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T Nishida

Publications and source records attributed to T Nishida.

At least 793 records · Page 44Linked to original sources
PubMed1967

Dissociation of low density lipoprotein-antibody precipitates at alkaline pH.

The effect of alkaline pH on the dissociation of immunoprecipitates of low density lipoproteins (LDL) of the S(f) 0-10 class was studied by immunological and ultracentrifugal methods. The precipitates prepared at the equivalence point were dissolved and centrifuged in sodium chloride solutions of density 1.063 and pH's between 10.25 and 11.5. Analytical centrifugation of the top fraction, which floated at density 1.063, after dialysis against 0.9% sodium chloride of pH 7.4 revealed the presence of LDL and of soluble LDL-antibody complex. The amount of soluble complex was greater for the preparations obtained at lower pH than those obtained at higher pH and was undetectable at pH 11.5. The yield of immunoglobulin from the bottom fractions was maximal when the pH of the centrifugation medium was 11.0. Below pH 11.0, the greatly reduced yield of immunoglobulin was due partly to incomplete dissociation and partly to aggregation of soluble complex, while above pH 11.0 the decreased yield was possibly due to alkaline denaturation of the globulin. The immunoglobulin separated at pH 11.0 and dialyzed to pH 7.4 was reprecipitatable by LDL, and the reactivity did not seem to be appreciably influenced by the alkaline treatment.

Alkalies↗
PubMedDate not supplied

Blood level of mitochondrial aspartate aminotransferase as an indicator of the extent of ischemic necrosis of the rat liver.

To assess the severity of ischemic liver injury, we examined release of mitochondrial aspartate aminotransferase (EC 2.6.1.1) and its cytoplasmic isozyme from the ischemic rat liver into the circulation. Their patterns of leakage were quite different: the level of cytoplasmic aspartate aminotransferase reached a peak soon after the circulation to the ischemic liver was restored, while that of mitochondrial aspartate aminotransferase increased slowly, reaching a maximum after more than 10 hr. On anoxic incubation of mitochondria isolated from the normal liver, oxidative phosphorylation capacity was lost within 2 hr, at which time no leakage of matrix enzymes was observed: more than 10 hr after-loss-of-oxidative phosphorylation were needed for the matrix enzymes to leak out of the mitochondrial membrane. Since the viability of cells is considered to depend on the capacity of oxidative phosphorylation, it is highly likely that the delayed appearance of mitochondrial aspartate aminotransferase in blood indicates the postmortem changes of injured cells. In fact, the cumulative activity of mitochondrial aspartate aminotransferase but not cytoplasmic aspartate aminotransferase in circulation after ischemic liver injury correlated fairly well with the decrease of total adenine nucleotides which were monitored to measure viable cells. The difference between mitochondrial aspartate aminotransferase and cytoplasmic aspartate aminotransferase as quantitative indices of hepatic necrosis may be due to the relative stability of the former and significant inactivation of the latter during hepatic ischemia. Therefore, the determination of mitochondrial aspartate aminotransferase in blood may be useful in the assessment of liver necrosis after ischemic injury.

Adenine Nucleotides↗
PubMedDate not supplied

Different responses in adult and neonatal hearts to changes in coronary perfusion pressure.

The influence of coronary perfusion pressure on neonatal heart function has not been evaluated. We compared the coronary perfusion pressure-cardiac function relationship between neonatal and adult hearts. Neonatal and adult rabbit hearts were examined. The coronary perfusion pressure was changed in increments of 10 mmHg. Coronary blood flow and left ventricular functions were measured at each coronary perfusion pressure. Autoregulatory capacity for coronary blood flow was quantified by calculating the autoregulation index. In neonatal hearts, left ventricular developed pressure was decreased at high perfusion pressure, whereas in adult hearts left ventricular developed pressure increased at high perfusion pressure. In neonatal hearts, left ventricular enddiastolic pressure was elevated at both low and high perfusion pressure, whereas in adult hearts left ventricular enddiastolic pressure remained constant at all perfusion pressures. Adult hearts exhibited coronary blood flow autoregulation in the perfusion pressure range between 40 and 90 mmHg. In contrast, neonatal hearts did not show autoregulation in any perfusion pressure range. In neonatal hearts, both low and high perfusion pressure caused deterioration in ventricular function attributable to the immaturity of coronary autoregulatory capacity. We conclude that coronary perfusion pressure should be controlled within a narrow range for neonates.

