Effect of Iron Doping in Ordered Nickel Oxide Thin Film Catalyst for the Oxygen Evolution Reaction.

Water splitting has emerged as a promising route for generating hydrogen as an alternative to conventional production methods. Finding affordable and scalable catalysts for the anodic half-reaction, the oxygen evolution reaction (OER), could help with its industrial widespread implementation. Iron-containing Ni-based catalysts have a competitive performance for the use in commercial alkaline electrolyzers.

Serological Antibodies against Kidney, Liver, and Spleen Membrane Antigens as Potential Biomarkers in Patients with Immune Disorders.

Immune disorders arise from complex genetic and environmental factors, which lead to dysregulation at the cellular and inflammatory levels and cause tissue damage. Recent research highlights the crucial role of reactive antibodies in autoimmune diseases and graft rejection, but their complex determination poses challenges for clinical use. Therefore, our study aimed to ascertain whether the presence of reactive antibodies against membrane antigens in tissues from both animal models and humans could serve as biomarkers in patients with autoimmune disorders.

Tracking the Evolution of Single-Atom Catalysts for the CO Electrocatalytic Reduction Using Operando X-ray Absorption Spectroscopy and Machine Learning.

Transition metal-nitrogen-doped carbons (TMNCs) are a promising class of catalysts for the CO electrochemical reduction reaction. In particular, high CO-to-CO conversion activities and selectivities were demonstrated for Ni-based TMNCs. Nonetheless, open questions remain about the nature, stability, and evolution of the Ni active sites during the reaction.

Monolithic All-Solid-State High-Voltage Li-Metal Thin-Film Rechargeable Battery.

The substitution of an organic liquid electrolyte with lithium-conducting solid materials is a promising approach to overcome the limitations associated with conventional lithium-ion batteries. These constraints include a reduced electrochemical stability window, high toxicity, flammability, and the formation of lithium dendrites. In this way, all-solid-state batteries present themselves as ideal candidates for improving energy density, environmental friendliness, and safety.

Single-nucleotide polymorphism associations with efficacy and toxicity in metastatic castration-resistant prostate cancer treated with cabazitaxel.

The aim of this study was to evaluate the impact of certain single-nucleotide polymorphisms (SNPs) in cabazitaxel activity and toxicity in patients with metastatic castration-resistant prostate cancer (mCRPC). 56 SNPs in five genes (, , , and ) were genotyped in 67 mCRPC patients and their correlation with outcomes analyzed. -rs151352 (hazard ratio: 0.

Revealing Li Metal Anode Surface Evolution upon Exposure to CO Using Ambient Pressure X-Ray Photoelectron Spectroscopy.

Because they deliver outstanding energy density, next-generation lithium metal batteries (LMBs) are essential to the advancement of both electric mobility and portable electronic devices. However, the high reactivity of metallic lithium surfaces leads to the low electrochemical performance of many secondary batteries. Besides, Li deposition is not uniform, which has been attributed to the low ionic conductivity of the anode surface.

Synergy between a Silver-Copper Surface Alloy Composition and Carbon Dioxide Adsorption and Activation.

Bimetallic electrocatalysts provide a promising strategy for improving performance, especially in the enhancement of selectivity of CO reduction reactions. However, the first step of CO activation on bimetallic materials remains obscure. Considering bimetallic silver-copper (AgCu) as an example, we coupled ambient pressure X-ray photoelectron spectroscopy (APXPS) and quantum mechanics (QM) to examine CO adsorption and activation on AgCu exposed to CO with and without HO at 298 K.

Identification and in vitro characterization of two new PCSK9 Gain of Function variants found in patients with Familial Hypercholesterolemia.

Familial hypercholesterolemia (FH) is an autosomal dominant disease caused by pathogenic variants in genes encoding for LDL receptor (LDLR), Apolipoprotein B and Proprotein convertase subtilisin/kexin type 9 (PCSK9). Among PCSK9 variants, only Gain-of- Function (GOF) variants lead to FH. Greater attention should be paid to the classification of variants as pathogenic.

Analysis of LDLR variants from homozygous FH patients carrying multiple mutations in the LDLR gene.

Background And Aims: Familial hypercholesterolemia (FH) is an autosomal dominant disease with widespread global prevalence that partially accounts for the high prevalence of premature coronary heart disease. Although the majority of research on FH has focused on single heterozygous LDLR mutations, there have been limited reports of double LDLR mutations on the same chromosome. The aim of this study was to gain insight into the clinical consequences of the presence of multiple mutations in the LDLR gene.

Structural changes induced by acidic pH in human apolipoprotein B-100.

Acidification in the endosome causes lipoprotein release by promoting a conformational change in the LDLR allowing its recycling and degradation of LDL. Notwithstanding conformational changes occurring in the LDLR have expanded considerably, structural changes occurring in LDL particles have not been fully explored yet. The objectives of the present work were to study structural changes occurring in apoB100 by infrared spectroscopy (IR) and also LDL size and morphology by dynamic light scattering (DLS) and electron microscopy (EM) at both pH 7.

The p.Leu167del Mutation in APOE Gene Causes Autosomal Dominant Hypercholesterolemia by Down-regulation of LDL Receptor Expression in Hepatocytes.

Context: The p.Leu167del mutation in the APOE gene has been associated with hyperlipidemia.

Objectives: Our objective was to determine the frequency of p.

Structural analysis of APOB variants, p.(Arg3527Gln), p.(Arg1164Thr) and p.(Gln4494del), causing Familial Hypercholesterolaemia provides novel insights into variant pathogenicity.

