Development and validation of the health literacy environment scale for Chinese hospitals from patients’ perspective

IntroductionWhile the research on improving individual health literacy by promoting individual skills and abilities is increasing, less attention has been paid to the complexities of the healthcare environment that may influence patients’ ability to access, understand, and apply health information and health services to make health decisions. This study aimed to develop and validate a Health Literacy Environment Scale (HLES) that is suitable for Chinese culture.MethodsThis study was conducted in two phases. First, using the Person-Centered Care (PCC) framework as a theoretical framework, initial items were developed by using the existing health literacy environment (HLE) related measurement tools, literature review, qualitative interviews, and the researcher’s clinical experience. Second, scale development was based on two rounds of Delphi expert consultation and a pre-test conducted with 20 hospitalized patients. Using 697 hospitalized patients from three sample hospitals, the initial scale was developed after item screening and its reliability and validity were evaluated.ResultsThe HLES comprised 30 items classified into three dimensions as follows: interpersonal (11 items), clinical (9 items), and structural (10 items) dimensions. The Cronbach’s α coefficient of the HLES was 0.960 and the intra-class correlation coefficient was 0.844. The confirmatory factor analysis verified the three-factor model after allowing for the correlation of five pairs of error terms. The goodness-of-fit indices signified a good fit for the model (χ2/df = 2.766, RMSEA = 0.069, RMR = 0.053, CFI = 0.902, IFI = 0.903, TLI = 0.893, GFI = 0.826, PNFI = 0.781, PCFI = 0.823, PGFI = 0.705). The item-content validity index ranged from 0.91 to 1.00, and the scale-content validity index was 0.90.ConclusionThe HLES had good reliability and validity and provides a patient perspective tool for evaluating HLE and a new perspective for improving health literacy in China. That is, healthcare organizations make it easier for patients to access, understand, and use health information and service. Further studies about the validity and reliability of HLE should include other districts and different tiers or types of healthcare organizations

Transcription Factor NFAT5 Promotes Glioblastoma Cell-driven Angiogenesis via SBF2-AS1/miR-338-3p-Mediated EGFL7 Expression Change

Glioblastoma (GBM) is the most aggressive primary intracranial tumor of adults and confers a poor prognosis due to high vascularization. Hence anti-angiogenic therapy has become a promising strategy for GBM treatment. In this study, the transcription factor nuclear factor of activated T-cells 5 (NFAT5) was significantly elevated in glioma samples and GBM cell lines, and positively correlated with glioma WHO grades. Knockdown of NFAT5 inhibited GBM cell-driven angiogenesis. Furthermore, long non-coding RNA SBF2 antisense RNA 1 (SBF2-AS1) was upregulated in glioma samples and knockdown of SBF2-AS1 impaired GBM-induced angiogenesis. Downregulation of NFAT5 decreased SBF2-AS1 expression at transcriptional level. In addition, knockdown of SBF2-AS1 repressed GBM cell-driven angiogenesis via enhancing the inhibitory effect of miR-338-3p on EGF like domain multiple 7 (EGFL7). In vivo study demonstrated that the combination of NFAT5 knockdown and SBF2-AS1 knockdown produced the smallest xenograft volume and the lowest microvessel density. NFAT5/SBF2-AS1/miR-338-3p/EGFL7 pathway may provide novel targets for glioma anti-angiogenic treatment

Analysis of the dermatophyte Trichophyton rubrum expressed sequence tags

BACKGROUND: Dermatophytes are the primary causative agent of dermatophytoses, a disease that affects billions of individuals worldwide. Trichophyton rubrum is the most common of the superficial fungi. Although T. rubrum is a recognized pathogen for humans, little is known about how its transcriptional pattern is related to development of the fungus and establishment of disease. It is therefore necessary to identify genes whose expression is relevant to growth, metabolism and virulence of T. rubrum. RESULTS: We generated 10 cDNA libraries covering nearly the entire growth phase and used them to isolate 11,085 unique expressed sequence tags (ESTs), including 3,816 contigs and 7,269 singletons. Comparisons with the GenBank non-redundant (NR) protein database revealed putative functions or matched homologs from other organisms for 7,764 (70%) of the ESTs. The remaining 3,321 (30%) of ESTs were only weakly similar or not similar to known sequences, suggesting that these ESTs represent novel genes. CONCLUSION: The present data provide a comprehensive view of fungal physiological processes including metabolism, sexual and asexual growth cycles, signal transduction and pathogenic mechanisms

The use of global transcriptional analysis to reveal the biological and cellular events involved in distinct development phases of Trichophyton rubrum conidial germination

