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

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William M. Armstead

Departments of Anesthesia and Pharmacology

University of Pennsylvania

Philadelphia

Pennsylvania 19104

USA

[email]@*.med.upenn.edu

Name/email consistency: high

 
 
 
 
 
 
 

Affiliation

  • Departments of Anesthesia and Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. 2000 - 2003

References

  1. Protein kinase C activation generates superoxide and contributes to impairment of cerebrovasodilation induced by G protein activation after brain injury. Armstead, W.M. Brain Res. (2003) [Pubmed]
  2. NOC/oFQ activates PKC and generates superoxide to impair hypotensive cerebrovasodilation after hypoxia/ischemia. Armstead, W. Med. Sci. Monit. (2002) [Pubmed]
  3. NOC/oFQ and NMDA contribute to piglet hypoxic ischemic hypotensive cerebrovasodilation impairment. Armstead, W.M. Pediatr. Res. (2002) [Pubmed]
  4. Protein tyrosine kinase and mitogen-activated protein kinase activation contribute to K(ATP) and K(ca) channel impairment after brain injury. Armstead, W.M. Brain Res. (2002) [Pubmed]
  5. Age-dependent NOC/oFQ contribution to impaired hypotensive cerebral hemodynamics after brain injury. Armstead, W.M. J. Neurotrauma (2002) [Pubmed]
  6. G protein activation elicits cerebrovasodilation through interaction with K(ATP) and K(Ca) channels. Armstead, W.M. Brain Res. (2002) [Pubmed]
  7. Role of Nociceptin/Orphanin FQ in the physiologic and pathologic control of the cerebral circulation. Armstead, W.M. Exp. Biol. Med. (Maywood) (2002) [Pubmed]
  8. Age dependent endothelin contribution to NOC/oFQ induced impairment of NMDA cerebrovasodilation after brain injury. Armstead, W.M. Peptides (2001) [Pubmed]
  9. Vasopressin-induced protein kinase C-dependent superoxide generation contributes to atp-sensitive potassium channel but not calcium-sensitive potassium channel function impairment after brain injury. Armstead, W.M. Stroke (2001) [Pubmed]
  10. Age-Dependent vasopressinergic modulation of Noc/oFQ-induced impairment of NMDA cerebrovasodilation after brain injury. Armstead, W.M. J. Neurotrauma (2001) [Pubmed]
  11. Vasopressin induced cyclooxygenase dependent superoxide generation contributes to K(+) channel function impairment after brain injury. Armstead, W.M. Brain Res. (2001) [Pubmed]
  12. Endothelin-Induced cyclooxygenase-dependent superoxide generation contributes to K+ channel functional impairment after brain injury. Armstead, W.M. J. Neurotrauma (2001) [Pubmed]
  13. Relationship between nociceptin/orphanin FQ and cerebral hemodynamics after hypoxia-ischemia in piglets. Armstead, W.M. Am. J. Physiol. Heart Circ. Physiol. (2000) [Pubmed]
  14. NOC/oFQ contributes to hypoxic-ischemic impairment of N-methyl-D-aspartate-induced cerebral vasodilation. Armstead, W.M. Brain Res. (2000) [Pubmed]
  15. Role of NOC/oFQ in impaired opioid-induced pial artery dilation following brain injury. Armstead, W.M. Brain Res. (2000) [Pubmed]
  16. Age-dependent cerebral hemodynamic effects of traumatic brain injury in newborn and juvenile pigs. Armstead, W.M. Microcirculation (2000) [Pubmed]
  17. Role of nociceptin/orphanin FQ in age-dependent cerebral hemodynamic effects of brain injury. Armstead, W.M. J. Neurotrauma (2000) [Pubmed]
  18. NOC/oFQ contributes to age-dependent impairment of NMDA-induced cerebrovasodilation after brain injury. Armstead, W.M. Am. J. Physiol. Heart Circ. Physiol. (2000) [Pubmed]
  19. NOC/oFQ PKC-dependent superoxide generation contributes to hypoxic-ischemic impairment of NMDA cerebrovasodilation. Armstead, W.M. Am. J. Physiol. Heart Circ. Physiol. (2000) [Pubmed]
  20. Role of altered cyclooxygenase metabolism in impaired cerebrovasodilation to nociceptin/orphanin FQ following brain injury. Armstead, W.M. Brain Res. Bull. (2000) [Pubmed]
 
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