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Articles by D Qi
Total Records ( 2 ) for D Qi
  D Qi , K Cai , O Wang , Z Li , J Chen , B Deng , L Qian and Y. Le

Amylin is the major component of pancreatic amyloid, which is implicated in the development of type 2 diabetes. It is costored with insulin in the secretory granules of pancreatic β-cells and cosecreted with insulin following stimulation with glucose. Here, we investigate the effect of fatty acids (FAs) on amylin expression and secretion by β-cells and explore the underlying mechanisms. Palmitate and oleate dose-dependently induced amylin mRNA accumulation in murine pancreatic β-cell line MIN6 and primary pancreatic islets. the inductive effect of FAs on amylin expression is independent of glucose concentration. FAs upregulated amylin expression at the transcriptional level, and FAs must be metabolized to induce amylin expression. FAs also significantly induced human amylin promoter activation. Pretreatment of MIN6 cells with Ca2+ chelator (EGTA, BAPTA-AM) PKC inhibitor Gö-6976 or protein synthesis inhibitor cycloheximide significantly inhibited FA-induced amylin mRNA expression. Transcription factors cAMP-responsive element-binding protein, pancreatic and duodenal homeobox factor-1, and peroxisome proliferator-activated receptor were not involved in FA-induced amylin expression. Palmitate and oleate both increased amylin and insulin release from MIN6 cells and stimulated amylin expression but had no effect on insulin expression. Mice refed with Intralipid had significantly higher levels of plasma FFA, amylin, and insulin than those refed with saline. These data demonstrate that FAs differently regulate amylin and insulin expression and induce both amylin and insulin release. Ca2+ and PKC signaling pathways and de novo-synthesized protein(s) were involved in FA-induced amylin expression. Induction of amylin production and release by FA may contribute to its biological functions under physiological conditions.

  T. V Glotzer , E. G Daoud , D. G Wyse , D. E Singer , M. D Ezekowitz , C Hilker , C Miller , D Qi and P. D. Ziegler

Background— It is unknown if brief episodes of device-detected atrial fibrillation (AF) increase thromboembolic event (TE) risk.

Methods and Results— TRENDS was a prospective, observational study enrolling patients with ≥1 stroke risk factor (heart failure, hypertension, age ≥65 years, diabetes, or prior TE) receiving pacemakers or defibrillators that monitor atrial tachycardia (AT)/AF burden (defined as the longest total AT/AF duration on any given day during the prior 30-day period). This time-varying exposure was updated daily during follow-up and related to TE risk. Annualized TE rates were determined according to AT/AF burden subsets: zero, low (<5.5 hours [median duration of subsets with nonzero burden]), and high (≥5.5 hours). A multivariate Cox model provided hazard ratios including terms for stroke risk factors and time-varying AT/AF burden and antithrombotic therapy. Patients (n=2486) had at least 30 days of device data for analysis. During a mean follow-up of 1.4 years, annualized TE risk (including transient ischemic attacks) was 1.1% for zero, 1.1% for low, and 2.4% for high burden subsets of 30-day windows. Compared with zero burden, adjusted hazard ratios (95% CIs) in the low and high burden subsets were 0.98 (0.34 to 2.82, P=0.97) and 2.20 (0.96 to 5.05, P=0.06), respectively.

Conclusions— The TE rate was low compared with patients with traditional AF with similar risk profiles. The data suggest that TE risk is a quantitative function of AT/AF burden. AT/AF burden ≥5.5 hours on any of 30 prior days appeared to double TE risk. Additional studies are needed to more precisely investigate the relationship between stroke risk and AT/AF burden.

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