Is Medical Director of the Adult Extracorporeal Membrane Oxygenation (ECMO) Program at Methodist Hospital, San Antonio, Texas. He is also the Medical Director of the Cardiovascular Intensive Care Unit at Methodist Healthcare System and the Texas IPS Critical Care Service Line (https://texasips.com/jeffrey-dellavol…). He also serves as chair of the Joint Society of Critical Care Medicine/Extracorporeal Life Support Organization Task Force and has created a platform for ECMO training and ECMO transport (https://ecmotransports.com/about/).
ECMO is a form of extracorporeal life support, providing prolonged cardiac and respiratory support to persons whose heart and lungs are unable to provide an adequate amount of oxygen, gas exchange or blood supply (perfusion) to sustain life.
Common treatments for Parkinson’s disease can address short-term symptoms, but can also cause extensive problems for patients in the long run. Namely, treatments can cause dyskinesia, a form of uncontrollable movements and postures.
In a recent study published in The Journal of Neuroscience, researchers at the University of Alabama at Birmingham took a different approach to dyskinesia and treated it like a “bad motor memory.” They found that blocking a protein called Activin A could halt dyskinesia symptoms and effectively erase the brain’s “bad memory” response to certain Parkinson’s treatments.
“Instead of looking for a completely alternative treatment, we wanted to see if there was a way to prevent dyskinesia from developing in the first place,” said David Figge, M.D., Ph.D., lead study author and assistant professor in the UAB Department of Pathology. “If dyskinesia does not occur, then patients could potentially stay on their Parkinson’s treatment for longer.”
Human brains outperform computers in many forms of processing and are far more energy efficient. What if we could harness their power in a new form of biological computing?
In multicellular organisms, many biological pathways exhibit a curious structure, involving sets of protein variants that bind or interact with one another in a many-to-many fashion. What functions do these seemingly complicated architectures provide? And can similar architectures be useful in synthetic biology? Here, Dr. Elowitz discusses recent work in his lab that shows how many-to-many circuits can function as versatile computational devices, explore the roles these computations play in natural biological contexts, and show how many-to-many architectures can be used to design synthetic multicellular behaviors.
About Michael Elowitz. Michael Elowitz is a Howard Hughes Medical Institute Investigator and Roscoe Gilkey Dickinson Professor of Biology and Biological Engineering at Caltech. Dr. Elowitz’s laboratory has introduced synthetic biology approaches to build and understand genetic circuits in living cells and tissues. As a graduate student with Stanislas Leibler, Elowitz developed the Repressilator, an artificial genetic clock that generates gene expression oscillations in individual E. coli cells. Since then, his lab has continued to design and build synthetic genetic circuits, bringing a “build to understand” approach to bacteria, yeast, and mammalian cells. He and his group have shown that gene expression is intrinsically stochastic, or ‘noisy’, and revealed how noise functions to enable probabilistic differentiation, time-based regulation, and other functions. Currently, Elowitz’s lab is bringing synthetic approaches to understand and program multicellular functions including multistability, cell-cell communication, epigenetic memory, and cell fate control, and to provide foundations for using biological circuits as therapeutic devices. His lab also co-develops systems such as “MEMOIR” that allows cells to record their own lineage histories and tools for RNA export, and precise gene expression. Elowitz received his PhD in Physics from Princeton University and did postdoctoral research at Rockefeller University. Honors include the HFSP Nakasone Award, MacArthur Fellowship, Presidential Early Career Award, Allen Distinguished Investigator Award, the American Academy of Arts and Sciences, and election to the National Academy of Sciences.
Summary: Researchers have discovered how glial cells can be reprogrammed into neurons through epigenetic modifications, offering hope for treating neurological disorders. This reprogramming involves complex molecular mechanisms, including the transcription factor Neurogenin2 and the newly identified protein YingYang1, which opens chromatin for reprogramming.
The study reveals how coordinated epigenome changes drive this process, potentially leading to new therapies for brain injury and neurodegenerative diseases.
Researchers have significantly improved gene-editing techniques. This new method, called eePASSIGE, can insert or replace entire genes in human cells with much higher efficiency than previous methods. This advancement could lead to a single gene therapy for diseases caused by various mutations in a single gene, like cystic fibrosis. Traditionally, gene therapy required a different treatment for each mutation.
EePASSIGE combines prime editing, which edits small stretches of DNA, with new enzymes that insert large pieces of DNA. This allows scientists to introduce a healthy copy of a gene directly where it belongs in the genome.
“This is one of the first examples of targeted gene integration with potential for therapeutic applications,” said Dr. David Liu, senior author of the study. “If these efficiencies translate to patients, many genetic diseases could be treated.”
Microbes that are used for health, agricultural, or other applications need to be able to withstand extreme conditions, and ideally the manufacturing processes used to make tablets for long-term storage. MIT researchers have now developed a new way to make microbes hardy enough to withstand these extreme conditions.
Their method involves mixing bacteria with food and drug additives from a list of compounds that the FDA classifies as “generally regarded as safe.” The researchers identified formulations that help to stabilize several different types of microbes, including yeast and bacteria, and they showed that these formulations could withstand high temperatures, radiation, and industrial processing that can damage unprotected microbes.
Researchers have developed a novel method for generating structured terahertz light beams using programmable spintronic emitters. This breakthrough offers a significant leap forward in terahertz technology, enabling the generation and manipulation of light with both spin and orbital angular momentum at these frequencies for the first time.
Terahertz radiation lies between microwaves and infrared light on the electromagnetic spectrum. It holds great promise for various applications, including security scanners, medical imaging, and ultrafast communication. However, generating and controlling terahertz light effectively has proven challenging.
This new research, published in eLight and led by Prof. Zhensheng Tao, Prof. Yizheng Wu from Fudan University and Prof. Yan Zhang from Capital Normal University, overcomes these limitations by employing programmable spintronic emitters based on exchange-biased magnetic multilayers. These devices consist of thin layers of magnetic and non-magnetic materials that convert laser-induced spin-polarized currents into broadband terahertz radiation.
Researchers from the Smart and Wireless Applications and Technologies Group (SWAT-UGR) have conducted two scientific studies aimed at answering a common question: understanding how electromagnetic waves propagate in the medium.
The increase in network speed opens the door to new possibilities, such as robotic surgery or virtual reality services.
A team of UGR researchers has examined the propagation of electromagnetic waves with the goal of enhancing the deployment of 5G and 6G networks. Additionally, the study results contribute to the development of Industry 4.0, which seeks to automate processes in factories using wireless technologies.
Researchers have developed a pH-responsive nanorobot system that changes confirmation in the tumor microenvironment to selectively kill cancer cells in mice.
Researchers at the Karolinska Institutet (Stockholm, Sweden) have recently developed a nanorobot system capable of killing cancer cells in mice. This system works by activating at lower pH, such as within the tumor microenvironment. It is hoped that this could serve as a proof-of-concept for similar stimulus-responsive nanorobotic approaches and introduce a new range of effective cancer therapeutics.
Certain membrane proteins capable of inducing apoptosis, a type of cell death, appear on the surface of both healthy and cancer cells. These proteins, often called death receptors, join and activate when in close proximity to each other. This closeness is induced by external factors binding to the cell surface.
