Role of oxidative stress and endoplasmic reticulum stress in drug-induced liver injury

The pathogenesis of drug-induced liver injury (DILI) is still in an early stage of research. However, investigators have shown that both oxidative stress and endoplasmic reticulum (ER) stress play a significant role in the pathological mechanism. However, there is little in-depth literature about these two mechanisms. In order to prevent and improve the clinical symptoms of DILI, it is particularly important to study its pathogenesis. In this review article, the role of ER and oxidative stress in DILI is thoroughly discussed

Gender differences in the clinical management of patients with angina pectoris: a cross-sectional survey in primary care

Non peer reviewedPublisher PD

NO-sGC Pathway Modulates Ca2+ Release and Muscle Contraction in Zebrafish Skeletal Muscle

Vertebrate skeletal muscle contraction and relaxation is a complex process that depends on Ca2+ ions to promote the interaction of actin and myosin. This process can be modulated by nitric oxide (NO), a gas molecule synthesized endogenously by (nitric oxide synthase) NOS isoforms. At nanomolar concentrations NO activates soluble guanylate cyclase (sGC), which in turn activates protein kinase G via conversion of GTP into cyclic GMP. Alternatively, NO post-translationally modifies proteins via S-nitrosylation of the thiol group of cysteine. However, the mechanisms of action of NO on Ca2+ homeostasis during muscle contraction are not fully understood and we hypothesize that NO exerts its effects on Ca2+ homeostasis in skeletal muscles mainly through negative modulation of Ca2+ release and Ca2+ uptake via the NO-sGC-PKG pathway. To address this, we used 5–7 days-post fecundation-larvae of zebrafish, a well-established animal model for physiological and pathophysiological muscle activity. We evaluated the response of muscle contraction and Ca2+ transients in presence of SNAP, a NO-donor, or L-NAME, an unspecific NOS blocker in combination with specific blockers of key proteins of Ca2+ homeostasis. We also evaluate the expression of NOS in combination with dihydropteridine receptor, ryanodine receptor and sarco/endoplasmic reticulum Ca2+ ATPase. We concluded that endogenous NO reduced force production through negative modulation of Ca2+ transients via the NO-sGC pathway. This effect could be reversed using an unspecific NOS blocker or sGC blocker

Power-Efficiency Evolution of Capacitive Sensor Interfaces

Recent years have witnessed an improvement in the energy efficiency of capacitive sensor interfaces by more than three orders of magnitude. This article reviews the architectural and circuit innovations that have contributed to this progress. The fundamental limit on the energy consumption of capacitive sensor interfaces is discussed, as well as the widely used figure-of-merit (FoM). Interfaces based on period modulation feature simple circuitry, but their power efficiency at higher resolution deteriorates. Those employing Δ Σ modulation achieve high resolution with improved efficiency but require operational transconductance amplifiers that do not easily scale with process and supply voltage. Interfaces using successive approximation techniques feature mostly digital circuitry achieving good power efficiency at medium resolution. To achieve higher resolution, they can also be employed as the front-end in a hybrid architecture, where a back-end based on Δ Σ modulation or a voltage-controlled oscillator (VCO) performs a fine measurement on the front-end's residue, resulting in high resolution and excellent energy efficiency simultaneously.Accepted author manuscriptElectronic Instrumentatio