Living-related liver transplantation despite major arterial and venous abnormalities.
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Biomedical subjects
Publications and source records attributed to T Ikegami.
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A 39-year-old female with AML (M2) underwent allogeneic bone marrow transplantation (BMT) on July 8th, 1991. The post transplantation course had been going well until day 85 post BMT, when severe hemorrhagic cystitis with right hydronephrosis and ureter stenosis developed. Adenovirus type 11 was isolated from the urine. She received instillations of prostaglandin E1 (PGE1) directly into the bladder after the appearance of clots in the urine. Complete resolution of hematuria was obtained by two courses of this treatment. PGE1 bladder instillations seem to be effective for the control of hematuria caused by severe hemorrhagic cystitis after BMT.
It has been reported that serum levels of thrombomodulin (TM) reflect endothelial damages in various diseases. We measured serum TM levels between day-10 and day 100 in 6 patients receiving allogeneic bone marrow transplantation. Serum TM levels were increased when patients had transplant related complications including graft versus host disease, hemorrhagic cystitis and interstitial pneumonitis. In patient without complications, serum TM levels were within normal limits. These results suggest that the serum TM level serves as a useful marker of treatment related toxicity and a predictor of complications after BMT.
The effects of birth season on the case fatality rate (CFR) of pulmonary tuberculosis were examined in case records of 9206 patients discharged during 1937-1965 from a national hospital for tuberculosis in Tokyo. The CFR was over 60% until 1945, then it decreased down to less than 9% after 1950. Male cases had little variation in their CFR by their birth season, while female cases had a significant variation and showed a significantly higher CFR than the male cases when they were born in January-June. The results suggest that the birth season had a significant influence on the prognosis of pulmonary tuberculosis.
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Five patients with abdominal tuberculous lymphadenitis were studied by ultrasound. The final diagnosis of tuberculosis was based on open biopsy in 2 patients, neck lymph node biopsy in 1, needle biopsy under ultrasound control in 2. Low-echoic and iso-echoic abdominal lymph nodes were seen in all patients and a mixed echoic lymph node was found in one of them. Enlarged, round or oval, lymph nodes were conglomeratically observed along the common hepatic artery, in the hepatoduodenal ligament and along the abdominal aorta. The size of the lymph node was found to be 20-70 mm. In one case, compression of the portal trunk and the common bile duct due to a large lymph node was observed, and arterioportography showed hepatopetal collateral veins. In the other case, multiple mass lesions in the liver and the spleen were observed. In the 4 patients who were observed by ultrasound at 2 months after anti-tuberculosis therapy, enlarged lymph nodes decreased and 3 of them changed from low-echo to iso-echo in the echo pattern. Of the 4 patients who were followed for more than 4 months, lymph nodes disappeared in 2 at 4 months and in one at 12 months. The remaining patient showed residual nodes which decreased in half at 8 months. Ultrasound is now used commonly in the examination of the abdomen, and there are cases of abdominal lymph nodes swelling due to varied diseases. In this study, there were no characteristic ultrasonographic findings in abdominal tuberculous lymphadenitis. So, it is difficult to diagnose the cause of abdominal lymph node swelling by only ultrasound.(ABSTRACT TRUNCATED AT 250 WORDS)
On the basis of vascular involvement, an open clinical trial was performed to determine whether or not the antithrombotic drug cilostazol (6-[4-(1-cyclohexyl-1H-tetrazol-5-yl) butoxy]-3,4-dihydro-2(1H)-quinolinone, OPC-13013, Pletaal, CAS 73963-72-1) applied as a single 100 mg tablet increases peripheral blood flow and prevents diabetic neuropathy in 30 patients with non-insulin dependent diabetes mellitus. The hemodynamic effects of this drug on the a. dorsalis pedis were examined using a new real-time two-dimensional Doppler echography. 1 h after oral administration of cilostazol, the cross-sectional area of the a. dorsalis pedis significantly increased from 2.2 +/- 0.2 to 2.9 +/- 0.3 mm2 (p less than 0.05). Also, the a. dorsalis pedis blood flow index significantly increased from 16 +/- 1 to 31 +/- 4 (p less than 0.05). Cilostazol did not affect plasma glucose level (from 213 +/- 14 to 198 +/- 15 mg/dl), but slightly plasma ratio of 6-keto PGF1a to TXB2 (from 0.71 +/- 0.09 to 0.83 +/- 0.12). These effects of cilostazol might ameliorate diabetic neuropathy by improving blood flow and preventing nerve tissue ischemia.
Platelet functions and morphological changes of megakaryocytes were investigated in three cases with chronic neutrophilic leukemia (CNL). The bleeding time was prolonged, the ADP, collagen, epinephrine-induced aggregation of platelets decreased in one case. The adhesiveness, epinephrine-induced aggregation and adenine nucleotide content of platelets decreased in one other case. Megakaryocyte size in CNL was larger than in CML and this difference of the megakaryocyte sizes was related to DNA content distribution of the megakaryocytes. Atypical megakaryocytes were apparently found in one case. The present study suggests that CNL is a stem cell disorder.
