Rapid identification and quantification of diquat in biological fluids within 30 s using a portable Raman spectrometer.

Rapid detection of diquat (DQ) is essential in clinical diagnosis and rescue. Here, we developed a fast, simple-yet-practical detection strategy for the reliable identification and quantification of DQ in biological fluids. Based on surface-enhanced Raman spectroscopy (SERS), point-of-care detection was realized under the acidic condition with gold nanoparticles as the substrate. Under optimal experimental conditions, the detection limits of the strategy were 17.5 ppb and 1.99 ppm in human urine and gastric juice, respectively. High specificity and selectivity of the SERS strategy were demonstrated using common pesticides and coexisting biological substances. The method was also used to detect biofluids from 5 patients and urine samples from 10 healthy volunteers. The results were in high agreement with spectrophotometric and clinical liquid chromatography-mass spectrometry methods. The volume of urine samples required for this technique is merely 20 µL, and no preparation of the samples is required. Compared to traditional methods used in clinical settings, SERS-based methods are capable of real-time measurements that accurately provide rapid detection and response in non-laboratory settings, with great potential for on-site and point-of-care testing.

Crotonaldehyde exposure induces liver dysfunction and mitochondrial energy metabolism disorder in rats.

Crotonaldehyde is a highly toxic pollutant, widely present in tobacco smoke and automobile exhaust. Exposure to crotonaldehyde can cause hepatotoxicity and induce liver tumors in rats; however, the underlying mechanism is unclear. Liver cells contain many mitochondria, which serve to maintain energy levels in the body. We hypothesized that the energy metabolism disorder caused by mitochondrial dysfunction is an important cause of liver injury in rats exposed to crotonaldehyde. To test this, we randomly divided 40 male Wistar rats into four groups, and provided crotonaldehyde at 0, 2.5, 4.5, and 8.5 mg/kg for 90 days by intragastric administration. The results showed that crotonaldehyde exposure caused damage to liver mitochondrial structure, reduced electron-transport chain activity and ATP levels, and interfered with mitochondrial DNA transcription. In response to increased crotonaldehyde exposure, rats exhibited increased reactive oxygen species levels, decreased superoxide dismutase and glutathione activity, and activation of the caspase-mediated apoptosis pathway, as well as elevated levels of alanine aminotransferase, aspartate aminotransferase, total bilirubin, and histopathological damage. Our findings, together with those of previous reports, should help elucidate the underlying mechanism of crotonaldehyde-induced mitochondrial dysfunction and energy metabolism disorder, and provide an important direction for the prevention and clinical intervention of liver diseases caused by crotonaldehyde and aldehydes with similar structures.

Ambient particulate matter compositions and increased oxidative stress: Exposure-response analysis among high-level exposed population.

BACKGROUND: Oxidative stress has been suggested to be one of the key drivers of health impact of particulate matter (PM). More studies on the oxidative potential of PM alone, but fewer studies have comprehensively evaluated the effects of external and internal exposure to PM compositions on oxidative stress in population. OBJECTIVE: To comprehensively investigate the exposure-response relationship between PM and its main compositions with oxidative stress indicators. METHODS: We conducted a cross-sectional study including 768 participants exposed to particulates. Environmental levels of fine particulate matter (PM2.5), polycyclic aromatic hydrocarbons (PAHs) and metals in PM were measured, and urinary levels of PAHs metabolites and metals were measured as internal dose, respectively. Multivariable linear regression models were used to analyze the correlations of PM exposure and urinary levels of 8-hydroxy-2́'-deoxyguanosine (8-OHdG), and 8-iso-prostaglandin-F2α (8-iso-PGF2α) and malondialdehyde (MDA). RESULTS: The concentration of both PM2.5 and total PAHs was significantly correlated with increased urinary 8-OHdG, 8-iso-PGF2α and MDA levels (all p < 0.05). The levels of 4 essential metals all showed significant exposure-response increase in urinary 8-OHdG in both current and non-current smokers (all p < 0.05); ambient selenium, cobalt and zinc were found to be significantly correlated with urinary 8-iso-PGF2α (p = 0.002, 0.003, 0.01, respectively); only selenium and cobalt were significantly correlated with urinary MDA (p < 0.001, 0.01, respectively). Furthermore, we found each one-unit increase in urinary total OH-PAHs generated a 0.32 increase in urinary 8-OHdG, a 0.22 increase in urinary 8-iso-PGF2α and a 0.19 increase in urinary MDA (all p < 0.001). Furthermore, it was found that the level of 12 urinary metals all showed significant and positive correlations with three oxidative stress biomarkers in all subjects (all p < 0.001). CONCLUSIONS: Our systematic molecular epidemiological study showed that particulate matter components could induce increased oxidative stress on DNA and lipid. It may be more important to monitor and control the harmful compositions in PM rather than overall particulate mass.

