Radiofrequency Catheter Ablation of Left Ventricular Outflow Tract Tachycardia from the Coronary Cusp: A New Approach to the Tachycardia Focus

INTRODUCTION: Idiopathic ventricular tachycardia (VT) originating from the left ventricular outflow tract (LVOT) is rare. Previously reported were two cases of LVOT tachycardia which were treated with radiofrequency (RF) catheter ablation through endocardial aortomitral continuity. We report here a case of a repetitive LVOT tachycardia in which the QRS morphology during VT exhibited an atypical left bundle branch block and inferior axis. Pace mapping revealed that the origin of this VT was very close to the left sinus of Valsalva. Transcoronary cusp RF catheter ablation abolished the VT in this patient and is a new approach for the treatment of this kind of VT. The application of this approach to the other types of VT has yet to be determined.     

Solid cell nests of the thyroid in medullary thyroid carcinoma

Solid cell nests of the thyroid gland were studied in 44 patients with medullary thyroid carcinoma. In 10 (22.7%) patients, solid cell nests were revealed in the vicinity of tumour foci (five cases) or in the contralateral thyroid lobe and isthmus (four cases); in one case the location was indeterminate. In all seven cases in which immunohistochemical studies were carried out, solid cell nests showed negative staining for thyroglobulin, calcitonin and chromogranin A, findings which were distinct from those in medullary thyroid carcinoma. It is therefore suggested that solid cell nests of the thyroid are not precursors of this tumour.     

Primary IgA Glomerulonephritis and Schonlein-Henoch Purpura Nephritis: Clinicopathological and Immunohistological Characteristics

A comparative analysis on clinicopathological and immunohistologicalcharacteristics was performed of 205 cases with primary IgAnephritis and 35 with Schönlein-Henoch purpura nephritis(purpura nephritis). Diagnostic criteria for primary IgA nephritiswere set out so that IgA was either the most prominent immunoglobulinor, at least, equal to IgG and/or IgM, if present, irrespectiveof mesangial or peripheral localization. In primary IgA nephritis,one half of the cases were discovered by asymptomatic proteinuria,and one-third presented recurrent upper respiratory tract infectionand gross hematuria, one-fourth abdominal pain and a few casesjoint pain, while purpura nephritis was associated with a significantlyhigher incidence of such systemic symptoms as abdominal andjoint pains, in addition to purpura. Both diseases shared atendency toward conspicuous hematuria in contrast to the modestproteinuria, with normal renal function in three-fourths totwo-thirds. Moreover, four of 35 with purpura nephritis showedpreceding proteinuria and had been regarded as primary IgA nephritisuntil purpura appeared. The glomerular pathology had a commonfeature in that there was frequent occurrence of mesangial proliferativeand focal and segmental lesions. The immunohistology in thetwo diseases was indistinguishable with regard to the glomerularimmunoglobulins and mediators, whether purpura was present orabsent. Thus, we propose a unifying concept that, by analogywith SLE, primary IgA nephritis may be regarded as ‘sinelupo,’ lying on one side of the nosological spectrum withless systemic symptoms, whereas purpura nephritis may occupythe other side with more systemic aspects. Furthermore, we confirmedthe epimembranous granular deposition of IgA in both diseasesas the most characteristic morphological expression of circulatingimmune complexes.     

PEPTIC ULCER: PATHOGENESIS,HEALING AND ANTI-ULCER DRUGS

Abstract At present, the evaluation of anti-ulcer drugs is generally accomplished simply by calculating the cumulative healing rate at a certain point of time during treatment, which does not implicate any analysis of the healing speed of the ulcer. If the cumulative healing rate of an ulcer is expressed as a function of drug administration time, t, then it will be possible to calculate parameters concerning the healing speed of ulcers and thus evaluate drug efficacy as the time series analysis of the cumulative healing rate. A new method of evaluating anti-ulcer drugs by a statistical analysis of healing speed is proposed. A non-linear regression analysis was performed between two variables, t (time of drug administration: week) and y (non-healing rate: %), to obtain the exponential function y = Ae^?kt. The theoretical values calculated from the exponential equation were in close proximity to the observed values. With this analysis, four parameters concerning the healing speed were defined, namely the healing rate constant, the initiation time of healing, the half-life of non-healing rate and the time necessary for 50% healing. With this method, the efficacy of drugs on peptic ulcer healing was dynamically analysed, the non-healing rate (y) being expressed as an exponential function of length of time (t) of treatment, thus obtaining digital parameters for healing speed.     

