Midwives' experiences of receiving maternity care and predictors of their overall birth experiences.

Background: Limited research has been conducted on midwives' experiences of receiving maternity care. Midwives may bring a degree of their own personal lives to their work, including their own birthing experience.

Aim: To explore midwives' experiences of giving birth and receiving maternity care and predictors of overall birth experience.

Optoelectronic Properties and Fluorescence Lifetime Imaging Application of Donor-Acceptor Dyads Derived From 2,6-DicarboxyBODIPY.

Donor-acceptor BODIPY dyads, functionalized at the 2 and 6 positions with benzyl ester (BDP-DE) or carboxylic acid (BDP-DA) groups, were synthesized and characterized for their optoelectronic properties. The introduction of carbonyl groups increased the reduction potential of the BODIPY core by 0.15-0.

Nutraceuticals silybin B, resveratrol, and epigallocatechin-3 gallate-bind to cardiac muscle troponin to restore the loss of lusitropy caused by cardiomyopathy mutations , , and .

Introduction: Adrenergic activation of protein kinase A (PKA) in cardiac muscle targets the sarcolemma, sarcoplasmic reticulum, and contractile apparatus to increase contractile force and heart rate. In the thin filaments of the contractile apparatus, cardiac troponin I (cTnI) Ser22 and Ser23 in the cardiac-specific N-terminal peptide (NcTnI: residues 1 to 32) are the targets for PKA phosphorylation. Phosphorylation causes a 2-3 fold decrease of affinity of cTn for Ca associated with a higher rate of Ca dissociation from cTnC leading to a faster relaxation rate of the cardiac muscle (lusitropy).

Astrocyte-dependent local neurite pruning in Beat-Va neurons.

Developmental neuronal remodeling is extensive and mechanistically diverse across the nervous system. We sought to identify Drosophila pupal neurons that underwent mechanistically new types of neuronal remodeling and describe remodeling Beat-VaM and Beat-VaL neurons. We show that Beat-VaM neurons produce highly branched neurites in the CNS during larval stages that undergo extensive local pruning.

An Ionic Sensor acts in Parallel to dSarm to Promote Neurodegeneration.

How neurons to sense when they are terminally dysfunctional and activate neurodegeneration remains poorly defined. The pro-degenerative NAD hydrolase dSarm/SARM1 can act as a metabolic sensor by detecting pathological changes in NAD /NMN and subsequently induce catastrophic axon degeneration. Here we show with-no-lysine kinase (dWnk), which can directly sense Cl , K and osmotic pressure, is required for neurodegeneration induced by depletion of the NAD biosynthetic enzyme dNmnat.