Apoptosis of lung cells regulated by mitochondrial signal pathway in crotonaldehyde-induced lung injury.

Crotonaldehyde, a highly toxic α, ß-unsaturated aldehyde, is a ubiquitous hazardous pollutant. Because of its extreme toxicity and ubiquity in all types of smoke, most current research focuses on the lung toxicity of such air pollutants. However, the specific mechanism of pulmonary toxicity caused by crotonaldehyde remains unclear, especially after long-term exposure to crotonaldehyde at low dose. Therefore, the aim of the present study is to determine whether crotonaldehyde-induced oxidative damage and inflammation promote apoptosis in rats via the mitochondrial pathway using histopathology, immunohistochemistry, biochemistry analysis and Western blot analysis. The results show that crotonaldehyde elicited oxidative damage and inflammation in rats in a concentration-dependent manner. Crotonaldehyde-induced lung injury which was confirmed by H&E, Masson's trichrome staining and TUNEL. And crotonaldehyde-induced lung cell apoptosis showed a concentration-response relationship. Immunohistochemistry and Western blot results showed that apoptotic mitochondrial signaling pathway is abnormally activated in crotonaldehyde-induced lung injury. Collectively, this study demonstrates that exposure of rats to crotonaldehyde induces lung injury by inducing apoptosis, which is related to oxidative damage and inflammation through mitochondrial pathway.

Behavioral Responses of Scolytus schevyrewi (Coleoptera: Curculionidae: Scolytinae) to Volatiles From Apricot Tree (Rosales: Rosaceae).

Scolytus schevyrewi Semenov (Coleoptera: Curculionidae: Scolytinae) is native to China and Central Asia. Damage by the adults and larvae weakens local apricot trees (Armeniaca spp.), often causing death to many host trees. In previous studies, freshly cut apricot logs were found to be highly attractive to S. schevyrewi adults. To explore the possibility of trapping and monitoring this bark beetle, we evaluated the effect of the apricot tree volatiles on S. schevyrewi behavior. Volatiles from the apricot logs were collected by headspace sampling and subjected to coupled gas chromatography-electroantennographic detection (GC-EAD) analysis. Behavioral responses to EAD-active compounds were assessed using two-choice Y-tube olfactometers. The results showed that the antennae of females responded to 21 volatile compounds from apricot logs. Seventeen compounds were confirmed with authentic compounds. The Y-olfactometer bioassays showed that at a stimulation dose of 100 µg, four compounds [(1S)-(-)-α-pinene, (±)-limonene, (1S)-(+)-3-carene, and 1-hexanol], and some binary mixtures of the four compounds [(1S)-(-)-α-pinene plus (±)-limonene; (1S)-(-)-α-pinene plus (1S)-(+)-3-carene; (1S)-(-)-α-pinene plus camphene; (1S)-(-)-α-pinene plus (±)-limonene, (1S)-(+)-3-carene, and 1-hexanol] were significantly attractive to both sexes (except (±)-limonene and (1S)-(+)-3-carene for males), suggesting that these compounds may play a role in host tree selection by S. schevyrewi and should be evaluated as lures for population monitoring. In contrast, octanal, nonanal, decanal, linalool and N,N-diethylformamide appeared to repel S. schevyrewi adults in Y-tube at the concentration tested.

Crotonaldehyde-induced alterations in testicular enzyme function and hormone levels, and apoptosis in the testes of male Wistar rats are associated with oxidative damage.

