She's single, so what? How are singles perceived compared with people who are married?

'In den vergangenen Jahrzehnten haben sich klassische Beziehungsmuster geändert. Neben der traditionellen Ehe finden sich heute nichteheliche Lebensgemeinschaften, Paare, die getrennte Haushalte führen (LATs) und gleichgeschlechtliche Paare. Daneben wurden Singles zu einer viel diskutierten Gruppe. In Anbetracht der Vielzahl an Lebensformen könnte man annehmen, dass negativ geprägte Stereotype gegenüber Singles zurückgegangen sind. Die Studie zeigt allerdings, dass noch immer verheiratete Personen positiver beurteilt werden als Singles. Beispielsweise werden Singles als einsamer, weniger einfühlsam und weniger fürsorglich eingeschätzt. Es zeigt sich aber auch eine tendenzielle Aufweichung des negativen Stereotyps: (jungen) Singles werden einige positive Eigenschaften zugeschrieben. Hierbei moderieren Merkmale der bewertenden Person die Einschätzung. Vor allem jüngere Frauen und ältere Singles haben ein relativ positives Bild von Singles und beurteilen sie im Vergleich zu verheirateten Personen als geselliger und weltgewandter.' (Autorenreferat)'Over the past few decades, relationship patterns have become more diverse. Besides classical marriage we find cohabitation, romantic partners living apart, and same-sex couples. Furthermore, single people have become an important and intensely discussed segment of society. Due to the increasing plurality of living arrangements, one might assume that stereotypes about singles have changed over the years. The study shows that married people are generally still seen more positively than singles. Singles were seen as more lonely, less warm and caring than married people. However, some positive features are ascribed to singles, too. Importantly, characteristics of the perceiver moderate his or her perceptions. Some groups rated single people as more sophisticated and sociable than married people.' (author's abstract

Re-examination of siRNA specificity questions role of PICH and Tao1 in the spindle checkpoint and identifies Mad2 as a sensitive target for small RNAs

The DNA-dependent adenosine triphosphatase (ATPase) Plk1-interacting checkpoint helicase (PICH) has recently been implicated in spindle checkpoint (SAC) signaling (Baumann et al., Cell 128(1):101–114, 2007). Depletion of PICH by siRNA abolished the SAC and resulted in an apparently selective loss of Mad2 from kinetochores, suggesting a role for PICH in the regulation of the Mad1–Mad2 interaction. An apparent rescue of SAC functionality by overexpression of PICH in PICH-depleted cells initially seemed to confirm a role for PICH in the SAC. However, we have subsequently discovered that all PICH-directed siRNA oligonucleotides that abolish the SAC also reduce Mad2 mRNA and protein expression. This reduction is functionally significant, as PICH siRNA does not abolish SAC activity in a cell line that harbors a bacterial artificial chromosome driving the expression of murine Mad2. Moreover, we identified several siRNA duplexes that effectively deplete PICH but do not significantly affect SAC functionality or Mad2 abundance or localization. Finally, we discovered that the ability of overexpressed PICH to restore SAC activity in PICH-depleted cells depends on sequestration of the mitotic kinase Plk1 rather than ATPase activity of PICH, pointing to an underlying mechanism of “bypass suppression.” In support of this view, depletion or inhibition of Plk1 also rescued SAC activity in cells harboring low levels of Mad2. This observation suggests that a reduction of Plk1 activity partially compensates for reduced Mad2 levels and argues that Plk1 normally reduces the strength of SAC signaling. Collectively, our results question the role of PICH in the SAC and instead identify Mad2 as a sensitive off target for small RNA duplexes. In support of the latter conclusion, our evidence suggests that an off-target effect on Mad2 may also contribute to explain the apparent role of the Tao1 kinase in SAC signaling (Draviam et al., Nat Cell Biol 9(5):556–564, 2007)

Desmoglein-1 regulates esophageal epithelial barrier function and immune responses in eosinophilic esophagitis

The desmosomal cadherin desmoglein-1 (DSG1) is an essential intercellular adhesion molecule that is altered in various human cutaneous disorders; however, its regulation and function in allergic disease remains unexplored. Herein, we demonstrate a specific reduction in DSG1 in esophageal biopsies from patients with eosinophilic esophagitis (EoE), an emerging allergic disorder characterized by chronic inflammation within the esophageal mucosa. Further, we show that DSG1 gene silencing weakens esophageal epithelial integrity, and induces cell separation and impaired barrier function (IBF) despite high levels of desmoglein-3 (DSG3). Moreover, DSG1 deficiency induces transcriptional changes that partially overlap with the transcriptome of inflamed esophageal mucosa; notably, periostin, a multipotent pro-inflammatory extracellular matrix molecule, is the top induced overlapping gene. We further demonstrate that IBF is a pathological feature in EoE, which can be partially induced through the downregulation of DSG1 by interleukin-13 (IL-13). Taken together, these data identify a functional role for DSG1 and its dysregulation by IL-13 in the pathophysiology of EoE and suggest that the loss of DSG1 may potentiate allergic inflammation through the induction of pro-inflammatory mediators such as periostin

p68/DdX5 supports β-Catenin & RNAP II during androgen receptor mediated transcription in prostate cancer

