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Aim: To describe the association between socio‐economic status and prevalence of key cardiovascular risk factors in people with type 2 diabetes in Scotland. Methods: A cross‐sectional study of 264 011 people with type 2 diabetes in Scotland in 2016 identified from the population‐based diabetes register. Socio‐economic status was defined using quintiles of the area‐based Scottish Index of Multiple Deprivation (SIMD) with quintile (Q)1 and Q5 used to identify the most‐ and least‐deprived fifths of the population, respectively. Logistic regression models adjusted for age, sex, health board, history of cardiovascular disease and duration of diabetes were used to estimate odds ratios (ORs) for Q1 compared with Q5 for each risk factor. Results: The mean (sd) age of the study population was 66.7 (12.8) years, 56% were men, 24% were in Q1 and 15% were in Q5. Crude prevalence in Q1/Q5 was 24%/8.8% for smoking, 62%/49% for BMI ≥ 30 kg/m2, 44%/40% for HbA1c ≥ 58 mmol/mol (7.5%), 31%/31% for systolic blood pressure (SBP) ≥ 140 mmHg, and 24%/25% for total cholesterol ≥ 5 mmol/l, respectively. ORs [95% confidence intervals (CI)] were 3.08 (2.95–3.21) for current smoking, 1.48 (1.44–1.52) for BMI ≥ 30 kg/m2, 1.11 (1.08–1.15) for HbA1c ≥ 58 mmol/mol (7.5%), 1.03 (1.00–1.06) for SBP ≥ 140 mmHg and 0.87 (0.84–0.90) for total cholesterol ≥ 5 mmol/l. Conclusions: Socio‐economic deprivation is associated with higher prevalence of smoking, BMI ≥ 30 kg/m2 and HbA1c ≥ 58 mmol/mol (7.5%), and lower prevalence of total cholesterol ≥ 5 mmol/l among people with type 2 diabetes in Scotland. Effective approaches to reducing inequalities are required as well as reducing risk factor prevalence across the whole population. What's new?: Socio‐economic deprivation is associated with increased risk of cardiovascular disease in people with diabetes.This study, using a national database of quarter of a million people, found that socio‐economic deprivation is strongly positively associated with smoking and obesity, modestly positively associated with above‐target HbA1c, and modestly negatively associated with above‐target cholesterol, with no evidence of an association with above‐target blood pressure.Inequalities appear to have widened over time.Our findings may enable more effective interventions to reduce these inequalities by targeted approaches in subgroups of the population. [ABSTRACT FROM AUTHOR]

Objective: To determine whether apoptosis contributes to hepatocyte loss in tunicamycin poisoning., Design: Groups of four guinea pigs were given 400 microg/kg of tunicamycin subcutaneously and killed at 24 h intervals up to 72 h post-injection. Livers were examined by routine histological methods and ancillary techniques (TUNEL staining, endonuclease activation, caspase activity, and electron microscopy) to ascertain whether any hepatocyte injury was apoptotic., Results: Many hepatocytes exposed to tunicamycin showed evidence of apoptosis in the form of nuclear karyorrhexis with chromatin margination and crescent formation, TUNEL-positivity, DNA laddering, elevated caspase activity and apoptotic body formation., Conclusion: Tunicamycin caused the death of many hepatocytes in the livers of guinea pigs by apoptosis.

Bcl-2 family of proteins are key regulators of apoptosis. Both proapoptotic and antiapoptotic members of this family are found in mammalian cells, but no such proteins have been described in insects. Here, we report the identification and characterization of Debcl, the first Bcl-2 homologue in Drosophila melanogaster. Structurally, Debcl is similar to Bax-like proapoptotic Bcl-2 family members. Ectopic expression of Debcl in cultured cells and in transgenic flies causes apoptosis, which is inhibited by coexpression of the baculovirus caspase inhibitor P35, indicating that Debcl is a proapoptotic protein that functions in a caspase-dependent manner. debcl expression correlates with developmental cell death in specific Drosophila tissues. We also show that debcl genetically interacts with diap1 and dark, and that debcl-mediated apoptosis is not affected by gene dosage of rpr, hid, and grim. Biochemically, Debcl can interact with several mammalian and viral prosurvival Bcl-2 family members, but not with the proapoptotic members, suggesting that it may regulate apoptosis by antagonizing prosurvival Bcl-2 proteins. RNA interference studies indicate that Debcl is required for developmental apoptosis in Drosophila embryos. These results suggest that the main components of the mammalian apoptosis machinery are conserved in insects.