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Biomedical subjects

S Nishida

Publications and source records attributed to S Nishida.

At least 307 records · Page 17Linked to original sources
PubMed1988

Provocation of a paradoxical growth hormone response to corticotropin-releasing hormone by pretreatment with metoclopramide in patients with acromegaly and normal subjects.

Two of 7 patients with acromegaly and one of 7 normal subjects exhibited a paradoxical rise in growth hormone (GH) to human corticotropin-releasing hormone (CRH) when pretreated with metoclopramide, although CRH alone did not induce an increase in GH. In one of these two patients with acromegaly, the GH increase to metoclopramide alone also reached the criteria of a paradoxical response. These two acromegalic patients showed a GH increase to metoclopramide pretreatment before and up to two months after surgery. In another acromegalic patient, whose GH level remained high 5 months after surgery, metoclopramide induced an increase in GH level, while in a patient who had an above-normal GH level 18 months after surgery, the resumption of physiological GH secretion after surgery was evidenced by a postoperative absence of a GH response to metoclopramide. It is suggested from these results that the GH response to metoclopramide and the metoclopramide-provoked GH response to CRH in patients with acromegaly result from the secretion of GH from nonadenomatous cells of the pituitary.

Acromegaly↗
PubMed1988

Harderian gland dependency of immunoglobulin A production in the lacrimal fluid of chicken.

Involvement of the Harderian gland (HG) in the production of lacrimal immunoglobulin (especially IgA) was investigated. The lacrimal concentration of each immunoglobulin class was not affected by surgical bursectomy but was reduced by cyclophosphamide (CY) and testosterone (TP) treatments. Surgical removal of the Harderian gland caused a remarkable reduction of both the lacrimal concentration of each immunoglobulin class and the specific antibody titre, and and IgA was almost undetectable. The lacrimal concentration of each immunoglobulin class, as well as the specific antibody titre, was not affected by surgical removal of the Lacrimal gland (LG). The route of antigen administration produced no difference in the class of lacrimal immunoglobulin produced. The results indicate that the production of immunoglobulin in chicken tears may be dependent on the HG and that lacrimal immunoglobulin may be synthesized and secreted locally in the HG. Lymphocytes of the HG are of bursa of Fabricius origin and are seeded into the HG prior to hatching and its lymphocytes do not appear to be involved in systemic immunity.

Aging↗
PubMed1987

Correlation between susceptibility to chloramphenicol, tetracycline and clindamycin, and serogroups of Clostridium difficile.

A total of 114 Clostridium difficile strains were analysed for a possible correlation between serological susceptibility to chloramphenicol, tetracycline and clindamycin, and serogrouping. All 17 chloramphenicol-resistant strains belonged to serovar I, while none of 32 tetracycline-resistant strains belonged to serovar I. All strains included in serovar III were tetracycline- and clindamycin-resistant.

Chloramphenicol↗
PubMed1987

Scalp topography of photic evoked potentials. Application of wave form decomposition technique.

A new method of wave form decomposition by using an evoked potential model was applied to the study of scalp topography of photic evoked potentials in 3 normal subjects. The parameters of the evoked potential model were composed of gain, natural frequency, damping ratio and time lag, and were determined in the frequency domain to minimize the square sums of the modeling error. By using the optimal model parameters, the wave form was decomposed into basic components. At least 4 components occurring within the initial 200 msec period after the stimulus onset were identified in all subjects and were shown to have different scalp distributions, suggesting different generator sources.

Adult↗
PubMed1987

Pituitary-adrenocortical response to metoclopramide in patients with acromegaly and prolactinoma: a clinical evaluation of catecholamine-mediated adrenocorticotropin secretion.

