The injury of fine particulate matter from cooking oil fumes on umbilical cord blood vessels in vitro.

Cooking oil fumes (COFs) derived PM2.5 is the major source of indoor air pollution in Asia. For this, a pregnant rat model within different doses of cooking oil fumes (COFs) derived PM2.5 was established in pregnancy in our research. Our previous studies have showed that exposure to COFs-derived PM2.5 was related to adverse pregnancy outcomes. However, the mechanisms of signaling pathways remain unknown. Therefore, this study aimed to investigate the underlying mechanisms induced by COFs-derived PM2.5 injury on umbilical cord blood vessels (UCs) in vitro. Exposure to COFs-derived PM2.5 resulted in changing the expression of eNOS, ET-1, ETRA, and ETRB. In additions, western blot analysis indicated that the HIF-1α/iNOS/NO signaling pathway and VEGF/VEGFR1/iNOS signaling pathway were involved in UCs injury triggered by COFs-derived PM2.5. In conclusion, our data suggested that exposure to COFs-derived PM2.5 resulted in increasing of oxidative stress and inflammation, as well as dysfunction of UCs.

Efficacy and Safety of Adjunctive Corticosteroids Therapy for Severe Community-Acquired Pneumonia in Adults: An Updated Systematic Review and Meta-Analysis.

BACKGROUND: Adjunctive corticosteroids therapy is an attractive option for community-acquired pneumonia (CAP) treatment. However, the effectiveness of adjunctive corticosteroids on mortality of CAP remains inconsistent, especially in severe CAP. We performed a meta-analysis to evaluate the efficacy and safety of adjunctive corticosteroids in severe CAP patients. METHODS: Three databases of PubMed, EMBASE and Cochrane Library were searched for related studies published in English up to December, 2015. Randomized controlled trials (RCTs) of corticosteroids in hospitalized adults with severe CAP were included. Meta-analysis was performed by a random-effect model with STATA 11.0 software. We estimated the summary risk ratios (RRs) or effect size (ES) with its corresponding 95% confidence interval (95%CI) to assess the outcomes. RESULTS: We included 8 RCTs enrolling 528 severe CAP patients. Adjunctive corticosteroids significantly reduced all-cause mortality (RR = 0.46, 95%CI: 0.28 to 0.77, p = 0.003), risk of adult respiratory distress syndrome (ARDS) (RR = 0.23, 95%CI: 0.07 to 0.80, p = 0.02) and need for mechanical ventilation (RR = 0.50, 95%CI: 0.27 to 0.92, p = 0.026). Adjunctive corticosteroids did not increase frequency of hyperglycemia requiring treatment (RR = 1.03, 95%CI: 0.61 to 1.72, p = 0.91) or gastrointestinal hemorrhage (RR = 0.66, 95%CI: 0.19 to 2.31, p = 0.52). In subgroup analysis by duration of corticosteroids, we found that prolonged corticosteroids therapy significantly reduced all-cause mortality (RR = 0.41, 95%CI: 0.20 to 0.83, p = 0.01) and length of hospital stay (-4.76 days, 95% CI:-8.13 to -1.40, p = 0.006). CONCLUSIONS: Results from this meta-analysis suggested that adjunctive corticosteroids therapy was safe and beneficial for severe CAP. In addition, prolonged corticosteroids therapy was more effective. These results should be confirmed by adequately powered studies in the future.

The structural and functional effects of fine particulate matter from cooking oil fumes on rat umbilical cord blood vessels.

A growing body of epidemiological evidence has supported the association between maternal exposure to airborne fine particulate matter (PM2.5) during pregnancy and adverse pregnancy outcomes. However, the specific biological mechanisms implicated in the causes of adverse pregnancy outcomes are not well defined. In this study, a pregnant rat model of exposure to different doses of cooking oil fumes (COFs)-derived PM2.5 by tail intravenous injection in different pregnant stages was established. The results indicated that exposure to COFs-derived PM2.5 was associated with adverse pregnancy outcomes, changed the structure of umbilical cord blood vessels, decreased the diameter and lumen area, and increased wall thickness. What's more, a significant increase of maximum contraction tension was observed in the early pregnancy high-dose exposure group and pregnant low-dose exposure group compared to the control group. Based on the maximum contraction tension, acetylcholine (ACh) did not induce vasodilation but caused a dose-dependent constriction, and there were significant differences in the two groups compared to the control group. Exposure to COFs-derived PM2.5 impaired the vasomotor function of umbilical veins by affecting the expression of NO and ET-1. This is the first study that evaluated the association of risk of adverse pregnancy outcomes and pregnant rats exposed to COFs-derived PM2.5 and primarily explored the potential mechanisms of umbilical cord blood vessels injury on a rat model. More detailed vitro and vivo studies are needed to further explore the mechanism in the future.