Goniodomin A,an Antifungal Polyether Macrolide,Increases the Filamentous Actin Content of 1321N1 Human Astrocytoma Cells

Goniodomin A, a polyether macrolide isolated from the dinoflagellate Goniodoma pseudogoniaulax, caused morphological change in 1321N1 human astrocytoma cells. Observation by scanning electron microscopy revealed that the shape of the cell became refractile from flat in response to goniodomin A. This morphological change was accompanied by the outgrowth of a needle-like structure from the cell surface. Goniodomin A increased the intracellular content of filamentous actin in a concentration- and time-dependent manner. It also caused the change in filamentous actin distribution in the cells. The elongation of filamentous actin was observed in goniodomin A-treated cells. These results suggest that goniodomin A induces morphological change by increasing the content of filamentous actin in non-muscle cells.     

Properties of the binding sites of [3H]9-methyl-7-bromoeudistomin D in bovine aortic smooth muscle microsomes

Abstract— [³H]9-Methyl-7-bromoeudistomin D ([³H]MBED), a powerful caffeine-like Ca²⁺ releaser, binds to the caffeine binding site of terminal cisternae of skeletal muscle sarcoplasmic reticulum and activates Ca²⁺-induced Ca²⁺ release. Properties of the binding site of [³H]MBED were investigated in aortic smooth muscle. The specific activity was higher in microsomes than in other fractions. [³H]MBED binding sites in smooth muscle microsomes were of a single class with a high affinity (K_D 50 Nm ), comparable with that in skeletal muscle sarcoplasmic reticulum. Caffeine competitively inhibited [³H]MBED binding, indicating MBED shares the same binding site with caffeine. Solubilization and fractionation of the microsomes gave two fractions of [³H]MBED binding activities. These results suggest that, in smooth muscle, there are multiple binding sites of [³H]MBED and caffeine, which might correspond to different pharmacological actions of caffeine on smooth muscle. Therefore, [³H]MBED, which binds to the different binding sites of caffeine, is useful as a probe for investigation of the actions of caffeine at the molecular level.     

Real-time monitoring of HCV-RNA by single tube assay kit and potential importance for predicting virological sustained response in patients with chronic hepatitis C

In an attempt to predict virological sustained responders among patients with chronic hepatitis C after interferon therapy, HCV-RNA in serum was measured by a one tube RT-PCR assay kit using the RNA corresponding to 5 μL serum (standard assay) or 300 μL serum (enhanced-sensitivity assay). Dilution analysis revealed that sensitivity of the ‘enhanced-sensitivity assay’ increased by 10–100-fold when compared with a ‘standard assay'. Using these assays, prospective study of interferon therapy on 38 HCV-RNA seropositive cases with chronic hepatitis (total amount 702 MU; duration of treatment 5–6 months) was performed. At the end of treatment, six were still positive and 32 became negative by the ‘standard assay', whereas an additional eight cases became positive (total 14 cases positive; the remaining 24 cases negative) by the ‘enhanced-sensitivity assay'. Hepatitis C viral RNA state at the end of treatment remained the same 6 months later in 23 cases (61%) by a ‘standard assay’ and in 31 (82%) by the ‘enhanced-sensitivity assay'. Of importance was that all patients (14 cases) demonstrating HCV-RNA in serum at the end of therapy, even by the ‘enhanced-sensitivity assay', did not show the disappearance of HCV-RNA in serum despite the long follow up. From these results, in order to improve our treatment efficacy, we should try to modify our treatment protocol to the extent that at least HCV-RNA becomes undetectable. That can be only feasible during treatment by real-time monitoring of HCV-RNA.     

Mechanism of mesaconitine-induced contractile response in guinea-pig ileum*

Mesaconitine (MA) caused contractions of the guinea-pig isolated ileum in a dose-dependent manner (10^?8 ?10^?5 g ml^?1), slightly potentiated the contractile response to acetylcholine (ACh) and histamine and enhanced responses to electrical stimulation. Repeated application of MA (10^?5 g ml^?1) produced tachyphylaxis. Atropine blocked contractions to MA (3 times 10^?7 g ml^?1), but only partially those to MA (10^?5 g ml^?1). Morphine, strychnine and hemicholinium-3, but not hexamethonium, also inhibited MA-induced contractions. Contractions produced by both doses of MA were abolished by cocaine, tetrodotoxin, or noradrenaline, or by previous cooling of the ileum. The atropine-resistant contractions produced by MA (10^?5 g ml^?1) were blocked by indomethacin. MA (3 times 10^?7 ?10^?5 g ml^?1) elicited a dose-dependent release of ACh from the isolated ileum which was blocked by treatment with tetrodotoxin or cocaine, or exclusion of calcium ions from the bath. It is concluded that the contractions induced by lower doses of MA are brought about by the release of ACh from the postganglionic cholinergic nerve and that the contractions by higher doses could also be mediated by release of prostaglandins from the ileum.