Crotonaldehyde is a hazardous pollutant present in cigarette smoke and automobile exhausts that is generated by lipid peroxidation, and harmful to reproductive organs. Although we are often exposed to low doses of crotonaldehyde daily, its adverse effects on the reproductive organs have not been fully elucidated. To elucidate them, we administered crotonaldehyde (0, 2.5, 4.5, and 8.5 mg/kg) by gavage for 150 days to male Wister rats, and evaluated its effect on their testicular tissues. Body weight, testis coefficient, sperm count, and motility decreased. Reactive oxygen species and malondialdehyde levels in the 8.5 and 4.5 mg/kg groups significantly increased as antioxidant enzyme activity decreased. Testicular cell apoptosis rate in the exposed groups increased. Testicular enzyme activity and reproductive hormone levels were significantly altered in the 8.5 and 4.5 mg/kg groups. Therefore, long-term exposure to crotonaldehyde may induce oxidative stress, resulting in testicular cell apoptosis, and testicular enzyme and hormone level alteration.

Derlin1 functions as an oncogene in cervical cancer via AKT/mTOR signaling pathway.

BACKGROUND: Cervical cancer (CC) ranks third in the morbidity and mortality of female cancer around the world. Derlin1 has been found to be overexpressed in several human cancers. However, it is still unclear about its roles in CC. The research aims to explore the relationship between Derlin1 and CC. METHODS: We purchased a human CC tissues microarray, which contained CC tissues and corresponding para-cancerous tissues from 93 patients with primary cervical squamous cell carcinoma. Immunohistochemical staining was used to confirm the expression of Derlin1 in these tissues. And we detected the differential expression of Derlin1 in cervical cancer cell lines and normal cervical epithelial cells (H8). Further, the cervical cancer cell lines SiHa and C33A were used as an in vitro model, which was down-regulated the expression of Derlin1 using siRNA interference technology. The effects of Derlin1 down-regulating in CC cell lines on cell proliferation and migration were detected by CCK8 assay and transwell assay, respectively. The effect of Derlin1 down-regulating on apoptosis was analyzed by flow cytometry, and apoptosis-related proteins were detected using western blotting. In-depth mechanisms were studied using western blotting. In addition, the effects of Derlin1 up-regulating in normal cervical epithelial cells also were exposed. RESULTS: Derlin1 was significantly elevated in CC tissues (81.7%, 76/93), and the expression of Derlin1 was positively correlated with the tumor size, pathological grade, and lymph node metastasis in CC patients. And Derlin1 was high expressed in cervical cancer cell lines compared to H8 cells. Knockdown of Derlin1 in cervical cancer cell lines inhibited cell proliferation and migration. Moreover, knockdown of Derlin1 induced apoptosis and affected the expression of apoptosis-related proteins, including Bcl-2, Bax, Bim, caspase3 and caspase9. Further experiments showed that AKT/mTOR signal pathway might be involve in this processes that knockdown of Derlin1 inhibited the expression of p-AKT and p-mTOR. Over-expression of Derlin1 in H8 cells promoted cell proliferation and migration via up-regulated the expression of p-AKT and p-mTOR. CONCLUSION: Derlin1 is an oncogene in CC via AKT/mTOR pathway. It might be a potential therapeutic target for CC.

Long-term exposure to crotonaldehyde causes heart and kidney dysfunction through induction of inflammatory and oxidative damage in male Wistar rats.

