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T Kenmochi

Publications and source records attributed to T Kenmochi.

81 records · Page 5Linked to original sources
PubMedDate not supplied

Protection of mouse islet isografts from nonspecific inflammatory damage by recipient treatment with nicotinamide and 15-deoxyspergualin.

The major cause of primary nonfunction of transplanted islets is nonspecific inflammation associated with the transplantation procedures. Using mouse islet isografts, we attempted to prevent graft loss mediated by nonspecific inflammation using recipient treatment with nicotinamide (NA) and 15-deoxyspergualin (DSG). Newborn BALB/c islets, ranging in numbers between 1200 and 1500, were transplanted into syngeneic adult mice made diabetic by intravenous injection of 200 mg/kg streptozotocin. Recipient mice were divided into the following four groups, based on the treatment protocol of NA and DSG: intraperitoneal injection (IP) of normal saline (Group 1), IP injection of 2500 mg/kg NA (Group 2), IP injection of 5 mg/kg DSG (Group 3), and IP injection of NA + DSG (Group 4). Treatment started Day -1 and continued until Day 9 (Day 0 is day of transplantation). Blood and urine glucose, body weight, and intravenous glucose tolerance tests (IV-GTT) were examined after transplantation. Reversal of diabetes, as indicated by normoglycemia and negative urine glucose, was higher in Groups 2 (75%), 3 (50%), and 4 (85.7%), compared to Group 1 (11.1%). Especially in Group 4, the endocrine function and morphology of grafted islets were well preserved as shown by K values of IV-GTT and histological studies. These results suggest the importance of islet protection from irreversible damage by nonspecific inflammation at earlier stages of implantation, and the effectiveness of a short course of treatment with NA and DSG.

Animals↗
PubMedDate not supplied

Combined therapy with radiofrequency thermal ablation and intra-arterial infusion chemotherapy for hepatic metastases from colorectal cancer.

BACKGROUND/AIMS: In this preliminary study, we investigated the efficacy of combined radiofrequency thermal ablation therapy (RFA) with hepatic arterial infusion chemotherapy (HAI) in the treatment of multiple liver metastases from colorectal cancer. METHODOLOGY: Nine patients with bilobular multiple metastases was treated. The number of nodules was 6.0 +/- 3.9 (range: 2-13), and the size was 2.1 +/- 1.0 cm (range: 0.5-4.8 cm) in diameter. RFA was performed using a RF generator operating at 460 kHz with a 15-gauge, 4-prong custom RF needle. Treatment temperature was kept at 90-110 degrees C for 5 min. 5-Fluorouracil (5-FU) was administered by weekly 750-1250 mg/body/5 h as the regimen of HAI. RESULTS: During a 15.2-month follow-up period, 6 of 9 patients survived more than 1 year. Three of the 6 survived more than 2 years. Serum CEA level in 5 patients dropped from 24.5 +/- 9.5 ng/ml to 10.3 +/- 5.5 ng/ml. Local recurrence was observed in 5 patients and new lesions in 4. Extrahepatic recurrence was observed in 5 patients. There were no serious complications but one HAI-related cerebral thrombosis. CONCLUSIONS: Combined RFA with HAI would be effective and safe. This modality provides a new option for the treatment of multiple liver metastases from colorectal cancer.

Adult↗
PubMedDate not supplied

Stromal thrombospondin-1 expression is correlated with progression of esophageal squamous cell carcinomas.

Thrombospondin-1 (TSP1) is an extracellular matrix glycoproteins that affecting cell adhesion, motility and growth. Based on its effects on tumors, TSP1 is thought to be a potential regulator of tumor growth and metastasis. In this study, we clarified TSP1 immunoreactivity in human esophageal squamous cell carcinoma and its clinicopathological significance. TSP1 immunoreactivity was detected mainly in the cancer stroma and was observed infrequently in cancer cells. According to the TNM classification, 70.6% (12/17) of the T3 esophageal cancers were TSP1-positive, while only 26.9% (7/26) of the Tis and T1 cancers showed TSP1 expression. Lymph node metastasis and venous involvement was frequently found in the TSP1-positive cases (71.4% and 80.0%, respectively) of esophageal squamous cell carcinoma (p < 0.001). This observation suggested that TSP1 expression plays an important role in cancer cell growth and metastasis of human esophageal squamous cell carcinomas, and that stromal TSP1 immunoreactivity is a good predictor of venous involvement and lymph node metastasis.

Aged↗
PubMedDate not supplied

Immunohistochemical MUC1 (DF3 antigen) expression of human esophageal squamous cell carcinoma.

