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Category: biotech/medical – Page 10

Machine learning method improves accuracy of inverse protein folding for drug design

An AI approach developed by researchers from the University of Sheffield and AstraZeneca, could make it easier to design proteins needed for new treatments.

In their study published in the journal Nature Machine Intelligence, Sheffield computer scientists in collaboration with AstraZeneca and the University of Southampton have developed a new machine learning framework that has shown the potential to be more accurate at inverse than existing state-of-the-art methods.

Inverse protein folding is a critical process for creating novel proteins. It is the process of identifying , the building blocks of proteins, that fold into a desired 3D protein structure and enable the protein to perform specific functions.

Scientists Discover Molecule That Blocks Aging And Dementia in Mice

Scientists are looking at ways to tackle Alzheimer’s and dementia from all kinds of angles, and a new study has identified the molecule hevin (or SPARCL-1) as a potential way of preventing cognitive decline.

Hevin is a protein naturally produced in the brain by cells called astrocytes. These support-worker cells look after the connections or synapses between neurons, and it’s thought that hevin plays a role in this essential work.

In this new study, researchers from the Federal University of Rio de Janeiro (UFRJ) and the University of São Paulo in Brazil boosted hevin production in the brains of both healthy mice and those with an Alzheimer’s-like disease.

Cancer Plasticity: The Shape-Shifting Threat Challenging Modern Treatments

Cancer plasticity allows tumor cells to change their identity, evade therapies, and adapt to environmental pressures, contributing to treatment resistance and metastasis. New research is targeting this adaptability through epigenetic drugs, immune checkpoint inhibitors, and strategies to limit phenotypic switching.

Previously uncharacterized gene necessary for DNA repair identified

Cells are constantly subjected to DNA damage from a range of internal and environmental sources. It is estimated that cells can experience as many as 100,000 DNA lesions per day. One of the most deleterious types of DNA lesions is the DNA double-strand break (DSB). Just one unrepaired DNA DSB may be enough to cause mutations or cell death leading to a wide range of pathologies including cancer, immune deficiency, premature aging and neurodegeneration.

To respond to the array of DNA lesions that occur, cells have developed a complex and coordinated series of steps involving DNA damage recognition, cell cycle arrest and signaling-induced activation of the DNA repair machinery—processes collectively referred to as the DNA damage response (DDR). In recent years, progress has been made in understanding how this process is initiated. However, the later stages of this process, including long range DNA end-resection, are not well understood.

In a new study published in Nature Cell Biology, researchers from Boston University Chobanian & Avedisian School of Medicine, Massachusetts General Hospital (MGH) and Harvard Medical School, identified several uncharacterized chromatin factors (proteins that regulate ) that are recruited to sites of DNA damage, including the gene ZNF280A. Importantly, this gene is hemizygously deleted—meaning one of the two copies of alleles is missing—in a subset of patients with a human developmental syndrome called 22q11.2 distal deletion syndrome.

Parkinson’s: an unknown treatment already transforming patients’ lives

A major medical breakthrough is giving new hope to those with Parkinson’s disease. Stem cell transplants into the brain are showing impressive results, leading to long-term improvements in motor symptoms for the first patients treated… Read more

First ancient genomes from the Green Sahara deciphered

The study provides critical new insights into the African Humid Period, a time between 14,500 and 5,000 years ago when the Sahara desert was a green savanna, rich in water bodies that facilitated human habitation and the spread of pastoralism. Later aridification turned this region into the world’s largest desert. Due to the extreme aridity of the region today, DNA preservation is poor, making this pioneering ancient DNA study all the more significant.

Genomic analyses reveal that the ancestry of the Takarkori rock shelter individuals primarily derives from a North African lineage that diverged from sub-Saharan African populations at about the same time as the modern human lineages that spread outside of Africa around 50,000 years ago. The newly described lineage remained isolated, revealing deep genetic continuity in North Africa during the late Ice Age. While this lineage no longer exists in unadmixed form, this ancestry is still a central genetic component of present-day North African people, highlighting their unique heritage.

An international team led by researchers from the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, has sequenced the first ancient genomes from the so-called Green Sahara, a period when the largest desert in the world temporarily turned into a humid savanna-like environment. By analyzing the DNA of two 7,000-year-old naturally mummified individuals excavated in the Takarkori rock shelter in southwestern Libya by the Archaeological Mission in the Sahara, Sapienza University of Rome, the team showed that they belonged to a long-isolated and now extinct North African human lineage. This group of cattle pastoralists has only a minor genetic component of non-African ancestry, suggesting that animal husbandry may have spread into the Green Sahara through cultural exchange rather than large-scale migrations.

Space conditions can cause gum inflammation and bone loss, say scientists

Living in zero gravity can lead to periodontitis, a common and serious condition where the gums become inflamed and the bone that supports teeth starts to break down, eventually leading to tooth loss, scientists reveal in a new study.

The scientists confirm their findings in a study published in the Journal of Periodontal Research, in which they try to understand how simulated —the near-weightless environment astronauts experience in space—might influence the development and severity of periodontitis.

The researchers carried out their experiment in a lab in which were used to test the impact of periodontitis in and on Earth. To simulate this, they used a special model where mice were placed in a position that mimics the effects of microgravity, and then gum disease was induced.

Advancing neuroscience research with high-speed, automated electrophysiology

Understanding the electrical activity of neurons is key to unlocking insights into neurological diseases. Yale researchers have unveiled a high-throughput automated method that captures the electrical activity of large numbers of neurons simultaneously and without bias.

This cutting-edge approach provides a powerful “functional fingerprint” of neuron populations in their natural state, opening new doors to understanding and treating neurological diseases. The work was published June 13 in Nature Protocols.

The patch-clamp technique has long been a gold standard for studying the electrical activity of neurons, the fundamental units of the nervous system. However, the manual execution of this approach is slow and labor-intensive. Recent advances in robotic patch-clamp technologies have improved speed and efficiency, but they are limited to artificially grown neurons rather than neurons in their native unmanipulated state.

Newly discovered mechanism of mitochondrial dysfunction in obesity may drive insulin resistance and type 2 diabetes

A newly discovered mechanism that leads to liver dysfunction may be a key factor in type 2 diabetes and other metabolic disorders in individuals with obesity, according to a new study led by Harvard T.H. Chan School of Public Health.

The dysfunction identified—dysregulated hepatic coenzyme Q metabolism—leads to excessive reactive oxygen species (ROS) produced by mitochondria at a single specific site in an enzyme called complex I. The researchers say the discovery offers a potential path for new, precise treatments for metabolic diseases.

“Our findings provide the first step toward solving a complex problem in the field of metabolic disease research that has stood for three decades,” said corresponding author Gökhan S. Hotamisligil, James Stevens Simmons Professor of Genetics and Metabolism.