Glutathione-binding proteins of Setaria digitata: antibody responses in human infected with Wuchereria bancrofti

Glutathione-s-transferase activity was determined in filarial parasites. The activity was detected in adult stages of cattle parasite Setaria digitata. It was absent in other stages of Setaria and also in infective larval stages of Wuchereria bancrofti and Brugia malayi. The activity was enhanced about twenty five fold following purification of adult setaria extracts on glutathione agarose column. Antibody (IgG and IgM) levels to the affinity purified proteins (SdGBP) were detected predominantly (90%) in Wuchereria bancrofti infected individuals compared with normal residents of endemic regions. IgA and IgE responses could not be detected. Filarial sera in contrast to non-filarial caused reduction in the enzymatic activities of Sd GBP. Micro-filaraemic sera after dielhylcarhamazine treatment resulted in enhanced reduction of enzymatic activity.     

Down to the Wire: Tricuspid Stenosis in the Setting of Multiple Pacing Leads

Tricuspid stenosis in the setting of endocardial pacing leads is a rare entity, attributed to infection or lead malposition. We report the case of a 37‐year‐old man without these risk factors, who presented with new onset severe tricuspid stenosis in the setting of multiple chronic pacing leads. (PACE 2010; e49–e52)     

Signet-ring cell carcinoid of the gallbladder

A case of signet-ring cell carcinoid of the gallbladder is reported. The tumour diffusely infiltrated the gallbladder wall and extensively ulcerated the mucosa. Neoplastic nests were composed of numerous signet-ring cells mixed with clear endocrine cells. The latter expressed chromogranin A, gastrin and somatostatin and contained neurosecretory granules. The diagnostic problem of differentiating between signet-ring cell carcinomas and composite adenocarcinoma-carcinoid tumours is discussed.     

Left Ventricular Ejection Fraction and Absence of ACE Inhibitor/Angiotensin II Receptor Blocker Predicts Appropriate Defibrillator Therapy in the Primary Prevention Population

Introduction: Implantable cardioverter defibrillators (ICD) significantly reduce mortality in patients with left ventricular (LV) dysfunction. However, little is known of the predictors of appropriate device activation in the primary prevention population. The aim of the present study was to determine predictors of appropriate device therapy in patients receiving ICDs for primary prevention. Methods & Results: One hundred twenty‐six patients with a left ventricular ejection fraction (LVEF) of < 35% and no prior documented ventricular arrhythmias underwent ICD implantation. The ICD implanted was single chamber in 60 (48%), dual chamber in 10 (8%), and biventricular in 56 (44%) patients and programmed with a single ventricular fibrillation (VF) zone at >180 beats per minute. Mean age was 58 ± 13 years and mean LVEF was 23 ± 7%. Fifty‐two percent had ischemic cardiomyopathy and 66% were New York Heart Association heart failure class II/III. During a mean follow‐up period of 589 ± 353 days, 17 (13%) patients received appropriate device therapy and three (4%) received inappropriate shocks. Appropriate ICD therapy was associated with reduced LVEF (mean 19.9% vs 23.7%, P = 0.02) and the patients were less likely to have received angiotensin‐converting enzyme inhibitor (ACEI) or angiotensin II receptor blockers (AIIRB) (65% vs 90%, P = 0.04). Multivariate analysis revealed lack of ACEI/AIIRB (odds ratio [OR]= 0.06, 95% confidence interval [CI]= 0.01–0.37, P = <0.01) and lower LVEF (OR = 0.88, 95% CI 0.79–0.98, P = 0.02) predicted appropriate device activation. There was no difference in transplant‐free survival between the appropriate therapy and no/inappropriate therapy groups, LVEF <20% and LVEF >20% group, and lack of ACEI/AIIRB and ACEI/AIIRB group. Conclusion: Appropriate device activation occurred in 13% of patients in a primary prevention population. LVEF and absence of ACEI/AIIRB predicted appropriate ICD therapy. (PACE 2010; 33:696–704)     

Effect of Dietary Administration of Lathyrus sativus Pulse on Intestinal Biochemical Parameters in Normal and Scorbutic Guinea Pigs

