The corona virus disease of 2019 pandemic caused by the SARS-CoV-2 virus continues to inflict significant morbidity and mortality around the globe. A variety of cardiovascular presentations of SARS-CoV-2 infection have been described so far. However, the impact of SARS-CoV-2 on the right ventricle is largely unknown. Due to its pathophysiologic relevance, the right ventricle finds itself in the eye of the storm of corona virus disease of 2019, placing it at higher risk of failure. Increased afterload from acute respiratory distress syndrome and pulmonary embolism, negative inotropic effects of cytokines, and direct angiotensin converting enzyme 2-mediated cardiac injury from SARS-CoV-2 are potential mechanisms of right ventricle dysfunction in corona virus disease of 2019. Early detection and treatment of right ventricle dysfunction may lead to decreased mortality and improved patient outcomes in corona virus disease of 2019.

Cardiovascular Diseases (CVDs) are the leading cause of death globally. More than 17 million people die worldwide from CVD per year. There is considerable evidence suggesting that estrogen modulates cardiovascular physiology and function in both health and disease, and that it could potentially serve as a cardioprotective agent. The effects of estrogen on cardiovascular function are mediated by nuclear and membrane estrogen receptors (ERs), including estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), and G-protein-coupled ER (GPR30 or GPER). Receptor binding in turn confers pleiotropic effects through both genomic and non-genomic signaling to maintain cardiovascular homeostasis. Each ER has been implicated in multiple pre-clinical cardiovascular disease models. This review will discuss current reports on the underlying molecular mechanisms of the ERs in regulating vascular pathology, with a special emphasis on hypertension, pulmonary hypertension, and atherosclerosis, as well as in regulating cardiac pathology, with a particular emphasis on ischemia/reperfusion injury, heart failure with reduced ejection fraction, and heart failure with preserved ejection fraction.

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A close association between microwave (MW) radiation exposure and neurobehavioral disorders has been postulated but the direct effects of MW radiation on central nervous system still remains contradictory. This study was performed to understand the effect of short (15 days) and long-term (30 and 60 days) low-level MW radiation exposure on hippocampus with special reference to spatial learning and memory and its underlying mechanism in Swiss strain male mice, Mus musculus. Twelve-weeks old mice were exposed to 2.45 GHz MW radiation (continuous-wave [CW] with overall average power density of 0.0248 mW/cm(2) and overall average whole body specific absorption rate value of 0.0146 W/Kg) for 2 h/day over a period of 15, 30, and 60 days). Spatial learning and memory was monitored by Morris Water Maze. We have checked the alterations in hippocampal oxidative/nitrosative stress, neuronal morphology, and expression of pro-apoptotic proteins (p53 and Bax), inactive executioner Caspase- (pro-Caspase-3), and uncleaved Poly (ADP-ribose) polymerase-1 in the hippocampal subfield neuronal and nonneuronal cells (DG, CA1, CA2, and CA3). We observed that, short-term as well as long-term 2.45 GHz MW radiation exposure increases the oxidative/nitrosative stress leading to enhanced apoptosis in hippocampal subfield neuronal and nonneuronal cells. Present findings also suggest that learning and spatial memory deficit which increases with the increased duration of MW exposure (15 < 30 < 60 days) is correlated with a decrease in hippocampal subfield neuronal arborization and dendritic spines. These findings led us to conclude that exposure to CW MW radiation leads to oxidative/nitrosative stress induced p53-dependent/independent activation of hippocampal neuronal and nonneuronal apoptosis associated with spatial memory loss.

Microwave (MW) radiation induced oxidative stress reduces dendritic arborization, spine density and number of hippocampal pyramidal neurons and hence, impair learning and spatial memory through p53-dependent/independent apoptosis of hippocampal neuronal and nonneuronal cells. However, the mechanisms responsible for MW radiation induced impairment in memory formation remains still unknown. This study elucidates the effect of short (15 days) and long-term (30 and 60 days) low level 2.45 GHz MW radiation-induced local stress on the hippocampal spatial memory formation pathway in adult male mice. Twelve-weeks old mice were exposed to 2.45 GHz MW radiation (continuous-wave with overall average Power density of 0.0248 mW/cm2 and overall average whole body SAR value of 0.0146 W/Kg) @ 2 h/d for 15, 30, and 60 days. Learning and spatial memory was assessed by 8-arm radial maze. We have investigated the alterations in serum corticosterone level and the expression of glucocorticoid receptor, corticotropin-releasing hormone (CRH), inducible nitric oxide synthase (i-NOS), iGluRs, PSD-95-neuronal NOS (n-NOS) system, protein kinase A, protein kinase Cε-ERK1/2-pERK1/2 in all the hippocampal subregions, viz. CA1, CA2, CA3, and DG through immunohistochemistry/immunofluorescence and alterations in the expression of hippocampal glucocorticoid receptor, CRH-receptor 1 (CRH-R1), cAMP-response element-binding (CREB), and phosphorylated-CREB (p-CREB) through western blot analysis. We observed that 2.45 GHz MW irradiated mice showed slow learning and significantly increased number of working and reference memory errors in radial maze task. Further, 2.45 GHz MW radiation exposure increases serum corticosterone level and the expression of CRH, CRH-R1, and i-NOS, while the expression of iGluRs, n-NOS, PSD-95, protein kinase Cε, protein kinase A, ERK-p-ERK, CREB, and p-CREB decreases in above mentioned hippocampal subregions in a duration dependent manner. Our findings led us to conclude that 2.45 GHz MW radiation exposure induced local stress suppresses signaling mechanism(s) of hippocampal memory formation.