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Biomedical subjects

S Todo

Publications and source records attributed to S Todo.

At least 505 records · Page 28Linked to original sources
PubMed1989

[Neurofibroma-associated left peroneal nerve palsy in a patient with acute lymphoblastic leukemia].

Peroneal nerve palsy developed in a patient with T cell-type acute lymphoblastic leukemia (ALL) is reported. In the fifth month after starting of chemotherapy against ALL, the patient, a 7-year-old girl, developed drop foot on the left. Three possibilities were considered as its pathogenesis; (1) VCR neuropathy, (2) neurotoxicity of intrathecal MTX, (3) leukemic invasion to the spinal canal. However, there was no evidence of leukemic invasion in any lumbar taps, and no improvement was obtained by cessation of VCR and intrathecal MTX. Examination by CT scan revealed tumors in the intervertebral (L5-S2) region, which was diagnosed to be neurofibromas by biopsy. The tumors compressed the left peroneal nerve and neurotoxicity of antineoplastic agents for ALL could be the cause of her drop foot.

Child↗
PubMed1989

Human leukemia cells and mature lymphocytes induce platelet aggregation after removal of cell surface sialic acid.

We examined platelet aggregating activity (PAA) of 5 human leukemia cell lines (HL-60, ML-1, HPB-ALL, RPMI-1788, K562), human mature lymphocytes and 2 human neuroblastoma lines (NCG, GOTO). Although intact cell suspensions of all leukemia cells and mature lymphocytes did not induce platelet aggregation, all cells exhibited PAA in both heparinized and citrated platelet rich plasma (PRP) following neuraminidase treatment (2 units/ml). In contrast, NCG and GOTO cells with PAA in intact cell suspensions were not affected by neuraminidase. PAA of HL-60 cells pre-cultured in the presence of tunicamycin (0.1-1.0 microgram/ml) to inhibit glycosylation decreased after neuraminidase treatment. Neuraminidase treatment had no effect on procoagulant activity of any of the cells examined. There was no difference in total sialic acid contents between human leukemia and neuroblastoma cells. These results suggest the cell surface glycoconjugates on hematopoietic cells play a role in PAA, and that sialic acid prevents their interaction with platelets.

Cell Membrane↗
PubMed1989

[An adolescent case of myelodysplastic syndrome following aplastic anemia].

A male with myelodysplastic syndrome (MDS) following aplastic anemia is reported. The patient had been diagnosed as aplastic anemia at 8 years of age, and treated with blood transfusions, anabolic and glucocorticoid steroid hormones. Over a period of subsequent twelve years, he had remission and deterioration. At the age of 21, the patient developed a sudden progression of severe anemia, when his bone marrow showed hyperplasia with prominent dyshematopoiesis and excess of blasts, compatible with MDS by the definition of FAB classification. He received low dose Ara-C therapy, which was ineffective. Nine months later he developed acute monocytic leukemia (M5b) and died. Chromosomal analysis revealed 46, XY at the onset of aplastic anemia, 46, XY, del (6) (q21 q27) at the MDS and 46, XY, -7, +21, 6q-/47, XY, +Y, -7, +21, 6q- at the acute leukemic stage.

Adult↗
PubMed1989

[Malignant lymphoma of the central nervous system in a boy with immotile cilia syndrome].

Malignant lymphoma of the central nervous system in a thirteen-year-old boy with immotile cilia syndrome (ICS) is reported. He had frequent upper respiratory tract infections, chronic sinusitis and pneumonia during in childhood. Bronchiectasis was demonstrated by bronchography. The diagnosis of ICS was confirmed by the lack of dynein arms of cila in the nasal mucosa with electronmicroscopy. In 1987, he complained of headache and vomiting and a space occupied mass lesion in the left frontoparietal lobe was found by head CT scan, which was subtotally resected. Histological studies showed large cell type non-Hodgikin lymphoma of B-cell phenotype. He received radiotherapy (41Gy) to the whole brain and systemic chemotherapy consisting of adriamycin, cyclophosphamide, vincristine, prednisolone, L-asparaginase and intrathecal methotrexate, and the patient maintained complete remission for eight months. However, relapse occurred and the patient died twelve months after the initiation of treatment.

Adolescent↗
PubMed1989

Pharmacokinetics of the cyclosporine-ketoconazole interaction in dogs.

