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971.
Maria A. Herreros Antonio Gonzalez-Bulnes Silvia Iñigo-Nuñez Ignacio Contreras-Solis Jose M. Ros Teresa Encinas 《Reproductive biology》2013,13(1):66-74
The aim of the present study was to determine the toxicokinetics of short-term exposures to di(2-ethylhexyl) phthalate (DEHP) and its effects on ovarian cyclicity and luteal function using a sheep experimental model. For establishing the model, we examined the clearance of DEHP after intravenous (i.v.) and intramuscular (i.m.) administration of a single dose of 25 mg/kg body weight (b.w.) and after i.m. administration of two different doses (25 and 50 mg/kg b.w.; DEHP25 and DEHP50, respectively) three times a week for two months. Results showed a significant, dose-dependent effect of DEHP administration, when compared to the control group (CTL; untreated ewes; n = 6), on the duration of the ewes’ estrous cycles (17.1 ± 0.5 days, CTL; 15.1 ± 0.9 days, DEHP25; 12.0 ± 0.8 days, DEHP50; p < 0.05); 94.9% of the cycles were of regular duration (15–19 days) in CTL, but only 51.1% and 25.4% in DEHP25 and DEHP50, respectively. Corpora lutea (CL) were smaller in DEHP50 than in DEHP25 (p < 0.05) and were smaller in both groups than in CTL (p < 0.005), but the maximum plasma concentrations of progesterone were greater (p < 0.05) in DEHP25 and DEHP50 than in CTL. In conclusion, the exposure of cycling ewes to DEHP causes shortening of the ovulatory cycles due mainly to a reduction in the size and lifespan of CL. However, the exposure to the phthalate is also associated with an increase in circulating concentrations of progesterone, suggesting the influence of DEHP on steroid metabolism. 相似文献
972.
973.
Michael R. Blatt Adrian Hills Zhong-Hua Chen Yizhou Wang Maria Papanatsiou Vigilio L. Lew 《Plant signaling & behavior》2013,8(1)
Much of the 70% of global water usage associated with agriculture passes through stomatal pores of plant leaves. The guard cells, which regulate these pores, thus have a profound influence on photosynthetic carbon assimilation and water use efficiency of plants. We recently demonstrated how quantitative mathematical modeling of guard cells with the OnGuard modeling software yields detail sufficient to guide phenotypic and mutational analysis. This advance represents an all-important step toward applications in directing “reverse-engineering” of guard cell function for improved water use efficiency and carbon assimilation. OnGuard is nonetheless challenging for those unfamiliar with a modeler’s way of thinking. In practice, each model construct represents a hypothesis under test, to be discarded, validated or refined by comparisons between model predictions and experimental results. The few guidelines set out here summarize the standard and logical starting points for users of the OnGuard software. 相似文献
974.
Jenny Hill Jenna Hoyt Anna Maria van Eijk Lauren D'Mello-Guyett Feiko O. ter Kuile Rick Steketee Helen Smith Jayne Webster 《PLoS medicine》2013,10(7)
Background
Malaria in pregnancy has important consequences for mother and baby. Coverage with the World Health Organization–recommended prevention strategy for pregnant women in sub-Saharan Africa of intermittent preventive treatment in pregnancy (IPTp) and insecticide-treated nets (ITNs) is low. We conducted a systematic review to explore factors affecting delivery, access, and use of IPTp and ITNs among healthcare providers and women.Methods and Results
We searched the Malaria in Pregnancy Library and Global Health Database from 1 January 1990 to 23 April 2013, without language restriction. Data extraction was performed by two investigators independently, and data was appraised for quality and content. Data on barriers and facilitators, and the effect of interventions, were explored using content analysis and narrative synthesis. We conducted a meta-analysis of determinants of IPTp and ITN uptake using random effects models, and performed subgroup analysis to evaluate consistency across interventions and study populations, countries, and enrolment sites. We did not perform a meta-ethnography of qualitative data.Ninety-eight articles were included, of which 20 were intervention studies. Key barriers to the provision of IPTp and ITNs were unclear policy and guidance on IPTp; general healthcare system issues, such as stockouts and user fees; health facility issues stemming from poor organisation, leading to poor quality of care; poor healthcare provider performance, including confusion over the timing of each IPTp dose; and women''s poor antenatal attendance, affecting IPTp uptake. Key determinants of IPTp coverage were education, knowledge about malaria/IPTp, socio-economic status, parity, and number and timing of antenatal clinic visits. Key determinants of ITN coverage were employment status, education, knowledge about malaria/ITNs, age, and marital status. Predictors showed regional variations.Conclusions
Delivery of ITNs through antenatal clinics presents fewer problems than delivery of IPTp. Many obstacles to IPTp delivery are relatively simple barriers that could be resolved in the short term. Other barriers are more entrenched within the overall healthcare system or socio-economic/cultural contexts, and will require medium- to long-term strategies. Please see later in the article for the Editors'' Summary 相似文献975.
Maria Rohm Anke Sommerfeld Daniela Strzoda Allan Jones Tjeerd P. Sijmonsma Gottfried Rudofsky Christian Wolfrum Carsten Sticht Norbert Gretz Maximilian Zeyda Lukas Leitner Peter P. Nawroth Thomas M. Stulnig Mauricio Berriel Diaz Alexandros Vegiopoulos Stephan Herzig 《Cell metabolism》2013,17(4):575-585
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976.
