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Biomedical subjects

S K Oh

Publications and source records attributed to S K Oh.

68 records · Page 4Linked to original sources

Differential effects of an immunosuppressive fraction from ascites fluid of patients with ovarian cancer on spontaneous and antibody-dependent cytotoxicity.

The ascites fluids from humans with cancer that has metastasized to the peritoneum is suppressive of the immune response both in vitro and in vivo. The active moiety is present in a high-molecular-weight fraction which elutes in the void volume of a Sephadex G-200 column. This fraction (designated Peak I) has been shown to inhibit a number of in vitro responses and will inhibit the antibody response to sheep red blood cells in vivo. In this report, the Peak I protein fraction from the ascites of patients with ovarian cancer is shown to inhibit spontaneous cytotoxicity of human mononuclear cells against the myeloid cell line K562 and against the T-lymphoid cell line Molt-4F. This fraction was active at concentrations of 1 to 3 mg/ml. In contrast to this finding, it was not possible to demonstrate an inhibition of antibody-dependent cell cytotoxicity against chicken red blood cells. Preincubation of the effector cells with Peak I prior to addition to the chicken red blood cell targets or modification of the antibody concentration in the assay did not result in suppression; in fact, in many experiments, the Peak I potentiated cytotoxicity against chicken red blood cells. The Peak I proteins were also tested in an antibody-dependent cell cytotoxicity assay against a transformed cell line (HeLa cells), and there was no significant suppression of cytotoxicity. Peak I protein fractions prepared as controls from normal human serum and a congestive heart failure fluid were not suppressive, whereas the Peak I fraction from a cirrhotic fluid was suppressive of natural killing activity.

Antibody-Dependent Cell Cytotoxicity↗

Present status of the zinc glycinate marker (ZGM).

ZGM was purified from both primary and metastatic colonic carcinomas demonstrably positive for ZGM by immunofluorescence microscopy. ZGM purification included preparative Pevikon electrophoresis, Sepharose 4B molecular exclusion chromatography and Con A-Sepharose affinity chromatography. ZGM had an alpha2 electrophoretic mobility, an estimated molecular weight by Sepharose 4B equal to or greater than 2 x 10(6), and did not bind to Con A-Sepharose, although having determinants with CEA-like activity. Its immunologic activity was resistant to trypsin or phospholipase A but not to neuraminidase. Antisera prepared to ZGM and absorbed with saliva, when tested by double immunodiffusion, formed a single precipitation line with saline extracts of colon tumors and did not cross-react with CEA, AFP, normal tissue extracts, ferritin, NCA, NCA-2, CSAp, blood groups A, B, H, Lewis antigen, or buffy coat, alpha-2 macroglobulin, saliva or ovarian cyst fluid. Immunofluorescence microscopy confirmed the presence of ZGM in 40 out of 45 adenocarcinomas of the GI tract staining primarily in tumors, the apical cytoplasm, and in grossly nonmalignant tissues, the deep crypts of the villi, while all of 22 non-GI tumors in the study were ZGM negative.

Antigens, Neoplasm↗

Tissue localization of zinc glycinate marker and carcinoembryonic antigen by immunofluorescence. I. Preparation of antisera against the zinc glycinate marker.

Antisera against the zinc glycinate marker (ZGM) were produced in New Zealand White rabbits with induced tolerance to normal tissue components and CEA, and in mature, previously uninoculated rabbits for use in immunofluorescent histologic localization of ZGM in colon cancers and other tissues. Analysis of the antisera by immunodiffusion and counterimmunoelectrophoretic techniques showed them to be specific for ZGM when tested with ZGM, carcinoembryonic antigen, normal tissue extracts, or cell elements of normal blood.

Animals↗

Tissue localization of zinc glycinate marker and carcinoembryonic antigen by immunofluorescence. II. Immunofluorescence microscopy.

Preliminary indirect immunofluorescence studies on the zinc glycinate marker (ZGM) were compared with carcinoembryonic antigen (CEA) immunofluorescence, ZGM, detected in 26 of 29 human colon adenocarcinomas, was associated with the epithelial component of the malignant glands. Fluorescence was generally less strong and more granular for ZGM than for CEA and was found in intraglandular spaces, luminal border areas, and cytoplasm. ZGM concentration and tissue localization appeared to be related to tumor differentiation. ZGM was also detected in benign colon mucosae (adjacent to and distant from the carcinomas) from patients with colon carcinoma, but differed from CEA in that it was present in the deep crypt portion only. Gastric, pancreatic, esophageal, and anal adenocarcinomas, as well as benign gastric pyloric and small bowel mucosae had detectable ZGM. CEA, but not ZGM, was observed in 20 nongastrointestinal carcinomas to date. Studies are under way to determine whether ZGM is a marker associated with colon and gastrointestinal adenocarcinoma specifically or undifferentiated crypt cells of the colon and digestive tract in general.

