Biomedical subjects
Publications and source records attributed to K Sue.
In supercritical water the rate of methanol oxidation was controlled by ionic behavior as follows: the oxidation rate of methanol decreased with increasing proton and hydroxide ion concentration, possibly due to stabilization of the reactant, while that of CO was suppressed by added protons and enhanced by added hydroxide ions.
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We report the case of a 14-year-old female with Yersinia mesenteric lymphadenitis presenting as a right lower abdominal mass. Although such cases are very rare, Yersinia infection should be considered in the differential diagnosis of a right lower abdominal mass.
The authors encountered a sibling case of Meckel's diverticulum in 9 and 11 year old Japanese boys. They were diagnosed using contrast examination and 99mTc-pertechnetate scintigraphy before operation. The familial tendency is one in every 2500 families. Only 15 cases of familial occurrence have been reported by five authors.
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A three year old boy with a 10 cm double-barrelled tubular duplication of the distal ileum is reported. He presented with a small bowel obstruction after a large meal of mandarin oranges. At laparotomy an obstruction of both lumens was found which communicated at both ends with the normal ileal lumen. Although cystic duplications of the small intestine are common, tubular duplications are relatively rare, especially an obstruction with impacted undigested foods.
A simulation model to predict the survival probability of individual patients with hepatocellular carcinoma (HCC) after therapy was derived from the results of various therapies and follow-up studies of 450 HCC patients. Twenty-two prognostically important variables were analyzed by Cox's proportional hazards model. The 9 significant variables that were extracted were used to build the simulation. In this model, S(t), the expected estimated survival rate for individual patient at time t (month), is calculated by the following equation: S(t) = (exp (-0.03655t) (exp [0.9479 ([portal vein invasion]-0.222) + 0.3846 ([tumor number]-2.00) + 0.2578 ([tumor size]-3.231) + 0.0742 ([loge AFP]-5.647) + 0.8184 ([metastasis]-0.036) + 0.2810 ([Child's class]-1.689)-0.7088 ([transcatheter arterial embolization]-0.578)-0.9746 ([percutaneous ethanol injection]-0.153)-0.5377 ([hepatectomy]-0.109)]) The validity of the model was assessed using a split-sample technique. This paper does not discuss the superiority or inferiority of the therapies, because some selection bias for prognostic factors among the therapies can not be completely excluded. But this model is proposed as a practical model to predict the survival of patients with HCC.
Obliteration for gastric or duodenal variceal hemorrhage was performed via transileocoecal or transhepatic portal catheterization in 8 patients with portal hypertension. The patients were 6 men and 2 women, whose average age was 59 years. All of the patients had cirrhosis of the liver. The obliteration was performed as an emergency procedure in 6 cases, and 2 patients were electively treated. Transileocoecal obliteration (TIO) and transhepatic obliteration (PTO) were selected for 6, and 2 patients, respectively. Variceal bleeding was successfully controlled in all patients after completion of the therapy. One patient died after 3 months when duodenal variceal bleeding recurred. Elective surgical operations were performed on 2 patients after the initial therapy, because the vein feeding toward the varices remained. Six of the patients have survived to date without bleeding. Transient oliguria and jaundice after the therapy were noticed in 2 patients. Histological examination revealed cast formation of polymerized cyanoacrylate in the obliterated gastric varices of 2 patients. TIO and PTO seem to be safe, effective procedures to stop bleeding from ectopic varices, gastric or duodenal. This therapy is useful either to obtain accurate information about the varices or to obliterate the collateral veins in patients with ruptured ectopic varices.
The effects of obliteration of portal systemic shunts (PSS) in 5 patients with non-cirrhotic hepatic encephalopathy is reported. All patients had a history of disturbance of consciousness for several years, and examinations revealed large PSS, most of which connecting the left gastric vein to the left renal vein. After the obliteration of PSS, portal vein pressure elevated, the shunt ratio of the portal blood flow decreased, the indocyanine green disappearance rate increased, and serum albumin increased. Blood ammonia (NH3) decreased significantly accompanied by disappearance of hepatic encephalopathy. This treatment may open a way to improve the quality of life in patients with large PSS without severe hepatic injury.
IFN-alpha was administered intermittently over a 6 month period in 39 patients with chronic non-A, non-B hepatitis confirmed by peritoneoscopy and liver biopsy. Three million units of IFN-alpha were administered 3 times a week for the first 6 months then twice, then once a week. In 26 patients (67%), GPT decreased and remained within the normal range during the course of administration, and in 9 patients (23%) GPT remained normal for over 6 months after the discontinuation of IFN-alpha. There was no significant difference of efficacy among 3 groups liver histology groups (CPH, CAH-2A, and CAH-2B), but GPT decreased significantly in patients with sporadic hepatitis compared to patients with a history of blood transfusion. Furthermore, GPT decreased significantly in patients with a history of a blood transfusion within the preceding 2 years compared to patients with a history of a blood transfusion over 7 years ago. GPT increased markedly after an early tapering to 2 doses weekly, but it did not increase after a 6 month administration. In conclusion, the long-term administration of 300 million unit IFN-alpha, 3 times weekly for 6 months, about 2.5 hundred million units in total, is thought to be an effective way to control chronic NANB hepatitis.
