[Measurement of 5'-nucleotidase activity. Basic study and clinical application].
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Biomedical subjects
Publications and source records attributed to S Ueda.
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Clinical trials were carried out with sulbactam/cefoperazone (SBT/CPZ) (combination ratio of 1:1) in pediatric infections. Results were as follows. The mean half-lives of SBT and CPZ in the serum following intravenous injection of SBT/CPZ were about 0.7 and 1.2 hours, respectively. Urinary excretions of SBT and CPZ within 6 hours after intravenous injection of SBT/CPZ were 81.9% and 28.1%, respectively. SBT/CPZ was administered to 33 pediatric patients with various infection; 18 respiratory tract infections, 12 urinary tract infections and 3 Salmonella enterocolitis. The overall efficacy rate was 87.9%. In particular, 7 of 8 urinary tract infections caused by beta-lactamase producing organisms were improved after administration of SBT/CPZ. Diarrhea in 8 and soft stool in 3 of 33 patients occurred, and slight elevation of GOT/GPT was observed in 2 patients.
A mouse hybridoma cell line producing monoclonal antibody, F10, was established from mice hyperimmunized with cells bearing adult T cell leukemia (ATL) virus (ATLV). F10 antibody reacted with an ATLV structural polypeptide ( gp21 ) with a m.w. of 21,000 that was glycosylated on cell surfaces. The gp21 was expressed on cell surfaces of all ATL-associated antigen (ATLA)-positive human cell lines but not on ATLA-negative cell lines nor peripheral blood leukocytes stimulated with mitogens. The gp21 was also detected with anti-ATLA-positive human serum, and the binding of F10 antibody to ATLA-positive cell surfaces was significantly blocked by pretreatment with anti-ATLA-positive human sera. Double immunofluorescence staining with F10 antibody and anti-ATLA-positive human serum caused co-capping on cell surfaces, which suggests that gp21 co-exists with other ATLV antigens expressed on cell surfaces. Immunoprecipitation studies also suggested that the gp21 is a minor component of the ATLV envelope.
Laboratory and clinical studies on ceftazidime ( CAZ ), a new cephem antibiotic, were carried out in the field of pediatrics. The results were as follows: Antibacterial activities of CAZ against clinically isolated strains of S. pneumoniae, H. influenzae, E. coli and P. aeruginosa were compared with those of cefotaxime (CTX), ceftizoxime (CZX), latamoxef ( LMOX ), cefoperazone (CPZ) and cefmetazole (CMZ), and also with cefsulodin (CFS) and gentamicin (GM) against P. aeruginosa. Against S. pneumoniae and H. influenzae, CAZ was almost as active as CTX, CZX and CPZ. Against E. coli, it was almost as active as CTX, CZX and LMOX . Against P. aeruginosa, it was almost as active as CFS and GM. Serum concentrations and urinary excretion rates after intravenous bolus injection of CAZ at doses of 20 mg/kg and 10 mg/kg for 5 minutes in each 2 cases (4 cases in total) were determined. The mean serum concentrations of CAZ were 78.9 and 52.0 micrograms/ml at 15 minutes, 38.5 and 27.4 micrograms/ml at 1 hour, and 6.5 and 4.8 micrograms/ml at 4 hours, with serum half-lives (T 1/2) of 1.39 and 1.80 hours respectively. Mean cumulative urinary excretion rate within 6 hours after administration was 84.6%. In a patient with chronic renal failure, serum half-life was 3.22 hours and urinary excretion rate within 6 hours was 22.8% (after intravenous bolus injection of CAZ at a dose of 10 mg/kg). CAZ was administered at a dose of 55.5 mg/kg by intravenous bolus injection to a child with purulent meningitis. The levels of CAZ in the cerebrospinal fluid (CSF) at 1 hour after administration were 2.7-38.9 micrograms/ml with CSF/Serum ratios of 3.2-28.8%. Forty-two pediatric patients with various bacterial infections (pyelonephritis 14, tonsillitis 1, bronchopneumonia 3, pneumonia 17, purulent meningitis 1, bacteremia 2, SSSS 1, enterocolitis 3) were treated with CAZ at a daily dose of 49-222 mg/kg t.i.d. or q.i.d. (as a rule 60 mg/kg t.i.d.). The efficacy rate was 97.6% clinically and 97.8% bacteriologically. No adverse reactions were observed except 1 case with mild diarrhea. Abnormal laboratory findings were also only mild; eosinophilia in 1, slight elevation of GOT in 5 and that of GOT & GPT in 3 cases. These results indicate the usefulness of CAZ in the treatment of bacterial infections in children.
