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Science: In my opinion the main cause of aging is the accumulation of mutations in DNA 🧬 more than telomere size reduction or “toxin’s”. But the control of these “toxins” together with drug’s that simulate the restriction of calories and the transfusion of blood from young people to old people. And future drugs to make the telomeres grow again.

These four treatments together maybe can promote life extension. I am also enthusiastic in regenerative treatment with stem cells and “replace” old organs by new one’s growing in lab from stem cells. However I believe that immortality only when you make the enzymes “fix” in 100% the mutations caused by radicals.


High levels of toxic chemicals in the body, such as formaldehyde, which is best known as an embalming agent, have recently been found to be naturally made by cells and also to cause ageing.

Leading scientists from Cornell University, the University of Oxford, the University of Cambridge and Cancer Research UK are trying to understand what causes the body to overproduce formaldehyde.

It is hoped that drugs may be able to lower levels of it in the body and reverse the ageing process.

Recent developments in various domains have led to a growing interest in the potential of artificial intelligence to enhance our lives and environments. In particular, the application of artificial intelligence in the management of complex human diseases, such as cancer, has garnered significant attention. The evolution of artificial intelligence is thought to be influenced by multiple factors, including human intervention and environmental factors. Similarly, tumors, being heterogeneous and complex diseases, continue to evolve due to changes in the physical, chemical, and biological environment. Additionally, the concept of cellular intelligence within biological systems has been recognized as a potential attribute of biological entities. Therefore, it is plausible that the tumor intelligence present in cancer cells of affected individuals could undergo super-evolution due to changes in the pro-tumor environment. Thus, a comparative analysis of the evolution of artificial intelligence and super-complex tumor intelligence could yield valuable insights to develop better artificial intelligence-based tools for cancer management.

Tumor evolution refers to the changes that occur in a cancerous tumor over time as it grows and spreads (Hanahan and Weinberg, 2011; Lyssiotis and Kimmelman, 2017). These changes are the result of genetic mutations and changes in gene expression that can give rise to new subpopulations of cells within the tumor (Lyssiotis and Kimmelman, 2017; Balaparya and De, 2018). Over time, these subpopulations may accumulate subsequent mutations that confer enhanced survival and heightened proliferative capacity, thereby culminating in the emergence of a more formidable tumor exhibiting either heightened aggressiveness or treatment resistance (Balaparya and De, 2018; Gui and Bivona, 2022; Shin and Cho, 2023). Tumor evolution can have important implications for cancer diagnosis and treatment.

Imagine an iPad that’s more than just an iPad—with a surface that can morph and deform, allowing you to draw 3D designs, create haiku that jump out from the screen and even hold your partner’s hand from an ocean away.

That’s the vision of a team of engineers from the University of Colorado Boulder. In a new study, they’ve created a one-of-a-kind shape-shifting display that fits on a card table. The device is made from a 10-by-10 grid of soft robotic “muscles” that can sense outside pressure and pop up to create patterns. It’s precise enough to generate scrolling text and fast enough to shake a chemistry beaker filled with fluid.

It may also deliver something even rarer: the sense of touch in a digital age.

New chemistry, new enzymology. With a new method that merges the best of two worlds—the unique and complementary activities of enzymes and small-molecule photochemistry—researchers at UC Santa Barbara have opened the door to new catalytic reactions. Their synergistic method allows for new products and can streamline existing processes, in particular, the synthesis of non-canonical amino acids, which are important for therapeutic purposes.

“This method solves what in my opinion is one of the most important problems in our field: how to develop new catalytic reactions in a general sense that are new to both biology and chemistry,” said chemistry Professor Yang Yang, an author of a paper that appears in the journal Science. “On top of that, the process is stereoselective, meaning it can select for a preferred “shape” of the resulting amino .”

The synergistic photobiocatalytic method consists of two co-occurring catalytic reactions. The photochemical reaction generates a short-lived intermediate molecule that works with the reactive intermediate of the enzymatic process, resulting in the amino acid.

Raman spectroscopy—a chemical analysis method that shines monochromatic light onto a sample and records the scattered light that emerges—has caused frustration among biomedical researchers for more than half a century. Due to the heat generated by the light, live proteins are nearly destroyed during the optical measurements, leading to diminishing and non-reproducible results. As of recently, however, those frustrations may now be a thing of the past.

A group of researchers with the Institute for Quantum Sciences and Engineering at Texas A&M University and the Texas A&M Engineering Experiment Station (TEES) have developed a new technique that allows low-concentration and low-dose screenings of protein-to-ligand interactions in physiologically relevant conditions.

