HbA1c variability, in addition to mean HbA1c, predicts incident hip fractures in Chinese people with type 2 diabetes.

Type 2 diabetes is associated with an increased risk of hip fractures. We hypothesize that long-term glycemic variability predicts incident hip fractures. We demonstrated that HbA1c variability predicted incident hip fractures independent of mean HbA1c, suggesting the potential benefits of minimizing glycemic variability in addition to optimizing mean glycemia for bone health. INTRODUCTION: Type 2 diabetes is associated with an increased risk of hip fractures, and a linear relationship between HbA1c levels and hip fracture incidence has been observed. We hypothesize that HbA1c variability also predicts incident hip fractures in type 2 diabetes. METHODS: Chinese individuals with type 2 diabetes aged ≥ 60 years were identified from electronic health records in Hong Kong between 2008 and 2012 and observed for incident hip fractures. Hip fracture was defined by the International Classification of Diseases (Ninth Revision) code 820. HbA1c variability was determined using standard deviation, adjusted standard deviation, and coefficient of variation of HbA1c measurements in the 5 years preceding the entry date. Multivariable Cox regression analysis was used to evaluate associations between HbA1c variability and incident hip fractures. RESULTS: A total of 83,282 participants were included. Their mean age was 71.3 ± 7.5 years, duration of diabetes 11.7 ± 7.7 years, baseline HbA1c 56.6 ± 13.5 mmol/mol (7.33 ± 1.23%), and median follow-up 6.8 years. All indices of HbA1c variability were significant independent predictors of incident hip fractures, with an adjusted hazard ratio of up to 1.29 (all p < 0.001), and remained to be independent predictors across groups of different intensity of glycemic control. Mean HbA1c ≥ 64 mmol/mol (8.0%) was associated with a 25% increase in incident hip fractures compared with mean HbA1c < 53 mmol/mol (7.0%). CONCLUSION: HbA1c variability is an independent positive predictor of hip fracture in type 2 diabetes, across the spectrum of varying degree of glycemic control, while a high HbA1c is also not advisable from the perspective of bone health.

Coexistence between colorectal cancer/adenoma and coronary artery disease: results from 1382 patients.

BACKGROUND: Common risk factors exist in colorectal neoplasia (cancer or adenoma) and coronary artery disease. AIM: To investigate in a retrospective study if there is coexistence of the two events in patients > OR =50 years. METHODS: Computer data on colonoscopies performed on symptomatic patients, the corresponding medical record and colonic histology in 1997-2000 were retrieved. History of coronary artery disease was recorded. To adjust for the factors of age and sex, bivariate logistic regression analysis was used to test for coexistence. RESULTS: 1382 patients were recruited. Colorectal neoplasia and history of coronary artery disease were present in 27% (373) and 12% (167) of patients, respectively. The mean age of patients was older in colorectal neoplasia+ (75 +/- 11 vs. 69 +/- 13 years, P < 0.0001) and in coronary artery disease+ (79 +/- 9 vs. 69 +/- 12 years, P < 0.0001) patients. Male was the predominant sex in colorectal neoplasia+: 33% vs. 22% (P < 0.0001), but not in coronary artery disease+ (P = 0.29). Colorectal neoplasia+ patients were more likely to have coronary artery disease+ [21.2% (79/373) vs. 8.8% (89/1098) (P < 0.0001)]. Bivariate logistic regression analysis showed strong association between the two events (OR: 2.12, 95% CI: 1.5, 3.0). CONCLUSION: There is strong coexistence of colorectal neoplasia and coronary artery disease, probably due to exposure to common risk factors.

Generation and Characterization of Patient-Specific iPSC Model for Cardiovascular Disease.

Advances in differentiation of cardiomyocytes from human induced pluripotent stem cell (hiPSC) were emerged as a tool for modeling of cardiovascular disease that recapitulates the phenotype for the purpose of drug screening, biomarker discovery, and testing of single-nucleotide polymorphism (SNP) as a modifier for disease stratification. Here, we describe the (1) retroviral reprogramming strategies in the generation of human iPSC, (2) methodology in characterization of iPSC in order to identify the stem cell clones with the best quality, and (3) protocol of cardiac differentiation by modulation of Wnt signaling and ß-catenin pathway.