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Biomedical subjects

M Nobunaga

Publications and source records attributed to M Nobunaga.

At least 91 records · Page 5Linked to original sources
PubMed1987

Generation of superoxide by immunologically stimulated normal human neutrophils and possible modulation by intracellular and extracellular SOD and rheumatoid factors.

Rheumatoid synovial fluids generated significantly greater amounts of superoxide, lysosomal enzymes, and superoxide dismutase from neutrophils into extracellular fluid than osteoarthritic synovial fluids. Rheumatoid factors isolated from serum suppressed superoxide-generating activity of performed immune complexes, but did not suppress that of intermediate-sized immune complexes isolated from RA serum. Synovial fluid neutrophils has a greater capacity to generate superoxide and lower intracellular superoxide dismutase activity, compared with peripheral neutrophils of the corresponding patients. These results suggest that neutrophil superoxide release may be modulated, both by rheumatoid factor and by intracellular and extracellular superoxide dismutase.

Acetylglucosaminidase↗
PubMed1987

Detection of low molecular weight IgM by immunoblot analysis in rheumatoid arthritis.

The immunoblot technique was used to detect low molecular weight IgM (LMWIgM) in the serum and synovial fluid (SF) of patients with rheumatoid arthritis (RA). LMWIgM was detected in 64% of 58 RA sera and in 47% of 17 RA SF. The levels of IgM and rheumatoid factor (RF) were significantly higher in the positive sera of LMWIgM. Sequential studies revealed that LMWIgM appeared in the serum while the titer of RF was high. Our analysis also suggested the presence of several other oligomeric LMWIgM with monomeric IgM.

Arthritis, Rheumatoid↗
PubMed1986

Superoxide generation by synovial fluid neutrophils enhanced by immune complexes and suppressed by rheumatoid factor in synovial fluid.

Synovial fluid (SF) from patients with rheumatoid arthritis (RA) enhanced superoxide generation by neutrophils isolated from RA SF, in contrast to SF from patients with osteoarthritis. These superoxide generation-enhancing substances may be intermediate-sized immune complexes and a complement C5-derived fragment. Rheumatoid factor (RF) isolated from RA SF suppressed superoxide generation-enhancing activity of aggregated IgG. Therefore, biologically active RF may block the interaction of the immune complexes with neutrophils accumulating in RA SF, and protect the joint tissue from the effects of oxygen radicals or proteases.

Antigen-Antibody Complex↗
PubMed1986

Influences of water deprivation and fasting on hypothalamic, pituitary and plasma opioid peptides and prolactin in rats.

To study the physiological roles of endogenous opioid peptides in drinking and feeding behaviors, the effects of water deprivation and fasting on plasma immunoreactive (IR) beta-endorphin (beta-end), IR-Antidiuretic hormone (ADH) and IR-Prolactin (Prl), pituitary IR-beta-end and IR-methionine-enkephalin (IR-Met-enk) and IR-ADH, and hypothalamic IR-beta-end and IR-Met-enk were observed in rats. The effects of water deprivation on hypothalamic dopaminergic system was also studied. In water deprived rats, plasma IR-beta-end and Prl were decreased significantly. In the neurointermediate lobe, IR-Met-enk, but not IR-beta-end, was decreased, although these peptides did not change in the anterior lobe and hypothalamus. Intraperitoneal injection of haloperidol reversed the decrease in plasma IR-beta-end in water deprived rats but did not change it in control rats. Subcutaneous injection of CB-154, on the other hand, decreased the plasma IR-beta-end in control rats but not in water deprived rats. The dopamine (DA) turnover rate in hypothalamus, in addition, was increased in water deprived rats as compared with controls. In fasted rats, IR-beta-end in plasma, but not in pituitary lobes and hypothalamus, was increased. The present results suggest that the increase of hypothalamic dopaminergic activity, in part, is related to the suppressed secretions of pituitary IR-beta-end and Prl in water deprivation, and plasma IR-beta-end play some roles in feeding behavior in rats.

Animals↗
PubMed1986

Influences of feeding and drinking on circadian rhythms of opioid peptides in plasma, hypothalamus and pituitary gland in rats.

