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Scientists testing a new method of sequencing single cells have unexpectedly changed our understanding of the rules of genetics.

The genome of a protist has revealed a seemingly unique divergence in the DNA

DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).

Scientists studied genetic samples from more than 7,000 people and linked three genetic variants, inherited from Neanderthals, to increased pain sensitivity.

Summary: Researchers unveil the medial septum’s pivotal role in orchestrating memory storage and recall through managing rapid brain wave cycles in the hippocampus. Employing various research methodologies, including optogenetics, the team observes how gamma oscillations, embedded in theta rhythms, facilitate seamless switching between memory encoding and retrieval.

These fast and slow gamma waves, crucial for memory functions, are dictated through two primary pathways via the medial septum, showcasing a sophisticated coordination in memory processes. This insight illuminates potential avenues for understanding and eventually addressing memory-related illnesses like dementia.

This is a bit technical. “nucleocytoplasmic compartmentalization assay”, Yeah buddy.

Life is dependent on the preservation and storage of information. The genome and epigenome are the two central storehouses of information in eukaryotes, and although they work interdependently, they are fundamentally quite different. Genetic information is consistent across all body cells throughout the life of an individual while epigenetic information varies between cells as well as changes over time and as per environment.

Researchers have identified several hallmarks of aging such as epigenetic alterations, genomic instability, cellular senescence, telomere attrition, mitochondrial dysfunction, and others [1]. These are known to play a role in the dysfunction and deterioration of cells with age. David Sinclair and other researchers have previously indicated that loss of epigenetic information can cause changes in gene expression, leading to cellular identity loss. Previous studies in mice have also shown that cell injuries such as cell crushing and DNA double-strand breaks can promote loss of epigenetic information which can accelerate aging along with age-related diseases [2].

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Some of nature’s mysteries have kept scientists busy for decades—for example, the processes that drive evolution. The question of whether certain differences between and within species are caused by natural selection or by chance processes divides evolutionary biologists even today. Now, an international team of researchers has teased apart a scientific debate concerning the evolutionary theories of Darwin and the Japanese geneticist Kimura. Their conclusion: the debate is unnecessarily convoluted by the co-existence of different interpretations.

Due to his contributions to geological and biological sciences, British naturalist Charles Darwin (1809–1882) is considered one of the most important natural scientists. His influential work “On the Origin of Species” (1859), with its strictly scientific explanation of the diversity of life, forms the basis of modern evolutionary biology. Darwin concluded that species evolve through natural selection: well-adapted organisms survive, others don’t.

However, by the end of the 1960s, the Japanese geneticist Motoo Kimura (1924–1994) proposed that at the genetic level, most changes in the course of evolution do not offer direct advantages or disadvantages to the individual but are simply neutral. According to his “Neutral Theory of Molecular Evolution,” first published in 1968, most of the genetic variation within and between species arises from random fluctuations of neutral mutations.

Centenarians, once considered rare, have become commonplace. Indeed, they are the fastest-growing demographic group of the world’s population, with numbers roughly doubling every ten years since the 1970s.

How long humans can live, and what determines a long and healthy life, have been of interest for as long as we know. Plato and Aristotle discussed and wrote about the ageing process over 2,300 years ago.

The pursuit of understanding the secrets behind exceptional longevity isn’t easy, however. It involves unravelling the complex interplay of genetic predisposition and lifestyle factors and how they interact throughout a person’s life.

New research that helps explain the molecular processes involved in the painful autoimmune disease ankylosing spondylitis, or AS, may reduce the guessing game that health care providers currently play while attempting to treat the condition.

A team from Oregon Health & Science University and the VA Portland Health Care System has found a specific kind of AS treatment that is effective when used by patients who have a particular genetic mutation. Their study was published today in the journal Annals of the Rheumatic Diseases, and its findings could lead to more targeted, timely and patient-specific treatment recommendations.

“This is the first time research has shown that we might be able to use genetic markers to determine which therapy ankylosing spondylitis patients should receive,” said the study’s senior researcher, Ruth Napier, Ph.D., assistant professor of molecular microbiology and immunology, arthritis and rheumatic disease in the OHSU School of Medicine, and principal investigator with VA Portland. “These promising findings are encouraging. This is the first time I can say that I’m on the cusp of making a difference for patients with ankylosing spondylitis who seek relief.”

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