Effect of individual-level and socioeconomic factors on long-term survival after cataract surgery over a 30-year period

Purpose: To evaluate survival and the risk for mortality after cataract surgery in relation to individual-level and socioeconomic factors in Scotland over 3 decades. Setting: Linked healthcare data, United Kingdom. Design: Representative population-based study. Methods: A 5% random sample of Scottish decedents linked to hospital records (1981 to 2012) was assessed. Survival time, survival probability, and determinants of mortality were evaluated after the first and second recorded hospital episodes for cataract surgery. Cox proportional-hazards regression models were used to assess the effect of individual-level and socioeconomic factors including age, geographic location, socioeconomic status, and comorbidity on mortality. Results: The study evaluated linked administrative healthcare data from 9228 deceased patients who had cataract surgery. The mean survival time was 2383 days ± 1853 (SD). The survival probability decreased from 98% 90 days after surgery to 22% at 10 years, 2% at 20 years, and 0% after 30 years. The mean age was 77 ± 9 years. Age (hazard ratio [HR] 3.66; 95% confidence interval [CI], 2.97-3.80; P < .001) and severe comorbidity (HR 1.68; 95% CI, 1.47-1.91; P < .001) were associated with an increased risk for mortality; women had a 20% lower risk than men (HR 0.80; 95% CI, 0.76-0.83; P < .001). Socioeconomic status and rural geographic locations were not linked to mortality. Conclusions: Long-term survival after cataract surgery was determined by individual-level characteristics reflecting the mortality patterns of aging populations. The mortality risk was independent of socioeconomic and geographic factors per se

The impact of alcohol pricing policies on public health in Hong Kong, China: A modelling study.

Background Contrary to most developed economies, Hong Kong has reduced and eliminated taxes on beer and wine over the last 15 years and observed increasing alcohol consumption. Methods We applied econometric epidemiological modelling to assess the impact of reverting ad valorem taxation to pre-2008 levels (20% on wine and 40% on beer) on consumption and health outcomes. We used 15 years of industry sales and pricing data (2004-2018) to derive 25 own-price and cross-price elasticity estimates. We applied risk functions from the World Health Organization 2018 Global Status Report to assess the impact on 25 alcohol-attributable conditions. Findings An estimated 616 deaths (91.3% in men) were attributable to alcohol in 2018. Raising taxes to pre-2008 levels is estimated to reduce consumption of pure alcohol consumption by 8.0%, 15.9%, and 31.1%; and reduce alcohol-attributable deaths by 11.6%, 21.8%, and 40.2% assuming 25%, 50% and 100% pass through rates of taxes to consumers. The largest projected decreases in alcohol-attributable mortality in absolute numbers are alcohol abuse, alcohol dependence, and alcoholic psychoses (wholly alcohol-attributable disorders). The largest absolute number of new alcohol-attributable cases in 2018 were hypertension, alcohol dependence and alcohol abuse; which are estimated to be reduced by 31.3%, 34.2%, and 34.3% respectively by raising taxes to pre-2008 levels. The alcohol-attributable health burden and absolute reductions in health harms are far greater in men. Interpretation Reversing the 2008 alcohol tax reductions is potentially effective in averting the alcohol-attributable health burden and thus mitigate against the avoidable harms of alcohol-related disease. Funding Health and Medical Research Fund, Food and Health Bureau of the Hong Kong SAR, China [03170067].fals

Profiling of the perturbed metabolomic state of mouse spleen during acute and chronic toxoplasmosis

