Management of recurrent ventricular tachyarrhythmias associated with Q-T prolongation

Eleven patients with acquired prolongation of the Q-Tc interval and recurrent ventricular tachyarrhythmias were studied. Five patients required 5 to 44 direct current shocks to correct prolonged ventricular tachyarrhythmias, and five were given at least two antiarrhythmic agents in an attempt to control the arrhythmias. In 4 of the 11 patients, when thioridazine, diuretic drugs and antiarrhythmic agents were withdrawn and hypokalemia or hypocalcemia corrected, ventricular tachyarrhythmias did not recur. The Q-Tc interval normalized in 2 to 3 days. Ventricular tachyarrhythmias were recurrent in the remaining seven patients, despite withdrawal of the drugs that caused the Q-Tc prolongation, attempted correction of hypokalemia when present and the administration of antiarrhythmic agents to four of the seven. All antiarrhythmic agents were then withdrawn in this group.

Immediately on the establishment of overdrive ventricular or atrioventricular sequential pacing in these patients, ventricular tachyarrhythmias were abolished. No breakthrough ventricular tachyarrhythmias occurred during temporary pacing. Temporary pacing was required for an average of 10 days and the Q-Tc interval normalized an average of 5 days from the onset of pacing. Three patients required a permanent pacemaker, one because of chronic complete heart block, one because of the sick sinus syndrome, and one because of frequent ventricular ectopic complexes complicating ischemic heart disease. All 11 patients survived their period of hospitalization.     

Diabetes enhances lipopolysaccharide-induced cardiac toxicity in the mouse model

Diabetic patients have a higher rate of mortality from sepsis than do their nondiabetic septic counterparts. The hypothesis in this study is that chronic diabetes may make cardiovascular systems more sensitive to septicemia. To test this hypothesis, the authors investigated the effect of diabetes on endotoxin-induced cardiac toxicity. Diabetes was induced in FVB mice by injecting a single dose (150 mg/kg) of streptozotocin. Two months after streptozotocin treatment, the diabetic mice were treated with lipopolysaccharide by intraperitoneal injection at 2 mg/kg. Cardiac toxicity was evaluated by measuring levels of serum cardiac enzymes and cardiac morphology at 1 h, 4.5 h, and 24 h after lipopolysaccharide treatment. Serum and cardiac tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were detected by enzyme-linked immunosorbent assay methods at 1 h and 4.5 h after lipopolysaccharide treatment. Lipopolysaccharide treatment did not significantly affect the diabetic manifestations, including decreased body weight gain and increased glycated hemoglobin and serum triglyceride levels. However, diabetes significantly enhanced lipopolysaccharide-induced cardiac toxicity, which was demonstrated by significant increases in the levels of cardiac enzymes such as creatine phosphokinase and troponin T, abnormal morphological changes examined under light microscope with hematoxylin and eosin staining, and oxidative damage to proteins detected by 3-nitrotyrosine staining. Lipopolysaccharide treatment significantly increased serum and cardiac TNF-α and IL-6 concentrations. Diabetes did not alter the effect of lipopolysaccharide on serum and cardiac TNF-α elevation, but it significantly enhanced lipopolysaccharide-induced cardiac IL-6 production. These results suggest that diabetes significantly enhances endotoxin-induced cardiac toxicity, possibly through mechanisms that involve inflammatory/acute-phase cytokines.     

Comparison between bacillus Calmette-Guérin and the A60 mycobacterial antigen complex used as cancer-preventive immunotherapies

Preparations of live or lysates ofMycobacterium bovis strain Calmette-Guérin (BCG) have long been used as treatments for a variety of cancer types, especially those involving the urinary tract, with varying success. This study was conducted to compare the antitumoral activity of BCG and the thermostable macromolecular antigen complex of BCG (A60) when used as preventive treatments, in conjunction with or without tumor antigens, against growth and dissemination of the EMT6 murine tumor cell line. It was demonstrated that tumor antigens alone did not significantly alter the oncological indexes, although a slight increase in both T lymphocyte and macrophage activations was found. It was further demonstrated that A60 induces a protective activity up to 40% greater than that of live BCG and that this protection was not accompanied by any of the adverse effects sometimes observed during BCG immunotherapy.Abbreviations BCGMycobacterium bovis strain Calmette-Guérin - A60 the thermostable macromolecular antigen complex ofM. bovis BCG - EMT6 murine transplantable mammary adenocarcinoma - ELISA enzyme-linked immunosorbent assay     

Combined glucose-6-phosphate dehydrogenase and glucosephosphate isomerase deficiency can alter clinical outcome

Glucosephosphate isomerase (GPI) deficiency in humans is an autosomal recessive disorder, which results in nonspherocytic hemolytic anemia of variable clinical expression. A 4-year-old female with severe congenital hemolytic anemia had low red cell GPI activity of 15.5 IU/g Hb (50% of normal mean) indicating GPI deficiency. Subsequent DNA sequence analysis revealed a novel homozygous 921C to G mutation in the GPI gene sequence, predicting a Phe307 to Leu replacement. Strikingly, the red cell GPI activity in this patient was higher than that found in a second patient expressing the same GPI variant, with a more severe clinical phenotype. We propose that the hemolysis in the first patient may be modified by an accompanying deficiency of glucose-6-phosphate dehydrogenase (G6PD). The proband's red cell G6PD activity was reduced at 4.5 IU/g Hb (50% of normal mean) and molecular studies revealed heterozygosity for the G6PD Viangchan mutation and a skewed pattern of X-chromosome inactivation, producing almost exclusive expression of the mutated allele. The G6PD Viangchan variant is characterised by severe enzyme deficiency, but not chronic hemolysis. This study suggests that the metabolic consequences of a combined deficiency of GPI and G6PD might be responsible for a different clinical outcome than predicted for either defect in isolation.     

