Exposure to serum perfluoroalkyl substances and biomarkers of liver function: The Korean national environmental health survey 2015-2017.

BACKGROUND: Exposure to perfluoroalkyl substances (PFAS) may increase the risk of liver disease by disrupting cholesterol and lipid synthesis/metabolism, leading to higher liver-enzyme concentrations. However, most studies assessing association between PFAS and liver enzymes focused on individual PFAS. Moreover, PFAS concentrations differ based on sex and obesity status, and it remains unclear whether these factors affect associations with liver function. Therefore, we examined the association between exposure to both individual and combined PFAS and liver-function biomarkers and assessed sex and obesity as effect modifiers in Korean adults. METHODS: We measured serum concentrations of the five most abundant PFAS (PFOA, PFOS, PFHxS, PFDA, PFNA) and three liver enzymes (alanine transaminase [ALT], aspartate aminotransferase [AST], γ-glutamyl transferase [GGT]) in 1404 adults from the Korean National Environmental Health Survey Cycle 3, 2015-2017. We used linear regression to evaluate associations between individual PFAS and liver-function biomarkers, assessing sex and obesity as possible effect modifiers, and performed Bayesian kernel machine regression and quantile g-computation to evaluate the overall effect of PFAS mixture on biomarkers of liver function. RESULTS: Among 1404 Korean adults, all five PFAS were detected. Geometric mean concentration was highest for PFOS (16.11 µg/L), followed by PFOA (5.83 µg/L), PFHxS (2.21 µg/L), PFNA (2.03 µg/L), and PFDA (1.06 µg/L). In multivariable linear regression, all PFAS were positively associated with ALT, AST, and GGT; 2-fold increase in each PFAS was associated with 3.4-8.6% higher ALT, 2.4-4.6% higher AST, and 4.6-11.1% higher GGT (all p < 0.05). Positive associations for PFOA, PFDA, and PFNA with AST were stronger in men, and positive associations for PFOS with ALT and GGT were stronger in women. Compared to obese participants, nonobese participants had higher average percent changes in each enzyme, particularly GGT, when individual PFAS concentration doubled. Additionally, increased exposure to PFAS mixtures was associated with higher ALT, AST, and GGT. In quantile g-computations, simultaneous quartile increase in all PFAS was significantly associated with 6.9% (95%CI: 3.7, 10.2) higher ALT, 4.5% (95%CI: 2.4, 6.6) higher AST, and 8.3% (95%CI: 3.7, 13.1) higher GGT levels, on average. CONCLUSIONS: Exposure to individual and combined PFAS is associated with higher liver enzymes in Korean adults, providing additional evidence for the association between PFAS exposure and risk of liver disease.

Nitrogen dioxide increases the risk of disease progression in idiopathic pulmonary fibrosis.

BACKGROUND AND OBJECTIVE: Air pollution affects clinical course and prognosis of idiopathic pulmonary fibrosis (IPF). However, the effect of individual exposure to air pollutants on disease progression is unclear. We aimed to identify the effect of individual exposure to nitrogen dioxide (NO2 ) and particulate matter (aerodynamic diameter ≤ 10 µm [PM10 ]) on disease progression in patients with IPF. METHODS: The serial lung function data of 946 IPF patients (mean age: 65.4 years, male: 80.9%) were analysed. Individual-level long-term exposures to NO2 and PM10 at the residential addresses of patients were estimated using a national-scale exposure prediction model, constructed based on air quality regulatory monitoring data. Progression was defined as a relative decline (≥10%) in forced vital capacity. Individual- and area-level covariates were adjusted in the primary analysis model. RESULTS: Overall, 547 patients (57.8%) experienced progression during a median follow-up of 1.0 year (interquartile range: 0.4-2.6 years). In the primary model, a 10-ppb increase in NO2 concentration was associated with a 10.5% increase in the risk of progression (hazard ratio [HR] = 1.105; 95% CI = 1.000-1.219) in patients with IPF. There was also an increasing trend of progression in patients with IPF according to the second to fourth quartiles of NO2 (Q2 [HR = 1.299; 95% CI = 0.972-1.735], Q3 [1.409; 1.001-1.984], Q4 [1.598; 1.106-2.310]) compared to the first quartile. We found no association between PM10 and progression in IPF patients. CONCLUSION: Our data suggest that increased individual exposure to NO2 can increase the risk of progression in patients with IPF.

