Plant DNA has become a frontier for artificial intelligence, with large language models turning genetic sequences into interpretable content for researchers. These tools treat bases like words, revealing hidden patterns that once eluded traditional methods.
A study published by Dr. Meiling Zou from Hainan University describes how language-based models interpret extensive plant genomes with remarkable precision.
To Shakespeare’s Hamlet, we humans are “the paragon of animals.” But recent advances in genetics are suggesting that humans are far from being evolution’s greatest achievement.
For example, humans have an exceptionally high proportion of fertilized eggs that have the wrong number of chromosomes and one of the highest rates of harmful genetic mutation.
In my new book, “The Evolution of Imperfection,” I suggest that two features of our biology explain why our genetics are in such a poor state. First, we evolved a lot of our human features when our populations were small, and second, we feed our young across a placenta.
Scientists have revealed a novel means of tracking everything from wildlife to illicit substances using environmental DNA detectable in the air around us.
The findings, outlined in a new study published in Nature Ecology & Evolution, show that tracking virtually anything using environmental DNA can be achieved as simply as capturing this ever-present genetic material from the air using a vacuum.
The discovery, made by a team led by David Duffy, Ph.D., reveals DNA as a powerful new tool for detecting and tracking living organisms and a range of substances in virtually any environment.
Scientists at the San Raffaele Telethon Institute for Gene Therapy (SR-Tiget), Milan, have found that gene editing using CRISPR-Cas9 in combination with AAV6 vectors can trigger inflammatory and senescence-like responses in blood stem cells, compromising their long-term ability to regenerate the blood system.
The study, published in Cell Reports Medicine, outlines new strategies to overcome this hurdle, improving both the safety and efficacy of gene-editing-based therapies for inherited blood disorders.
The research was led by Dr. Raffaella Di Micco, group leader at SR-Tiget, New York Stem Cell Foundation Robertson Investigator and Associate Professor at the School for Advanced Studies (IUSS) of Pavia, in collaboration with Professor Luigi Naldini, Director of SR-Tiget, and several European research partners.
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The researchers are especially interested in how our bodies maintain balance. Metabolic homeostasis, the fancy term for it, may have shaped more traits than we realize.
And as diets continue to change today, our ancient genetic choices could still be nudging us in new directions.
The study is published in the journal Cell Genomics.
We are currently facing the possibility of achieving immortality for humans by 2030. This prediction comes from renowned futurist Ray Kurzweil, who has a history of making accurate predictions. He anticipates that with the ongoing progress in genetics, robotics, and nanotechnology, we will soon have nanobots coursing through our bloodstream, which could enable us to live forever. It’s truly remarkable to consider that this could be a reality within just seven years.
Nanobots, which are small robots sized between 50–100 nm in width, are currently being used in various clinical medical applications. They are used in research as DNA probes, imaging materials for cells, and targeted delivery vehicles for cells. According to Kurzweil, nanobots represent the future of medicine.
They will be capable of repairing our bodies at a cellular level, making us resistant to diseases, aging, and, ultimately death. Additionally, he theorizes that humans may be able to transfer their consciousness into digital form, leading to immortality.
Ischaemic heart disease remains the main cause of death worldwide. 1 Within its multifactorial aetiology low-density lipoprotein (LDL) and other apolipoprotein (apo) B-containing lipoproteins play a central, causal role, promoting the development of the underlying process of atherosclerosis. The use of statins and other drugs—ezetimibe, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, bempedoic acid—to lower LDL is a central strategy in the prevention of atherosclerotic cardiovascular disease (ASCVD) in both primary and secondary settings. 2 However, in many individuals, a substantial ASCVD risk remains after LDL-cholesterol (LDL-C) goal achievement, and elevated plasma triglyceride (TG) is recognised as an important component of this residual risk. 3 Plasma TG, or more specifically TG-rich lipoproteins (TRL), is therefore an additional target for lipid-lowering therapy. Outcome studies of TG lowering using classical drugs such as fibrates and high-dose niacin when added to statins failed to demonstrate further ASCVD risk reduction, although retrospective analyses suggest that subgroups characterised by high TG and low high-density lipoprotein (HDL) may have positive results. 4–7 An alternative approach, treatment with high-dose eicosapentaenoic acid (EPA), has been shown to reduce cardiovascular risk in patients with (and without) hypertriglyceridaemia who are on statins. 8–10
This review explores the concepts behind, and practical implementation of, an evidence-based therapeutic strategy that tailors further intervention according to the plasma lipid profile in patients on standard statin therapy who are often undertreated. 11
Genetic analyses provide robust evidence that elevated TG is a causal risk factor for ASCVD 12 13 and underpin the finding from epidemiological studies that raised TG levels are positively and linearly related to cardiovascular risk (figure 1A). 14 15 The importance of these observations is that they reveal an often unaddressed major risk factor that is of particular relevance in people with obesity or type 2 diabetes in whom TG levels are frequently elevated. 16 Further, outcome trials have shown that elevated TG levels (again especially in type 2 diabetics) are associated with high residual cardiovascular risk in statin-treated patients with established cardiovascular disease, even if they have well-controlled LDL-C. 17–19.