Measurement of the branching ratio of the decay KL0--> micro micro.
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Biomedical subjects
Publications and source records attributed to T Kishida.
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We examined host ability to produce alpha- and gamma-interferon on a large scale by culturing 2 ml of peripheral blood for 20 hr with Sendai virus or concanavalin A as inducer of alpha- or gamma-interferon, respectively. Production of gamma- but not alpha-interferon was lower in females (n = 351) than in males (n = 531) (P less than 0.001). Both alpha- and gamma-interferon production declined gradually with ageing. The production of alpha-interferon (3,233 +/- 1,773 IU/ml) and gamma-interferon (19 +/- 20 IU/ml) in rheumatoid arthritis patients was significantly lower than the values found in total and age-matched healthy donors (P less than 0.01). These results suggest that interferon production is dependent on age and sex and is significantly lower in patients with rheumatoid arthritis.
Interferon-alpha (IFN-alpha) production was investigated in whole-blood cultures of 66 bladder cancer patients and 65 control subjects. IFN synthesis was induced with Sendai virus, and IFN activity was assayed in FL cells challenged with vesicular stomatitis virus (VSV). The mean levels of the IFN-alpha produced were 5,724 +/- 2,288 IU/ml in the control subjects and 4,800 +/- 2,353 IU/ml in the bladder cancer patients. IFN-alpha production was significantly suppressed in the bladder cancer patients compared with that in the control subjects (P less than 0.05). The impairment in IFN-alpha production correlated with the tumor grade, and it was shown that the tendency toward decreased IFN-alpha production was closely associated with the advancement of the tumor stage. Our results suggested that the decreased IFN-alpha production may contribute to the disordered immunoregulation in bladder cancer patients.
BALB/c mice were immunized with alpha 2-seminoglycoprotein (A2SGP), the lymph node cells were fused with P3U1 myeloma cells and cultured by the conventional technique. Four antibody-producing hybridoma clones were established and antibody-containing ascitic fluid obtained. The antibody was directed to the protein backbone of A2SGP and not to ABH antigenic determinants and did not cross-react with saliva or vaginal secretions. When tested in an indirect ELISA the anti-A2SGP antibody had a titer of 512000. The anti-A2SGP was used in a capture ELISA (or sandwich ELISA) in which wells were coated with this antibody to capture A2SGP in semen, and the captured A2SGP was detected with anti-A, anti-B or anti-H-peroxidase conjugate and peroxidase-labeled second antibody. This ELISA allowed correct ABO grouping even of 1:12,800 or higher dilutions of semen. When the ELISA was applied to ABO grouping of seminal fluids mixed with vaginal secretions only the seminal ABH antigens could be detected. The results strongly suggest the potential usefulness of monoclonal anti-A2SGP in the investigation of rape cases.
A Japanese family with unusual segregation of GM phenotype was found in connection with a case of disputed paternity. Typing for 27 hemogenetic marker systems revealed apparent nonmaternity in the GM system alone. When tested for 14 GM allotypes, the alleged father, the mother, and the child were of the GM A,F,Z N B0,1,3,4,5,S,T,U; GM A,Z N' G,U; and GM A,Z N' B0,3,5,S,T types, respectively. The results of a family study strongly suggested that a GM silent allele was responsible for the apparent nonmaternity; however, definitive evidence could not be obtained.
The effects of dietary pantethine levels on the contents and compositions of fatty acids and on the levels of lipid peroxides were investigated with rat liver and its S-9 fraction under administration of 0 (non), 0.2 (low dose), and 0.35 ml (high dose) of autoxidized linoleate (AL) per 100 g body weight of the rats per day for 5 days. AL having 800 meq/kg of peroxide value (PV) and 1,700 meq/kg of carbonyl value (CV) was dosed to the rats of each group given drinking water containing 0 mg% (deficient), 6.25 mg% (adequate), and 125 mg% pantethine (excess). In the pantethine-deficient and -adequate groups, the contents of fatty acids both in the liver homogenate and in the S-9 fraction were correspondingly decreased by increasing dose levels of AL, and the decrease was remarkable especially in the pantethine-deficient group, but was not significant in the pantethine-excess group even by a high dose of AL. Particularly, in the high dose of AL, the notable decreases of oleic acid (C18:1) contents in both the liver and the S-9 fraction were observed in rats of the pantethine-deficient and -adequate groups. The thiobarbituric acid (TBA) values in the liver homogenate and the S-9 fraction were increased correspondingly by increasing dose levels of AL, and the increases were repressed in the pantethine-excess group.
We reviewed retrospectively the medical records of 70 patients treated for prostate cancer who were followed for more than 10 years or until they died. All patients were treated by hormonal therapy and 54 of 70 patients (77 per cent) were combined with castration. Of 70 patients 10 (14.3 per cent) are alive now with an average follow up for 180.5 months. Of 60 patients with stage A and B only 3 died of the tumor. Of 56 patients with stage C and D, 10 and 18 patients died of the tumor, respectively. From the point of pathology, none of the patients with well differentiated adenocarcinoma died of the tumor. And in patients with stage A and B, pathologically well and moderately differentiated adenocarcinoma, there were no cancer death. On the other hand, a group of patients of poorly differentiated adenocarcinoma had a poor prognosis. In cases with well differentiated adenocarcinoma who discontinued hormonal medication (diethylstilbestrol diphosphate) no patients died of the tumor. From these observations we consider that, after long term hormonal medication, we can stop the hormonal medication for patients who have no positive prostate biopsy results for 4 years with well differentiated adenocarcinoma of stage A and B.
