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Biomedical subjects

K Ando

Publications and source records attributed to K Ando.

At least 559 records · Page 31Linked to original sources

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↗

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↗

Evidence for increased sympatho-adrenomedullary activity in young subjects with borderline hypertension.

Three different studies were performed to estimate the sympatho-adrenomedullary activity in young subjects with borderline hypertension (BHT, n = 40), compared with age-matched normotensive subjects (NT, n = 24). In the first study, 23 BHT and 9 NT were subjected to isometric stress by maintaining handgrip at the 30% level of maximal voluntary contraction for 3 min. The response of plasma total catecholamines at the second and third min during the isometric exercise were greater in BHT than in NT (98.9 +/- 24.3 vs. 18.0 +/- 30.7 and 93.0 +/- 12.6 vs. 47.1 +/- 15.4 pg/ml, respectively, p less than 0.05). In the second study, the effects of intravenous glucagon injection (1 USP unit) were studied in 12 BHT and 9 NT. The increments of plasma epinephrine (E) at 2 and 3 min after injection were significantly greater in BHT than those in NT: 44.1 +/- 12.3 vs. 5.1 +/- 4.4 pg/ml, and 68.9 +/- 13.2 vs 32.1 +/- 8.9 pg/ml, respectively, p less than 0.05. In the last study, the pressor effects of intravenous norepinephrine (NE) infusion (100 and 200 ng/kg/min for 15 min) were examined in 17 BHT and 15 NT under three different sodium balances: regular customary diet, treatment with diuretics and high-sodium diet. Treatment with diuretics decreased and high-sodium diet increased the pressor response to NE in both groups, but there were no significant differences in NE reactivity between 2 groups throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗

[Changes in movement and ataxic gait with development in genetically ataxic mice: a comparison with the level of cerebellar cyclic nucleotide].

Spontaneous movement and ataxic gait in ataxic mice showing various pathological changes in the cerebellum were investigated according to developmental stage by the open-field method of comparison with normal mice. As the cerebellum contains relatively high levels of cyclic nucleotide, its concentrations was measured by radioimmunoassay to elucidate the correlation between spontaneous movement and ataxic gait and the neurological changes. The movements of Rolling Mouse Nagoya (RMN), Weaver and Reeler mice without Purkinje Cell Degeneration (PCD) were found to decrease at 4 and 12 weeks of age. The degree of ataxic gait worsen in RMN, was unchanged in Reeler and improved in Weaver and PCD mice. The cerebellar c-GMP concentration of ataxic mice was decreased, while no significant changes in c-AMP concentration were found in comparison with normal mice. With development, the level of cerebellar c-GMP in Weaver mice increased, but this was not apparent in RMN, Reeler or PCD mice. The results of this investigation indicated that there may be some relation between the degree of ataxic gait and the level of cerebellar c-GMP in Weaver mice.

Animals↗

[Elevated immunoreactive-somatostatin levels in the brain of ataxic mutant mice].

Immunoreactive-somatostatin (IR-SRIF) levels were investigated in the brain of 4 types of ataxic mice (Rolling Mouse Nagoya, Weaver, PCD, Staggerer) with different cerebellar pathologies. IR-SRIF concentrations (ng/mg) were found to be significantly elevated in both cerebellum and cerebrum of all ataxic mutant mice, IR-SRIF (ng/organ) was found to be increased in the cerebellum and cerebrum in Rolling Mouse Nagoya and PCD compared with control mice. The gel-filtration profile (Sephadex G-50) in the cerebellar extracts of Rolling Mouse Nagoya proved to be identical to that of control mice. Three peaks of IR-SRIF were found to be uniformly elevated in Rolling Mouse Nagoya, with the highest peak coinciding with authentic somatostatin-14. The present results suggest that elevated levels of IR-SRIF in the brain may play a role in the mechanism underlying the manifestation of ataxia in ataxic mutant mice, especially in Rolling Mouse Nagoya and PCD.

Animals↗

The presence of atrial natriuretic peptide in canine cerebrospinal fluid and its possible origin in the brain.

