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Biomedical subjects

K Isobe

Publications and source records attributed to K Isobe.

At least 271 records · Page 15Linked to original sources
PubMed1989

Donor Igh-linked genetic control of allotype-specific antibody response.

Immunogenicity of allogeneic immunoglobulins in mice were studied, measuring the allotype-specific antibody activity by agglutination of allogeneic antibody-coated red blood cells. It was found that the serum from C.B-20 mice (Ighb, BALB/c-congenic) was uniquely immunogenic in BALB/c mice for allotype antibody response. Whereas the C57BL/6 (Ighb) serum was immunogenic only when heat aggregated and/or combined with adjuvant, the ultracentrifugation-deaggregated C.B-20 serum was definitely immunogenic when administered in a moderate dose (100 microliters/mouse). Even more surprising was the fast that very low doses (0.01-0.1 microliter) of soluble C.B-20 serum, but not C57BL/6 serum, down regulated the allotype-specific response effectively. Genetic analysis on congenic mice suggested that the immunogenicity is controlled by donor Igh or Igh-V (Id-C.B) inasmuch as the serum from BALB/c-congenic C.B-20 (Igh-VbCb), but not BALB/c-congenic BAB/14 (Igh-VaCb), mice was active in BALB/c mice in soluble form. Further studies showed that the Id-C.B was dominantly expressed on the immunoglobulins of (BALB/c x C.B-20)F1 and (C56BL/6 X C.B-20)F1 strains, and was originally derived from the C57BL/Ka strain. The major determinant for the antibody production was encoded in Igh-C, but not in Igh-V. It is suggested that Id-C.B controls the allotype-specific antibody response in an unusual manner, possibly acting as a unique determinant activating helper T cells.

Animals↗
PubMed1989

Mode of alloantibody-mediated blockade of allo-sensitization for tumor allograft rejection.

The mode of alloantibody-mediated inhibition of allo-sensitization for tumor allograft rejection was studied. Relatively small amounts of anti-H-2d alloantiserum administered shortly before or after injection of allogeneic spleen cells blocked the allo-sensitization for second-set tumor allograft rejection. In contrast, the alloantiserum injected shortly before inoculation of tumor barely enhanced the tumor growth. The passively administered alloantiserum inhibited the sensitization for allospecific cytotoxic T lymphocyte responses in vitro. Further study revealed that the allo-sensitization could be blocked with antiserum specific against only one of the expressed H-2 antigens on stimulator cells. Correspondingly, H-2Dd-monospecific monoclonal antibody (IgG2a) was effective in inhibiting the sensitization with cells expressing multiple H-2 alloantigens. These results suggest that antibody-mediated inactivation of stimulator cells as a whole is an important mechanism of the allograft enhancement.

Animals↗
PubMed1989

Carbohydrates mediate tissue type-specific membrane activity for Thy-1 alloantibody response.

Thymocyte membrane fragments (TMF) but not brain cell membrane fragments (BMF) show a unique activity for inducing Thy-1 alloantibody response. Treatment of TMF with alpha-mannosidase or endoglycosidase-H greatly diminished this activity but not the serological Thy-1 antigenicity. This suggested that the TMF activity is supported by high mannose type N-linked oligosaccharides on the TMF. On the other hand, treatment with neuraminidase made otherwise silent BMF definitely active for the antibody response and this activity was abolished by further treatment with endoglycosidase-D. This demonstrated that BMF have a latent activity which is mediated by complex type N-linked oligosaccharides normally masked with sialic acids. It was concluded that two types of N-linked oligosaccharides as well as sialic acids mediate at least in part the tissue type-specific membrane activity for Thy-1 alloantibody response.

Animals↗
PubMed1989

Long-term results of spinal instrumentation surgery for scoliosis five years or more after surgery, in patients over twenty-three years of age.

From 1967 to 1981, 311 scoliotic patients treated at Chiba University, with a minimum follow-up of 5 years and aged more than 23 years, were selected for this study. Seventy-two were males and 239 were females, whose age at operation ranged from 9 to 44 years, with an average of 16.5 years. The operative procedures were one-stage Harrington procedure in 179 cases, staged procedure in 108 cases, anterior procedure in 20 cases, and combined anteroposterior fusion in four cases. Including 198 patients examined physically, a total of 263 patients (54 males and 209 females) have responded to a questionnaire or were interviewed by telephone. In general, 85% of the patients were satisfied with the result of the operation for the control of spinal deformity, improvement of the cosmesis, and increase in physical and social activity.

Activities of Daily Living↗
PubMed1989

Rat mesangial cells actively produce phosphatidylinositol-anchored Thy-1.

