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T Tobe

Publications and source records attributed to T Tobe.

At least 379 records · Page 21Linked to original sources
PubMed1986

[Role of hepatic resection in multiple combination therapy of hepatocellular carcinoma].

UNLABELLED: Recently, resectable hepatocellular carcinoma (HC-C) has been increasing. However, it has not been established whether or not hepatectomy is beneficial in achieving long survival in HCC patients. The present study was aimed at evaluating whether hepatic resection could lead to long survival by retrospectively analyzing cumulative survival rate. One hundred twenty-three cases underwent hepatic resection for HCC between 1977 and 1985. Their post-operative cumulative survival rates including operative death were 65, 34 and 27% for 1, 3 and 5 years, respectively. The 3-year survival rates for stages 1, 2, 3 and 4 were 55, 48, 27 and 0%, respectively. When the survival rate was analyzed by curability, the 3-year survival rates were 68 and 28% for curative and non-curative operations. In our department, 18 cases have survived over 3 years after hepatectomy. The macroscopical appearance of their tumors was characterized by encapsulation, with no tumor thrombosis in the portal vein. Tumor size or satellite lesions did not necessarily affect long survival. CONCLUSIONS: Liver resection for hepatoma patients at stage I and II can be expected to bring about long-term survival.

Carcinoma, Hepatocellular↗
PubMed1986

[An in vitro sensitivity assay for anti-cancer agents by measuring the inhibition rate of DNA synthesis (3H-thymidine uptake of cancer cells). II. Clinical study of 110 cases of breast cancer].

The sensitivity of cancer cells to anti-cancer agents (ACA) was assessed in 110 cases of breast cancer (87 primary cases and 23 recurrent cases). The cancer cells were cultured with ACAs: Mitomycin C (MMC), Adriamycin (ADR), 5-Fluorouracil (5-FU), Cytosine Arabinoside (Ara-C), Carboquone (CQ), Nimustine Hydrochloride (ACNU), Cis-platinum Diammine Dichloride (CPDD) or Vincristine (VCR) for 3 days and their sensitivity was estimated by the inhibition rate (I.R.) of DNA synthesis (3H-thymidine uptake) of cancer cells. The DNA synthesis was higher in recurrent cases than in primary cases. The primary cases showed high sensitivity to ADR or CQ, and the recurrent cases showed high sensitivity to ADR. Histologically, papillotubular or medullary tubular carcinoma showed high sensitivity to CQ, and scirrhous carcinoma showed high sensitivity to ADR, CQ or 5-FU. The sensitivities of medullary tubular or scirrhous carcinoma to ADR, 5-FU and CQ in patients with stage III and IV were lower than those in patients with stages I and II. No difference of ACA sensitivity was observed between estrogen receptor (+) and (-) cases. All recurrent cases were treated with 5-FU or its derivatives. The 50% survival period in the 5-FU high sensitivity (I.R. greater than 80%) group was 7.0 months and that of the low sensitivity (I.R. less than 80%) group 3.0 months, respectively.

Adenocarcinoma↗
PubMed1986

[Augmentation of the anti-tumor activity of regional lymph node lymphocytes and spleen cells of tumor-bearing mice by culture with T cell growth factor in vitro--a comparison of the intestinal cancer model and footpad cancer model].

The anti-tumor activity of regional lymph node lymphocytes (RLNL) of DS mice bearing syngeneic carcinoma SC42 was observed both in intestinal cancer model and in footpad cancer model, while neither spleen cells (SPLC) nor distant lymph node lymphocytes showed any activity in Winn's tumor neutralizing test. This anti-tumor activity of RLNL was tumor specific examining between SC42 and SC115. RLNL in both cancer models did not show any cytotoxic activity against SC42 measured by 51Cr release test. However, after 9 days of culture with lectin-free T cell growth factor (LF-TCGF), the cytotoxic activity against SC42 of RLNL was induced in both cancer models. Cultured SPLC showed the cytotoxic activity against SC42 only in intestinal cancer model. Any lymphocytes from normal mice showed no cytotoxic activity against SC42 after culture with LF-TCGF. Moreover, the cytotoxic activity of cultured RLNL was tumor specific between SC42 and SC115, while that of cultured SPLC was non-specific. These results indicated that RLNL was immunologically important in tumor bearing host and the immunological significance of spleen was different between intestinal cancer and cancer of other sites.

Animals↗
PubMed1986

[Effect of combined immunotherapy using two different BRMs; OK-432 and IL-2-cultured lymphocytes].

We have developed an adoptive immunotherapy (AIT) system using syngeneic tumor-bearer-spleen cells cultured with interleukin-2 (IL-2) and soluble tumor extract. The therapeutic effect of the AIT was significantly augmented by in vivo local preadministration of a streptococcal preparation, OK-432. The previous report demonstrated a mechanism in which OK-432 augments the effect of AIT. That is, OK-432 induces IL-2 in vivo and prolongs the in vivo life span of cultured, IL-2-dependent lymphocytes (CL). This paper describes another mechanism, that is, the synergism between CL and OK-432-induced host lymphocytes. Fresh spleen cells (FSC) obtained from mice in complete remission after chemotherapy (cyclophosphamide, 100 mg/kg) showed a clear synergistic anti-tumor effect on CL, when both were injected i.p. into MOPC104E-bearing BALB/c mice which had been inoculated i.p. with 1 X 10(5) tumor cells 5 days previously. The effect was greatest when the FSC: CL ratio was 4:1, whereas the administration of either FSC or CL alone had little effect. The effector population of CL that exhibited synergism on FSC was Lyt 2+, cytotoxic T cells. FSC and CL both needed a tumor-specific combination. In addition, OK-432-induced tumor-infiltrating, intraperitoneal lymphocytes had a similar synergistic effect on CL as assessed by the transplantability of intraperitoneal cells. Probably because of this mechanism, OK-432 showed a much higher augmenting effect on AIT using CL than in vivo administration of IL-2. This therapy system using OK-432 and CL is a proper model which, through combined use of different, correlated BRMs, may bring a great effect whereas the effect of single BRM is weak.

