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Biomedical subjects

K Mizoguchi

Publications and source records attributed to K Mizoguchi.

At least 109 records · Page 6Linked to original sources
PubMed1988

Glycolipids of rat glomerular mesangial cells: antibody against the cells reacts specifically to isoglobotetraosylceramide.

Cultured rat glomerular mesangial cells had relatively simple glycolipid composition which comprised mainly monoglycosylceramide, diglycosylceramide, isoglobotetraosylceramide and GM3. Beside these glycolipids, sulfatide, polar gangliosides and an unknown neutral glycolipid were detected in whole kidney and tubules. Polyclonal antibody against the cultured rat mesangial cells, which induced glomerular injury in vivo, bound specifically with isoglobotetraosylceramide.

Animals↗
PubMed1987

Familial apoceruloplasmin deficiency associated with blepharospasm and retinal degeneration.

A 52-year-old woman had a newly recognized disorder of familial hypoceruloplasminemia, blepharospasm, retinal degeneration, and high-density areas in CT of the basal ganglia and liver scan. Immunofixation electrophoresis disclosed apoceruloplasmin deficiency. Kinetic, x-ray analysis, and histochemical study showed accumulation of iron in liver and brain, but not of copper. Intestinal copper absorption was reduced, but liver uptake was increased. Ceruloplasmin is involved in iron metabolism, and the findings suggest that hypoceruloplasminemia due to lack of apoceruloplasmin was causally linked to the iron deposition in basal ganglia and other organs, leading to blepharospasm and retinal degeneration.

Apoproteins↗
PubMed1987

Water intoxication due to excessive water intake: observation of initiation stage.

A patient who had experienced water intoxication despite normal renal function and normal urinary diluting ability was observed during the initiation stage of hyponatremia. Upon the excessive water intake (10 to 15 L) for several days, he developed moderate hyponatremia (121 mEq/L) and headache, an early symptom frequently seen in water intoxication. During this period, his urine was maximally dilute (50 to 60 mOsm/kg H2O), and his urinary sodium excretion increased. This report suggests that 10 to 15 L of water intake for several days can cause water intoxication in subjects with normal urinary diluting ability and that the increase in sodium excretion is prerequisite for the high urine flow rate.

Adult↗
PubMed1986

Augmentation of antibody responses of mice to inhaled protein antigens by simultaneously inhaled bacterial lipopolysaccharides.

Serum antibody responses of mice to repeatedly inhaled protein antigens such as bovine serum albumin and ovalbumin, plus or minus bacterial lipopolysaccharide (LPS) in the form of an aerosol were studied. Results showed that the levels of responses to inhaled protein antigens varied, depending on the mouse strain-antigen combination and that LPS inhaled simultaneously with the antigens definitely augmented the responses which were not otherwise very high. LPS extracted from Klebsiella O3 (LPS-K) but not LPS from Escherichia coli O55 (LPS-E), which was inhaled at the time of initial inhalation of antigen, significantly intensified the priming for the secondary antibody response to the antigen subsequently inhaled. Both LPS-K and LPS-E, however, definitely acted to augment the response when they were inhaled repeatedly together with the antigen. Oral administration of antigen or antigen plus LPS-K did not induce any detectable antibody response in our experiment, ruling out the possibility that the antigen and LPS stimulated the immune system via alimentary canal rather than via lung. Tissue distribution of the radioactivity soon after inhalation of 131I-labeled antigen and decay speed of the radioactivity were not significantly changed by LPS-K inhaled simultaneously. This suggested that the augmentation of responses was not mediated by the action of LPS to modulate the air-blood barrier against the entry of antigen via lung. All the results prove for the first time that inhaled LPS displays a definite adjuvant action on antibody responses to inhaled antigens.

Adjuvants, Immunologic↗
PubMed1986

[Abnormal cerebrospinal fluid plasma cells in a case of myeloma].

Cerebrospinal fluid (CSF) involvement in myeloma is rarely seen. Recently we experienced a case with this lesion. A 70-year-old man developed consciousness level disorder during the course of bronchopneumonia. Neurological examination revealed stuporous consciousness, neck stiffness and Kernig's sign. Immunoelectrophoresis showed monoclonal IgG in serum. CSF which was obtained through lumbar puncture was clear and its pressure was 155 mm H2O. It contained 207 white cells/3 mm3; glucose, 54 mg/dl; and protein, 33 mg/dl. The differential count of the CSF was (in %) monocytes, 48.0; plasma cells, 25.5; neutrocytes, 15.5; and lymphocytes, 11.0. Cytoplasm and nucleus of the plasma cells were in various sizes. Some irregular multiple nuclei, flaming cells and grape cells were also observed in them. The cytoplasm of the plasma cells fluoresced with antisera against lambda chains IgG. The value of immunofluorescent technique in identifying plasma cells in the CSF is emphasized.