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The augmenting effect of vaccinia virus infection of tumor cells on induction of tumor-specific resistance was examined in mice. C3H/HeN mice were primed intraperitoneally (ip) with live vaccinia virus after whole-body irradiation with 250 rad of X-rays. Three weeks later the mice were immunized ip 3 times at weekly intervals with syngeneic murine hepatoma MH134 or spontaneous myeloma X5563 which had been infected in vitro with vaccinia virus and subsequently irradiated with 7000 rad of X-rays. One week after the third immunization, the mice were challenged with 1 X 10(5) viable cells of MH134 or X5563 ip or 1 X 10(6) tumor cells intradermally (id). On ip challenge with viable MH134 cells all mice that had not been pretreated died within 3 weeks due to ascites tumor out-growth, whereas all mice that had been vaccinia virus-primed and immunized with vaccinia virus-infected MH134 cells survived. On ip challenge with X5563 cells, the percentage survival of vaccinia virus-primed and vaccinia virus-modified tumor-immunized mice was 80%. On id challenge with MH134 and X5563 tumor cells, in un-treated mice tumors grew to more than 5 mm in diameter within 3 weeks, whereas 90% and 60%, respectively, of the mice that had been vaccinia virus-primed and immunized with vaccinia virus-infected tumor cells showed no tumor out-growth. Pretreatment by only immunization with vaccinia virus-infected cells or vaccinia virus-priming and immunization with virus non-infected tumor cells were not effective for preventing induction of tumor-resistance to either ip or id challenge with MH134 or X5563 tumor cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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Expression of heterophile Hanganutziu-Deicher (HD) antigen on the cell surface of various human malignant tumor tissues was studied by membrane immunofluorescence staining with chicken antiserum against N-glycolylneuraminyllactosylceramide (HD3) and fluorescein-conjugated rabbit anti-chicken IgG. The HD antigen was demonstrated in samples from 38 of 77 (38/77, 49%) cases, consisting of gastric (9/16), breast (8/14), colorectal (3/12), nasopharyngeal (4/7), and uterine (2/3) carcinomas, leukemias (5/10), malignant lymphomas (2/5), and other cancers (5/10). Histological examination indicated that expression of the antigen by the gastric, colorectal and breast carcinomas and leukemias was not related to their histological types. The cytoplasm and the surface of the malignant glandular epithelial cells were both specifically stained by immunofluorescence staining of frozen sections in one colon adenocarcinoma. Glycosphingolipids (GSLs) were extracted from the colon cancer tissue and two HD antigen-active GSLs were detected on thin-layer chromatography (TLC) by enzyme-immunostaining using affinity-purified chicken anti-HD3 and horseradish peroxidase-conjugated rabbit anti-chicken IgG. One migrated to the same position as HD3 on TLC, and the other to a position similar to that of authentic N-glycolylneuraminylneolactotetraosylceramide.
Two hybridoma clones producing monoclonal antibodies were obtained from mice immunized with the Marek's disease (MD)-lymphoblastoid cell line MSB1. These monoclonal antibodies reacted with the surface of MD-lymphoblastoid cell lines at higher titers than with avian lymphoid leukosis cell lines or with normal chicken thymus, bursa or peripheral blood lymphocytes. The serological specificity of these monoclonal antibodies seemed to correspond with that of rabbit antiserum reactive with MD tumor-associated surface antigen (MATSA).
