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The Nursing Clinics of North America
|
September 1, 1985
Space nursing. A professional challenge
M M Perrin
Immunology
|
May 1, 1990
Defective macrophage antigen presentation following haemorrhage is associated with the loss of MHC class II (Ia) antigens
A Ayala, M M Perrin, I H Chaudry
Cytokine
|
January 1, 1992
Differential effects of hemorrhage on Kupffer cells: decreased antigen presentation despite increased inflammatory cytokine (IL-1, IL-6 and TNF) release
A Ayala, M M Perrin, W Ertel, et al.
The Journal of Surgical Research
|
June 1, 1992
Sepsis induces an early increased spontaneous release of hepatocellular stimulatory factor (interleukin-6) by Kupffer cells in both endotoxin tolerant and intolerant mice
A Ayala, M M Perrin, P Wang, et al.
Immunology
|
July 1, 1993
The release of transforming growth factor-beta following haemorrhage: its role as a mediator of host immunosuppression
A Ayala, D R Meldrum, M M Perrin, et al.
Archives of Surgery (Chicago, Ill. : 1960)
|
January 1, 1990
Enhanced susceptibility to sepsis after simple hemorrhage. Depression of Fc and C3b receptor-mediated phagocytosis
A Ayala, M M Perrin, M A Wagner, et al.
Journal of Immunology (Baltimore, Md. : 1950)
|
December 15, 1991
Hemorrhage induces enhanced Kupffer cell cytotoxicity while decreasing peritoneal or splenic macrophage capacity. Involvement of cell-associated tumor necrosis factor and reactive nitrogen
A Ayala, M M Perrin, P Wang, et al.
Cytokine
|
May 1, 1990
Hemorrhage induces an increase in serum TNF which is not associated with elevated levels of endotoxin
A Ayala, M M Perrin, D R Meldrum, et al.
Immunology
|
October 1, 1991
Anti-TNF monoclonal antibodies prevent haemorrhage-induced suppression of Kupffer cell antigen presentation and MHC class II antigen expression
W Ertel, M H Morrison, A Ayala, et al.
Circulatory Shock
|
March 1, 1992
Polymicrobial sepsis selectively activates peritoneal but not alveolar macrophages to release inflammatory mediators (interleukins-1 and -6 and tumor necrosis factor)
A Ayala, M M Perrin, J M Kisala, et al.
Page
of 2
Search research articles
Search
Showing results (1-10 of 17) with videos related to
Sort By:
Page
of 2
The Nursing Clinics of North America
|
September 1, 1985
Space nursing. A professional challenge
M M Perrin
Immunology
|
May 1, 1990
Defective macrophage antigen presentation following haemorrhage is associated with the loss of MHC class II (Ia) antigens
A Ayala, M M Perrin, I H Chaudry
Cytokine
|
January 1, 1992
Differential effects of hemorrhage on Kupffer cells: decreased antigen presentation despite increased inflammatory cytokine (IL-1, IL-6 and TNF) release
A Ayala, M M Perrin, W Ertel, et al.
The Journal of Surgical Research
|
June 1, 1992
Sepsis induces an early increased spontaneous release of hepatocellular stimulatory factor (interleukin-6) by Kupffer cells in both endotoxin tolerant and intolerant mice
A Ayala, M M Perrin, P Wang, et al.
Immunology
|
July 1, 1993
The release of transforming growth factor-beta following haemorrhage: its role as a mediator of host immunosuppression
A Ayala, D R Meldrum, M M Perrin, et al.
Archives of Surgery (Chicago, Ill. : 1960)
|
January 1, 1990
Enhanced susceptibility to sepsis after simple hemorrhage. Depression of Fc and C3b receptor-mediated phagocytosis
A Ayala, M M Perrin, M A Wagner, et al.
Journal of Immunology (Baltimore, Md. : 1950)
|
December 15, 1991
Hemorrhage induces enhanced Kupffer cell cytotoxicity while decreasing peritoneal or splenic macrophage capacity. Involvement of cell-associated tumor necrosis factor and reactive nitrogen
A Ayala, M M Perrin, P Wang, et al.
Cytokine
|
May 1, 1990
Hemorrhage induces an increase in serum TNF which is not associated with elevated levels of endotoxin
A Ayala, M M Perrin, D R Meldrum, et al.
Immunology
|
October 1, 1991
Anti-TNF monoclonal antibodies prevent haemorrhage-induced suppression of Kupffer cell antigen presentation and MHC class II antigen expression
W Ertel, M H Morrison, A Ayala, et al.
Circulatory Shock
|
March 1, 1992
Polymicrobial sepsis selectively activates peritoneal but not alveolar macrophages to release inflammatory mediators (interleukins-1 and -6 and tumor necrosis factor)
A Ayala, M M Perrin, J M Kisala, et al.
Page
of 2