We provide evidence that the mesangial cells of rat kidney glomeruli express Thy-1 as a phosphatidylinositol-anchored protein. Both the mesangial area of kidney, examined in tissue sections, and mesangial cells maintained in culture for more than 3 months, showed prominent immunofluorescence staining with an anti-Thy-1 monoclonal antibody (OX7); this staining was almost completely abolished by pretreating kidney sections or mesangial cells with the phosphatidylinositol-specific enzyme, phospholipase C. By Northern blotting, mesangial cells were shown to express mRNA of an appropriate size, hybridizing to a mouse Thy-1.1-specific probe.

Animals↗
PubMed1989

[Early diagnosis of the cervical incompetency by the ultrasonography].

To establish a reliable method for diagnosing cervical incompetency, we observed changes in the cervix by ultrasonography and tried to settle the criteria for early diagnosis. The ultrasonographic evaluation of the cervix was performed by real time B mode scanning (Aloka Echo camera SSD 650 with attached sector scanner using 3.5 MHZ transducers). The cervical length was defined as the distance from the lower edge of the fetal membranes to the edge of the portio vaginalis. In the case of normal pregnancy, the cervical length increased gradually from 14 to 24 weeks of gestation and then decreased gradually. In the case of patients who delivered before 33 weeks of gestation, the cervical length was less than -ISD. 78 of 79 cases in whom bulging of the membranes was not seen delivered at term, but 9 of 33 cases with bulging membranes delivered preterm (chi2, p less than 0.001). The criteria of cervical incompetency based on ultrasonographic findings are as follows: 1. Bulging of the fetal membranes into the endocervical canal 2. Shortening of the cervix a. the cervical length less than -ISD of the mean value b. the decrease in cervical length before 24 weeks of gestation

Cervix Uteri↗
PubMed1989

[Simultaneous, multiple hypertensive intracerebral hematomas: report of 5 cases and review of literature].

Five cases of multiple hypertensive intracerebral hematomas which occurred simultaneously but in different locations were described in this report. The diagnoses of all five cases were established by computed tomography, and the location of the hematomas was as follows; case 1. bilateral putamen, case 2. bilateral thalamus and right parietal subcortex, case 3. cerebellum and left thalamus, cases 4 and 5. cerebellum and right putamen. These represented 0.7% of all the patients (679 cases) who suffered from hypertensive intracerebral hematoma and were admitted to our two institutions in the last five years. We also reviewed the other 11 cases which have been reported in literature, and the total 16 cases were analyzed with respect to clinical characteristics, pathogenesis of multiple hematomas, indication of operation and prognosis. 1. The age distribution had a peak in the 70's and was similar to that of single hematoma. 2. Sixteen cases had 34 intracerebral hematomas. Eleven cases had bilateral supratentorial lesions. Four cases had cerebellar and supratentorial lesions. The remaining had two supratentorial lesions ipsilaterally. The distribution of 34 hematomas (16 in cerebral basal ganglia, 10 in thalamus, 4 in cerebellum, 4 in cerebral subcortex and none in pons) was well correlated to the distribution of usual hypertensive intracerebral hematomas. 3. The clinical symptoms were characterized by severe consciousness disturbance and severe neurological deficits. Their outcome was poor. 4. As for the possible mechanism of simultaneous multiple hemorrhages, we suspected either that two or more primary bleedings occurred simultaneously in the different regions, or that a primary bleeding was followed a short time after by a secondary bleeding in the other site.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Lack of D-amino-acid oxidase activity causes a specific renal aminoaciduria in the mouse.

Thin-layer chromatography and amino acid analysis showed that urine of mutant ddY/DAO- mice lacking D-amino-acid oxidase activity contained more serine, proline, alanine and methionine than that of normal ddY/DAO+ mice. Among these four, an increase in alanine was conspicuous. However, the urinary levels of 11 other amino acids and glucose were not different between the ddY/DAO- and ddY/DAO+ mice. Amino acid analysis showed that the plasma levels of serine, proline and methionine were not elevated in the ddY/DAO- mice, though a slight increase in alanine was observed. Genetic crosses showed that aminoaciduria and lack of D-amino-acid oxidase activity were concomitantly transmitted as a set through generations. These results indicated that the lack of enzyme activity caused a specific renal aminoaciduria. Whether this enzyme merely diminishes the D-amino acid load presented for reabsorption, or actually participates catalytically in the reabsorption process, remains undetermined.

Amino Acids↗
PubMed1988

Induction and characterization of minor histocompatibility antigens. Specific primary cytotoxic T lymphocyte responses in vitro.