Adult↗
PubMedDate not supplied

Study of HLA class I restriction and the directed antigens of cytotoxic T lymphocytes at the tumor sites of ovarian cancer.

The molecular basis of T-cell-mediated recognition of ovarian cancer cells remains to be fully addressed. In this study we investigated HLA class I restriction and directed antigens of cytotoxic T lymphocytes (CTL) at the sites of ovarian cancer. Three HLA-class-I-restricted CTL lines were established from the tumor sites of ovarian cancer by culturing tumor-infiltrating lymphocytes or tumor-associated ascitic lymphocytes with interleukin-2: (1) HLA-A2402-restricted and ovarian-adenocarcinoma-specific CTL, (2) HLA-A2-restricted CTL recognizing histologically different cancers, and (3) HLA-B52-restricted and ovarian-cancer-specific CTL. HLA-A0201, HLA-A0206 and HLA-A0207 tumor cells were lysed by the HLA-A2-restricted CTL. HLA-B52 restriction of the third CTL line was confirmed by the transfection of HLA-B5201 cDNA into the tumor cells. The HLA-A2-restricted CTL recognized the SART-1, but not the MAGE-1 or MAGE-3 antigen. These results may facilitate a better understanding of the molecular basis of tumor-specific immunity at the tumor site of ovarian cancer.

Animals↗
PubMedDate not supplied

Prognostic significance of proliferative cell nuclear antigen in carcinoma of the extrahepatic bile duct.

Bile duct cancers are still difficult to cure, and even if curatively resected locoregional recurrences are frequent. Biologic proliferative activity of the cancer may influence postoperative recurrence and the prognosis. A retrospective study was performed with the medical records of 44 consecutive patients who underwent surgery for histologically extrahepatic bile duct cancer (stage 3 or 4) at Osaka Police Hospital during the period 1980 to 1992. Univariate analysis suggested that the stage according to the UICC classification, curability, DNA ploidy, proliferating cell nuclear antigen (PCNA), S-phase and G2M-phase fractions, and histologic differentiation were significant prognostic factors. The Cox's proportional hazard model indicated that PCNA and histologic differentiation were independent prognostic factors for crude and cause-specific survival. When PCNA was omitted from the analysis, DNA ploidy and histologic differentiation were independent prognostic factors for both crude and cause-specific survival. These results suggested that proliferative activity influenced the postoperative prognosis of extrahepatic bile duct cancer.

Bile Duct Neoplasms↗
PubMedDate not supplied

Preventing human CD8+ cytotoxic T lymphocyte-mediated cytotoxicity against swine endothelial cells by overexpression of human decoy Fas antigen.

Although the birth of homozygous alpha1, 3 galactosyltransferase gene-knockout pigs raised hopes for an imminent breakthrough in the prevention in the antibody-mediated rejection of pig to human discordant xenotransplants, human CD8(+) cytotoxic T lymphocyte (CTL)-mediated killing may represent a new immunological barrier to long-term survival in xenograft recipients. In this study, we demonstrated that the cytotoxicity of human CD8(+) CTL against swine endothelial cells (SEC) is highly detrimental and mediated at least in part by the Fas/FasL pathway. To prevent this CTL-mediated xenocytotoxicity, we overexpressed the human decoy Fas antigen, which does not contain a death domain in its cytoplasmic region, by means of binding competition with endogenous pig Fas antigen on SEC for the common ligand, human FasL. Furthermore, we generated a membrane-bound form of human FasL that cannot be cleaved by a putative metalloproteinase to produce a soluble form, which was assessed as an inhibitor of CTL cytotoxicity. Both human decoy Fas and membrane-bound FasL were effective to prevent CTL-mediated killing, suggesting that these novel molecules may represent a step forward toward preventing CD8(+) CTL-mediated xenograft rejection. The combined expression of both molecules may be more beneficial to protect xenograft cells.

Animals↗