Glycemic control and comprehensive metabolic risk factors control in older adults with type 2 diabetes.

BACKGROUND: Older adults with type 2 diabetes are prone to multiple metabolic abnormalities. However, data from these patients on comprehensive metabolic risk factors control are limited. METHODS: The present study included 2736 older adults aged 60 to 90 years with type 2 diabetes from 114 hospitals across 22 provinces in China. Metabolic abnormalities, including hypertension, dyslipidemia, hyperuricemia, and obesity, were recorded. Comprehensive metabolic risk factors control included the control of hemoglobin A1c (HbA1c) level, blood pressure, serum lipids level, serum uric acid level, and body mass index. The target glycemic control was defined as HbA1c <7%. RESULTS: The proportion of older adults who achieved the HbA1c target was 23.0%. The glycemic control rate increased with the number of metabolic abnormalities increased. The patients who had all four metabolic abnormalities had 4.05 times (95% confidence interval: 2.16, 7.61) the odd to meet glycemic target than those with none of metabolic abnormalities. However, only 4.6% of patients met the targets for all 5 metabolic risk factors. The comprehensive rate of all 5 factors in control decreased from 13.4% to 0% with the number of metabolic abnormalities increased. CONCLUSION: The glycemic control rate and the comprehensive metabolic risk factors control rate were 23.0% and 4.6%, respectively. As the number of metabolic abnormalities increased, the number of risk factor targets achieved decreased. Our findings suggest that a strategy for comprehensive control is urgently needed in older adults with type 2 diabetes, especially in those with co-existing metabolic abnormalities.

KIF3B Promotes the Proliferation of Pancreatic Cancer.

Background: Kinesin Family Member 3B (KIF3B) is one of the most ubiquitously expressed KIFs, which is related to numerous physiological responses. KIF3B has also been implicated in carcinogenesis such as in hepatocellular carcinoma cells. However, the expression of KIF3B has not been studied in pancreatic cancer along with its clinical significance. Methods: Immunohistochemical assays were performed to detect the expression levels of KIF3B in the tumor tissues and adjacent non-tumor tissues. Patients were sequentially divided into different expression levels of KIF3B group based on the staining intensity of FKIF3B in tumor tissues. The link between KIF3B expression and clinical characteristics were investigated, and the role of KIF3B on pancreatic cancer cell proliferation was detected by colony formation and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, respectively. And the proliferation related proteins such as Ki67 and proliferating cell nuclear antigen (PCNA) were detected by Western blot. The possible effects of KIF3B on tumor growth were assessed in vivo. Results: KIF3B was highly expressed in human pancreatic cancer tissues. We also found KIF3B was significantly associated to the pTNM stage (*p = 0.018), lymph node metastasis (*p = 0.040) and vascular invasion (*p = 0.034). We reported that increased expression of KIF3B was significantly correlated with poor clinical outcome in our clinical cohort of pancreatic cancer. Furthermore, functional assays revealed that knockdown KIF3B in vitro and in vivo might inhibit cancer cells proliferation by affecting Ki67 and PCNA. Conclusions: Our data suggested that KIF3B was associated with pancreatic cancer malignant progression especially proliferation. Hence, KIF3B might serve as a potential therapy target of pancreatic cancer in clinical treatment.