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OBJECTIVES: Coronavirus disease 2019 (COVID-19) represents a major pandemic threat that has spread to more than 212 countries with more than 432,902 recorded deaths and 7,898,442 confirmed cases worldwide so far (on June 14, 2020). It is crucial to investigate the spatial drivers to prevent and control the epidemic of COVID-19. METHODS: This is the first comprehensive study of COVID-19 in Iran; and it carries out spatial modeling, risk mapping, change detection, and outbreak trend analysis of the disease spread. Four main steps were taken: comparison of Iranian coronavirus data with the global trends, prediction of mortality trends using regression modeling, spatial modeling, risk mapping, and change detection using the random forest (RF) machine learning technique (MLT), and validation of the modeled risk map. RESULTS: The results show that from February 19 to June 14, 2020, the average growth rates (GR) of COVID-19 deaths and the total number of COVID-19 cases in Iran were 1.08 and 1.10, respectively. Based on the World Health Organisation (WHO) data, Iran's fatality rate (deaths/0.1M pop) is 10.53. Other countries' fatality rates were, for comparison, Belgium - 83.32, UK - 61.39, Spain - 58.04, Italy - 56.73, Sweden - 48.28, France - 45.04, USA - 35.52, Canada - 21.49, Brazil - 20.10, Peru - 19.70, Chile - 16.20, Mexico- 12.80, and Germany - 10.58. The fatality rate for China is 0.32 (deaths/0.1M pop). Over time, the heatmap of the infected areas identified two critical time intervals for the COVID-19 outbreak in Iran. The provinces were classified in terms of disease and death rates into a large primary group and three provinces that had critical outbreaks were separate from the others. The heatmap of countries of the world shows that China and Italy were distinguished from other countries in terms of nine viral infection-related parameters. The regression models for death cases showed an increasing trend but with some evidence of turning. A polynomial relationship was identified between the coronavirus infection rate and the province population density. Also, a third-degree polynomial regression model for deaths showed an increasing trend recently, indicating that subsequent measures taken to cope with the outbreak have been insufficient and ineffective. The general trend of deaths in Iran is similar to the world's, but Iran's shows lower volatility. Change detection of COVID-19 risk maps with a random forest model for the period from March 11 to March 18 showed an increasing trend of COVID-19 in Iran's provinces. It is worth noting that using the LASSO MLT to evaluate variables' importance, indicated that the most important variables were the distance from bus stations, bakeries, hospitals, mosques, ATMs (automated teller machines), banks, and the minimum temperature of the coldest month. CONCLUSIONS: We believe that this study's risk maps are the primary, fundamental step to take for managing and controlling COVID-19 in Iran and its provinces.

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INTRODUCTION: Estrogen and prolactin affect vitamin D metabolism. In conditions such as pregnancy and lactation, their interaction in regulating vitamin D metabolism and circulating FGF23 is not clearly defined. The aim of this study is to investigate this interaction in female rats. METHOD: This study was performed on 50 female adult rats, which were divided into five groups of Sham, ovariectomized rats (O), and three groups of ovariectomized rats were indicated with prolactin alone (OP), estradiol alone (OE), and a combination of estradiol and prolactin (OEP). Serum levels of 25(OH)D, 1,25(OH)2D3, FGF23, PTH, vitamin D-binding protein, calcium, and phosphorous were evaluated. RESULTS: Serum 1,25(OH)2D3 and PTH in OE were higher than the O group (P < 0.001 and P = 0.003, respectively). Serum FGF23 in the OE group was lower than the O group (P = 0.016). Serum 1,25(OH)2D3 increased in OP compared to the O group (P < 0.001) and OE group (P < 0.001). Serum FGF23 in OP was lower than the O group (P = 0.04). Furthermore, combining estradiol and prolactin showed no extra effect on increasing serum 1,25(OH)2D3. Serum 1,25(OH)2D3 was positively correlated with serum prolactin levels (r = 0.318, P = 0.017) in all five groups. CONCLUSION: It is suggested that estradiol could increase 1,25(OH)2D3 by elevating PTH and decreasing serum FGF23; however, prolactin was able to increase 1,25(OH)2D3 by lowering serum FGF23. Moreover, prolactin was shown to be more potent in augmenting serum 1,25(OH)2D3 than estrogen itself, which is important in maternal and fetal calcium supply during late pregnancy and lactation.