Treatment, beginning in November 1986, of chemotherapy with cisplatin (CDDP) was given to a 4-year-old girl with unresectable hepatoblastoma. Laparotomy for excision was performed after 16 months of therapy. The solution of CDDP was administered by dropping intravenously (DIV therapy) or intrahepatic arterially (IA therapy), and a suspension of crystalline CDDP with Lipiodol containing phosphatidylcholine was injected intrahepatic arterially (CDDP-suspension therapy). To evaluate the safety and effect of CDDP-suspension therapy in this case, toxicity and antitumor effect were investigated by comparison with DIV therapy. Under chemotherapy with CDDP, logarithm of alpha-fetoprotein reduced linearly. When a slope (k) of the regression line was defined as a constant of AFP reduction rate, k was -0.0072. AFP reduction rate under CDDP-suspension therapy (k = -0.0097, 12/1987-6/1988) was more rapid than that under DIV therapy (k = -0.0053, 2/1987-12/1987), and AFP reduced completely in June of 1988. The CDDP-suspension therapy may be suggestive of more effective treatment. Platinum (Pt) concentration in serum, urine and hepatic specimens was determined in order to investigate CDDP pharmacokinetics. The area under serum concentration (AUC) per doses and renal elimination rate were lower values under CDDP-suspension therapy. In the hepatic specimen, Pt concentration was significantly higher at the site where Lipiodol was localized. These results suggested that CDDP-suspension therapy delayed CDDP distribution and reduced toxicity. After CDDP-suspension therapy, reversible toxicity to the liver was observed. However, that to kidney or to blood components was less severe than after DIV therapy. After multiple DIV therapy, serum creatinine and blood urea nitrogen increased gradually in the course of therapy, while they tended to recovery after multiple CDDP-suspension therapy.
Two cases with unresectable hepatoblastoma were treated by intrahepatic arterial injections of cisplatin-phosphatidylcholine-Lipiodol suspension (CPLS), combined with systemic chemotherapy. Unfortunately, the first patient who was given three injections of CPLS in association with systemic chemotherapy died of progressive disease 18 months after the commencement of the therapy. However, the second patient who received about 1 year of systemic chemotherapy followed by three injections of CPLS prior to subtotal tumor resection, plus four injections after surgery, is now alive and healthy 22 months after the commencement of treatment, with no detectable serum alpha-fetoprotein (AFP), although the AFP level on admission was 695,000 ng/ml. In the surgical specimens of case 2, there were areas with Lipiodol deposits rich in platinum and replaced by marked fibrosis around necrotic tumor nodules. Intrahepatic arterial injection of CPLS in combination with systemic chemotherapy and surgery should be considered as an effective method for unresectable cases.
A new immunotherapy for hepatocellular carcinoma (HCC) using Freund's adjuvant and recombinant interleukin-2 (IL-2) combined with conventional transarterial chemoembolization therapy was performed. In 16 patients with HCC and one patient with metastatic liver cancer receiving this therapy, decrease and suppression of reelevation of alpha-fetoprotein after therapy was observed. Disappearance of tumor thrombi of HCC in the main portal vein was observed in a patient, and decrease of carcinoembryonic antigen was also observed in a patient with metastatic liver cancer. The present therapy using Freund's adjuvant and IL-2 is likely to open a new avenue for the treatment of patients with advanced liver cancer.
Combined effects of vitamin E (alpha-tocopherol) and cisplatin on the growth of two murine neuroblastomas (C1300, NS-20) was investigated in vivo. Five groups of mice were prepared; group 1 were fed the control diet, group 2 were fed a vitamin E-deficient diet, group 3 were fed a vitamin E-supplemented diet, group 4 were fed the control diet and plus vitamin E solution given intraperitoneally during the treatment (solvent i.p. group), and group 5 were given vitamin E in the same manner (20 mg/kg/day; vitamin E i.p. group). Cisplatin (6 mg/kg) was injected intraperitoneally into the mice of each group during the treatment. In case of the C1300 neuroblastoma, the antitumor activity of cisplatin was most enhanced in the mice receiving vitamin E i.p., and the intra-tumor vitamin E and platinum levels were significantly higher in this group than in the other groups (P less than 0.01, and P less than 0.05 respectively). In contrast, in animals transplanted with the NS-20 murine neuroblastoma, which proved to be a cisplatin-tolerant tumor in separate experiments, no combined effect of those drugs was observed, although the intra-tumor level of platinum was elevated. The possibility was that vitamin E increases the influx of cisplatin into the tumor cells and acts after incorporation of cisplatin through the plasma membrane. Vitamin E did not accentuate the cisplatin-induced renal impairment in vitamin E-loaded groups. Those results suggested that vitamin E should be considered as a co-agent of cisplatin for the treatment of neuroblastoma.
Four cloned murine neuroblastomas were implanted intramuscularly into the left thigh of adult A/Jax mice. Cyclophosphamide, cisplatin, adriamycin, imidazole carboxamide, and vincristine were administered intraperitoneally, in a dose of one third to one fourth of a median lethal dose, every week after the implantation until all the mice died. The effects of continuous long-term chemotherapy, particularly on clonal differences, were then assessed. Cyclophosphamide was most effective for four murine neuroblastomas, and cisplatin was the next most effective drug. Cisplatin was not effective in the NS-20 cell line, a cholinergic cloned neuroblastoma. The C 1300 cell line (wild type) was tolerant to adriamycin, imidazole carboxamide, and vincristine. The N-18 cell line (an inactive clone) exhibited tolerance of adriamycin and imidazole carboxamide. In the N1E-115 cell line, an adrenergic clone, tumor growth was inhibited by all the drugs given. We conclude from this study that drug sensitivity differs with the clone, and that there are clones resistant to each drug.
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