[Self-Management Education in Rural Older Adults With Diabetes].

Diabetes is one of the most prevalent chronic diseases affecting public health. The Taiwan government implemented the Diabetes Shared Care Program to deliver continuous medical care and provide health education in order to help clients with diabetes learn self-management. However, rural older adults with diabetes often have poor access to medical resources and thus face obstacles to obtaining and using the services of this program. This paper introduces the current status of the Diabetes Shared Care Program, discusses the concept of self-management education and support for diabetes cases, and proposes community-based strategies, including (1) provide DSMES (diabetes self-management education and support) with multi-types of services, (2) increase non-professional personnel training, and (3) provide culture-congruent health education, in order to strengthen the diabetes self-management capabilities of rural older adults.

Glycolic acid attenuates UVB-induced aquaporin-3, matrix metalloproteinase-9 expression, and collagen degradation in keratinocytes and mouse skin.

Ultraviolet-B exposure causes an inflammatory response, photoaged skin, and degradation of extracellular matrix proteins including collagen and elastin. The regulation of these genes was suggested as an important mechanism to attenuate skin aging. Glycolic acid (GA) is commonly present in fruits and recently used to treat dermatological diseases. We reported that GA slows down cell inflammation and aging caused by UVB. Little is known about GA retarding the skin premature senescence or how to impede these events. To investigate the potential of GA to regulate the expression of MMPs and collagen, GA was topically applied onto human keratinocytes and the C57BL/6J mice dorsal skin. In the present study, we demonstrated that GA reduced UVB-induced type-I procollagen expression and secretory collagen levels. GA reverted and dose-dependently increased the level of aquaporin-3 (AQP3), the expression of which was down-regulated by UVB. The UV-induced MMP-9 level and activity were reduced by GA pre-treatment. Concomitantly, GA reverted mitogen-activated protein kinase (MMP-9) activation and inhibited the extracellular signal-regulated kinase activation (p38, pERK) triggered by UVB. The animal model also presented that GA attenuated the wrinkles caused by UVB on the mouse dorsal skin. Finally, GA triggers the transient receptor potential vanilloid-1 (TRPV-1) channel to initiate the anti-photoaging mechanism in keratinocytes. These findings clearly indicated that the mechanisms of GA promote skin protection against UVB-induced photoaging and wrinkle formation. GA might be an important reagent and more widely used to prevent UVB-induced skin aging.

How mental health nurses improve their critical thinking through problem-based learning.

Critical thinking has been regarded as one of the most important elements for nurses to improve quality of patient care. The aim of this study was to use problem-based learning (PBL) as a method in a continuing education program to evaluate nurses' critical thinking skills. A quasiexperimental study design was carried out. The "Critical Thinking Disposition Inventory" in Chinese was used for data collection. The results indicated significant improvement after PBL continuous education, notably in the dimensions of systematic analysis and curiosity. Content analysis extracted four themes: (a) changes in linear thinking required, (b) logical and systematic thinking required performance improved, (3) integration of prior knowledge and clinical application, and (4) brainstorming learning strategy. The study supports PBL as a continuing education strategy for mental health nurses, and that systematic analysis and curiosity effectively facilitate the development of critical thinking.

[Strategy for promoting evidence-based nursing practice in hospital].

Evidence-based practice has been demonstrated to improve quality of care, increase patients' satisfaction, and reduce the costs of medical care. Therefore, evidence-based practice is now central to the clinical decision-making process and to achieving better quality of care. Today, it is one of the important indicators of core competences for healthcare providers and accreditation for healthcare and educational systems. Further, evidence-based practice encourages in-school and continuous education programs to integrate evidence-based elements and concepts into curricula. Healthcare facilities and professional organizations proactively host campaigns and encourage healthcare providers to participate in evidence-based related training courses. However, the clinical evidence-based practice progress is slow. The general lack of a model for organizational follow-up may be a key factor associated with the slow adoption phenomenon. The authors provide a brief introduction to the evidence-based practice model, then described how it may be successfully translated through a staged process into the evidence-based practices of organizational cultures. This article may be used as a reference by healthcare facilities to promote evidence-based nursing practice.

Glutathione S-transferase mu2 suppresses cancer cell metastasis in non-small cell lung cancer.

Glutathione S-transferase mu2 (GST-M2) is a phase II detoxification enzyme. Low expression of GST-M2 in lung cancers is due to hypermethylation of its promoter. Lung cancer with the GST mu-null genotype is associated with shorter survival. However, a correlation between GST-M2 and important clinical parameters, as well as the migration of GST-M2-defective cells in lung cancer, has not been established. In the present study, we investigate the role of GST-M2 in cell migration and actin disassembly in lung cancer cells. GST-M2 and CCN2 mRNA levels were significantly reduced in non-small cell lung cancer (NSCLC) tumors when compared with matched normal lung tissues in 82 patients with NSCLC. We found that high expressions of both GST-M2 and CCN2 are correlated with favorable survival of patients with lung cancer when compared with similar patients without GST-M2 or CCN2 expression. GST-M2 can induce CCN2 expression by driving the CCN2 proximal promoter. Overexpression of GST-M2 decreases the formation of filopodia, resulting in remodeling of the reorganized cytoskeletons. Overexpression of GST-M2 significantly suppressed cancer cell migration on wound-healing assay. In addition, overexpression of GST-M2 dramatically reduced tumor growth and metastasis in a xenograft mouse model. These data highlight the potential of GST-M2 as a novel tumor suppressor. GST-M2 increases the expression of CCN2 in lung cancer cells, which inhibits cancer cell migration in lung cancer and animal models.

Epigenetic mechanisms for silencing glutathione S-transferase m2 expression by hypermethylated specificity protein 1 binding in lung cancer.

BACKGROUND: Glutathione S-transferases M2 (GST-M2) is a detoxifying enzyme. Low expression levels of GST-M2 have been detected in lung cancer cells. However, little is known about the regulation of GST-M2 in lung cancer cells. In this study, the authors investigated the epigenetic regulatory mechanisms of GST-M2 in lung cancer cells. METHODS: The authors evaluated the promoter methylation of GST-M2 in lung cancer cells after treatment with the DNA methyltransferase (DNMT) inhibitor 5'-aza-2'-deoxycytidine (5'-aza-dC). Reporter activity assays, chromatin immunoprecipitation (ChIP), electrophoretic mobility-shift assays, and small interfering RNA (siRNA) assays were used to determine whether the methylation of specificity protein 1 (Sp1) affected binding to the GST-M2 promoter or regulated GST-M2 transcription. Real-time polymerase chain reaction was used to determine GST-M2 and DNMT-3b messenger RNA levels in 73 nonsmall cell lung cancer (NSCLC) tissues. RESULTS: GST-M2 expression was restored after treatment with 5'-aza-dC in lung cancer cells. GST-M2 exhibited high frequency of promoter hypermethylation in lung cancer cells and NSCLC tumor tissues. CpG hypermethylation abated Sp1 binding to the GST-M2 promoter in lung cancer. Knockdown of Sp1 in normal lung cells reduced GST-M2 expression, and silencing of DNMT-3b increased GST-M2 expression in lung cancer cells. In addition, DNMT-3b expression was significantly higher in lung tumors with low levels of GST-M2 expression than in lung tumors with high levels of GST-M2 expression, especially among women and among patients who had stage I disease. CONCLUSIONS: Epigenetic silencing of GST-M2 was distinguished from Sp1-mediated GST-M2 transcriptional expression. The authors concluded that this represents a mechanism that leads to decreased expression of GST-M2 in lung cancer cells.