Toggle light / dark theme

This past year, global attention has been focused on geo-strategic issues, such as the devastating war in Ukraine, which has dislocated many and caused immense suffering. Attention has also been focused on the recovery from the COVID pandemic, which was the overriding concern over the past three years. And finally, the economic destruction wrought by rapidly ramped interest rates which have targeted all sectors of the economy, particularly technology. But despite all this negativity, the business of building the future continues. There has been progress across major axes of computing, from visualization to AI and new types of processors (quantum).


With immense progress in technology, what might we look forward to in 2023?

Though it is a cornerstone of virtually every process that occurs in living organisms, the proper folding and transport of biological proteins is a notoriously difficult and time-consuming process to experimentally study.

In a new paper published in eLife, researchers in the School of Biological Sciences and the School of Computer Science have shown that AF2Complex may be able to lend a hand.

Building on the models of DeepMind’s AlphaFold 2, a machine learning tool able to predict the detailed three-dimensional structures of individual proteins, AF2Complex—short for AlphaFold 2 Complex—is a deep learning tool designed to predict the physical interactions of multiple proteins. With these predictions, AF2Complex is able to calculate which proteins are likely to interact with each other to form functional complexes in unprecedented detail.

This week our guest is business and technology reporter, Peter Ward. Earlier this year, Peter released his book The Price of Immortality: The Race to Live Forever, where he investigates the many movements and organizations that are seeking to extend human life, from the Church of Perpetual Life in Florida, to some of the biggest tech giants in Silicon Valley.

In this episode, we explore Peter’s findings, which takes us on a tour from cryonics to mind uploading, from supplements to gene editing, and much more. Along the way, we discuss the details of how one might actually achieve immortality, the details of senescent cells and telomeres, whether it’s better to live healthy than to live long, the scams and failures that seem to dominate the space, as well as the efforts that seem most promising.

Find Peter’s work on PenguinRandomHouse.com or follow him at twitter.com/PeterWardJourno.

Host: steven parton — linkedin / twitter.

Music by: Amine el Filali.

Many cancer cells never leave their original tumors. Some cancer cells evolve the ability to migrate to other tissues, but once there cannot manage to form new tumors, and so remain dormant. The deadliest cancer cells are those that can not only migrate to, but also thrive and multiply in distant tissues.

These metastatic are responsible for most of the deaths associated with cancer. Understanding what enables some cancer cells to metastasize—to spread and form new tumors—is an important goal for researchers, as it will help them develop therapies to prevent or reverse those deadly occurrences.

Past research from Whitehead Institute Member Robert Weinberg and others suggests that cancer cells are best able to form metastatic tumors when the cells are in a particular state called the quasi-mesenchymal (qM) state. New research from Weinberg and Arthur Lambert, once a postdoc in Weinberg’s lab and now an associate director of translational medicine at AstraZeneca, has identified two gene-regulating molecules as important for keeping cancer cells in the qM state.

Immunotherapy, including immune checkpoint inhibitors (ICIs), has changed the landscape of cancer treatment in the last decade. Immunotherapies, treatments targeting a patient’s immune system instead of the cancer itself, work on cancers considered “hot,” indicating that the tumor contains immune cells and factors which favor an anti-tumor immune response. Cancers that respond to immune-based therapies are known as “immunogenic” since the treatment can stimulate the immune response.

On the other hand, “cold” cancers, characterized as “non-immunogenic,” fail to respond to immunotherapies. One cancer understood as refractory to immune-based regimens is pancreatic ductal adenocarcinoma (PDAC), a highly aggressive pancreatic malignancy where less than 10% of patients survive five years past diagnosis. ICIs, including those targeting PD-L1 and CTLA-4 lack the efficacy to impact survival outcomes in PDAC patients significantly. Further, estimates project that by 2030, PDAC will rise to the second-highest cause of cancer-related deaths. Thus, there remains a significant need to develop novel and practical strategies to treat patients with this disease.

