World’s first pig lung transplant in brain-dead man lasts nine days in China.
In a medical first, a pig lung was transplanted into a brain-dead human, where it functioned for nine days.
Surgeons at Guangzhou Medical University, China, performed the cross-species lung transplantation.
The recipient, a 39-year-old man who had suffered a brain hemorrhage, received the left lung from a Chinese Bama Xiang pig that had undergone genetic modifications.
Translocations are chromosomal “cut and paste” errors that drive many lymphomas, a type of blood cancer and the sixth most common form of cancer overall. This includes mantle cell lymphoma, a rare but aggressive subtype diagnosed in about one in every 100,000 people each year.
A study by researchers at the Centre for Genomic Regulation (CRG) in Barcelona, has shown a new way translocations promote cancer. The translocation most typically found in mantle cell lymphoma drags a powerful regulatory element into a new area of the human genome, where its new position allows it to boost the activity of not just one but 50 genes at once.
The discovery of this genome rewiring mechanism shows the traditional focus on the handful of genes at chromosomal breakpoints is too narrow. The study also greatly expands the list of potential drug targets for mantle cell lymphoma, for which there is no known cure.
Scientists at the Medical Research Council’s Laboratory of Molecular Biology say they’ve engineered a bacteria whose genetic code is more efficient than any other lifeform on Earth.
They call their creation “Syn57,” a bioengineered strain of E. coli — yes, the same bad boy that can make you extremely sick if you eat an undercooked hot dog — which uses seven less codons than all life on earth. A codon, put simply, is a three-letter sequence found in DNA and RNA which delivers instructions for amino acids, a fundamental “building block” of life.
For the past billions years or so, all known life on earth has used 64 codons. Scientists cracked the code detailing which codons corresponded to which amino acids — mapping the standard genetic code, in other words — in 1966, revealing only 20 total amino acids.
Researchers at VCU Massey Comprehensive Cancer Center have developed a new computational tool called Vesalius, which could help clinicians understand the complex relationships between cancer cells and their surrounding cells, leading to potential discoveries regarding the development of hard-to-treat cancers.
Findings from a new study, published in Nature Communications, could help guide the identification of predictive biomarkers for multiple cancers and better inform the effectiveness of different treatment options based on individuals’ specific type of disease.
Rajan Gogna, Ph.D., member of the Developmental Therapeutics research program at Massey and assistant professor in the VCU School of Medicine’s Department of Human and Molecular Genetics, and a team of collaborators were driven by the goal of interpreting extensive amounts of data in a meaningful way.
Researchers from University of California San Diego Sanford Stem Cell Institute have developed a novel method to stimulate and mature human brain organoids using graphene, a one-atom-thick sheet of carbon. Published in Nature Communications, the study introduces Graphene-Mediated Optical Stimulation (GraMOS), a safe, non-genetic, biocompatible, non-damaging way to influence neural activity over days to weeks. The approach accelerates brain organoid development — especially important for modeling age-related conditions like Alzheimer’s disease — and even allows them to control robotic devices in real time.
“This is a game-changer for brain research,” said Alysson Muotri, Ph.D., corresponding author, professor of pediatrics, and director of the UC San Diego Sanford Stem Cell Institute Integrated Space Stem Cell Orbital Research Center. “We can now speed up brain organoid maturation without altering their genetic code, opening doors for disease research, brain–machine interfaces and other systems combining living brain cells with technology.”
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Chronic pain is life-changing and considered one of the leading causes of disability worldwide, making daily life difficult for millions of people around the world, and exacerbating personal and economic burdens. Despite established theories about the molecular mechanisms behind it, scientists have been unable to identify the specific processes in the body responsible, until now.
In an exciting collaboration, a team led by NDCN’s Professor David Bennett, and Professor Simon Newstead in the Department of Biochemistry and Kavli Institute for NanoScience Discovery, have identified a new genetic link to pain, determined the structure of the molecular transporter that this gene encodes, and linked its function to pain.
The findings of the research offers a promising, new, specific target against which to develop a drug to alleviate chronic pain. The paper “SLC45A4 is a pain gene encoding a neuronal polyamine transporter” is published in Nature.
A large international study led by researchers at the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, shows that major depressive disorder (MDD) not only increases risk for a wide range of diseases and social problems, but is also partly driven by factors such as loneliness, obesity, smoking, and chronic pain.
The study, published in Nature Mental Health, applied genetic methods to systematically test which traits are causes, and which are consequences, of depression. The findings highlight the double burden of MDD: it both arises from and contributes to poor health, making prevention and treatment particularly urgent.
“We show that depression sits at the center of a web of health problems,” says Joëlle Pasman, research associate at Amsterdam UMC and Karolinska Institutet, who led the study. “It is not only a debilitating condition in itself but also increases the risk of many diseases, while at the same time being triggered by social, behavioral, and medical factors.”