Sign number 7: Gut issues. Zinc: -Aids hydrochloric acid (HCl) production (the production of H ions (the acid component of HCl) relies on the enzyme carbonic anhydrase (specifically isoforms I and II), which is a zinc-dependent enzyme) Is essential for the structure and function of the proteins that form TJs (like ZO-1, occludin and claudin-1). -Is necessary for the continuous self-renewal and regeneration of intestinal epithelial cells. -Deficiency has been linked to lower microbial diversity and an imbalance of beneficial versus potentially harmful bacteria. -Is crucial for "nutritional immunity" (the host's immune system uses this to sequester zinc to fight off infections. However, a systemic zinc deficiency can give pathogenic bacteria an advantage in competing for the available zinc, potentially leading to increased colonization and infection). -Is crucial for maintaining the structure of the microvilli (tiny projections in the small intestine that absorb nutrients). -Is a cofactor for several digestive enzymes. -Is essential for electrolyte/fluid balance (in cases of deficiency, the body may have difficulty regulating ion transport across the intestinal wall, which can lead to excessive water secretion and diarrhea).

Longer answer: Functional MRI studies of the coupling of pressure waves in brain vascular is followed by a pressure wave in cerebral spinal fluid during deep sleep cycles. These cycles can apparently be entrained by light and or music. I believe the key is the frequency. I interpret this method as a treatment for those who are unable to obtain sufficient deep sleep. Meditative practices probably do the same. I hypothesize that the coupling of the glymphatic system clears amyloid through the available brain apoe isoforms and relevant transport proteins. Functional MRI studies during sleep demonstrate at least part of this hypothesis. Molecular studies of apoE clearance of cholesterol together with separate studies of apoE clearance of amyloid are supportive of this hypothesis. Unfortunately, scientific studies typically do not have sufficient funds to do molecular analysis on CSF and fMRI in sleeping individuals. I for one would never submit myself to such an investigative trial, but that doesn't mean it doesn't work!

@grok cool, where does chirality stand in relation to the isoforms? what are the best ways to implement the long read RNA tech to map these isoforms with the SNV present there appropriately? what would the best SOPs for best resolution and accurate and precise mapping of the variations here both genetically and chemical structure wise?

Jonas Gustavson presents data on long-read RNA seq from the 1000 genomes project and its power to detect isoforms that were not known from short read data. #eshg2026

🚨 New preprint alert! We used IntAct Ultrastructure Expansion microscopy to map actin isoforms in 3D🤯 Check out this gorgeous 3D volume of U2OS cells - revealing diverse filament networks including the elusive nuclear actin filaments! #cytoskeleton #microscopy #actin

Excited to share our PLOS Biology paper! 🎉 Using IntAct‑U‑ExM, we achieved super‑resolution imaging of actin isoforms. With @anubhav_dhar, I explored neuronal actin rings & synaptic architecture. Grateful to @deepak_iisc & @syncellbiolab doi.org/10.1371/journal.pbio… #IISc #UExm

ANCHOR aggregates read evidence within UMIs through a Beta-binomial model that can abstain when allelic evidence is ambiguous. Isoforms are defined from observed splice structure rather than reference transcript assignment, allowing allele-specific splice patterns to be retained.

ANCHOR aggregates read evidence within UMIs through a Beta-binomial model that can abstain when allelic evidence is ambiguous. Isoforms are defined from observed splice structure rather than reference transcript assignment, allowing allele-specific splice patterns to be retained.

Corrigendum to "Expression profiling of GP63 isoforms with predicted nuclear localization signals in Leishmania (Viannia) braziliensis" [Experimental Parasitology 286 (2026) 109155] dlvr.it/TT0qXq PubMed

Dopaminergic Neurons / GABA / Excitotoxicity/ LRRK2-G2019S/ Striatum Our results demonstrate, for the first time, that LRRK2 G2019S induces a significant reduction in GABA-evoked current amplitudes. Moreover, we identified an altered distribution of receptor isoforms in pathological tissue, affecting both tonic and phasic GABA currents. Specifically, synaptic GABAA receptors containing the γ2 subunit were functionally modulated by LRRK2 G2019S. The reduced availability of gephyrin in the presence of the G2019S variant may impair the gephyrin–GABAA receptor complex, leading to decreased receptor surface expression and further shifting the glutamate/GABA current ratio toward excitatory dominance. This is supported by the increased activity of AMPA and NMDA receptors observed in the pathological striatum. LRRK2 G2019S disrupts GABAergic signaling and shifts excitatory/inhibitory balance in the striatum | bioRxiv share.google/63RBFSl9JWFP4GB…

Congratulations to Harry and Alishba on our new review:The Multi-System Roles of Dp71 Dystrophin Isoforms in Duchenne Muscular Dystrophy We summarize Dp71 roles in brain, retina, skeletal/cardiac muscle, and emerging therapeutic strategies mdpi.com/3930242 @MDPIOpenAccess