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)

LEW with BDE-heart graft received 0 (control), 15, or 40 mg cyclosporine (CsA)/kg b. wt. per day. On postoperative days 3, 5, 7, 10, and 14 in four animals each weight and cell count of thymus and spleen were determined, and thymus and spleen cell subpopulations were examined with monoclonal antibodies. The same tests were performed in FiS heart graft recipients without immunosuppression and ungrafted LEW which received 15 or 40 mg CsA. We expressed alterations in thymocyte subpopulations by using the differentiation ratio (DR), i.e., differentiated in % of all T-cells and by the ratio of helper to suppressor/cytotoxic T-cells (Th-Ts/c). In graft rejection the thymus showed no significant change in DR or Th-Ts/c. However, in the CsA-induced graft tolerance DR was elevated and at the same time Th-Ts/c declined, both showing maximum values on days 5 and 7 and a return to normal thereafter. FiS graft recipients exhibited similar thymus alterations as tolerant recipients, but less marked. In CsA-treated ungrafted LEW, elevation of DR was slight after 15 mg but very strong after 40 mg CsA (93% on day 7), and it did not return to normal in the latter group. Th-Ts/c was decreased in these ungrafted animals, but not as strongly as in tolerant graft recipients. Such thymus alterations were not observed in graft rejection. Spleen weights were strongly increased in graft rejection and unchanged in graft tolerance. Splenic Ts/c and Th-Ts/s were increased in CsA-treated tolerant recipients but not in graft rejection. We conclude that elevation of DR and decline of thymic Th-Ts/c in the initial postoperative phase are indicators of graft tolerance in organ recipients.
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PMID:Significance of thymus differential ratio in immunologic status of graft tolerance. 306 60

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

Myelodysplastic syndrome is a clonal process characterized by ineffective hematopoiesis and progression to acute leukemia. Although many myelodysplastic syndrome and leukemic patients have compromised immunity, the role of underlying mutations in regulating immune function is poorly understood. Recent studies show that NUP98-HOXD13 (NHD13) fusion gene results in myelodysplastic syndrome and impairs lymphocyte differentiation in transgenic mice. In our studies, we sought to elucidate the mechanism by which NHD13 affects B-lymphocyte development and function. Based on our preliminary findings that transgenic mice had increased levels of IgM and reduced IgG1 and IgE, we hypothesized that the fusion gene might impair class switch recombination (CSR). Mice were immunologically challenged with dinitrophenol. NHD13 mice showed a marked reduction in B-lymphocyte differentiation in their bone marrow and spleen following dinitrophenol stimulation and had reduced production of dinitrophenol-specific antibodies. Spleen follicles from these mice were small and hypocellular, indicating failure of clonal expansion. When isolated NHD13 B lymphocytes were stimulated in vitro using Escherichia coli lipopolysaccharide or lipopolysaccharide + interleukin-4, they failed to undergo sufficient CSR and proliferation. Taken together, our findings show that expression of NUP98-HOXD13 impairs CSR and reduces the antibody-mediated immune response, in addition to its role in leukemia. Further delineation of the NUP98-HOXD13 transgene may reveal novel pathways involved in CSR.
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PMID:A NUP98-HOXD13 leukemic fusion gene leads to impaired class switch recombination and antibody production. 2261 70