The use of a gonadal vein interposition graft to replace a polar artery in renal transplantation.
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Biomedical subjects
Publications and source records attributed to P Joshi.
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A 77-year-old man underwent repair of a vesicocolic fistula following which he had a protracted stay in the intensive care unit due to recurrent septicaemia, which was initially caused by bowel anastomosis breakdown. Management included central venous cannulation and pulmonary artery catheter monitoring. A septic, mobile right atrial thrombus developed, which was successfully treated. The literature on this condition is reviewed.
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Lymphocyte inhibitory factor (LyIF) and lymphocyte chemotactic factor (LCF) were produced by sensitized thymic (T) and bursal (B) cells and thymic (T) cells, respectively. The passage of sensitized T and B cells through a Sephadex G-10 column abrogated the ability of T cells to produce LyIF and LCF while B cells remained capable of producing LyIF. The return of macrophages to the adherent cell depleted population reconstituted the T cells' ability to produce LyIF and LCF. These data suggest a greater macrophage dependency of thymic cells than bursal cells in the production of lymphokines.
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Bursal (B) and thymic (T) lymphocytes from chickens sensitized to Mycobacterium tuberculosis (PPD) or human gamma globulin (hGG) produced an avian lymphocyte-inhibitory factor designated as LyIF-PPD or LyIF-hGG, respectively. A chemotactic factor (LCF) for peripheral blood leukocytes was elaborated only by T-cells sensitized to PPD and hGG. These factors were partially purified by HPLC and were characterized physiochemically. Maximum inhibitory activity for LyIF-PPD and LyIF-hGG occurred in peak fractions corresponding to molecular weight ranges of 29,000 to 52,000 daltons and 15,000 to 29,000 daltons, respectively. The inhibitory activity of B- and T-LyIF-hGG was lost after chymotrypsin and neuraminidase treatment. Maximum chemotactic activity for LCF-PPD and LCF-hGG was in peak HPLC fractions corresponding to molecular weight ranges of 9,000 to 16,000 daltons and 8,000 to 16,500 daltons, respectively. Chemotactic activity of LCF-PPD and LCF-hGG was lost following chymotrypsin treatment while it was not reduced after neuraminidase treatment. Both inhibitory and chemotactic activities were stable at 56 C for 30 min and resistant to changes in pH from 5 to 9. The precursor molecule for the lymphokine is made after antigen immunization, but activated in the presence of the sensitizing agent.
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The membrane phospholipid organization in Plasmodium falciparum-infected human erythrocytes was analysed by employing phospholipase A2 and Merocyanine 540 as external membrane probes. Both bee venom and pancreatic phospholipases A2 failed to hydrolyse phosphatidylserine in uninfected human red cells isolated from in vitro P. falciparum cultures. However, these enzymes under identical conditions readily degraded this aminophospholipid in P. falciparum-infected erythrocytes. Phosphatidylethanolamine hydrolysis also increased in parasitized cells. The degree to which these aminophospholipids were cleaved by the enzymes in intact infected cells depended on the developmental stage of the intracellular parasite, and was maximum at the schizont stage. This was consistent with the finding that the 'fluid-sensing' fluorescent dye, Merocyanine 540, readily labelled both the schizont and trophozoite-infected cells but not the fresh, uninfected or ring-infected erythrocytes. These results demonstrate that P. falciparum produces stage-dependent changes in the membrane phospholipid organization of its host erythrocyte.
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The membrane phospholipid organization in monkey erythrocytes harbouring different developmental stages of the simian malarial parasite Plasmodium knowlesi was studied using phospholipase A2 from two different sources and Merocyanine 540 as the external-membrane probes. Experiments were done to confirm that the phospholipases did not penetrate into the infected cells or hydrolyse phospholipids during membrane isolation. The parasite-free erythrocyte membrane was isolated by differential centrifugation or by using the cationic beads Affi-Gel 731. The purity of the membranes was established by optical and electron microscopy, and by assaying the parasite-specific enzyme glutamate dehydrogenase. About 10% of the phosphatidylethanolamine and none of phosphatidylserine were hydrolysed by the phospholipases in intact normal monkey erythrocytes. However, accessibility of these aminophospholipids to the enzymes was significantly enhanced in the infected cells under identical conditions. The degree of this enhancement depended on the developmental stage of the intracellular parasite, but not on the parasitaemia levels in the infected monkeys, and increased with the parasite growth inside the cells. Analogously, Merocyanine 540 was found to label the trophozoite- or schizont-infected erythrocytes, but not the ring-infected or normal cells. These results demonstrate that the intracellular malarial parasite produces stage-dependent alterations in the membrane phospholipid organization of its host erythrocyte.
A new surgical technique to close bladder defects using well vascularized myouterine flap is described. The flap serves as a temporary scaffold while the bladder is being bridged by natural bladder regeneration. The advantage of this flap is that it is not a free flap, being well vascularized through its pedicle, enhancing optimal bladder regeneration. This technique may be a useful surgical alternative for repair of large bladder defects.
Previous studies (Gupta et al. (1982) Nature 299, 259-261) have shown that nonparasitized erythrocytes of Plasmodium knowlesi-infected monkeys contain the procoagulant phospholipid phosphatidylserine (PS) in the outer-half of their membrane bilayer. A reinvestigation of this problem has now revealed that in acute P. knowlesi infection, at least 30% of the infected animals do not have this abnormality. However, PS externalization was a consistent feature in the uninfected red cells of chronically infected animals. Also, a similar membrane change was observed in the red cells of uninfected splenectomized monkeys. These results strongly suggest that spleen plays an important role in maintaining the exclusive inner distribution of PS in the normal erythrocyte membrane, and that partial migration of this lipid to the outer monolayer in nonparasitized erythrocytes could be attributed to an abnormal physiology of this organ in malarial infection.
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Three hundred twenty-six patients treated at New York University from 1970 to 1982 were studied for survival in relationship to surgical stage, type of therapy, and pathologic characterization of the primary tumor. At the time of diagnosis 25.5 per cent of tumors were Stage I, 15 per cent Stage II, 28.5 per cent Stage III, and 31 per cent Stage IV. The retrospective study showed that patients with tumor confined within the capsule achieved the highest five- and ten-year survivals of 88 per cent and 66 per cent, respectively. Survivals decreased as tumor invaded perirenal fat (67% and 35%) or regional lymph nodes (17% and 5%). Tumor invasion into the renal vein alone did not significantly change five-year survival (84%) but lowered ten-year survival to 45 per cent. Patients with metastases at the time of nephrectomy did poorly regardless of site of metastases or kind of adjuvant therapy, except for those managed by surgical extirpation of the secondary lesion. Certain tumor characteristics were associated with a better prognosis, e.g., size below 5 cm in diameter, lack of invasion of collecting system, perirenal fat or regional lymph nodes, and predominance of clear or granular cells growing into a recognizable histologic pattern.
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