For the protein qubit to “encode” more information about what is going on inside a cell, the fluorescent protein needs to be genetically engineered to match the protein scientists want to observe in a given cell. The glowing protein is then attached to the target protein and zapped with a laser so it reaches a state of superposition, turning it into a nano-probe that picks up what is happening in the cell. From there, scientists can infer how a certain biological process happens, what the beginnings of a genetic disease look like, or how cells respond to certain treatments.
And eventually, this kind of sensing could be used in non-biological applications as well.
“Directed evolution on our EYFP qubit could be used to optimize its optical and spin properties and even reveal unexpected insights into qubit physics,” the researchers said. “Protein-based qubits are positioned to take advantage of techniques from both quantum information sciences and bioengineering, with potentially transformative possibilities in both fields.”
When cells are healthy, we don’t expect them to suddenly change cell types. A skin cell on your hand won’t naturally morph into a brain cell, and vice versa. That’s thanks to epigenetic memory, which enables the expression of various genes to “lock in” throughout a cell’s lifetime. Failure of this memory can lead to diseases, such as cancer.
Traditionally, scientists have thought that epigenetic memory locks genes either “on” or “off” — either fully activated or fully repressed, like a permanent Lite-Brite pattern. But MIT engineers have found that the picture has many more shades.
In a new study appearing today in Cell Genomics, the team reports that a cell’s memory is set not by on/off switching but through a more graded, dimmer-like dial of gene expression.
Spinal Cord Restoration, Head Transplants & Beyond — The Rise And Future Of Transplantation Neurosurgery — Dr. Michael Lebenstein-Gumovski, Ph.D. — Senior Scientific Officer, Sklifosovsky Emergency Medicine Institute, Moscow, Russian Federation
Dr. Michael Lebenstein-Gumovski, Ph.D. is Senior Scientific Officer and Neurosurgeon, in the Neurosurgery Department, of the Sklifosovsky Clinical and Research Institute for Emergency Medicine, Moscow, Russian Federation (https://sklif.mos.ru/), where his team is engaged in both neurosurgical and experimental practice, conducting advanced research in the field of spinal cord injury restoration, spinal cord transplantation and head transplantation.
The Sklifosovsky Institute for Emergency Medicine is a large multidisciplinary scientific and practical center dealing with problems of emergency medical care, emergency surgery, resuscitation, combined and burn trauma, emergency cardiology and acute poisoning.
Since 2013, Dr. Lebenstein-Gumovski has been studying spinal cord injury, and also developing methods for restoring the full functional and morphological repair of the spinal cord.
Dr. Lebenstein-Gumovski’s work is aimed at studying the effect of fusogens on nervous tissue, developing new methods and techniques for treating spinal cord injury, developing methods for its resection and transplantation. The lab develops and studies various methods of neuroprotection, combining methods to achieve better results and the current focus is the study of combination fusogen-induced (PEG-chitosan, Neuro-PEG) axonal restoration of the spinal cord after its complete transection.
Like bees breathing life into gardens, providing pollen and making flowers blossom, little cellular machines called mitochondria breathe life into our bodies, buzzing with energy as they produce the fuel that powers each of our cells. Maintaining mitochondrial metabolism requires input from many molecules and proteins—some of which have yet to be discovered.
Salk Institute researchers are taking a closer look at whether mitochondria rely on microproteins—small proteins that have been difficult to find and, consequently, underestimated for their role in health and disease. In their new study, a microprotein discovered just last year at Salk, called SLC35A4-MP, was found to play a critical role in upholding mitochondrial structure and regulating metabolic stress in mouse fat cells. The findings plant the seed for future microprotein-based treatments for obesity, aging, and other mitochondrial disorders.
The study, published in Science Advances on August 29, 2025, is part of a series of recent discoveries at Salk that showcase the functional importance of microproteins in cellular biology, metabolism, and stress.
EVANSTON, IL. — With the power to rewrite the genetic code underlying countless diseases, CRISPR holds immense promise to revolutionize medicine. But until scientists can deliver its gene-editing machinery safely and efficiently into relevant cells and tissues, that promise will remain out of reach.
Now, Northwestern University chemists have unveiled a new type of nanostructure that dramatically improves CRISPR delivery and potentially extends its scope of utility.
Called lipid nanoparticle spherical nucleic acids (LNP-SNAs), these tiny structures carry the full set of CRISPR editing tools — Cas9 enzymes, guide RNA and a DNA repair template — wrapped in a dense, protective shell of DNA. Not only does this DNA coating shield its cargo, but it also dictates which organs and tissues the LNP-SNAs travel to and makes it easier for them to enter cells.
New system delivers CRISPR machinery more safely and effectively into cells.
Lymphoid structures and thermogenic adipose tissue interplay!
The presence of active thermogenic adipose tissue (TAT) has been related to better cardiometabolic health.
While immunity and metabolism were once considered distinct domains, emerging evidence highlights the critical role of infiltrated immune cells in orchestrating the development and activation of TAT. Despite this novel function of infiltrated immune cells, scarce research has focused on the role that organized lymphoid structures like lymph nodes (LNs) and lymphatics exert on TAT metabolism.
The presence of peripheral LNs relates to a higher browning and thermogenic capacity of the surrounding fat, at least in part, through the secretion of factors like IL-33 and CCL22, and the higher number of BST2-beige adipocyte progenitors compared to more distant fat.
The lymphatic vasculature also influences TAT function and adaptive thermogenesis through the secretion of neurotensin by the lymphatic endothelial cells.
Future research should elucidate whether exploiting the lymphoid tissue– TAT axis could constitute a potential therapeutic target to activate TAT. #sciencenewshighlights #ScienceMission https://sciencemission.com/lymphoid-structures-and-thermogenic-adipose-tissue