Long-term exposure to particulate air pollution and incidence of Parkinson's disease: A nationwide population-based cohort study in South Korea.

There has been increasing interest in the neurological impact of particulate matter (PM). However, its association with the incidence of Parkinson's disease (PD) remains unclear. We selected 313,355 participants satisfying inclusion criteria from the National Health Insurance Service-National Sample Cohort based on the nationwide population of South Korea, and followed them up from January 2007 through December 2015. Individual-level long-term PM exposure was assessed as the five time-varying average concentrations estimated for the previous 1, 2, 3, 4 and 5 years on each year (until censored or event occurred) at the district-level residential addresses of participants using a previously validated prediction model. Incident PD was defined as the first diagnosis accompanied by anti-PD medication prescription from 2007 through 2015. Time-varying Cox proportional hazards models were employed to estimate the hazard ratio (HR) of incident PD for long-term PM exposure, adjusting for individual- and area-level covariates. During the 8 years (2,745,389 person-years) of follow-up for a total of 313,355 participants (mean [range] age, 48.9 [19-87] years; 169,571 males [54.1%]), 2621 participants (0.8%) developed PD. The HR of incident PD per interquartile range (3.3 µg/m3) increase in fine PM (PM2.5) for the previous 1 year was 1.08 (95% confidence interval: 1.01-1.19). In subgroup-specific analyses, HRs for PM2.5 were significant among older participants, males, participants living in metropolitan cities, ibuprofen users, and participants with comorbidities (HR: 1.10-1.20). Long-term exposure to PM2.5 might play a role in PD development.

Different Mortality Risks of Long-Term Exposure to Particulate Matter across Different Cancer Sites.

Particulate matter (PM) air pollution has challenged the global community and the International Agency for Research on Cancer (IARC) classified airborne particulate matter as carcinogenic to humans. However, while most studies of cancer examined a single cancer type using different cohorts, few studies compared the associations of PM between different cancer types. We aimed to compare the association of long-term exposure to PM (PM10 and PM2.5) and cancer mortality across 17 different types of cancer using a population-based cohort in the Seoul Metropolitan Area (SMA), South Korea; Our study population includes 87,608 subjects (mean age: 46.58 years) residing in the SMA from the National Health Insurance Services-National Sample cohort (NHIS-NSC) and followed up for 2007-2015. We used the time-dependent Cox proportional hazards model to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs) of each cancer mortality per 10 µg/m3 increase in PM concentrations, after adjusting for individual and areal characteristics. During eight years of follow-up, 1487 people died with any of 17 cancer types. Lung cancer death was the highest, followed by liver and stomach cancer. Although we did not find the association for all cancer types, possibly because of limited cancer cases, HRs of PM2.5 were relatively high for lung, stomach, pancreas, non-Hodgkin's lymphoma, prostate, esophagus, oral and pharynx, and brain cancer mortality (HRs = 1.44-7.14). High HRs for pancreas, non-Hodgkin's lymphoma, esophagus, and oral and pharynx cancer were also seen for PM10; our findings suggest PM air pollution as a potential risk factor of cancer mortality for upper digestive tracts, mouth, pancreas, and non-Hodgkin's lymphoma in a highly urbanized population with high exposure to PM for a long time.

Impact of limited residential address on health effect analysis of predicted air pollution in a simulation study.

BACKGROUND: Recent epidemiological studies of air pollution have adopted spatially-resolved prediction models to estimate air pollution concentrations at people's homes. However, the benefit of these models was limited in many studies that used existing health data relying on incomplete addresses resulting from confidentiality concerns or lack of interest when designed. OBJECTIVE: This simulation study aimed to understand the impact of incomplete addresses on health effect estimation based on the association between particulate matter with diameter ≤10 µm (PM10) and low birth weight (LBW). METHODS: We generated true annual average concentrations of PM10 at 46,007 mothers' homes and their LBW status, using the parameters obtained from our data analysis and a previous study in Seoul, Korea. Then, we hypothesized that mothers' address information is limited to the district and compared the properties of their health effect estimates of PM10 with those using complete addresses. We performed this comparison across eight environmental scenarios that represent various spatial distributions of PM10 and nine exposure prediction methods that provide different sets of predicted PM10 concentrations of mothers. RESULTS: We observed increased bias and root mean square error consistently across all environmental scenarios and prediction methods using incomplete addresses compared to complete addresses. However, the bias related to incomplete addresses decreased when we used population-representative exposures averaged to the district from predicted PM10 at census tract centroids. SIGNIFICANCE: Our simulation study suggested that individual exposure estimated by prediction approaches and averaged across population-representative points can provide improved accuracy in health effect estimates when complete address data are unavailable. IMPACT STATEMENT: Our simulation study focused on a common and practical challenge of limited address information in air pollution epidemiology, and investigated its impact on health effect analysis. Cohort studies of air pollution have developed advanced exposure prediction model to allow the estimation of individual-level long-term air pollution concentrations at people's addresses. However, it is common that address information of existing health data is available at the coarse spatial scale such as city, district, and zip code area. Our findings can help understand the possible consequences of limited address information and provide practical guidance in achieving the accuracy in health effect analysis.

