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Objective: To investigate the influence and critical windows of prenatal exposure to pyrethroid pesticides (PYRs) on neurodevelopment of 2-year-old children. Methods: The subjects of this study were derived from the Xuanwei Birth Cohort. A total of 482 pregnant women who participated in the rural district of Xuanwei birth cohort from January 2016 to December 2018 were included. Maternal urinary concentrations of PYRs metabolites during 8-12 gestational weeks, 20-23 gestational weeks and 32-35 gestational weeks were measured with ultra high performance liquid chromatography system coupled with a tandem mass spectrometry detector. Child neurodevelopment was evaluated with the Bayley Scales of Infant and Toddler Development-Third Edition at 2 years of age. Multivariate linear regression models and binary logistic regression models were used to assess the association between PYRs exposure during pregnancy and children's neurodevelopment. Results: A total of 360 mother-child pairs had complete data on maternal urinary PYRs metabolites detection and children's neurodevelopment assessment. The detection rate of any one PYRs metabolites during the first, second and third trimester were 93.6% (337/360), 90.8% (327/360) and 94.2% (339/360), respectively. The neurodevelopmental scores of Cognitive, Language, Motor, Social-Emotional, and Adaptive Behavior of 2-year-old children were (102.3±18.9), (100.2±16.3), (102.0±20.3), (107.8±23.3) and (85.8±18.6) points, respectively. After controlling for confounding factors, 4-fluoro-3-phenoxybenzoic acid (4F3PBA, one of PYRs metabolites) exposure in the first trimester reduced Motor (β=-5.02, 95%CI: -9.08, -0.97) and Adaptive Behavior (β=-4.12, 95%CI:-7.92, -0.32) scores of 2-year-old children, and increased risk of developmental delay of adaptive behavior (OR=2.07, 95%CI:1.13-3.82). Conclusion: PYRs exposure during the first trimester of pregnancy may affect neurodevelopment of 2-year-old children, and the first trimester may be the critical window.
Subject(s)
Child, Preschool , Female , Humans , Infant , Pregnancy , Birth Cohort , Child Development , Cohort Studies , Maternal Exposure/adverse effects , Pesticides/adverse effects , Pregnancy Trimester, Third , Prenatal Exposure Delayed Effects/chemically induced , Pyrethrins/metabolismABSTRACT
Objective To investigate the level and relevant factors of pyrethroid pesticide exposure among pregnant women during the first trimester in rural areas of Yunnan province,and to provide basic data for further study and provide a basis for the formulation of intervention measures to reduce exposure.Methods According to the birth cohort of rural Yunnan built in 2014, pregnant women in the first trimester were recruited in two townships of an agricultural county who were confirmed pregnant and continued pregnancy in antenatal clinics. The concentration of the metabolites of the pesticides in the urine of women was determined by super high performance liquid chromatography and the contact status of pyrethroid pesticides was analyzed using a questionnaire survey. Results A total of 419 women in the first trimester were surveyed and 94.51% of women detected at least one of the pyrethroid metabolites, among which the detection rates of 3－Phenoxybenzoic acid (3－PBA), cis－/trans－3－ (2, 2－Dichloroethenyl)－2, 2－dimethyl－cyclopropanecarboxylate (cis－/trans－DCCA) and 4－fluoro－3－phenoxybenzoic acid (4－F－3－PBA) were 79.47%, 62.05% and 24.58%,and the median concentrations were 3.53 ng/mL, 14.80 ng/m L and less than the minimum detection limit 0.4 ng/m L.Only 12 people (2.95%) reported that they had exposure to pesticides.Self－reported exposure rate was not consistent with the actual exposure rate.Multivariate linear regression analysis showed that the season was a factor affecting the level of three metabolites in women in the first trimester. Higher lever was found in women in spring (t=2.147,P=0.032), summer (t=2.144,P=0.035) and winter (t=2.453,P=0.015) compared to those in autumn.Conclusion Pyrethroid pesticides were widely exposed in the pregnant women in rural areas of Yunnan province. Some women have higher exposure level, which is related to the season.
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Objective:To better understand the pathogenesis of obstructive jaundice (O J),a variety of rat OJ and biliary drainage models have been tried;however,complications are still common.We aimed to establish a stable rat model of OJ using microsurgical techniques,and to assess its reversal by internal bile drainage(IBD).Methods:After the pilot study,we developed a standardized surgical procedure.All operations were carried out under an operating microscope.In the first laparotomy,the proximal common bile duct (CBD) of the rat was ligated and transected.A tube was introduced into the distal end of the duct,and the other end of the tube was sealed and fixed.In the second laparotomy,the drainage tube was inserted into the (by now markedly dilated) proximal CBD,and ligated into position.We evaluated the general condition of the rats,the status of the liver and pancreas before and after IBD.Results:Complications such as intestinal reflux and bile duct blockage,were not found.Pancreatic injury was not evident by day 4 after the first laparotomy.After biliary drainage,the serum glucose and albumin concentration rapidly returned to normal levels.Liver weight/body weight ratio increased.The biochemical indicators and ultrasonographic elastography results for the liver gradually returned to normal.Conclusion:Using microsurgical techniques,we have developed a stable rat model of OJ reversed by IBD.
