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Subject neutrophils

Superoxide is formed (reaction 1) in the red blood cell by the auto-oxidation of hemoglobin to methemo-globin (approximately 3% of hemoglobin in human red blood cells has been calculated to auto-oxidize per day) in other tissues, it is formed by the action of enzymes such as cytochrome P450 reductase and xanthine oxidase. When stimulated by contact with bacteria, neutrophils exhibit a respiratory burst (see below) and produce superoxide in a reaction catalyzed by NADPH oxidase (reaction 2). Superoxide spontaneously dismu-tates to form H2O2 and O2 however, the rate of this same reaction is speeded up tremendously by the action of the enzyme superoxide dismutase (reaction 3). Hydrogen peroxide is subject to a number of fates. The enzyme catalase, present in many types of cells, converts... [Pg.611]

Meltzer, S., Goldberg, B., Lad, P. and Easton, J. (1989). Superoxide generation and its modulation by adenosine in neutrophils of subjects with asthma. J. Allergy Clin. Immunol. 83, 960-966. [Pg.230]

Lee SC, Brummet ME, Shahabuddin S, et al. Cutaneous injection of human subjects with macrophage inflammatory protein-1 alpha induces significant recruitment of neutrophils and monocytes. J Immunol 2000 164 3392-3401. [Pg.83]

A study of 148000 subjects by Lanza and colleagues (1987) reported 36 individuals with myeloperoxidase deficiency, 10 of whom were completely deficient a further 2 individuals with total deficiency were identified from familial studies. Of the 12 patients with total deficiency, 7 had either benign or malignant tumours, but none was undergoing radio- or chemotherapy at the time of analysis hence, the myeloperoxidase deficiency could not be attributed, in these cases, to the therapy used for treatment of the malignant disease. These findings imply either that the tumour somehow affects the expression of myeloperoxidase in these patients, or that myeloperoxidase-deficient individuals perhaps have an increased incidence of tumours. Much follow-up work is needed for these studies on myeloperoxidase-deficient neutrophils in order to evaluate these proposals. [Pg.276]

CGD) Defect due to mutation in neutrophil enzyme NADPH oxidase gene coding for any one of the four subunits of the enzyme Patients subject to recurrent infections by catalase-positive organisms and to granuloma formation X-Unked mutation more severe... [Pg.253]

The finely tuned hematopoietic system, however, sometimes breaks down. Neutropenia—decreased blood neutrophil numbers below 1800 cells/mm —is a clinical condition in which neutrophilic leukocytes in the blood fall two standard deviations below normal. Leukopenia and granulocytopenia are terms that are generally used interchangeably with neutropenia. Recurrent infections which typically are inconsequential in healthy subjects, could produce significant consequences in neutropenia, and can be devastating for immunocompromised patients. There are many acquired causes of neutropenia, with... [Pg.132]

Lysis of antibody-coated red cells through the products of the respiratory burst appears to be linked to phagocytosis Neutrophils from patients with chronic granulomatous disease lysed antibody-coated erythrocytes less effectively than PMNs from norma subjects in suspension, but when phagocytosis was prevented by attachment of the erythrocytes to plastic or by treatment with colchicine, PMNs from the patients with chronic granulomatous disease lysed the red cells normally. [Pg.60]

The Hi Receptor and its Ligands. The H receptor mediates effects, through an increase in cyclic adenosine monophosphate (cAMP). such as gastric acid secretion relaxation of airway smooth muscle and of pulmonary vessels increased lower airway mucus secretion esophageal contraclion inhibition of basophil, but not mas cell histamine release inhibition of neutrophil activation and induction or suppressor T cells. There is no evidence that the H- receptor causes significant modulation of lung function in the healthy human subject or in the asthmatic. [Pg.777]

In addition to the classical symptoms of zinc deficiency mentioned above, the following unusual conditions have been reported liver and spleen enlargement, abnormal dark adaptation and abnormalities of taste. Several laboratory procedures for diagnosing zinc deficiency are available. Measurement of zinc levels in plasma is useful in certain cases. Levels of zinc in the red cells and hair may be used for assessment of body zinc status. More accurate and useful parameters are neutrophil zinc determination and quantitative assay of alkaline phosphatase activity in neutrophils. Determination of zinc in 24 h urine may help diagnose deficiency if sickle cell disease, chronic renal disease and liver cirrhosis are ruled out. A metabolic balance study may clearly distinguish zinc-deficient subjects. [Pg.765]

It is well recognized that antithyroid drugs, and especially propylthiouracil, can be associated with development of anti-neutrophil cytoplasmic antibody (ANCA)-positive vasculitis, often manifesting as renal disease. Atypical presentations, with pyoderma gangrenosum (49) and progressive bilateral sensorineural hearing loss (50), have been described in separate case reports of subjects taking propylthiouracil. [Pg.349]

The neutrophil-mediated clearance was expressed as a Michaelis-Menten function, because G-CSF receptor binding is subject to saturation. The product of kcat and the ratio of ANC and ANC at baseline is the maximum velocity of drug elimination from this pathway, km is the Michaelis constant, and C is the pegfilgrastim concentration. CL2 denotes the linear clearance pathway. [Pg.380]

In an interesting experimental protocol, Silvestro et al. (1993) utilized HPLC-mass spectrometry with an ion spray (electrospray) interface for determination of PAF and lysoPAF in human PMN (neutrophils). Both unstimulated and stimulated (with complement-activated zymosan) cells were used as starting material. The total lipids were isolated in the usual way, and the PAF was isolated and purified by a combination of thin-layer chromatography, HPLC, and silica chromatography. This final PAF preparation was subjected to a bioassay with the inclusion of 3H 16 0 PAF to monitor recoveries. [Pg.173]


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