In epidemiology, the basic reproduction number (R0) is a term that describes the expected number of infections generated by 1 case in a susceptible population. At the beginning of the coronavirus disease 2019 (COVID-19) pandemic, R0 was frequently referenced by the public health community and the wider public. However, this metric is often misused or misinterpreted. Moreover, the complexity of the process of estimating R0 has caused difficulties for a substantial number of researchers. In this article, in order to increase the accessibility of this concept, we address several misconceptions related to the threshold characteristics of R0 and the effective reproduction number (Rt). Moreover, the appropriate interpretation of the metrics is discussed. R0 should be considered as a population-averaged value that pools the contact structure according to a stochastic transmission process. Furthermore, it is necessary to understand the unavoidable time lag for Rt due to the incubation period of the disease.
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Objectives The outbreak of coronavirus disease 2019 (COVID-19) is one of the main public health challenges currently facing the world. Because of its high transmissibility, COVID-19 has already caused extensive morbidity and mortality in many countries throughout the world. An accurate estimation of the basic reproduction number (R0) of COVID-19 would be beneficial for prevention programs. In light of discrepancies in original research on this issue, this systematic review and meta-analysis aimed to estimate the pooled R0 for COVID-19 in the current outbreak.
Methods International databases (including Google Scholar, Science Direct, PubMed, and Scopus) were searched to identify studies conducted regarding the R0 of COVID-19. Articles were searched using the following keywords: “COVID-19” and “basic reproduction number” or “R0.” The heterogeneity among studies was assessed using the I2 index, the Cochran Q test, and T2. A random-effects model was used to estimate R0 in this study.
Results The mean reported R0 in the identified articles was 3.38±1.40, with a range of 1.90 to 6.49. According to the results of the random-effects model, the pooled R0 for COVID-19 was estimated as 3.32 (95% confidence interval, 2.81 to 3.82). According to the results of the meta-regression analysis, the type of model used to estimate R0 did not have a significant effect on heterogeneity among studies (p=0.81).
Conclusions Considering the estimated R0 for COVID-19, reducing the number of contacts within the population is a necessary step to control the epidemic. The estimated overall R0 was higher than the World Health Organization estimate.
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Ho Kyung Sung, Seung Hyun Ma, Ji-Yeob Choi, Yunji Hwang, Choonghyun Ahn, Byoung-Gie Kim, Yong-Man Kim, Jae Weon Kim, Sokbom Kang, Jaehoon Kim, Tae Jin Kim, Keun-Young Yoo, Daehee Kang, Suekyung Park
J Prev Med Public Health. 2016;49(6):349-366. Published online September 8, 2016
Objectives We conducted a systematic review and meta-analysis to summarize current evidence regarding the association of parity and duration of breastfeeding with the risk of epithelial ovarian cancer (EOC).
Methods A systematic search of relevant studies published by December 31, 2015 was performed in PubMed and EMBASE. A random-effect model was used to obtain the summary relative risks (RRs) and 95% confidence intervals (CIs).
Results Thirty-two studies had parity categories of 1, 2, and ≥3. The summary RRs for EOC were 0.72 (95% CI, 0.65 to 0.79), 0.57 (95% CI, 0.49 to 0.65), and 0.46 (95% CI, 0.41 to 0.52), respectively. Small to moderate heterogeneity was observed for one birth (p<0.01; Q=59.46; I2=47.9%). Fifteen studies had breastfeeding categories of <6 months, 6-12 months, and >13 months. The summary RRs were 0.79 (95% CI, 0.72 to 0.87), 0.72 (95% CI, 0.64 to 0.81), and 0.67 (95% CI, 0.56 to 0.79), respectively. Only small heterogeneity was observed for <6 months of breastfeeding (p=0.17; Q=18.79, I2=25.5%). Compared to nulliparous women with no history of breastfeeding, the joint effects of two births and <6 months of breastfeeding resulted in a 0.5-fold reduced risk for EOC.
Conclusions The first birth and breastfeeding for <6 months were associated with significant reductions in EOC risk.
Summary
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OBJECTIVES Evidence for an effect of reproductive factors on colorectal carcinogenesis is not yet consistent. Little research has been conducted to investigate whether reproductive factors were associated with colorectal adenomas that are the precursors of colorectal cancer. We evaluated the relationships between reproductive factors and the degree of dysplasia of the colorectal adenoma and cancer as colorectal adenoma-carcinoma sequence. METHODS: For this study, 241 adenoma cases with histo-pathologically confirmed incident colorectal adenoma, 76 cancer cases with colorectal cancer and 1677 controls were collected from Our Lady of Mercy Hospital, The Catholic University of Korea, during 1994-1999. Before colonoscopy, information on demographic characteristics, reproductive factors, life style habits and dietary intake were obtained by interviewed questionnaire. Adjusted OR and 95% CI were estimated by using polytomous logistic regression model. Potential confounders that were selected based on the goodness of fit statistics and interaction between risk factors were considered in this adjustment. The Wald statistic was calculated to test the heterogeneity of the odds ratios for each case. RESULTS: Postmenopausal women with natural menopause were found to be positively associated with the risk of mild dysplasia adenoma (multivariate-adjusted OR : 2.59, 95% CI=1.1-6.2). Parity was found to be negatively associated with the risk of colorectal cancer (age-adjusted OR : 0.40, 95% CI=0.2-0.9), but did not significantly decrease the risk of colorectal cancer (multivariate-adjusted OR : 0.95, 95% CI=0.3-2.9). No associations were seen between age at menarche, breast feeding, induced abortion, oral contraceptive use, menopausal types, menopausal age or hormone replacement therapy (HRT) and the degree of dysplasia of the colorectal adenoma and cancer. However, none of these associations differed significantly between the degree of dysplasia of the colorectal adenoma and cancer. CONCLUSIONS: These findings suggest that postmenopausal women with natural menopause may experience increased risk of mild dysplasia adenoma among colorectal adenoma-carcinoma sequence.