Association between long-term exposure to high levels of ambient air pollution and incidence of lung cancer in a population-based cohort.

Although outdoor air pollution including particulate matter (PM) was classified as carcinogenic to humans based on accumulating epidemiological evidence, these findings were suggested mostly from low-dose environments in North America and Europe. We aimed to examine the association of long-term exposure to PM ≤ 10 and 2.5 µm in diameter (PM10 and PM2.5) and nitrogen dioxide (NO2) with lung cancer incidence using a population-based cohort in the Seoul Metropolitan Area (SMA), South Korea. Our study included 83,478 people residing in the SMA and followed up for 2007-2015 from the National Health Insurance Service-National Sample Cohort. This cohort was constructed based on the National Health Insurance database that contains sociodemographic and medical information under universal health coverage. Individual long-term concentrations of PM10, PM2.5, and NO2 were estimated at people's district-level and annually-updated residential addresses for the previous 5 years by using previously-validated prediction models. We applied a time-dependent Cox proportional hazards model and estimated hazard ratios (HRs) per 10 µg/m3 and 10 ppb increases in PM and NO2, respectively, after adjusting for individual characteristics. During 9 years of follow-up, 489 lung cancer new cases occurred (714,012 person-year). The adjusted HRs for PM10 were greater than 1 but statistically non-significant (HR = 1.15; 95% CI = 0.88-1.52). We also did not find associations for PM2.5 and NO2. Despite null associations for the total population, our subgroup analysis suggested associations with PM in family members with cancer (PM10: HR = 2.59, 95% CI = 1.26-5.32; PM2.5: 5.55, 1.09-27.91) and in those who have smoked more than 1 pack per day (1.77, 0.96-3.25; 3.81, 1.00-14.44) or for less than 20 years (2.81; 1.13-7.07; 2.02, 0.21-19.23). Our study based on a highly urbanized population exposed to relatively high air pollution provides no evidence of the association between PM and lung cancer incidence in the total population but indicates the potential susceptibility in heavy smokers for relatively short periods and family members of cancer patients. Future studies should re-examine the association using improved exposure assessment and extended population.

Outdoor air pollution and diminished ovarian reserve among infertile Korean women.

BACKGROUND: Mounting evidence implicates an association between ambient air pollution and impaired reproductive potential of human. Our study aimed to assess the association between air pollution and ovarian reserve in young, infertile women. METHODS: Our study included 2276 Korean women who attended a single fertility center in 2016-2018. Women's exposure to air pollution was assessed using concentrations of particulate matter (PM10 and PM2.5), nitrogen dioxide (NO2), carbon monoxide (CO), sulfur dioxide (SO2), and ozone (O3) that had been collected at 269 air quality monitoring sites. Exposure estimates were computed for 1, 3, 6, and 12 months prior to the ovarian reserve tests. Anti-Müllerian hormone (AMH) ratio (defined as an observed-to-expected AMH based on age) and low AMH (defined as < 0.5 ng/mL) were employed as indicators of ovarian reserve. We included a clustering effect of 177 districts in generalized estimating equations approach. A secondary analysis was conducted restricting the analyses to Seoul residents to examine the association in highly urbanized setting. RESULTS: The mean age was 36.6 ± 4.2 years and AMH level was 3.3 ± 3.1 ng/mL in the study population. Average AMH ratio was 0.8 ± 0.7 and low AMH was observed in 10.3% of women (n=235). The average concentration of six air pollutants was not different between the normal ovarian reserve and low AMH groups for all averaging periods. In multivariable models, an interquartile range (IQR)-increase in 1 month-average PM10 was associated with decrease in AMH ratio among total population (ß= -0.06, 95% confidence interval: -0.11, 0.00). When we restrict our analysis to those living in Seoul, IQR-increases in 1 and 12 month-average PM2.5 were associated with 3% (95% CI: -0.07, 0.00) and 10% (95% CI: -0.18, -0.01) decrease in AMH ratio. The ORs per IQR increase in the six air pollutants were close to null in total population and Seoul residents. CONCLUSIONS: In a cohort of infertile Korean women, there was a suggestive evidence of the negative association between ambient PM concentration and ovarian reserve, highlighting the potential adverse impact of air pollution on women's fertility.