Objective In order to investigate that ascorbic acid deficiency is responcible for lathyrus toxicity, the effect of dietary feeding of lathyrus pulse in normal and scorbutic guinea pigs for 3 months, on intestinal biochemical parameters was undertaken. Methods The intestinal brush border membrane (BBM) marker and xenobiotic metabolising enzymes (XME) were assayed. Results Exposure to 80% lathyrus alone and in scorbutic conditions showed significant inhibition of alkaline phosphatase (28%-30%), sucrase (19%) and γ-glutamyl transpeptidase (GGT) (15%-27%) enzymes, while Ca2 -Mg2 -ATPase was significantly inhibited (38%) in scorbutic plus lathyrus treated group. The phase I XME (AHH) remained unchanged while the phase II enzyme glutathione-S-tranferase (GST) was significantly decreased (20%-22%) in lathyrus and scorbutic plus lathyrus treated groups. Quinone reductase (QR) activity was found to be significantly decreased in lathyrus exposed group (20%). The intestinal biomarker contents including hexose (2     

Prazosin modulates rapid eye movement sleep deprivation-induced changes in body temperature in rats

Prolonged rapid eye movement sleep deprivation (REMSD) causes hypothermia and death; however, the effect of deprivation within 24 h and its mechanism(s) of action were unknown. Based on existing reports we argued that REMSD should, at least initially, induce hyperthermia and the death upon prolonged deprivation could be due to persistent hypothermia. We proposed that noradrenaline (NA), which modulates body temperature and is increased upon REMSD, may be involved in REMSD- associated body temperature changes. Adult male Wistar rats were REM sleep deprived for 6–9 days by the classical flower pot method; suitable free moving, large platform and recovery controls were carried out. The rectal temperature (Trec) was recorded every minute for 1 h, or once daily, or before and after i.p. injection of prazosin, an alpha-1 adrenergic antagonist. The Trec was indeed elevated within 24 h of REMSD which decreased steadily, despite continuation of deprivation. Prazosin injection into the deprived rats reduced the Trec within 30 min, and the duration of effect was comparable to its pharmacological half life. The findings have been explained on the basis of REMSD-induced elevated NA level, which has opposite actions on the peripheral and the central nervous systems. We propose that REMSD-associated immediate increase in Trec is due to increased Na-K ATPase as well as metabolic activities and peripheral vasoconstriction. However, upon prolonged deprivation, probably the persistent effect of NA on the central thermoregulatory sites induced sustained hypothermia, which if remained uncontrolled, results in death. Thus, our findings suggest that peripheral prazosin injection in REMSD would not bring the body temperature to normal, rather might become counterproductive.     

Endogenous ouabain-like compounds in locus coeruleus modulate rapid eye movement sleep in rats

Although the detailed mechanism of spontaneous generation and regulation of rapid eye movement sleep (REMS) is yet unknown, it has been reported that noradrenergic REM-OFF neurons in the locus coeruleus (LC) cease firing during REMS and, if they are kept active, REMS is significantly reduced. On the other hand, the activity as well as expression of Na-K ATPase has been shown to increase in the LC following REMS deprivation. Ouabain is a specific inhibitor of Na-K ATPase, and endogenous ouabain-like compounds are present in the brain. These findings led us to propose that a decrease in the level of ouabain-like compounds spontaneously available in and around the LC would stimulate and increase the REM-OFF neuronal activities in this region and thus would reduce REMS. To test this hypothesis, we generated anti-ouabain antibodies and then microinjected it bilaterally into the LC in freely moving chronically prepared rats and recorded electrophysiological signals for evaluation of sleep−wakefulness states; suitable control experiments were also conducted. Injection of anti-ouabain antibodies into the LC, but not into adjacent brain areas, significantly reduced percent REMS (mean ± SEM) from 7.12 (±0.74) to 3.63 (±0.65). The decrease in REMS was due to reduction in the mean frequency of REMS episode, which is likely due to increased excitation of the LC REM-OFF neurons. Control microinjections of normal IgG did not elicit this effect. These results support our hypothesis that interactions of naturally available endogenous ouabain-like compounds with the Na-K ATPase in the LC modulate spontaneous REMS.