Maria Cecilia Rey Moreno Karma C. Fussell Sibylle Gröters Steffen Schneider Volker Strauss Stefan Stinchcombe Ivana Fegert Mariana Veras Bennard van Ravenzwaay 《Birth defects research. Part B, Developmental and reproductive toxicology》2013,98(3):208-221
Epoxiconazole (CAS‐No. 133855‐98‐8) was recently shown to cause both a marked depletion of maternal estradiol blood levels and a significantly increased incidence of late fetal mortality when administered to pregnant rats throughout gestation (GD 7–18 or 21); estradiol supplementation prevented this epoxiconazole effect in rats (Stinchcombe et al., 2013), indicating that epoxiconazole‐mediated estradiol depletion is a critical key event for induction of late fetal resorptions in rats. For further elucidation of the mode of action, the placentas from these modified prenatal developmental toxicity experiments with 23 and 50 mg/kg bw/d epoxiconazole were subjected to a detailed histopathological examination. This revealed dose‐dependent placental degeneration characterized by cystic dilation of maternal sinuses in the labyrinth, leading to rupture of the interhemal membrane. Concomitant degeneration occurred in the trophospongium. Both placentas supporting live fetuses and late fetal resorptions were affected; the highest degree of severity was observed in placentas with late resorptions. Placental degeneration correlated with a severe decline in maternal serum estradiol concentration. Supplementation with 0.5 and 1.0 μg of the synthetic estrogen estradiol cyclopentylpropionate per day reduced the severity of the degeneration in placentas with live fetuses. The present study demonstrates that both the placental degeneration and the increased incidence of late fetal resorptions are due to decreased levels of estrogen, since estrogen supplementation ameliorates the former and abolishes the latter. Birth Defects Res (Part B) 98:208–221, 2013. © 2013 Wiley Periodicals, Inc. 相似文献
977.
Steffen Schneider Thomas Hofmann Stefan Stinchcombe Maria Cecilia Rey Moreno Ivana Fegert Volker Strauss Sibylle Gröters Eric Fabian Jutta Thiaener Karma C. Fussell Bennard van Ravenzwaay 《Birth defects research. Part B, Developmental and reproductive toxicology》2013,98(3):230-246
Epoxiconazole, a triazole‐based fungicide, was tested in toxicokinetic, prenatal and pre‐postnatal toxicity studies in guinea pigs, following oral (gavage) administration at several dose levels (high dose: 90 mg/kg body weight per day). Maternal toxicity was evidenced by slightly increased abortion rates and by histopathological changes in adrenal glands, suggesting maternal stress. No compound‐related increase in the incidence of malformations or variations was observed in the prenatal study. In the pre‐postnatal study, epoxiconazole did not adversely affect gestation length, parturition, or postnatal growth and development. Administration of epoxiconazole did not alter circulating estradiol levels. Histopathological examination of the placentas did not reveal compound‐related effects. The results in guinea pigs are strikingly different to those observed in pregnant rats, in which maternal estrogen depletion, pathological alteration of placentas, increased gestation length, late fetal death, and dystocia were observed after administration of epoxiconazole. In the studies reported here, analysis of maternal plasma concentrations and metabolism after administration of radiolabeled epoxiconazole demonstrated that the different results in rats and guinea pigs were not due to different exposures of the animals. A comprehensive comparison of hormonal regulation of pregnancy and birth in murid rodents and primates indicates that the effects on pregnancy and parturition observed in rats are not applicable to humans. In contrast, the pregnant guinea pig shares many similarities to pregnant humans regarding hormonal regulation and is therefore considered to be a suitable species for extrapolation of related effects to humans. Birth Defects Res (Part B) 98:230–246, 2013. © 2013 Wiley Periodicals, Inc. 相似文献
978.
Marion Sourisseau Maria L. Michta Chati Zony Benjamin Israelow Sharon E. Hopcraft Christopher M. Narbus Ana Parra Martín Matthew J. Evans 《PLoS pathogens》2013,9(3)
Hepatitis C virus (HCV) is a major cause of liver disease worldwide. A better understanding of its life cycle, including the process of host cell entry, is important for the development of HCV therapies and model systems. Based on the requirement for numerous host factors, including the two tight junction proteins claudin-1 (CLDN1) and occludin (OCLN), HCV cell entry has been proposed to be a multi-step process. The lack of OCLN-specific inhibitors has prevented a comprehensive analysis of this process. To study the role of OCLN in HCV cell entry, we created OCLN mutants whose HCV cell entry activities could be inhibited by antibodies. These mutants were expressed in polarized HepG2 cells engineered to support the complete HCV life cycle by CD81 and miR-122 expression and synchronized infection assays were performed to define the kinetics of HCV cell entry. During these studies, OCLN utilization differences between HCV isolates were observed, supporting a model that HCV directly interacts with OCLN. In HepG2 cells, both HCV cell entry and tight junction formation were impaired by OCLN silencing and restored by expression of antibody regulatable OCLN mutant. Synchronized infection assays showed that glycosaminoglycans and SR-BI mediated host cell binding, while CD81, CLDN1 and OCLN all acted sequentially at a post-binding stage prior to endosomal acidification. These results fit a model where the tight junction region is the last to be encountered by the virion prior to internalization. 相似文献
979.
980.