Nitrogen dioxide increases the risk of mortality in idiopathic pulmonary fibrosis.

Ambient air pollution is associated with the prognosis of idiopathic pulmonary fibrosis (IPF) patients. We aimed to identify the impacts of individual exposure to particulate matter with a 50% cut-off aerodynamic diameter of 10 µm (PM10) and nitrogen dioxide (NO2) on IPF patients' mortality.1114 patients (mean age 65.7 years; male 80.5%) diagnosed with IPF between 1995 and 2016 were included in this study. Individual-level long-term concentrations of PM10 and NO2 at residential addresses of patients were estimated using a national-scale exposure prediction model. The effect of PM10 and NO2 on mortality was estimated using a Cox proportional hazards model adjusted for individual- and area-level covariates.The median follow-up period was 3.8 years and 69.5% of the patients died or underwent lung transplantation. When adjusted for individual- and area-level covariates, a 10 ppb increase in NO2 concentration was associated with a 17% increase in mortality (hazard ratio (HR) 1.172, 95% CI 1.030-1.344; p=0.016). When IPF patients were stratified by age (≥65 versus <65 years) or by sex, NO2 was a significant prognostic factor for mortality in the elderly (HR 1.331, 95% CI 1.010-1.598; p=0.010). When stratified by age and sex jointly, NO2 showed the stronger association with mortality in elderly males (HR 1.305, 95% CI 1.072-1.598; p=0.008) than in other groups. PM10 was not associated with IPF mortality in all patients and in subgroups stratified by age or sex.Our findings suggest that increased exposure to NO2 can increase the risk of mortality in patients with IPF, specifically in elderly males.

Anti-Helicobacter pylori activity of acomplex mixture of Lactobacillus paracasei HP7 including the extract of Perilla frutescens var. acuta and Glycyrrhiza glabra.

The effect of standard therapeutic strategies on Helicobacter pylori infection is diminished over time owing to the emergence of drug resistant strains. In this study, we would like to confirm the enhanced effect of L. paracasei HP7, which has been reported to exert antibacterial and gastric mucosal protective effects, in combination with Perilla frutescens var. acuta (P. frutescens)and Glycyrrhiza glabra (G. glabra) extracts. P. frutescens extract and G. glabra extract were found to inhibit the growth of H. pylori in a concentration-dependent manner, and the combination of L. paracasei HP7 and P. frutescens extract and G. glabra extract effectively inhibited H. pylori from attaching to AGS a gastric epithelial cells. Moreover, L. paracasei HP7 complex mixture containing P. frutescens and G. glabra extracts has been shown to inhibit H. pylori virulence genes such as AlpA, CagA, FlaA and UreA. When H. pylori-infected mice were administered a complex mixture of L. paracasei HP7 containing P. frutescens and G. glabra extract, the infection rate of H. pylori was significantly reduced. In addition, the L. paracasei HP7 complex mixture significantly reduced serum IL-8 levels and stomach inflammation in H. pylori infected mice. These results suggest that a complex mixture of L. paracasei HP7 containing P. frutescens and G. glabra extracts may be an alternative to treating diseases caused by H. pylori infection.

Incident cardiovascular disease and particulate matter air pollution in South Korea using a population-based and nationwide cohort of 0.2 million adults.

