Predictive value of serum uric acid on cardiovascular disease and all-cause mortality in urban Chinese patients.

BACKGROUND: The association between increased serum uric acid (SUA) levels and cardiovascular risk has been debated for decades. Several large studies have provided conflicting results regarding the clinical significance of elevated SUA levels in cardiovascular disease (CVD) or cerebrovascular disease. The aim of this study was to investigate the relationship between SUA and CVD and all-cause mortality and their potential diagnostic value. METHODS: A total of 3570 in-patients ranging in age from 56 to 95 years (mean (67.36 +/- 11.36) years) were selected from 20 hospitals in Beijing and Shanghai. A carefully designed questionnaire was used to gather baseline data of each patient. All patients were divided into two main groups according to their SUA levels: high SUA and normal SUA groups. Serum indices and other important parameters were measured. RESULTS: Compared with normal SUA group, high SUA group had significant difference in systolic blood pressure (SBP), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), body mass index (BMI), and age (P < 0.05 or P < 0.01). High SUA prevailed in female and patients with history of essential hypertension, while history of smoking and diabetes showed no significant difference between two groups. All-cause and CVD mortality occurred more frequently in high SUA group than in normal SUA group. In the accumulative survival analysis, high SUA group had lower survival rate than normal SUA group both in CVD and all-cause mortality. COX regression analysis indicated that the history of smoking, age and high SUA were independent risk factors for the development of CVD. CONCLUSIONS: These preliminary observations suggest that patients with high SUA levels would face higher risk of mortality. SUA measurement may be applied as a routine predictor for clinical assessment.

[Effects of double-stranded RNA poly(I:C) on matrix metalloproteinase mRNA expression in human nasal polyp epithelial cells].

OBJECTIVE: Chronic rhinosinusitis was often exacerbated by viral infection. A disruption of the mechanisms that regulate the activity of matrix metalloproteinases (MMPs) during viral infection was one possible mechanism responsible for the exacerbation. The purpose of study was to achieve a better understanding of MMP expression in nasal epithelial cells after viral infection. METHODS: Human nasal epithelial cells were isolated from nasal polyp specimens obtained during endoscopic endonasal surgery in chronic rhinosinusitis patients. The expression of MMP-2, MMP-9, and tissue inhibitor of metalloproteinase (TIMP)-1 mRNA in primary human nasal polyp epithelial cells after double stranded RNA (ds RNA) stimulation were investigated. RESULTS: Among the genes whose expression was evaluated, only expression of MMP-9 mRNA increased significantly after dsRNA stimulation (22.61 +/- 5.47 fold increase, Z = -2.52, P = 0.012). CONCLUSIONS: The significant up-regulation of MMP-9 mRNA, which was not modulated by TIMP-1, was an additional source of increased proteolytic activity in virus-infected upper airways that might contribute to the exacerbation of chronic rhinosinusitis with nasal polyps.

[The characteristics during exercise test in long QT syndrome patients and the effects of left cardiac sympathetic denervation].

OBJECTIVE: To explore the mechanism of the left cardiac sympathetic denervation (LCSD) surgery to reduce the incidence of cardiac events for long QT syndrome (LQTS) patients. METHODS: 12 LQTS patients were selected to do exercise test (ET) to mimic sympathetic activation. The dynamic alterations on ECG during exercise and recovery phases (Rec) were observed and the exercise test characteristics for LQTS patients before and after surgery were summarized and compared. RESULTS: The QTc at resting was shortened from 0.54 s +/- 0.04 s to 0.50 s +/- 0.04 s, P = 0.026, while the maximum heart rate during exercise decreased from 141 beat/min +/- 18 beat/min to 124 beat/min +/- 14 beat/min, P = 0.003. QTc was shortened during exercise, however, it was prolonged during the early recovery phase (before ET 0.54 s +/- 0.02 s, ET 10 min 0.46 s +/- 0.02 s, Rec 4 min 0.55 s +/- 0.03 s); LCSD could reduce such abrupt alteration of QTc during early recovery phase (after surgery: before ET 0.53 s +/- 0.03 s, ET 10 min 0.48 s +/- 0.03 s, Rec 4 min 0.53 s +/- 0.05 s). QT/RR interval slope, representing the adaptation response of QT interval to heart rate, became steeper after exercise (from 0.61 +/- 0.06 to 0.71 +/- 0.07 after exercise, P < 0.01). LCSD made the slopes become less steep both before exercise (from 0.61 +/- 0.06 before surgery to 0.55 +/- 0.07 after surgery, P = 0.013) and after exercise (from 0.71 +/- 0.07 before surgery to 0.66 +/- 0.06 after surgery, P = 0.018). Notched T wave alterations occurred in 7 patients at the end of exercise and/or during early recovery phase before surgery, and LCSD diminished such alteration in 4 patients. CONCLUSION: The slope between QT and RR both the pre-exercise and post-exercise slopes, interval becomes less steep after LCSD, which suggests that exaggerated delay in repolarization with decreasing heart rate for LQTS patients is improved by LCSD. This may be one of the mechanisms of LCSD efficacy for treating LQTS patients. Exercise test is one of tools to evaluate the effect of LCSD on LQTS patients.

A novel missense mutation of the ATP2A2 gene in a Chinese family with Darier's disease.

Darier's disease (DD) is an autosomal dominant skin disorder that is characterized by multiple keratotic papules, focal loss of adhesion and abnormal keratinization. Mutations in the ATP2A2 gene encoding sarco/endoplasmic reticulum calcium pumping ATPase type 2 have been identified as the molecular basis of DD. We report here a three-generation family with DD, and examined ATP2A2 gene mutations in this family by direct sequencing. A novel missense mutation A-->G was identified in exon 12, nucleotide 1704, which leads to the substitution of lysine by arginine at codon 514 (K514R). This study contributes to the database on ATP2A2 in DD, and further illustrates the extensive diversity of mutational events that lead to the different phenotypes of DD.