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Biomedical subjects

T Kanai

Publications and source records attributed to T Kanai.

At least 163 records · Page 9Linked to original sources
PubMed1994

Decrease in 6R-5,6,7,8-tetrahydrobiopterin content in cerebrospinal fluid of autistic patients.

The levels of pterin compounds in the lumbar cerebrospinal fluid (CSF) of ten neurologically normal and twenty autistic children were measured by two different liquid chromatographic systems, a conventional and a newly developed direct method. Among pterin compounds 7,8-dihydroneopterin (NH2) and 6R-5,6,7,8-tetrahydrobiopterin (R-BH4) levels in autistic children were significantly reduced to 66.1 and 41.5%, respectively, of those found in the controls. The autistic children were divided into three subgroups according to their CSF homovanillic acid (HVA) level and age: the group with an elevated HVA level, the younger (< 7 year old) group with a normal HVA level, and the older (> 7 year old) group with a normal HVA level. In comparison, the further reduction was observed in NH2 and R-BH4 levels in the younger group and in the 7,8-dihydropterin (PH2) level in the group with an elevated HVA level. Thus, these results suggest that the endogenous biosynthesis of R-BH4 in the brain may be reduced in autistic children as compared with that in neurologically normal children.

Adolescent↗
PubMed1994

Electron spin resonance signals of non-heme iron as an indicator of ischemia-reperfusion injury of the liver.

Although many different methods have been proposed to assess the viability of preserved or reperfused liver, none of them are definitive. In this study, we investigated the usefulness of electron spin resonance (ESR) spectrometry in the rat liver ischemia model. Ischemia was induced in Wistar rats weighing 250-300 g by clamping the portal triad. At 15, 30, 60, or 90 min after the clamping, the liver was reperfused by removing the clamp. Liver specimens obtained before and after the clamping and also 30 min after reperfusion were frozen with liquid nitrogen and analyzed at 140K by ESR spectrometry. Two significant signals of g-values of 2.0 and 1.96 were observed with the fresh liver. The former was thought to be a mixture of CoQ, flavin, and succinate radicals. The intensity of this signal did not change throughout the experimental period. The latter was regarded as the signal from non-heme irons of mitochondria. The intensity of this signal decreased as the ischemic time became longer (the ratio to the signal intensity of the fresh liver was 0.69 +/- 0.19, 0.22 +/- 0.08, 0.20 +/- 0.05, and 0.18 +/- 0.09 at the end of 15, 30, 60, and 90 min of ischemia, respectively). After reperfusion, each ratio recovered to 0.95 +/- 0.12, 0.77 +/- 0.06, 0.56 +/- 0.15, and 0.37 +/- 0.20, respectively. This suggests that detectable signals with Fe(II)-Fe(III) decreased and became undetectable as the reduced form of non-heme irons under the anoxic state. Then, after reperfusion, the reduced form of non-heme irons decreased and the oxidized form increased. Incomplete recovery was thought to be due to decrease in the viability or function of liver cells. ATP and energy charge had the same tendency as the non-heme iron signal observed with ESR. There was a significant correlation between the non-heme iron signal and energy charge (y = 0.73x + 0.32, r = 0.78, P < 0.001), demonstrating that the signal intensity reflects the viability or function of liver cells. This study suggests that the signal from non-heme irons detected by ESR can be a good parameter of the metabolic state of the liver in ischemia and reperfusion. This method is simple and quick and should be applicable in clinical liver transplantation.

Adenosine Diphosphate↗
PubMed1994

New development of transarterial immunoembolization (TIE) for therapy of hepatocellular carcinoma with intrahepatic metastases.

