Exposure to ambient particulate matter affects semen quality: A case study in Wenzhou, China.

BACKGROUND: Particulate matter (PM), including PM2.5 (PM ≤ 2.5 µm in aerodynamic diameter) and PM10 (PM ≤ 10 µm in aerodynamic diameter), is a component of air pollutants, which is linked to semen quality. However, the available evidence of association needs to be strengthened, and some studies have conflicting results. OBJECTIVES: To evaluate the potential impacts of PM on semen quality during the full (0-90 days before semen examination) and three key sperm development windows (0-9, 10-14, and 70-90 days before semen examination). METHODS: We included 1494 infertile men in the main urban area in Wenzhou, China, who had undergone semen examinations for fertility between 2014 and 2019. The impacts were assessed by multivariable linear regression models. RESULTS: Overall, during the full sperm development window, PM2.5 and PM10 exposures were associated with declined progressive sperm motility (%) (ß: -0.6; 95% confidence intervals (CIs): -1.07, -0.13 and -0.46; -0.59, -0.33) and total sperm motility (%) (-1.95; -2.67, -1.23 and -1.32; -1.82, -0.82), and associated with increased sperm concentration (106 /ml) (0.02; 0.006, 0.023 and 0.007; 0.001, 0.013) and total sperm number (106 ) (0.02; 0.01, 0.03 and 0.011; 0.004, 0.017). Furthermore, only PM2.5 exposure during the 10-14 days window was significantly associated with declined progressive motility (%) (-0.207; -0.395, -0.023). CONCLUSIONS: During the full sperm development window, PM exposure has an adverse impact on sperm motility and positive impacts on sperm concentration and total sperm number. The adverse impact was more severe in the 10-14 days window.

The Association between Spatial-Temporal Distribution of Prostate Cancer and Environmental Factors in Mainland China.

BACKGROUND: In China, the incidence and mortality of prostate cancer are increasing. In this study, we analyzed the spatial-temporal distribution characteristics of prostate cancer incidence and mortality in China and explored the potential associations of socioeconomic, ecological, and meteorologic conditions. METHODS: Spatial-temporal scan statistics were used to analyze the spatial-temporal patterns of prostate cancer in China from 2012 to 2016. Spatial regression models and the Geodetector method were used to explore the potential associations of anthropogenic and natural factors with prostate cancer. RESULTS: The incidence and mortality of prostate cancer in China from 2012 to 2016 rapidly increased. The high incidence and mortality clusters were concentrated in the economically developed Yangtze River Delta region along the southeast coast. Among the 14 selected environmental factors, gross domestic product (GDP) per capita, population density, comprehensive index of environmental pollution discharge, accessibility of health care resources, urbanization rate, and nitrogen dioxide (NO2) had significant positive correlations with prostate cancer incidence and mortality. GDP per capita, urbanization rate, and population density had high explanatory power. CONCLUSIONS: The high-concentration areas for prostate cancer are located in more economically developed cities. The index of environmental pollution discharge, NO2, and prostate cancer incidence and mortality were positively correlated. The government should advocate increasing the use of clean energy while strengthening the regulation of industrial production to reduce pollutant emissions. IMPACT: To inform the development of prevention and control strategies for prostate cancer in China.

[Effects of Magnolol combined with Gefitinib on A549 non-small cell lung cancer cells].

