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Category: genetics – Page 190

Groundbreaking Discoveries About Human Brain and Neuronal Complexity

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Hello and welcome! My name is Anton and in this video, we will talk about recent discoveries about human brain and various types of neuronal cells.
Links:
https://www.nature.com/articles/d41586-023-03192-2
https://nemoarchive.org/
https://www.science.org/collections/brain-cell-census.
https://www.science.org/doi/10.1126/science.adc8810
https://news.rub.de/english/press-releases/2022-06-0…ir-neurons.
https://www.nature.com/articles/s41559-022-01933-6
https://www.nature.com/articles/s41586-023-06502-w.
https://www.nature.com/articles/s41593-023-01284-w.
https://elifesciences.org/articles/76143
Previous video on major discoveries: https://youtu.be/iGdFh3ENjzc.
More about Neanderthals: https://youtu.be/BvrBl9-TbBs.
#brain #neuron #neuroscience.

0:00 Recent papers on the human brain.
1:00 Human brain atlas and 3,000 new types of cells.
2:00 What was this collaboration for?
2:40 Unexpected complexity of cells in certain brain parts.
4:00 Are there a lot of individual differences? Yes!
4:40 Physical structure appears same across species.
5:10 Genetic activity is very different though.
5:35 Human disorders are unique to humans.
6:30 Unusual layers protecting the brain — SLYM
7:38 Axons turned out to be more unusual, especially in other species.
9:35 Shape of the brain suggests apes and humans are similar only until adolescence.
12:15 Hippocampus in humans is unique focusing on vision…explaining art?
13:48 New memory cell discovered.
15:45 Limitations.

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Study: Novel small molecule 5D4 disrupts several molecular pathways that lead to cancer growth

Researchers at Baylor College of Medicine have identified a small molecule named 5D4 that can suppress the growth of breast and ovarian cancers in animal models. 5D4 works by binding to TopBP1 protein in cancer cells, disrupting its interactions with several pathways that promote cancer growth. Combining 5D4 with another cancer inhibitor, talazoparib, enhances the effectiveness of the anti-cancer activity.

The study, published in the Proceedings of the National Academy of Sciences, strongly supports continuing the investigation toward further developing this strategy for clinical use.

“Cancer development involves many steps of genetic alterations and signaling pathway deregulation. About 10 years ago, our team discovered that protein TopBP1 is at a convergent point of multiple cellular pathways involved in cancer growth and progression, making it a potential candidate for targeted cancer therapy,” said corresponding author Dr. Weei-Chin Lin, professor of medicine-hematology and oncology and of molecular and cellular biology at Baylor. He also is a member of Baylor’s Dan L Duncan Comprehensive Cancer Center. “Our idea was to identify molecules that would bind to TopBP1 and interfere with its interactions with molecular pathways that promote cancer growth.”

23AndMe Hacker Leaks New Tranche of Stolen Data

A threat actor who claimed responsibility for the compromise of the 23AndMe site earlier this month has released a new dataset, including the records of more than 4 million people’s genetic ancestry.

The cybercriminal, known by the handle Golem, alleges in a cybercrime Dark Web forum the stolen data includes information on, “the wealthiest people living in the US and Western Europe,” according to reports.

23andMe spokesperson Andy Kill said in a statement the organization is still trying to confirm whether the most recently leaked data is genuine.

23 Younger Biological Age: Supplements, Diet (Blood Test #6 in 2023)

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Genetic Factors that Could Extend the Life of Golden Retrievers

One of the most popular dog breeds is the Golden Retriever. Unfortunately, these dogs are also at high risk for developing cancer. New research has investigated genetic factors that may be able to extend the lives of these beloved dogs. This work focused on longevity genes instead of those that have been associated with cancer, and led to the identification of gene variants that could extend the dogs’ lifespan by as much as two years. The findings have been reported in GeroScience.

While most golden retrievers are predisposed to cancer, some of these dogs can live to be as old as 15 or 16 years. So the researchers thought that there might be genetic factors that were mitigating the effect of the cancer-related genes, noted co-corresponding study author Robert Rebhun, Maxine Adler Endowed Chair in oncology at the UC Davis School of Veterinary Medicine. The gene that had this effect was HER4.

