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Nvidia has achieved a historic milestone. The chipmaker is now the world’s most valuable listed company. Its market capitalization has surpassed five trillion dollars. This surge places Nvidia ahead of tech giants like Alphabet and Apple. The company’s success is driven by its crucial role in supplying GPUs for artificial intelligence models. Nvidia’s stock performance reflects its strong market position.
Gene therapy is an emerging and powerful therapeutic tool to deliver functional genetic material to cells in order to correct a defective gene. During the past decades, several studies have demonstrated the potential of AAV-based gene therapies for the treatment of neurodegenerative diseases. While some clinical studies have failed to demonstrate therapeutic efficacy, the use of AAV as a delivery tool has demonstrated to be safe. Here, we discuss the past, current and future perspectives of gene therapies for neurodegenerative diseases. We also discuss the current advances on the newly emerging RNAi-based gene therapies which has been widely studied in preclinical model and recently also made it to the clinic.
Gene therapy is an emerging therapeutic tool used to deliver functional genetic material to cells in order to correct a defective gene. By delivering a copy of a therapeutic gene to affected cells, the product encoded by that gene [i.e., its messenger RNA (mRNA) and/or proteins] will be continuously synthesized within the cell, utilizing the cell’s own transcriptional and translational machinery (Porada et al., 2013). The main advantage of this technology is that it offers a potentially life-long therapeutic effect without the need for repeated administration. Gene therapy can be used to correct defective genes by introducing a functional copy of the gene, by silencing a mutant allele using RNA interference (RNAi), by introducing a disease-modifying gene, or by using gene-editing technology (Grimm and Kay, 2007; Dow et al., 2015; Saraiva et al., 2016).
Gene therapy vectors can be either viral or non-viral. Different physical and chemical systems can be applied to deliver therapeutic genes to cells without the need of a viral vector. Non-viral vectors have no size limitation for the therapeutic gene, generally have a low immunogenicity risk, and can be produced at relatively low costs (Nayerossadat et al., 2012). However, due to the fact that high therapeutic doses are required when using non-viral technologies, and the resulting gene expression is generally transient, most gene therapies now rely on viral vectors. Numerous viral vector types have been tested in clinic, including vaccinia, measles, vesicular stomatitis virus (VSV), polio, reovirus, adenovirus, lentivirus, γ-retrovirus, herpes simplex virus (HSV) and adeno-associated virus (AAV) (Lundstrom, 2018).
Among older adults, longer and more frequent daytime napping, especially in the morning, was associated with higher AllCauseMortality, supporting wearable sleep assessment for risk evaluation.
Question Are objectively measured daytime nap characteristics, including duration, frequency, variability, and timing, associated with all-cause mortality among community-dwelling older adults?
Findings In this prospective cohort study of 1,338 adults aged 56 years or older, longer and more frequent daytime napping, as well as morning napping, were associated with higher all-cause mortality. Variability in nap duration was not associated with mortality.
Meaning The findings suggest longer and more frequent, particularly morning, napping may be a behavioral marker of increased mortality risk in late life, underscoring the potential clinical value of incorporating wearable device–based nap assessments into routine health monitoring.
A protein long understood to drive inflammation by producing nitric oxide has a second, previously unknown role—it physically binds to another key protein inside cells to directly modulate the immune response. The discovery, published in Nature Metabolism, could open new routes to treating conditions such as cardiovascular disease, arthritis, Crohn’s and other inflammatory diseases.
When the immune system detects infection or injury, it triggers inflammation to fight back. That response is essential, but it must be carefully controlled. If it runs too hard for too long, it causes the tissue damage that underlies many chronic diseases. Understanding the molecular switches that regulate inflammation—and finding new ways to target them—is one of the biggest challenges in modern medicine.
Researchers from the University of Surrey and the University of Oxford have identified one such switch. They have shown that inducible nitric oxide synthase (iNOS)—a protein that produces nitric oxide during inflammation—can also bind directly to a second protein, IRG1, inside mitochondria. That physical interaction blocks IRG1 from producing itaconate, a metabolite that acts as a brake on the inflammatory response.
