TREATMENT OF GOUT WITH ALTERNATE-DAY HYPO-URICAEMIC DRUGS

In the treatment of gout, an alternate-day hypo-uricaemic drugwas tried in order to reduce the amount of hypo-uricaemic drugprescribed and to lessen its possible side-effects. The serumurate level in the alternate-day therapy with benzbromarone(100 mg/day) was higher than that found with daily therapy,but was conversely lower than that in half-dose daily therapy.The serum urate level in alternate-day therapy with five hypo-uricaemicdrugs increased by 0.7 mg to 1.4 mg/100 ml, compared with thatin the daily therapy. The incidence of hyperuricaemia (serumuric acid over 7 mg/100 ml) in alternate-day therapy with along-acting hypo-uricaemic drug was relatively low (0 % forbucolome, 20 % for probenecid and 25.0 % for benzbromarone).The incidence of hyperuricaemia in alternate-day therapy withsulphinpyrazone and allopurinol was 42.9 % and 66.7 %, respectively.The frequency of gouty attacks in alternate-day therapy withfive drugs was not significantly different, when compared withdaily therapy.     

Pulmonary surfactant transport in alveolar type II cells

Abstract:   Pulmonary surfactant (PS) is a mixture of several lipids (mainly phosphatidylcholine; PC) and four apoproteins (A, B, C and D). The classical hypothesis of PS transport suggests that PS is synthesized in the endoplasmic reticulum and transported to the lamellar body (LB) via the Golgi apparatus. However, recent studies have raised questions regarding this single route. This study examined, independently, the intracellular trafficking route of three different components of PS, that is, PC, SP-A and SP-B. Alveolar type II cells were isolated from Sprague–Dawley rats or Japanese white rabbits. The cells were cultured with either [³H]choline or [³⁵S]methionine/cysteine with or without brefeldin A, which disassembles the Golgi apparatus. LB was purified from disintegrated cells with sucrose density gradient centrifugation. [³H]PC was extracted from radiolabeled media, cells, and the LB fraction with Bligh–Dyer's method. [³⁵S]SP-A or [³⁵S]SP-B was immunoprecipitated from each sample with a specific antibody. [³H]PC was transported and stored to the LB via a Golgi-independent pathway. [³⁵S]SP-A was transported to the Golgi apparatus, underwent glycosylation, and was then constitutively secreted. The secreted [³⁵S]SP-A was re-uptaken into the LB. [³⁵S]SP-B was transported and stored to the LB via the Golgi-dependent pathway. These results indicate that, rather than a single route, surfactant components take different pathways to reside in the LB. These different pathways may reflect the different nature and role of each surfactant component such as surface tension-lowering activity and innate host defense.     

Intraoperative transesophageal echocardiography for inferior vena caval tumor thrombus in renal cell carcinoma

BACKGROUND: We investigated the advantages of intraoperative transesophageal echocardiography (TEE) during inferior vena caval tumor thrombectomy in renal cell carcinoma (RCC). METHODS: Five patients with RCC that extended into the inferior vena cava (IVC) underwent radical nephrectomy. To remove the tumor thrombus in the IVC, an inflated Fogarty balloon catheter was used to pull the thrombus below the level of the hepatic veins with real-time TEE monitoring. RESULTS: In all cases, TEE monitoring during surgery provided an accurate and excellent view of the IVC thrombus. TEE was particularly helpful for the thrombectomy to minimize hepatic mobilization by using occlusion balloon catheter in two patients whose thrombus extended to the intrahepatic IVC. CONCLUSIONS: Intraoperative real-time TEE monitoring is a safe, minimally invasive technique that can provide accurate information regarding the presence and extent of IVC involvement, guidance for placement of a vena caval clamp, confirmation of complete removal of the IVC thrombus and intervention using catheters to assist in thrombectomy.     

Transient Manifestation of Antegrade Conduction Over a Kent Bundle After Ventricular Pacing

Postventricular Pacing Preexcitation. Antegrade conduction over a Kent bundle was transiently manifested after the cessation of ventricular overdrive pacing in two patients; otherwise, the heart behaved as if it had a concealed accessory pathway. Conventional electrophysiologic study suggested either a longitudinal dissociation of an accessory pathway or closely located double accessory pathways. The mechanism of the transient manifestation of ventricular preexcitation was discussed. (J Cardiovasc Electrophysiol, Vol. 3, pp. 423–430, October 1992)     

Mechanisms and significance of proteinuria

Summary: Glomerular permselectivity is determined by complex interactions of the glomerular basement membrane (GBM) and the endothelial and epithelial cells of the glomerular capillary wall. Proteinuria may result acutely from functional changes in filtration, and be quickly reversible. Chronic structural changes may also contribute to proteinuria in many disease settings by affecting the components of the glomerular capillary wall (GCW). Thus, glomerular epithelial cell abnormalities are prominent in both minimal change disease and focal segmental glomerulosclerosis, whereas altered GBM thickness and composition are major features in diabetic nephropathy and Alport syndrome. A multitude of pathologic stimuli appear to influence proteinuria, including the renin-angiotensin system and numerous other cytokines. Human and experimental data indicate a heterogeneity of mechanisms in different diseases manifesting proteinuria which are associated with a range of structural appearances from normal morphology to a severely damaged GCW. Current therapeutic trials in progressive human renal diseases have focused on the potential benefits of angiotensin converting enzyme inhibitor (ACEI). Encouraging results indicate amelioration of both functional and structural components of proteinuria, as well as a benefit on sclerosis, although the latter effect has so far only been documented in animal studies. Advances in molecular technologies may allow identification of more specific abnormalities in the GCW which underlie proteinuria. Further understanding of these abnormalities will direct future therapy at the specific defect in each disease setting.