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Background The association between passive smoking (PS) and cardiovascular disease (CVD) has not yet been fully clarified. Objective This meta‐analysis was performed to evaluate the association between PS and the incidence of CVDs and mortality due to CVD. Methods PubMed/Medicine, Science Direct, Scopus, Web of Knowledge, and ProQuest were searched to identify observational studies that met the inclusion criteria without time, language, age, gender, ethnicity, and design restrictions until July 30, 2018. In case–control studies, relative risk (RR) with 95% confidence interval (CI) was calculated for the relationship between PS and CVD incidence. Also, in cohort studies, hazard ratio (HR) with 95% CI was calculated for the relationship between PS and CVD mortality. Results Eighteen studies (10 cohort and 8 case–control studies) were included with 10,672 participants (2,542 cases and 8,130 controls) in case–control studies and 2,313,935 participants in cohort studies. This meta‐analysis in case–control studies revealed that the PS could increase the risk of CVD incidence by 28% (adjusted RR = 1.28 [95% CI 1.09, 1.50]), where the highest risk was associated with those who were exposed to second‐hand smoke at home and at work (Adjusted RR = 1.41 [95% CI 0.73, 2.70]). Also, the meta‐analysis in cohort studies indicated that PS was associated with a 12% higher increase in the risk of CVD mortality (Adjusted HR = 1.12 [95% CI 1.06, 1.20]) with the highest risk of mortality being observed for those who were exposed to second‐hand smoking at home, work, and public places (Adjusted HR = 1.26 [95% CI 1.13, 1.40]). Conclusions PS is significantly associated with an increased risk of incidence and mortality of CVD.

IMPORTANCEThe prevalence and severity of long-term health complications after exposure to sulfur mustard are unknown.OBJECTIVE To investigate the long-term health outcomes among survivors exposed to sulfur mustard during the Iran-Iraq War. DESIGN, SETTING, AND PARTICIPANTSIn this retrospective cohort study, late-onset health complications of 64 190 Iranian survivors exposed to sulfur mustard during the Iran-Iraq War from 1980 to 1988 were investigated using descriptive statistics. Data involving affected organs and symptom severity were extracted from the Veterans and Martyr Affair Foundation (VMAF) database from 1980 to 2019. Assessments were conducted across 3 groups depending on whether survivors were (1) evacuated and admitted (EA) to a hospital; (2) not evacuated or admitted (NEA) to a hospital; or (3) evacuation or admission status was not documented. EXPOSURES Analysis of chronic symptom severity following exposure to sulfur mustard. MAIN OUTCOMES AND MEASURESMild, moderate, or severe rankings of symptoms in lungs, eyes, and skin of survivors exposed to sulfur mustard using data from the VMAF database. RESULTSOf 64 190 chemical survivors registered in the VMAF database, 60 861 met the inclusion criteria. Of the included survivors, 98.0% were male, and the mean (SD) age was 23.5 (7.7) years.Most survivors (53 675 [88.2%]) had no symptoms or mild lesions, and 7186 survivors (11.8%) had moderate or severe complications. Moderate to severe lung (6540 [10.7%]), eye (335 [0.6%]), or skin (725 [1.2%]) injuries were documented in the exposed population. The proportion of moderate plus severe late complications in eyes was 3 times as high in male survivors compared with female survivors (0.6% [95% CI, 0.53%-0.65%] vs 0.2% [95% CI, 0.09%-0.73%]; P < .001), whereas dermal complications were significantly more common in female survivors (3.9% [95% CI, 2.92%-5.11%] vs 1.14% [95% CI, 1.06%-1.23%]; P < .001). Mild lung lesions were more prevalent in the NEA group than in the EA group (73.9% [95% CI, 73.4%-74.4%] vs 11.0% [95% CI, 10.6%-11.3%]; P < .001). In the NEA group, 83.2% (n = 23 866) developed lung injuries that were mostly mild or moderate, whereas 77% (n = 24 766) of the EA group did not develop lung injuries (P < .001). CONCLUSIONS AND RELEVANCEThe present study found sex differences in the frequencies of eye and skin complications following sulfur mustard exposure, and lung complications were more prevalent years after sulfur mustard exposure than soon after exposure. Mild lung lesions were observed more frequently among sulfur mustard-exposed survivors who had not been evacuated or hospitalized than among those who had been evacuated or hospitalized. These differences may be due to physiological response or dose of exposure. Close monitoring over an extended period may be required for detection of late pulmonary complications in individuals exposed to sulfur mustard.

International research collaborations improve individual, institutional and governmental capacities to respond to health crises and inequalities but may be greatly affected by political environments. Iran ranks highly in tertiary education, productivity growth, knowledge impact and successful patent applications. In many countries, economic hardship has correlated with increased international research collaborations. Some have hypothesised that financial constraint drives scholars to seek outside collaborations for cost and risk sharing, and to access funding, materials and patient populations otherwise unavailable. This paper explores the history and importance of US political sanctions on the health of Iran’s academic sector. Although Iran’s international research collaborations increased during periods of increased sanctions, the Pearson correlation coefficient between gross domestic product and international research collaborations was not significant (r=0.183, p=0.417). This indicates that other factors are at least in part responsible. Additionally, we found Iran’s quantitative (eg, publication number) and qualitative (eg, visibility indices) publishing metrics to be discordant (two-tailed Mann–Kendall trend; p<0.0002 for both). Reasons for this are multifactorial, including increased indexing of Iranian journals, willingness of lower visibility journals to handle manuscripts with Iranian authors, widespread linkage of career advancement to science visibility indices, and others. During periods of increased sanctions, Iranian scholars were increasingly denied opportunities to publish scientific findings, attend scientific meetings, access to essential medical and laboratory supplies and information resources. We conclude that academic boycotts violate researchers’ freedom and curtail progress. Free exchange of ideas irrespective of creed is needed to optimize global scientific progress.

