Toggle light / dark theme

Abstract: Immune signaling and function in neurodegeneration:

Yvonne L. Latour & Dorian B. McGavern contribute a Review to the JCI Series on Neurodegeneration, discussing signaling pathways, cellular players, and immune responses shared across multiple neurodegenerative diseases, while considering external factors that may influence CNS disease progression. Neurodegeneration.


Viral Immunology and Intravital Imaging Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, Maryland, USA.

Lifestyle-Driven Variations in Nutrimiromic MicroRNA Expression Patterns across and beyond Genders

The importance of diet and lifestyle in maintaining overall health has long been recognised. MicroRNAs (miRNAs) have emerged as key players in the intricate interplay between health and disease. This study, including 305 participants, examined the role of miRNAs from capillary blood as indicators of individual physiological characteristics, diet, and lifestyle influences. Key findings include specific miRNAs associated with inflammatory processes and dietary patterns. Notably, miR-155 was associated with subjects with metabolic diseases and upregulated in age. Additionally, the study revealed diet-related miRNA expressions: high consumption of vegetables, fruits, and whole grains correlated with increased levels of miR-let-7a and miR-328, both implicated in anti-inflammatory pathways, and decreased expression of pro-inflammatory miR-21.

Unlocking secrets of human development: How early nerve cell choices shape the peripheral nervous system

Millions of neurons branch throughout our bodies, keeping them in close communication with our brains. This peripheral network begins to take shape long before birth, as the cells of a growing embryo move into position and adopt their specialized roles. This crucial stage of human development can’t be monitored directly, but by examining genetic clues that linger in adult cells, scientists have now gained surprising insights into the developmental origins of the peripheral nervous system.

Researchers led by Xiaoxu Yang, Ph.D., at University of Utah Health, and Keng Ioi Vong, Ph.D., and Joseph Gleeson, M.D., at the University of California San Diego, have discovered that within the first few weeks of development, some of an embryo’s cells have already been selected to take on particular roles in the peripheral nervous system. Their findings, recently reported in the journal Nature, overturn longstanding assumptions in biology.

Their discovery could change the way scientists think about treatments for a variety of childhood diseases that begin in the cells of the peripheral nervous system.

Abstract: In obesity, the heart muscle can thicken, preventing it from relaxing properly between beats

While diet and inflammation likely contribute, the underlying molecular mechanism has been unclear.

https://doi.org/10.1172/JCI196238 Here, Junichi Sadoshima & team find direct stimulation of IL-6 transcription by PPARα in cardiomyocytes plays an important role in mediating the initial development of obesity cardiomyopathy.

The figure indicates binding of PPARα to NFkB (via PLA assay).


1Rutgers New Jersey Medical School Department of Cell Biology and Molecular Medicine, Rutgers Biomedical and Health Sciences, Newark, New Jersey, USA.

2Precision Medicine Research Center, College of Medicine, The Catholic University of Korea, Seoul, Korea.

Address correspondence to: Junichi Sadoshima, Cardiovascular Research Institute, Rutgers Biomedical and Health Science, 185 South Orange Ave., MSB G609, Newark, New Jersey, 7,103, USA. Phone 973.972.8619; Email: sadoshju@njms.rutgers.edu.

A missing link in how the brain regulates appetite

Bile acids at the center of hepato-ocular crosstalk.

Hepatic dysfunction with ocular pathology has been linked to dysregulated bile acid metabolism.

Bile acid imbalance has been shown to drive ocular injury along the gut-liver-eye axis through direct cytotoxicity, disruption of retinal and lens homeostasis mediated by FXR and TGR5 signaling, and immune activation and these mechanisms are implicated across a spectrum of conditions, ranging from inborn metabolic disorders to acquired cholestatic diseases.

The researchers in this review discuss translational potential of targeting bile acid homeostasis and summarize emerging therapeutic strategies, including bile acid-based interventions, targeted drug delivery, and microbiome modulation, that aim to restore systemic bile acid balance.

Thus, bile acid homeostasis act as a unifying therapeutic framework for hepato-ocular comorbidities. sciencenewshighlights ScienceMission https://sciencemission.com/Hepato-ocular-crosstalk


Health sciences.

Low-frequency wireless sensor tracks artery stiffening in real time with less interference

Wireless sensors used in wearable smart devices and medical equipment must be capable of detecting minute changes while maintaining high operational stability. However, existing technologies often utilize excessively high frequencies, leading to electromagnetic interference (EMI) or potential health risks to the human body. To address these fundamental issues, a Korean research team has developed a low-frequency-based wireless sensor technology.

A joint research team, led by Professor Seungyoung Ahn from the KAIST Cho Chun Shik Graduate School of Mobility and Professor Do Hwan Kim from the Department of Chemical Engineering at Hanyang University, has developed the “WiLECS” (Wireless Ionic-Electronic Coupling System), a low-frequency wireless electrochemical sensing platform that combines ion-based materials with wireless power transfer technology. The research is published in the journal Nature Communications.

Conventional wireless sensors suffer from low capacitance (the ability to store electrical charge), requiring high frequencies in the megahertz (MHz) range to compensate. However, these high-frequency methods can cause tissue heating or signal instability, limiting their practical application in clinical medical settings.

NIH-funded breakthrough shrinks CRISPR for precision delivery in the body

Smaller gene-editing system could expand treatment options for cancer, ALS and other diseases.

A National Institutes of Health (NIH)-funded research team has discovered an enhanced CRISPR gene-editing system that could enable targeted delivery inside the human body — a key step toward broader clinical use. Researchers identified a naturally occurring enzyme, Al3Cas12f, that is small enough to fit into adeno-associated virus vectors, a leading targeted delivery method for gene therapies. They then engineered an enhanced version that dramatically improved gene-editing performance in human cells.

The advance addresses a major limitation in CRISPR technology. Commonly used gene-editing proteins are too large for targeted delivery systems, restricting clinical applications to cells modified outside the body, such as blood and bone marrow.

The Fight For Slow And Boring Research

Great article. I should note that it actually has nothing to do with slow and boring research — it’s about the importance of scientists practicing good communication and public engagement to facilitate fundraising from non-governmental sources.


As federal research funding shrinks, scientists are looking to other sources of support. Can they learn to sell their work without selling out?

Since the middle of the twentieth century, the National Institutes of Health and the National Science Foundation have embodied an imperfect social contract: Federal agencies would fund basic research at scale, and in return, that research would serve the public good through medical advances, technological progress, and economic growth.

For scientists, this system created a reliable pathway: Do good work, write strong grants, and federal agencies would keep your lab running. It was never a perfectly fair system, but it was predictable enough that you could build a life around it. If your work was solid and your grants were strong, the system would fund you.

Mitochondria-Derived Vesicles and Mitochondrial Extracellular Vesicles in Health and Cardiovascular Disease

@CircRes Compendium on Migration of Mitochondria Beyond Cell Boundary.

Authored by Drs. Rapushi & colleagues.


Mitochondria-derived vesicles (MDVs) and mitochondrial extracellular vesicles (mitoEVs) represent 2 related extensions of mitochondrial dynamics that link organelle maintenance to communication within and between cells. MDVs are small vesicles that bud directly from mitochondria, selectively packaging components of the outer membrane, inner membrane, or matrix. They serve as a localized quality control mechanism that removes oxidized or damaged material without engaging the entire mitophagic machinery. After budding, MDVs typically enter the endolysosomal pathway, where they can fuse with late endosomes or lysosomes for cargo degradation. A subset of MDVs also targets other organelles, particularly peroxisomes, contributing to organelle crosstalk, lipid metabolism, and redox balance.

/* */