In addition to physical health, the COVID-19 pandemic has affected the global economy and mental health significantly. The economic and social consequence has sparked many psychological mediators. In severe cases, they led to suicidal behavior in individuals like as seen in the 1918-1919 flu pandemic and in the 2003 severe acute respiratory syndrome (SARS) epidemic. Previously, a few articles have been published with regard to COVID-19 suicides in Bangladesh. However, all these articles talked about sporadic cases of suicides with no clear picture of the holistic overview of suicides in Bangladesh. Herein, we looked into all COVID-19 suicide cases from March 01, 2020, to July 31, 2020, as reported in Bangladeshi media. Our study also reports the risk factors contributing to suicidal incidents. Moreover, we also identified the impact of gender, profession, and COVID-19 diagnosis status on committing suicide. This study will shed light on the topic with a clear understanding of the causalities influencing individuals to suicide. Furthermore, it will help the policymakers to take necessary actions to prevent any further suicides.

Background: We reported previously that α _1B ‐AR (α _1B ‐adrenoceptor) and AVPR1A (arginine vasopressin receptor 1A) heteromerize with CCR1 (C‐C motif [chemokine] receptor 1) in human monocytes, through which CCR1 is controlled. Whether CCR1 affects α _1B ‐AR and AVPR1A signaling and whether such complexes are detectable in human vascular smooth muscle cells (hVSMCs) is unknown. Methods and Results: Bioluminescence resonance energy transfer suggested that the receptors can form hetero‐oligomeric complexes. Activation of CCR1 with CCL23 (chemokine [C‐C motif] ligand 23) increased the efficacy of aVP (arginine vasopressin)‐stimulated AVPR1A and reduced the efficacy of phenylephrine‐stimulated α _1b ‐AR to activate guanine nucleotide‐binding protein G(q) subunit alpha (Gαq) in cells coexpressing all 3 receptors. Although CCL23 increased the efficacy of aVP and phenylephrine to recruit β‐arrestin to AVPR1A and α _1b ‐AR, respectively, when CCR1 is coexpressed, CCL23 did not affect β‐arrestin recruitment to agonist‐stimulated AVPR1A and α _1b ‐AR when all 3 receptors are present. Proximity ligation assays suggested that such receptor complexes are expressed in hVSMCs. Proximity ligation assays after small interfering RNA knockdown of each receptor showed that interactions between CCR1 and AVPR1A depend on the presence of α _1B ‐AR, whereas interactions between CCR1 and α _1B ‐AR and between α _1B ‐AR and AVPR1A are not affected by the presence of the third receptor partner. CCL23 increased IP3 (inositol trisphosphate) production and gel contraction of hVSMCs upon aVP stimulation and inhibited IP3 production and gel contraction of hVSMCs upon phenylephrine stimulation. Conclusions: Our findings suggest that CCR1 within functional heteromeric complexes with α _1B ‐AR and AVPR1A modulates the efficacy of α _1B ‐AR and AVPR1A in hVSMCs to activate downstream signaling cascades that mediate vasoconstriction and control vascular tone.

β-adrenoceptor (β-AR) agonists are known to antagonize thrombin-induced impairment (TII) of bovine and ovine lung endothelial barrier function. The effects of adrenoceptor agonists and other vasoactive agents on human lung microvascular endothelial cell (HULEC-5a) barrier function upon thrombin exposure have not been studied. Furthermore, it is unknown whether the in vitro effects of adrenoceptor agonists translate to lung protective effects in vivo. We observed that epinephrine, norepinephrine, and phenylephrine enhanced normal and prevented TII of HULEC-5a barrier function. Arginine vasopressin and angiotensin II were ineffective. α_1B-, α_2A/B-, and β_1/2-ARs were detectable in HULEC-5a by RT-PCR. Propranolol but not doxazosin blocked the effects of all adrenoceptor agonists. Phenylephrine stimulated β₂-AR-mediated Gαs activation with 13-fold lower potency than epinephrine. The EC₅₀ to inhibit TII of HULEC-5a barrier function was 1.8 ± 1.9 nM for epinephrine and >100 nM for phenylephrine. After hemorrhagic shock and fluid resuscitation in rats, Evans blue extravasation into the lung increased threefold (p < 0.01 vs. sham). Single low-dose (1.8 μg/kg) epinephrine administration at the beginning of resuscitation had no effects on blood pressure and reduced Evans blue extravasation by 60% (p < 0.05 vs. vehicle). Our findings confirm the effects of β-adrenoceptor agonists in HULEC-5a and suggest that low-dose β-adrenoceptor agonist treatment protects lung vascular barrier function after traumatic hemorrhagic shock.