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OBJECTIVE: To study the effect of valdecoxib and pirarubicina combination on cell cycle and apoptosis of human lung cancer A549 cell line in vitro. METHODS: MTT assay was used to analyze the effect of valdecoxib and pirarubicina on the growth of human lung cancer A549 cell line. The median-effect principle was applied to determine the combination effect of valdecoxib and pirarubicina. Flow cytometry (FCM) was used to observe the cell cycle and apoptosis. The expressions of Bcl-2, Bax, and Caspase-3 were detected by western blotting. RESULTS: The inhibition ratio of A549 cell in valdecoxib and pirarubicina combination group was increased compared with their respective application, and CI<1. In valdecoxib and pirarubicina combination group, the apoptosis rate and the expression of Bax and Caspase-3 was increased, and the expression of Bcl-2 was decresed. CONCLUSION: Valdecoxib and pirarubicina combination has synergistic effect, which is partly due to the increase of the apoptosis rate.
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<p><b>OBJECTIVE</b>To evaluate the underestimation of papillary breast lesions diagnosed at ultrasound-guided breast biopsy.</p><p><b>METHODS</b>Totally 4453 ultrasound-guided visible breast lesions that were identified in the Department of Ultrasound, Chinese PLA General Hospital, from April 2005 to April 2012 were retrospectively reviewed. Of 207 papillary lesions that were detected by histologic findings of ultrasound-guided core needle biopsy(US-CNB), 90 underwent surgical excision, 110 were followed up for at least one year, and 7 were lost to follow-up. The histological findings of the US-CNB and the findings of surgical excision were compared to analyze the underestimation rates according to the Breast Imaging Reporting and Data System(BI-RADS)categories of American College of Radiology(ACR)and biopsy methods.</p><p><b>RESULTS</b>Of the 90 papillary lesions underwent surgical excision, 29(32.2%)were underestimated, and 22 malignant lesions were underestimated(24.4%). Of the 23 papillomata with atypical ductal hyperplasia(IDP+ADH), 11(47.8%)were upgraded to malignant. Of the 137 benign intraductal papilloma(IDP)with concordance imaging-histologic findings, 8 lesions were underestimated(5.8%), whereas 10 out of 25(40.0%)IDP with diacordant imaging-histologic findings were underestimated. In total, 17.9% understimation were biopsied by 18G core needle biopsy(CNB)(P=0.017)and 16.0% by 16G CNB(P=0.023), which were significantly higher than vacuum-assisted biopsy(VAB).</p><p><b>CONCLUSIONS</b>VAB is more accurate than 16G or 18G CNB in detecting papillary breast lesions. For high underestimations of IDP+ADH and IDP with discordant imaging-histologic findings, VAB or surgical excisions should be performed.</p>
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Female , Humans , Biopsy, Needle , Methods , Breast , Breast Neoplasms , Diagnosis , Hyperplasia , Retrospective Studies , Ultrasonography, MammaryABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of rosuvastatin on monocrotaline (MCT)-induced pulmonary artery hypertension in rats.</p><p><b>METHODS</b>Pulmonary arterial hypertension was induced by a single subcutaneous injection of monocrotaline (50 mg/kg) in rats. In the prevention protocol, 32 male Sprague-Dawley rats were randomly divided into four groups (n = 8 each): low-dose rosuvastatin prevention group (2 mg×kg(-1)×d(-1)), high-dose rosuvastatin prevention group (10 mg×kg(-1)×d(-1)), pulmonary arterial hypertension group, normal control group. Beginning on the MCT injection day, rats were treated with rosuvastatin by daily gavage for 4 weeks. Normal control group and pulmonary arterial hypertension group received vehicle by gavage. In the treatment protocol, 52 male Sprague-Dawley rats were randomly divided into four groups (n = 13 each): low-dose rosuvastatin treatment group (2 mg×kg(-1)×d(-1)), high-dose rosuvastatin treatment group (10 mg×kg(-1)×d(-1)), pulmonary arterial hypertension group, normal control group. Four weeks after MCT injection, rats were treated with rosuvastatin by daily gavage for 4 weeks. Normal control group and pulmonary arterial hypertension group received vehicle by gavage. At the end of study, survival rates, mean pulmonary arterial pressure (mPAP), wall thickness of small pulmonary artery and right ventricular hypertrophy among groups were compared. The expression levels of proliferating cell nuclear antigen (PCNA) and endothelial nitricoxide synthase (eNOS) protein in small pulmonary artery, the expression levels of Rho kinase 1(ROCK-1) and eNOS mRNA in lung tissue were also detected.</p><p><b>RESULTS</b>All rats in the prevention protocol survived. Rosuvastatin treatment improved survival in the treatment protocol (58%, 75% vs.30%, P < 0.05). Rosuvastatin therapy in both preventive or treatment protocols significantly lowered mPAP [prevention protocol: (27.53 ± 3.43), (25.72 ± 1.76) vs. (36.05 ± 2.45) mm Hg (1 mm Hg = 0.133 kPa), P < 0.01; treatment protocol: (30.39 ± 3.17), (27.59 ± 1.99) vs. (40.68 ± 1.39) mm Hg, P < 0.01], reduced thickening of small pulmonary artery wall (P < 0.01) and right ventricular hypertrophy (P < 0.01). Rosuvastatin also inhibited PCNA expression of SMC (P < 0.01), restored eNOS expression of EC (P < 0.05) and inhibited ROCK-1 mRNA expressions in lung tissue (P < 0.05).</p><p><b>CONCLUSIONS</b>Rosuvastatin therapy reduced mPAP in monocrotaline-induced pulmonary arterial hypertension rat model and this effect is linked with inhibition of ROCK-1 expression, inhibition of smooth muscle cell proliferation and restoration of endothelial cell functions.</p>