Air Pollution and the Risk of Birth Defects in Anqing City, China.

OBJECTIVE: This study aimed to explore evidence for the influence of air pollution on the risk of birth defects in China and contribute to establish prevention strategies. METHODS: We conducted a retrospective cohort study in Anqing city, Eastern China, from 2010 to 2012. Binary logistic regression models were used to estimate odds ratios (ORs) per 10 µg/m3 change for SO2, NO2, and PM10. RESULTS: For continuous exposure to SO2 (10 µg/m increase), the adjusted OR for birth defects is 1.20 [95% confidence interval (95% CI) 1.09 to 1.29] in the preconception. A 10 µg/m increase in SO2 (adjusted OR 1.26, 95% CI 1.15 to 1.36) during the second trimester is strongly associated with birth defects. No associations have been observed for NO2 and PM10. CONCLUSION: The results suggested that exposure to ambient SO2 during pregnancy may increase the risk of birth defects.

Short-term exposure to particulate air pollution and risk of myocardial infarction: a systematic review and meta-analysis.

A growing number of studies have associated short-term exposure to ambient particulate matter air pollution (PM) and risk of specific cardiovascular events, just as myocardial infarction (MI). However, the results of the recent studies were inconsistent; therefore, a systematic review and meta-analysis was performed. To synthetically quantify the association between short-term exposure to PM and risk of MI, a meta-analysis was conducted to combine the estimates of effect for a relationship between short-term exposure to PM10, PM2.5 (particulate matter ≤ 10 µm, 2.5 µm in diameter) and risk of MI. Electronic database searches for all relevant published studies were updated in January 2015. And, a random-effects model was performed to estimate pooled relative risk (RR) and 95 % confidence intervals (95 % CI). Thirty-one published observational epidemiological studies were identified. Risk of MI was significantly associated with per 10 µg/m(3) increment in PM10 (OR = 1.005; 95 % CI 1.001-1.008) and PM2.5 (OR = 1.022; 95 % CI 1.015-1.030). The risk of PM2.5 exposure was relatively greater than PM10. In the subgroup analysis by study design, location, quality score, and lag exposure, the results were basically consistent with the former overall results in PM2.5 but slightly changed in PM10. Short-term exposure to particulate matter (PM2.5, PM10) was a risk factor for MI, and the results further confirmed the discovery in the previous meta-analysis.

Association between maternal tumor necrosis factor-α G308A polymorphism and interferon-γ A874T polymorphism and risk of preterm birth: a meta-analysis.

OBJECTIVE(S): This article was undertaken to investigate the association between tumor necrosis factor-α (TNF-α) G308A polymorphism and interferon-γ (INF-γ) A874T polymorphism and risk of preterm birth (PTB) by performing a meta-analysis of available studies. STUDY DESIGN: Articles were chosen based on PubMed, EMBASE, Web of science, and China Biology Medicine (CBM) databases with no language restriction from their inceptions to 1 March, 2014. Specific inclusion criteria were used to evaluate articles. Meta-analysis was performed by using a random or fixed effect model with STATA 11.0 software. We estimated the summary odds ratios (ORs) with its corresponding 95% confidence interval (95%CI) to assess the association. RESULTS: 21 eligible case-control studies with a total of 2103 cases and 5070 controls were finally included into this meta-analysis. Pooled analysis showed that A allele of TNF-α G308A was not associated with increased PTB risk (OR=0.84, 95%CI: 0.65-1.07, p=0.167 for G vs. A). Stratifying analysis for ethnicity and different definition of PTB also indicated that A allele was not associated with increased PTB risk. However, the meta-analysis showed that INF-γ A874T polymorphism was associated with the increased risk of PTB (OR=1.14, 95%CI: 1.11-1.73, p=0.004 for A vs. T). Stratifying analysis was not performed due to the small sample size. CONCLUSION(S): TNF-α G308A polymorphism was not associated with an increased risk of PTB, but INF-γ A874T polymorphism may contribute to increasing susceptibility to PTB. Detection of polymorphism of INF-γ A874T might be a promising biomarker for the diagnosis and prognosis of preterm delivery.