Aged↗
PubMed1986

[A case of peptostreptococcal meningitis associated with subarachnoid hemorrhage and subdural hematoma].

A very rare case of peptostreptococcal meningitis associated with subarachnoid hemorrhage and subdural hematoma was reported. A 25-year-old man was admitted to St. Mary's Hospital on November 6, 1984 with a few day's history of headache and low grade fever. On admission, he had high grade fever (39.2 degrees C) and tachycardia (110/min). There were no neurological deficits other than neck stiffness and Kernig's sign. The cerebrospinal fluid (CSF) which was obtained through lumbar puncture showed watery clear appearance, white cell count of 32/3 mm3 (mononuclear: polymorphonuclear = 4:5), protein 76 mg/dl and glucose 8 mg/dl. It was found to be sterile. However, peptostreptococcus was found in his peripheral blood culture. He was diagnosed peptostreptococcal meningitis. After administration of antibiotics, laboratory test result of CSF improved gradually so as his meningeal irritation signs. After 25 days of hospitalization, he developed suddenly severe headache. CSF showed bloody and xanthochromic appearance, and CT scan revealed a subdural hematoma in the left fronto-temporal convexity. Although we suspected formation of mycotic aneurysm caused by the meningitis and its rupture, cerebral angiography revealed no abnormality except for the findings of subdural hematoma. The subdural hematoma was completely absorbed and he was discharged 79 days after admission without having any neurological deficit. We concluded that such a mycotic aneurysm was too small to be detected by the cerebral angiography.

Adult↗
PubMed1986

[A family of hereditary communicating hydrocephalus with trigonocephaly].

We studied a family of hereditary hydrocephalus with trigonocephaly, affecting eight members (four males and four females) across two generations. A proband in this family was 51 year old man, who complained of nonprogressive gait disturbance after the age of 20 years. He was admitted to our hospital because of non-neurological disease. Accidentally urinary incontinence appeared and then CT scan was performed, which revealed marked dilatation of the lateral ventricles. He was short stature and showed trigonocephalic forehead, but his head circumference was 56 cm. Mild dementia, spastic gait and hyperreflexia were observed on neurological examinations. A lumbar puncture disclosed that cerebrospinal fluid pressure was 115 mm H2O and sugar, protein and cells were normal. His skull X-ray film demonstrated temporal buldging of the calvarium, but its breadth length and height were within normal limits. Sagittal, coronal and lomboid sutures were not fused. However, skull bones were thinned and the top of dorsum sellae was erosive. A marked symmetrical dilatation of lateral, third and fourth ventricles were found in CT scan, to the contrary, bilateral Sylvian fissures and cortical sulci were slightly widened. On R.I. cisternography, ventricular reflux was noted during 3 to 72 hours after the injection. No accumulation of R. I. was observed in the parasagital region. In the arterial phase of the right carotid angiography, slight displacement was noted in Sylvian branches of bilateral middle cerebral arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Depression of afferent arc of the in vivo cytotoxic T-cell immunity by bacterial lipopolysaccharides.

The afferent arc of the in vivo cytotoxic T-cell immunity assessed by second set rejection of ascitic allogeneic tumors was shown to be depressed by bacterial lipopolysaccharide (LPS) that was administered simultaneously with or 1 day before injection of allogeneic spleen cells as stimulators. Two different LPSs from Escherichia coli O55 and Klebsiella O3 displayed similar activities whereas dextran sulfate, concanavalin A, or poly A:U was not effective. Stimulator activities of allogeneic cells was not directly modified by LPS. Any definite suppressor activity on afferent or efferent arc of the T-cell response was not demonstrable in mice receiving LPS and allogeneic cells. Further, the LPS effect for immune depression was not diminished by whole body X-ray irradiation to the recipient at 300 R, which ablated the B-cell reactivity to LPS for polyclonal activation, or by treatment of the recipient with carrageenan, a known toxic agent to macrophages. It was suggested from these results that LPS suppresses the cytotoxic T-cell immunity by modulating responder T cells to be temporarily refractory to the allogeneic stimulus rather than by activating suppressor cells such as radiation-sensitive lymphocytes and carrageenan-sensitive macrophages.

