Workplace health promotion programs should be tailored according to individual needs and efficient intervention. This study aimed to determine the effects of nutrition and exercise health behaviors ...on predicted risk for cardiovascular disease (CVD) when body mass index (BMI) is considered. In total, 3350 Taiwanese workers were included in this cross-sectional study. A self-reported questionnaire was used to measure their nutrition and exercise behaviors. Data on anthropometric values, biochemical blood determinations, and predicted CVD risk (using the Framingham risk score) were collected. In multiple regression analyses, the nutrition behavior score was independently and negatively associated with CVD risk. Exercise was not significantly associated with the risk. However, the interactive effect of exercise and BMI on CVD risk was evident. When stratified by BMI levels, associations between exercise and CVD risk were statistically significant for ideal weight and overweight subgroups. In conclusion, nutrition behavior plays an important role in predicting the CVD risk. Exercise behavior is also a significant predictor for ideal weight and overweight workers. Notably, for underweight or obese workers, maintaining health-promoting exercise seems insufficient to prevent the CVD. In order to improve workers' cardiovascular health, more specific health-promoting strategies should be developed to suit the different BMI levels.
► We identify CCAR1 to directly interact with Ngn3. ► CCAR1 is co-localized with Ngn3 in the nucleus. ► CCAR1 cooperates with Ngn3 in activating NeuroD expression. ► CCAR1 is required for ...Ngn3-mediated PANC-1 transdifferentiation.
Neurogenin3 (Ngn3) is a basic helix-loop-helix transcription factor that specifies pancreatic endocrine cell fates during pancreas development. It can also initiate a transdifferentiation program when expressed in pancreatic exocrine and ductal cells. However, how Ngn3 initiates a transcriptional cascade to achieve endocrine differentiation is still poorly understood. Here, we show that cell cycle and apoptosis regulator 1 (CCAR1), which is a transcriptional coactivator for nuclear receptors, also interacts with Ngn3. The association between Ngn3 and CCAR1 was verified by pull-down assays and co-immunoprecipitation analyses. Using gene reporter assays, we found that CCAR1 is essential for Ngn3 to activate the expression of the reporter genes containing the NeuroD promoter. Moreover, down-regulation of endogenous CCAR1 in the PANC-1 pancreatic ductal cell line inhibits the transdifferentiation program initiated by Ngn3. CCAR1 is, therefore, a novel partner of Ngn3 in mediating endocrine differentiation.
Autophagy is an intracellular process in which a portion of cytoplasm is transported into vacuoles for recycling. Physiological roles of autophagy in plants include recycling nutrients during ...senescence, sustaining life during starvation, and the formation of central digestive vacuoles. The regulation of autophagy and the formation of autophagosomes, spherical double membrane structures containing cytoplasm moving toward vacuoles, are poorly understood. HVA22 is a gene originally cloned from barley (Hordeum vulgare), which is highly induced by abscisic acid and environmental stress. Homologs of HVA22 include Yop1 in yeast, TB2/DP1 in human, and AtHVA22a to -e in Arabidopsis (Arabidopsis thaliana). Reverse genetics followed by a cell biology approach were employed to study the function of HVA22 homologs. The AtHVA22d RNA interference (RNAi) Arabidopsis plants produced small siliques with reduced seed yield. This phenotype cosegregated with the RNAi transgene. Causes of the reduced seed yield include short filaments, defective carpels, and dysfunctional pollen grains. Enhanced autophagy was observed in the filament cells. The number of autophagosomes in root tips of RNAi plants was also increased dramatically. The yop1 deletion mutant of Saccharomyces cerevisiae was used to verify our hypothesis that HVA22 homologs are suppressors of autophagy. Autophagy activity of this mutant during nitrogen starvation increased in 5 min and reached a plateau after 2 h, with about 80% of cells showing autophagy, while the wild-type cells exhibited low levels of autophagy following 8 h of nitrogen starvation. We conclude that HVA22 homologs function as suppressors of autophagy in both plants and yeast. Potential mechanisms of this suppression and the roles of abscisic acid-induced HVA22 expression in vegetative and reproductive tissues are discussed.
The purpose of this study is to explore the relationships among social support, professional empowerment, and nursing career development and to identify the significant factors that affect nursing ...career development among male nurses. A cross-sectional survey design was used with 314 male nurses in Taiwan. Social support and professional empowerment were significantly and positively correlated with nursing career development among male nurses. Social support, professional empowerment, salary, type of institution, type of clinical level, and nursing discipline were identified as factors that significantly influenced nursing career development. Together, they accounted for 55.9% of the total variation. Professional empowerment was the most critical predictor of nursing career development and accounted for 47.7% of the variation. Nursing managers should follow male nurses’ empowerment with interest and specifically address professional empowerment to promote male nurses’ career development.
