Calcium intake in health maintenance - a systematic review

Peer reviewe

Increased activity of Piezo1 channel in red blood cells is associated with Alzheimer's disease-related dementia

INTRODUCTION: Red blood cells (RBCs) are crucial for oxygen delivery to active tissues and endure significant mechanical forces in the microcirculatory bed. The enrichment of mechanosensitive Piezo1 channels, linked to the cytoskeleton, aids RBCs in navigating the narrow capillaries. In Alzheimer’s disease (AD), impaired brain microcirculation may necessitate enhanced Piezo1 function in RBCs. METHODS: With micropipette aspiration and flow cytometry technics, we evaluated, using the specific Piezo1 agonist Yoda1, AD-related alterations in the biomechanical properties of RBCs from cognitively healthy patients (HC) and individuals with mild cognitive impairment (MCI) and AD. RESULTS: We show that beta-amyloid (Aβ) peptides alter the biomechanical properties of RBCs. We observed significantly higher Yoda1-induced calcium responses in RBCs in individuals with MCI and AD compared to RBCs from age-matched HC

Marine Tourism Development in the Arkhangelsk Region, Russian Arctic : Stakeholder’s Perspectives

Author's accepted version (postprint).This is an Accepted Manuscript of an article published by Springer in Springer Polar Sciences on (07/03/2020).Available online: https://link.springer.com/chapter/10.1007%2F978-3-030-28404-6_17acceptedVersio

Noncompaction of the Ventricular Myocardium Is Associated with a De Novo Mutation in the β-Myosin Heavy Chain Gene

Noncompaction of the ventricular myocardium (NVM) is the morphological hallmark of a rare familial or sporadic unclassified heart disease of heterogeneous origin. NVM results presumably from a congenital developmental error and has been traced back to single point mutations in various genes. The objective of this study was to determine the underlying genetic defect in a large German family suffering from NVM. Twenty four family members were clinically assessed using advanced imaging techniques. For molecular characterization, a genome-wide linkage analysis was undertaken and the disease locus was mapped to chromosome 14ptel-14q12. Subsequently, two genes of the disease interval, MYH6 and MYH7 (encoding the α- and β-myosin heavy chain, respectively) were sequenced, leading to the identification of a previously unknown de novo missense mutation, c.842G>C, in the gene MYH7. The mutation affects a highly conserved amino acid in the myosin subfragment-1 (R281T). In silico simulations suggest that the mutation R281T prevents the formation of a salt bridge between residues R281 and D325, thereby destabilizing the myosin head. The mutation was exclusively present in morphologically affected family members. A few members of the family displayed NVM in combination with other heart defects, such as dislocation of the tricuspid valve (Ebstein's anomaly, EA) and atrial septal defect (ASD). A high degree of clinical variability was observed, ranging from the absence of symptoms in childhood to cardiac death in the third decade of life. The data presented in this report provide first evidence that a mutation in a sarcomeric protein can cause noncompaction of the ventricular myocardium