WBC、IL-6对急性心肌梗死患者近期预后的影响

目的 观察急性心肌梗死（AMI）患者人院外周血白细胞（WBC）总数、血浆白细胞介素-6（IL-6）对近期预后的影响。方法 首发AMI患者103例，通过检测WBC、IL-6，以发病后30天内是否发生心血管不良事件（包括心源性死亡、心力衰竭、心源性休克、恶性心律失常）为观察终点。结果 36例发生心血管事件组外周血WBC总数和IL-6显著高于67例无心血管事件组。AMI时外周血WBC总数和IL-6水平为发生心血管事件的预测因素。结论 WBC、IL-6与AMI患者近期预后相关。     

贵州江口土家族男性葡萄糖-6-磷酸脱氢酶缺陷症的基因频率调查

目的 调查贵州省江口土家族男性葡萄糖-6-磷酸脱氢酶（G6PD）缺陷症的基因频率。方法 2002年10-11月随机选取227名江口当地土家族男性居民，采用四氮唑蓝（NBT）纸片定性法初筛G6PD缺陷症。G6PD／6PGD比值法定量确诊。结果 对贵州省江口县227名土家族男性进行筛查，共检出17例G6PD缺陷阳性。其基因频率为0．0749。结论 通过对贵州土家族G6PD缺乏症基因频率的调查和分析，初步了解了贵州省土家族G6PD缺乏症的分布特征。为该地区预防该疾病、指导临床、提高少数民族的素质及研究该民族起源提供了一定的依据。     

Synergistic action of famotidine and chlorpheniramine on acetic acid-induced chronic gastric ulcer in rats

AIM: To assess the synergistic action of famotidine (FMD) and chlorpheniramine (CPA) on acetic acid-induced chronic gastric ulcer in rats. METHODS: Chronic gastric lesions were induced in male Sprague-Dawley (SD) rats by serosal application of the acetic acid. Forty SD rats were randomly divided into blank group (n=8), control group (n=8), FMD group (n = 8), CPA group (n=8), and FMD+CPA group (n=8). Each group was given intraperitoneally (i.p.) 0.5 mL/100 g distilled water, 9 g/L NaCl saline, 4 mg/kg FMD, 10 mg/kg CPA, 4 mg/kg FMD+10 mg/kg CPA, respectively, daily for 10 d. On d 10, ulcer area was determined by planimetry. The level of myeloperoxidase (MPO) in the liver homogenation was determined by biochemical methods and the plasma levels of 6-ketoprostaglandin F1 alpha (6-keto-PGFia) and IL-8 were determined by radioimmunoassay. RESULTS: The synergistic effects of FMD+CPA group on the lesion, IL-8, 6-keto-PGFia and MPO were confirmed. The effect of FMD+CPA group was significantly different as compared to the control and FMD groups. The lesion (mm2) was reduced from 40.18±2.6 in control group to 6.83±2.97 in PMD+CPA group, P<0.01, and from 32.9±3.27 in FMD group to 6.83±2.97 in PMD+CPA group, P<0.01. The plasma levels of IL-8 decreased from 0.69±0.11 ng/L in control group to 0.4±0.04 ng/L in PMD+CPA group, P<0.01, and from 0.51±0.08 ng/L in FMD group to 0.4±0.04 ng/L in PMD+CPA group, P<0.05. The level of 6-keto-PGFia increased from 7.55±1.65 ng/L in control group to 16.62±0.97 ng/L in PMD+CPA group, P<0.01, and from 13.15±1.48 ng/L in FMD group to 16.62±0.97 ng/L in PMD+CPA group, P<0.05. The levels of MPO in the liver homogenate decreased from 9.12±2.05 u/L in control group to 4.33±0.95 u/L in PMD+CPA group, P<0.01, and from 8.3±1.29 u/L in FMD group to 4.33±0.95 u/L, P<0.01. CONCLUSION: The synergistic action of FMD and CPA on acetic acid-induced chronic gastric ulcer in rats decreases the incidence of ulcer and also enhances the healing of ulcer.     

Maternal Physical Activity Is Associated With Improved Blood Pressure Regulation During Late Pregnancy

Background

Cardiovagal baroreflex gain (cBRG) reflects an individual's ability to buffer swings in blood pressure. It is not well understood how this mechanism is influenced by physical activity in pregnancy. Because pregnant women tend to engage in low levels of moderate-to-vigorous physical activity (MVPA) and high levels of sedentary behaviour, we sought to determine the influence of MVPA and sedentary behaviour on cBRG and mean arterial pressure (MAP) in pregnancy.

Biochemical and molecular characterization of a new sporadic glucose-6-phosphate dehydrogenase variant described in Italy: G6PD Modena

Summary. A new glucose-6-phosphate dehydrogenase variant detected in an Italian man from the Po delata is described and designated as G6PD Modena. Biochemical characterization of the variant enzyme revealed an activity 21% of normal, a slow electrophoretic mobility, increased K_m value for NADP, decreased K_m value for G6P and a complete absence of NADPH inhibition, which could account for the apparently nonhaemolytic feature of this variant. The cloning and sequencing of the G6PD Modena allele showed a GC transition at nucleotide 844 in exon VIII causing a Asp His amino acid substitution. On the basis of biochemical characterization, G6PD Modena is classified as a genuine variant but it has the same mutation as G6PD Seattle-like.