Chae Kwan Lee, Seog Hyun Kim, Deog Hwan Moon, Jeong Ho Kim, Byung Chul Son, Dae Hwan Kim, Chang Hee Lee, Hwi Dong Kim, Jung Won Kim, Jong Eun Kim, Chae Un Lee
OBJECTIVE The aim of this study was to investigate the effects of bisphenol A (BPA), an estrogen-like environmental endocrine disrupter, on the placental function and reproduction in rats. The mRNA levels of the placental prolactin-growth hormone (PRL-GH) gene family, placental trophoblast cell frequency and reproductive data were analyzed. METHODS: The pregnancies of F344 Fisher rats (160 g +/- 20 g) were detected by the presence of the copulatory plug or sperm in the vaginal smear, which marked Day 0 of pregnancy. Pregnant rats were divided into three groups. The control group was intraperitoneally injected with a sesame oil vehicle. The two remaining groups were injected with 50 or 500 mg/kg B.W/day of BPA, resuspended in sesame oil, on either days 7 to 11 or 16 to 20 of pregnancy, with the rats sacrificed on either day 11 or 20, respectively. The mRNA levels of PRL-GH and Pit-1a and b isotype genes were analyzed by Northern blot hybridization and reverse transcription-polymerase chain reaction. The hormone concentrations were analyzed by radioimmunoassay, and the frequency of the placental trophoblast cells observed by a histochemical study. Reproductive data, such as the placental weight and litter size, were surveyed on day 20. The fetal weight was surveyed for 4 weeks after birth. A statistical analysis was carried out using the SAS program (version 8.1). RESULTS: The mRNA levels of the PRL-GH gene family, such as placental lactogen I, Iv and II, prolactin like protein A, C and Cv, and decidual prolactin-related protein were significantly reduced due to BPA exposure. The mRNA levels of the Pit-1a and b isotype genes, which induce the expression of the PRL-GH gene family in the rat placenta, were also reduced due to BPA exposure. The PL-Iv and PL-II concentrations were reduced in the BPA exposed group. During the middle to last stage of pregnancy (Days 11-20), a high dose of BPA exposure reduced the frequency of spongiotrophoblast cells, which are responsible for the secretion of the PRL-GH hormones. Reproductive data, such as the placental and fetal weights and the litter size, were reduced, but that of the pregnancy period was extended in the BPA exposed compared to the control group. CONCLUSIONS: BPA disrupts the placental functions in rats, which leads to reproductive disorders.
OBJECTIONS: This study aimed to investigate the toxic effects of chromium (VI) on the placental function and reproduction in rats. For the study, the placental prolactin-growth hormone (PRL-GH) gene expression, placental trophoblast cell differentiation and reproductive data were analyzed. METHODS: The pregnancies of F344 Fisher rats were checked by the presence of a copulatory plug or sperm in the vaginal smear, which was defined as day 0 of the pregnancy. Pregnant rats were divided into the three groups. The control group was given tap water (chromium level < 0.001 ppm) and the remaining groups were given 250 or 750 ppm of chromium (VI) [as potassium dichromate], from day 7 to 19 of the pregnancy. Rats were sacrificed at days 11 and 20 of pregnancy. The mRNA levels of PRL-GH and Pit-1a and b isotype genes were analyzed by Northern blot hybridization and reverse transcriptionpolymerase chain reaction (RT-PCR). The hormonal concentration was analyzed by radioimmunoassay, and the differentiation of placental trophoblast cells were observed by histochemical studies. Reproductive data, such as placental and fetal weights, pregnancy period, and litter size, were surveyed at day 20 of pregnancy and after birth. A statistical analysis was carried out using the SAS program (version 8.1). RESULTS: The mRNA levels of the prolactin-growth hormone (PRL-GH) family of genes were dose dependently reduced by chromium exposure. The mRNA levels of Pit-1a and b isotype genes that induce the expression of the PRL-GH family of genes were also reduced by chromium exposure. The PRL-GH hormonal concentration in the rat placenta, fetus and maternal blood were decreased by chromium exposure. In the middle stage of pregnancy (day 11), a high dose of chromium suppressed the differentiation of spongiotrophoblast cells that secret the PRLGH hormones. In the last stage of pregnancy (day 20), a high dose of chromium induced apoptosis of placental cells. Reproductive data, such as placental and fetal weights, litter size, were reduced, but the pregnancy period was extended in the group exposed to chromium compared with the controls. CONCLUSION: Chromium (VI) disrupts the ordered functions of the placenta, which leads to reproductive disorders in rats.