A definite cytotoxic activity was developed in a BALB/c (H-2d) anti-DBA/2 primary mixed leukocyte culture (MLC), which received interleukin 2 (IL-2) on day 3 of culture. This cytotoxic activity was minor histocompatibility antigens (MIHA)-specific at the stimulator level, and was not developed in a syngeneic (BALB/c anti-BALB/c) MLC. The addition of IL-2 on day 3 of culture was crucial; no or very weak cytotoxic activity was developed in MLC receiving IL-2 on day 0 or on both day 0 and day 3. Only appropriate MIHA-allogeneic tumor cells were lysed as the target of the cytotoxic activity. The cytotoxic activity seemed MIHA-specific also at the target level; it lysed tumor cells of DBA/2 mouse origin but not those of BALB/c (syngeneic) origin. Phenotypes of the cytotoxic effector cell were Thy-1+ Lyt-2+. We concluded from these results that MIHA-specific cytotoxic T lymphocytes (CTL) were generated in the MIHA-allogeneic primary MLC. In this newly developed system, we studied genetic and antigenic requirements for primary anti-MIHA CTL responses in vitro. We demonstrated; among spleen cells (SC) of seven B10 H-2-congenic strains only SC of B10.D2 strain whose major histocompatibility complex (MHC) (H-2d) was compatible with the responder MHC effectively stimulated responder BALB/c (H-2d) SC for an anti-MIHA (DBA-C57BL-common) CTL response. Similarly, only SC of two out of seven C x B recombinant inbred strains (C x B.H and C x B.D), which were compatible at the MHC with responder SC, activated responder BALB/c SC for the response. The possibility that cells responding to H-2 alloantigens suppressed the anti-MIHA response was ruled out. Additional experiments showed that compatibility at the H-2K-end or the H-2D-end of the MHC was sufficient for a definite anti-MIHA response. These provided formal evidence that primary anti-MIHA CTL responses in vitro were MHC-restricted at the stimulator level. We then showed that sonication-disrupted SC or Sephadex G-10 column-passed nonadherent SC failed to stimulate responder SC for a primary anti-MIHA CTL response, whereas G-10-passed nonadherent SC responded well to adherent stimulator cells. Further study demonstrated that Ia+ adherent cells were the most active cell type as stimulator. Finally, we confirmed that the primary anti-MIHA CTL responses to adherent stimulator cells was MHC-restricted.

Animals↗
PubMed1988

Excessive urinary excretion of methionine in mutant mice lacking D-amino-acid oxidase activity.

Thin-layer chromatography and amino acid analysis showed that mutant (ddY/DAO-) mice lacking D-amino-acid oxidase activity excreted about 3.5 times more methionine in urine than did normal (ddY/DAO+) mice. High-performance liquid chromatography using a chiral column showed that approximately 82% of urinary methionine of the ddY/DAO- mice had the D-configuration. Analysis revealed that the mouse diet used contained 0.04% free methionine and that approximately 46% of methionine was the D-isomer. When the ddY/DAO- mice were given a diet containing a low level of supplementary DL-methionine or a diet without D-methionine, they excreted the normal levels of methionine. These results indicate that the ddY/DAO- mice were unable to metabolize D-methionine and excrete it in urine.

Amino Acids↗
PubMed1988

Further evidence for H-2-unrestricted induction of minor histocompatibility antigens-specific T cell immunity in vivo.

Antigenic requirements for inducing minor histocompatibility antigens (MIHA)-specific T cell immunity for second set rejection (SSR) of a MIHA-allogeneic tumor were studied. An intravenous injection of surprisingly small numbers (10(4)-10(5] of live allogenetic spleen cells (SC) effectively primed mice for SSR of the allogeneic tumor, and this immunity was developed as early as 2-3 days after injection of the SC. In contrast, sonication-disrupted allogeneic SC, which should be readily processed by host antigen presenting cells (APC), were not active as immunogens, even at a dose 1000 times higher than the minimum effective dose of live SC. The possibility that host APC preferentially receive MIHA antigens shed by live allogeneic SC for T cell activation was ruled out. These results demonstrated that antigen processing via conventional pathways is very little involved in the mechanism of T cell activation. Under such restricted experimental conditions, the induction phase but not the effector phase of the MIHA-specific T cell immunity was shown to be H-2-unrestricted.

Animals↗
PubMed1988

Biphasic radiation-sensitivity of the transplantation immunity for rejection of an allogeneic ascites tumor.