Numerous clinical reports have documented an increase in trough blood concentrations of cyclosporine in transplant recipients treated concomitantly with ketoconazole. The objective of this study was to elucidate the mechanism(s) underlying the cyclosporine-ketoconazole interaction using a choledochoureterostomy dog model. Five male beagle dogs received a 4 mg/kg, i.v. bolus dose of cyclosporine either alone or on day seven of a 10-day, 13 mg/kg/day, oral dosing regimen of ketoconazole. Blood samples were collected prior to and at predetermined times for 60 hrs after the cyclosporine dose, while the bile/urine mixture was collected quantitatively for 96 hours after the cyclosporine dose. Ketoconazole decreased the systemic clearance of cyclosporine from 7.0 ml/min/kg to 2.5 ml/min/kg. The terminal disposition rate constant was also decreased significantly from 0.0794 to 0.0354 hrs-1. Ketoconazole caused no significant changes in cyclosporine steady state volume of distribution, or plasma unbound fraction. Ketoconazole did not significantly alter the excretion of cyclosporine and various cyclosporine metabolites in the bile/urine mixture. Inhibition of hepatic drug metabolizing enzymes appears to be the primary reason for the ketoconazole induced elevation in cyclosporine concentration.

Animals↗
PubMed1988

Treatment of hepatic epithelioid hemangioendothelioma with liver transplantation.

Ten patients received liver transplants for unresectable epithelioid hemangioendothelioma (EHE). At the time of transplantation, four patients had microscopic metastases to the hilar lymph nodes, and one of the four also had metastases to a rib. The fifth patient had metastases to the lung, pleura, and diaphragm. The remaining five patients were believed to be free of metastatic disease. Two of these five patients died of metastatic disease at 3 and 16 months, respectively, after transplantation. Interestingly, all five patients with metastatic involvement are currently alive 40.6 +/- 22 months (mean +/- standard error of mean [SEM]) after transplantation, although one of these patients currently has metastatic disease to the lungs and mediastinum. Thus, the projected 5-year actuarial survival rate is 76%, with two patients at risk after the third year. In conclusion, liver transplantation is a reasonable procedure for bulky, otherwise unresectable, EHE even in the presence of metastatic disease.

Adult↗
PubMed1988

Orthotopic liver transplantation for alcoholic cirrhosis.

Fifteen patients with Laennec's cirrhosis underwent orthotopic liver transplantation between 1963 and the end of 1979. The first eight patients died perioperatively or within two months, but four of the next seven patients had long survival; three are still alive after 11 to 14 years. After the introduction of cyclosporine therapy, 41 more patients with alcoholic cirrhosis were treated with liver transplantation from 1980 to June 1987. The one-year survival is 73.2%, and, after one to three years, 28 (68%) of the recipients are living. Of the 35 patients in the combined old and new series who lived for six months or longer, only two returned to alcohol abuse. Social and vocational rehabilitation has been the rule in these recipients who were selected primarily because of urgency of need, because they or their families insisted on treatment, and because they and their families thereby committed themselves to long-standing programs of alcoholism care.

Adult↗
PubMed1988

High serum ferritin level as a marker of malignant histiocytosis and virus-associated hemophagocytic syndrome.

Serum ferritin level was measured serially in three malignant histiocytosis (MH) and five virus-associated hemophagocytic syndrome (VAHS) patients. Serum ferritin levels were greater than 1000 ng/ml at the early phase of disease. When disseminated intravascular coagulation (DIC) developed in patients, serum ferritin levels elevated further to greater than 12,000 ng/ml. MH patients were treated by combination chemotherapy, and VAHS patients were given prednisone. Each MH and VAHS patient died within 1 week from the onset of DIC, without decrease of serum ferritin level. One MH patient with continued high serum ferritin levels for 3 months after DIC also died. The remaining patients with decreased serum ferritin values less than 1000 ng/ml at 3 months after DIC are now alive with normal serum ferritin levels. These results suggest that serum ferritin level in histiocytic proliferative disorders is a useful indicator of disease activity in both neoplastic and reactive conditions rather than only a marker of malignant process.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1988

Induction of S 100 protein by 5-bromo-2'-deoxyuridine in human neuroblastoma cell lines.

