Objective: This study investigated the associations of breakfast skipping with obesity and health-related quality of life (QOL). We also tested the hypothesis that there is a dose-dependent relationship between frequency of breakfast consumption and prevalence of obesity. Subjects and Design: This cross-section study used a national representative sample (n ¼ 15 340) from the 2005 Taiwan National Health Interview Survey. Breakfast skippers were defined as those who ate breakfast about once a week or less often and those who never ate breakfast. Individuals were classified as 'obese' if their body mass index was X27. Health-related QOL was assessed using the Medical Outcome Studies 36-Item Short-Form (SF-36) Health Survey. Logistic regression was used to examine the odds ratio of obesity and associated 95% confidence intervals (CIs) in breakfast skippers compared with breakfast eaters. Multivariable logistic regression modeling was used to adjust all risk estimates for covariates. Results: The unadjusted odds ratio of obesity in breakfast skippers was 1.23 (95% CI: 1.06, 1.43). The odds of developing obesity for breakfast skippers was 1.34 (95% CI: 1.15, 1.56) controlling for age, sex, marital status, educational level, monthly income, smoking, alcohol, betel nut chewing and exercise habit. The Cochran-Armitage trend test revealed that the prevalence rate of obesity decreased as the frequency of breakfast consumption increased (P ¼ 0.005). Breakfast skippers had significantly worse health-related QOL than breakfast eaters (Po0.001). Moreover, breakfast skippers had significantly lower scores in 5 out of 8 domain scores of the SF-36, namely general health perceptions (Po0.001), vitality (Po0.001), social functioning (P ¼ 0.036), emotional role (Po0.001) and mental health (Po0.001).

BackgroundTuberculous pleurisy is traditionally indicated by extreme lymphocytosis in pleural fluid and low yield of effusion culture. However, there is considerable inconsistency among previous study results. In addition, these data should be updated due to early effusion studies and advances in culture methods.MethodsFrom January 2004 to June 2009, patients with tuberculous pleurisy were retrospectively identified from the mycobacteriology laboratories and the pathology and tuberculosis registration databases of two hospitals in Taiwan where tuberculosis is endemic. Pleural fluid characteristics and yields of mycobacterial cultures using liquid media were evaluated.ResultsA total of 382 patients with tuberculous pleurisy were identified. The median lymphocyte percentage of total cells in pleural fluids was 84% (IQR 64–95%) and 17% of cases had a lymphocyte percentage of <50%. The lymphocyte percentage was negatively associated with the probability of a positive effusion culture (OR 0.97; 95% CI 0.96 to 0.99). The diagnostic yields were 63% for effusion culture, 48% for sputum culture, 79% for the combination of effusion and sputum cultures, and 74% for histological examination of pleural biopsy specimens.ConclusionThe degree of lymphocyte predominance in tuberculous pleurisy was lower than was previously thought. The lymphocyte percentage in pleural fluid was negatively associated with the probability of a positive effusion culture. With the implementation of a liquid culture method, the sensitivity of effusion culture was much higher than has been previously reported, and the combination of effusion and sputum cultures provided a good diagnostic yield.

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In this study, we examined the relationship between astrocyte activation in the cuneate nucleus (CN) and behavioral hypersensitivity after chronic constriction injury (CCI) of the median nerve. In addition, we also examined the effects of pre-emptive treatment with a number of drugs on astrocyte activation and hypersensitivity development in this model. Using immunohistochemistry and immunoblotting, little glial fibrillary acidic protein (GFAP; an astrocyte marker) immunoreactivity was detected in the CN of the normal rats. As early as 3 days after CCI, there was a significant increase in GFAP immunoreactivity in the lesion side of CN, and this reached a maximum at 7 days, and was followed by a decline. Counting of GFAP-immunoreactive astrocytes revealed that astrocytic hypertrophy, but not proliferation, contributes to increased GFAP immunoreactivity. Furthermore, microinjection of the glial activation inhibitor, fluorocitrate, into the CN at 3 days after CCI attenuated injury-induced behavioral hypersensitivity in a dose-dependent manner. These results suggest that median nerve injury-induced astrocytic activation in the CN modulated the development of behavioral hypersensitivity. Animals received MK-801 (glutamate N-methyl-d-aspartate (NMDA) receptor antagonist), clonidine (alpha(2)-adrenoreceptor agonist), tetrodotoxin (TTX, sodium channel blocker) or lidocaine (local anesthetic) 30 min prior to median nerve CCI. Pre-treatment with MK-801, TTX, and 2% lidocaine, but not clonidine, attenuated GFAP immunoreactivity and behavioral hypersensitivity following median nerve injury. In conclusion, suppressing reactions to injury, such as the generation of ectopic discharges and activation of NMDA receptors, can decrease astrocyte activation in the CN and attenuate neuropathic pain sensations.

This study aimed to investigate the association of fasting insulin and glucose levels with hepatocellular carcinoma (HCC) risk in a case-cohort study within a cohort (1989-2006) of 2903 male government employees chronically infected with hepatitis B virus (HBV) in Taiwan. Insulin, glucose and HBV-related factors were assayed in baseline plasma among 124 HCC cases and a random subcohort of 1084 of the total cohort. After adjustment for demographics and HBV-related factors, including viral load and genotype, the HCC risk was higher for the highest [>6.10 μU/ml, hazard ratio (HR) = 2.36, 95% confidence interval (CI): 1.43-3.90] and lowest (<2.75 μU/ml, HR = 1.57, 95% CI: 0.96-2.58) categories of insulin, compared with insulin of 2.75-4.10 μU/ml. The dose-response relationship between insulin and HCC varied by follow-up time, with stronger association for the HCC cases that occurred ≥8 years after baseline (P for trend <0.0001). The effect of higher insulin on HCC risk remained after adjustment for other metabolic factors, and was fairly consistent across strata of age, body mass index, and HBV genotypic variants. However, it was more profound among those with viral load <4.39 log(10) copies/ml at recruitment (>6.10 μU/ml, HR = 6.15, 95% CI: 2.48-15.22). Higher insulin was also associated with an increased risk for cirrhosis diagnosed by ultrasonography and elevated alanine aminotransferase. No association with either cirrhosis or HCC was noted for glucose or diabetes after adjusting for insulin. In conclusion, elevated insulin levels are an independent risk factor for HCC among HBV carriers, especially for those with lower viral load.

It was hypothesized that the suppressive effect of diosgenin (1) on the intestinal T helper (Th)2 responses is associated with an enhancement of the regulatory T-cell immunity. Ovalbumin (OVA)-sensitized BALB/c mice were gavaged daily with 1 and received repeatedly oral OVA challenges to induce intestinal allergic responses. The expression of Th2- and Treg-related cytokines and transcription factors was examined by immunohistochemical staining and RT-PCR. Administration of 1 markedly attenuated the intestinal expression of interleukin (IL)-4 and GATA3. In addition, administration of 1 reversed the diminished density of intestinal Foxp3(+) cells induced by OVA oral challenges and enhanced the expression of IL-10 by Foxp3(+) cells markedly. These results suggest that the suppressive effect of 1 on allergen-induced intestinal Th2 responses is closely associated with an up-regulation of the regulatory T-cell immunity in the inflammatory site.

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