Physical activity, smoking, and the incidence of clinically diagnosed insomnia

OBJECTIVE: This study was designed to examine the independent and combined associations of physical activity and smoking on the incidence of doctor-diagnosed insomnia using a nationally representative sample over seven years, taking into account other relevant covariates. METHODS: Participants aged 18 years or older in the 2005 Taiwan National Health Interview Survey (NHIS) with links to National Health Insurance (NHI) claim data between 2005 and 2012 and without diagnosed insomnia before 2005, were selected into this study (n = 12,728). Participants were classified as having insomnia with International Classification of Diseases, Ninth Revision (ICD-9) CM codes 307.41, 307.42, or 780.52. Self-reported smoking status and frequency, duration, and types of leisure-time and non−leisure-time physical activities were collected. Metabolic equivalent (MET) intensity levels for each activity were assigned, and weekly energy expenditure of each activity was calculated and summed. RESULTS: Inactive participants had a higher risk of incident insomnia [hazard ratio (HR) = 1.22, 95% confidence interval (CI) = 1.06–1.42, p = 0.007] than the active group, and ever-smokers were more likely to have incident insomnia than never smokers (HR = 1.45, 95% CI = 1.20–1.76, p < 0.001). Compared with the nonsmoker/active group, the ever-smoker/inactive group had a higher risk of incident insomnia (HR = 1.78, 95% CI = 1.41–2.25, p < 0.001). Sensitivity analyses excluding individuals diagnosed with other sleep disorders or mental disorders yielded similar results, with the ever-smoker/inactive group having the highest risk of insomnia. CONCLUSIONS: Inactive adults and smokers are at higher risk for incident insomnia, highlighting the importance of a healthy lifestyle and pointing to strategies such as encouraging smoking cessation and physical activity to avoid insomnia among adults

Prospective association between late-life physical activity and hospital care utilisation: a 7-year nationwide follow-up study

BACKGROUND: It is still equivocal whether there is a potential role of late-life physical activity in ameliorating the challenges of increasing healthcare expenditure due to the consequence of global population ageing. OBJECTIVE: this study aimed to examine the prospective association between physical activity and subsequent hospital care utilisation in older adults and to explore the optimal dose of physical activity required to reduce hospital care utilisation. DESIGN: this was a prospective cohort study based on the data from the Taiwan 2005 National Health Interview Survey, which were linked to the 2005-12 claims data from the National Health Insurance system. PARTICIPANTS: 1,760 older adults aged 65 or more. METHODS: the frequency, duration and intensity for physical activity were assessed, and total physical activity energy expenditure was estimated. The average annualised hospital care utilisation for the period 2006 through 2012, including number of hospitalisations, number of days in hospital and the costs of hospitalisation, were calculated. RESULTS: older adults engaging in at least moderate volume of physical activity (≥1,000 kcal/week) experienced fewer subsequent hospital admissions and fewer days in hospital than did sedentary individuals, after adjusting for covariates. Trends for reduced hospitalisation costs were also found. These associations persisted in sensitivity analyses, including tests of reverse causation. CONCLUSION: this study has provided evidence that older adults who are at least moderately active may minimise utilisation of hospital care services. The findings highlight the importance of maintaining a physically active lifestyle in later life

Cyclin D 1‐induced proliferation is independent of beta‐catenin in H ead and N eck C ancer

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/106775/1/odi12124.pd

Non-Coding Keratin Variants Associate with Liver Fibrosis Progression in Patients with Hemochromatosis

Background: Keratins 8 and 18 (K8/K18) are intermediate filament proteins that protect the liver from various forms of injury. Exonic K8/K18 variants associate with adverse outcome in acute liver failure and with liver fibrosis progression in patients with chronic hepatitis C infection or primary biliary cirrhosis. Given the association of K8/K18 variants with endstage liver disease and progression in several chronic liver disorders, we studied the importance of keratin variants in patients with hemochromatosis. Methods: The entire K8/K18 exonic regions were analyzed in 162 hemochromatosis patients carrying homozygous C282Y HFE (hemochromatosis gene) mutations. 234 liver-healthy subjects were used as controls. Exonic regions were PCRamplified and analyzed using denaturing high-performance liquid chromatography and DNA sequencing. Previouslygenerated transgenic mice overexpressing K8 G62C were studied for their susceptibility to iron overload. Susceptibility to iron toxicity of primary hepatocytes that express K8 wild-type and G62C was also assessed. Results: We identified amino-acid-altering keratin heterozygous variants in 10 of 162 hemochromatosis patients (6.2%) and non-coding heterozygous variants in 6 additional patients (3.7%). Two novel K8 variants (Q169E/R275W) were found. K8 R341H was the most common amino-acid altering variant (4 patients), and exclusively associated with an intronic KRT8 IVS7+10delC deletion. Intronic, but not amino-acid-altering variants associated with the development of liver fibrosis. I

Sphingosine 1-phosphate receptor 4 promotes nonalcoholic steatohepatitis by activating NLRP3 inflammasome

BACKGROUND & AIMS: Sphingosine 1-phosphate receptors (S1PRs) are a group of G-protein-coupled receptors that confer a broad range of functional effects in chronic inflammatory and metabolic diseases. S1PRs also may mediate the development of nonalcoholic steatohepatitis (NASH), but the specific subtypes involved and the mechanism of action are unclear. METHODS: We investigated which type of S1PR isoforms is activated in various murine models of NASH. The mechanism of action of S1PR4 was examined in hepatic macrophages isolated from high-fat, high-cholesterol diet (HFHCD)-fed mice. We developed a selective S1PR4 functional antagonist by screening the fingolimod (2-amino-2-[2-(4- n-octylphenyl)ethyl]-1,3-propanediol hydrochloride)-like sphingolipid-focused library. RESULTS: The livers of various mouse models of NASH as well as hepatic macrophages showed high expression of S1pr4. Moreover, in a cohort of NASH patients, expression of S1PR4 was 6-fold higher than those of healthy controls. S1pr4(++/-) mice were protected from HFHCD-induced NASH and hepatic fibrosis without changes in steatosis. S1pr4 depletion in hepatic macrophages inhibited lipopolysaccharide-mediated Ca++ release and deactivated the Nod-like receptor pyrin domaincontainning protein 3 (NLRP3) inflammasome. S1P increased the expression of S1pr4 in hepatic macrophages and activated NLRP3 inflammasome through inositol trisphosphate/inositol trisphosphate-receptor-dependent [Ca++] signaling. To further clarify the biological function of S1PR4, we developed SLB736, a novel selective functional antagonist of SIPR4. Similar to S1pr4(+/-) mice, administration of SLB736 to HFHCD-fed mice prevented the development of NASH and hepatic fibrosis, but not steatosis, by deactivating the NLRP3 inflammasome. CONCLUSIONS: S1PR4 may be a new therapeutic target for NASH that mediates the activation of NLRP3 inflammasome in hepatic macrophages

The impact of SARS on hospital performance

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