Nasal polyposis is characterised by persistent inflammation of the upper airways. Autophagy has been implicated in many chronic inflammatory diseases. Whether autophagy plays a role in nasal polyp ...(NP) inflammation is completely unknown and deserves investigation.
LC3 and COX-2 expression, the common autophagy and inflammation indicators, respectively, was analysed by immunoblotting in fresh tissues of NP and control nasal mucosa (NM). Primary cultures of NP-derived fibroblasts (NPDFs) and NMDFs were established for in vitro studies. Autophagy was induced by amino acid starvation and LC3 ectopic overexpression or inhibited by 3-methyladenine in the fibroblasts. Inflammation was induced by IL1-β and TNF-α. LC3 and COX-2 expression was confirmed in NP specimens by immunohistochemistry.
LC3 expression was decreased while COX-2 expression was significantly increased in fresh NP tissues compared with the NM control. In NMDFs and NPDFs, autophagy induction by starvation and LC3 overexpression downregulated COX-2 expression. Conversely, autophagy inhibition by 3-methyladenine enhanced COX-2 expression. However, IL1-β and TNF-α had no effect on autophagy. Immunohistochemical studies on the NP specimens showed that most displayed low LC3 expression, whereas COX-2 was highly expressed in >50% of the specimens. Examination of two consecutive NP sections from the same tissue blocks revealed a negative correlation between LC3 and COX-2 expression.
Autophagy is deficient in NP tissues and COX-2 is negatively regulated by autophagy in NP-derived fibroblasts. Since COX-2 is essential for the production of pro-inflammatory mediators, this study might help interpret persistent mucosal inflammation in NP. Attenuation of inflammation by restoring autophagy might be a therapeutic strategy for treating NP.
Background/Purpose Oral squamous cell carcinoma (OSCC) is an aggressive tumor and its occurrence in Taiwan is closely related to chronic smoking, alcohol consumption, and especially to betel quid ...chewing. It became the fourth most common malignant tumor of Taiwanese men in 2006. Unfortunately, there are few biomarkers for diagnosis and treatment of this disease. Methods To find potential markers, two domestic cell lines (OC2 and OCSL) derived from different grades of OSCC were established and their proteins were compared by global proteomic analysis. The expression differences of GRP78 protein in these two cell lines and clinical samples from OSCC patients were verified. Results Of the 11 candidate proteins expressed differentially in both cell lines, six heat shock protein 90 kDa beta member 1 (94 kDa glucose-regulated protein; GRP94), protein disulfide-isomerase precursor, vimentin, tubulin beta-2C chain, 78 kDa glucose-regulated protein precursor (GRP78), and annexin A2 were increased in OC2 cells (low-grade OSCC), and five (heat shock protein 90-beta, annexin A1, stress-induced phosphoprotein 1, elongation factor-2, and integrin alpha-3 precursor) were increased in OCSL cells (high-grade OSCC). Some of these proteins have been previously associated with malignant tumors, but no previous association of GRP78 with OSCC has been reported. GRP78 protein expression in these two OSCC cell lines was confirmed by Western blotting. Immunohistochemical staining of clinical samples from OSCC patients revealed that decreased GRP78 protein expression was significantly correlated with advance tumor stage ( p < 0.001) and neck lymph node metastasis ( p = 0.001). Conclusion GRP78 protein is a possible biomarker of oral cancer in Taiwan.
Betel quid (BQ)-chewing oral cancer is a prevalent disease in many countries of Southeast Asia. Yet, the precise disease mechanism remains largely unknown. Here, we show that BQ extract-induced cell ...motility in three oral cancer cells (Ca9-22, SAS, and SCC9) presumably involves the Src family kinases (SFKs). Besides, BQ extract can markedly induce cell migration of wild type mouse embryonic fibroblasts (MEFs) but not MEFs lacking three SFK members, namely, Src, Yes, and Fyn, indicating the requirement of SFKs for BQ-induced cell motility. Betel quid extract can also elevate cellular SFK activities because phosphorylation of tyrosine 416 at the catalytic domain is increased, which in turn promotes phosphorylation of an in vitro substrate, enolase. Furthermore, we identified that areca nut, a major component of BQ, is the key factor accounting for BQ-induced cell migration and invasion through SFKs-mediated signaling pathways. Immunohistochemistry revealed that, particularly in BQ-chewing cases, the activity of SFKs was significantly higher in tumor-adjacent mucosa than that in solid tumor areas (P < .01). These results suggest a possible role of SFKs in tumor-host interface and thus in early tumor invasion in vivo. Consistent with this is the observation that activation of SFKs is colocalized with invasive tumor fronts in oral squamous cell carcinoma. Together, we conclude that SFKs may represent a potential biomarker of invasion and therapeutic target in BQ-induced oral cancer.
