Background: The Wnt signaling pathway is a conserved pathway and plays a crucial role in regulating trophoblast functions. Abnormal expression of the Wnt pathway may result in the dysfunction of the trophoblast that can contribute to the pathogenesis of preeclampsia (PE). However, published data regarding the association between Wnt pathway and PE in human pregnancy is rare. Objective: The aims of this study were to investigate the expression pattern of Wnt2 and secreted frizzled-related protein 4 (sFRP4) in the third trimester human placenta and to evaluate the relationship between changes in placental Wnt2 and sFRP4 expression and severe PE. Methods: The expression of Wnt2 and sFRP4 in normal and severe PE placentas was examined using immunohistochemistry (IHC), real-time polymerase chain reaction, and Western blot. Results: Compared to the controls, the relative expression of Wnt2 messenger RNA was remarkably downregulated in the PE placentas, while there was no significant difference in sFRP4 between the 2 groups. The IHC indicated that Wnt2 and sFRP4 were expressed predominantly in the villous syncytiotrophoblast and the extravillous trophoblast, whereas Wnt2 in the control group showed higher staining intensity than in the PE group, and sFRP4 in the PE group had a higher staining intensity than in the control group. Furthermore, the results of the Western blots were consistent with the IHC. Conclusions: The Wnt signaling pathway was detected in human third trimester placentas, and the decreased placental expression of Wnt2 and increased placental expression of sFRP4 may be associated with the pathogenesis of severe PE.

This paper aims to reveal the relationship and structure of library and information science (LIS) journals in China. 24 core LIS journals in China are selected and the relevant data of journal co-citation are retrieved from Chinese Journal Full-Text Database constructed by China National Knowledge Infrastructure during the period of 1999-2009. By calculating mean co-citation frequencies and correlation coefficients, we find that there is a strong relationship among LIS journals in China. Utilizing the methods of cluster analysis, multidimensional scaling analysis and factor analysis, we analyze the data of journal co-citation. LIS journals in China are divided into four clusters. The relatedness among journals is shown manifestly through their locations in the two-dimensional map. A three-factor solution is obtained with the factor loading of each journal. Finally, we interpret and discuss the results to get some conclusions and also expect to describe the network characters of journal co-citation in future research.

Hormones, notably estrogens, are pivotal in the origins of breast cancer but androgenic effects, while supported by persistence of AR expression in breast cancers, remain controversial. This study determined the role of the androgen actions via androgen receptor (AR) in experimental mammary cancer. Androgen-resistant female and male mice (ARKO) were generated using Cre/loxP technique and featured a global AR inactivation. The effect of AR inactivation and influence of genetic background on 7,12-dimethylbenz[a]anthracene (DMBA)-induced tumorigenesis was confirmed using two separate ARKO models with different genetic backgrounds. The onset of palpable mammary tumors was significantly faster in ARKO females (median time 22 vs 34 weeks, respectively; (p = 0.0024; multivariate Cox regression) compared to WT and independent of the mouse genetic background. The cumulative incidence at 9 months was 81 ± 10% [mean ± SE] for ARKO compared to 50 ± 13% in WT females. The increased DMBA susceptibility of ARKO females was associated with a higher epithelial proliferation index but not with major structural or receptor (estrogen or progesterone) expression differences between the virgin WT or ARKO female mammary glands. AR inactivation allowed substantial ductal extension in ARKO males while WT males displayed only rudimentary epithelial branches or complete regression of epithelial structures. Yet, DMBA did not induce epithelial mammary tumors in WT or ARKO males, demonstrating that AR inactivation alone is insufficient to promote mammary tumors. These results demonstrate that AR inactivation accelerates mammary carcinogenesis in female mice exposed to the chemical carcinogen DMBA regardless of mouse genetic background but require prior exposure to endogenous ovarian hormones.

We present a catalog containing 839 candidate post–common envelope systems. Common envelope evolution is very important in stellar astrophysics, particularly in the context of very compact and short-period binaries, including cataclysmic variables, as progenitors of, e.g., supernovae Type Ia or mergers of black holes and/or neutron stars. At the same time, it is a barely understood process in binary evolution. Due to limitations, since partially remedied, on direct simulation, early investigations were mainly focused on providing analytic prescriptions of the outcome of common envelope evolution. In recent years, detailed hydrodynamical calculations have produced deeper insight into the previously elusive process of envelope ejection. However, a direct link between the observations and theory of this relatively short-lived phase in binary evolution has not been forthcoming. Therefore, the main insight to be gained from observations has to be derived from the current state of systems likely to have gone through a common envelope. Here we present an extensive catalog of such observations as found in the literature. The aim of this paper is to provide a reliable set of data, obtained from observations, to be used in the theoretical modeling of common envelope evolution. In this catalog, the former common envelope donor star is commonly observed as a white dwarf or hot subdwarf star. This catalog includes period and mass estimates wherever obtainable. Some binaries are borderline cases to allow an investigation of the transition between a common envelope formation and other mass-transfer processes.