Lifeboat Foundation

Unnecessary playing with nature.

In January, Bennett’s doctors offered him the chance to receive a heart from a pig. He took it. “I know it’s a shot in the dark, but it’s my last choice,” he said in a press release from the University of Maryland Medical Center in Baltimore, where he was being treated. On 7 January, doctors transplanted the heart, which had been genetically modified so that the human body would tolerate it.

Bennett survived for eight weeks with his new heart before his body shut down. After his death, the research team learnt that the transplanted organ was infected with a pig herpesvirus that had not been detected by tests¹.

Continue reading “Will pigs solve the organ crisis? The future of animal-to-human transplants” »

The discovery could lead to potential future targeted therapies and treatments for this brain disorder.

Researchers have found two novel genes that increase an individual’s risk of developing Alzheimer’s disease (AD). This disorder is the leading cause of dementia and has an estimated heritability —genetic factor causing variation in the population, or an inherited trait— of 70%.

Digicomphoto/iStock.

Continue reading “The world’s largest Alzheimer’s study has made a gene discovery that could lead to treatments” »

A University of Maryland researcher and colleagues found that the fungus Metarhizium robertsii removes mercury from the soil around plant roots, and from fresh and saltwater. The researchers also genetically engineered the fungus to amplify its mercury detoxifying effects.

Mercury pollution of soil and water is a worldwide threat to public health. This new work suggests Metarhizium could provide an inexpensive and efficient way to protect crops grown in polluted areas and remediate mercury-laden waterways.

The study, which was conducted by UMD professor of entomology Raymond St. Leger and researchers in the laboratory of his former post-doctoral fellow, Weiguo Fang (now at Zhejiang University in Hangzhou, China), was published in Proceedings of the National Academy of Sciences (PNAS) on November 14, 2022.

New research from the University of California, Irvine, suggests aging is an important component of retinal ganglion cell death in glaucoma, and that novel pathways can be targeted when designing new treatments for glaucoma patients.

The study was published today in Aging Cell. Along with her colleagues, Dorota Skowronska‐Krawczyk, Ph.D., assistant professor in the Departments of Physiology & Biophysics and Ophthalmology and the faculty of the Center for Translational Vision Research at the UCI School of Medicine, describes the transcriptional and epigenetic changes happening in aging retina.

The team shows how stress, such as intraocular pressure (IOP) elevation in the eye, causes retinal tissue to undergo epigenetic and transcriptional changes similar to natural aging. And, how in young retinal tissue, repetitive stress induces features of accelerated aging including the accelerated epigenetic age.

Circa 2012

Researchers have identified seven genetic markers linked with a woman’s breast size, according to a new study.

While it’s was known that breast size is in part heritable, the study is the first to find specific genetic factors that are associated with differences in breast size, the researchers said.

Circa 2017 face_with_colon_three

Study of more than 195,000 people finds 16 common genetic variants associated with muscle strength and gives insight into underlying biological mechanisms.

Sponsored by Kishore Tipirneni’s new book “A New Eden” available here: https://getbook.at/NewEden | Abiogenesis – origin of life. Living matter from non-living matter. The origin of living organisms from inorganic or non-living material is called abiogenesis. But abiogenesis is not evolution.

Despite the incredible variations of life we see today, at the fundamental level, all living things contain three elements: Nucleic acids, Proteins, and lipids. These three things had to have been present in order for life to start.

Continue reading “How did life begin? Abiogenesis. Origin of life from nonliving matter” »

New research at the University of Chicago has found that the same machinery used by mammalian cells to drive cellular differentiation also plays a critical role in activating genes in yeast in response to environmental stress.

The results, which were published in Molecular Cell, suggest that these machines, known as transcriptional condensates, are an ancient, conserved tool used by eukaryotic cells to promote high level gene expression for over a billion years. The findings are helping to not only better explain how cells respond dynamically to environmental cues but also have implications for understanding human diseases such as cancer and neurodegeneration.

The study extends existing research on transcriptional condensates in mammalian cells into yeast and their heat shock response—how cells respond to high temperatures. “The heat shock response is ancient,” said David Pincus, Ph.D., Assistant Professor of Molecular Genetics and Cell Biology at UChicago. “This response existed long before there were people—long before there were even yeast. It predates the split between prokaryotes and eukaryotes, so it’s a really fundamental and important cellular response.”

A research team has identified a molecular target that could open up new therapeutic options to treat aging-associated diseases like Parkinson’s. Scientists at the University of Cologne have discovered how cells can eliminate mutated mitochondrial DNA (mtDNA). Mitochondria are the powerhouses of our cells. Due to their evolutionary descent from bacteria, they still have genetic material packaged in chromosome-like structures (nucleoids). They convert the chemical energy in our food into a biologically usable form. A team of researchers from the University of Cologne’s Physiology Centre at the Faculty of Medicine, the Centre for Molecular Medicine Cologne (CMMC) and the CECAD Cluster of Excellence for Aging Research has now shown that mutations of the mtDNA lead to a local rearrangement of proteins in the mitochondrial membrane. The mutated mtDNA is targeted, eliminated, and subjected to autophagy, the cellular ‘waste disposal’. The results have appeared in Nature Communications under the title ‘Mitochondrial membrane proteins and VPS35 orchestrate selective removal of mtDNA’.

In many tissues, mutations in mtDNA accumulate as a result of normal aging. These kinds of mutations are an important cause of many aging-associated diseases. There are thousands of copies mtDNA in every cell, so mitochondrial function is only impaired when the percentage of mutated mtDNA molecules exceeds a certain threshold value. It has long been established that mitochondrial damage, including acute mtDNA damage, triggers the process of mitophagy. In this process, dysfunctional mitochondrial parts are selectively degraded and recycled.

Dr David Pla-Martin, the lead author of the current study, explained the details: ‘What is new in our study is that this mechanism does not affect the cells’ endowment with mitochondria, but only clears out the damaged mtDNA. By labelling neighbouring proteins — so-called proximity labelling — we showed that mtDNA damage leads to the recruitment of endosomes in close proximity to nucleoids.’ Their removal is coordinated by the interaction of the nucleoid protein Twinkle and the mitochondrial membrane proteins SAMM50 and ATAD3 controls their distribution, SAMM50 induces the release and transfer of the nucleoid to the so-called endosomes. ‘This additionally prevents the activation of an immune response. The protein VPS35, the main component of the retromer, mediates the maturation of early endosomes into late autophagy vesicles, where degradation and recycling ultimately take place,’ said Pla-Martin.