied from computer models and which interactions may exist between β-amyloid peptide and big dynorphin, to determine its role in β-amyloid accumulation.

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