TruDiagnostic and Harvard announce new multi omic informed biological aging clock

A study published today by scientists from Harvard University and epigenetic research company TruDiagnostic has shed light on the reasons why our bodies are aging on a cellular level, laying the foundations for medical based treatment options to reduce the risk of age-related death and disease in highly targeted ways.

Longevity. Technology: Age is the number one risk factor for most chronic diseases and death across the world. Epigenetics (or the way our genes are put to use throughout our bodies) has emerged as a crucial method of evaluating health, and while previous DNA methylation clocks could determine how advanced one’s body has aged, they have not yet been able to provide information to the reasons why someone might have accelerated or decelerated aging outcomes.

“In our research, we set out to create the best method to quantify the biological aging process. However, aging is extremely complex,” explains Harvard Medical School Associate Professor Dr Jessica Lasky-Su. “To solve this issue of complexity, our approach was to gather data across multiple sources of information. We chose to do this by building one of the most robust aging datasets in the world by quantifying patients’ proteomics, metabolomics, clinical histories and DNA methylation.”

Creating Sapient Technology and Cyborg Rights Should Happen Soon

Here’s my latest Opinion piece just out for Newsweek…focusing on cyborg rights.

Over the past half-century, the microprocessor’s capacity has doubled approximately every 18–24 months, and some experts predict that by 2030, machine intelligence could surpass human capabilities. The question then arises: When machines reach human-level intelligence, should they be granted protection and rights? Will they desire and perhaps even demand such rights?

Beyond advancements in microprocessors, we’re witnessing breakthroughs in genetic editing, stem cells, and 3D bioprinting, all which also hold the potential to help create cyborg entities displaying consciousness and intelligence. Notably, Yale University’s experiments stimulating dead pig brains have ignited debates in the animal rights realm, raising questions about the ethical implications of reviving consciousness.

Amid these emerging scientific frontiers, a void in ethical guidelines exists, akin to the Wild West of the impending cyborg age. To address these ethical challenges, a slew of futurist-oriented bills of rights have emerged in the last decade. One of the most prominent is the Transhumanist Bill of Rights, which is in its third revision through crowdsourcing and was published verbatim by Wired in 2018.

These cyborg bills encompass a broad array of protections, including safeguards for thinking robots, gender recognition for virtual intelligences, regulations for genetically engineered sapient beings, and the defense of freedoms for biohackers modifying their bodies. Some also incorporate tech-driven rules to combat environmental threats like asteroids, pandemics, and nuclear war.

Vocal functional flexibility in the grunts of young chimpanzees

Half a century after its foundation, the neutral theory of molecular evolution continues to attract controversy. The debate has been hampered by the coexistence of different interpretations of the core proposition of the neutral theory, the ‘neutral mutation–random drift’ hypothesis. In this review, we trace the origins of these ambiguities and suggest potential solutions. We highlight the difference between the original, the revised and the nearly neutral hypothesis, and re-emphasise that none of them equates to the null hypothesis of strict neutrality. We distinguish the neutral hypothesis of protein evolution, the main focus of the ongoing debate, from the neutral hypotheses of genomic and functional DNA evolution, which for many species are generally accepted. We advocate a further distinction between a narrow and an extended neutral hypothesis (of which the latter posits that random non-conservative amino acid substitutions can cause non-ecological phenotypic divergence), and we discuss the implications for evolutionary biology beyond the domain of molecular evolution. We furthermore point out that the debate has widened from its initial focus on point mutations, and also concerns the fitness effects of large-scale mutations, which can alter the dosage of genes and regulatory sequences. We evaluate the validity of neutralist and selectionist arguments and find that the tested predictions, apart from being sensitive to violation of underlying assumptions, are often derived from the null hypothesis of strict neutrality, or equally consistent with the opposing selectionist hypothesis, except when assuming molecular panselectionism. Our review aims to facilitate a constructive neutralist–selectionist debate, and thereby to contribute to answering a key question of evolutionary biology: what proportions of amino acid and nucleotide substitutions and polymorphisms are adaptive?

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