Background: HPV has been found repeatedly in esophageal carcinoma tissues. However, reported detection rates of HPV DNA in these tumors have varied markedly. Differences in detection methods, sample types, and geographic regions of sample origin have been suggested as potential causes of this discrepancy.Methods: HPV L1 DNA and HPV genotypes were evaluated in 435 esophageal carcinoma specimens collected from four geographic regions with different ethnicities including Anyang in north China, Shantou in south China, Xinjiang in west China, and the United States. The HPV L1 fragment was detected using SPF1/GP6+ primers. HPV genotyping was performed using genotype specific PCR.Results: Two hundred and forty four of 435 samples (56.1%) tested positive for HPV L1. Significant differences in detection rate were observed neither among the three areas of China nor between China and the US. HPV6, 16, 18, 26, 45, 56, 57, and 58 were identified in L1 positive samples. HPV16 and 57 were the most common types in all regions, followed by HPV26 and HPV18.Conclusions: HPV infection is common in esophageal carcinoma independent of region and ethnic group of origin. Findings in this study raise the possibility that HPV is involved in esophageal carcinogenesis. Further investigation with a larger sample size over broader geographic areas may be warranted.

Background: Thrombospondin1 (THBS1), cystene-rich protein 61 (Cyr61) and connective tissue growth factor (CTGF) are all involved in the transforming growth factor-beta (TGF-β) signal pathway, which plays an important role in the tumorigenesis. The purpose of this study is to explore the expression and prognostic significance of these proteins in esophageal squamous cell carcinoma (ESCC).Methods: We used immunohistochemistry and western blotting to examine the expression status of THBS1, Cyr61 and CTGF in ESCC. Correlations of THBS1, Cyr61 and CTGF over-expressions with various clinicopathologic factors were also determined by using the Chi-square test or Fisher's exact probability test. Survival analysis was assessed by the Kaplan-Meier analysis and the log-rank test. Relative risk was evaluated by the multivariate Cox proportional hazards model.Results: THBS1, Cyr61 and CTGF were all over-expressed in ESCC. THBS1 over-expression was significantly associated with TNM stage (P= 0.029) and regional lymph node involvement (P= 0.026). Kaplan-Meier survival analysis showed that over-expression of THBS1, Cyr61 or CTGF was related to poor survival of ESCC patients (P= 0.042,P= 0.020,P= 0.018, respectively). Multivariate Cox analysis demonstrated that Cyr61 and CTGF were independent factors in prognosis of ESCC.Conclusion: Cyr61, CTGF and THBS1 were all over-expressed in ESCC and might be new molecular markers to predict the prognosis of ESCC patients.

Early life represents a critical period for the development and growth of the lungs. Adverse exposures in this stage may drive the development of chronic obstructive pulmonary disease (COPD). Thus, we quantitatively evaluated the impact of different early life exposures on COPD in adulthood. The PubMed, Embase and Cochrane Library electronic databases were searched for articles published from January 2001 to October 2020. A total of 30 studies (795,935 participants) met the criteria and were included in the review. We found a significant association of COPD with childhood serious respiratory infections, pneumonia or bronchitis (pooled adjusted OR [aOR], 2.23 [95% CI, 1.63–3.07]). The probability of COPD was increased 3.45‐fold for children with than without asthma (pooled aOR, 3.45 [95% CI, 2.37–5.02]). In addition, the probability of COPD was associated with maternal smoking (pooled aOR, 1.42 [95% CI, 1.17–1.72]), any child maltreatment (pooled aOR, 1.30 [95% CI, 1.18–1.42]) and low birth weight (pooled aOR, 1.58 [95% CI, 1.08–2.32]) but not childhood environmental tobacco smoke exposure (pooled aOR, 1.15 [0.83–1.61]) or premature birth (pooled aOR, 1.17 [95% CI, 0.87–1.58]). Furthermore, subgroup analyses revealed that probability was increased for only women with childhood physical abuse, sexual abuse and exposure to intimate partner violence. Factors resulting in COPD in adults could trace back to early life. Childhood respiratory disease, maltreatment, maternal smoking and low birth weight increase the risk of COPD. Promising advances in prevention strategies for early life exposures could markedly decrease the risk of COPD.

Background: Human papillomavirus (HPV) infection is a major risk factor for the development of nearly all cases of cervical cancer worldwide. The presence of HPV DNA in cases of esophageal squamous-cell carcinoma (ESCC) has been reported repeatedly from Shantou, China, and other regions with a high incidence of esophageal carcinoma (EC). However, unlike in cervical squamous-cell carcinoma (CSCC), in ESCC, the characteristics of HPV are unclear. Thus, the role of high-risk HPV types in the carcinogenesis of ESCC remains uncertain. Methods: Seventy cases of ESCC with 60 controls and 39 cases of CSCC with 54 controls collected from patients in Shantou region in China were compared for the distributions of HPV-16, -18 and -58; viral load; and viral integration using real-time PCR assay and HPV-16 expression using immunostaining. Results: The detection rates and viral loads of HR-HPV infection were significantly lower in ESCC than in CSCC (50.0% vs. 79.48%, P = 0.005; 2.55 ± 3.19 vs. 361.29 ± 441.75, P = 0.002, respectively). The combined integration level of HPV-16, -18 and -58 was slightly lower in ESCC than in CSCC (P = 0.022). HPV-16 expression was detected in 59.26% of ESCC tissue and significantly associated with tumour grade (P = 0.027). Conclusions: High levels of HR-HPV expression and integration may be an indicator of the risk of ESCC, at least for patients in the Shantou region of China. However, a relatively low HPV copy number and infection rate in ESCC is unlikely to play an essential a role in the carcinogenesis of ESCC as in cervical cancer. Factors other than HR-HPV infection may contribute to the carcinogenesis of ESCC.