We evaluated the effects of recombinant human granulocyte colony stimulating factor (rhG-CSF) given to 30 patients with hematological malignancies after cytotoxic chemotherapy. The first course of chemotherapy was not treated with rhG-CSF (control), and in the second to fourth courses, rhG-CSF was given by one of the following three ways to the patients (not necessarily in this order): 1) 10 days of administration starting 48 hr after chemotherapy, 2) 5 days of administration starting 48 hr after chemotherapy, and 3) 5 days of administration after the leukocyte counts reached to less than 2,000/microliters. The leukocyte nadirs were significantly higher in the course with 10 days of administration compared with the control course. The time needed for recovery from the leukocyte nadir was significantly shorter in 10-day course and 5-day course after the leukocyte counts reached to less than 2,000/microliters. The therapy spans became significantly shorter with all of the three patterns of administration of rhG-CSF compared with the control course. The number of days on which the leukocyte counts became less than 2,000/microliters were significantly fewer in 10-day course and 5-day course after the leukocyte counts became less than 2,000/microliters. These findings showed that rhG-CSF prevented severe neutropenia after cytotoxic chemotherapy, and (or) assisted the rapid recovery from neutropenia. These effects depend on the timing of its administration.
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The present paper reports seven families with an atypical segregation pattern which we have recently found during paternity testing. In one family, heterozygous mother-child incompatibility (1B2A and 1A2B) in the PGM1 system was observed. This could be explained by an intragenic recombination between the PGM1*1B and PBM1*2A alleles giving rise to the PGM1*2B allele. In the other families, two types of new GC variants with two pairs of double band were identified. These variants (GC*1S1A2 and GC*1F1A2) were presumed to have arisen from the duplication of two GC*1 alleles.
Thirty-seven patients with malignant lymphoma were treated with mitoxantrone, ifosfamide, vindesine, and prednisolone. The time among courses was not fixed, being decided by the time for recovery from the leukopenia caused by the treatment. The drug dose was adjusted after the initial course. Of the 12 patients treated for the first time, eight had a complete remission and two had a partial response. Of the 18 patients who relapsed after another drug regimen, six had a complete remission and seven had a partial response. The SD of the leukocyte nadirs decreased after the first course, and time needed for recovery from leukopenia tended to shorten during treatment. Side effects seemed mild, and we can use many drugs safely in a short term without long drug-free intervals. Response rates were satisfactory, compared with other report, so this method of timing the start of courses with adjustment of the dose seems useful.
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An anti-G1M F monoclonal antibody was produced by immunization of mice with a single dose of F(ab')2 fragments of normal IgG1-enriched IgG and subsequent fusion of their lymph node cells with P3U1 myeloma cells. Antibody specificity was tested by an ELISA in microtiter plates coated with allotype positive or negative IgG. The usefulness of the antibody as a G1M F typing reagent in inhibition and direct immobilization-type ELISAs and dot immunobinding was demonstrated by re-typing of 100 GM-allotyping control sera. The advantages and disadvantages of these assay methods are discussed.
Automated measurement of trypsin inhibitor in urine was performed with good precision using the COBAS FARA. Elevated levels of both trypsin inhibitor in urine and acute phase proteins in serum were shown in most cases of major abdominal surgery. We suggest that the automated assay of urinary trypsin inhibitor might be useful for the clinical diagnosis of acute phase response.
Dilutions of 100 serum samples of various GM phenotypes were dotted onto a nitrocellulose membrane. The serum dot-blots were detected with peroxidase-labeled anti-G3M T monoclonal antibody (anti-G3M T MAb). Up to a 1 : 256 dilution could be G3M T-typed correctly. By use of anti-G3M T MAb and peroxidase-labeled anti-mouse IgG or the biotin-avidin system instead of use of labeled anti-G3M T MAb, up to a 1 : 512 or 1 : 1024, respectively, dilution was typable. As with previous work with G3M G MAb, the dot immunobinding (DIB) method for G3M T typing was found very simple and practical.
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Interferon-alpha (IFN-alpha) producing capacity was measured in 47 patients with prostatic cancer by whole blood assay. The mean IFN-alpha producing capacity of prostatic cancer patients was 3657 IU/ml, which indicated a significantly (p less than 0.005) lower value than that in healthy male aged 50 years or more. IFN-alpha producing capacity in patients with Stage D disease was lower than that with Stage A, B or C. The higher the grade of the disease, the lower tended to be the capacity. A certain relationship was suspected between IFN-alpha producing capacity and the prognosis of each patient. In particular, in patients with prostatic cancer in Stage D, the prognosis was worse in low IFN-alpha producing capacity group (less than 3000 IU/ml) than in normal or high IFN-alpha producing capacity group (greater than or equal to 3000 IU/ml). It was considered that IFN-alpha producing capacity might be useful in developing the prognosis of patients with prostatic cancer.
Sialyl Lewisx-i (SLX) was found in more than 40% of patients with acute leukemia or chronic myelogenous leukemia, and in about 20% of those with myelodysplastic syndrome or malignant lymphoma. This tumor marker was absent in all patients with polycythemia vera, essential thrombocythemia, primary myelofibrosis, chronic lymphatic leukemia, multiple myeloma, and those with acute leukemia or malignant lymphoma in remission. The marker was found in 8% and of the patients with idiopathic thrombocytopenic purpura and 33% of those with autoimmune hemolytic anemia but in no patient with aplastic anemia or megaloblastic anemia. Immunostaining with SLX antibody showed that tumor cells of the patients with high levels of serum SLX were producing the SLX antigen. The detection of this marker in the serum is thought to be useful not only in the diagnosis but also in the observation of the recurrence of the diseases.