Background Online misinformation proliferation during the COVID-19 pandemic has become a major public health concern. Objective We aimed to assess the prevalence of COVID-19 misinformation exposure and beliefs, associated factors including psychological distress with misinformation exposure, and the associations between COVID-19 knowledge and number of preventive behaviors. Methods A cross-sectional online survey was conducted with 1049 South Korean adults in April 2020. Respondents were asked about receiving COVID-19 misinformation using 12 items identified by the World Health Organization. Logistic regression was used to compute adjusted odds ratios (aORs) for the association of receiving misinformation with sociodemographic characteristics, source of information, COVID-19 misinformation belief, and psychological distress, as well as the associations of COVID-19 misinformation belief with COVID-19 knowledge and the number of COVID-19 preventive behaviors among those who received the misinformation. All data were weighted according to the Korea census data in 2018. Results Overall, 67.78% (n=711) of respondents reported exposure to at least one COVID-19 misinformation item. Misinformation exposure was associated with younger age, higher education levels, and lower income. Sources of information associated with misinformation exposure were social networking services (aOR 1.67, 95% CI 1.20-2.32) and instant messaging (aOR 1.79, 1.27-2.51). Misinformation exposure was also associated with psychological distress including anxiety (aOR 1.80, 1.24-2.61), depressive (aOR 1.47, 1.09-2.00), and posttraumatic stress disorder symptoms (aOR 1.97, 1.42-2.73), as well as misinformation belief (aOR 7.33, 5.17-10.38). Misinformation belief was associated with poorer COVID-19 knowledge (high: aOR 0.62, 0.45-0.84) and fewer preventive behaviors (≥7 behaviors: aOR 0.54, 0.39-0.74). Conclusions COVID-19 misinformation exposure was associated with misinformation belief, while misinformation belief was associated with fewer preventive behaviors. Given the potential of misinformation to undermine global efforts in COVID-19 disease control, up-to-date public health strategies are required to counter the proliferation of misinformation.

Introduction With the advent of genetically modified mice, it seems particularly advantageous to develop a mouse model of diabetic erectile dysfunction. Aim To establish a mouse model of type I diabetes by implementation of either multiple low-dose streptozotocin (STZ) protocol or single high-dose STZ protocol and to evaluate morphologic alterations in the cavernous tissue and subsequent derangements in penile hemodynamics in vivo. Methods Eight-week-old C57BL/6J mice were divided into three groups: a control group, a group administered the multiple low-dose STZ protocol (50 mg/kg × 5 days), and a group administered the single high-dose STZ protocol (200 mg/kg). Main Outcome Measures After 8 weeks, erectile function was measured by electrical stimulation of the cavernous nerve. The penis was then harvested and stained with hydroethidine (in situ analysis of superoxide anion), TUNEL, or antibodies to nitrotyrosine (marker of peroxynitrite formation), PECAM-1, smooth muscle α-actin, and phospho-eNOS. Penis specimens from a separate group of animals were used for phospho-eNOS and eNOS western blot or cGMP determination. Results Erectile function was significantly less in diabetic groups than in control group. The generation of superoxide anion and nitrotyrosine and the number of apoptotic cells in both cavernous endothelial and smooth muscle cells were significantly higher in diabetic groups than in control group. Cavernous tissue phospho-eNOS and cGMP expression and the number of endothelial and smooth muscle cells were lower in diabetic groups than in control group. Both diabetic models resulted in similar structural and functional derangements in the corpus cavernosum; however, the mortality rate was higher in mice receiving single high-dose of STZ than in those receiving multiple low-doses. Conclusion The mouse model of type I diabetes is useful and technically feasible for the study of the pathophysiologic mechanisms involved in diabetic erectile dysfunction.

Introduction With the advent of genetically engineered mice, it seems important to develop a mouse model of cavernous nerve injury (CNI). Aim To establish a mouse model of CNI induced either by nerve crushing or by neurectomy and to evaluate time-dependent derangements in penile hemodynamics in vivo and subsequent histologic alterations in the cavernous tissue. Methods Twelve-week-old C57BL/6J mice were divided into 4 groups (N=36 per group): control, sham operation, bilateral cavernous nerve crush, and bilateral cavernous neurectomy group. Main Outcome Measures Three days and 1, 2, 4, 8, and 12 weeks after CNI, erectile function was measured by electrical stimulation of the cavernous nerve. The penis was then harvested and TUNEL was performed. Immunohistochemical analysis was performed assaying for caspase-3, transforming growth factor-β1 (TGF-β1), phospho-Smad2, PECAM-1, factor VIII, and smooth muscle α-actin. The numbers of apoptotic cells and phospho-Smad2-immunopositive cells in endothelial cells or smooth muscle cells were counted. Results Erectile function was significantly less in the cavernous nerve crushing and neurectomy groups than in the control or sham group. This difference was observed at the earliest time point assayed (day 3) and persisted up to 4 weeks after nerve crushing and to 12 weeks after neurectomy. The apoptotic index peaked at 1 or 2 weeks after CNI and decreased thereafter. Cavernous TGF-β1 and phospho-Smad expression was also increased after CNI. The numbers of apoptotic cells and phospho-Smad2-immunopositive cells in cavernous endothelial cells and smooth muscle cells were significantly greater in the cavernous nerve crush and cavernous neurectomy groups than in the control or sham group. Conclusion The mouse is a useful model for studying pathophysiologic mechanisms involved in erectile dysfunction after CNI. Early intervention to prevent apoptosis in smooth muscle cells and endothelial cells or to inhibit cavernous tissue fibrosis is required to restore erectile function.

OBJECTIVEPatients with diabetic erectile dysfunction often have severe endothelial dysfunction and respond poorly to oral phosphodiesterase-5 inhibitors. We examined the effectiveness of the potent angiopoietin-1 (Ang1) variant, cartilage oligomeric matrix protein (COMP)-Ang1, in promoting cavernous endothelial regeneration and restoring erectile function in diabetic animals.RESEARCH DESIGN AND METHODSFour groups of mice were used: controls; streptozotocin (STZ)-induced diabetic mice; STZ-induced diabetic mice treated with repeated intracavernous injections of PBS; and STZ-induced diabetic mice treated with COMP-Ang1 protein (days −3 and 0). Two and 4 weeks after treatment, we measured erectile function by electrical stimulation of the cavernous nerve. The penis was harvested for histologic examinations, Western blot analysis, and cGMP quantification. We also performed a vascular permeability test.RESULTSLocal delivery of the COMP-Ang1 protein significantly increased cavernous endothelial proliferation, endothelial nitric oxide (NO) synthase (NOS) phosphorylation, and cGMP expression compared with that in the untreated or PBS-treated STZ-induced diabetic group. The changes in the group that received COMP-Ang1 restored erectile function up to 4 weeks after treatment. Endothelial protective effects, such as marked decreases in the expression of p47phox and inducible NOS, in the generation of superoxide anion and nitrotyrosine, and in the number of apoptotic cells in the corpus cavernosum tissue, were noted in COMP-Ang1–treated STZ-induced diabetic mice. An intracavernous injection of COMP-Ang1 completely restored endothelial cell-cell junction proteins and decreased cavernous endothelial permeability. COMP-Ang1–induced promotion of cavernous angiogenesis and erectile function was abolished by the NOS inhibitor, N-nitro-L-arginine methyl ester, but not by the NADPH oxidase inhibitor, apocynin.CONCLUSIONSThese findings support the concept of cavernous endothelial regeneration by use of the recombinant Ang1 protein as a curative therapy for diabetic erectile dysfunction.

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