BACKGROUND: While many studies reported the association between long-term exposure to particulate matter air pollution (PM) and cardiovascular disease (CVD), few studies focused on incidence with relatively high-dose exposure using a nationwide cohort. This study aimed to investigate the association between long-term exposure to PM10 and PM2.5 and incidence of CVD in a nationwide and population-based cohort in South Korea where the annual average concentration of PM2.5 is above 20 µg/m3. METHODS: We selected 196,167 adults in the National Health Insurance Service-National Sample Cohort (NHIS-NSC) constructed based on the entire South Korean population. Incidence of four CVD subtypes including ischemic heart disease (IHD), myocardial infarction, heart failure, and stroke, and total CVD including all four was identified as the first diagnosis for 2007-2015. To assess individual exposures, we used annually-updated district-level residential addresses and district-specific PM concentrations predicted by a previously developed universal kriging prediction model. We computed individual-level long-term PM concentrations for four exposure windows: previous 1, 3, and 5 year(s) and 5 years before baseline. We applied time-dependent Cox proportional hazards models to estimate hazard ratios (HRs) of incident CVDs per 10 µg/m3 increase in PM10 and PM2.5 after adjusting for individual- and area-level characteristics. RESULTS: During 1,578,846 person-year, there were 33,580 cases of total incident CVD. Average PM10 and PM2.5 concentrations for the previous 5 years were 52.3 and 28.1 µg/m3, respectively. A 10 µg/m3 increase in PM2.5 exposed for the previous 5 years was associated with 4 and 10% increases in the incidence of total CVD (95% confidence interval: 0-9%) and IHD (4-16%), respectively. HRs tended to be higher with earlier exposure for IHD and more recent exposure for stroke. The estimated shape of the concentration-response relationship showed non-linear patterns. We did not find evidence of the association for PM10. CONCLUSIONS: Using a population-based nationwide cohort exposed to relatively high PM concentration, this study confirmed the association between PM2.5 and CVD incidence that was reported in previous studies mostly with low-dose environments. The magnitude and the shape of the association were generally consistent with previous findings.

Spatial heterogeneity in the association between particulate matter air pollution and low birth weight in South Korea.

As many studies showed the spatial heterogeneity in the association between particulate matter (PM) air pollution and low birth weight (LBW), few studies focused on the variation of local associations at the national scale and related areal characteristics. This study aimed to explore different approaches to estimating local effects of PM with an aerodynamic diameter ≤10 µm (PM10) on LBW across 235 districts in South Korea, to investigate the spatial pattern of local associations, and to examine the relationship with local socio-demographic and environmental characteristics. LBW was identified in 5,692,650 mothers from birth certificate data for 2001-2013. We estimated individual annual-average concentrations of PM10 at centroids of mothers' residential districts by using a previously-validated prediction model. Then, we estimated district-specific odds ratios of LBW for PM10 using modified geographically weighted logistic regression. Here, we applied four approaches with different neighborhood definitions: the distance-based approach within 20- and 40-km bandwidth and the hybrid approach replacing with adjacent districts for urban districts <100 km2. In addition, we compared district-specific socioeconomic indicators and emission estimates across three groups of districts that showed significantly positive, no, and significantly negative associations. Medians of district-specific estimates of four approaches were similar to the global estimate and between each other. However, their variability differed with some unreasonably high estimates when a small distance was applied as the neighborhood definition, although spatial pattern was generally similar among the four. The hybrid approach based on the different neighborhood definition by urban and rural areas provided stable risk estimates. Higher risk districts in rural areas were found in more socioeconomically-deprived areas, whereas urban areas showed higher risk districts when their air pollution emissions were higher. Our approach and findings will help identify high risk areas and enhance understanding of geographic determinants.

Association of short- and long-term exposure to air pollution with atrial fibrillation.

BACKGROUND: Atrial fibrillation is a common cardiac arrhythmia and an important risk factor for stroke and cardiovascular morbidity. However, there is limited evidence regarding the association of air pollution with atrial fibrillation. This study aimed to compare the short-term and long-term effects of air pollution on atrial fibrillation. DESIGN: A nationwide cohort from the Korean general population. METHODS: Different analytical approaches were used for short-term and long-term effects. For the analysis of short-term effects, the daily incidence of emergency admissions for atrial fibrillation was identified. The relationship of atrial fibrillation with air pollutants, including PM2.5 (particulate matter ≤ 2.5 µm in aerodynamic diameter), PM10, carbon monoxide, sulphur dioxide, nitrogen dioxide and ozone, was analysed using a time-series analysis. The long-term effects of air pollution were analysed for subjects aged ≥30 years who resided in Seoul between 2007 and 2015 and had no history of atrial fibrillation. RESULTS: During the study period, 1137 emergency visits were identified in Seoul as being associated with atrial fibrillation. A 10-µg/m3 increase in ambient PM2.5 was shown to significantly increase emergency admissions by 4.5% at lag day 3 (p = 0.038). No other pollutants showed a significant relationship with emergency atrial fibrillation admission. Among 124,010 residents in Seoul, 1903 developed atrial fibrillation at a median follow-up of 9.5 years (1.95 per 1000 person-years). Long-term exposure to air pollution had no significant impact on atrial fibrillation occurrence (p = 0.830 for PM2.5). CONCLUSION: This study suggests that short-term exposure to PM2.5 triggers atrial fibrillation. However, we found no evidence linking atrial fibrillation with long-term exposure to air pollution.

