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Biomedical subjects

M Nagata

Publications and source records attributed to M Nagata.

At least 397 records · Page 22Linked to original sources
PubMed1991

[Bronchial lavage in the treatment of status asthmaticus].

Bronchial lavage was performed in 10 cases with status asthmaticus who were mechanically ventilated. The mean value of PaCO2 was 64.4 +/- 17.4 Torr before bronchial lavage, and it significantly decreased to 51.9 +/- 11.0 Torr after lavage. In 7 out the 10 cases, bronchial lavage was judged to be effective from the clinical point of view. In 5 cases with values of PaCO2 of over 55 Torr before lavage, massive mucus plugs were recovered. Bronchial lavage was judged to be effective in all of them, whereas three out of the another five cases whose values of PaCO2 were less than 55 Torr showed exacerbation of hypercapnia, and the state of asthma worsened and/or continued for a longer period. The ratio of PaO2/FiO2 did not improve even in effective cases. These results indicated that bronchial lavage is a useful tool to improve the hypercapnic state in patient with status asthmaticus being mechanically ventilated, if the value of PaCO2 is over 55 Torr.

Adult↗
PubMed1991

[The effect of long-term physical training on asymptomatic patients with myocardial infarction].

To examine the long-term effect of intense physical training on exercise capacity of patients with myocardial infarction(MI), multiphasic treadmill stress test(MTST) with modified Bruce protocol was performed repeatedly in 10 patients with training(Ex) and in 6 without training(C). In C, heart rate(HR), systolic blood pressure(SBP), or pressure rate product (PRP: HR X SBP/10(-2)) at any stage of MTST was unchanged for 3 years after MI. In Ex, these indices were unchanged at rest, but at stage 4 of MTST decreased significantly as follows: HR 119 +/- 20.4 to 108.6 +/- 16.0/min(p less than 0.05), SBP 151.6 +/- 24.0 to 137.0 +/- 17.5 mmHg(p less than 0.05), PRP 181.9 +/- 49.5 to 153.3 +/- 29.7(p less than 0.05). These indices at maximal exercise increased significantly after one year of training. One year of training in asymptomatic patients with MI reduced of myocardial oxygen consumption index during exercise at given work rate and increased maximal exercise capacity. With continued training these beneficial effects can be maintained for additional 2 years.

Blood Pressure↗
PubMed1991

[Routine use of the internal mammary artery for aorto-coronary bypass surgery].

Internal mammary artery (IMA) grafts have excellent long-term patency rate and result in improved late survival. Conventional use of IMA was only for selected cases. Elder or acute myocardial infarction case had been excluded from IMA use. During past 30 months we extended the indication of the IMA use for all the ACB case. The present study was undertaken to assess the possibility of routine use of the a IMA for aorto-coronary bypass (ACB). From Nov. 1987 through May 1990, we performed consecutive 110 ACB with the protocol "routine use of the IMA for all the ACB surgery". The 78 men and 32 women (29%) had a mean age of 64 years old (range 38 to 80 years old). Thirty-five patients (32%) were 70 years of age or older. Eighty-four patients had stable angina, nineteen patients had unstable angina, seven patients had acute myocardial infarction. IMA was used in 106 patients (96%). An average of 3.6 coronary arteries per patient were bypassed, and 1.6 distal anastomosis per patient were made with IMA. Combined cardiac surgery was performed in 8 cases (ventricular septal rupture repair: 2 cases, coronary endarterectomy: 4 cases, left ventricular aneurysm resection: 1 case, mitral commissurotomy: 1 case). Post operative complication due to IMA use were infrequent and operative mortality was 6.3%. In summary, routine use of the IMA for ACB surgery was possible method as if in high risked cases (elder or poor left ventricular function). We believe this method result in improved late result. We concluded routine use of the IMA for ACB was possible and usefull method.

Adult↗
PubMed1990

Production of active and passive anaphylactic shock in the WBB6F1 mouse, a mast cell-deficient strain.

