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No association with neck CT (HR 1.07, 95% CI 0.80; 1.43) was observed.
In our study population, a similar risk of cataract with head, neck or the rest of the body CT was detected.
In our study population, a similar risk of cataract with head, neck or the rest of the body CT was detected.
To compare the changes in the measurement of corneal densitometry and total corneal higher-order aberrations (HOAs) between topical tacrolimus and transepithelial phototherapeutic keratectomy (Te-PTK) in the treatment of adenoviral corneal subepithelial infiltrates (SEIs).
This is an interventional prospective randomized study, including 63 eyes of 35 patients with symptomatic adenoviral corneal SEIs for at least 6months. All patients underwent previous topical steroid therapy associated with unsatisfactory response and/or complications. Patients were assigned into three groups (1) Te-PTK group Te-PTK with MMC 0.02% was performed by a Technolas; Teneo excimer laser; (2) tacrolimus group tacrolimus 0.03% ointment was applied once daily for 2-6months; the endpoint of treatment was based on the improvement in the corneal densitometry, BCVA, and OSDI; and (3) control group no intervention was done. BCVA, corneal densitometry, and total corneal higher-order aberrations (HOAs) evaluation using Pentacam HR were icantly lower in Te-PTK and tacrolimus groups than the control group.
Te-PTK and topical tacrolimus are effective methods for the treatment of adenoviral corneal SEIs improving visual acuity, corneal densitometry, and corneal HOA. The densitometry program of the Pentacam may give an objective guide for the treatment of adenoviral corneal SEIs.
ClinicalTrials.gov ID is NCT04267991.
ClinicalTrials.gov ID is NCT04267991.Monoamine oxidases (MAOs) are involved in the oxidative deamination of different amines and neurotransmitters. This pointed them as potential targets for several disorders and along the last 70 years a wide variety of MAO inhibitors have been developed as successful drugs for the treatment of complex diseases, being the first drugs approved for depression in the late 1950s. The discovery of two MAO isozymes (MAO-A and B) with different substrate selectivity and tissue expression patterns led to novel therapeutic approaches and to the development of new classes of inhibitors, such as selective irreversible and reversible MAO-B inhibitors and reversible MAO-A inhibitors. Significantly, MAO-B inhibitors constitute a widely studied group of compounds, some of them approved for the treatment of Parkinson's disease. Further applications are under development for the treatment of Alzheimer's disease, amyotrophic lateral sclerosis, and cardiovascular diseases, among others. This review summarizes the most important aspects regarding the development and clinical use of MAO inhibitors, going through mechanistic and structural details, new indications, and future perspectives. Monoamine oxidases (MAOs) catalyze the oxidative deamination of different amines and neurotransmitters. The two different isozymes, MAO-A and MAO-B, are located at the outer mitochondrial membrane in different tissues. The enzymatic reaction involves formation of the corresponding aldehyde and releasing hydrogen peroxide (H2O2) and ammonia or a substituted amine depending on the substrate. MAO's role in neurotransmitter metabolism made them targets for major depression and Parkinson's disease, among other neurodegenerative diseases. Currently, these compounds are being studied for other diseases such as cardiovascular ones.
To summarise the advances that have been made from 2017 in dual, triple, and quadruple low-dose combination therapy for treating high blood pressure.
Many people require multiple blood pressure lowering medicines to achieve target blood pressures, and initiating treatment with combination blood pressure lowering therapy is being increasingly investigated and recommended. Low-dose combinations of blood pressure lowering provide more effective blood pressure lowering, with fewer adverse events. Recent advances include listing of four dual combinations on the WHO Essential Medicines List, completion of a triple half-dose combination trial, and a pilot of quadruple quarter-dose combination, and recent cardiovascular polypill trials have included two blood pressure lowering medicines at low dose. These trials all demonstrated improvements in achieving blood pressure targets with low-dose combination therapy. Low-dose combination therapy is a promising option for initial treatment of hypertension that appears ts a promising option for initial treatment of hypertension that appears to be safe and effective. Larger trials of triple and quadruple low-dose combination therapy in multiple locations are underway and should provide stronger evidence of efficacy as well as information on the side effect profile.
The main goal of this article is to discuss the role of the epithelial sodium channel (ENaC) in extracellular fluid and blood pressure regulation.
Besides its role in sodium handling in the kidney, recent studies have found that ENaC expressed in other cells including immune cells can influence blood pressure via extra-renal mechanisms. Dendritic cells (DCs) are activated and contribute to salt-sensitive hypertension in an ENaC-dependent manner. We discuss recent studies on how ENaC is regulated in both the kidney and other sites including the vascular smooth muscles, endothelial cells, and immune cells. We also discuss how this extra-renal ENaC can play a role in salt-sensitive hypertension and its promise as a novel therapeutic target. The role of ENaC in blood pressure regulation in the kidney has been well studied. Recent human gene sequencing efforts have identified thousands of variants among the genes encoding ENaC, and research efforts to determine if these variants and their expression in extra-rpression in extra-renal tissue play a role in hypertension will advance our understanding of the pathogenesis of ENaC-mediated cardiovascular disease and lead to novel therapeutic targets.
To review current literature on endothelial dysfunction with previous coronaviruses, and present available data on the role of endothelial dysfunction in coronavirus disease-2019 (COVID-19) infection in terms of pathophysiology and clinical phenotype RECENT FINDINGS Recent evidence suggests that signs and symptoms of severe COVID-19 infection resemble the clinical phenotype of endothelial dysfunction, implicating mutual pathophysiological pathways. Dysfunction of endothelial cells is believed to mediate a variety of viral infections, including those caused by previous coronaviruses. click here Experience from previous coronaviruses has triggered hypotheses on the role of endothelial dysfunction in the pathophysiology of SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), which are currently being tested in preclinical and clinical studies. Endothelial dysfunction is the common denominator of multiple clinical aspects of severe COVID-19 infection that have been problematic for treating physicians. Given the global impact of this pandemic, better understanding of the pathophysiology could significantly affect management of patients.