Anionic biosurfactant surfactin-mediated gold nanoparticles were synthesized for the first time in this study. Differing proton concentrations is believed to cause structural changes in the ...lipopeptide surfactin used to stabilize the gold nanoparticles in aqueous solution, the effects of which on the morphology of the nanoparticles were investigated. Synthesis of gold nanoparticles by borohydrate reduction was performed at three pH levels (pH 5, 7 and 9) and two different temperatures, and the nanoparticles were characterized by UV-visible spectroscopy, X-ray diffraction and transmission electron microscopy. The UV-vis spectra showed a blue shift with increasing pH from 5 to 9 (from 528 to 566 nm) at both 4 degrees C and room temperature. The nanoparticles synthesized at pH 7 and 9 remained stable for 2 months, while aggregates were observed at pH 5 within 24 h. TEM micrographs revealed that the mean particle size was about 13.11, 8.16 and 4.70 nm at pH 5, 9 and 7, respectively, at 4 degrees C. The nanoparticles formed at pH 7 were uniform in shape and size, and polydispersed and anisotropic at pH 5 and 9. The nanoparticles synthesized at room temperature were monodispersed and were more uniform as compared with those formed at 4 degrees C. This report describes the use of a renewable and environmentally green and biodegradable surfactant as a template and stabilizing agent in the synthesis of gold nanoparticles.
► Muscarinic M4 receptor mediates betel quid-induced oral cancer cell migration. ► Betel quid can selectively bind to muscarinic M4 receptor in vitro. ► Muscarinic M4 receptor is required for betel ...quid-induced cancer cell migration. ► Betel quid-induced cell migration was mediated through M4 receptor
→
SFKs
→
ERK1/2.
Betel quid (BQ) is a widely accepted etiological factor for oral squamous cell carcinoma (OSCC) in Southeast Asia, but how BQ chewing leads to oral carcinogenesis remains to be elucidated. We have previously demonstrated that the activation of Src family kinases (SFKs) is critical for BQ-induced oral cancer cell motility. Here we investigate whether this biological effect is mediated by specific membrane receptors in oral cancer cells. We found that BQ-induced activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and cell migration could be inhibited by atropine, suggesting the involvement of the muscarinic receptor family. The enhanced activities of ERK1/2 and cell migration were significantly counteracted by PD102807, the selective antagonist of muscarinic M4 receptor. Moreover, cold BQ extract effectively competed with a known ligand,
3H-
N-methyl scopolamine, for binding to muscarinic M4 receptor in vitro, thereby implying that BQ could activate motility-promoting signaling pathways through direct interaction with the receptor. The requirement of muscarinic M4 receptor for BQ-induced oral cancer cell migration was demonstrated by knockdown of the receptor using RNA interference (RNAi). Remarkably, ectopic expression of muscarinic M4 receptor in two oral cancer cell lines, Ca9-22 and SCC-9, further augmented BQ-induced cell migration by 83% and 99%, respectively. Finally, we verified that BQ-induced oral cancer cell migration was mediated through a muscarinic M4 receptor
→
SFKs
→
ERK1/2 signaling pathway. Thus, our findings have identified a novel signaling cascade mediating BQ-induced oral cancer cell motility, which could be a therapeutic target for BQ-related oral malignancies.
Background: Nasal polyposis is characterised by persistent inflammation of the upper airways. Autophagy has been implicated in many chronic inflammatory diseases. Whether autophagy plays a role in ...nasal polyp (NP) inflammation is completely unknown and deserves investigation. Methods: LC3 and COX-2 expression, the common autophagy and inflammation indicators, respectively, was analysed by immunoblotting in fresh tissues of NP and control nasal mucosa (NM). Primary cultures of NP-derived fibroblasts (NPDFs) and NMDFs were established for in vitro studies. Autophagy was induced by amino acid starvation and LC3 ectopic overexpression or inhibited by 3-methyladenine in the fibroblasts. Inflammation was induced by IL1-β and TNF-α. LC3 and COX-2 expression was confirmed in NP specimens by immunohistochemistry. Results: LC3 expression was decreased while COX-2 expression was significantly increased in fresh NP tissues compared with the NM control. In NMDFs and NPDFs, autophagy induction by starvation and LC3 overexpression downregulated COX-2 expression. Conversely, autophagy inhibition by 3-methyladenine enhanced COX-2 expression. However, IL1-β and TNF-α had no effect on autophagy. Immunohistochemical studies on the NP specimens showed that most displayed low LC3 expression, whereas COX-2 was highly expressed in >50% of the specimens. Examination of two consecutive NP sections from the same tissue blocks revealed a negative correlation between LC3 and COX-2 expression. Conclusion: Autophagy is deficient in NP tissues and COX-2 is negatively regulated by autophagy in NP-derived fibroblasts. Since COX-2 is essential for the production of pro-inflammatory mediators, this study might help interpret persistent mucosal inflammation in NP. Attenuation of inflammation by restoring autophagy might be a therapeutic strategy for treating NP.
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