Proactive behaviors and health care workers: A systematic review.

Background: Proactive behaviors at work refer to discretionary actions among workers that are self-starting, change oriented, and future focused. Proactive behaviors reflect the idiosyncratic actions by individual workers that shape the delivery and experience of professional services, highlight a bottom-up perspective on workers' agency and motivation that can influence organizational practices, and are associated with a variety of employee and organizational outcomes.

Purpose: This systematic review aims to understand the various forms of proactive behaviors in health care workers that have been studied, and how these proactive behaviors are associated with employee-level outcomes and quality of care.

Work Engagement and Patient Quality of Care: A Meta-Analysis and Systematic Review.

Past research has demonstrated that work engagement among health care professionals influences patient quality of care. There is, however, no estimate of the strength of this relationship, and existing reviews have not always explained conflicting findings. We conduct a meta-analysis and review of 25 articles, and find a small to medium mean effect size ( = .

Snail induces epithelial cell extrusion by regulating RhoA contractile signalling and cell-matrix adhesion.

Cell extrusion is a morphogenetic process that is implicated in epithelial homeostasis and elicited by stimuli ranging from apoptosis to oncogenic transformation. To explore whether the morphogenetic transcription factor Snail (SNAI1) induces extrusion, we inducibly expressed a stabilized Snail transgene in confluent MCF-7 monolayers. When expressed in small clusters (less than three cells) within otherwise wild-type confluent monolayers, Snail expression induced apical cell extrusion.

Coronin 1B supports RhoA signaling at cell-cell junctions through Myosin II.

Non-muscle myosin II (NMII) motor proteins are responsible for generating contractile forces inside eukaryotic cells. There is also a growing interest in the capacity for these motor proteins to influence cell signaling through scaffolding, especially in the context of RhoA GTPase signaling. We previously showed that NMIIA accumulation and stability within specific regions of the cell cortex, such as the zonula adherens (ZA), allows the formation of a stable RhoA signaling zone.

Biomechanical guidance helps elongate a lumen.

Transporting epithelia commonly consist of tubes that mediate between the body and its environment. Lumen formation is closely linked to epithelial morphogenesis, but an open question is how luminal symmetry is broken to generate tubes rather than hollow cysts. A report about the biomechanics of intercellular contacts might now provide some answers.

Towards a mechanistic understanding of lipodystrophy and seipin functions.

CGL (Congenital generalized lipodystrophy) is a genetic disorder characterized by near complete loss of adipose tissue along with increased ectopic fat storage in other organs including liver and muscle. Of the four CGL types, BSCL2 (Berardinelli-Seip Congenital lipodystrophy type 2), resulting from mutations in the BSCL2/seipin gene, exhibits the most severe lipodystrophic phenotype with loss of both metabolic and mechanical adipose depots. The majority of Seipin mutations cause C-terminal truncations, along with a handful of point mutations.

Frequent co-expression of miRNA-5p and -3p species and cross-targeting in induced pluripotent stem cells.

Background: A miRNA precursor generally gives rise to one major miRNA species derived from the 5' arm, and are called miRNA-5p. However, more recent studies have shown co-expression of miRNA-5p and -3p, albeit in different concentrations, in cancer cells targeting different sets of transcripts. Co-expression and regulation of the -5p and -3p miRNA species in stem cells, particularly in the reprogramming process, have not been studied.

Suppression of adipogenesis by pathogenic seipin mutant is associated with inflammatory response.

Background: While pathogenic mutations in BSCL2/Seipin cause congenital generalized lipodystrophy, the underlying mechanism is largely unknown. In this study, we investigated whether and how the pathogenic missense A212P mutation of Seipin (Seipin-A212P) inhibits adipogenesis.

Methodology/results: We analyzed gene expression and lipid accumulation in stable 3T3-L1 cell lines expressing wild type (3T3-WT), non-lipodystrophic mutants N88S (3T3-N88S) and S90L (3T3-S90L), or lipodystrophic mutant A212P Seipin (3T3-A212P).

TCPTP regulates SFK and STAT3 signaling and is lost in triple-negative breast cancers.

Tyrosine phosphorylation-dependent signaling, as mediated by members of the epidermal growth factor receptor (EGFR) family (ErbB1 to -4) of protein tyrosine kinases (PTKs), Src family PTKs (SFKs), and cytokines such as interleukin-6 (IL-6) that signal via signal transducer and activator of transcription 3 (STAT3), is critical to the development and progression of many human breast cancers. EGFR, SFKs, and STAT3 can serve as substrates for the protein tyrosine phosphatase TCPTP (PTPN2). Here we report that TCPTP protein levels are decreased in a subset of breast cancer cell lines in vitro and that TCPTP protein is absent in a large proportion of "triple-negative" primary human breast cancers.