Synthesis of heterometallic metal–organic frameworks and their performance as electrocatalyst for CO2 reduction

Herein we report the solventless synthesis and doping of the benchmark HKUST-1(Cu) as a facile route to afford heterometallic metal–organic frameworks (MOFs) having proficient behavior as electrocatalytic materials in the reduction of carbon dioxide. Zn(ii), Ru(iii) and Pd(ii) were selected as doping metals (M_D) with the aim of partially replacing the Cu(ii) atoms of the pristine structure to afford HKUST-1(Cu,M_D) type materials. Apart from the high yield and good crystallinity of the obtained materials, the extremely high reagent concentration that the reaction conditions imply makes it feasible to control dopant loading in all cases. Prepared samples were processed as electrodes and assembled in a continuous flow filter-press electrochemical cell. Faraday efficiency to methanol and ethanol at Ru(iii)-based electrodes resulted in activity as high as 47.2%, although the activity of the material decayed with time. The interplay of the dopant metal and copper(ii), and the long-term performance are also discussed.

The solventless synthesis of heterometallic metal–organic frameworks and their proficient behavior as electrocatalysts in the CO₂ reduction to alcohols is presented.     

Postpartum depression in Mexican women with autoimmune rheumatic diseases

Clinical Rheumatology -     

Syncope in Patients With Severe Aortic Stenosis: More Than Just an Obstruction Issue

BackgroundSevere aortic stenosis (AoS) is considered a primary cause of syncope. However, other mechanisms may be present in these patients and accurate diagnosis can have important clinical implications. The aim of this study is to assess the different etiologies of syncope in patients with severe AoS and the impact on prognosis of attaining a certain or highly probable diagnosis for the syncope.MethodsOut of a cohort of 331 patients with AoS and syncope, 61 had severe AoS and were included in the study. Main cause of syncope and adverse cardiac events were assessed.ResultsIn 40 patients (65.6%), we reached a certain or highly probable diagnosis of the main cause of the syncope. AoS was considered the primary cause of the syncope in only 7 patients (17.5% of the patients with known etiology). Atrioventricular block (14 patients, 35.0%) and vasovagal syncope (6 patients, 15.0%) were the most frequently diagnosed causes. The presence of a known cause for syncope during the admission was not associated with a lower incidence of recurrence during follow-up (hazard ratio [HR] 0.69, 95% confidence interval [CI] 0.20-2.40). Syncope of unknown etiology was independently associated with greater mortality during 1-year follow-up (HR 5.4, 95% CI 1.3-21.6) and 3-year follow-up (HR 3.5, 95% CI 1.2-10.3).ConclusionsIn a high proportion of patients with severe AoS admitted for syncope, the valvulopathy was not the main cause of the syncope. Syncope in two-thirds of this population was caused by either bradyarrhythmia or reflex causes. Syncope of unknown cause was associated with increased short- and medium-term mortality, independently from treatment of the valve disease. An exhaustive work-up should be conducted to determine the main cause for syncope.     

Exploring the fuzzy border between senolytics and senomorphics with chemoinformatics and systems pharmacology

Biogerontology - Senescent cells accumulate within tissues during aging and secrete an array of pro-inflammatory molecules known as senescent-associated secretory phenotype (SASP), which contribute...     

Hemodynamic evaluation of stenotic cardiac valves: II. Modification of the simplified valve formula for mitral and aortic valve area calculation

Since the introduction by Gorlin and Gorlin of the hydraulic formulae for calculating valve area, it has become the best parameter for quantitating valve stenosis. Recently Hakki et al proposed a simplified formula for valve area calculation that does not take into account either heart rate (HR) or left ventricular filling or ejection time. The purpose of this study was to analyze the validity of Hakki's formulae under different physiological conditions and to propose an easy correction to improve its accuracy. Our study suggests: (1) that an easy correction for heart rate in certain cases, dividing by 1.35 when HR less than 75 beats per min in mitral stenosis and when HR greater than 90 beats per min in aortic stenosis, significantly improves the accuracy and validity of Hakki's formulae (p less than 0.02 and p less than 0.05); (2) the instantaneous valve gradients (peak gradient for aortic stenosis and average of instantaneous early, middle, and late diastolic gradients for mitral stenosis) are as valid as mean planimetric gradients for valve area calculation. Thus the simplified formulae proposed in this study allow mitral and aortic valve area calculations by means of instantaneous gradients, cardiac output, and heart rate.     

Tissue distribution and subcellular localization of the cardiac sodium channel during mouse heart development

AIMS: The aim of this study was to analyse the mRNA expression levels and protein distribution of the cardiac sodium channel Scn5a/Nav1.5 during mouse cardiogenesis. METHODS AND RESULTS: Scn5a mRNA levels were determined by real-time RT-PCR using embryonic hearts ranging from E9.5 to E17.5 as well as postnatal and adult hearts. In addition, Scn5a protein (Nav1.5) distribution was analysed by immunohistochemistry and confocal microscopy. Scn5a mRNA levels displayed a peak at stage E11.5, decreased during the subsequent stages and then steadily increased from E17.5 onwards, and throughout the postnatal to the adult stages. Immunohistochemistry experiments revealed comparable distribution of Nav1.5 between the different cardiac chambers at early embryonic stages. During the foetal stages, Nav1.5 showed an enhanced expression in the trabeculated myocardium and in the bundle branches. At the subcellular level, Nav1.5 and Scn1b double-immunostaining analysis is consistent with the presence of both sodium channel subunits in the T-tubule system and the intercalated discs. CONCLUSION: Our results demonstrate that the cardiac sodium channel, Nav1.5, shows a dynamic expression pattern during mouse heart development, indicating that it could play an important role in the acquisition of a mature pattern of conduction and contraction during cardiogenesis.     

Current and future treatment of chest pain of presumed esophageal origin

Patients with chest pain of presumed esophageal origin should be reassured and should undergo an esophageal manometry study. In patients with spastic esophageal disorders, a trial with calcium channel blockers or low-dose antidepressants used as visceral analgesics is the best approach. Inpatients with non GERD-related, nonspastic esophageal motility disorder, low-dose antidepressants seem reasonable. Anxiolytics are useful in patients with panic disorders, and psychological interventions (eg, cognitive-behavioral therapy) are also valuable, mainly in patients in whom reassurance is not sufficient to avoid the misinterpretation of their symptoms. In the future, visceral sensitivity modifying agents such as serotoninergic agonists or antagonists may become the cornerstone of therapy in patients with chest pain of presumed esophageal origin.Combinations of different approaches, such as proton pump inhibitors and psychotropic or antinociceptive agents, should also be evaluated in clinical trials.