No abstract

Accurate and comprehensive testing is crucial for practitioners to portray the pandemic. Without testing there is no data; yet, the exact number of infected people cannot be determined due to the lack of comprehensive testing. The number of seropositive for SARS‐CoV‐2 infection is obviously relative to the extent of testing. However, the true number of infections might be still far higher than the reported values. To compare the countries based on the number of seropositive for SARS‐CoV‐2 infection is misleading, as there may not be enough tests being carried out to properly monitor the outbreak. In this paper, we closely look through the COVID‐19 testing results. Herein, we try to draw conclusions based on the reported data: first, the presence of a possible relationship between COVID‐19 transition and patients' age will be assessed. Then, the COVID‐19 case fatality rate (CFR) is compared with the age‐demographic data for different countries. Based on the results, a method for estimating a lower bound (minimum) for the number of actual positive cases will be developed and validated. Results of this study have shown that CFR is a metric reflecting the spread of the virus, but is a factor of the extent of testing and does not necessarily show the real size of the outbreak. Moreover, no large difference in susceptibility by age has been found. The results suggest the similarity between the age distribution of COVID‐19 and the population age‐demographic is improving over the course of the pandemic. In addition, countries with lower CFRs have a more similar COVID‐19 age distribution, which is a result of more comprehensive testing. Finally, a method for estimation of the real number of infected people based on the age distributions, reported CFRs, and the extent of testing will be developed and validated.

No abstract

Seizure occurs as a result of uncontrolled electrical disturbances within the brain. Various biomolecules such as N‐methyl‐D‐aspartate (NMDA), nitric oxide (NO), and cAMP response element‐binding protein (CREB) have been implicated in the pathophysiology of seizure. Sumatriptan is a specific 5‐Hydroxytryptamine 1B/1D receptor agonist and has neuroprotective effects in various neuropsychiatric disorders. In the current study, we tried to investigate the possible interaction of sumatriptan with NMDA/NO and CREB signaling pathway in PTZ induced seizure. For this purpose, various agonist and antagonist of NMDA such as MK‐801 and Ketamine, NO precursor L‐ARG, and NOS inhibitors L‐NAME and 7‐NI were co‐administered with sumatriptan in PTZ induced seizure model. The level of nitrite in mice hippocampus was determined by Griess reaction. The gene expression of NR1, NR2A, NR2B, and CREB were quantified by quantitative real time‐polymerase chain reaction (qRT‐PCR). Furthermore, the involved neuronal nitric oxide synthase (nNOS) protein expression was examined via western blot analysis. Effective dose of sumatriptan (1.2 mg/kg) alone and subeffective dose of sumatriptan (0.3 mg/kg) in combination with NMDA and/or NO antagonist showed significant (P < 0.001) anticonvulsant activity in mice. Furthermore, sumatriptan significantly inhibited the PTZ‐induced mRNA expression of NR2A (P < 0.0001), NR2B (P < 0.05), and CREB (P < 0.01). Also, the expression of nNOS protein in PTZ treated group was reversed by sumatriptan (P < 0.01). Hence, current findings suggest that the anticonvulsant effect of sumatriptan was due to down regulation of NMDA/NO and CREB signaling pathway.