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Estrogen deficiency induced by hyperprolactinemia can reduce bone mineral density. Hyperprolactinemia through other mechanisms other than estrogen deficiency, with direct effect on the bone might cause bone loss in women. The present study evaluated the effect of prolactin itself and in combination with estrogen on bone mineral density of female rats. This study was performed on 50 adult female rats divided into five groups; included (a) Sham, (b) Ovariectomized rats; and (c-e) included ovariectomized rats were given prolactin alone, prolactin + estradiol and estradiol, respectively. Bone mineral density (BMD) and vitamin D metabolism parameters were checked in all groups before and after the study. There was no significant difference in baseline values of these parameters. Estradiol could increase 1,25(OH)2D3 and PTH levels and decrease serum ALP level. In addition, Prolactin could increase serum 1,25(OH)2D3 and ALP levels and decrease tibia BMD significantly without any change in PTH level. Combination of estradiol and prolactin could increase serum 1,25(OH)2D3 and PTH and tibia BMD compared with OVX group. Combination of estradiol and prolactin could significantly increase tibia BMD, in ovariectomized rats. We hypothesized that this combination could improve bone loss secondary to hyperprolactinemia by elevated PTH.

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Testosterone is an essential hormone to maintain bone integrity; however, the effect of aromatase enzyme in androgen-induced bone maintenance remains somewhat unclear. The present study evaluated the effect of testosterone itself and combined with letrozole, an aromatase inhibitor, on bone mineral density of male rats. Total of 48 male rats were divided into 4 equal groups (n = 12/group); sham group, O: orchiectomy, O + T: orchiectomized rats treated with testosterone, O + T + L: orchiectomized rats treated with combination of testosterone and letrozole. Bone density (BMD), bone markers, and vitamin D metabolism parameters were checked in all groups before and after the study. There was no significant difference in baseline values of these parameters, but at the end of the study there was a significant decrease in delta BMD at both lumbar and femor in orchiectomized rats in comparison with the sham group (p < 0.001, p < 0.001, respectively). Both testosterone and its combination with letrozole increased lumbar and femoral BMD of orchiectomized rats, with a higher increase in lumbar BMD in O + T group. CTX were higher in O group rats. The present study showed a major role for testosterone on BMD maintenance in male rats. However, testosterone has a potent effect on lumbar BMD, by the aromatization to estradiol.

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BACKGROUND: The etiology of the Behçet disease (BD) has remained obscured. There have been studies to show the association of BD to infections like herpes simplex, hepatitis, and parvovirus B19 however, the findings are rather controversial. MATERIALS AND METHODS: We selected 55 patients with the best matched symptoms of BD and measured the loads of B19 DNA in their plasma by quantitative real time PCR and verified their seropositivity by ELISA. All findings were compared to the results from 42 healthy persons. RESULTS: Patients showed a wide spectrum of BD symptoms. Serologic studies showed high prevalence of B19 IgG among the tested patients which was not statistically different with the healthy population (72.7% vs. 85.7%, respectively). Similarly, the prevalence of B19 IgM between patients and controls was not different (18% vs. 11.9%, respectively). No correlation was found between the presence of anti-B19 antibodies and the clinical observations. Only one person from the patient and control groups had detectable levels of B19 DNA without any difference or correlation with the disease symptoms. CONCLUSION: Our data could not establish an association between B19 parvovirus infection and Behçet disease, although there have been reports of such correlation. Nevertheless, there might be indirect relation in genetically susceptible individuals after viral infections. More studies on designed animal models and surveys on patients should be done to resolve this controversy.