Series — Clinical Trials on Alzheimer’s Disease (CTAD) 2022: Part 1 of 14: Dare We Say Consensus Achieved: Lecanemab Slows the Disease Part 2 of 14: Brexpiprazole Eases Agitation in People with AD; So Does Being in a Trial Part 3 of 14: Two New Stabs at Vaccinating People Against Pathologic Tau Part 4 of 14: Cognitive Tests Taken at Home Are on Par with In-Clinic Assessments Part 5 of 14: In Small Trial, Gene Therapy Spurs ApoE2 Production Part 6 of 14: Donanemab Mops Up Plaque Faster Than Aduhelm Part 7 of 14: Gantenerumab Mystery: How Did It Lose Potency in Phase 3? Part 8 of 14: Could Personalizing Multimodal Interventions Give Them Oomph?

Nuclear physicists have found a new way to use the Relativistic Heavy Ion Collider (RHIC)—a particle collider at the U.S. Department of Energy’s (DOE) Brookhaven National Laboratory—to see the shape and details inside atomic nuclei. The method relies on particles of light that surround gold ions as they speed around the collider and a new type of quantum entanglement that’s never been seen before.

Through a series of quantum fluctuations, the particles of light (a.k.a. photons) interact with gluons—gluelike particles that hold quarks together within the protons and neutrons of nuclei. Those interactions produce an intermediate particle that quickly decays into two differently charged “pions” (π). By measuring the velocity and angles at which these π+ and π- particles strike RHIC’s STAR detector, the scientists can backtrack to get crucial information about the photon—and use that to map out the arrangement of gluons within the nucleus with higher precision than ever before.

“This technique is similar to the way doctors use positron emission tomography (PET scans) to see what’s happening inside the brain and other body parts,” said former Brookhaven Lab physicist James Daniel Brandenburg, a member of the STAR collaboration who joined The Ohio State University as an assistant professor in January 2023. “But in this case, we’re talking about mapping out features on the scale of femtometers —quadrillionths of a meter—the size of an individual proton.”

Many applications, from fiber-optic telecommunications to biomedical imaging processes require substances that emit light in the near-infrared range (NIR). A research team in Switzerland has now developed the first chromium complex that emits light in the coveted, longer wavelength NIR-II range. In the journal Angewandte Chemie, the team has introduced the underlying concept: a drastic change in the electronic structure of the chromium caused by the specially tailored ligands that envelop it.

Many materials that emit NIR light are based on expensive or rare metal complexes. Cheaper alternatives that emit in the NIR-I range between 700 and 950 nm have been developed but NIR-II-emitting complexes of non– remain extremely rare. Luminescence in the NIR-II range (1000 to 1,700 nm) is, for example, particularly advantageous for in vivo imaging because this light penetrates very far into tissues.

The luminescence of complexes is based on the excitement of electrons, through the absorption of light, for example. When the excited electron drops back down to its , part of the energy is emitted as radiation. The wavelength of this radiation depends on the energetic differences between the electronic states. In complexes, these are significantly determined by the type and arrangement of the ligands bound to the metal.

An international research group has for the first time reconstructed ancestors dating back 2.6 billion years of the well-known CRISPR-Cas system, and studied their evolution over time. The results suggest that the revitalized systems not only work, but are more versatile than current versions and could have revolutionary applications. Nature Microbiology has published the results of this research, which, in the opinion of the research team, “opens up new avenues for gene editing.”

The project, led by Ikerbasque research professor Rául Pérez-Jiménez of CIC nanoGUNE, involves teams from the Spanish National Research Council, the University of Alicante, the Rare Diseases Networking Biomedical Research Center (CIBERER), the Ramón y Cajal Hospital-IRYCIS and other national and international institutions.

The acronym CRISPR refers to the repeated sequences present in the DNA of bacteria and archaea (prokaryotic organisms). Among the repeats, these microorganisms harbor fragments of genetic material from viruses that infected their ancestors; that enables them to recognize a repeat infection and defend themselves by cutting the invaders’ DNA using Cas proteins associated with these repeats. It is a mechanism (CRISPR-Cas system) of antiviral defense. This ability to recognize DNA sequences is the basis of their usefulness, and they act as if they were molecular scissors. Nowadays CRISPR-Cas technology enables pieces of genetic material to be cut and pasted into any cell, so that it can be used to edit DNA.