Transplantation immunity for second-set rejection of an allogeneic ascites tumor was induced by sensitizing mice with H-2-identical allogeneic spleen cells, and radiation-sensitivity of this immunity was studied. The immunity was not severely affected by 400 rads whole-body X-ray irradiation given at one day before the initial antigenic stimulation. In contrast, it was totally inactivated by 300-400 rads irradiation that was given one day before tumor challenge. An adoptive cell transfer experiment showed that alloreactive memory cells responsible for the immunity were unexpectedly highly radiosensitive. The immunity (memory), however, became resistant to 400 rads irradiation soon (one day) after challenge with the allogeneic tumor, and was resistant to 1500 rads for rejection of the tumor that was challenged at the second time when the initially challenged tumor was rejected. Corresponding to these observations, cells for allospecific CTL responses in peritoneal cavity of mice showed corresponding biphasic radiation-sensitivity.

Animals↗
PubMed1988

Augmentation by Corynebacterium liquefaciens of erythrocyte surface H-2 expression and alloimmunogenicity for antibody responses.

Intravenous injection of killed Corynebacterium liquefaciens induced a population of red blood cells that expressed both H-2K and H-2D antigens at exceptionally high density and displayed augmented immunogenicity for H-2 alloantigen-specific B cell activation. Injection of killed Escherichia coli or E. coli lipopolysaccharide was ineffective for the generation of such RBC. RBC that express H-2 antigens at high density first appeared at 7 days after injection of C. liquefaciens. These RBC persisted for more than 50 days, although they lost H-2 antigens gradually with time. The observed phenomenon was not due to enhanced erythropoiesis and peripheral release of immature RBC (reticulocytes); populations of both mature and immature RBC of mice injected with C. liquefaciens expressed H-2 antigens at high density, whereas those from normal mice or mice injected with phenyl hydrazine did not. Appearance of RBC expressing H-2 antigens at high density was preceded by a temporal increase in H-2 expression of bone marrow cells that included precursors of RBC. It was concluded that RBC expressing H-2 antigens at high density were descendants of bone marrow cells whose H-2 expression was augmented by C. liquefaciens. The present communication would be the 1st report of the bacteria-mediated augmentation of cell surface expression and activity of major-histocompatibility-complex class I antigens on host cells in vivo.

Animals↗
PubMed1988

Dynamics of cytotoxic T lymphocyte precursors in vivo assessed by change in the radiation sensitivity. Evidence for development of radiation-sensitive memory cells without clonal expansion.

The dynamics of cytotoxic T lymphocyte precursors (CTL-p) in mice injected with allogeneic spleen cells (SC) was studied with special reference to changes in their radiation sensitivity. Whole-body 400 rad X-ray irradiation of allo-SC-primed and unprimed mice virtually abolished the capacity of their SC to proliferate and to generate CTL in primary or secondary mixed leucocyte culture (MLC). However, the impaired ability of SC to generate CTL in the primary MLC was restored by interleukin 2 (IL-2). This showed that helper cells whose activity was replaceable with IL-2 (IL-2-producing cells) were functionally more radiation-sensitive than CTL-p in unprimed mice. In contrast, the radiation-impaired activity in secondary MLC was not restored by IL-2, suggesting that memory CTL-p in allo-SC-primed mice were unexpectedly sensitive to radiation. The D37 values determined from the percentage of residual CTL-p activity of SC in bulk cultures 1 day after irradiation were 525 rad for virgin CTL-p and 75 rad for memory CTL-p. Further studies demonstrated that the radiation-sensitive memory CTL-p were generated from relatively radiation-resistant precursors, largely independent of radiation-sensitive IL-2-producing cells and of cellular proliferation. The mean frequency of CTL-p in SC measured by limiting dilution assay was not significantly increased by the priming. This supports our conclusion that the development of the memory CTL-p activity in allo-SC-primed mice did not depend on clonal expansion. Whole-body 400 rad-irradiation reduced the frequency of CTL-p in SC from unprimed mice to 1/2-1/3 and that in SC from allo-SC-primed mice to 1/8-1/15. This supports the view that the majority of radiation-resistant virgin CTL-p functionally mature to radiation-sensitive memory CTL-p without cellular proliferation in allo-SC-primed mice.

Animals↗
PubMed1988

[A myelographic study of idiopathic scoliosis--with special reference to its clinical significance].