The presence of atrial natriuretic peptide (ANP) in canine cerebrospinal fluid (CSF) was clearly demonstrated and an attempt was made to determine its origin as either the brain or the atrium. The concentration of ANP in canine CSF was 0.78 +/- 0.37 pmol/l (n = 31) and showed no evident correlation with that in plasma (r = 0.12). Physiological doses of human alpha-ANP (alpha-hANP) were continuously infused intravenously into nine dogs, and ANP concentrations in CSF and plasma were examined six to eight times within a 120-min period following this. The ANP level in CSF was not influenced by the systemic administration of alpha-hANP up to 180 min. Only one low molecular weight peak corresponding to alpha-hANP could be obtained from the CSF samples, while both low and high molecular weight peaks were observed for plasma ANP by gel permeation chromatography. In the atrial and hypothalamic tissue extracts the same kinds of peaks were also evident. These results prove the presence of ANP in canine CSF and that it does not come from blood that has seeped across the blood-CSF barriers, but suggest that it may originate from the brain.

Animals↗

Response of atrial natriuretic peptide in plasma and urine to changes in dietary intake of sodium chloride in man.

Plasma concentration and urinary excretion of immunoreactive human atrial natriuretic peptide (ir-hANP), aldosterone, and vasopressin were measured, and renal function and blood pressure were determined in six healthy male subjects in three periods of different sodium intake: the control (172 mEq/day), low (20 mEq/day), and high (285 mEq/day) sodium period. Both plasma concentration and urinary excretion of ir-hANP increased significantly in the high sodium period but did not change between the control and low sodium periods. On the contrary, aldosterone increased and vasopressin decreased in the low sodium period but did not change between the control and high sodium periods. These results may point out the reciprocal action of both endocrine systems. The glomerular filtration rate changed in parallel with sodium intake whereas the fractional excretion of sodium decreased only in the low sodium period, probably reflecting the action of aldosterone. It is concluded from these results that the atrial peptide may be an important component in the regulation of body fluid in the high sodium loading of physiological range but its action may be limited to the control of glomerular filtration rate.

Adult↗

Gracile axonal dystrophy (GAD), a new neurological mutant in the mouse.

A new neurological mutant has been found in the F2 offspring of CBA/Nga and RFM/Nga mice. Affected mice exhibited ataxia beginning at about 80 days of age, followed by tremor, difficulty in moving, and muscular atrophy of the hind limbs. The neurological signs became progressively severe, and death occurred by 5 to 6 months of age. Since the animals could be distinguished from normal mice by the abnormal positions of the hind limbs when the mouse was hung by the tail after 1 month of age, they could be bred until onset of the signs. Pathological examination revealed neuroaxonal dystrophy and degeneration in the gracile nucleus of the medulla oblongata and the gracile fascicules of the spinal cord, which could be the main cause of the clinical signs. The mutation is inherited as an autosomal recessive trait. It was, therefore, named gracile axonal dystrophy (GAD) with the gene symbol gad. The mice could be a new pathological model for the study of neuroaxonal dystrophy.

Animals↗

Antitumor and antimetastatic activity of an antibiotic, ascofuranone, and activation of phagocytes.

Ascofuranone demonstrated antitumor activity against FM3A murine mammary carcinoma, implanted in the peritoneal cavity of syngeneic mice, C3H/He. It was more effective by treatment prior to implantation than by that after implantation. Treatment with ascofuranone also increased splenic cytotoxicity and phagocytic activity of host animal cells. Moreover, ascofuranone induced inflammatory cells in the peritoneal cavity which are mainly composed of polymorphonuclear leukocytes and macrophages. These cells are more potent in cytotoxicity against FM3A cells than with resident peritoneal cells. The antitumor activity of ascofuranone was suppressed by ip administration of silica, just prior to tumor implantation. These results suggest that the prophylactic antitumor activity of ascofuranone is expressed through the activation of phagocytes. Ascofuranone also suppressed pulmonary metastasis of B16 melanoma and Lewis lung carcinoma. Treatment after tumor implantation failed to suppress the metastasis. Single treatment of ascofuranone 4 days prior to implantation decreased the metastasis of Lewis lung carcinoma but not that of B16, whereas single treatment of ascofuranone 24 hours prior to the tumor implantation decreased the metastasis of B16 but not that of Lewis lung carcinoma.

Animals↗

[Cystitis in 8 patients treated with tranilast].

We encountered 8 cases of cystitis probably caused by Tranilast. Bladder biopsy performed on 6 of the 8 cases revealed eosinophilic cystitis in 3 cases. In the lymphocyte stimulation test using Tranilast as an antigen, a positive and false positive reaction was seen in one case each. This disease seemed to occur as a result of allergy of the bladder specific to Tranilast.

Adult↗