Changes of plasma, hypothalamic and pituitary immunoreactive beta-endorphin (IR-beta-end), methionine-enkephalin (IR-Met-enk) and ACTH (IR-ACTH) were studied under various conditions of feeding and watering in rats. When rats were fed from 17:00 to 09:00 hr and water was given ad lib, plasma IR-beta-end and IR-ACTH had parallel circadian rhythms with a peak before feeding and drinking. In the hypothalamus, IR-beta-end and IR-Met-enk showed parallel circadian rhythms with a decrease before these behaviors. When rats were fed from 09:00 to 17:00 hr, the peaks of plasma IR-beta-end and IR-ACTH shifted to one hour before the onset of feeding and drinking. When feeding and watering were restricted to 17:00-09:00 hr and 09:00-12:00 hr respectively, plasma IR-beta-end and IR-ACTH exhibited parallel circadian rhythms with two separate peaks at one hour before drinking and feeding, respectively. In the hypothalamus, IR-beta-end, IR-Met-enk and IR-ACTH showed parallel circadian rhythms with a decrease before feeding but not before drinking. When rats were fed from 17:00 to 20:00 hr, plasma IR-beta-end increased and neurohypophysial IR-beta-end and IR-Met-enk decreased at 16:00 hr, one hour before feeding. It was observed that locomotor activities increased at the time of transition from light to dark and at one hour before the onset of feeding and drinking. The present results suggest that endogenous opioid peptides may have some physiological roles in feeding and drinking behaviors.

Adrenocorticotropic Hormone↗
PubMed1986

Serum alkaline ribonuclease derived from vascular endothelial cells is raised in patients with rheumatoid vasculitis.

We investigated the mechanisms of the marked increase of alkaline ribonuclease (RNase) in the sera of patients with rheumatoid arthritis associated with vasculitis. Among various tissues examined, blood vessels contained higher levels of alkaline RNase than acid RNase. Cultured human endothelial cells contained significantly higher amounts of alkaline RNase than acid RNase. In contrast, acid RNase was predominant in most other tissues and cells. Endothelial cells cultured with sera from patients with vasculitis released alkaline RNase into the extracellular medium. The phosphocellulose chromatographic profile of these sera differed from that of sera from healthy subjects. These results imply that the alkaline RNase in sera of patients with vasculitis is derived from blood vessels, probably from endothelial cells.

Arthritis, Rheumatoid↗
PubMed1985

Human vascular smooth muscle cells and endothelial cells lack catalase activity and are susceptible to hydrogen peroxide.

51Cr release as lytic and cell detachment as nonlytic injury were employed to estimate neutrophil-mediated injury of cultured human vascular smooth muscle cells and endothelial cells. The reagents hydrogen peroxide or hypoxanthine-xanthine oxidase produced dose-dependent killing and nonlytic cell detachment, which were specifically inhibited by catalase but not by superoxide dismutase. The concentration of hydrogen peroxide or xanthine oxidase to induce cell detachment was less than lytic dose, suggesting that cell detachment was a much more sensitive assay of injury. Neutrophil-mediated cell lysis averaged 15% at most and was mostly dependent on hydrogen peroxide, while neutrophil-mediated cell detachment was nearly 100% and its dependency on hydrogen peroxide varied from 46% to 60%. These results suggest that vascular smooth muscle cells and endothelial cells in neutrophil-mediated events are destroyed by a hydrogen peroxide-dependent process, mainly via a nonlytic cell detachment mechanism. There was no striking difference of sensitivity to hydrogen peroxide between vascular smooth muscle cells and endothelial cells. Vascular smooth muscle cells and endothelial cells contained fairly high concentrations of superoxide dismutase, but not catalase, activity. The sensitivity of these cells to hydrogen peroxide but not to superoxide may arise from the fact that these cells lack intracellular catalase activity. The injury of vascular cells, which constitute important components of blood vessels, may lead to vascular injury and subsequent tissue damage.

Blood Vessels↗
PubMed1984

A case of scleroderma with Sjögren's syndrome developed after mammoplasty.

A case of scleroderma and Sjögren's syndrome, which occurred 9 years after mammoplasty, was reported. The association between mammoplasty and connective tissue disorders was considered to be more than coincidental. The prolonged hypersensitization by injected material may be responsible for the development of connective tissue disorders, that is, a human adjuvant disease.

Breast↗
PubMed1984

Human umbilical cord vein smooth muscle cells lack receptors for C3b and the Fc portion of immunoglobulin G.

