Background-While a close association between gastric mucosa associated lymphoid tissue (MALT) lymphoma andHelicobacter pylori infection has been established, there are still cases which do not respond to H pylori eradication. Aims-To investigate the clinicopathological factors which may help predict the therapeutic eYcacy of H pylori eradication in gastric MALT lymphoma. Patients-Forty one patients with gastric MALT lymphoma, including low and high grade lesions. Methods-After endosonographic staging was determined, H pylori was eradicated in all patients, and the subsequent gastric pathological course was then investigated. Results-Complete regression of MALT lymphoma was observed in 29(71%) patients, partial regression in five (12%), and no regression in seven (17%). Twenty six (93%) of 28 MALT lymphomas restricted to the mucosa but only three (23%) of 13 lymphomas which invaded the deep portion of the submucosa or beyond completely regressed. Kaplan-Meier analysis for the probability of complete regression of MALT lymphoma revealed a significant diVerence between tumours restricted to the mucosa and those invading the submucosa deeply or beyond (p<0.05). Neither the presence of a high grade component, perigastric lymphadenopathy, nor clinical staging prior to eradication correlated with the probability of lymphoma regression. Conclusions-Assessment of deep submucosal invasion by endosonography is valuable for predicting the eYcacy of H pylori eradication in gastric MALT lymphoma. (Gut 2001;48:454-460)

We studied the mechanism of hemorrhagic infarction after acute cerebral embolism in 160 patients by brain computed tomography and angiography. Hemorrhagic infarction during the month after the embolic event was evident in 65 patients (40.6%). Initial angiography a median of 1.5 (range 1-60) days after the event revealed occlusion of the cerebral arteries in 117 of 142 patients (82.4%), and reopening of the vessels was observed in 56 (94.9%) of 59 patients who had follow-up angiography a median of 20 (range 3-47) days after the event. The incidence of hemorrhagic infarction was higher in patients ^70 years old (31 of 61, 50.8%) than in those aged 50-69 years (27 of 72, 37.5%) or <50 years (seven of 27, 25.9%) (2=70 vs. <50, /><0.05). In patients with moderate or large infarcts, hemorrhagic infarction developed in 50.0% or 51.5%, respectively, while in those with small infarcts it developed in only 2.9% (p<0.05). No correlation was found between hemorrhagic infarction and history of hypertension or blood pressure during the acute stage of stroke. Thrombolytk and/or anticoagulant therapy did not affect the incidence of hemorrhagic infarction (40.0% with vs. 40.7% without therapy) but tended to cause massive hematoma. Our results indicate that hemorrhagic transformation in cerebral embolism is caused not only by reopening of the occluded vessels but also by other factors such as age and size of the infarct. Hypertension per se seems to be less important for hemorrhagic infarction. Anticoagulants and/or thrombolytk agents should be carefully administered i n the elderly and i n patients with large infarcts. (Stroke 1989;20:598-603)

SUMMARYThe long chain fatty acid composition of phospholipids in colonic mucosa was determined by high performance liquid chromatography in nine patients with active ulcerative colitis and eight healthy controls. The arachidonic acid composition was 12*5±1-4 mol % (mean±2 SEM) in the inflamed colonic mucosa from the patients with active ulcerative colitis and 6-8±1*2 mol % in the intact mucosa from healthy controls (p<0001). In the inflamed colonic mucosa, oleic acid and palmitoleic acid were concomitantly decreased (p<0001 and p<0-02, respectively), while docosahexaenoic acid was increased (p<005). Histopathological examination showed that there was a three fold increase in the cell density of inflammatory infiltrate in the lamina propria of the inflamed colonic mucosa (p<0-001). The cell density of inflammatory infiltrate correlated with the arachidonic acid composition of phospholipids in colonic mucosa (r=089, p<0005). These findings indicate that inflammation alters the long chain fatty acid composition of phospholipids in colonic mucosa. The observed increase in the arachidonic acid composition of phospholipids in inflamed colonic mucosa may contribute to the enhanced arachidonic acid metabolism in patients with active ulcerative colitis.Arachidonic acid, incorporated into the two position of phospholipids,' is an integral component of cell membranes,2 and its metabolites formed via both the cyclooxygenase and lipoxygenase pathways are thought to be an important mediator of inflammation in ulcerative colitis.' Raised concentrations of prostaglandins are found in inflamed colonic mucosa, serum, urine, and stool of patients with active ulcerative colitis.' Sharon and Stenson7 have recently reported that rectal biopsy specimens from patients with active ulcerative colitis contain large amounts of lipoxygenase products, 5-hydroxyeicosatetra-enoic acid (5-HETE) and leucotriene B4, potent chemotactic agents recruiting neutrophils into areas of inflammation.-'2 A likely explanation

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SUMMARY A pathological examination was performed on normotensive rats (NTR) and spontaneously hypertensive rats (SHR) following bilateral common carotid artery ligation. After ligation, diffuse and extensive cerebral infarcts in the carotid artery territory occurred frequently in SHR, while NTR occasionally had wellcircumscribed small infarcts.The posterior communicating arteries, which are the major anastomotic channels connecting the carotid and vertebrobasilar systems, did not show any anomalies and were well developed in SHR and NTR. Vascular changes secondary to hypertension, such as fibrinoid necrosis or thickening of the wall, were not observed in SHR. Because of the paucity of structural difference of the blood vessels, the more diffuse and extensive cerebral infarcts in SHR after carotid occlusion were attributed to the hemodynamic difference rather than the morphological difference between the two groups.The results of the present experiment suggest that hypertension per se, i.e., hemodynamic factors, may be operative for the development of cerebral infarction.Introduction SPONTANEOUSLY hypertensive rats (SHR) had a marked increase in lactate and lactate-pyruvate ratio of the brain following bilateral common carotid artery ligation and an early mortality, while a slight increase in metabolites and a lower mortality were observed in normotensive rats (NTR). 13 To elucidate the cause of the susceptibility of SHR to brain ischemia, a pathological study of the rat brain was performed.