Familial hypercholesterolaemia (FH) is an inherited autosomal dominant disorder resulting from defects in the low-density lipoprotein receptor (LDLR), in the apolipoprotein B (APOB) or in the proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. In the majority of the cases FH is caused by mutations occurring within LDLR, while only few mutations in APOB and PCSK9 have been proved to cause disease. p.

Adenylate Cyclase Toxin promotes bacterial internalisation into non phagocytic cells.

Bordetella pertussis causes whooping cough, a respiratory infectious disease that is the fifth largest cause of vaccine-preventable death in infants. Though historically considered an extracellular pathogen, this bacterium has been detected both in vitro and in vivo inside phagocytic and non-phagocytic cells. However the precise mechanism used by B.

The importance of an integrated analysis of clinical, molecular, and functional data for the genetic diagnosis of familial hypercholesterolemia.

Purpose: Familial hypercholesterolemia (FH) is one of the most common monogenic disorders, and the high concentrations of low-density lipoprotein (LDL) cholesterol presented since birth confers on these patients an increased cardiovascular risk. More than 1,600 alterations have been described in the LDL receptor gene (LDLR), but a large number need to be validated as mutations causing disease to establish a diagnosis of FH. This study aims to characterize, both at the phenotypic and genotypic levels, families with a clinical diagnosis of FH and present evidence for the importance of the integration of clinical, molecular, and functional data for the correct diagnosis of patients with FH.

Activity-associated effect of LDL receptor missense variants located in the cysteine-rich repeats.

Background: The LDL receptor (LDLR) is a Class I transmembrane protein critical for the clearance of cholesterol-containing lipoprotein particles. The N-terminal domain of the LDLR harbours the ligand-binding domain consisting of seven cysteine-rich repeats of approximately 40 amino acids each. Mutations in the LDLR binding domain may result in loss of receptor activity leading to familial hypercholesterolemia (FH).

Advantages and versatility of fluorescence-based methodology to characterize the functionality of LDLR and class mutation assignment.

Familial hypercholesterolemia (FH) is a common autosomal codominant disease with a frequency of 1:500 individuals in its heterozygous form. The genetic basis of FH is most commonly mutations within the LDLR gene. Assessing the pathogenicity of LDLR variants is particularly important to give a patient a definitive diagnosis of FH.

Functional characterization and classification of frequent low-density lipoprotein receptor variants.

Familial hypercholesterolemia (FH) is an autosomal-dominant disorder mostly caused by mutations in the low-density lipoprotein receptor (LDLR) gene leading to increased risk for premature cardiovascular diseases. According to functional studies, LDLR mutations may be classified into five classes. The main objective of this study was to characterize seven LDLR variants previously detected in FH patients.

Functional assembly of Kv7.1/Kv7.5 channels with emerging properties on vascular muscle physiology.

Objective: Voltage-dependent K(+) (Kv) channels from the Kv7 family are expressed in blood vessels and contribute to cardiovascular physiology. Although Kv7 channel blockers trigger muscle contractions, Kv7 activators act as vasorelaxants. Kv7.

Novel functional APOB mutations outside LDL-binding region causing familial hypercholesterolaemia.

Familial hypercholesterolaemia (FH) is characterized by increased circulating low-density lipoprotein (LDL) cholesterol leading to premature atherosclerosis and coronary heart disease. Although FH is usually caused by mutations in LDLR, mutations in APOB and PCSK9 also cause FH but only a few mutations have been reported, APOB p.R3527Q being the most common.

Ca2+ influx and tyrosine kinases trigger Bordetella adenylate cyclase toxin (ACT) endocytosis. Cell physiology and expression of the CD11b/CD18 integrin major determinants of the entry route.

Humans infected with Bordetella pertussis, the whooping cough bacterium, show evidences of impaired host defenses. This pathogenic bacterium produces a unique adenylate cyclase toxin (ACT) which enters human phagocytes and catalyzes the unregulated formation of cAMP, hampering important bactericidal functions of these immune cells that eventually cause cell death by apoptosis and/or necrosis. Additionally, ACT permeabilizes cells through pore formation in the target cell membrane.

Factors associated with cortisol levels and health in 5-6-year-old children.

Objectives: This study assesses the relationships between social context (family and inter-peer context), stress, and illness in 5-6-year-old children.

Methods: To this end, data were collected on spontaneous social interpeer behavior; families provided data on stress, anxiety, and parental acceptance-rejection; and the children's pediatricians provided data relative to their health. Data on stress-related hormones (cortisol) were collected using saliva samples.

Calpain-Mediated Processing of Adenylate Cyclase Toxin Generates a Cytosolic Soluble Catalytically Active N-Terminal Domain.

Bordetella pertussis, the whooping cough pathogen, secretes several virulence factors among which adenylate cyclase toxin (ACT) is essential for establishment of the disease in the respiratory tract. ACT weakens host defenses by suppressing important bactericidal activities of the phagocytic cells. Up to now, it was believed that cell intoxication by ACT was a consequence of the accumulation of abnormally high levels of cAMP, generated exclusively beneath the host plasma membrane by the toxin N-terminal catalytic adenylate cyclase (AC) domain, upon its direct translocation across the lipid bilayer.

[Fospropofol: A new prodrug of propofol].

The development of new propofol formulations has advanced rapidly in the last ten years with the achievement of the marketing a new prodrug of propofol: fospropofol, pharmacologically different from the original compound. It is a water soluble compound that requires metabolism of the prodrug to propofol, which leads to a time delay between its administration and the appearance of its pharmacological effect. Its pharmacokinetic and pharmacodynamic characteristics are different to the original formula.