Crotonaldehyde is a ubiquitous hazardous pollutant, present in cigarette smoke and automobile exhaust and is endogenously generated by lipid peroxidation. Most of the current studies focus on its lung toxicity. However, there have been few investigations on the cardiac and renal toxicity caused by crotonaldehyde exposure. We hypothesized that oral intake of crotonaldehyde can cause inflammatory and oxidative/nitrosative damage to the heart and kidneys. Therefore, we treated male rats with crotonaldehyde by gavage at 0, 2.5, 4.5, and 8.5 mg/kg/day for 120 d and evaluated the alterations in histological and serological parameters, oxidative state, and inflammation responses to explore the roles of crotonaldehyde-induced oxidative/nitrosative stress and inflammation in the heart and kidney dysfunction and to explore the relationship between heart and kidney dysfunction. We found that body weight increment, as well as heart and kidney coefficients decreased with an increasing crotonaldehyde dosage. Histological examinations indicated that crotonaldehyde exposure led to focal myocardial necrosis, cardiac fibrosis, renal tubular epithelial cell edema, and renal lymphocyte infiltration. We also assessed the impact of crotonaldehyde treatment on oxidative/nitrosative stress markers, antioxidant enzymes, inflammatory biomarkers, heart/kidney functional markers, and angiotensin II-aldosterone-brain natriuretic peptide (AngII-ALD-BNP) levels. Overall, we found that proinflammatory cytokine and malondialdehyde levels increased in a dose-dependent manner. Furthermore, crotonaldehyde treatment (4.5 and 8.5 mg/kg) significantly prevented the upregulation of antioxidant enzyme activity, thereby increasing oxidative/nitrosative stress (p < 0.05). Moreover, we found that the levels of AngII and ALD increased, whereas the levels of BNP decreased, consistent with heart and kidney dysfunction. Collectively, these results suggest that long-term, low-dose crotonaldehyde exposure leads to an imbalance in AngII-ALD-BNP levels, which mediates cardiac hemodynamic changes causing internal oxidative/nitrosative stress and inflammatory reactions, leading to renal and cardiac dysfunction in male rats.

Derlin1 functions as an oncogene in cervical cancer via AKT/mTOR signaling pathway

BACKGROUND: Cervical cancer (CC) ranks third in the morbidity and mortality of female cancer around the world. Derlin1 has been found to be overexpressed in several human cancers. However, it is still unclear about its roles in CC. The research aims to explore the relationship between Derlin1 and CC. METHODS: We purchased a human CC tissues microarray, which contained CC tissues and corresponding para-cancerous tissues from 93 patients with primary cervical squamous cell carcinoma. Immunohistochemical staining was used to confirm the expression of Derlin1 in these tissues. And we detected the differential expression of Derlin1 in cervical cancer cell lines and normal cervical epithelial cells (H8). Further, the cervical cancer cell lines SiHa and C33A were used as an in vitro model, which was down-regulated the expression of Derlin1 using siRNA interference technology. The effects of Derlin1 down-regulating in CC cell lines on cell proliferation and migration were detected by CCK8 assay and transwell assay, respectively. The effect of Derlin1 down-regulating on apoptosis was analyzed by flow cytometry, and apoptosis-related proteins were detected using western blotting. In-depth mechanisms were studied using western blotting. In addition, the effects of Derlin1 up-regulating in normal cervical epithelial cells also were exposed. RESULTS: Derlin1 was significantly elevated in CC tissues (81.7%, 76/93), and the expression of Derlin 1 was positively correlated with the tumor size, pathological grade, and lymph node metastasis in CC patients. And Derlin 1 was high expressed in cervical cancer cell lines compared to H8 cells. Knockdown of Derlin 1 in cervical cancer cell lines inhibited cell proliferation and migration. Moreover, knockdown of Derlin 1 induced apoptosis and affected the expression of apoptosis-related proteins, including Bcl-2, Bax, Bim, caspase3 and caspase9. Further experiments showed that AKT/mTOR signal pathway might be involve in this processes that knockdown of Derlin 1 inhibited the expression of p-AKT and p-mTOR. Over-expression of Derlin 1 in H8 cells promoted cell proliferation and migration via up-regulated the expression of p-AKT and p-mTOR. CONCLUSION: Derlin 1 is an oncogene in CC via AKT/mTOR pathway. It might be a potential therapeutic target for CC.

Declining Pulmonary Function in Populations with Long-term Exposure to Polycyclic Aromatic Hydrocarbons-Enriched PM2.5.