Jessica A. Regan & Svati H. Shah Comment on Yonekawa et al.: https://doi.org/10.1172/JCI198708 aneurysm.
Address correspondence to: Jessica A. Regan, Duke Molecular Physiology Institute Duke University School of Medicine, 300 N. Duke Street, Carmichael Building, Durham, North Carolina, 27,701, USA. Email: jessica.a.regan@duke.edu.
A new laboratory technique for measuring how quickly cells penetrate and pass through a porous membrane and reach the opposite side could help identify cancer cells with the greatest potential to spread in the human body.
The method relies on tiny electrodes placed on either side of an artificial membrane. The electrodes measure changes in electrical resistance as cells pass through the material. The most aggressive cancer cells pass through the membrane more rapidly than other cells.
The illustration depicts cells (green and blue) moving through a membrane (grey) studded with microelectrodes (gold rings).
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We present a novel microfluidic device capable of electrically interrogating both surfaces of a porous membrane quantitatively and in real time using electrical impedance spectroscopy to monitor cell migration. This device holds patterned gold electrodes on both sides of the membrane, which enable independent impedance measurements on each side of the membrane. We introduce the term cross-over cell migration (CoCM) to describe this dual-sided approach, which allows precise monitoring of cells at their seeding location and as they move through a porous membrane. To ensure reliable tracking, we developed a normalization method, the CoCM index, that allows us to compare both membrane surfaces directly in real-time. Human renal carcinoma cells (786-O) were passively seeded in the device’s top microfluidic chamber, and we collected impedance data from both sides of the membrane surfaces simultaneously over a three-day period. These measurements successfully captured the onset and progression of cell migration across the membrane interface. We tracked the cells with fluorescence imaging in parallel to validate our impedance data. As cells appeared in focus on the bottom-side electrode surface, their numbers kept increasing over the course of our experiment. The CoCM index decreased by about 20% in the top chamber and increased by approximately 15% in the bottom chamber. Symmetrical CoCM index trends appeared after 40 h, consistent with the fluorescent images captured. Finally, we performed live-cell fluorescence assays to confirm post-experiment cell viability and to quantify migrated cells, further validating our CoCM platform measurements. This platform is a valuable tool not only for real-time and quantitative cell migration studies of cancer and other cells in bulk but also for future studies of single-cell migration processes.
The retina, the thin layer of tissue at the back of the eye, is made up of photoreceptor cells that convert visible light into electrical signals, which is essential for human vision. Some diseases, such as retinal degeneration, cause these photoreceptor cells to stop working, which results in blindness. Researchers at Yonsei University, the Institute for Basic Science (IBS) and other institutes in the Republic of Korea have recently developed a new artificial retina that could partly restore vision in people with damaged retinas.
The new device, introduced in a paper published in Nature Electronics, works by detecting near-infrared light and converting it into electrical signals, which stimulate another type of cells in the retina that are undamaged.
“Many people suffer from blindness due to retinal diseases that cause photoreceptor degeneration,” wrote Won Gi Chung, Inhea Jeong and their colleagues in their paper. “Electrical stimulation of retinal neurons can recreate the action potentials associated with seeing that are generated by these cells. We report a thin artificial retina that can be adhered to the epiretinal surface and can convert near-infrared (NIR) light into electrical stimuli that selectively stimulate ganglion cells.”
Urea is an extremely important chemical, especially for fertilizers. But, making urea is energy intensive and relies heavily on fossil fuels. However, new findings from Griffith University and the Queensland University of Technology have highlighted new ways to produce urea electrochemically, using electricity and waste gases such as carbon monoxide (CO) and nitrogen oxides (NO) instead.
The paper, “Machine Learning-Assisted Design Framework of Carbon Edge-Dominated Dual-Atom Catalysts for Urea Electrosynthesis,” has been published in ASC Nano.
“The challenge is that when CO and NO react on a catalyst, they usually don’t form urea,” said co-lead author Professor Qin Li from Griffith University.