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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Neutrophils

 
 
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Disease relevance of Neutrophils

 

Psychiatry related information on Neutrophils

 

High impact information on Neutrophils

 

Chemical compound and disease context of Neutrophils

 

Biological context of Neutrophils

 

Anatomical context of Neutrophils

  • Administration of recombinant GM-CSF resulted in dose-dependent increases in circulating leukocytes and in increases in circulating neutrophils, eosinophils, and monocytes [25].
  • The serums of five patients with idiopathic neutropeniaopsonized normal neutrophils, causing them to be ingested by rabbit macrophages or else to activate glucose oxidation rates of other normal neutrophils by at least twice the rate of controls [26].
  • The adherence of neutrophils to bovine endothelial-cell monolayers pretreated with leukotriene B4 was inhibited completely, and their average chemotactic response to leukotriene B4 was inhibited by 70 per cent, as compared with values determined before the diet was begun and six weeks after its discontinuation [27].
  • F(ab')2 fragments of a monoclonal antibody, 25E11, raised against activated large granular lymphocytes, inhibited killing by natural killer cells, blocked the binding of fibronectin-coated particles by monocytes, and stimulated neutrophils to exhibit increased antibody-dependent killing [28].
  • Results. Treatment with granulocyte CSF accelerated the recovery of neutrophils significantly (P less than 0.01), shortening it by about a week, but it had no effect on platelet recovery [29].
 

Associations of Neutrophils with chemical compounds

 

Gene context of Neutrophils

  • Granulocyte colony-stimulating factor (G-CSF) is a cytokine that regulates the proliferation and differentiation of neutrophils [35].
  • Thus, matrilysin-mediated shedding of syndecan-1/KC complexes from the mucosal surface directs and confines neutrophil influx to sites of injury [4].
  • Cells transfected with VCAM-1 bind the human leukemia lines Jurkat, Ramos, Raji, HL60, and THP1, but not peripheral blood neutrophils [36].
  • In matrilysin null mice, neutrophils remained confined in the interstitium of injured lungs and did not advance into the alveolar space [4].
  • EPIs inhibit the growth of epithelial cells but induce them to secrete the neutrophil attractant IL-8, while PEPI blocks neutrophil activation by tumor necrosis factor, preventing release of oxidants and proteases [37].
 

Analytical, diagnostic and therapeutic context of Neutrophils

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