Background Toxoplasma gondii, a common opportunistic protozoan, is a leading cause of illness and mortality among immunosuppressed individuals and during congenital infections. Current therapeutic strategies for toxoplasmosis are not fully effective at curtailing disease progression in these cases. Given the parasite ability to influence host immunity and metabolism, understanding of the metabolic alterations in the host’s immune organs during T. gondii infection may enhance the understanding of the molecular mechanisms that define the pathophysiology of T. gondii infection. Methods We investigated the global metabolic changes in the spleen of BALB/c mice at early and late stage of infection with T. gondii using LC-MS/MS-based metabolomics. Multivariate data analysis methods, principal components analysis (PCA) and partial least squares discriminant analysis (PLS-DA), were used to identify metabolites that are influenced by T. gondii infection. Results Multivariate analyses clearly separated the metabolites of spleen of infected and control mice. A total of 132 differential metabolites were identified, 23 metabolites from acutely infected versus control mice and 109 metabolites from chronically infected versus control mice. Lipids, hormones, lactones, acids, peptides, antibiotics, alkaloids and natural toxins were the most influenced chemical groups. There were 12 shared differential metabolites between acutely infected versus control mice and chronically infected versus control mice, of which 4,4-Dimethyl-5alpha-cholesta-8,14,24-trien-3beta-ol was significantly upregulated and ubiquinone-8 was significantly downregulated. Major perturbed metabolic pathways included primary bile acid biosynthesis, steroid hormone biosynthesis, biotin metabolism, and steroid biosynthesis, with arachidonic acid metabolism being the most significantly impacted pathway. These metabolic changes suggest a multifactorial nature of the immunometabolic responses of mouse spleen to T. gondii infection. Conclusions This study demonstrated that T. gondii infection can cause significant metabolomic alterations in the spleen of infected mice. These findings provide new insights into the molecular mechanisms that underpin the pathogenesis of T. gondii infection

The mechanisms of action of metformin

Metformin is a widely-used drug that results in clear benefits in relation to glucose metabolism and diabetes-related complications. The mechanisms underlying these benefits are complex and still not fully understood. Physiologically, metformin has been shown to reduce hepatic glucose production, yet not all of its effects can be explained by this mechanism and there is increasing evidence of a key role for the gut. At the molecular level the findings vary depending on the doses of metformin used and duration of treatment, with clear differences between acute and chronic administration. Metformin has been shown to act via both AMP-activated protein kinase (AMPK)-dependent and AMPK-independent mechanisms; by inhibition of mitochondrial respiration but also perhaps by inhibition of mitochondrial glycerophosphate dehydrogenase, and a mechanism involving the lysosome. In the last 10 years, we have moved from a simple picture, that metformin improves glycaemia by acting on the liver via AMPK activation, to a much more complex picture reflecting its multiple modes of action. More work is required to truly understand how this drug works in its target population: individuals with type 2 diabetes

Search for new physics in the multijet and missing transverse momentum final state in proton-proton collisions at √s=8 Tev

Peer reviewe

Study of hadronic event-shape variables in multijet final states in pp collisions at √s=7 TeV

Peer reviewe

Measurement of Higgs boson production and properties in the WW decay channel with leptonic final states

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An administrative data merging solution for dealing with missing data in a clinical registry: adaptation from ICD-9 to ICD-10

<p>Abstract</p> <p>Background</p> <p>We have previously described a method for dealing with missing data in a prospective cardiac registry initiative. The method involves merging registry data to corresponding ICD-9-CM administrative data to fill in missing data 'holes'. Here, we describe the process of translating our data merging solution to ICD-10, and then validating its performance.</p> <p>Methods</p> <p>A multi-step translation process was undertaken to produce an ICD-10 algorithm, and merging was then implemented to produce complete datasets for 1995–2001 based on the ICD-9-CM coding algorithm, and for 2002–2005 based on the ICD-10 algorithm. We used cardiac registry data for patients undergoing cardiac catheterization in fiscal years 1995–2005. The corresponding administrative data records were coded in ICD-9-CM for 1995–2001 and in ICD-10 for 2002–2005. The resulting datasets were then evaluated for their ability to predict death at one year.</p> <p>Results</p> <p>The prevalence of the individual clinical risk factors increased gradually across years. There was, however, no evidence of either an abrupt drop or rise in prevalence of any of the risk factors. The performance of the new data merging model was comparable to that of our previously reported methodology: c-statistic = 0.788 (95% CI 0.775, 0.802) for the ICD-10 model versus c-statistic = 0.784 (95% CI 0.780, 0.790) for the ICD-9-CM model. The two models also exhibited similar goodness-of-fit.</p> <p>Conclusion</p> <p>The ICD-10 implementation of our data merging method performs as well as the previously-validated ICD-9-CM method. Such methodological research is an essential prerequisite for research with administrative data now that most health systems are transitioning to ICD-10.</p

Constraints on parton distribution functions and extraction of the strong coupling constant from the inclusive jet cross section in pp collisions at √s=7 TeV

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Study of double parton scattering using W+2-jet events in proton-proton collisions at √s=7 TeV

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