A general viscosity model of Campi Flegrei (Italy) melts

Viscosities of shoshonitic and latitic melts, relevant to the Campi Flegrei caldera magmas, have been experimentally determined at atmospheric pressure and 0.5 GPa, temperatures between 840 K and 1870 K, and H2O contents from 0.02 to 3.30 wt%. The concentric cylinder technique was employed at atmospheric pressure to determine viscosity of nominally anhydrous melts in the viscosity range of 101.5 - 103 Pa·s. The micropenetration technique was used to determine the viscosity of hydrous and anhydrous melts at atmospheric pressure in the high viscosity range (1010 Pa·s). Falling sphere experiments were performed at 0.5 GPa in the low viscosity range (from 100.35 to 102.79 Pa·s) in order to obtain viscosity data of anhydrous and hydrous melts. The combination of data obtained from the three different techniques adopted permits a general description of viscosity as a function of temperature and water content using the following modified VFT equation: where η is the viscosity in Pa·s, T the temperature in K, w the H2O content in wt%, and a, b, c, d, e, g are the VFT parameters. This model reproduces the experimental data (95 measurements) with a 1σ standard deviation of 0.19 and 0.22 log units for shoshonite and latite, respectively. The proposed model has been applied also to a more evolved composition (trachyte) from the same area in order to create a general model applicable to the whole compositional range of Campi Flegrei products. Moreover, speed data have been used to constrain the ascent velocity of latitic, shoshonitic, and trachytic melts within dikes. Using petrological data and volcanological information (geometrical parameters of the eruptive fissure and depth of magma storage), we estimate a time scale for the ascent of melt from 9 km to 4 km depth (where deep and shallow reservoirs, respectively, are located) in the order of few minutes. Such a rapid ascent should be taken into account for the hazard assessment in the Campi Flegrei area

Idiopathic sensorineural hearing loss is associated with endothelial dysfunction

Hearing impairment is the most prevalent sensory deficit [1]. Sensorineural hearing loss (SNHL) is the most common type of permanent hearing loss and it occurswhen there is damage to the inner ear (cochlea), or to the nerve pathways fromthe inner ear to the brain.Most of the time, SNHL cannot be medically or surgically corrected. SNHL can result from genetic, environmental, or combined etiologies that prevent normal function of hearing, but, despite detailed investigation, the main cause remains usually unknown. Clinical and experimental studies have shown that ischemia contributes to several SNHL [2], suchas sudden sensoneural hearing loss, presbyacusis and noise-induced hearing loss. All of these SNHL can be related to alteration in blood flow [3]. The aim of the study is finding a relationship between idiopathic SNHL and endothelial dysfunction

Understanding the heart-brain axis response in COVID-19 patients: A suggestive perspective for therapeutic development

In-depth characterization of heart-brain communication in critically ill patients with severe acute respiratory failure is attracting significant interest in the COronaVIrus Disease 19 (COVID-19) pandemic era during intensive care unit (ICU) stay and after ICU or hospital discharge. Emerging research has provided new insights into pathogenic role of the deregulation of the heart-brain axis (HBA), a bidirectional flow of information, in leading to severe multiorgan disease syndrome (MODS) in patients with confirmed infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Noteworthy, HBA dysfunction may worsen the outcome of the COVID-19 patients. In this review, we discuss the critical role HBA plays in both promoting and limiting MODS in COVID-19. We also highlight the role of HBA as new target for novel therapeutic strategies in COVID-19 in order to open new translational frontiers of care. This is a translational perspective from the Italian Society of Cardiovascular Researches

Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial

Background: The EMPA KIDNEY trial showed that empagliflozin reduced the risk of the primary composite outcome of kidney disease progression or cardiovascular death in patients with chronic kidney disease mainly through slowing progression. We aimed to assess how effects of empagliflozin might differ by primary kidney disease across its broad population. Methods: EMPA-KIDNEY, a randomised, controlled, phase 3 trial, was conducted at 241 centres in eight countries (Canada, China, Germany, Italy, Japan, Malaysia, the UK, and the USA). Patients were eligible if their estimated glomerular filtration rate (eGFR) was 20 to less than 45 mL/min per 1·73 m2, or 45 to less than 90 mL/min per 1·73 m2 with a urinary albumin-to-creatinine ratio (uACR) of 200 mg/g or higher at screening. They were randomly assigned (1:1) to 10 mg oral empagliflozin once daily or matching placebo. Effects on kidney disease progression (defined as a sustained ≥40% eGFR decline from randomisation, end-stage kidney disease, a sustained eGFR below 10 mL/min per 1·73 m2, or death from kidney failure) were assessed using prespecified Cox models, and eGFR slope analyses used shared parameter models. Subgroup comparisons were performed by including relevant interaction terms in models. EMPA-KIDNEY is registered with ClinicalTrials.gov, NCT03594110. Findings: Between May 15, 2019, and April 16, 2021, 6609 participants were randomly assigned and followed up for a median of 2·0 years (IQR 1·5–2·4). Prespecified subgroupings by primary kidney disease included 2057 (31·1%) participants with diabetic kidney disease, 1669 (25·3%) with glomerular disease, 1445 (21·9%) with hypertensive or renovascular disease, and 1438 (21·8%) with other or unknown causes. Kidney disease progression occurred in 384 (11·6%) of 3304 patients in the empagliflozin group and 504 (15·2%) of 3305 patients in the placebo group (hazard ratio 0·71 [95% CI 0·62–0·81]), with no evidence that the relative effect size varied significantly by primary kidney disease (pheterogeneity=0·62). The between-group difference in chronic eGFR slopes (ie, from 2 months to final follow-up) was 1·37 mL/min per 1·73 m2 per year (95% CI 1·16–1·59), representing a 50% (42–58) reduction in the rate of chronic eGFR decline. This relative effect of empagliflozin on chronic eGFR slope was similar in analyses by different primary kidney diseases, including in explorations by type of glomerular disease and diabetes (p values for heterogeneity all >0·1). Interpretation: In a broad range of patients with chronic kidney disease at risk of progression, including a wide range of non-diabetic causes of chronic kidney disease, empagliflozin reduced risk of kidney disease progression. Relative effect sizes were broadly similar irrespective of the cause of primary kidney disease, suggesting that SGLT2 inhibitors should be part of a standard of care to minimise risk of kidney failure in chronic kidney disease. Funding: Boehringer Ingelheim, Eli Lilly, and UK Medical Research Council

Clopidogrel reloading in patients undergoing percutaneous coronary intervention on chronic clopidogrel therapy: results of the ARMYDA-4 RELOAD (Antiplatelet therapy for Reduction of MYocardial Damage during Angioplasty) randomized trial

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