The DEAD box RNA helicase p68 (Ddx5) is an important androgen receptor (AR) transcriptional co-activator in prostate cancer (PCa) and is over-expressed in late stage disease. β-Catenin is a multifunctional protein with important structural and signalling functions which is up-regulated in PCa and similar to p68, interacts with the AR to co-activate expression of AR target genes. Importantly, p68 forms complexes with nuclear β-Catenin and promotes gene transcription in colon cancer indicating a functional interplay between these two proteins in cancer progression. In this study, we explore the relationship of p68 and β-Catenin in PCa to assess their potential co-operation in AR-dependent gene expression, which may be of importance in the development of castrate resistant prostate cancer (CRPCa). We use immunoprecipitation to demonstrate a novel interaction between p68 and β-Catenin in the nucleus of PCa cells, which is androgen dependent in LNCaP cells but androgen independent in a hormone refractory derivative of the same cell line (representative of the CRPCa disease type). Enhanced AR activity is seen in androgen-dependent luciferase reporter assays upon transient co-transfection of p68 and β-Catenin as an additive effect, and p68-depleted Chromatin-Immunoprecipitation (ChIP) showed a decrease in the recruitment of the AR and β-Catenin to androgen responsive promoter regions. In addition, we found p68 immunoprecipitated with the processive and non-processive form of RNA polymerase II (RNAP II) and show p68 recruited to elongating regions of the AR mediated PSA gene, suggesting a role for p68 in facilitating RNAP II transcription of AR mediated genes. These results suggest p68 is important in facilitating β-Catenin and AR transcriptional activity in PCa cells

Quantitative Mass Spectrometry Analysis Reveals Similar Substrate Consensus Motif for Human Mps1 Kinase and Plk1

Background Members of the Mps1 kinase family play an essential and evolutionarily conserved role in the spindle assembly checkpoint (SAC), a surveillance mechanism that ensures accurate chromosome segregation during mitosis. Human Mps1 (hMps1) is highly phosphorylated during mitosis and many phosphorylation sites have been identified. However, the upstream kinases responsible for these phosphorylations are not presently known. Methodology/Principal Findings Here, we identify 29 in vivo phosphorylation sites in hMps1. While in vivo analyses indicate that Aurora B and hMps1 activity are required for mitotic hyper-phosphorylation of hMps1, in vitro kinase assays show that Cdk1, MAPK, Plk1 and hMps1 itself can directly phosphorylate hMps1. Although Aurora B poorly phosphorylates hMps1 in vitro, it positively regulates the localization of Mps1 to kinetochores in vivo. Most importantly, quantitative mass spectrometry analysis demonstrates that at least 12 sites within hMps1 can be attributed to autophosphorylation. Remarkably, these hMps1 autophosphorylation sites closely resemble the consensus motif of Plk1, demonstrating that these two mitotic kinases share a similar substrate consensus. Conclusions/Significance hMps1 kinase is regulated by Aurora B kinase and its autophosphorylation. Analysis on hMps1 autophosphorylation sites demonstrates that hMps1 has a substrate preference similar to Plk1 kinase

Effect of apoptosis in neural stem cells treated with sevoflurane

BACKGROUND: At present, sevoflurane inhalation anesthesia used on infants is well-known. But long-time exposure to inhalation anesthetic could cause neurologic disorder, especially nerve degeneration in infant and developing brain. The central nervous system degeneration of infants could affect the memory and cognitive function. γ-Aminobutyric acid (GABA) is a known inhibitory neurotransmitter in central nervous system. Inhalation anesthetic sevoflurane may activate GABA(A) receptor to inhibit central nervous system, leading to apoptosis of neural degeneration, cognitive dysfunction in the critical period of brain development. METHODS: Neural stem cells were derived from Wistar embryos, cultured in vitro. Third generation of neural stem cells were randomly divided into four groups according to cultured suspension: Sevoflurane group (Group S), GABA(A) receptor antagonists, Bicuculline group (Group B), Sevoflurane + GABA(A) receptor antagonists, Bicuculline group (Group S + B), dimethyl sulphoxide (DMSO) group (Group D). Group B and Group D did not receive sevoflurane preconditioning. Group S and Group S + B were pretreated with 1 minimum alveolar concentration (MAC) sevoflurane for 0 h, 3 h, 6 h, and 12 h. Group S + B and Group B were pretreated with bicuculline (10 uM). Group D was treated with DMSO (10 uL/mL). After treatments above, all groups were cultured for 48 h. Then we measured the cells viability by Cell Counting Kit (CCK-8) assay, cytotoxicity by Lactate Dehydrogenase (LDH) assay, apoptosis ratio with Annexin V/propidium iodide (PI) staining by flow cytometry, and the expression of GABA(A)R, anti-apoptotic protein Bcl-2, pro-apoptotic protein Bax and Caspase-3 by western blotting. RESULTS: After exposing to sevoflurane for 0 h, 3 h, 6 h, and 12 h with 1MAC, we found that cell viability obviously decreased and cytotoxicity increased in time-dependent way. And Annexin V/PI staining indicated increased apoptosis ratio by flow cytometry. The protein level of GABA(A) receptor, pro-apoptotic protein Bax and apoptosis protein Caspase-3 increased; while anti-apoptotic protein Bcl-2 decreased. And bicuculline could reverse all detrimental results caused by sevoflurane. CONCLUSION: Sevoflurane can inhibit the central nervous system by activating GABA(A), resulting in apoptosis of neural stem cells, thus leading to the NSCs degeneration

