Purpose of Review 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. 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. Summary 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.

Aims Transient Receptor Potential Melastatin 7 (TRPM7) cation channel is a chanzyme (channel + kinase) that influences cellular Mg2+ homeostasis and vascular signalling. However, the pathophysiological significance of TRPM7 in the cardiovascular system is unclear. The aim of this study was to investigate the role of this chanzyme in the cardiovascular system focusing on inflammation and fibrosis. Methods and results TRPM7-deficient mice with deletion of the kinase domain (TRPM7+/Δkinase) were studied and molecular mechanisms investigated in TRPM7+/Δkinase bone marrow-derived macrophages (BMDM) and co-culture systems with cardiac fibroblasts. TRPM7-deficient mice had significant cardiac hypertrophy, fibrosis, and inflammation. Cardiac collagen and fibronectin content, expression of pro-inflammatory mediators (SMAD3, TGFβ) and cytokines [interleukin (IL)-6, IL-10, IL-12, tumour necrosis factor-α] and phosphorylation of the pro-inflammatory signalling molecule Stat1, were increased in TRPM7+/Δkinase mice. These processes were associated with infiltration of inflammatory cells (F4/80+CD206+ cardiac macrophages) and increased galectin-3 expression. Cardiac [Mg2+]i, but not [Ca2+]i, was reduced in TRPM7+/Δkinase mice. Calpain, a downstream TRPM7 target, was upregulated (increased expression and activation) in TRPM7+/Δkinase hearts. Vascular functional and inflammatory responses, assessed in vivo by intra-vital microscopy, demonstrated impaired neutrophil rolling, increased neutrophil: endothelial attachment and transmigration of leucocytes in TRPM7+/Δkinase mice. TRPM7+/Δkinase BMDMs had increased levels of galectin-3, IL-10, and IL-6. In co-culture systems, TRPM7+/Δkinase macrophages increased expression of fibronectin, proliferating cell nuclear antigen, and TGFβ in cardiac fibroblasts from wild-type mice, effects ameliorated by MgCl2 treatment. Conclusions We identify a novel anti-inflammatory and anti-fibrotic role for TRPM7 and suggest that its protective effects are mediated, in part, through Mg2+-sensitive processes.

A growing amount of literature has explored mainly the role of depression (and/or anxiety) in patients with rheumatic disorders. We aimed at determining the prevalence of depression, anxiety, and their association with quality of life among patients attending a rheumatology clinic, focusing on data regarding concomitant psychiatric treatment. Depression, anxiety, and quality of life were assessed using the Zung Self-Rating Depression Scale, the Hamilton Anxiety Scale, and the Health Assessment Questionnaire, respectively. Overall, 514 rheumatologic patients were studied. Depression and anxiety were documented in 21.8 and 30.8 % of the population, respectively, and correlated significantly with quality of life. Only 13.4 % of patients with depressive symptoms and 12.1 % of patients with anxiety symptoms were receiving antidepressant or antianxiety medication. Given the wide therapeutic armamentarium available nowadays for the management of depression and anxiety, an increased awareness among physicians dealing with rheumatologic patients is warranted in order to integrate detection and effective treatment of anxiety and depression into the routine clinical practice. Special attention should be paid to female patients, patients with longer disease duration, and/or those with established disability.

Purpose: Retinal image registration is a useful tool for medical professionals. However, performance evaluation of registration methods has not been consistently assessed in the literature. To address that, a dataset comprised of retinal image pairs annotated with ground truth and an evaluation protocol for registration methods is proposed.Methods: The dataset is comprised by 134 retinal fundus image pairs. These pairs are classified into three categories, according to characteristics that are relevant to indicative registration applications. Such characteristics are the degree of overlap between images and the presence/absence of anatomical differences. Ground truth in the form of corresponding image points and a protocol to evaluate registration performance are provided.Results: The proposed protocol is shown to enable quantitative and comparative evaluation of retinal registration methods under a variety of conditions.Conclusion: This work enables the fair comparison of retinal registration methods. It also helps researchers to select the registration method that is most appropriate given a specific target use.

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This study shows for the first time an association between quantitatively assessed retinal abnormalities and increased arterial stiffness in a sample of early-stage hypertensive and normotensive individuals, suggesting that micro- and macrocirculation impairment in hypertension is a dynamic, mutual, interdependent process present from its very early stages. Given the predictive value of both retinal arteriolar narrowing and arterial stiffness in terms of cardiovascular mortality and morbidity, identification of combined micro- and macrovascular damage might be helpful in cardiovascular risk stratification of hypertensive patients.

Arterial hypertension represents a leading cause of cardiovascular mortality and morbidity worldwide through its detrimental effects on target organs. Therefore, the early identification and appropriate management of high-risk patients emerges as extremely important. Given that the microvasculature is subject to a series of morphological and functional changes under the continuous effect of high blood pressure, research over the last years has gradually moved toward the identification of specific microcirculatory alterations that may serve as early prognostic markers of cardiovascular risk. Dermal capillaries represent an "open window" for the in vivo study of human microcirculation that has been long used mainly for the study of rheumatic diseases. However, capillaroscopy has been relatively understudied and only recently applied in the field of hypertension. Capillaroscopy represents a forthcoming promising estimate of the microvascular status in hypertensive patients, with capillary rarefaction representing the most typical finding. The present review aims at summarizing available evidence and the main findings, as well as the premises and promises, of capillary rarefaction as a tool for evaluating patients with hypertension.

Currently the treatment mainstay of sepsis is early and appropriate antibiotic therapy, accompanied by aggressive fluid administration, the use of vasopressors when needed and the prompt initiation of measures to support each failing organ. Activated protein C and hydrocortisone, when used accordingly can affect mortality. As the pathophysiologic events that take place during sepsis are being elucidated, new molecules that target each step of those pathways are being tested. However, a lot of those molecules affect various mediators of the sepsis cascade including inflammatory cytokines, cellular receptors, nuclear transcription factors, coagulation activators and apoptosis regulators. Over the last decade, a multitude of clinical trials and animal studies have investigated strategies that aimed to restore immune homeostasis either by reducing inflammation or by stimulating the innate and adaptive immune responses. Antibiotics, statins and other molecules with multipotent immunomodulatory actions have also been studied in the treatment of sepsis.