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Category: biotech/medical – Page 114

Researchers found that neural crest stem cells are uniquely capable of reprogramming, challenging current reprogramming theories and opening possibilities for stem cell-based treatments.

A research team from the University of Toronto has identified that neural crest stem cells, a group of cells found in the skin and other parts of the body, are the origin of reprogrammed neurons previously found by other scientists.

Their findings refute the popular theory in cellular reprogramming that any developed cell can be induced to switch its identity to a completely unrelated cell type through the infusion of transcription factors. The team proposes an alternative theory: there is one rare stem cell type that is unique in its ability to be reprogrammed into different types of cells.

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Carbon is a gregarious little atom, bending over backwards to link with a wide variety of elements in what is collectively referred to as organic chemistry. Life itself wouldn’t be possible without carbon’s knack for making connections.

Yet even this friendly fellow has its limits. Take Bredt’s rule for instance, which says stable two-laned connections known as covalent double bonds won’t form adjacent to any V-shaped bridges that happen to form across ‘bicyclic’ molecules.

Now a team of chemists from the University of California, Los Angeles has uncovered a solution that violates Bredt’s century-old rule. This encourages future drug research to explore the use of molecules that we thought could not exist.

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Google DeepMind has unexpectedly released the source code and model weights of AlphaFold 3 for academic use, marking a significant advance that could accelerate scientific discovery and drug development. The surprise announcement comes just weeks after the system’s creators, Demis Hassabis and John Jumper, were awarded the 2024 Nobel Prize in Chemistry for their work on protein structure prediction.

AlphaFold 3 represents a quantum leap beyond its predecessors. While AlphaFold 2 could predict protein structures, version 3 can model the complex interactions between proteins, DNA, RNA, and small molecules — the fundamental processes of life. This matters because understanding these molecular interactions drives modern drug discovery and disease treatment. Traditional methods of studying these interactions often require months of laboratory work and millions in research funding — with no guarantee of success.

The system’s ability to predict how proteins interact with DNA, RNA, and small molecules transforms it from a specialized tool into a comprehensive solution for studying molecular biology. This broader capability opens new paths for understanding cellular processes, from gene regulation to drug metabolism, at a scale previously out of reach.

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How organisms age is a question with broad implications for human health. In mammals, DNA methylation is a biomarker for biological age, which may predict age more accurately than date of birth. However, limitations in mammalian models make it difficult to identify mechanisms underpinning age-related DNA methylation changes. Here, we show that the short-lived model plant Arabidopsis thaliana exhibits a loss of epigenetic integrity during aging, causing heterochromatin DNA methylation decay and the expression of transposable elements. We show that the rate of epigenetic aging can be manipulated by extending or curtailing lifespan, and that shoot apical meristems are protected from this aging process. We demonstrate that a program of transcriptional repression suppresses DNA methylation maintenance pathways during aging, and that mutants of this mechanism display a complete absence of epigenetic decay. This presents a new paradigm in which a gene regulatory program sets the rate of epigenomic information loss during aging.

The authors have declared no competing interest.

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A multi-institutional group of researchers led by the Hubrecht Institute and Roche’s Institute of Human Biology has developed strategies to identify regulators of intestinal hormone secretion. In response to incoming food, these hormones are secreted by rare hormone producing cells in the gut and play key roles in managing digestion and appetite. The team has developed new tools to identify potential ‘nutrient sensors’ on these hormone producing cells and study their function. This could result in new strategies to interfere with the release of these hormones and provide avenues for the treatment of a variety of metabolic or gut motility disorders. The work will be presented in an article in Science, on October 18th.

The intestine acts as a vital barrier. It protects the body from harmful bacteria and highly dynamic pH levels, while allowing nutrients and vitamins to enter the bloodstream. The gut is also home to endocrine cells, which secrete many hormones that regulate bodily functions. These enteroendocrine cells (EECs, endocrine cells of the gut) are very rare cells that release hormones in response to various triggers, such as stretching of the stomach, energy levels and nutrients from food. These hormones in turn regulate key aspects of physiology in response to the incoming food, such as digestion and appetite. Thus, EECs are the body’s first responders to incoming food, and instruct and prepare the rest of the body for what is coming.

Medications that mimic gut hormones, most famously GLP-1, are very promising for the treatment of multiple metabolic diseases. Directly manipulating EECs to adjust hormone secretion could open up new therapeutic options. However, it has been challenging to understand how gut hormone release can be influenced effectively. Researchers have had trouble identifying the sensors on EECs, because EECs themselves represent less than 1% of cells in the intestinal epithelium, and in addition the sensors on these EECs are expressed in low amounts. Current studies mainly rely on mouse models, even though the signals to which mouse EECs respond are likely different compared to those to which human EECs respond. Therefore, new models and approaches were required to study these signals.

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Scientists from Vilnius University’s (VU) Life Sciences Center (LSC) have discovered a unique way for cells to silence specific genes without cutting DNA. This research, led by Prof. Patrick Pausch and published in the journal Nature Communications, reveals a new way to silence genes that is akin to pressing a “pause” button on certain genetic instructions within cells.

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Macrophages are associated with many human diseases but are challenging to study in vivo. Here, Ginhoux and colleagues discuss how iMacs — macrophages generated from induced pluripotent stem (iPS) cells — can enable disease modelling, including through the use of patient-derived iPS cells and 3D organoid co-culture systems. Ultimately, these iMac-based approaches can improve our understanding of macrophage biology in both health and disease.

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A team of EU scientists is developing a new advanced camera that uses photonics to reveal what the eye cannot see. This innovative system is being developed to transform various industries, including vertical farming. It will allow farmers growing crops like salads, herbs, and microgreens to detect plant diseases early, monitor crop health with precision, and optimise harvest times — boosting yields by up to 20%.

A new European consortium funded under the Photonics Partnership is developing a new imaging platform that ensures everything from crops to factory products is of the highest quality by detecting things humans simply cannot.

Called ‘HyperImage’, the project aims to revolutionise quality assurance and operational efficiency across different sectors. This high-tech imaging system uses AI machine learning algorithms to identify objects for more precise decision-making.

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Abstract. Type H vessels have been proven to couple angiogenesis and osteogenesis. The decline of type H vessels contributes to bone loss in the aging process. Aging is accompanied by the accumulation of advanced oxidation protein products (AOPPs). However, whether AOPP accumulation is involved in age-related decline of type H vessels is unclear. Here, we show that the increase of AOPP levels in plasma and bone were correlated with the decline of type H vessels and loss of bone mass in old mice. Exposure of microvascular endothelial cells to AOPPs significantly inhibited cell proliferation, migration, and tube formation, increased NADPH oxidase activity and excessive reactive oxygen species generation, upregulated the expression of vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1, and eventually impaired angiogenesis, which was alleviated by redox modulator N-acetylcysteine and NADPH oxidase inhibitor apocynin. Furthermore, reduced AOPP accumulation by NAC treatment was able to alleviate significantly the decline of type H vessels, bone mass loss and deterioration of bone microstructure in old mice. Collectively, these findings suggest that AOPPs accumulation contributes to the decline of type H vessels in the aging process, and illuminate a novel potential mechanism underlying age-related bone loss.

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