Animals↗
PubMed1985

Genetic and stimulatory cell type requirements for inducing class I major histocompatibility complex alloantigen-specific in vivo cytotoxic T cell immunity.

Current interpretation based on analytical in vitro works that actions of Ia antigens and accessory cells such as macrophages and dendritic cells are crucial for inducing cytotoxic T cell responses to class I major histocompatibility complex (MHC) alloantigens has been challenged by experiments performed in a newly developed system handling in vivo cytotoxic T cell immunity. We first characterized the transplantation immunity for second-set rejection of ascitic tumor allografts as principally induced by allogeneic stimulator cells via direct pathway, and as exclusively mediated by class I MHC alloantigen-specific in vivo cytotoxic T cell activity. By comparison of activities of limiting effective doses (10(4)-10(5) cells per mouse) of various stimulator cells in this defined system, we could demonstrate that genetic disparity at the D region of H-2 to the recipient is just enough for inducing the immunity, and presence of allogeneic or syngeneic Ia antigens in addition to H-2D alloantigens on stimulator cells does not give any premium effect. Further study revealed that allogeneic peritoneal cells rich in macrophages or glass-adherent spleen cells enriched for dendritic cells are not stronger stimulators than allogeneic adherent cell-depleted spleen cells and semi-allogeneic thymocytes. These results fit with the alternative concept that the physiological pathway inducing in vivo cytotoxic T cell immunity for graft rejection entirely depends on class I MHC antigens on live lymphocytes as self-supported stimulators, and does not crucially involve additional stimulator activities of Ia antigens and special accessory cell types, which must be in vivo concerned with induction of other types of transplantation immunity.

Animals↗
PubMed1985

Ontogeny of the transplantation immunity of mice for rejecting ascitic allogeneic tumors.

Ontogeny of the murine transplantation immunity for rejecting ascitic allogeneic tumors (chemically-induced RG lymphoma and L1210 leukemia) as a model of in vivo cytotoxic T cell immunity was studied. Challenge by 10(6) to 10(7) allogeneic tumor cells per 20 g body weight (b.w.) of the mouse was fatal to 1-3 day-old mice, whereas 7-30 day-old mice rejected the tumor. In newborn mice however some yet undetermined mechanism worked to temporally depress the initial tumor growth. Injection of low (10(6) cells per 20 g b.w.) to moderate (10(7)) doses of semiallogeneic spleen cells into newborn mice prepared for second set rejection of the tumor carrying the same alloantigens as the spleen cells, although injection of high dose (3 X 10(8)) cells reduced the tumor rejecting immunity. This second set rejection occurred even against the allogeneic tumor inoculated as early as 3 days old, if the mice had been primed with the alloantigens at birth. It appears therefore that newborn and early suckling mice are protected from tumor invasion by cytotoxic immunity more powerfully than expected from earlier in vitro works.

Age Factors↗
PubMed1985

Immune reactivity of allogeneically pregnant mice to paternal MHC antigens on fetal and placental cells assessed by second set rejection of ascites tumor cells.

In vivo immunogenicity of fetus- and placenta-derived cells as well as the immune reactivity of pregnant mice to fetal cells were examined for graft rejecting response (GRR). Systemic administration of small numbers of fetal cells but not placental cells from allogeneically pregnant mice (10(6) cells per mouse) or adult allogeneic spleen cells (10(4) cells) sensitized mice for second-set rejection of an ascitic tumor bearing paternal major histocompatibility complex (MHC) antigens. Despite this fact and the known positive humoral response, pregnant and parous mice are not even minimally sensitized with fetal MHC antigens for GRR transplacentally. Nevertheless, any pregnancy-related systemically active control, which would selectively prevent the mother from being sensitized for GRR by limiting numbers of semi-allogeneic fetal cells, was not demonstrable in either allogeneically or syngeneically pregnant mice. Irrespective of pregnancy, mice did not, however, respond to repeated administration of very small numbers of allogeneic spleen cells (5 X 10(2) cells per mouse) for graft rejection. These findings support the notion that deviation of maternal immunity to fetal antigens away from harmful GRR is mediated principally by local mechanisms which inhibit fetal cells from gaining access to the mother for GRR, and additionally by the innate inability of mice to respond to very small numbers of allogeneic cells that might escape past the local maternal-fetal barrier.

Animals↗