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  • Treatment  (2)
  • Nitric oxide  (1)
  • Secretoneurin  (1)
  • 1
    ISSN: 0014-5793
    Keywords: Chemotaxis ; Monocyte ; Neurogenic inflammation ; Secretogranin II ; Secretoneurin
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Nitric oxide ; Respiratory burst ; Ischemia ; Reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In animal studies of myocardial ischemia/reperfusion l-arginine reduces necrotic injury by preservation of endothelial function and attenuation of neutrophil accumulation in ischemic cardiac tissue. Because release of oxygen radical species by circulating neutrophils is important in endothelial function and ischemia-reperfusion injury, this study investigated the effect of intravenous administration of L-arginine on the in vitro release of superoxide anion of neutrophils in healthy young adults. Neutrophils were obtained at various time points before, during, and after infusion of l-arginine (17 mg kg−1 min−1 for 30 min) and analyzed for superoxide dismutase inhibitable reduction of ferricytochrome c. The spontaneously occurring respiratory burst of polymorphonuclear leukocytes at basal conditions was compared with that after triggering by 1 μmol/l formylpeptide or 50 ng/ml phorbolester. Infusion of l-arginine inhibited both basal (P 〈 0.01) and formylpeptide-triggered (P 〈 0.05) release of superoxide anion did, but not affect release stimulated by phorbol 12-myristate 13-acetate. Pretreatment of neutrophils with 1 mmol/l l-arginine in vitro also significantly reduced formylpeptide-triggered (1 μmol/l) superoxide anion release, suggesting that the affects observed after in vivo pretreatment may be due to direct action of l-arginine on neutrophils. These findings demonstrate the ability of L-arginine to reduce release of oxygen radical species by circulating neutrophils in man.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1912
    Keywords: Growth hormone deficiency ; Neutrophils ; Monocytes ; Respiratory burst ; Chemotaxis ; Treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The observations that growth hormone primes neutrophils and stimulates various activities of monocytes suggested that it plays a role in the regulation of leukocyte biology. The in vivo reduction of growth hormone levels may be responsible for to the functional impairment of leukocytes observed in growth hormone deficient children. Whether leukocyte function is impaired in growth hormone deficient adults is not known as yet. We therefore studied superoxide anion release from neutrophils and chemotaxis of monocytes in 15 patients with adult-onset growth hormone deficiency before and after a period of 6 months of replacement therapy with recombinant human growth hormone. Analyses were performed by comparing functions of the leukocytes from these patients with those from age and sex-matched healthy control subjects. Before growth hormone treatment, patients received appropriate replacement therapy with thyroid, adrenal and gonadal hormones. The dose of recombinant human growth hormone was 0.25–0.5 U/kg/week (0.013–0.026 mg/kg/day) throughout the whole period of replacement therapy. In growth hormone deficient subjects, formylpeptide-triggered release of superoxide anions from neutrophils was significantly suppressed by about 40% before treatment as compared to healthy control subjects. After 6 months of replacement therapy, neutrophil superoxide anion release was similar in patients and healthy individuals. Neither before nor after replacement therapy, however, was there a difference in monocyte migration between control and growth hormone deficient subjects. These data indicate that neutrophil function is somehow altered in growth hormone deficient patients, even when receiving appropriate therapy with thyroid, adrenal and gonadal hormones, but that neutrophil function can be restored to near normalcy by growth hormone replacement therapy. This would suggest that suppressed neutrophil respiratory burst is due to the deficiency in growth hormone.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1912
    Keywords: Key words Growth hormone deficiency ; Neutrophils ; Monocytes ; Respiratory burst ; Chemotaxis ; Treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The observations that growth hormone primes neutrophils and stimulates various activities of monocytes suggested that it plays a role in the regulation of leukocyte biology. The in vivo reduction of growth hormone levels may be responsible for to the functional impairment of leukocytes observed in growth hormone deficient children. Whether leukocyte function is impaired in growth hormone deficient adults is not known as yet. We therefore studied superoxide anion release from neutrophils and chemotaxis of monocytes in 15 patients with adult-onset growth hormone deficiency before and after a period of 6 months of replacement therapy with recombinant human growth hormone. Analyses were performed by comparing functions of the leukocytes from these patients with those from age and sex-matched healthy control subjects. Before growth hormone treatment, patients received appropriate replacement therapy with thyroid, adrenal and gonadal hormones. The dose of recombinant human growth hormone was 0.25–0.5 U/kg/week (0.013–0.026 mg/kg/day) throughout the whole period of replacement therapy. In growth hormone deficient subjects, formylpeptide-triggered release of superoxide anions from neutrophils was significantly suppressed by about 40% before treatment as compared to healthy control subjects. After 6 months of replacement therapy, neutrophil superoxide anion release was similar in patients and healthy individuals. Neither before nor after replacement therapy, however, was there a difference in monocyte migration between control and growth hormone deficient subjects. These data indicate that neutrophil function is somehow altered in growth hormone deficient patients, even when receiving appropriate therapy with thyroid, adrenal and gonadal hormones, but that neutrophil function can be restored to near normalcy by growth hormone replacement therapy. This would suggest that suppressed neutrophil respiratory burst is due to the deficiency in growth hormone.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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