The role of mast cells in active and passive anaphylactic shock was examined using the WBB6F1 mouse, a genetically mast cell-deficient strain. Lethal anaphylactic shock occurred at high incidence rates in mice actively sensitized to bovine serum albumin (BSA). The reaction was specific to BSA since the shock could not be elicited by human or guinea pig serum albumin in these animals. Lethal shock could be prevented by CV-3988 but not by cyproheptadine, which suggests that the shock is mediated by PAF but not by histamine and serotonin. Similarly, lethal shock was provoked by homologous antigens in mice which had been passively sensitized with allogeneic anti-benzylpenicilloyl (BPO) IgG1 monoclonal antibody or with allogeneic or xenogeneic anti-BSA antiserum, but not in those sensitized with allogeneic anti-BPO IgE monoclonal antibody. These findings suggest that mast cells are not necessarily required for anaphylactic shock in the mouse.

Anaphylaxis↗
PubMed1990

[Studies on the pathogenesis of type I diabetes mellitus--destruction of pancreatic beta cells by cytotoxic T lymphocytes in nonobese diabetic mice].

Proliferation of islet-associated leukocytes occurred when isolated islets from 20 week-old female Non-obese Diabetic (NOD) mice were cultured with 10 U/ml recombinant interleukin-2 (rIL-2) for 7 days. Co-culture of these lymphocytes with freshly-isolated islets from 6-8 week-old NOD donors in the presence of 1 U/ml rIL-2 produced islet structural deformation within 24 h and islet cytolysis within 48 h. Three lines of evidence suggest that leukocytes were cytotoxic T lymphocytes (CTL) specific for islet cells. First, these proliferating cells adhered to NOD islets at 6 h and specifically killed islets after 48 h of culture, but the cytoadherence of these cells to the other organs including thyroid, pancreatic exocrine glands and liver from NOD mice could not be observed and the shape of tissue clumps hardly deformed after culture for 48 h. The accumulated insulin release from NOD islets to the medium after 6 h of culture was significantly increased in the presence of islet-derived cells compared with the insulin release in the absence of cells. On the contrary, lactic dehydrogenase activity released from liver and amylase activity from pancreatic exocrine glands showed on difference between with and without these cells for 6h of culture. Second, a flow cytometric analysis showed that these cells consisted of 96%Thy1.2, 70%Lyt2, and 8%L3T4-positive cells. After treatment with monoclonal anti-Thy1.2 or Lyt2 antibody and complement, these cells lost their activity to destroy NOD islets. However, these cells still had a full killing activity after the depletion of L3T4-positive cells. Third, islets of NOD (H-2 genotype KdDb), B10.GD (H-2KdDb), BALB/cA (H-2d), and DBA/2N (H-2d) were susceptible to destructive activity of these cells, whereas islets of NON (H-2b), C57BL/6N (H-2b), C57BL/10J (H-2b), and C3H/He (H-2k) mice remained intact. Furthermore, anti-Kd monoclonal antibody could prevent islet-specific cytolysis of these cells. These results suggest that CTL expressing Thy1.2 and Lyt2 phenotypes appear to recognize islet cell antigen with restriction of major histocompatibility complex (MHC) class H-2Kd and then destroy pancreatic beta cells in NOD mice.

Animals↗
PubMed1990

Human gamma delta T-cell receptor-positive cell-mediated inhibition of erythropoiesis in vitro in a patient with type I autoimmune polyglandular syndrome and pure red blood cell aplasia.

