Psychological insulin resistance and its impact on self-management in type II diabetes mellitus patients treated with insulin therapy.

AIMS: Psychological insulin resistance is a common barrier to initiation and persistence with insulin therapy that affects approximately 42.7% of people living with type II diabetes mellitus, which may negatively impact self-management. This study aimed to assess patients' levels of psychological insulin resistance and to identify factors associated with self-management in patients with type II diabetes mellitus treated with insulin therapy. METHODS: We adopted a cross-sectional design. Subjects from the metabolism and endocrinology outpatient departments of a regional teaching hospital in central Taiwan were recruited by consecutive sampling. Patients were assessed for psychological insulin resistance and self-management using the barriers to insulin treatment questionnaire and the partners in health scale. RESULTS: A total of 222 patients with type II diabetes mellitus were recruited. Patients had an average psychological insulin resistance score of 3.14 (maximum of 8). Positive self-management was associated with insulin therapy injection by patient, fewer expectations regarding positive insulin-related outcomes, no diabetes-related complications, less fear of injection and self-testing, no hypoglycaemia within the previous year, and younger age. CONCLUSION: Insulin therapy injection by patient and no diabetes-related complications were the most common factors associated with overall self-management and with each domain of self-management in patients with type II diabetes mellitus treated with insulin therapy. Insulin therapy education should be offered to improve patients' beliefs about insulin therapy and enhance patients' ability to perform self-management.

Perceived stigma and depression in initially diagnosed pulmonary tuberculosis patients.

AIMS AND OBJECTIVES: To investigate the status of tuberculosis stigma and depression among tuberculosis patients, to examine the relationship between demographics and tuberculosis stigma and depression among tuberculosis patients, and to identify the predictors of depression among tuberculosis patients. BACKGROUND: After the diagnosis of tuberculosis, patients suffer from disease symptoms and disease-related stigma. Depression is also a major concern in tuberculosis patients. DESIGN: A cross-sectional design was used in this study. METHODS: A total of 84 subjects, obtained through convenience sampling, enrolled in this study, which was conducted from 1 March 2013-30 December 2014. Data were collected using a structured questionnaire with a demographic component, the Tuberculosis-related Stigma Scale, and the Beck Depression Inventory-II. Data were analysed, using spss Version 20. Independent t tests, Pearson's correlation coefficient tests and analyses of variance were used for analysis of patient demographic characteristics, disease characteristics, and the correlation between stigma and depression. Multiple linear regression was used for determining the predictors of depression. RESULTS: The results showed that not disclosing one's illness to others was associated with tuberculosis stigma and depression. Multiple linear regression analysis indicated that patient-perceived tuberculosis stigma and body mass index accounted for 34% of the variation in depression. CONCLUSIONS: These results can serve as a reference for clinical healthcare providers to understand perceived stigma and depression in initially diagnosed tuberculosis patients. RELEVANCE TO CLINICAL PRACTICE: An intervention to reduce patient tuberculosis stigma, such as improving community healthcare education or offering mental health outreach, has great potential to lower the level of depression among patients with tuberculosis.

A novel oncogenic role of inositol phosphatase SHIP2 in ER-negative breast cancer stem cells: involvement of JNK/vimentin activation.

Overexpression of SH2-containing-5'-inositol phosphatase-2 (SHIP2) correlates with poor survival in breast cancer. However, its role in breast cancer stem cells (BCSCs) remains unclear. Here, we showed that the percentage of SHIP2(+) cells was positively correlated with that of CD24(-) CD44(+) cells in 60 breast cancer specimens. Among 20 estrogen receptor (ER)-negative samples, 17 had greater SHIP2 expression in CD24(-) CD44(+) subpopulation than the remaining subpopulation. Data mining of microarray analysis of 295 breast tumors showed a significant correlation of higher SHIP2 expression with distant metastasis. Examination of patient-derived mouse xenografts revealed that SHIP2 protein and its tyrosine 1135 phosphorylation were significantly higher in BCSCs, identified as CD24(-) CD44(+) or aldehyde dehydrogenase (ALDH(+)), than non-BCSCs. SHIP2 silencing or inhibitor of SHIP2 phosphatase significantly decreased mammosphere-forming efficiency, ALDH(+) subpopulation in vitro and tumorigenicity of BCSCs in vivo. Overexpression of SHIP2 enhanced the expression of epithelial-mesenchymal transition markers including vimentin (VIM), which was mainly expressed in ER-negative breast cancer cells with higher level in mammospheres than monolayer culture. Ablation of c-Jun N-terminal kinase 1 (JNK1), JNK2, or VIM diminished the increased ALDH(+) population and tumorigenicity, induced by SHIP2 overexpression. BCSCs displayed greater expression of phospho-JNK than non-BCSCs and silencing of JNK suppressed SHIP2-mediated upregulation of VIM. Furthermore, SHIP2 overexpression enhanced Akt activation, but Akt inhibition failed to influence SHIP2-induced phospho-JNK/VIM upregulation. In conclusion, SHIP2 plays a key role in BCSCs of ER-negative breast cancers through activation of Akt and JNK with upregulation of VIM and may serve as a target for therapy directed at BCSCs.