Narcissism in patients admitted to psychiatric acute wards: its relation to violence, suicidality and other psychopathology

<p>Abstract</p> <p>Background</p> <p>The objective was to examine various aspects of narcissism in patients admitted to acute psychiatric wards and to compare their level of narcissism to that of an age- and gender-matched sample from the general population (NORM).</p> <p>Methods</p> <p>This cross-sectional study interviewed 186 eligible acute psychiatric patients with the Brief Psychiatric Rating Scale (BPRS) and the Global Assessment of Functioning (GAF). The patients filled in the Narcissistic Personality Inventory-21 item version (NPI-21), The Hospital Anxiety and Depression Scale (HADS) and the Rosenberg Self-Esteem Scale. High and low narcissism was defined by the median of the total NPI-21 score. An age- and gender-matched control sample from the general population also scored the NPI-21 (NORM).</p> <p>Results</p> <p>Being male, involuntary admitted, having diagnosis of schizophrenia, higher self-esteem, and severe violence were significantly associated with high narcissism, and so were also low levels of suicidality, depression, anxiety and GAF scores. Severe violence and high self-esteem were significantly associated with high narcissism in multivariable analyses. The NPI-21 and its subscales showed test-retest correlations ≥0.83, while the BPRS and the HADS showed lower correlations, confirming the trait character of the NPI-21. Depression and suicidality were negatively associated with the NPI-21 total score and all its subscales, while positive association was observed with grandiosity. No significant differences were observed between patients and NORM on the NPI-21 total score or any of the NPI subscales.</p> <p>Conclusion</p> <p>Narcissism in the psychiatric patients was significantly associated with violence, suicidality and other symptoms relevant for management and treatment planning. Due to its trait character, use of the NPI-21 in acute psychiatric patients can give important clinical information. The similar level of narcissism found in patients and NORM is in need of further examination.</p

Organization of multiprotein complexes at cell–cell junctions

The formation of stable cell–cell contacts is required for the generation of barrier-forming sheets of epithelial and endothelial cells. During various physiological processes like tissue development, wound healing or tumorigenesis, cellular junctions are reorganized to allow the release or the incorporation of individual cells. Cell–cell contact formation is regulated by multiprotein complexes which are localized at specific structures along the lateral cell junctions like the tight junctions and adherens junctions and which are targeted to these site through their association with cell adhesion molecules. Recent evidence indicates that several major protein complexes exist which have distinct functions during junction formation. However, this evidence also indicates that their composition is dynamic and subject to changes depending on the state of junction maturation. Thus, cell–cell contact formation and integrity is regulated by a complex network of protein complexes. Imbalancing this network by oncogenic proteins or pathogens results in barrier breakdown and eventually in cancer. Here, I will review the molecular organization of the major multiprotein complexes at junctions of epithelial cells and discuss their function in cell–cell contact formation and maintenance

Consistency and flexibility in solving spatial tasks: different horses show different cognitive styles

Individual animals vary in their behaviour and reactions to novel situations. These differences may extend to differences in cognition among individuals. We tested twenty-six horses for their ability to detour around symmetric and asymmetric obstacles. All of the animals were able to get around the barrier to reach a food target, but varied in their approach. Some horses moved slowly but were more accurate in choosing the shortest way. Other horses acted quickly, consistently detoured in the same direction, and did not reliably choose the shortest way. The remaining horses shifted from a faster, directionally consistent response with the symmetric barrier, to a slower but more accurate response with the asymmetric barrier. The asymmetric barrier induced a reduction in heart rate variability, suggesting that this is a more demanding task. The different approaches used to solve the asymmetric task may reflect distinct cognitive styles in horses, which vary among individuals, and could be linked to different personality traits. Understanding equine behaviour and cognition can inform horse welfare and management