This study assesses the effects of long-term exposure to ambient air pollutants on inflammatory response and lung function. We selected 390 male coke oven workers with exposure to polycyclic aromatic hydrocarbons (PAHs) and fine particulate matter (PM2.5) and 115 control workers. The average duration in the exposed group was 9.10 years. The total amount of PAHs was more enriched in PM2.5 which collected from the coke oven workshops compared with the control areas. Correspondingly, the internal PAHs exposure indicated by urinary 1-hydroxypyrene (1-OHP) in the exposure group increased 25.7-fold compared to that of the control group. Moreover, the increasing level of urinary 1-OHP was associated with the decrease of forced expiratory volume in 1 s to forced vital capacity ratio (FEV1/FVC). In non-current smokers of exposure group, inverse correlation of 1-OHP with FEV1/FVC was also found. Particularly, an exposure duration-dependent decline in FEV1/FVC and mean forced expiratory flow between 25% and 75% of forced vital capacity (FEF25-75%) indicated that small airways were functionally obstructed. Furthermore, the increasing serum high-sensitivity C-reactive protein (hs-CRP) was correlated with the decline in pulmonary function in all subjects. These findings provide a clue that long-term exposure to PAHs-enriched PM2.5 impairs pulmonary function in occupational population.

Reduced serum club cell protein as a pulmonary damage marker for chronic fine particulate matter exposure in Chinese population.

BACKGROUND: Exposure to fine particulate matter (PM2.5) pollution is associated with increased morbidity and mortality from respiratory diseases. However, few population-based studies have been conducted to assess the alterations in circulating pulmonary proteins due to long-term PM2.5 exposure. METHODS: We designed a two-stage study. In the first stage (training set), we assessed the associations between PM2.5 exposure and levels of pulmonary damage markers (CC16, SP-A and SP-D) and lung function in a coke oven emission (COE) cohort with 558 coke plant workers and 210 controls. In the second stage (validation set), significant initial findings were validated by an independent diesel engine exhaust (DEE) cohort with 50 DEE exposed workers and 50 controls. RESULTS: Serum CC16 levels decreased in a dose response manner in association with both external and internal PM2.5 exposures in the two cohorts. In the training set, serum CC16 levels decreased with increasing duration of occupational PM2.5 exposure history. An interquartile range (IQR) (122.0µg/m3) increase in PM2.5 was associated with a 5.76% decrease in serum CC16 levels, whereas an IQR (1.06µmol/mol creatinine) increase in urinary 1-hydroxypyrene (1-OHP) concentration was associated with a 5.36% decrease in serum CC16 levels in the COE cohort. In the validation set, the concentration of serum CC16 in the PM2.5 exposed group was 22.42% lower than that of the controls and an IQR (1.24µmol/mol creatinine) increase in urinary 1-OHP concentration was associated with a 12.24% decrease in serum CC16 levels in the DEE cohort. CONCLUSIONS: Serum CC16 levels may be a sensitive marker for pulmonary damage in populations with high PM2.5 exposure.

A genetic variant of miR-335 binding site in the ERBB4 3'-UTR is associated with prognosis of ovary cancer.

Ovarian cancer is one of the leading gynecologic malignancies globally, the 5-year survival rate for patients with advanced stage ovarian cancer is very low. Our objective was to test the hypothesis that miR-335 was associated with the survival of patients with ovarian cancer. Bioinformatics tools and luciferase report assay were used to select the target of miR-335, and real-time PCR was used to detect the expression of miR-335 and ERBB4 in different genotype groups. Finally, Cox regression and Kaplan-Meier analyses were used to assess the relationship of ERBB4 genotype and survival of ovary cancer. Firstly, individuals carried ERBB4 rs186724 GG genotype had poorer overall survival compared with those carried CC/CT genotypes in ovarian cancer, while the participants with rs1836724 GA genotype had the same overall survival with that in participants with rs1836724 AA genotype in accordance with the result of Cox regression and Kaplan-Meier analyses. Then according to result of the in-silicon analysis, ERBB4 was the target of miR-335, and rs1836724 was located on 3'UTR of ERBB4, the binding site of miR-335, and miR-335 inhibited the expression of ERBB4 and this regulation was more suppressed when the G allele replaced by the variant A allele. Finally, miR-335 was similar among GG, GA, and AA groups, and ERBB4 level was higher in GG group. Finally, malignant grade is apparently higher in GG group than the other group. The data indicated that the ERBB4 rs1836724 polymorphism was associated with the survival of ovarian cancer.