This study was undertaken to produce experimental autoimmune hepatitis in mice, and to examine the role of liver specific lipoprotein (LSP), if any, and of cellular immunity in such a model. After immunization of three strains of mice (C57BL/6, C3H/He and BALB/c) with syngeneic crude liver proteins, most prominent liver changes histologically mimicking human hepatitis were produced in the liver of C57BL/6 (B6) mice. Antigenic and immunogenic activity of LSP in the crude liver proteins was decreased by the treatment of freezing and thawing, and the recovery of the antigenic activity seemed to correlate with the susceptibility of immunized mice to the induction of liver damage. Autoantibody against LSP was demonstrated in the serum of immunized B6 mice, but not in the sera of other strains after immunization. It was also found that EDTA contained in the buffer used for purification of LSP distinctly suppressed lymphocyte activity in vivo and in vitro. With the use of EDTA free LSP, it was shown that spleen cells of immunized B6 mice (especially of T cell enriched fraction) had a high reactivity studied by lymphocyte transformation test. Further examination showed that EDTA free LSP could induce mild liver lesions and lymphocyte reactivity against LSP, although neither histological change nor lymphocyte reactivity was found in the liver of B6 mice immunized with EDTA containing LSP.
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Adult identical twins with Moyamoya disease are reported. Laboratory examinations such as blood types, AB, Rh(+), HLA (human leucocytic antigen) analysis [AW26(9), A26(10), BW62(15), BW61(40), CW3], and finger prints, and hairs confirmed that two patients were identical twins. Both had normal serum immunoglobulin levels and no anti-DNA antibodies. Patient No. 1, a 39-year-old female, was admitted to our service with chief complaints of nausea, vomiting and left hemiparesis with sudden onset on Oct 31, 1981. The patient had an episode of tetraplegia that occurred suddenly at 4 years of her age and lasted about a week. Motor weakness had completely disappeared but moderate mental retardation remained. She had been employed just prior to this attack. CT and angiographic examinations revealed ventricular hemorrhage with Moyamoya disease, which had miliary aneurysm in the branch of the right posterior choroidal artery. The operation of encephalomyosynangiosis was performed on her left hemisphere. The postoperative course was uneventful. Patient No. 2, the twin sister of patient No. 1, was in good health and mental state until 19 years of her age, when she suddenly lost consciousness and developed hemiparesis. After this attack, her motor function had recovered well. However, mental ability gradually deteriorated and she was admitted to a psychiatric ward. CT examination and angiographic studies were performed on Oct 12, 1982, and she was diagnosed as having Moyamoya disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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Painting of tributyl-tin oxide on the skin induced a secondary Fanconi syndrome in guinea pigs. In the urine of these animals, excretion of sodium, chloride, phosphate, glucose and many kinds of amino acids increased and reached a maximum between day 40 and 50. In sera, the concentrations of phosphate and certain amino acids were low due to excessive loss into urine. Histological examination of the kidney revealed damage to the tubular epithelium with no glomerular change. It was also found that cytochrome P-450 in the kidney and 1-25-dihydroxy vitamin D in serum were reduced in the tin-treated animals. It is most likely that tributyl-tin oxide caused a secondary Fanconi syndrome as defined by renal tubular disturbances represented by glucosuria, generalized amino aciduria, phosphaturia, and hypophosphatemia.
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The antitumor effect of human leukocyte interferon was investigated on ten patients with malignant brain tumor. In eight cases of primary tumor, IFN alone was administered when their recurrent sign was evident. A dose of 3 X 10(6) IU or 1 X 10(6) IU of IFN was injected intramuscularly two or three times a week in high-dose group, while a dose of 5 X 10(4) IU once a week in low-dose group. No remarkable side effects including bone marrow depression were noted. Natural killer activity was enhanced and immunologic skin reaction manifested. Partial remission of more than 50% decrease of tumor volume calculated on CT scan was seen in two cases in the low-dose group for about 3-6 months. Complete remission could not be obtained by IFN alone. Our pilot study has shown that IFN alone will not be effective against progressive malignant brain tumors by general administration. Further investigation should be carried out to improve the use of IFN therapy in malignant brain tumor.