Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathophysiological impact of infections with chloroquine-susceptible (CQS) and chloroquine-resistant (CQR) strains of Plasmodium berghei in Mastomys natalensis was studied with respect to changes in polyamine profiles in various tissues. Both CQS and CQR infections produced similar changes in polyamine profiles of various tissues. Maximum increase was recorded in spleen followed by liver and lungs. Renal, cardiac and cerebral tissues did not register significant changes. An increase in spermidine level was more prominent as compared to putrescine and spermine, leading to an overall increase in spermidine/spermine ratio. This ratio is an important index of cellular proliferation. Liver did not show considerable change in the activities of ornithine decarboxylase and S-adenosyl methionine decarboxylase, the regulatory enzymes of the polyamine biosynthetic pathway. Spleen however, registered marked induction of both the enzymes which was more prominent in the CQS infection than CQR. Normal erythrocytes contained traces of polyamine while the erythrocytes loaded with P. berghei parasites exhibited appreciably higher polyamine levels. Spermidine was detected in about five-fold higher concentrations than putrescine and spermine which were detected in equimolar levels. Again, CQS as well as CQR P. berghei, exhibited qualitatively and quantitatively similar polyamine profiles thus ruling out a role of polyamines in CQ-resistance in malaria.
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PMID:Polyamine metabolism in various tissues during pathogenesis of chloroquine-susceptible and resistant malaria. 941 68

This study evaluated the long-term effects of distal splenorenal shunt with splenopancreatic disconnection (DSRS-SPD) on portal hypertension (PH) in biliary atresia (BA) patients. Five patients with BA underwent DSRS-SPD at the age of 3.3 to 8.5 years. They had been free from jaundice after hepatic portoenterostomy (HPE); however, they gradually developed gastroesophageal varices and hypersplenism. Portal venous pressure after anastomosis was 37.2 +/- 6.1 cmH2O, as high as that before anastomosis (37.8 +/- 3.3 cmH2O). Postoperatively, liver function tests became worse within 2 weeks; however, they returned to preoperative levels within 1 month without any further treatment. No patient developed a significant encephalopathy throughout the observed period. During follow-up of 4 to 12 years, the shunt was patent in all patients. Spleen size decreased after operation. Abdominal-wall venous dilatation completely disappeared in two of four patients. The platelet counts gradually increased and were significantly higher 3 years (126.6 +/- 59.3 x 10(3)/mm3) after DSRS-SPD than preoperative values (66.0 +/- 24.2 x 10(3)/mm3). White blood cell counts showed no significant changes. No patient developed a gastrointestinal hemorrhage postoperatively, although three had had repeated hemorrhages before the operation. Two patients showed disappearance of varices endoscopically at 2 years and 7 months after DSRS-SPD, respectively, but had recurrent varices at 7 and 11 years, respectively. The endoscopic findings regarding varices 3 to 7 years after DSRS-SPD were as follows: decreased number (80%); decreased length (40%); improvement of form (20%); improvement of fundamental color (60%); disappearance of red-color sign (100%); disappearance of gastric varices (75%); and disappearance of acute gastric mucosal lesions (100%). Although one patient later underwent liver transplantation because of progression of liver cirrhosis, all five are doing well. From these results, DSRS-SPD may prove to be a safe and feasible procedure for intrahepatic PH after HPE for BA and may improve gastroesophageal varices and hypersplenism on long-term follow-up.
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PMID:Distal splenorenal shunt with splenopancreatic disconnection for portal hypertension in biliary atresia. 1007 38