Analysis of Blood Concentrations of Zinc, Germanium, and Lead and Relevant Environmental Factors in a Population Sample from Shandong Province, China.

Trace elements, including zinc (Zn) and germanium (Ge), are essential for health; deficiency or excess levels of trace elements results is harmful. As a result of industrial and agricultural production, Pb widely exists in people's living environment. It is absorbed mainly through the respiratory and digestive tracts, producing systemic harm. Reference values for a normal, healthy population are necessary for health assessment, prevention and treatment of related diseases, and evaluation of occupational exposures. Reference ranges for the Chinese population have not been established. From March 2009 to February 2010; we collected data and blood samples (n = 1302) from residents aged 6-60 years living in Shandong Province, China. We measured blood concentrations of Zn, Ge, and Pb using inductively coupled plasma mass spectrometry to determine reference ranges. Results were stratified by factors likely to affect the concentrations of these trace elements: sex, use of cosmetics or hair dye, age, alcohol intake, smoking habits, and consumption of fried food. The overall geometric mean (GM) concentrations (95% confidence interval) were 3.14 (3.08-3.20) mg/L for Zn, 19.9 (19.3-20.6) µg/L for Ge, and 24.1 (23.2-25.1) µg/L for Pb. Blood Zn concentrations were higher in women than in men (p < 0.001), while the opposite was found for Pb (p < 0.001) and sex did not influence Ge (p = 0.095). Alcohol use was associated with higher blood concentrations of Zn (p = 0.002), Ge (p = 0.002), and Pb (p = 0.001). The GM concentration of Zn was highest in 20-30-year-olds (p < 0.001), while Pb concentrations were highest in 12-16-year-olds (p < 0.001). Use of hair dye was associated with lower blood concentrations of Ge (p < 0.05). GM blood concentrations of Pb differed significantly between those who consumed fried foods 1-2 times/month (18.7 µg/L), 1-2 times/week (20.9 µg/L), and every day (28.5 µg/L; p < 0.001). Blood Pb concentrations were higher in subjects who used cosmetics (p < 0.05), hair dye (p < 0.05), and who smoked cigarettes (p < 0.001) than in those who did not.

Inhibition of gap junction intercellular communication is involved in silica nanoparticles-induced H9c2 cardiomyocytes apoptosis via the mitochondrial pathway.

Gap junction intercellular communication (GJIC) between cardiomyocytes is essential for synchronous heart contraction and relies on connexin-containing channels. Connexin 43 (Cx43) is a major component involved in GJIC in heart tissue, and its abnormal expression is closely associated with various cardiac diseases. Silica nanoparticles (SNPs) are known to induce cardiovascular toxicity. However, the mechanisms through which GJIC plays a role in cardiomyocytes apoptosis induced by SNPs remain unknown. The aim of the present study is to determine whether SNPs-decreased GJIC promotes apoptosis in rat cardiomyocytes cell line (H9c2 cells) via the mitochondrial pathway using CCK-8 Kit, scrape-loading dye transfer technique, Annexin V/PI double-staining assays, and Western blot analysis. The results showed that SNPs elicited cytotoxicity in H9c2 cells in a time- and concentration-dependent manner. SNPs also reduced GJIC in H9c2 cells in a concentration-dependent manner through downregulation of Cx43 and upregulation of P-Cx43. Inhibition of gap junctions by gap junction blocker carbenoxolone disodium resulted in decreased survival and increased apoptosis, whereas enhancement of the gap junctions by retinoic acid led to enhanced survival but decreased apoptosis. Furthermore, SNPs-induced apoptosis through the disrupted functional gap junction was correlated with abnormal expressions of the proteins involved in the mitochondrial pathway-related apoptosis such as Bcl-2/Bax, cytochrome C, Caspase-9, and Caspase-3. Taken together, our results provide the first evidence that SNPs-decreased GJIC promotes apoptosis in cardiomyocytes via the mitochondrial pathway. In addition, downregulation of GJIC by SNPs in cardiomyocytes is mediated through downregulation of Cx43 and upregulation of P-Cx43. These results suggest that in rat cardiomyocytes cell line, GJIC plays a protective role in SNPs-induced apoptosis and that GJIC may be one of the targets for SNPs-induced biological effects.