Short-term effects of air pollution on blood pressure.

Elevated blood pressure (BP) has been proposed as a possible pathophysiological mechanism linking exposure to ambient air pollution and the increased risk of cardiovascular mortality and morbidity. In this study, we investigated the hourly relationship between ambient air pollutants and BP. BP measurements were extracted from the electronic health record database of the Seoul National University Bundang Hospital from February 2015 to June 2017. A total of 98,577 individual BP measurements were matched to the hourly levels of air pollutants. A generalized additive model was constructed for hour lags of 0-8 of air pollutants adjusting for age, sex, meteorological variables, and time trend. Systolic BP was shown to be significantly lower at 2-4 hours and 3-5 hours after increased levels of SO2 and CO, respectively (0.24 mmHg and 0.26 mmHg for an interquartile range, respectively). In contrast, O3 and NO2 were associated with significantly increased systolic BP at 3-5 lag hours and at 0-2 lag hours, respectively. BP elevation in association with O3 and NO2 was shown to be significantly greater in hypertensive patients than normotensive subjects. Our findings suggest that short-term exposure to air pollution may be associated with elevated BP.

Anti-Helicobacter pylori activity and inhibition of gastritis by Allium hookeri extract.

Allium hookeri is widely consumed plant as a vegetable and herbal medicine in southeastern Asia. Allium hookeri has been reported antioxidant, improvement of bone health and antidiabetic effects. In the present study, we investigated the potential inhibitory effect of Allium hookeri extract (AHE) on Helicobacter pylori. The in vitro anti-bacterial activities of AHE were determined by disk agar diffusion method. Also, the inhibition effect of the AHE on H. pylori infection was investigated using a mouse model. H. pylori colonization was confirmed by rapid urease tests, as described previously. Mucosal damage was evaluated grossly and histologically according to previously described criteria. As the results of the disk agar diffusion assay, CLR, AMX and MTZ inhibited the bacterial growth with inhibition zone of 19.2, 15.2 and 7.5 mm, respectively. AHE 100 µg/mL showed an inhibition zone value of 20.6 mm. Rapid urease tests of the mice stomachs demonstrated a significant reduction in H. pylori colonization. In addition to the therapeutic effect against H. pylori infection, the AHE reduced mucosal inflammation and epithelial damages in the stomach of H. pylori-infected mice. These results demonstrate that the AHE successfully cured an H. pylori infection and treated the H. pylori infection. This AHE could be a promising treatment for patients with gastric complaints including gastritis caused by H. pylori.

Anti-coccidial activity of the ethanol extract of Tribulus terrestris fruits on Eimeria tenella.

Anti-coccidial effects of the fruits of Tribulus terrestris (Tribuli fructus) ethanol extract (TTE) were studied with animal experiment following per oral administration with Eimeria (E.) tenella. This experiment was performed on the 3-day-old chicks (n=30). The animals were divided with 3 groups; TFE 15mg per animal+infected (n=10), TTE untreated+infected (n=10) and non-infected control (n=10). Animals were administrated with or without TTE during 1 week, and then inoculated with E. tenella. The anti-coccidial activity were evaluated with oocysts shedding numbers in stools, body weights changes and food intake changes. The TTE-inoclated animals revealed significantly decreased stool oocysts numbers (P<0.05) when compared to the TTE untreated animals. Also, TTE-treated animals showed more increased body weight gains (P<0.05) than the TTE untreated animals. These results demonstrate that TTE produce anticoccidial activities against E. tenella. TTE could be a promising treatment for the coccidiosis.

In vitro and in vivo inhibition of Helicobacter pylori by Lactobacilllus paracasei HP7.