The prognosis of patients with multiple hepatocellular carcinoma (HCC) remains disappointing. In this study, we devised a new therapeutic modality for HCC consisting of transarterial immunoembolization (TIE) using OK-432 and fibrinogen and then analyzed the preliminary results. In the first series, we applied the treatment to 19 patients with advanced HCC who had proved to be insensitive to several previous conventional treatments. In all, 14 patients (74%) with unresected HCC have currently survived for between 2 and 16 months after TIE. The remaining 5 patients died at 17, 14, 8, 7, and 4 months after TIE. The serum levels of tumor markers decreased in all of the patients, and a marked reduction in tumor size was observed in six patients after TIE. A high fever occurred in all cases, and abdominal pain and loss of appetite were also observed after TIE. However, deterioration of liver function was negligible. After confirmation of the safety of this method, we started a second study series in which this TIE treatment was selected as the first choice. Six patients have been treated to date. All patients in this group underwent hepatic resection at 6-48 days following TIE. Histological examination of the resected specimens following TIE showed massive infiltration of mononuclear cells around tumor cell nests and lytic necrosis as well as coagulation necrosis of the main tumor and the intrahepatic metastases. In conclusion, our results indicate that TIE may be a safe and promising therapy for patients with HCC.

Adult↗
PubMed1994

Type-IV collagenase and tissue inhibitor of metalloproteinase in ovarian cancer tissues.

OBJECTIVE: We examined the specific expression of gelatinase/type-IV collagenase and tissue inhibitor of metalloproteinase (TIMP) in clinical ovarian cancer tissue. METHODS: Molecular weight-specific gelatinase/type-IV collagenase activity was examined by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis in which substrate was included (zymography). The expression of TIMP mRNA was examined by Northern blot analysis. RESULTS: Zymography revealed that in ovarian cancer the activity of a 92-kDa gelatinase/type-IV collagenase was always greater than that of a 64-kDa gelatinase/type-IV collagenase in contrast to the situation in the normal ovary. Northern blot analysis revealed no remarkable difference of TIMP mRNA expression between cancer and normal ovarian tissues. CONCLUSIONS: These results indicate that the higher activity of the 92-kDa gelatinase/type-IV collagenase enzyme, relative to that of the 64-kDa enzyme, is involved in the malignant phenotype of ovarian cancer, while the inhibitor of these enzymes, TIMP, is distributed in a widespread fashion in the tissue, and its levels are not correlated with the malignancy.

Adenocarcinoma, Clear Cell↗
PubMed1994

Crystalline inclusions in the glomerular podocytes in a patient with benign monoclonal gammopathy and focal segmental glomerulosclerosis.

We report a case of a 40-year-old woman with benign monoclonal gammopathy who developed focal segmental glomerulosclerosis associated with widespread deposition of large crystalline inclusions in the glomerular podocytes. Electron microscopy showed that the crystalline structures were electron dense and needle shaped or polygonal. At a higher magnification, they were seen to be surrounded by unit membranes and to feature a longitudinal filamentous substructure. These inclusions showed positive immunohistochemical staining for kappa light chain. Clinically, the patient had shown nephrotic syndrome on the first medical examination, and later revealed chronic renal failure and monoclonal gammopathy of the immunoglobulin G kappa type, but no evidence of multiple myeloma or other lymphoproliferative diseases. This patient seems to have had a rare form of glomerular involvement associated with benign monoclonal gammopathy.

Adult↗
PubMed1994

Low temperature collagenase digestion for islet isolation from 48-hour cold-preserved rat pancreas.

We examined the efficacy of relatively low temperature collagenase digestion at 20 degrees C on the yield and viability of islets after long-term cold preservation. Wistar rat pancreases were distended with University of Wisconsin solution via a pancreatic duct at the time of harvesting to which collagenase and 2.5 mM calcium chloride were added. The pancreases were cold-preserved at 4 degrees C for 24 or 48 hr. After storage, they were incubated for collagenase digestion at 37 degrees C or 20 degrees C for various incubation periods to obtain the peak yield. At 20 degrees C, in vitro collagenase activity measured by the FALGPA method was one fourth of that at 37 degrees C, and pancreases were well digested with a prolonged digestion period (60-90 min vs. 15-20 min for the 37 degrees C group). In vitro insulin secretion of islets isolated from freshly removed pancreases was maintained at 20 degrees C for 120 min in University of Wisconsin solution as compared with 30 min at 37 degrees C. Therefore, the preserved pancreases used in this study were incubated either at 37 degrees C or 20 degrees C at various times in order to obtain peak islet yields. The islet yields from 24-hr cold-preserved pancreases at 37 degrees C and 20 degrees C digestion were 573 +/- 59/rat (n = 6) and 497 +/- 84/rat (n = 11), respectively, and those from 48-hr cold-preserved pancreases were 395 +/- 113/rat (n = 6) and 414 +/- 75/rat (n = 6), respectively. The yields from 24- and 48-hr cold-preserved pancreases were significantly low compared with 635 +/- 52/rat for fresh pancreases (n = 15), but there was no significant difference between the 2 methods. The viability of the isolated islets, which was examined by transplantation to streptozotocin-induced diabetic C57BL/6 mice, showed a significant difference in the capacity to ameliorate diabetes. The functional success rate of islet transplantation after 24-hr cold preservation was equally good (8/8 for 37 degrees C group vs. 9/10 for 20 degrees C group), but the rate for those from 48-hr cold-preserved pancreases was significantly better with digestion at 20 degrees C than at 37 degrees C (1/8 for 37 degrees C group vs. 7/8 for 20 degrees C group, P < 0.05). We concluded that viable islets can be isolated from 48-hr cold-preserved pancreases with the low temperature collagenase digestion method, which shows promise as a modality for successful clinical islet transplantation.