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Recently, many of studies have illustrated that the new pandemic SARS-CoV-2 can affect Central Nervous System through olfactory bulb. In addition to investigating anosmia or hyposmia induced by this virus, the quantitative analysis was needed to clarify the taste and smell disorder of the new corona virus . The four basic taste quality with five concentrations for sweet, sour, bitter and salty were administered in to 75 subject divided in to three groups: COVID-19 patients with taste disorder, COVID-19 patients without taste disorder and control group. The results indicated the increment of sweet (2.68±0.14), sour (3.34±0.12) and bitter (3.39±0.2) thresholds in COVID-19 patients with taste disorder in comparison with patients without taste disorder that the threshold were: 2±0.16, 2.11±0.2 and 2.55±0.5 for sweet, sour and bitter respectively. On the other-hand the patients inversely showed significant decrease in salty taste threshold (0.51±0.03) compared to COVID-19 positive control groups (1.11±0.11). Additionally, despite taste disorder in almost all of patients with smell deficiency, only 30% of cases with taste disorder reported smell deficiency. It may be concluded that some of taste disorders in patients with COVID-19 disorder could be associated with taste receptors dysfunction or the spread of infection to the cranial nerves responsible for conduction of tastes sensation.

The endogenous cyclic adenosine monophosphate (AMP) antagonist, cyclic PIP, has been identified as a prostaglandylinositol cyclic phosphate. It inhibits protein kinase A 100% and activates protein serine phosphatase about sevenfold. It is biosynthesized by an enzyme of the plasma membrane when the assay mixture contains adenosine triphosphate (ATP), Mg2+, prostaglandin E and a novel inositol polyphosphate, which cannot be substituted by commercially available inositol phosphates. This novel inositol polyphosphate is a very labile compound. On anion exchange chromatography it elutes in the range of ATP, which may indicate the presence of three phosphate groups. It adsorbs on charcoal, which suggests the presence of a hydrophobic component, possibly a guanosine. Pyrophosphates obtained from inositol 1,4- and inositol 2,4-bisphosphate are accepted by cyclic PIP synthetase for the synthesis of cyclic PIP. The biosynthesis is characterized by enzyme kinetic parameters like dependence on time, enzyme and substrate concentration. The pH optimum of the enzyme is in the range 7.5-8. The enzyme functions optimally with prostaglandin E and poorly with prostaglandin A as the substrate. The presence of fluoride in the assay causes a three- to fourfold increase in cyclic PIP synthesis, which may be correlated with activation via G proteins. These data support previous reports on the chemical structure and action of cyclic PIP. With respect to the possible isomers of cyclic PIP, these indicate that it is most likely the C4-hydroxyl group of the inositol which binds the C15-hydroxyl group of prostaglandin E. A model of hormone-stimulated synthesis of cyclic PIP is proposed: phospholipase A2 and phospholipase C, activated by G proteins upon alpha-adrenergic stimulation, liberate either unsaturated fatty acids or inositol phosphates, which are transformed to prostaglandins and to novel inositol polyphosphate with an energy-rich bond. The cyclic PIP synthetase combines these two substrates to cyclic PIP.

M1 muscarinic receptor plays a fundamental role in memory and is closely associated with Alzheimer's disease (AD); it has long been assumed as a therapeutic goal. By activating of the cholinergic receptor vitamin E helps with memory retention. But effects of vitamin E on density of M1 muscarinic receptor-immunoreactive (ir) neurons remain poorly understood. The present research aimed to examine the chronic administration effect of vitamin E against scopolamine-induced memory loss and the number of M1 muscarinic receptor-ir neurons of the hippocampus in male rats. Randomly, 42 adult male Wistar rats were divided to six groups: control, Sham-saline: receiving scopolamine + saline, Sham-sesame oil: receiving scopolamine + sesame oil and three experimental groups: receiving scopolamine + vitamin E with different doses (25, 50, and 100 mg/kg/day, i.p.) for 14 days. The passive avoidance task was used for the memory test. Twenty-four hours after behavioral tests, rats' brains were taken and fixed, and after tissue processing, sections were stained using the immunohistochemical technique for M1 muscarinic receptor-ir neurons and cresyl violet for neurons. The injection of scopolamine to rats caused memory impairment and vitamin E treatment could ameliorate it. In the scopolamine-treated groups, the number of CA1 and CA3 pyramidal and dentate gyrus (DG) granular neurons was decreased significantly as compared to the control group. Vitamin E treatment significantly increased neuron numbers in the CA1 and CA3 areas of the hippocampus and DG area. Treatment with vitamin E for 14 days could compensate the loss of M1 muscarinic receptor-immunoreactive neuron numbers induced by scopolamine in the hippocampus. The most effective vitamin E dose was 50 mg/kg/day in this study. In conclusion, vitamin E can compensate the neuronal loss in the hippocampal formation and also it can raise the density of M1 receptor-ir muscarinic neurons after an injection of scopolamine.