The gamma delta T-cell receptor-positive (gamma delta TCR+) lymphocytes were markedly expanded up to 68% of peripheral blood lymphocytes in a case with type I autoimmune polyglandular syndrome and pure red blood cell aplasia (PRCA). The gamma delta TCR+ cells showed CD4 negative, 16% dim-CD8 positive and 10% to 46% human leukocyte antigen-D-related (HLA-DR) positive, and exhibited no monoclonality as assessed by the patterns of TCR gene rearrangements. Functional studies revealed that the proliferative responses of the patient's peripheral blood mononuclear cells (PBMC) were severely depressed to candida antigen, alloantigens, and autoantigens (non-T cells). The gamma delta TCR+ cells had no suppressive effect on the proliferative response of the alpha beta TCR+ cells to candida. The patient's PBMC, isolated gamma delta TCR+ cells but not alpha beta TCR+ cells, exhibited non-major histocompatibility complex (MHC)-restricted cytotoxicity. Furthermore, the patient's PBMC and isolated gamma delta TCR+ cells inhibited burst-forming units-erythroid (BFU-E), but not colony-forming units/granulocyte-macrophage (CFU-GM). Supernatants derived from the patient's T cells similarly inhibited BFU-E but not CFU-GM. The clinical course of the patient also showed a close correlation between the decreased number of total lymphocyte counts, especially HLA-DR + gamma delta TCR+ cell counts, and recovery from PRCA. These observations suggest that the gamma delta TCR+ cells might be functional in vivo and involved in the pathogenesis of PRCA in this patient.

Adult↗
PubMed1990

Radioimmunoassay of glioma-associated antigen in cerebrospinal fluid and its usefulness for the diagnosis and monitoring of human glioma.

Quantitative determination of human glioma-associated antigen in cerebrospinal fluids (CSFs) obtained from 66 patients with a variety of neurological diseases was performed by solid-phase radioimmunoassay with a monoclonal antibody (G-22). In this system, the minimum detectable amount of the antigen in the CSF was 8 ng/ml. It was demonstrated that CSF diagnosis of glioblastoma might be possible in the case of small tumors with a diameter of less than 2 cm. CSFs obtained from all 18 patients with glioma were positive and the level varied from 11.2 to 186.1 ng/ml. The antigen level in the cystic fluid of the tumor was higher than that in CSF. There was a tendency for the antigen level in CSF to be correlated with the tumor size and the type of histology. The malignant types of glioblastoma or medulloblastoma showed higher levels than the benign type of ependymoma and astrocytoma. Most types of non-gliomatous brain tumor were negative except immature teratoma, meningioma with central neurofibromatosis, and metastatic brain tumor from lung cancer. We also noted that tumor progression or regression of malignant glioma could be predicted by the monitoring of the antigen in the CSF.

Adult↗
PubMed1990

Anti-interleukin 2 receptor antibody attenuates low-dose streptozotocin-induced diabetes in mice.

Recent evidence indicates that activated T cells and macrophages play an important role in the induction of insulitis and diabetes in certain strains of mice treated with multiple subdiabetogenic doses of streptozotocin. In the present study, we treated C57BL/6J mice with five daily doses of 40 mg/ml streptozotocin and examined the prophylactic effect of an anti-interleukin 2 receptor monoclonal antibody (PC61). In mice treated with streptozotocin, interleukin 2 receptor-positive mononuclear cells were shown to infiltrate into the islets and soluble interleukin 2 receptors in the sera were significantly increased compared with control mice. The administration of PC61 to the mice attenuated the insulitis, and diminished interleukin 2 receptor-positive cells from islets and soluble interleukin 2 receptors in the sera. Moreover, the administration of PC61 significantly reduced the development of hyperglycaemia shown in these mice (12.8 +/- 1.1 mmol/l vs 18.5 +/- 0.7 mmol/l, p less than 0.005). As judged by flow cytometric analysis, this antibody did not cause any changes in either spleen cell counts or T cell subsets. Interleukin 2 receptors were expressed on a minor population of spleen cells regardless of treatment with PC61 (STZ + normal rat IgG: 2.1 +/- 0.3%, STZ + PC61: 2.4 +/- 0.3%). Even after stimulation of spleen cells with concanavalin A or alloantigen, interleukin 2 receptor expression was not significantly different between the two groups. Our studies suggest that interleukin 2 receptor-positive activated T cells or macrophages are important in the development of multi-low-dose streptozotocin diabetes and that an anti-interleukin 2 receptor antibody can attenuate this process.