Titled thermostable-Raman-interaction-profiling (TRIP), this new approach is a paradigm-shifting answer to a long-standing problem that provides label-free, highly reproducible Raman spectroscopy measurements. The researchers published their findings in the Proceedings of the National Academy of Sciences.

Plastic waste is a problem. Most plastics can’t be recycled, and many use finite, polluting petrochemicals as the basic ingredients. But that’s changing. In a study published today in Nature Sustainability, researchers successfully engineered microbes to make biological alternatives for the starting ingredients in an infinitely recyclable plastic known as poly(diketoenamine), or PDK.

The finding comes from collaboration among experts at three facilities at the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab): the Molecular Foundry, the Joint BioEnergy Institute (JBEI), and the Advanced Light Source.

“This is the first time that bioproducts have been integrated to make a PDK that is predominantly bio-based,” said Brett Helms, staff scientist at the Molecular Foundry who led the project. “And it’s the first time that you see a bio-advantage over using petrochemicals, both with respect to the material’s properties and the cost of producing it at scale.”

Exercise gives your brain a “bubble bath of neurochemicals,” says Wendy Suzuki, a professor of neural science.

Up next, Forensic accountant explains why fraud thrives on Wall Street.
â–ș https://youtu.be/GHKyDYtKGEg.

Exercise can have surprisingly transformative impacts on the brain, according neuroscientist Wendy Suzuki. It has the power not only to boost mood and focus due to the increase in neurotransmitters like dopamine, serotonin, and noradrenaline, but also contributes to long-term brain health. Exercise stimulates the growth of new brain cells, particularly in the hippocampus, improving long-term memory and increasing its volume. Suzuki notes that you don’t have to become a marathon runner to obtain these benefits — even just 10 minutes of walking per day can have noticeable benefits. It just takes a bit of willpower and experimentation.

0:00 My exercise epiphany.
1:35 What is “runner’s high”?
2:40 The hippocampus & prefrontal cortex.
3:32 Neuroplasticity: It’s never too late to move your body.

Read the video transcript â–ș https://bigthink.com/series/the-big-think-interview/how-the-
escription.

About Wendy Suzuki:

Fragile X syndrome is a genetic disorder caused by a mutation in a gene that lies at the tip of the X chromosome. It is linked to autism spectrum disorders.

People with fragile X experience a range of symptoms that include cognitive impairment, developmental and speech delays and hyperactivity. They may also have some physical features such as large ears and foreheads, flabby muscles and poor coordination.

Along with our colleagues Jonathan Watts and Elizabeth Berry-Kravis, we are a team of scientists with expertise in molecular biology, nucleic acid chemistry and pediatric neurology.

For more information on mental health or #YaleMedicine, visit: https://www.yalemedicine.org/conditions/topics/mental-health.

For many people, depression turns out to be one of the most disabling illnesses that we have in society. Despite the treatments that we have available, many people are not responding that well. It’s a disorder that can be very disabling in society. It’s also a disorder that has medical consequences. By understand the neurobiology of depression we hope to be able more to find the right treatment for the patient suffering from this disease. The current standard of care for the treatment of depression is based on what we call the monoamine deficiency hypothesis. Essentially, presuming that one of three neurotransmitters in the brain is deficient or underactive. But the reality is, there are more than 100 neurotransmitters in the brain. And billions of connections between neurons. So we know that that’s a limited hypothesis. Neurotransmitters can be thought of as the chemical messengers within the brain, it’s what helps one cell in the brain communicate with another, to pass that message along from one brain region to another. For decades, we thought that the primary pathology, the primary cause of depression was some abnormality in these neurotransmitters, specifically serotonin or norepinephrine. However, norepinephrine and serotonin did not seem to be able to account for this cause, or to cause the symptoms of depression in people who had major depression. Instead, the chemical messengers between the nerve cells in the higher centers of the brain, which include glutamate and GABA, were possibilities as alternative causes for the symptoms of depression. When you’re exposed to severe and chronic stress like people experience when they have depression, you lose some of the connections between the nerve cells. The communication in these circuits becomes inefficient and noisy, we think that the loss of these synaptic connections contributes to the biology of depression. There are clear differences between a healthy brain and a depressed brain. And the exciting thing is, when you treat that depression effectively, the brain goes back to looking like a healthy brain, both at the cellular level and at a global scale. It’s critical to understand the neurobiology of depression and how the brain plays a role in that for two main reasons. One, it helps us understand how the disease develops and progresses, and we can start to target treatments based on that. We are in a new era of psychiatry. This is a paradigm shift, away from a model of monoaminergic deficiency to a fuller understanding of the brain as a complex neurochemical organ. All of the research is driven by the imperative to alleviate human suffering. Depression is one of the most substantial contributors to human suffering. The opportunity to make even a tiny dent in that is an incredible opportunity.