Lifeboat Foundation

Insilico Medicine, a clinical-stage generative AI-driven drug discovery company has announced that the company has used Microsoft BioGPT to identify targets against both the aging process and major age-related diseases.

Longevity. Technology: ChatGPT – the AI chatbot – can craft poems, write webcode and plan holidays. Large language models (LLMs) are the cornerstone of chatbots like GPT-4; trained on vast amounts of text data, they have been contributing to advances in diverse fields including literature, art and science – but their potential in the complex realms of biology and genomics has yet to be fully unlocked.

The new shots could make malaria protection more plentiful and affordable.

The effect of a TE on its host can be classified analogous to the effect of point mutations. In the majority of cases, the consequences of a TE their activity (transposition to a new genomic site) is either neutral or deleterious. The latter occurs, when TEs disrupt genes and their functions, or when, they trigger de-novo genomic instability by transposition or TE-mediated chromosomal rearrangements, which can lead to disease^{1, 3}. TEs can occasionally have a positive impact on the host genome, for example, by impacting gene regulatory networks. In the British peppered moth (Biston betularia), a TE inserted within the first intron of the cortex gene, resulted in increased transcription levels, subsequently affecting cell cycle regulation during wing-disc development through the amount of cortex protein product, resulting in the iconic melanic form⁴. However, more research is needed to understand these different evolutionary impacts that TEs can have when interacting with their host genome.

The increased accessibility to high throughput sequencing technologies has greatly increased our ability to analyse genetic differences caused by changes at the nucleotide level, and patterns of natural selection on coding sequences, and simultaneously allowed us to disentangle phenotypic differences at the nucleotide level. Mounting evidence has started to shed light on non-coding regions having important effects on genomic variation³. While TEs can be found in the genomes of virtually all organisms, large proportions of TEs are often absent from reference genomes, as their repetitive nature impedes their assembly and can result in collapsed regions within the reference genome^{2, 5}. These difficulties have led to an increased demand for reference genomes that are of a higher quality and are more complete. More importantly, a new demand for high-quality annotations of non-coding regions in reference genomes has surfaced. Annotations of non-coding regions are imperative to study the evolution of these regions between and within species. Improvements in sequencing techniques, especially the addition of long-read sequencing, and improved bioinformatic analytical tools are resulting in the assembly of increasingly gapless reference genomes, enabling the curation of high-quality TE annotations.

The current efforts of large consortia, such as the VGP⁶ and the B10K⁷ to create high-quality references for a wide variety of organisms provide invaluable data to improve our endeavours for a better understanding of TEs. With these new resources we can take our research into TEs and their effects on host genomes further, for example, to better understand the evolution of complex traits across phylogenomic scales. One such a complex trait is seasonal bird migration and recent research across a migratory divide in willow warblers identified a diagnostic TE correlated with migratory direction⁸. Here we focus on the Eurasian blackcap (Sylvia atricapilla), another iconic model species for bird migration, and consequently, the resource published here may be able to add insight to the quest to resolve the genetic background of migratory behaviour.

Genome engineering may be the future of medicine, but it relies on evolutionary advances made billions of years ago in primordial bacteria, the original masters of gene editing.

Modern day genome engineers like Columbia’s Sam Sternberg are always looking forward, modifying these ancient systems and pushing them to perform ever more complex feats of gene editing.

But to uncover new tools, it sometimes pays to look backward in time to understand how bacteria first created the original systems, and why.

A new CRISPR-based gene-editing tool has been developed which could lead to better treatments for patients with genetic disorders. The tool is an enzyme, AsCas12f, which has been modified to offer the same effectiveness but at one-third the size of the Cas9 enzyme commonly used for gene editing. The compact size means that more of it can be packed into carrier viruses and delivered into living cells, making it more efficient.

Researchers created a library of possible AsCas12f mutations and then combined selected ones to engineer an AsCas12f enzyme with 10 times more editing ability than the original unmutated type. This engineered AsCas12f has already been successfully tested in mice and has the potential to be used for new, more effective treatments for patients in the future.