The effect of growth phase on enzymatic activities of the de novo and salvage pathways for purine and pyrimidine nucleotide synthesis was studied in a hepatocyte-derived cell line from the rat. The cells were in lag phase after plating for 36 h; log phase started at 48 h and persisted up to 120 h of culture. Then the cells stopped growing and entered into plateau phase (144 h). In non-proliferating cells (144 h of culture) the basal activities of the enzymes of purine de novo biosynthesis were 1.7- to 6.8-fold higher than in normal rat liver, those of pyrimidine de novo synthesis showed 0.6- to 30-fold increase in activity. The purine salvage enzymes were unchanged, and the pyrimidine salvage enzymes were 3.1- to 7.4-fold higher compared to normal liver. During the growth cycle all enzymes except the purine salvage enzymes, which did not change, showed a peak in activity at 72 h of culture (log phase). The increase in activity in log phase compared to plateau phase was 1.3- to 2.4-fold for purine de novo synthetic enzymes, 1.1- to 2.4-fold for pyrimidine de novo enzymes, and 1.4- to 4.7-fold for pyrimidine salvage enzymes. The specific activities of the enzymes in exponentially growing cells were comparable either to that in 24-h regenerating liver, or to that in hepatomas of low or medium growth rate. It was concluded that the enzymatic pattern and metabolic state of the cells shared some features with regenerating liver, others with tumors, although they were not tumorigenic after transplantation into athymic nude mice.
Using plateau phase C3H 10T1/2 cells, we studied the effect of multiple-dose irradiation on the repair capacity of cells after further irradiation. Cells were irradiated with repeated doses of 2.5 Gy delivered two fractions per day at 6 to 7 hours interval. The cell survival after exposure to 1 to 9 fractions was lower above 5 fractions as compared to that predicted by calculating from single dose survival curve by assuming that cells retain their capacity to repair radiation damage after each fraction. Repair kinetics experiments showed that cells were less able to repair potentially lethal damage after test dose following multiple dose irradiations. There was, however, no difference in the ability to repair sublethal damage and potentially lethal damage sensitive to anisotonic treatment in preirradiated and untreated cells. Thus, it would appear that an enhancement of the lethal expression of potentially lethal damage of three types of damage may, at least in part, contribute to the difference between the cell survival curve after multiple fractions and that predicted by calculation.
The study was performed to obtain a relationship between the pulmonary blood flow and the tau b (time constant) calculated from multiple-breath nitrous oxide (N2O) washout curve. Elimination of N2O depends on pulmonary blood flow and alveolar ventilation. From the theoretical consideration, tau b can be calculated by the following formula; tau b = Vd[1/Qt-Qs) + 0.47/VA) Vd = N2O volume of distribution in the body Qt = cardiac output, Qs = shunt blood flow VA = alveolar ventilation. Relationship between observed Qt-Qs and observed tau b was admitted to the predicted formula. The method was compared with the thermodilution method in almost simultaneous measurement of the cardiac output. A good correlation was obtained between them (r = 0.87). Washout curve of nitrous oxide can be used for a reliable measurement of pulmonary perfusion.
A case of chronic myelogenous leukemia (CML) with marked thrombocytosis and its megakaryokinetics were reported. Patient was 57-year old woman who had a marked thrombocytosis (1,413 x 10(3)/microliters) and a bone marrow megakaryocytosis. Bone marrow karyotype demonstrated Ph1 chromosome in all cells examined. However, on physical examination, there was no splenomegaly. CBC showed no immature myeloid cells, and neutrophil alkaline phosphatase was elevated. These manifestations were consistent with so called essential thrombocythemia (ET) with Ph1 chromosome reported by Nissenblatt. To know the megakaryokinetics of this case, we examined the number of colony forming unit-megakaryocyte (CFU-M), platelet glycoprotein (PGP) IIb/IIIa positive cells, cytoplasmic area, and DNA content, comparing with those of normal subjects, CML, and ET. We found a marked increase of CFU-M and PGP IIb/IIIa positive cells, but in contrast, decreased DNA content and cytoplasmic area. This pattern of megakaryokinetics was consistent with that of CML. We conclude that ET with Ph1 chromosome may be a variant of CML rather than ET itself.
The flux activities of de novo and salvage purine synthesis were compared in rat hepatoma 3924A cells in various growth phases. The initial rate assays of [14C]adenine, [14C]hypoxanthine, and [14C]guanine incorporation yielded Michaelis-Menten kinetics with Kms of 5, 7, and 7 microM, respectively. After replating plateau phase cells in lag and log phases the activity of purine de novo pathway increased 4.5- to 8-fold with a preferential rise in guanylate synthesis, whereas purine salvage activities increased only 1.6- to 2.1-fold. However, for the syntheses of IMP, AMP, and GMP, the activities of purine salvage pathways were 2- to 7-fold, 5- to 28-fold, and 2- to 32-fold higher than those of the de novo purine pathway. Treatment of cells with acivicin, an inhibitor of the activity of amidophosphoribosyltransferase, phosphoribosylformylglycinamidine synthase, and GMP synthase, inhibited the flux activities of de novo purine, adenylate, and guanylate syntheses to 37, 73, and 3% of the controls and decreased the concentration of GTP to 42%; the concentration of ATP did not change and that of 5-phosphoribosyl 1-pyrophosphate increased 3.1-fold. Under these conditions the activities of salvage synthesis from hypoxanthine and guanine were enhanced 2.5-fold. Treatment of hepatoma cells with IMP dehydrogenase inhibitors, tiazofurin, ribavirin, and 4-carbamoylimidazolium 5-olate, to block de novo guanylate synthesis accelerated the flux activity of guanine salvage pathway. The higher capacity of purine salvage pathway than that of the de novo one and the further rise of the activity in response to the drugs targeted against the de novo pathway highlight the important role salvage synthesis might play in circumventing the impact of antimetabolites of de novo purine synthesis in cancer chemotherapy.
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Explore the source record for details and available documents.
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