Effects of the Calcium Antagonist AE0047 on the Development of Neurological Deficit and Infarction after Middle Cerebral Artery Occlusion in Stroke-prone Spontaneously Hypertensive Rats

AE0047 [4-(4-benzhydrylpiperazino)phenethyl methyl 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridine dicarboxylate dihydrochloride] is a new dihydropyridine calcium antagonist with protective effects against cerebral ischaemia and the occurrence of stroke in several animal models. We investigated the effects of AE0047 on focal ischaemia induced by middle cerebral artery occlusion in stroke-prone spontaneously hypertensive rats. AE0047 at a dose causing 20 or 40% systemic hypotension (1 or 3 mg kg^?) was given orally twice, 15 min and 24 h after occlusion. The neurological status of animals was investigated 2, 24 and 48 h after occlusion. Infarct area of brain was measured 48 h after occlusion. Middle cerebral artery occlusion resulted in the progressive deterioration of neurological status and large infarction in middle cerebral artery territories with 40% mortality. AE0047 dose-dependently attenuated the deterioration of neurological status, and reduced mortality to 0 or 10%. AE0047 significantly reduced infarct size and left/right hemispheric area ratio, an index of brain swelling. These results suggest that AE0047 has the ability to ameliorate ischaemic cerebral stroke in hypertensive patients.     

Xanthogranulomatous pyelonephritis with a renocolic fistula caused by a parapelvic cyst

Fistula formation between the upper urinary tract and bowel is an uncommon complication in urogenital diseases. We present a rare case of focal xanthogranulomatous pyelonephritis with a renocolic fistula. This is the first case where a parapelvic cyst obstructs the caliceal outflow and leads to the formation of a renocolic fistula in renal inflammatory disease. It is difficult to make a preoperative diagnosis of focal xanthogranulomatous pyelonephritis with widespread involvement that is caused by non-calculous urinary tract obstruction.     

Suppression of the Murine Gut Mucosal IgA Response to Cholera Toxin with Oral Cyclosporine

The gut mucosal immune system may be a primary target for manyingested chemicals. Methods have been developed to examine theeffects of chemicals on the systemic humoral immune response;however, studies to evaluate various methods of assessing thelocal gut mucosal immune response in a toxicology assay havebeen limited. The objectives of this study were to examine theeffects of the known immunosuppressive compound, cyclosporine(CYS), on the generation of a cholera toxin (CT)-specific gutmucosal IgA response and evaluate the methods used to measurethe gut IgA response. Groups of female B6C3F1 mice were leftuntreated or were treated daily, p.o., with corn oil (vehicle)or CYS at doses of 10 and 50 mg/kg for 20 days. On Days 3 and13, mice were sensitized p.o. with CT. On Day 21, mice wereterminated, gut washings were collected, and lamina proprialymphocytes were extracted from gut tissue with collagenasetreatment. Cholera toxin-specific IgA in the gut washings wasmeasured by an ELISA. The numbers of CT-specific IgA (CT-IgA)and total IgA antibody-forming cells (spot-forming cells, SFC)obtained from the lamina propria were determined by the ELISPOTmethod. A dose of 50 mg/kg CYS produced a significant decreasein the amount of CT-IgA in gut washings. This dose also decreasedthe number of cells recovered from the lamina propria by atleast 50%. The amount of CT-specific SFC/million lamina propriacells decreased with a dose of 10 mg/kg CYS, whereas 50 mg/kgCYS did not alter the response. When the CT-IgA SFC responsewas calculated on the basis of lamina propria cells obtainedper mouse, both the 10 and 50 mg/kg dose were found to suppressthe response by at least 50% of control. The amount of IgA-SFC/totallamina propria cells obtained per mouse was also found to bedecreased with a dose of 50 mg/kg. Thus, the results indicatethat oral exposure to CYS results in a suppressed CT-specificIgA response. In comparing the two endpoints, measurement ofCT-specific SFC was a more sensitive indicator. However, collectionof gut washings and measurement of CT-IgA by ELISA is much easierthan the labor-intensive methods required to isolate laminapropria lymphocytes.     

Desquamative interstitial pneumonia may progress to lung fibrosis as characterized radiologically

Background and objective: In some patients, desquamative interstitial pneumonia may progress to lung fibrosis. The aim of this study was to assess the long‐term radiological follow‐up results in patients with desquamative interstitial pneumonia. Methods: Among 75 patients suspected of having desquamative interstitial pneumonia, 31 who fulfilled the criteria were included in this study. Clinical characteristics at presentation, responses to treatment and long‐term follow‐up were evaluated. Results: The 31 patients were predominantly males (94%), and the mean age was 55 years; 93% (28/30) had a history of smoking. The clinical findings included high serum levels of lactate dehydrogenase and immunoglobulin G. Bronchoalveolar lavage (26 patients, 84% of cases) frequently showed an increased percentage of eosinophils (mean 17%). Computed tomography (CT) or high resolution (HR) CT at presentation showed ground glass opacities and/or consolidation in all patients, with one third of patients also showing thin‐walled cysts within the ground glass opacities. There was no honeycombing on CT or HRCT scans at presentation. Corticosteroid therapy was effective early in the course of the disease; long‐term follow‐up (mean 99 months) of 31 patients showed only one death due to progression of the disease, but long‐term follow‐up of 14 patients (mean 125 months) by HRCT showed the development of new thin‐walled cysts and honeycombing in five and lung cancer in four patients, respectively. Conclusions: In a proportion of patients, desquamative interstitial pneumonia may progress to lung fibrosis with honeycombing on HRCT, despite therapy.