<p>Abstract</p> <p>Background</p> <p>Conidia are considered to be the primary cause of infections by <it>Trichophyton rubrum</it>.</p> <p>Results</p> <p>We have developed a cDNA microarray containing 10250 ESTs to monitor the transcriptional strategy of conidial germination. A total of 1561 genes that had their expression levels specially altered in the process were obtained and hierarchically clustered with respect to their expression profiles. By functional analysis, we provided a global view of an important biological system related to conidial germination, including characterization of the pattern of gene expression at sequential developmental phases, and changes of gene expression profiles corresponding to morphological transitions. We matched the EST sequences to GO terms in the <it>Saccharomyces </it>Genome Database (SGD). A number of homologues of <it>Saccharomyces cerevisiae </it>genes related to signalling pathways and some important cellular processes were found to be involved in <it>T. rubrum </it>germination. These genes and signalling pathways may play roles in distinct steps, such as activating conidial germination, maintenance of isotropic growth, establishment of cell polarity and morphological transitions.</p> <p>Conclusion</p> <p>Our results may provide insights into molecular mechanisms of conidial germination at the cell level, and may enhance our understanding of regulation of gene expression related to the morphological construction of <it>T. rubrum</it>.</p

Fibronectin Promotes the Malignancy of Glioma Stem-Like Cells Via Modulation of Cell Adhesion, Differentiation, Proliferation and Chemoresistance

Glioma stem-like cells (GSCs) are regarded as the sources of oncogenesis, recurrence, invasion and chemoresistance in malignant gliomas. Growing evidence suggests that the microenvironment surrounding GSCs interacts with tumor cells to influence biological behavior; however, the functional mechanisms involved are still unclear. In the present study, we investigated the modulation of GSCs triggered by fibronectin (FN), a main component of the extracellular matrix (ECM), in terms of cell adhesion, differentiation, proliferation and chemoresistance. We demonstrated that pre-coated FN prompted increased adherence by GSCs, with increased matrix metallopeptidases (MMPs)-2 and -9 expression, in a concentration-dependent manner. Decreases in sox-2 and nestin levels, and increased levels of glial fibrillary acidic protein (GFAP) and β-tubulin were also found in GSCs, indicating cell differentiation driven by FN. Further investigation revealed that FN promoted cell growth, as demonstrated by the elevation of Ki-67, with the activation of p-ERK1/2 and cyclin D1 also evident. In addition, FN suppressed p53-mediated apoptosis and upregulated P-glycoprotein expression, making GSCs more chemoresistant to alkylating agents such as carmustine. In contrast, this effect was reversed by an integrin inhibitor, cilengitide. Activation of the focal adhesion kinase/paxillin/AKT signaling pathway was involved in the modulation of GSCs by FN. Focusing on the interactions between tumor cells and the ECM may be an encouraging aspect of research on novel chemotherapeutic therapies in future

Security Issues on Spectral-Phase-Encoded Optical CDMA with Phase-masking Scheme&amp;quot;, OFC

Abstract: This paper proposes a time-varying phase-masking scheme for OCDMA security enhancement. We provide a quantitative analysis of its confidentiality. Analytical results indicate that the phase-masking scheme increases the difficulty of interception and achieves low data interception rates

Endothelial Monocyte-Activating Polypeptide-II Induces BNIP3-Mediated Mitophagy to Enhance Temozolomide Cytotoxicity of Glioma Stem Cells via Down-Regulating MiR-24-3p

Preliminary studies have shown that endothelial-monocyte-activating polypeptide-II (EMAP-II) and temozolomide (TMZ) alone can exert cytotoxic effects on glioma cells. This study explored whether EMAP-II can enhance the cytotoxic effects of TMZ on glioma stem cells (GSCs) and the possible mechanisms associated with Bcl-2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3)-mediated mitophagy facilitated by miR-24-3p regulation. The combination of TMZ and EMAP-II significantly inhibited GSCs viability, migration, and invasion, resulting in upregulation of the autophagy biomarker microtubule-associated protein one light chain 3 (LC3)-II/I but down-regulation of the proteins P62, TOMM 20 and CYPD, changes indicative of the occurrence of mitophagy. BNIP3 expression increased significantly in GSCs after treatment with the combination of TMZ and EMAP-II. BNIP3 overexpression strengthened the cytotoxic effects of EMAP-II and TMZ by inducing mitophagy. The combination of EMAP-II and TMZ decreased the expression of miR-24-3p, whose target gene was BNIP3. MiR-24-3p inhibited mitophagy and promoted proliferation, migration and invasion by down-regulating BNIP3 in GSCs. Furthermore, nude mice subjected to miR-24-3p silencing combined with EMAP-II and TMZ treatment displayed the smallest tumors and the longest survival rate. According to the above results, we concluded that EMAP-II enhanced the cytotoxic effects of TMZ on GSCs' proliferation, migration and invasion both in vitro and in vivo