Evaluation of prognostic factors for secondary cytoreductive surgery in Chinese patients with recurrent epithelial ovarian carcinoma.

OBJECTIVE: Secondary cytoreductive surgery (SCS) is reported to be beneficial for patients with recurrent epithelial ovarian carcinoma (EOC). The current study is to evaluate risk factors that would affect the surgical optimal resection rate and prognosis of recurrent EOC after SCS in Chinese patients. METHODS: In our study, 44 patients with recurrent EOC treated with SCS at Shandong Cancer Hospital were retrospectively reviewed. Patient characteristics were collected and multivariate logistic regression was used to analyze factors that affect the optimal surgical resection rate. The overall survival rate was calculated by the Kaplan-Meier method. Cox proportional-hazards regression was used to analyze risk factors that affect the overall survival of these patients. RESULTS: 90.9% (40/44) patients achieved optimal cytoreductive surgery. Logistic regression did not find any factor that affects the optimal surgical resection rate. Among 24 cases that received chemotherapy before SCS, 18 cases achieved good response and thus had a better survival rate after SCS. Multivariate Cox proportional hazard regression analysis indicated that differentiation, the extent of surgical resection during the initial surgery, and course and efficacy of chemotherapy prior to SCS, and efficacy of chemotherapy after the first recurrence significantly correlated with survival of patients with recurrent cancer (P < 0.05; OR < 1). CONCLUSION: Selection of patients that are suitable to perform SCS will enhance the optimal surgical resection rate. The prognosis of Chinese patients with recurrent EOC after SCS is affected by histologic grade, the extent of residual disease and the effect of chemotherapy after first relapse.

Malathion-induced testicular toxicity is associated with spermatogenic apoptosis and alterations in testicular enzymes and hormone levels in male Wistar rats.

Malathion has a broad range of toxicities while its reproductive effects have not been fully elucidated. In this study, we treated animals with malathion by gavage at doses of 0, 33.75, 54, and 108 mg/kg for 60 days and evaluated the alterations in histology, biochemistry and serology. Malathion caused the reduction in the sperm counts and motility. The reduced body and testis weights were coupled with mild to severe degenerative changes in seminiferous tubules. We found malathion at 54 mg/kg increased spermatogenic apoptosis rate which was confirmed by changes in protein expression of Bax and Bcl-2. The activities of testicular enzymes including ACP, LDH and γ-GT were significantly altered with the reduced level of reproductive hormones such as LH, FSH and T. These results indicate that malathion can elicit deleterious effects on reproductive system of rats. The abnormal levels of hormones and apoptotic proteins induced by malathion may play important roles.

[Expression of heat shock protein 70 and its mRNA in career exposure to manganese].

OBJECTIVE: To analyze the expression levels of heat shock protein70 (HSPs70) and HSPs70 mRNA in different exposure to manganese, and research the neuroprotective effect on the career exposure to manganese. METHODS: From 2008 to 2009, with cross-sectional study design, and in a locomotive and rolling stock works, by stratified random sampling method, the exposed sample consisted of 180 welders from different welding shops and 100 unexposed in the last three years, non-welder controls with age-matched workers of similar socioeconomic status from the same industry. The control workers had not been exposed to neurotoxic chemicals. The mRNA expressions of four different metabolic enzyme were detected by SYBR Green I quantitative real-time polymerase chain reaction. The expression levels of the two enzymes mRNA in different exposure to manganese were analyzed. The expressions of HSPs70 were detected by Western blot. The concentration of air manganese was determined by GFAAS. The average concentration of 8 h time (8h-TWA) was used to express the level of individual exposure to manganese, according to the air manganese workplace occupational exposure limit (8h-TWA=0.15 mg/m3), the exposed group is divided into high exposed group (>0.15 mg/m3) and low exposure group (<0.15 mg/m3). RESULTS: The individuals exposed to manganese dose of exposed group ((0.25±0.31) mg/m3) was higher than the control group ((0.06±0.02) mg/m3) (t=6.15, P=0.001); individuals exposed to manganese dose of high exposure group for (0.42±0.34) mg/m3, which was higher than low exposure group (0.09±0.07) mg/m3 (t=9.80, P=0.001). HSPs70 mRNA and protein of exposure group (5.65±0.21, 3.26±0.15) were higher than the reference group (0.41±0.03, 1.32±0.12) (t=18.91, t=8.68, P=0.001). HSP70 mRNA and protein of high exposure group (6.48±0.37, 3.67±0.26) were higher than the low exposure group (5.15±0.23, 3.02±0.19) (t=3.24, t=2.01, P=0.003, P=0.043). CONCLUSION: The expression of peripheral blood lymphocytes HSPs70 level and HSPs70 mRNA workers exposed to manganese increased and protect nerve cells from related to Mn stimulation induced lipid peroxidation damag.