Oxidative stress, apoptosis, and cell cycle arrest are induced in primary fetal alveolar type II epithelial cells exposed to fine particulate matter from cooking oil fumes.

Epidemiological studies demonstrate a linkage between morbidity and mortality and particulate matter (PM), particularly fine particulate matter (PM2.5) that can readily penetrate into the lungs and are therefore more likely to increase the incidence of respiratory and cardiovascular diseases. The present study investigated the compositions of cooking oil fume (COF)-derived PM2.5, which is the major source of indoor pollution in China. Furthermore, oxidative stress, cytotoxicity, apoptosis, and cell cycle arrest induced by COF-derived PM2.5 in primary fetal alveolar type II epithelial cells (AEC II cells) were also detected. N-acetyl-L-cysteine (NAC), a radical scavenger, was used to identify the role of oxidative stress in the abovementioned processes. Our results suggested that compositions of COF-derived PM2.5 are obviously different to PM2.5 derived from other sources, and COF-derived PM2.5 led to cell death, oxidative stress, apoptosis, and G0/G1 cell arrest in primary fetal AEC II cells. Furthermore, the results also showed that COF-derived PM2.5 induced apoptosis through the endoplasmic reticulum (ER) stress pathway, which is indicated by the increased expression of ER stress-related apoptotic markers, namely GRP78 and caspase-12. Besides, the induction of oxidative stress, cytotoxicity, apoptosis, and cell cycle arrest was reversed by pretreatment with NAC. These findings strongly suggested that COF-derived PM2.5-induced toxicity in primary fetal AEC II cells is mediated by increased oxidative stress, accompanied by ER stress which results in apoptosis.

Maternal exposure to fine particulate matter (PM2.5) and pregnancy outcomes: a meta-analysis.

A growing body of evidence has investigated the association between maternal exposure to PM2.5 (particulate matter with aerodynamic diameter 2.5 µm) during pregnancy and adverse pregnancy outcomes. However, the results of those studies are not consistent. To synthetically quantify the relationship between maternal exposure to PM2.5 during pregnancy and pregnancy outcomes (the change in birth weight, low birth weight (LBW), preterm birth (PTB), small for gestational age (SGA), and stillbirth), a meta-analysis of 25 published observational epidemiological studies that met our selection criteria was conducted. Results suggested a 10 µg/m(3) increase in PM2.5 was positively associated with LBW (odds ratio (OR) = 1.05; 95 % confidence interval (CI), 1.02-1.07), PTB (OR = 1.10; 95 % CI, 1.03-1.18), and SGA (OR = 1.15; 95 % CI, 1.10-1.20) based on entire pregnancy exposure, and pooled estimate of decrease in birth weight was 14.58 g (95 % CI, 9.86-19.31); however, there was no evidence of a statistically significant effect of per 10 µg/m(3) increase in PM2.5 exposure on the risk of stillbirth (OR = 1.18; 95 % CI, 0.69-2.04). With respect to three different gestation periods, no significant risks were found in PTB, stillbirth, and the first trimester on the change of birth weight with a 10 µg/m(3) increase in PM2.5. In this study, a comprehensive quantitative analysis of the results show that PM2.5 can increase the risk of LBW, PTB, and SGA; pregnant women need to take effective measures to reduce PM2.5 exposure.

Association between ubiquitin carboxy-terminal hydrolase-L1 S18Y variant and risk of Parkinson's disease: the impact of ethnicity and onset age.