Objective: To investigate the synergistic effects of magnolol and gefitinib on non-small cell lung cancer A549 cells. Methods: A549 cells were treated with Magnolol (6.25～500 µmol/L) or gefitinib (6.25～500 µmol/L) for 24 h, respectively, and the cell viability was detected by cell counting Kit-8 (CCK-8) experiment (n=3). Magnolol 100 µmol/L and gefitinib 5 µmol/L were selected in the following experiments (n=3, 24 h). Control group, magnolol group, gefitinib group and magnolol+gefitinib group were set up for factorial analysis. Colony formation experiment was applied to detect the cell proliferation. Western blot was used to detect protein expressions. Flow cytometry was applied to test cell apoptosis and sorting CD44+ and CD133+ cells. Results: Compared with the control group, the colony formation rate of Magnolol or Gefitinib groups was decreased significantly (P＜0.05); the apoptosis rate was increased significantly (P＜0.05); the number of CD44+ and CD133+ cells was reduced significantly (P＜0.05); the expressions of Ki67, PCNA, and stem cell marker proteins SOX2 and OCT4 were down-regulated (P＜0.05); and the ratio of Bax/Bcl-2 was increased significantly (P＜0.05). Compared with the Magnolol group or Gefitinib group, the Magnolol+Gefitinib group further promoted the above changes (P＜0.05), and the apoptosis rate, the ratio of Bax/Bcl-2, SOX2 and OCT4 all showed interactions between magnolol and gefitinib (P＜0.05). Conclusion: Magnolol and gefitinib promote the apoptosis of A549 cells and inhibit its stem cell-like properties, and the effect of the two combined is better than separated administration. Magnolol and gefitinib have interactive effects on A549 cells.

Spatial-temporal characteristics of AIDS incidences in Mainland China.

OBJECT: Revealed the spatial-temporal patterns of acquired immune deficiency syndrome (AIDS) incidences in Mainland China. METHODS: Empirical orthogonal function (EOF) technique was applied to analyze the major spatial distribution modes and the temporal changes of AIDS incidences in Mainland China during 2002-2017. RESULTS: The annual average AIDS incidences increased from 0.06 per 100 000 in 2002 to 4.15 per 100 000 in 2017, with an annual average increase of 0.31 per 100 000. The southwest regions were high-incidence areas, as well as Xinjiang province in the northwest. There were two typical spatial modes. EOF 1 represented an isodirectional spatial pattern that the incidences were relatively high in general, and the fluctuation ranges were relatively high in the southwest and northeast. EOF 2 represented a reverse spatial pattern that the incidences were relatively high (or low) in Guangxi, Yunnan, Xinjiang, Shanghai, and Henan, yet were relatively low (or high) in the remaining regions. CONCLUSION: The AIDS incidences in Mainland China were relatively low during 2002-2010, yet were kept in a relatively high level since 2012. The prevention and control of AIDS need further development, especially in the southwest regions.

LINC00467 promotes cell proliferation and stemness in lung adenocarcinoma by sponging miR-4779 and miR-7978.

Lung adenocarcinoma (LAD), as one of the most common types of lung tumors, is lethal and malignant. Long noncoding RNAs (lncRNAs) play important roles in various cancers according to many previous studies. LINC00467 was proposed to be a tumor promoter. Despite the validated promotive effect of LINC00467 on neuroblastoma progression, its regulatory mechanism in LAD remains unclear. In this study, LINC00467 expressed higher in LAD tissues and cell lines, and increased LINC00467 indicated a poor prognosis. Knockdown of LINC00467 inhibited cell proliferation, the expressions of tumor stem cell-related genes, and cell spheroid formation ability, while it promoted cell apoptosis. miR-4779 and miR-7978 were reported to play antitumor roles in several cancers before. LINC00467 could combine with miR-4779 and miR-7978, and negatively regulated miR-4779 and miR-7978. miR-4779 and miR-7978 inhibitor could partly rescue the LINC00467 knockdown-induced influence on cell proliferation, apoptosis, and stemness. In a word, this study innovatively investigated the mechanism of LINC00467 in LAD and verified LINC00467 exerted its carcinogenesis function by sponging miR-4779 and miR-7978, which may become a catalyst for generating new therapeutic targets for LAD treatment.

CCR7 preservation via histone deacetylase inhibition promotes epithelial-mesenchymal transition of hepatocellular carcinoma cells.