Adenocarcinoma↗

Soluble HL-A antigens in serum. I. Isolation and purification.

A new method was developed which utilizes fractional salting out, gel filtration, ion exchange chromatography and polyacrylamide gel electrophoresis for the isolation and purification of soluble HL-A antigens from serum. The method produced purified antigens possessing HL-A 5,9 specificities with yield up to 60% of that detected in the original serum. Up to 150-fold increase in specific HL-A antigenic activity above that in the starting material could be achieved as measured by the ability of the purified antigens to specifically inhibit the cytotoxic activity of HL-A alloantisera against selected target cells. Electrophoretically purified HL-A antigens with different specificities appear to have a similar molecular size, i.e. 33 000, but differ in their electric charge properties, beta2-microglobulin (beta2m) seems to be noncovalently associated with HL-A antigens present in serum, but during purification beta2m in progressively lost until at the final purification by polyacrylamide gel electrophoresis, the material is completely devoid of beta2m.

Chemical Precipitation↗

Management of ileal perforation due to typhoid fever.

The results of the surgical management of 161 cases of ileal perforation due to typhoid fever are presented. Most were seen after an illness of 2-4 weeks, and because of delays in seeking hospital admission, more than half were explored more than 24 hours after their perforation occurred. All patients were prepared for operation with nasogastric suction, intravenous fluids, and antibiotics. At laparotomy, 80% had considerable quantities of pus and small bowel contents in the peritoneal cavity and the remainder had localized abscesses; there were no instances of localization of the perforation. One hundred three of these patients underwent simple closure of their perforations, while 43 underwent small bowel resection, usually because of multiple perforations. Exteriorization or drainage were performed only in patients too sick to tolerate a more appropriate procedure. The overall mortality was 9.9%. The authors believe that typhoid perforations can best be dealt with at operation. Delay in operative intervention adversely affects the survival rate after surgery. Chloramphenicol is used as the drug of choice.

Chloramphenicol↗

Recombinant human growth hormone decreases lung and liver tissue lipid peroxidation and increases antioxidant activity after thermal injury in rats.

The combination of increased oxidant with decreased endogenous polypeptide and protein antioxidant activity corresponds to a decrease in cellular energetics and cell membrane lipid peroxidation. Providing large doses of growth hormone has been shown to preserve cell mass and organ function after burn injury. The role of growth hormone in oxidant injury has not been defined. We determined whether growth hormone altered the degree of lung and liver lipid peroxidation and the activity of glutathione and catalase in lung and liver tissue after burn injury. Four groups of 40 rats each were studied for 48 hours, with 1 group receiving a 20% full-thickness burn, 1 group treated with growth hormone after 20% full-thickness burn injury, a control group, and a growth hormone alone-treated group. We found increased lipid peroxidation, measured as malondialdehyde, in lung and liver tissue, and a decrease in glutathione and catalase activities during the 48-hour post-burn period. The addition of growth hormone prevented the lipid peroxidation and significantly increased tissue glutathione and catalase activities with respect to control values. Growth hormone alone also increased endogenous antioxidant levels. We conclude that growth hormone given after burn injury decreases oxidant stress by producing a significant increase in the endogenous antioxidants glutathione and catalase.

Analysis of Variance↗

Expression of phospholipase C-gamma 1 and its transcriptional regulators in breast cancer tissues.

BACKGROUND: PLC-gamma 1 is activated through direct interaction with growth factor receptor tyrosine kinase but little is known about the mechanisms controlling PLC-gamma 1 expression and its biological significance. MATERIALS AND METHODS: Using immunoblotting, we evaluated PLC-gamma 1 protein overexpression in twenty breast cancer tissues. The expression of binding protein to GES1, GES2 and GES3, located in transcriptional regulator (GPE1) was found by electrophoretic mobility shift assay (EMSA). We also determined whether there was any correlation between prognostic factors (numbers of metastatic axillary nodes, histologic grade, c-erbB2, p53, and E-cadherin) and the overexpression of PLC-gamma 1 protein. RESULT: On immunoblotting, 17 of 20 breast cancer tissues showed overexpression of PLC-gamma 1, a result of which was corresponded to that of immunohistochemistry. The binding proteins to GES1, GES2 and GES3 were overexpressed only when PLC-gamma 1 protein overexpression was apparent. Positive expression of E-cadherin only was significantly associated with PLC-gamma 1 protein overexpression (x = 0.607, p = 0.045). CONCLUSION: GPE1 binding proteins might be the transcriptional regulator in PLC-gamma 1 overexpression and the relationship between expression of PLC-gamma 1 and E-cadherin would require further elucidation.

Base Sequence↗