By now you have probably heard of CRISPR, the gene-editing tool which enables researchers to replace and alter segments of DNA. Like genetic tailors, scientists have been experimenting with “snipping away” the genes that make mosquitoes malaria carriers, altering food crops to be more nutritious and delicious, and in recent years begun human trials to overcome some of the most challenging diseases and genetic disorders.

Stem cells from the human stomach can be converted into cells that secrete insulin in response to rising blood sugar levels, offering a promising approach to treating diabetes, according to a preclinical study from researchers at Weill Cornell Medicine.

In the study, which appeared April 27 in Nature Cell Biology, the researchers showed that they could take stem cells obtained from human stomach tissue and reprogram them directly—with strikingly high efficiency—into cells that closely resemble pancreatic insulin-secreting cells known as beta cells. Transplants of small groups of these cells reversed disease signs in a mouse model of diabetes.

“This is a proof-of-concept study that gives us a solid foundation for developing a treatment, based on patients’ own cells, for type 1 diabetes and severe type 2 diabetes,” said study senior author Dr. Joe Zhou, an associate professor of regenerative medicine and a member of the Hartman Institute for Therapeutic Organ Regeneration at Weill Cornell Medicine.

Ageing has always been inevitable but fasting, epigenetic reprogramming and parabiosis are just some of the scientific techniques that seem to help people stay young. Might the Peter Pan dream become real?

00:00 — Can science turn back the clock?
01:01 — Centenarians.
02:51 — What is ageing?
04:51 — Dietary restriction.
06:00 — Roundworms.
07:55 — Epigenetics.
09:43 — Blood and guts.
11:40 — Senolytics.
12:38 — Metformin.
13:51 — Anti-ageing treatments are coming.

Continue reading “Longevity: can ageing be reversed?” »

September is Thyroid Cancer Awareness Month, which makes this a good time to learn about treating thyroid cancer.

Nearly 44,000 new cases of thyroid cancer will be diagnosed in the U.S. this year, and more than 2,000 people will die of the disease, according to the American Cancer Society.

Thyroid cancer occurs in the cells of the thyroid, a butterfly-shaped gland at the base of your neck. Your thyroid produces hormones that regulate your heart rate, blood pressure, body temperature and weight.

Ribonucleic acid (RNA) is a molecule which is present in cells and made of genetic material to help build proteins necessary for cell function. RNA provides a template for the construction of proteins and is essential for cell and organism life. Immune cells rely on these proteins, including CD8⁺ or cytotoxic T cells which are responsible for killing invading pathogens. Importantly, cytotoxic T cells are a major component of the memory immune response. A pool of T cells specifically designed to recognize an invader is stored for future invasion of that particular pathogen. For example, once these cells are exposed to an invading antigen or protein, the immune system will expand T cells specific to that antigen and remember the antigen next time it enters the body. Vaccines work in a similar way by introducing a foreign antigen to the body, so the immune system is ready if the pathogen ever enters your body in the future. Only a small set of T cells that expand survive and it is unclear how this process occurs.

Recently a team of researchers at the University of Massachusetts Amherst (UMass) demonstrated that a single strand of RNA governs a T cells ability to recognize and kill tumors. The single strand of RNA is known as let-7 and is a microRNA, which is responsible for gene expression regulation. The recent discovery may improve vaccine development and cellular memory to enhance immunotherapy against cancers. Immunotherapy is a general term referring to cancer therapies that try to activate the immune system to kill the tumor compared to other drugs that try to directly kill the tumor with chemicals, such as chemotherapy.

The report published in Nature Communications identified that the microRNA, let-7, may enhance memory of T cells. Researchers led by Dr. Leonid Pobezinsky, Associate Professor of Veterinary and Animal Sciences at UMass, further built on our understanding of how T cells form immune memory. Pobezinsky and colleagues found that a small piece of microRNA that has been present throughout evolution is expressed in memory cells. Additionally, they found that more let-7 a cell has, the more likely that cell will recognize a cancer cell and kill it. The increased let-7 also indicates that the cell will turn into a memory cell after being exposed to an antigen. The regulation of enhanced memory T cells by let-7 is an integral process key to fight infections. This is a critical finding, especially because memory cells retain stem-like characteristics and can survive for decades.