The effectiveness of a transtheoretical model-based smoking cessation intervention for rural smokers: A quasi-experimental longitudinal study.

OBJECTIVE: Cigarette smoking is highly prevalent, despite being a primary preventable cause of disease and mortality. This study examined the effect of a Transtheoretical Model (TTM)-based psychoeducational intervention for smoking cessation (SC) on knowledge, SC-related parameters, and progression through the TTM stages of change among rural smokers. METHODS: This quasi-experimental study recruited 200 smokers from an outpatient clinic. The comparison group was recruited before the experimental group to address possible self-selection bias. Structured questionnaires were administered pre- and post-intervention (three months) and at follow-up (six months). RESULTS: A generalised estimation equation model indicated that the TTM-based intervention significantly increased participants' SC-knowledge and improved progression through TTM stages by the six-month follow-up. No significant group differences were found in self-efficacy and nicotine dependence scores or daily cigarette consumption. CONCLUSIONS: A TTM-based intervention enhances SC-knowledge and fosters progress through change stages. However, it does not directly impact nicotine dependence or cigarette consumption. Outpatient settings may employ TTM-based programmes for SC education and motivation. Detecting anticipated effects may require a longer intervention duration exceeding six months. PRACTICE IMPLICATIONS: Such TTM-based programmes may facilitate SC-knowledge and motivation in outpatient settings. Further research to comprehend patients' context and experiences during the stages of change is required.

The expression and significance of insulin-like growth factor-1 receptor and its pathway on breast cancer stem/progenitors.

INTRODUCTION: Dysregulation of the insulin-like growth factor-1 receptor (IGF-1R)/phosphatidylinositol-3-kinase (PI3K)/Akt pathway was shown to correlate with breast cancer disease progression. Cancer stem cells are a subpopulation within cancer cells that participate in tumor initiation, radio/chemoresistance and metastasis. In breast cancer, breast cancer stem cells (BCSCs) were identified as CD24-CD44+ cells or cells with high intracellular aldehyde dehydrogenase activity (ALDH+). Elucidation of the role of IGF-1R in BCSCs is crucial to the design of breast cancer therapies targeting BCSCs. METHODS: IGF-1R expression in BCSCs and noncancer stem cells sorted from xenografts of human primary breast cancers was examined by fluorescence-activated cell sorting (FACS), western blot analysis and immunoprecipitation. The role of IGF-1R in BCSCs was assessed by IGF-1R blockade with chemical inhibitor and gene silencing. Involvement of PI3K/Akt/mammalian target of rapamycin (mTOR) as the downstream pathway was studied by their phosphorylation status upon IGF-1R inhibition and the effects of chemical inhibitors of these signaling molecules on BCSCs. We also studied 16 clinical specimens of breast cancer for the expression of phosphor-Akt in the BCSCs by FACS. RESULTS: Expression of phosphorylated IGF-1R was greater in BCSCs than in non-BCSCs from xenografts of human breast cancer, which were supported by western blot and immunoprecipitation experiments. The sorted IGF-1R-expressing cells displayed features of cancer stem/progenitors such as mammosphere formation in vitro and tumorigenicity in vivo, both of which were suppressed by knockdown of IGF-1R. A specific inhibitor of the IGF-1R, picropodophyllin suppressed phospho-AktSer473 and preferentially decreased ALDH+ BCSC populations of human breast cancer cells. Furthermore, picropodophyllin inhibited the capacity of CD24-CD44+ BCSCs to undergo the epithelial-mesenchymal transition process with downregulation of mesenchymal markers. Inhibitors of signal molecules downstream of IGF-1R including PI3K/Akt/mTOR also reduced the ALDH+ population of breast cancer cells. Furthermore, the mTOR inhibitor, rapamycin, suppressed BCSCs in vitro and in vivo. CONCLUSION: Our data support the notion that IGF-1R is a marker of stemness, and IGF-1R and its downstream PI3K/Akt/mTOR pathway are attractive targets for therapy directed against breast cancer stem/progenitors.