Animals↗
PubMed1986

[Selective arterial secretin injection test for localization of gastrinoma].

We have already shown that gastrinomas release gastrin when stimulated with secretin in vitro. In order to ascertain whether this is true in vivo and whether the reaction is clinically useful in the localization of gastrinomas, secretin was injected into a feeding artery of the gastrinoma in four patients, and blood samples were taken from a peripheral artery (PA) and the hepatic vein (HV) for determination of immunoreactive gastrin (IRG) and immunoreactive insulin (IRI) levels. When secretin was injected into a feeding artery of the gastrinoma, IRG rose within 40 seconds in the HV and within 60 seconds in the PA. When secretin was injected into a nonfeeder, IRG did not rise for 2 min in the PA. This test was performed to two of the postgastrectomized patients and a patient with hypergastrinemia due to atrophic gastritis. In these patients, IRG in the hepatic vein did not rise for two minutes. It was concluded that secretin directly stimulates gastrinomas to release gastrin in vivo and that the selective arterial secretin injection test is helpful in determining the location of the gastrinoma.

Adult↗
PubMed1986

A secured technique for pancreatojejunal anastomosis in pancreaticoduodenectomy.

In order to avoid complications after pancreaticoduodenectomy, a simple and safe technique for pancreatojejunal anastomosis was developed. After resection of the pancreas, a vinyl chloride tube with a circumferential knot is inserted into the pancreatic duct and tied with a Dexon suture. Pancreatojejunal anastomosis is performed by approximating the seromuscular layer of the jejunum around the opening to the parenchymal tissue of the pancreas with interrupted nylon sutures, eliminating the need for direct anastomosis between the duct and jejunum. The knot on the tube prevents the tube from dislodging, and pancreatic juice is completely drained until the tube is safely removed two to three weeks after the operation.

Duodenum↗
PubMed1985

Effect of synthetic neuromedin C, a decapeptide of gastrin-releasing peptide (GRP [18-27]), on blood flow and exocrine secretion of the pancreas in dogs.

Neuromedin C, the smaller molecular form of gastrin releasing peptide (GRP [18-27]), has been recently identified from canine intestinal muscle and porcine spinal cord. This study was conducted to determine if this newly identified peptide retains biological activity on canine pancreas in vivo. Intravenous injection of graded doses of synthetic Neuromedin C caused a marked increase of systemic blood pressure and initial reduction of pancreatic blood flow in eleven anesthetized dogs, as measured by Laser Doppler Flowmetry. Flow volume and protein output of pancreatic juice were also increased by Neuromedin C in a dose-related manner in six dogs. These results suggest that this peptide is one of the biologically active forms of mammalian bombesin-like peptides and may possess physiological significance as a novel neuropeptide.

Amino Acid Sequence↗
PubMed1985

Changes in coenzyme Q level in mitochondria of cirrhotic rat liver.

In the cirrhotic rat liver induced by carbon tetrachloride and phenobarbitone, the concentrations of mitochondrial Coenzyme Q were measured in comparison with other respiratory components. The concentration of cytochrome a(+a3) and Coenzyme Q significantly increased in the cirrhotic liver, without any changes in the ratio of Coenzyme Q to cytochrome a(+a3). It is suggested that such increase of Coenzyme Q plays an important role as one of the adaptive responses to compensate for the prolonged metabolic overload on the mitochondrial respiratory assembly. Also, from the findings that the concentrations of cytochrome a(+a3) in the mitochondria of cirrhotic liver increase concomitant with the severity of cirrhosis, it is suggested that the rise of Coenzyme Q levels may be one of the indicators for the decreased functional reserve capacity in liver cirrhosis.

Animals↗
PubMed1985

Teratogenic effects of carcinogenic agents on limb regeneration in the Japanese newt Cynops pyrrhogaster.

Normal regeneration of the amputated forelimb of the Japanese newt Cynops pyrrhogaster and regeneration after a single intraperitoneal injection of three potent mutagenic/carcinogenic agents was investigated. Three dose levels of each agent and controls were tested for teratogenicity in this newt model with the following chemicals: N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), 4-nitro-quinoline-1-oxide, and 2-(2-furyl)-3-(5-nitrofuryl)acrylamide. These chemicals were administered at 10 days (late dedifferentiation stage), 20 days (late bud stage), and 30 days (early digits stage) after amputation at the midforelimb. A total of 628 newts, with 16-20 animals per group, were used. Normal forelimb regeneration in Cynops pyrrhogaster closely paralleled that reported for other species. A variety of deformities, including syndactyly, polydactyly, oligodactyly, brachydactyly, and digital branching, were occasionally observed in control regenerating forelimbs, with syndactyly occurring at highest incidence (17.5%). All three mutagens at all tested dose levels enhanced the incidence of teratogenic changes, though increases were not always statistically significant. MNNG, particularly when administered at the time of initial chondrogenesis (20 days, late bud stage), was especially teratogenic. The type of forelimb deformity was not mutagen-specific in this experiment. As Cynops pyrrhogaster is easily and inexpensively maintained and tolerates surgery well, this model with the regenerating forelimb should prove useful for further studies on teratogen screening. Also, studies directed toward mutagenic and epigenetic effects of exogenous agents on rapidly proliferating and differentiating tissues can be investigated with this model, which obviates transplacental excursion and metabolism of test compounds.

4-Nitroquinoline-1-oxide↗