The Ubiquitin carboxy-terminal hydrolase-L1 (UCHL1) is a candidate risk gene for Parkinson' disease (PD), and a function SNP (rs5030732) in the coding region of this gene has been studied for the association with the disease extensively among worldwide populations, but the results were inconsistent and controversial. Here, to estimate the association between UCHL1 S18Y polymorphism and risk of PD in general population, we conducted a systematic meta-analysis by combining all available case-control subjects in Asian, European, and American populations, with a total of 7742 PD cases and 8850 healthy controls, and the pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) for UCHL1 S18Y polymorphism and PD were calculated using the Mantel-Haenszel method with a fixed- or random-effects model. Subgroup analysis was also performed in different onset age-matched groups. Among high-quality studies, UCHL1 S18Y polymorphism was moderately associated with the risk of PD (allele contrasts, OR = 1.063, 95% CI 1.008-1.122; p = 0.024; regressive genetic model, OR = 1.078, 95% CI 1.005-1.157; p = 0.035). When stratifying for ethnicity, none association were observed in subgroups. Analysis of early-onset PD (EOPD) and late-onset PD (LOPD) revealed that the polymorphism was not associated with the risk of PD. In conclusion, our meta-analysis suggests that UCHL1 S18Y polymorphism is moderately associated with susceptibility to PD, and more studies are needed to confirm our conclusion.

Plasminogen activator inhibitor-1 -675 4G/5G polymorphism and polycystic ovary syndrome risk: a meta analysis.

PURPOSE: Several studies have reported that excessive amounts of plasminogen activator inhibitor-1(PAI-1) might increase the incidence of polycystic ovary syndrome(PCOS), but so far the published results were inconsistent. The aim of this study was to further investigate the association between PAI-1 gene polymorphism and the susceptibility to PCOS by performing a meta-analysis. METHODS: A comprehensive literature search for relevant studies was conducted on google scholar, PubMed, the Chinese National Knowledge Infrastructure (CNKI) and the Chinese Biomedical Literature Database (CBM). This meta-analysis was performed using the STATA 11.0 software and the pooled odds ratio (OR) with 95% confidence interval (CI) was calculated. RESULTS: Ten case-control studies were included in this meta-analysis with a total of 2,079 cases and 1,556 controls. The results showed that PAI-1 -675 4G/5G polymorphism may increase the risk of PCOS, especially among Asian populations. However, there was no statistically significant association between the polymorphism and PCOS risk in Caucasians. CONCLUSION: Our meta-analysis suggests that PAI-1 -675 4G/5G polymorphism may contribute to increasing susceptibility to PCOS in Asians. Detection of the PAI-1 gene polymorphism might be a promising biomarker for the susceptibility of PCOS.

The association between the C-509T and T869C polymorphisms of TGF-ß1 gene and the risk of asthma: a meta-analysis.

Asthma is a complex multigenic disease in which gene-environment interactions play a critical role in disease onset and progression. Transforming growth factor-ß1 (TGF-ß1) is one of several candidate locus for the pathogenesis of asthma, and is highly polymorphic. To derive a more precise estimation of the relationship between the T869C and C-509T polymorphisms of the TGF-ß1 gene and asthma, a meta-analysis of 24 published case-control studies was conducted. 20 studies for C-509T polymorphism and 8 studies for T869C polymorphism were included. The pooled odds ratios were calculated respectively for allele contrasts, additive genetic model, dominant genetic model and recessive genetic model. Subgroup analyses were also performed by ethnicity, age, atopic status and asthma severity for two gene polymorphisms. In regard to T869C polymorphism, significant associations with asthma were observed in recessive (OR 1.23, 95%CI 1.00-1.51 and P=0.047), additive and allele models. In the subgroup analysis by age, significant risks were also found in the recessive model for adults (OR 1.31, 95%CI 1.02-1.69 and P=0.032), atopic asthma (OR 1.63, 95%CI 1.07-2.49 and P=0.023). With respect to C-509T polymorphism, significant associations with asthma were demonstrated in the overall analysis and subgroup analyses in the dominant model for Asian (OR 1.37, 95%CI 1.04-1.81 and P=0.025), Adults (OR 1.26, 95%CI 1.02-1.56 and P=0.035), Children (OR 1.19, 95%CI 1.01-1.40 and P=0.034). Potentially functional TGF-ß1 C-509T and T869C polymorphisms may be risk factors for asthma susceptibility.