The efficacy of standard therapeutic strategies for Helicobacter pylori (H. pylori) infection is decreasing over time due to the emergence of drug-resistant strains. As an alternative, the present study investigated the capacity of Lactobacilllus paracasei (L. paracasei) HP7, isolated from kimchi, to inhibit H. pylori growth. The effects of L. paracasei HP7 on H. pylori adhesion and H. pylori-induced inflammation were examined in AGS human gastric adenocarcinoma epithelial cells and a mouse model of H. pylori SS1 infection. L. paracasei HP7 reduced H. pylori adhesion to AGS cells and suppressed the inflammatory response in infected cells by downregulating interleukin-8. H. pylori colonization in the stomach of C57BL/6 mice was demonstrated by rapid urease test, and results showed significant decrease in mice post-treated with L. paracasei HP7. Additionally, L. paracasei HP7 decreased gastric inflammation and epithelial lesions in the stomach of H. pylori-infected mice. These results demonstrate that L. paracasei HP7 treatment can inhibit H. pylori growth and is thus a promising treatment for patients with gastric symptoms such as gastritis that are caused by H. pylori infection.

Association between Long-Term Exposure to Particulate Matter Air Pollution and Mortality in a South Korean National Cohort: Comparison across Different Exposure Assessment Approaches.

Increasing numbers of cohort studies have reported that long-term exposure to ambient particulate matter is associated with mortality. However, there has been little evidence from Asian countries. We aimed to explore the association between long-term exposure to particulate matter with a diameter ≤10 µm (PM10) and mortality in South Korea, using a nationwide population-based cohort and an improved exposure assessment (EA) incorporating time-varying concentrations and residential addresses (EA1). We also compared the association across different EA approaches. We used information from 275,337 people who underwent health screening from 2002 to 2006 and who had follow-up data for 12 years in the National Health Insurance Service-National Sample Cohort. Individual exposures were computed as 5-year averages using predicted residential district-specific annual-average PM10 concentrations for 2002-2006. We estimated hazard ratios (HRs) of non-accidental and five cause-specific mortalities per 10 µg/m³ increase in PM10 using the Cox proportional hazards model. Then, we compared the association of EA1 with three other approaches based on time-varying concentrations and/or addresses: predictions in each year and addresses at baseline (EA2); predictions at baseline and addresses in each year (EA3); and predictions and addresses at baseline (EA4). We found a marginal association between long-term PM10 and non-accidental mortality. The HRs of five cause-specific mortalities were mostly higher than that of non-accidental mortality, but statistically insignificant. In the comparison between EA approaches, the HRs of EA1 were similar to those of EA2 but higher than EA3 and EA4. Our findings confirmed the association between long-term exposure to PM10 and mortality based on a population-representative cohort in South Korea, and suggested the importance of assessing individual exposure incorporating air pollution changes over time.

Multiple roles of RARRES1 in prostate cancer: Autophagy induction and angiogenesis inhibition.

BACKGROUND: Prostate cancer (PCa) poses a major health concern in men worldwide. Retinoic Acid Receptor Responder (RARRES1)/ Tazarotene-induced gene-1 (TIG-1) is a putative tumor suppressor gene that exerts its tumor suppressor function via unknown mechanisms. Epigenetic silencing of RARRES1 leads to its loss in several types of cancer, including PCa. Determining the molecular mechanisms that mediate the tumor suppressor role of RARRES1 in PCa is the focus of our study. FINDINGS: Our data indicates that RARRES1 over expression in PCa cell lines represses mitogen-activated protein kinase (MAPK) activation. RARRES1 expression induces the levels of autophagy-related genes, beclin, ATG3 and increases LC3B-II conversion. A significant induction of SIRT1 along with mTOR inhibition is noted on RARRES1 expression. Furthermore, RARRES1 over expression elevates the levels of the antioxidant enzyme, catalase. Our results also indicate that RARRES1 expression inhibits angiogenesis in endothelial cells. CONCLUSIONS: In summary, the data presented here indicate that forced expression of RARRES1 in PCa cells (a) induces ER stress and autophagic response; (b) increases SIRT1 levels; and (c) higher levels of anti-oxidant enzymes. Our study also implicates the role of RARRES1 as a novel anti-angiogenic molecule. Overall this study reports the molecular players that RARRES1 modulates to serve as a tumor suppressor molecule. Future studies will help determine the in vivo mechanisms by which RARRES1 may serve as a target for therapeutic intervention both in cancer and in angiogenesis-related disorders.