Animals↗
PubMed1994

A potential immunosuppressive effect of anti-lymphocyte function-associated antigen-1 monoclonal antibody on islet transplantation.

The immunosuppressive potentials of mAbs to lymphocyte function-associated antigen-1 (LFA-1) and CD2 molecules were examined in murine islet transplantation. Crude digested islets from BALB/c (H-2d) mice were transplanted into the renal subcapsular space of streptozotocin-induced diabetic C57BL/6 (H-2b) mice. The rat mAbs of KBA (anti-LFA-1) and RM2-1 (anti-CD2) were given intraperitoneally immediately after transplantation and on the first day after grafting at a dose of 0.1 mg/mouse/day. In nontreated animals, the islet allografts were acutely rejected with a mean survival time (MST) of 19.6 +/- 8.3 days. Control isotype-matched anti-CD18 treatment did not prolong the MST of 12.8 +/- 1.6 days. Anti-LFA-1 treatment alone produced indefinite survival in 5 of 10 recipients with MST of 72.2 +/- 33.4 days. Anti-CD2 treatment failed to do so, although MST was marginally prolonged to 32.8 +/- 20.5 days. When both mAbs were given together, additional benefit with anti-CD2 treatment was not observed (MST: 77.4 +/- 31.1 days). In spite of the unresponsiveness to islet allografts, the animals did not suffer from any severe infectious disease. Mice bearing long-term functioning islets rejected third-party skin grafts as well as islet donor strain skin grafts. The long-term surviving islet allografts were also rejected coincidentally. These results indicate that a perioperative short course of anti-LFA-1 mAb treatment can induce unresponsiveness to islet allografts, although it is not systemic, and that costimulatory signals through these adhesion molecules play a central role in inducing an immune response leading to rejection of the allografted islets.

Animals↗
PubMed1994

Cytoprotective effect of prostaglandin I2 analogues on superoxide-induced hepatocyte injury.

BACKGROUND: Prostaglandin I2 (PGI2) analogues have been suggested to protect the liver from ischemia-reperfusion injury, but the exact mechanism remains to be proved. METHODS: Primary cultured rat hepatocytes were exposed to superoxide generated by mixing hypoxanthine and xanthine oxidase, and changes in cell viability, cytosolic free calcium concentration ([Ca2+]i), and adenosine 3',5'-cyclic monophosphate (cAMP) concentration were assessed. The PGI2 analogue (OP2507 or OP41483) at 1 to 100 ng/ml was given as treatment. RESULTS: PGI2 analogues suppressed hepatocyte death in a dose-dependent manner (p < 0.01; OP2507 at 10 and 100 ng/ml, OP41483 at 100 ng/ml). At the end of 1-hour preincubation with OP2507, a significant rise in cAMP concentration was observed. Moreover, addition of dibutyryl cAMP suppressed hepatocyte death. A rise in [Ca2+]i, which preceded cell death, was prevented by PGI2 analogues or dibutyryl cAMP. CONCLUSIONS: The increase in cellular cAMP followed by suppression of [Ca2+]i elevation might be the major cause of the cytoprotective effect of PGI2 analogues in superoxide-induced hepatocyte injury.

Animals↗