The simultaneous effect of 5-bromo-2'-deoxyuridine (BrdUrd) on cell growth, morphological changes, and cellular contents of S 100 (S 100ao and S 100b) protein and neuron specific enolase was investigated in human neuroblastoma cells in culture. Among four cell lines (NCG, SK-N-DZ, GOTO, NB-1), GOTO was the most affected. With 5 micrograms/ml BrdUrd, the growth of this cell line was significantly inhibited to 14.5% of the control on day 6, in association with morphological changes into flat-type cells and an increase of S 100 protein. S 100ao protein was increased from 37 to 211,000 pg/mg protein (5,600-fold) and S 100b protein from less than 25 to 623 pg/mg protein. The induction of S 100 protein was also seen in SK-N-DZ but not in NCG and NB-1. In GOTO the induction of S 100 protein occurred in a dose- and time-dependent manner by the treatment with BrdUrd. On the other hand, after exposure to BrdUrd, neuron specific enolase decreased in NB-1 and SK-N-DZ and increased in GOTO. These results suggest that although heterogeneous certain neuroblastoma cell lines could be differentiated into S 100 protein-positive cells that may represent glial or Schwann cells and that the effect of BrdUrd is exerted bidirectionally in neuroblastoma differentiation.

Bromodeoxyuridine↗
PubMed1988

Right trisegmentectomy with a synthetic vena cava graft.

In the course of a right trisegmentectomy of the liver, nearly the entire length of the retrohepatic vena cava was replaced with a Dacron graft. Patency of the graft was proved by a venacavogram a year later.

Blood Vessel Prosthesis↗
PubMed1988

Renal artery reconstruction for harvesting injuries in kidney transplantation with particular reference to the use of vascular allografts.

At the University of Pittsburgh during the calendar year 1986, an arterial injury occurred during harvesting in 20 (7.5%) of the 270 grafts used to perform kidney transplantation (KTx). Four cases required reconstruction, using extension iliac arterial allografts from cadaveric donors of the same blood type; 6 patients, remodelling of the aortic patch in multiple arteries; 4 cases, repairs for injuries to the smaller segmental/polar arteries; 6 cases, a combination of the above techniques. These ex vivo arterial reconstructions are described and the use of donor arterial homografts is emphasized. No deaths have occurred at an average follow-up of 19 months. The postoperative acute tubular necrosis (ATN) rate was significantly higher (90%) compared with non-reconstructed kidneys during the same year (30%). The 1-year graft survival of kidneys undergoing arterial reconstruction (75%) was statistically no different than the overall kidney-transplant survival. Whenever extension iliac allografts were utilized, the cyclosporin-steroid immunosuppression required to control the kidney rejection contributed to the long-term patency rate of the graft. Since the number of organs available for grafting is limited, reconstruction of injured renal vessels has become justified, allowing valuable kidneys to be used that would otherwise be lost.

Adult↗
PubMed1988

Role of adenosine 3'5'-cyclic monophosphate in antineoplastic effect of prostaglandins (PGE1, PGE2, PGD2 and PGA1) on human neuroblastoma cells.

To determine the role of adenosine 3'5'-cyclic monophosphate (cAMP) in the antineoplastic effect of prostaglandins (PGE1, PGE2, PGD2 and PGA1), we studied 2 cell lines of human neuroblastoma; i.e. GOTO and SK-N-DZ. PGE1 or E2 at 30 micrograms/ml and PGD2 or PGA1 at 5 micrograms/ml were cytotoxic to these neuroblastoma cells. In both cell lines, increase of intracellular cAMP was closely associated with E-type PGs cytotoxicity, however, in PGD2, or PGA1 cytotoxicity, cAMP increase was observed only in GOTO cells. Pretreatment of GOTO cells with 5 micrograms/ml PGE2 for 24 hr caused a desensitization of cAMP responses to PGE1, PGD2 or PGA1 only in association with a reduced cytotoxicity of PGE1. On the other hand, PGE2-pretreated SK-N-DZ cells resulted in a desensitization in response to PGE1, but not to other PGs, without affecting the cytotoxicity of these PGs. A decreased [3H]PGE1 binding similarly occurred in either the PGE2-pretreated GOTO or SK-N-DZ cells. However, cholera toxin- or forskolin-induced cAMP production was suppressed only in the pretreated GOTO cells. cAMP response by forskolin rather increased in the pretreated SK-N-DZ cells. These results indicate that antineoplastic effect of E type PGs mediates through cAMP, but not that of PGD2 and PGA1 and that PGE2 pretreatment may cause a down regulation of PGE1 receptor site in both cell lines. It is also suggested that PGE2 pretreatment results in a heterologous desensitization in GOTO and a homologous desensitization in SK-N-DZ cells.

Alprostadil↗