We have demonstrated that metoclopramide stimulates cortisol secretion at least in part by a stress-mediated effect in normal men. To examine further the effect of the drug on the hypothalamo-pituitary adrenal system, we studied the cortisol response to 20 mg metoclopramide in patients with acromegaly, prolactinomas, and functional hyperprolactinemia and compared the results with the responses to insulin-induced hypoglycemia. In some patients, the effects of metoclopramide on CRH-induced ACTH and cortisol increase were studied to determine whether a change in dopaminergic (catecholaminergic) activity altered CRH stimulation of pituitary-adrenal function. No cortisol response to 20 mg metoclopramide occurred in 13 tests on 8 of 9 patients with prolactinoma or acromegaly with hyperprolactinemia, whereas both acromegalic patients without hyperprolactinemia had a response. All of the patients had a normal cortisol response to insulin-induced hypoglycemia. Pretreatment with metoclopramide enhanced the CRH-induced cortisol increase from 30-120 min after CRH in normal men, but only at 15 and 30 min in 5 agromegalic patients. The results suggest that metoclopramide acts in the hypothalamus to release ACTH through a dopamine antagonist-mediated (catecholaminergic) mechanism, and that metoclopramide may act additively with CRH to stimulate ACTH secretion in normal men. The absence of a metoclopramide-induced cortisol response in patients with acromegaly or prolactinomas and the absence of a normal cortisol response to metoclopramide-CRH in acromegalic patients could be due to endogenous catecholamine deficiency in these patients.

Acromegaly↗
PubMed1987

Immunohistochemical change of actin in experimental myocardial ischemia. Its usefulness to detect very early myocardial damages.

Pathomorphological diagnosis of acute myocardial infarction has many problems in human autopsy materials less than 4 to 6 hours after clinical onset and in rats 2 to 3 hours after experimental coronary occlusion. Since immunohistochemical reaction depends on the antigen determinant site of the material, changes in the reaction may reflect alterations at the molecular level in myocardial fibers. With this consideration in mind, the effectiveness of diagnosing infarction at the earliest (possible) stage, and the changes of actin filaments were investigated through experiments, using immunohistochemical methods involving anti-actin antibodies produced from chicken gizzards in our laboratory. The left coronary arteries of rats were ligated to produce ischemia. Dehydrogenases were shown to be still present by triphenyltetrazolium chloride (TTC) reaction, but the anti-actin antibody reaction had disappeared in areas corresponding to the ischemic sites. However, on electron microscopic examination of these sites, actin fibers were clearly revealed. In the case of ischemia lasting for more than 6 hours, the anti-actin antibody reaction had disappeared, corresponding to the disappearance of the TTC reaction. At this stage, myocardial actin fibers were revealed by electron microscopic examination. These results indicate that ischemia induces some type of biochemical degeneration at the molecular level of myocardial actin, most likely the change of actin polymerization. Moreover, they show that the anti-actin antibody technique is capable of detecting such very early degenerative and ischemic changes proving itself to be better suited for determining the range and degree of early infarction.

Actins↗
PubMed1987

[Granulopoietic effects of lentinan, an antitumor polysaccharide in BALB/c nude mice].

The effect of lentinan on granulopoiesis in BALB/c nude mice (Nu/Nu) was compared with that in their heterozygotes (Nu/+). Lentinan-injected Nu/+ showed enhanced serum colony-stimulating activity (CSA), and increased diphasically granulocyte-macrophage colony forming cells (GM-CFC) in bone marrow and spleen (i.e., first peak on day 1-2 and second peak on day 6). On the other hand, in Nu/Nu, lentinan did not enhance serum CSA, although the control level was higher than the enhanced level in Nu/+. Monophasic increase in GM-CFC was observed in Nu/Nu, but the second peak seen in Nu/+ was not observed. Reconstitution of Nu/+ splenocytes to Nu/Nu increased GM-CFC on day 6, and the increase was augmented by lentinan administration. These results suggest that mature T-cells participate in regulation of granulopoiesis in vivo and that lentinan augments granulopoiesis at least in part via mature T-cell populations.

Animals↗
PubMed1987

[Granulopoietic effects of lentinan in mice: effects on GM-CFC and 5-FU-induced leukopenia].

