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LEV is upon us.


OpenAI chief executive Sam Altman, who provided the initial $180mn to seed the start-up, will put in more money in the series A. The company is in talks with family offices, venture capitalists and sovereign wealth funds, as well as a US “hyperscaler” data centre to provide computing power to run the AI models it uses to create and test its treatments.

In partnership with OpenAI, the start-up has built a bespoke AI model that designs proteins to temporarily turn regular cells into stem cells, which it says can reverse their ageing process.

The San Francisco-based biotech will use the money to fund clinical trials for three drugs, including a potential treatment for Alzheimer’s disease, which will be tested in an early stage study in Australia this year. It is also working on drugs for rejuvenating blood and brain cells.

Engineered enzymes are poised to have transformative impacts across applications in energy, materials, biotechnology, and medicine. Recently, machine learning has emerged as a useful tool for enzyme engineering. Now, a team of bioengineers and synthetic biologists says they have developed a machine-learning guided platform that can design thousands of new enzymes, predict how they will behave in the real world, and test their performance across multiple chemical reactions.

Their results are published in Nature Communications in an article titled, “Accelerated enzyme engineering by machine-learning guided cell-free expression,” and led by researchers at Stanford University and Northwestern University.

“Enzyme engineering is limited by the challenge of rapidly generating and using large datasets of sequence-function relationships for predictive design,” the researchers wrote. “To address this challenge, we develop a machine learning (ML)-guided platform that integrates cell-free DNA assembly, cell-free gene expression, and functional assays to rapidly map fitness landscapes across protein sequence space and optimize enzymes for multiple, distinct chemical reactions.”

A study by the University of the Basque Country (UPV/EHU) demonstrates that the drug WIN55,212–2 protects the brain and reverses early cognitive damage caused by dementia, while also explaining its mechanism of action.

Over two decades of research conducted by the Neurochemistry and Neurodegeneration group at UPV/EHU, led by Dr. Rafael Rodríguez-Puertas, has uncovered a promising pathway for developing therapies aimed at improving memory in cases of cognitive impairment caused by neurodegenerative diseases like Alzheimer’s.

Alzheimer’s disease is a progressive neurological disorder that primarily affects older adults, leading to memory loss, cognitive decline, and behavioral changes. It is the most common cause of dementia. The disease is characterized by the buildup of amyloid plaques and tau tangles in the brain, which disrupt cell function and communication. There is currently no cure, and treatments focus on managing symptoms and improving quality of life.

A research team at KAIST has identified the core gene expression networks regulated by key proteins that fundamentally drive phenomena such as cancer development, metastasis, tissue differentiation from stem cells, and neural activation processes. This discovery lays the foundation for developing innovative therapeutic technologies.

A joint research team led by Professors Seyun Kim, Gwangrog Lee, and Won-Ki Cho from the Department of Biological Sciences has uncovered essential mechanisms controlling gene expression in animal cells.

The findings were published on January 7 in the journal Nucleic Acids Research in a paper titled “Single-molecule analysis reveals that IPMK enhances the DNA-binding activity of the transcription factor SRF.”

Cancer cells need to acquire a different metabolic state than that of non-tumor cells in order to proliferate, invade, and metastasize. During cancer progression, cancer cells encounter various kinds of metabolic stress. First, tumor microenvironments are generally hypoxic and acidic and have a distinct nutrient composition compared to non-tumor tissues from the primary site, which forces cancer cells to adapt in order to grow and invade in these environments. Second, to enter and survive in vessels, cancer cells must reprogram their metabolic state, allowing for anchorage-independent growth that induces extensive oxidative stress in cancer cells. Finally, once cancer cells colonize other organs, they must adapt to quite distinct metabolic environments than those present in primary sites [1]. Overall, because cancer cells need to reprogram their metabolic state during each step of cancer progression, metabolic reprogramming has been recognized as one of the hallmarks of cancer [2].

Elucidating the mechanisms underlying metabolic reprogramming during cancer progression can reveal the metabolic vulnerabilities of cancer cells. This may ultimately result in the identification of new therapeutic targets for cancer and improvement of patients’ prognosis. In this review, we describe each step of the metabolic reprogramming that occurs in cancer cells during cancer progression, including during growth and invasion in primary sites, survival in vessels, and colonization of other organs. Finally, we also describe emerging therapeutic strategies that target cancer-specific metabolism.

Can a file be stored on DNA? What would be the advantages of such storage? And what developments can we expect in the future? All these answers in 12 minutes!

0:00 — Introduction.
2:00 — Inspiration from life, DNA
3:24 — Storing files.
7:35 — A technology under development.
10:51 — Conclusion.

Video produced for EchoSciences Sud Provence-Alpes-Côte d’Azur https://www.echosciences-paca.fr with CNRS research director Marc Antonini (I3S — CNRS/UCA). Based on an original idea by Play Azur Prod. Video coordinated by Gulliver https://www.gulliver-sciences.fr and Play Azur Prod: https://playazur-prod.fr/

Calculations and sources of the figures :

The core components of CRISPR-based genome-editing therapies are bacterial proteins called nucleases that can stimulate unwanted immune responses in people, increasing the chances of side effects and making these therapies potentially less effective.

Researchers at the Broad Institute of MIT and Harvard and Cyrus Biotechnology have now engineered two CRISPR nucleases, Cas9 and Cas12, to mask them from the immune system. The team identified protein sequences on each nuclease that trigger the immune system and used computational modeling to design new versions that evade immune recognition. The engineered enzymes had similar gene-editing efficiency and reduced immune responses compared to standard nucleases in mice.

Appearing today in Nature Communications, the findings could help pave the way for safer, more efficient gene therapies. The study was led by Feng Zhang, a core institute member at the Broad and an Investigator at the McGovern Institute for Brain Research at MIT.

A new study by researchers at the Department of Molecular Medicine at SDU sheds light on one of the most severe consequences of stroke: damage to the brain’s “cables”—the so-called nerve fibers—which leads to permanent impairments. The study, published in The Journal of Pathology, which is based on unique tissue samples from Denmark’s Brain Bank located at SDU, may pave the way for new treatments that help the brain repair itself.

A stroke occurs when the to part of the brain is blocked, leading to brain damage. Following an injury, the brain tries to repair the damaged nerve fibers by re-establishing their insulating layer, called myelin. Unfortunately, the often succeeds only partially, meaning many patients experience lasting damage to their physical and mental functions.

According to Professor Kate Lykke Lambertsen, one of the study’s lead authors, the brain has the resources to repair itself, “We need to find ways to help the cells complete their work, even under difficult conditions.”