The phosphatidylinositol 3-kinase (PI3K)-AKT signaling pathway is one of the most critical and extensively investigated signaling pathways. It is the central regulator of various cellular processes including cell growth, proliferation, metabolism, and survival. Hyperactivation of PI3K-AKT signaling is highly related to a significant number of human diseases, particularly cancers.
The intricate relationship between hydrogen sulfide (H2S), gut microbiota, and sirtuins (SIRTs) can be seen as a paradigm axis in maintaining cellular homeostasis, modulating oxidative stress, and promoting mitochondrial health, which together play a pivotal role in aging and neurodegenerative diseases. H2S, a gasotransmitter synthesized endogenously and by specific gut microbiota, acts as a potent modulator of mitochondrial function and oxidative stress, protecting against cellular damage. Through sulfate-reducing bacteria, gut microbiota influences systemic H2S levels, creating a link between gut health and metabolic processes. Dysbiosis, or an imbalance in microbial populations, can alter H2S production, impair mitochondrial function, increase oxidative stress, and heighten inflammation, all contributing factors in neurodegenerative diseases such as Alzheimer’s and Parkinson’s.
Scientists in Japan have created hybrid plant-animal cells, essentially making animal cells that can gain energy from sunlight like plants. The breakthrough could have major benefits for growing organs and tissues for transplant, or lab-grown meat.
Animal and plant cells have different energy-producing structures inside them. For animals, that’s mitochondria, which convert chemical energy from food into a form that our cells can use. Plants and algae, meanwhile, use chloroplasts, which perform photosynthesis to generate energy from sunlight to power their cells.
In a new study led by the University of Tokyo, the team inserted chloroplasts into animal cells, and found that they continued to perform photosynthetic functions for at least two days. The chloroplasts were sourced from red algae, while the animal cells were cultured from hamsters.
The researchers’ recently published study describes a way to re-activate apoptosis in mutated cells, which would amount to forcing cancer to self-destruct through a bioengineered, bonding molecule.
Gerald Crabtree, one of the study’s authors and a professor of development biology, said he had the idea while hiking through Kings Mountain, California, during the pandemic period. The new compound would have to bind two proteins which already exist in the cancerous cells, turning apoptosis back on and making the cancer kill itself.
“We essentially want to have the same kind of specificity that can eliminate 60 billion cells with no bystanders,” Crabtree said, so that no cell gets destroyed if it isn’t the proper target of this new killing mechanism. The two proteins in question are known as BCL6, an oncogene which suppresses apoptosis-promoting genes in the B-cell lymphoma, and CDK9, an enzyme that catalyzes gene activation instead.
In recent years, standing has been touted as a remedy to a sedentary lifestyle, especially for desk workers who spend long hours seated at their screens.
But a new study from researchers in Australia and the Netherlands has found standing for long periods of time might not be much better than sitting after all – and actually comes with its own life-threatening risks.
Just under seven years of data from 83,013 adults were collected as part of the UK Biobank, using wrist-worn devices to track their activity, sleep, and sedentary time. The amount of time individuals spent standing and sitting was matched with incidences of cardiovascular diseases – coronary heart disease, heart failure and stroke – as well as circulatory diseases – low blood pressure on standing, varicose veins, chronic venous insufficiency, and venous ulcers.
Marking a major breakthrough in medical development, scientists have used AI to design antibodies from scratch.
Adeno-associated virus (AAV) is a well-known gene delivery tool with a wide range of applications, including as a vector for gene therapies. However, the molecular mechanism of its cell entry remains unknown. Here, we performed coarse-grained molecular dynamics simulations of the AAV serotype 2 (AAV2) capsid and the universal AAV receptor (AAVR) in a model plasma membrane environment. Our simulations show that binding of the AAV2 capsid to the membrane induces membrane curvature, along with the recruitment and clustering of GM3 lipids around the AAV2 capsid. We also found that the AAVR binds to the AAV2 capsid at the VR-I loops using its PKD2 and PKD3 domains, whose binding poses differs from previous structural studies. These first molecular-level insights into AAV2 membrane interactions suggest a complex process during the initial phase of AAV2 capsid internalization.
The small-scale FDA-cleared trial is designed to evaluate both the safety and initial efficacy of RB-ADSCs in nine patients with Alzheimer’s. Regeneration Biomedical’s CTAD presentation focused on the first three enrolled patients, who each received a single dose of RB-ADSCs delivered directly into the lateral ventricles of the brain using an “Ommaya reservoir” – a device implanted under the scalp to bypass the blood-brain barrier, a major obstacle in Alzheimer’s treatments.
Biomarker analysis at the 12-week mark demonstrated reductions in both p-Tau and amyloid-beta – two proteins strongly associated with Alzheimer’s disease progression. In cerebrospinal fluid (CSF) samples from the three patients, p-Tau levels decreased to “normal” levels, while amyloid PET scans also showed a reduction in amyloid buildup.
Regeneration Biomedical also reported its treatment produced signs of cognitive improvement, with two of the three patients showing increased Mini-Mental State Examination (MMSE) scores, a common measure of cognitive function.
In a groundbreaking Nature paper, researchers have developed synthetic regulatory sequences that could prevent targeted gene therapies from having effects in unwanted cell types.
More than methylation
While methylation is the most well-known regulator of gene expression, it isn’t the only thing that determines what is to be expressed when. Cis-regulatory elements (CREs), so called because they sit near the DNA sequences they regulate, are responsible for expressing the genes that are specific to each cell type [1]. While they are technically non-coding, as they do not directly code for functional proteins, CREs are critical to epigenomic function.
Murata is branching out from its usual ceramic components with the launch of flexible, stretchable electronics — a Stretchable Printed Circuit (SPC) platform it says is ideally positioned for wearable and medical devices.
In recent years, in the medical field, to make more accurate diagnoses, the…
Bendy, soft, stretchy devices target the wearable and medical markets.