C57BL mice were injected intravenously with an antitumor immunopotentiating polysaccharide, lentinan, to assess its effect on granulopoiesis in normal mice as well as its ability to enhance the recovery from leukopenia induced by 5-fluorouracil (5-FU). Lentinan increased neutrophils and monocytes in peripheral blood as well as granulocyte-macrophage progenitor cells (GM-CFC) in spleen and bone marrow. Administration of 5-FU induced a significant decrease in GM-CFC from day 1 to day 6, and thereafter the number of GM-CFC rebounded. The administration of 5-FU also suppressed white blood cells such as neutrophils, monocytes and lymphocytes. Injection of lentinan one day after 5-FU resulted in prompt restoration of the leukopenia through the recovery of neutrophils, monocytes and lymphocytes as well as prompt and marked rebound of GM-CFC. These results suggest that lentinan may contribute to the recovery from some of the hematopoietic depression in clinical chemoimmunotherapy.

Animals↗
PubMed1987

Fine structural significance of bone corpuscle-shaped pigmentation in the human retinal pigment degeneration.

Two cases of advanced RPD were observed their trypsin digested vascular trees and retinal substructures, especially RPE and pigmented cells in the neural retina. In the both eyes the visual cell was almost completely degenerated to disappear except posterior regions and apical part of RPE came to contact with neural retina or external limiting membrane formed by tight junction between adjacent Müller cell processes. Occasionally RPE in the equatorial region had completely disappeared and was replaced by Müller cell processes which was directly apposed to the Bruch's membrane. Pigmented cells were observed at almost all levels of the neural retina and along the intraretinal capillary. Pigmented cells were classified into three types. The first type of the cell was corresponded with the macrophage in the substructural features. The second type of the cell was RPE proliferated or migrated into the neural retina forming bone corpuscle-shape pigmentation in the retina and along the intraretinal capillary. Müller cell processes also indicated up-taking pigment granules, that is, the third type of the pigmented cell.

Adult↗
PubMed1986

A new approach for the enzymatic estimation of infarct size: serum peak creatine kinase and time to peak creatine kinase activity.

The relations of several creatine kinase (CK) variables to angiographic left ventricular ejection fraction and abnormally contracting segments in the chronic phase were examined in 2 groups of patients with a first anterior acute myocardial infarction. In group A (n = 22), emergency coronary angiography was performed and nonsurgical early reperfusion was attempted. Such an early revascularization, which was considered partially present in group B (n = 16), which received conventional therapy, shifted the CK time-activity curve to the left and altered its relation to angiographic cardiac function. At similar levels of peak CK, myocardial damage was significantly smaller in patients with successful thrombolysis than in those with unsuccessful reperfusion and conventional therapy (p less than 0.01). In patients whose infarct was considered to be moderate according to peak CK (1,000 to 3,000 U/liter), there was significant correlation between time to peak CK and left ventricular ejection fraction or percent abnormally contracting segments irrespective of their group. The results suggest that one should take into account rapid washout and shorter time to peak CK when estimating enzymatic infarct size in humans. The multivariate analysis of cardiac function with peak CK and time to peak CK resulted in a closer correlation in all patients. Such a correction in the time to peak CK may be a clinically useful approach for better interpretation of infarct size.

Aged↗
PubMed1986

Pathogenesis of angina pectoris in patients with one-vessel disease: possible role of dynamic coronary obstruction.

We examined the pathogenesis of angina pectoris in 101 patients with one-vessel disease except those with 99% to 100% occlusion. The attacks could not be induced or could not be reproducibly induced by maximal treadmill exercise at the same hour of different days within a week period in 54 (53.5%) of the patients. In the 47 patients whose attacks were reproducibly induced by the exercise, propranolol, 80 mg orally, did not suppress the attacks in 41 (87.2%) of the patients. Diltiazem, 90 mg, and nifedipine, 20 mg given orally, suppressed the attacks completely in 39 (83.0%) of the 47 patients and in 36 (81.8%) of the 44 patients, respectively. Coronary arteriography showed that dynamic obstruction of the artery supplying the area of myocardium represented by ST segment deviation appeared during the attacks and disappeared with subsidence of the attacks in all 55 patients in whom coronary arteriography was done during the attack. We conclude that angina pectoris is usually caused not by increased myocardial oxygen demand but by dynamic coronary obstruction or by a combination of both in most patients with one-vessel disease.

Adult↗