The effects of Histone deacetylase (HDAC) inhibition on epithelial-mesenchymal transition (EMT) differs in various types of cancers. However, its function in hepatocellular carcinoma (HCC) is not well-explored. In this study, we investigated the effect of HDAC inhibition on EMT in HCC cells by using trichostatin A (TSA) and valproic acid (VPA). The results showed that TSA/VPA significantly induced EMT phenotype, as demonstrated by the decreased level of E-cadherin, increased level of N-cadherin, vimentin, Twist and snail, and enhanced capacity of cell migration and invasion. In addition, CCR7 was speculated and confirmed as a function target of HDAC inhibition. CCR7 promotes the progression of HCC and is associated with poor survival. Knockdown of CCR7 significantly attenuated the effect of TSA on EMT. Moreover, our results demonstrated that HDAC inhibition up-regulates CCR7 via reversing the promoter hypoacetylation and increasing CCR7 transcription. Taken together, our study has identified the function of HDAC in EMT of HCC and suggested a novel mechanism through which TSA/VPA exerts its carcinogenic roles in HCC. HDAC inhibitors require careful caution before their application as new anticancer drugs.

Evaluation of ascitic soluble human leukocyte antigen-G for distinguishing malignant ascites from benign ascites.

The overexpression of soluble human leukocyte antigen-G is associated with malignant tumours. The purpose of our study was to detect soluble human leukocyte antigen-G concentrations in ascites and to evaluate the value of ascitic soluble human leukocyte antigen-G for the diagnosis of malignant ascites. Enzyme-linked immunosorbent assay was used to detect soluble human leukocyte antigen-G levels in 64 patients with malignant ascites and 30 patients with benign ascites. Receiver operating characteristic curves were used to evaluate the diagnostic efficacy of ascitic soluble human leukocyte antigen-G for the detection of malignant ascites. Ascitic soluble human leukocyte antigen-G levels were significantly higher in the malignant ascites group than in the benign ascites group (20.718 ± 3.215 versus 12.467 ± 3.678 µg/L, t = 7.425, p < 0.001). The area under the receiver operating characteristic curve for ascitic soluble human leukocyte antigen-G was 0.957 (95% confidence interval, 0.872-0.992). At a cut-off value of 19.60 µg/L, the sensitivity and specificity of ascitic soluble human leukocyte antigen-G were 87.5% (95% confidence interval, 71.0%-96.5%) and 100% (95% confidence interval, 88.4%-100%), respectively. With respect to area under the receiver operating characteristic curve, sensitivity and specificity, ascitic carcinoembryonic antigen (0.810, 68.75% and 83.33%, respectively) and carbohydrate antigen 19-9 (0.710, 65.63% and 70%, respectively) significantly differed (all p < 0.05). In malignant ascites that were cytology-negative and biopsy-positive, the rate of positivity for ascitic soluble human leukocyte antigen-G was 75%, which was higher than the corresponding rates for ascitic carcinoembryonic antigen (31.25%) and carbohydrate antigen 19-9 (6.25%; both p < 0.05). In conclusion, The detection of ascitic soluble human leukocyte antigen-G exhibited good performance for diagnosing malignant ascites, and particularly those that were cytology-negative and biopsy-positive.

Let-7a inhibits tumor cell growth and metastasis by directly targeting RTKN in human colon cancer.

Colorectal cancer (CRC) is the third most common cancer worldwide, with high morbidity. MicroRNAs (miRNAs) are endogenous small RNAs that play important roles in regulating multiple biological and pathologic processes. The differential expression of miRNAs in CRC was first reported in 2003. Accumulated evidence indicates that lethal-7a (let-7a, miRNA) generally functions as a tumor suppressor in several human cancers. However, the role of let-7a in human colon cancer remains unclear. The aim of this study was to investigate the biological functions of let-7a and its potential role in colon cancer. We first discovered that let-7a level was significantly decreased in colon cancer tissues and cell lines (HT-29, HCT-116, LoVo, SW480, and SW620). To explore the effects of let-7a on colon cancer, let-7a over-expressed HCT-116 and SW620 cells were constructed. Further studies demonstrated that over-expressed let-7a could remarkably inhibit HCT-116 and SW620 cell growth and metastasis by directly down-regulating Rhotekin (RTKN). When RTKN was reintroduced into let-7a mimic transfected HCT-116 or SW620 cells, the inhibition effects of let-7a on colon cancer cell growth and metastasis were markedly reversed. In conclusion, our research shows that let-7a can inhibit tumor cell growth and metastasis by directly targeting RTKN in human colon cancer.