MUC1 (DF3 antigen) is a member of a family of high molecular weight glycoproteins. Recent studies have demonstrated that MUC1 is expressed in tumors of various human organs and may function as an anti-adhesion molecule that inhibits cell-to-cell adhesion, inducing tumor metastasis. However, expression patterns of MUC1 have not yet been established in human esophageal carcinomas. In this study, we examined MUC1 expression and its histopathological localization in human esophageal squamous cell carcinoma. MUC1 immunoreactivity was found in 17 (32.1%) out of 53 esophageal squamous cell carcinomas, regardless of the depth of tumor invasion, vascular invasion or lymph node status. MUC1 expression was detected in the intramucosal part in 28.3% (15 out of 53) and in the invasive part in 32.6% (14 out of 43) of the esophageal carcinomas (no significant difference). These observations suggested that expression of MUC1 is an early event in cancer progression, but that it is not significantly associated with metastasis of human esophageal carcinomas.

Aged↗
PubMedDate not supplied

Arterio-portal shunt in liver rescued by hepatectomy after arterial embolization.

Arterio-portal shunts are generally treated with transcatheter arterial embolization, as a therapeutic measure for bleeding of esophageal varices. However, transcatheter arterial embolization is frequently associated with reestablishment of arterio-portal shunts. We now report our experience with partial hepatectomy to remove the arterio-portal shunt associated with esophageal varices, which recurred after transcatheter arterial embolization. The patient was a 60-year-old female, who had massive hematemesis caused by rupture of esophageal varices. Doppler sonography and arteriography demonstrated an arterio-portal shunt in the right anterior superior segment of the liver. Temporary hemostasis was achieved with transcatheter arterial embolization, however, hemorrhage recurred one month later. The second transcatheter arterial embolization failed to manage the shunt and varices. The patient developed hepatic coma. After recovery from coma, she was referred to our hospital. We carried out partial hepatectomy, which provided remarkable hemodynamic improvement; the portal vein flow changed from hepatofugal to hepatopetal. Esophageal varices and hepatic coma have totally disappeared. This patient has had no complaint and has remained free of esophageal varices, for 3 years postoperatively. She is having a normal life. The partial hepatectomy to remove the arterio-portal shunt induced complete resolution of the arterio-portal shunt, as well as dramatic improvement in portal flow and hepatic coma. Our experience in the present case suggests that partial hepatectomy should be considered as a radical therapy for arterio-portal shunt, without insistence on transcatheter arterial embolization.

Arteriovenous Fistula↗
PubMedDate not supplied

In vitro metabolism of dorzolamide, a novel potent carbonic anhydrase inhibitor, in rat liver microsomes.

The in vitro metabolism of dorzolamide, a potent carbonic anhydrase inhibitor, was investigated using liver microsomes from Sprague-Dawley rats. The liver microsomes metabolized dorzolamide to an N-deethylated form, whereas N-deethylation of dorzolamide was not detected in 10,000g supernatant from the small intestine, brain, heart, lung, kidney and spleen, or the cytosol fraction of liver. The dorzolamide N-deethylase activity was not detected without an NADPH-generating system and was inhibited by classical inhibitors for cytochrome P450, metyrapone and n-octylamine. Orphenadrine and diphenhydramine (specific inhibitors for CYP2B1/2), diethyldithiocarbamate, disulfiram and isoniazid (inhibitors for CYP2E1), troleandomycin (inhibitor for CYP3A), and testosterone inactivated dorzolamide N-deethylase activity. On the other hand, ajmalicine, a specific inhibitor for CYP2D1, did not inhibit the reaction. With phenobarbital-induced microsomes, 66%, 72%, 36%, and 53% of the 2 beta-, 6 beta-, 16 alpha-, and 16 beta-testosterone hydroxylase activities were inhibited by 5 mM dorzolamide, respectively, whereas the 2 alpha-hydroxylase activity was not inactivated. Antisera against rat CYP2B1, CYP2E1, and CYP3A2 suppressed dorzolamide N-deethylase activity by 52%, 43% and 46%, respectively, whereas only 18% and 15% of the activity were inhibited by anti-CYP1A1 and anti-CYP4A1 antibodies, respectively. Analysis of the N-deethylase reactions using Eadie-Scatchard plots showed high- and low-affinity components in rat liver microsomes. The high-affinity reaction was induced with phenobarbital and dexamethasone, but not with 3-methylcholanthrene. These results suggest that CYP2B, CYP2E1, and CYP3A subfamilies are involved in the dorzolamide N-deethylation in rat liver microsomes.

Animals↗