Animals↗
PubMed1990

Increased levels of beta-human atrial natriuretic peptide-like immunoreactivity in chronically overloaded atrial tissue.

The levels and molecular form of atrial natriuretic peptide-like immunoreactivity (ANP-LI) in human atrial tissue were investigated. The levels of right atrial ANP-LI were significantly higher in mitral disease than in other cardiac or noncardiac diseases. The increased ANP-LI was mainly accounted for by an increase in beta-human ANP-LI (beta-hANP-LI). Both total ANP-LI and beta-hANP-LI levels were associated with the presence of atrial fibrillation and with increased atrial pressure. Plasma beta-hANP-LI levels were also increased in mitral disease. These results suggest that human atrium with hemodynamic overloads is characterized by increased tissue levels of ANP and by a shift to the beta-hANP form.

Adult↗
PubMed1990

Acute leukemia with normal platelet count at diagnosis.

Thirty-six (17.8%) of 202 children with acute lymphoblastic leukemia (ALL) and 2 (3.7%) of 54 children with acute nonlymphoblastic leukemia (ANLL) had a platelet count over 150 x 10(9)/l at diagnosis. Children with ALL and a platelet count over 150 x 10(9)/l were analysed in detail. The ALL patients without thrombocytopenia tended to be male predominant and had less frequent bleeding manifestations (p less than 0.01). These patients without thrombocytopenia had also significantly less marked leukocytosis (p less than 0.01), less severe anemia (p less than 0.05) and lower percentages of bone marrow blasts (p less than 0.05) than those with thrombocytopenia. In addition, ALL patients without thrombocytopenia had a significantly higher probability of continuous complete remission than those with thrombocytopenia (p less than 0.01).

Child↗
PubMed1990

Bile salt-induced disintegration of egg phosphatidylcholine liposomes: a kinetic study based on turbidity changes.

The disintegration kinetics of egg phosphatidylcholine small unilamellar liposomes in various bile salts (nine species) were investigated by monitoring turbidity changes with a stopped-flow apparatus. The pseudo-first-order rate constants obtained as a function of bile salt concentration (up to 25 mM) were analyzed based on a two-step model in which a penetration-saturation step of bile salt into the bilayer and a lamellar-micellar transition step were assumed for the disintegration mechanism of the bilayer. The order of the rate of the penetration-saturation step, which is assumed to be a measure of the disintegration ability, was as follows: SCDOC greater than SDOC greater than STCDOC greater than STDOC greater than STC greater than SC greater than SGCDOC greater than SGDOC greater than SGC. The results indicated that (1) the dihydroxy bile salts have a greater disintegration ability than the corresponding trihydroxy bile salts, (2) the chenodeoxy bile salts have a greater ability than the corresponding deoxy-bile salts regardless of non-conjugated or conjugated form, (3) the taurine conjugates always have a greater ability than the glycine conjugates. The penetration-saturation rate of the bile salts against the lipid bilayer depends considerably on the chemical nature of each bile salt, varying by a factor of about 10(5). In the conjugated bile salts alone, they were in a narrower range of a factor of 10(3). The physical integrity of liposomes can hardly be maintained in the bile salt-rich intestinal tract but the resulting mixed micelles may contribute substantially to solubilization and enhanced delivery of drugs.

Bile Acids and Salts↗
PubMed1990

Central inhibition of gastric motility by intravenously administered nicotine in rats.

Effects of intravenously (i.v.) administered nicotine on gastric motility were investigated in urethane-anesthetized rats in which an intragastric balloon had been placed. I.v. administered nicotine at 75-300 nmole/kg dose-dependently decreased gastric motility. Decrease in gastric motility induced by nicotine at the dose of 300 nmole/kg was inhibited by intracisternally administered hexamethonium. Gastric motility was also decreased by intracisternally applied nicotine (1-10 nmole). These doses were much smaller than those by the intracerebroventricular route in our previous report. Bilateral vagotomy significantly suppressed basal gastric motility. In bilaterally vagotomized animals, nicotine at 1 mumole/kg but not 300 nmole/kg given i.v. significantly decreased the gastric motility maintained at a normal level by electrical stimulation of the vagus nerve. This nicotine-induced decrease in gastric motility, under conditions of electrical stimulation of the vagus nerve, was inhibited by pretreatment with phentolamine. These results suggest that a smaller dose of nicotine given i.v. activates nicotinic receptors in the brainstem and elicits vagally-mediated inhibition of gastric motility. Activation of peripheral alpha-adrenergic mechanisms together with that of central nicotinic mechanisms may be involved in the decreasing effects of a larger dose of nicotine on gastric motility.

