To address the socioeconomic and psychological impact of COVID-19 pandemic on individuals belonging to different developing countries. METHODOLOGYA cross-sectional study was conducted from March 2020 to June 2020 in different developing countries around the world. All consenting individuals who were 18 years or older, with access to the internet were included in the study. The individuals who did not speak English language, had no computer skills, and were younger than 18 years were excluded from the study. The survey started with recording socio-demographic information followed by administration of generalized anxiety disorder questionnaire (GAD-7). The severity of anxiety levels and degree of worrying were associated with sociodemographic characteristics and financial stability of participants. A p-value of <0.05 was considered as statistically significant. RESULTSA total of 552 individuals participated in the study with a mean age of 27.10(6.44) years. It was found that 94(17%) participants were given a temporary layoff while 26(4.7%) individuals were permanently terminated from their jobs amid the pandemic.

Prompt reperfusion is vital to resuscitating ischemic myocardium. However, cardiomyocyte death still occurs due to ischemia-reperfusion (I/R) injury, which is mediated in part by oxidative stress. Major sources of reactive oxygen species (ROS) during I/R are NADPH oxidase (NOX-2) and mitochondria, which are principally activated by protein kinase C βII (PKCβII). Previously, myristic acid (Myr) and trans-activator of transcription (Tat) conjugated PKCβII inhibitor (Myr-Tat-PKCβII-; N-Myr-Tat-CC-SLNPEWNET) exhibited cardioprotective effects in ex vivo rat hearts. In this study, we hypothesize that Myr-Tat-PKCβII- will mitigate cardiac injury in an in vivo porcine myocardial I/R model compared to scrambled peptide controls. Male Yorkshire pigs (38-50kg) underwent regional I(1hr)/R(3hrs) through balloon-assisted occlusion of the second diagonal branch of the left anterior descending coronary artery (LAD) supplying ~40% of the anterior portion of the myocardium. During reperfusion (balloon deflation), a bolus of Myr-Tat-PKCβII- or scrambled control was infused into the LAD. Cardiac function was evaluated as the relative change in ejection fraction (EF) at the end of 3hr reperfusion compared to baseline. Serial measurements of serum creatine phosphokinase (CPK), troponin I, and myoglobin were evaluated to assess cardiac injury. Post-reperfused hearts were stained with Evans Blue dye to identify the area at risk (AR) and 1% triphenyltetrazolium chloride to demarcate the area of necrosis (AN). Infarct size (AN/AR), EF, and cardiac injury markers were analyzed via Student’s t-test. Myr-Tat-PKCβII- preserved EF with a relative change of 1.2±2.8% compared to 8.9±2.2% in control hearts (p<0.05) from mean baseline EF (61.4±0.5%). Myr-Tat-PKCβII- significantly decreased myoglobin levels at 1hr reperfusion (135±132ng/mL, n=4) compared to scrambled control (1022±346ng/mL, n=3 p<0.05). Myr-Tat-PKCβII- reduced infarct size to 13.5±3.9% (n=4) compared to scrambled control hearts (27.5±7.9%, n=6). CPK and troponin I levels were comparable in both groups. These results suggest Myr-Tat-PKCβII- mitigates cardiac injury when given at reperfusion onset. Future studies will examine Myr-Tat-PKCβII- in an 8 week in-vivo, porcine MI survival study.

Ischemic heart disease remains the leading cause of death worldwide. Pharmacological agents that mimic the cardioprotective effects of ischemic preconditioning may have therapeutic potential as a secondary prevention strategy to resist infarction from subsequent cardiovascular events. Increased left ventricular end diastolic pressure (LVEDP) during ischemia, or ischemic peak pressure (IPP), is known to be correlated to infarct size. Recently our laboratory demonstrated that naltrindole (NTI), a selective delta opioid receptor antagonist, reduces IPP and infarct size when given prior to ischemia (preconditioning) in a Langendorff rat heart model. The purpose of this study was to examine the effects of NTI analogues naltriben (NTB, delta opioid receptor antagonist) and guanidinonaltrindole (GNTI, kappa opioid receptor antagonist) compared to NTI. Nor‐binaltrophine (BNI, kappa opioid receptor antagonist) and naloxone (NX, broad‐spectrum opioid receptor antagonist) were tested to evaluate cardioprotection by other opioid receptor antagonists. Isolated hearts from male Sprague‐Dawley rats (~300g) were subjected to 30‐min global ischemia (I)/45‐min reperfusion (R) with treatments infused for 5 min before I and during the first 5 min of R. LV cardiac function was measured using a pressure transducer. At the end of reperfusion, infarct size was assessed using 1% triphenyltetrazolium chloride staining and defined as infarcted tissue/total area at risk. Data were evaluated using ANOVA Student‐Neuman‐Keuls post‐hoc analysis. Control I/R hearts demonstrated an IPP of 39±3 mmHg compared to pre‐ischemic LVEDP of 9±1 mmHg at baseline (n=12, p<0.01), resulting in substantial infarct at the end of 45 min R (32±4%). NTI (n=7) and NTB (n=6) elicited cardiodepressive effects during preconditioning by reducing the maximal rate in the rise of LV pressure (dP/dt max) to 1581±379 mmHg/s and 929±243 mmHg/s, respectively, compared to control (2471±72 mmHg/s, p<0.01). IPP was reduced by NTI (18±3 mmHg/s) and NTB (15±3 mmHg/s) compared to all groups (p<0.05). Post‐reperfused dP/dt max and infarct size was most improved following NTI (1830±90 mmHg/s, 7±2%) and NTB (1846±140 mmHg/s, 7±2%) pretreatment, compared to control (777±142 mmHg/s, 32±4%, p<0.01). GNTI reduced infarct size (17 ± 4%, n=6, p<0.05), but did not exert a negative inotropic effect. Cardiac function and infarct size did not improve with BNI (n=7) or NX (n=6) pretreatment. These results suggest that NTI and analogues, GNTI and NTB, are cardioprotective against myocardial I/R injury. The negative inotropic effects of NTI and NTB were associated with ~75% reduction in infarct size compared to control. GNTI decreased infarct size by ~50% and these results suggest that NTI, NTB, and GNTI exert tissue‐salvaging effects independent of delta or kappa opioid receptor antagonism. In future studies, we will examine different ischemic time points to administer NTI and its analogues to determine optimal cardioprotection and investigate downstream effects on calcium handling.