Under apparently normal conditions, the smooth muscle cells obtained from veins of human umbilical cord do not possess receptors for C3b or the Fc portion of IgG. These receptors were not expressed even after exposure to neutrophil lysate or a superoxide-generating system. The lack of these receptors argues against the possibility that smooth muscle cells participate in the pathogenesis of immune complex diseases through binding of C3b or Fc fragments.

Cells, Cultured↗
PubMed1984

Human plasma proopiomelanocortin N-terminal peptide and adrenocorticotropin: circadian rhythm, dexamethasone suppression, and corticotropin-releasing hormone stimulation.

The circadian rhythm, suppression with dexamethasone, and stimulation by corticotropin-releasing hormone (CRH) of plasma immunoreactive (IR) proopiomelanocortin N-terminal (NT) and IR-ACTH were studied in nine normal subjects and two patients with Addison's disease. The RIA for human NT (hNT) used was specific for NT except for partial cross-reactivity with gamma 2MSH. In normal subjects, plasma IR-hNT and IR-ACTH had almost parallel circadian rhythms and were suppressed by dexamethasone. The mean plasma levels of IR-hNT and IR-ACTH at 0800 h were 140 +/- 23 (SD) and 23 +/- 5 pg/ml, respectively. Plasma IR-hNT increased in parallel with IR-ACTH 15 to 30 min after iv injection of 100 micrograms ovine CRH. Maximum percent increases in plasma IR-hNT and IR-ACTH were 185 +/- 47 and 235 +/- 10%, respectively. In Addison's disease, on the other hand, plasma levels of IR-hNT and IR-ACTH were markedly elevated and the circadian rhythms were parallel. The mean plasma IR-hNT and IR-ACTH levels at 0900 h were 4363 and 1750 pg/ml, respectively. These results suggest that plasma hNT and ACTH are produced from a common precursor in the pituitary gland and secreted concomitantly under various physiological conditions such as stimulation by CRH and inhibition by glucocorticoid.

Addison Disease↗
PubMed1984

Chemotactic activity generated in human serum from the fifth component of complement by hydrogen peroxide.

Exposure of normal human serum to various concentrations of hydrogen peroxide as low as 68.8 microM resulted in the generation of chemotactic activity for human neutrophils, which was inhibited by adding catalase prior to the exposure. Maximum chemotactic activity was obtained by hydrogen peroxide at a concentration of 1.1 mM, and the concentration greater than 1.1 mM expressed decreased activity. On the contrary, hydrogen peroxide less than 1.1 mM produced dose-dependent chemotactic activity. The generation of chemotactic activity is initiated at an incubation time of 5 minutes, and subsequently increases with up to 90 minutes. The suppression of chemotactic activity was minimum even after 180 minutes. The maximum activity was obtained by 1024-fold dilution of serum treated with 13.8 mM hydrogen peroxide. These results suggest that the disappearance of chemotactic activity at the high-dose range of hydrogen peroxide is due to neutrophil deactivation rather than inactivation of the chemotactic activity after it was generated. Similarly, purified human C5 exposed to hydrogen peroxide generated chemotactic activity. The chemotactic activity was inhibitable by antiserum to human C5. The molecular weight of chemotactically active substance was approximately 15,000. The generation of chemotactic activity was not inhibited by addition of EGTA or EDTA. These results imply that hydrogen peroxide generates C5a-like chemotactic factor through hydrolysis of C5.

Aminopeptidases↗
PubMed1983

Serum factors from patients with systemic lupus erythematosus enhancing superoxide generation by normal neutrophils.

It has been suggested that human neutrophils exposed to performed immune complexes or activated complement fragments generate O2- anions in extracellular medium. In vivo studies have revealed that oxygen intermediates produced by immune complex-activated neutrophils play an important role in subsequent tissue damage. Since it is difficult to obtain direct evidence that O2- is released into plasma in patients with systemic lupus erythematosus (SLE), we studied the capacities of their sera to stimulate O2- release by human neutrophils in vitro. Sera from patients with SLE significantly enhanced O2- generation by neutrophils compared to normal sera. The enhancing activity of serum in the induction of increased O2- generation correlated positively with the presence of serum immune complexes and negatively with serum complement levels. The enhancing factors were analyzed by serum fractionation on Sephadex G-200 gel filtration, and were concluded to be immune complexes of intermediate size containing an activated complement fragment.

Cytochrome c Group↗