Lower risk of primary Sjogren’s syndrome in patients with dengue virus infection: a nationwide cohort study in Taiwan

Clinical Rheumatology - The data concerning the association between dengue viruses (DV) infection and autoimmune diseases (ADs) remain unclear and are scarce. This nationwide population-based...     

The effect of fluvastatin on fibrinolytic factors in patients with hypercholesterolemia

Several studies have shown cardiovascular benefit in treating hypercholesterolemia with HMG-CoA reductase inhibitor. However, in addition to the lowering of cholesterol, the beneficial effects of this inhibitor reflect other pharmacological activities. Whether these beneficial effects are partly mediated by changes in fibrinolytic factors remains to be proven, since clinical studies on the effects of HMG-CoA reductase inhibitors on fibrinolytic factors have not yielded consistent results. The purpose of this study was to evaluate the effects of fluvastatin on fibrinolytic factors in hypercholesterolemic patients. After 6 weeks on a low-fat, low-cholesterol diet, 23 outpatients known to have primary hypercholesterolemia with low density lipoprotein cholesterol (LDL-C) > or = 130 mg/dl with at least 2 risk factors or fasting LDL-C > or = 160 mg/dl were selected for the study. Venous blood samples were collected at baseline and at 8 weeks after fluvastatin therapy (40 mg/day) to measure of tissue plasminogen activator (t-PA), plasminogen activators inhibitor-1 (PAI-1), fibrinogen, D-dimer and lipid profile. After 8 weeks of therapy, fluvastatin reduced serum cholesterol by 11% (261.9 mg/dl vs 233.2 mg/dl, P < 0.01) and LDL-C by 22% (191.9 mg/dl vs 149.3 mg/dl, P < 0.01). D-dimer was significantly decreased (0.38 ng/L vs 0.28 ng/L, P = 0.02) and tPA, PAI-1 and fibrinogen tended to decrease after therapy. Fluvastatin therapy improved fibrinolytic profile; the result of this study may in part explain the benefit of HMG-CoA reductase inhibitor on cardiovascular system other than lipid lowering.     

Anatomic problems associated with arterial switch procedures for double outlet right ventricle with subpulmonary ventricular septal defect

Two cases of double outlet right ventricle with subpulmonary ventricular septal defect treated by arterial switch operations are reported. The anatomical problems of coronary artery transfer, occult outflow tract obstruction and position of the pulmonary bifurcation are discussed. Cases of double outlet right ventricle and subpulmonary ventricular septal defect with anterior-to-posterior relation of the great arteries are suited to the repair techniques pioneered by Jatene for complete transposition and ventricular septal defect. Cases in which the great arteries are side-by-side pose more difficult problems, partly because of the more complex and varied anatomy of the coronary arteries, and because of the spatial relation of the roots of the great arteries. Although it may be possible to overcome these technical problems, we have reservations about the reproducibility of such a procedure. We believe, however, that cases of this type are best treated without recourse to "inflow" correction. The options are either the arterial switch procedure or a modified Rastelli operation.     

A review of the coronary venous system: a road less travelled.

Compared with the coronary arterial system, less attention has been paid to the coronary venous system. In the current era, there are therapeutic options for arrhythmias and for heart failure that use the coronary venous system to access target areas. We review the arrangement of the main cardiac veins to provide a morphologic background to interventionists. In general, the venous system is a useful conduit for delivery of percutaneous transcatheter treatment. But, variability in terms of valves, diameter, angulation, extent of muscular sleeves, proximity to other cardiac structures, and cross-over spatial relationship with branches of coronary arteries have implications for practitioners seeking to make use of the system.     

The influence of age and gender on HLA-DR in Chinese child-onset type 1 diabetes mellitus patients

To further clarify the association of HLA DR alleles with type 1 diabetes mellitus and the influence of age-onset and gender on type 1 diabetes, we investigated HLA-DR in 76 child onset Chinese (36 males) type 1 diabetes patients and 154 normal controls by using PCR-SSP (sequence specific primer). The mean age of onset of diabetes patients was 8.43 +/- 3.96 year-old. Our results revealed that the frequencies of DR3, DR4 and DR9 in diabetes patients were significantly higher than those in control group (all P < 0.01). The susceptible alleles were DR3, DR4, DR9, with relative risks of 8.25, 2.57 and 2.67, respectively. The protective alleles to type 1 diabetes were DR 2, DR8, DR11 and DR12 with relative risk of 0.24, 0.15, 0.16 and 0.39, respectively. There were no significant differences between the frequencies of HLA DR 3, DR4, DR9, DR3/4, DR3/9 and DR4/9 in male and female diabetic children. We divided the diabetes patients into three groups according to their age of onset (1-5 years old, 6-10 years old and 11-17 years old). There was a trend that the frequencies of DR9 decreased with the increase of age at onset, but there was no significant difference of DR3, DR4, DR9, DR3/4, DR3/9 and DR4/9 frequencies between diabetes children with age onset 0-10 years and 11-17 years. As to the influence of gender on the HLA genotypes, the frequency of DR3/4 decreased with the increase of age at onset for male patients and the frequency of DR3/4 increased with the increase of age at onset for female patients.     

Cardiac fibroblasts produce leukemia inhibitory factor and endothelin, which combine to induce cardiac myocyte hypertrophy in vitro

Cardiac fibroblasts in culture produce factor(s) that induce hypertrophy of neonatal rat ventricular myocytes in vitro. As in vivo, the myocyte hypertrophy response in culture is characterized by an increase in cell size and contractile protein content, and by the activation of embryonic genes, including the gene for atrial natriuretic peptide. The purpose of this study was to identify the factor(s) produced by fibroblasts that induce myocyte hypertrophy. The fibroblast hypertrophy activity was inhibited using a combination of the endothelin A receptor blocker BQ-123 and an antibody to leukemia inhibitory factor. The individual antagonists each caused a partial inhibition. The mRNAs for both leukemia inhibitory factor and endothelin were detected by RT-PCR analysis and the concentration of both proteins was determined to be approximately 200 pmol/L in the conditioned medium using immunoassays. Purified leukemia inhibitory factor and endothelin each induced distinctive morphological changes in the myocytes. Their combination generated a different morphology similar to that induced by fibroblast conditioned medium. Each factor also induced atrial natriuretic peptide production, but both were required for the myocytes to produce the levels measured after exposure to fibroblast conditioned medium. These results show that hypertrophy activity produced by cardiac fibroblasts in culture is a result of leukemia inhibitory factor and endothelin.