The purpose of this study was to investigate the concealed anomaly of the spinal cord in the so-called idiopathic scoliosis. Thirty-three patients with idiopathic scoliotic curvatures underwent metrizamide myelography before surgery from 1979 through 1985. Spinal cord anomalies were found in 8 of the 33 patients (abnormal group). They were 3 patients with Arnold-Chiari malformation with syringomyelia, 3 with syringomyelia and 2 with "narrowed dural tube". The remaining 25 patients (normal group) gave us the standard values for myelographic measurements with which we compared quantitatively the size of dural tube and spinal cord in the normal and abnormal groups. The abnormal group was classified into three types: type I was swollen spinal cord with normal dural tube; type II was swollen spinal cord with narrowed dural tube; and type III was normal spinal cord with narrowed dural tube. In conclusion myelography and myelographic measurements are essential for idiopathic scoliotic patients who will undergo spinal correction and fusion operations.

Adolescent↗
PubMed1987

Dynamics of generation of antigen loss variants from L1210 murine leukemia clones detected by a tumor-specific T-cell clone.

Originally T-cell clone K7L-sensitive L1210 murine leukemia clones were tested for their capacity to generate K7L-insensitive variants at various times after cloning. All of the L1210 clones (L1210/1, -2, -4, and -7) maintained in vitro for 1 month were severely inhibited in their growth in the culture in which K7L was added and in mice given injections of K7L at the initial stage. This indicated that any L1210 clone tested was not a mixture of K7L-sensitive and K7L-insensitive clones at the time of cloning. By both in vivo and in vitro K7L-mediated tumor suppression assays, K7L-insensitive antigen loss variants were then found to be generated from some (L1210/4, L1210/7) but not other (L1210/1, L1210/2) originally K7L-sensitive L1210 clones during 1 month of maintenance. Ratios of variant cells to total clone cells 1 month after cloning were estimated around 0.1% for L1210/7, 0.01% for L1210/4, and less than 0.001% (undetectable) for L1210/1 and L1210/2. Neither L1210/1 nor L1210/2 generated detectable K7L-insensitive variant cells during long-term (14-month) maintenance. All of the ten subclones of L1210/7 which were obtained 7 or 11 months after the initial cloning of L1210/7 were K7L sensitive, and not all the subclones generated K7L-insensitive variants in 1-2 months of maintenance after recloning. However, all of the subclones of L1210/7 which were maintained for 7 months generated antigen loss variants. All eight clone cells obtained from original L1210 and K7L-insensitive L1210 expressed H-2Kd and H-2Dd antigens detected by H-2Kd or Dd-specific cytotoxic T-lymphocyte clones or monoclonal antibodies. These results suggest that the antigen loss variants arise in originally K7L-sensitive L1210 clones at different times after cloning, and the probability of generation of the variants is clonally determined. The antigen loss variants seem to be generated by rare (once per 1 to 2 months or less frequent) chance with unproportionally rapid growth rather than by more frequent development for simple accumulation. The ratio of K7L-insensitive variant cells to total L1210/7 cells did not increase progressively during long-term (13 months or more) maintenance in vivo or in vitro and was always below 0.1%. It was suggested that the population size of antigen loss variants was controlled biphasically.

Animals↗
PubMed1987

Development of host-dependent high-grade tumor-specific immunity through a novel mechanism triggered by the Lyt-2+ tumor-specific T cell clone (K7L) that induces temporal growth of L1210 leukemia-K7L-variant.

When a murine leukemia L1210-specific Lyt-2+ T cell clone, K7L, was injected i.p. into CD2F1 mice together with L1210, the normal growth of L1210 in the peritoneal cavity of the mice at the early stage (days 0 to 5) was strongly inhibited, but L1210 grew progressively at the middle-stage (days 5 to 10), and then was rejected at the late stage (days 10 to 20). The mice thus survived for long times (more than 60 days), whereas the normal control injected with L1210 alone died within 14 days. The L1210 that grew at the middle stage in mice initially inoculated with L1210 together with K7L was a K7L-insensitive (K7L-) variant. All of eight tumor clones established from L1210-K7L- by limiting dilution was insensitive to the antitumor activity of K7L, and this property of tumor clones was stable after repeated in vitro passage. The initial depression of the L1210 growth by K7L followed by growth and rejection of the variant L1210-K7L- by the host T cell activity was then found to prepare a strong, long-lasting (more than 3 mo) immunity to protect mice against the high-dose (10(7) cells per mouse) challenge of original L1210. Corresponding to this result, definite tumor (L1210)-specific cytotoxic T lymphocyte (CTL) activity against both variant and original L1210 targets was developed by antigen (L1210) restimulation in the culture of spleen cells from these mice, but was not increased to a detectable level before L1210-K7L- variant started to grow. It was suggested that the 1210-K7L- variant and the original L1210 should have the common tumor-specific antigen that was independent of the K7L-reactive antigen, and that original L1210, whose growth was retarded by K7L, primed the host with the common antigen to be enormously boosted by the subsequently growing L1210-K7L- variant.

Animals↗