Anesthesia↗
PubMed1990

Impaired mitogen-induced expression of high-affinity interleukin 2 receptors on spleen cells from NOD/Shi/Kbe mice.

The immune abnormalities of NOD mice, a model of human type I (insulin-dependent) diabetes, have been postulated to be T-lymphocyte dependent. We measured responsiveness to exogenous interleukin 2 (IL-2) and IL-2 production in spleen mononuclear cells from female NOD/Shi/Kbe mice after stimulating the cells with concanavalin A (ConA blasts) or phytohemagglutinin (PHA blasts). Exogenous IL-2 produced significantly lower proliferative responses in each blast from 3- and 10-wk-old NOD/Shi/Kbe mice than from control strains. IL-2 production in NOD/Shi/Kbe mice was inclined to decrease but not significantly compared with controls. Even sufficient amounts of recombinant IL-2 (rIL-2) or IL-1 (rIL-1), added with mitogens to the preculture medium, failed to provoke normal proliferative responses from NOD/Shi/Kbe mouse cells. To clarify the reason for this defect, we investigated the expression of IL-2 receptors (IL-2Rs) on mitogen-activated cells with anti-IL-2R monoclonal antibody (PC61) and radiolabeled IL-2. Cytofluorometry showed no significant difference between strains in the number of PC61+ ConA and PHA blasts. However, Scatchard analysis with 125I-labeled IL-2 showed that the number of high-affinity IL-2Rs (H-IL-2Rs), the mediators of the biological activity of IL-2, was decreased in NOD/Shi/Kbe mice compared with controls, whereas the number of low-affinity IL-2Rs (L-IL-2Rs) was not different. Separating the L3T4+ and Lyt-2+ populations of T lymphocytes by cell sorting showed both to be deficient in H-IL-2Rs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Active and passive cutaneous anaphylaxis in WBB6F1 mouse, a mast cell-deficient strain.

WBB6F1 mouse, a mast cell-deficient strain, was tested for active and passive cutaneous anaphylactic reactions. Active cutaneous anaphylaxis was not produced in mice which had been immunized for 1 to 2 weeks by an intraperitoneal injection of bovine serum albumin with either adjuvant, Freund's complete adjuvant or Bordetella pertussis organisms, even though circulatory IgE and IgG1 antibodies were raised. Passive cutaneous anaphylaxis (PCA) was also absent, when the mice had been sensitized with allogeneic IgE or IgG1 monoclonal antibodies. However, obvious PCA was produced when allogeneic or xenogeneic hyperimmune serum was employed. These findings indicate that mast cells are not necessarily needed for the production of PCA. Some mechanism quite different from the well-elucidated mechanism, i.e., IgE- or IgG1 antibody-triggered histamine release from mast cells, seems to be operative.

Animals↗
PubMed1990

Serum granulocyte colony-stimulating factor levels in chronic neutropenia of infancy.

Eight infants with chronic neutropenia ranging in age from 1 to 13 months were studied for serum granulocyte colony-stimulating factor (G-CSF) levels. Serum G-CSF levels were elevated, especially when peripheral blood absolute neutrophil counts (ANC) were under 500/microliter in seven patients with autoimmune neutropenia. On the other hand, in a patient with congenital agranulocytosis (Kostmann type), G-CSF levels were below the sensitivity of the assay (less than 50 pg/ml) despite severe neutropenia (less than 100/microliter).

Autoantibodies↗