Effects of formaldehyde on lymphocyte subsets and cytokines in the peripheral blood of exposed workers.

Formaldehyde (FA) is a well-known irritant, and it is suggested to increase the risk of immune diseases and cancer. The present study aimed to evaluate the distribution of major lymphocyte subsets and cytokine expression profiles in the peripheral blood of FA-exposed workers. A total of 118 FA-exposed workers and 79 controls were enrolled in the study. High performance liquid chromatography, flow cytometry, and cytometric bead array were used to analyze FA in air sample and formic acid in urine, blood lymphocyte subpopulations, and serum cytokines, respectively. The FA-exposed workers were divided into low and high exposure groups according to their exposure levels. The results showed that both the low and high FA-exposed groups had a significant increase of formic acid in urine when compared to the controls. Both the low and high exposure groups had a significant increase in the percentage of B cells (CD19+) compared to the control group (p<0.01). A significant increase in the percentage of the natural killer (NK) cells (CD56+) was observed in the low exposure group compared to the control (p = 0.013). Moreover, the FA-exposed workers in both exposure groups showed a significant higher level of IL-10 but lower level of IL-8 than the control (p<0.01). Subjects in the high exposure group had a higher level of IL-4 but a lower level of IFN-γ than the control (p<0.05). Finally, there is a significant correlation between the levels of IL-10, IL-4, and IL-8 and formic acid (p<0.05). The findings from the present study may explain, at least in part, the association between FA exposure and immune diseases and cancer.

[Influence of genetic polymorphisms of epoxide hydrolase 1 on metabolism of styrene in body].

OBJECTIVE: To investigate the role of genetic polymorphisms of epoxide hydrolase 1 (EPHX1) in the metabolism of styrene in vivo. METHODS: Fifty-six styrene-exposed workers, who worked in the painting workshop of an enterprise for manufacturing glass fiber-reinforced plastic yachts in Shandong Province, China for over one year and were protected in approximately the same way, were selected as study subjects. The 8-hour time-weighted average concentration (8 h-TWA) of styrene and the concentrations of mandelic acid (MA) and phenyl glyoxylic acid (PGA) as urinary metabolites were measured. The genetic polymorphisms of EPHX1 were detected by polymerase chain reaction-restriction fragment length polymorphism analysis. RESULTS: The urinary concentrations of MA and PGA were 177.25±82.36 mg/g Cr and 145.91±69.73 mg/g Cr, respectively, and the 8 h-TWA of styrene was 133.28±95.81 mg/m3. Urinary concentrations of MA and PGA were positively correlated with 8 h-TWA of styrene (R=0.861, P < 0.05; R=0.868, P < 0.05). The subjects were divided into high-exposure group (8 h-TWA >50 mg/m(3)) and low-exposure group (8 h-TWA ≤ 50 mg/m(3), and in the two groups, the urinary concentrations of MA and PGA were significantly higher in the individuals carrying high-activity genotypes of EPHX1 than in those carrying low-activity genotypes of EPHX1 (P < 0.05). CONCLUSION: Genetic polymorphisms of EPHX1 play an important role in the metabolic process of styrene in vivo.