Characterization of early and terminal complement proteins associated with polymorphonuclear leukocytes in vitro and in vivo after spinal cord injury.

Membrane attack complex formation on yeast as trigger of selective release of terminal complement proteins from human polymorphonuclear leukocytes.

Activation of complement pathways after contusion-induced spinal cord injury.

Studies on the mechanism of bacterial resistance to complement-mediated killing. VI. IgG increases the bactericidal efficiency of C5b-9 for E. coli 0111B4 by acting at a step before C5 cleavage.

Human polymorphonuclear leukocytes store large amounts of terminal complement components C7 and C6, which may be released on stimulation.

Attenuation of experimental allergic encephalomyelitis in complement component 6-deficient rats is associated with reduced complement C9 deposition, P-selectin expression, and cellular infiltrate in spinal cords.

Complement fixation by pemphigus antibody. V. Assembly of the membrane attack complex on cultured human keratinocytes.

Increased growth factor expression and cell proliferation after contusive spinal cord injury.

Activation of human complement by IgG antisperm antibody and the demonstration of C3 and C5b-9-mediated immune injury to human sperm.

Dynamics of the inflammatory response after murine spinal cord injury revealed by flow cytometry.

The killer molecule of complement.

Upregulation of EphA3 receptor after spinal cord injury.

Soluble complement receptor type 1 inhibits the complement pathway and prevents contractile failure in the postischemic heart. Evidence that complement activation is required for neutrophil-mediated reperfusion injury.

Antibody-mediated complement activation on nucleated cells. A quantitative analysis of the individual reaction steps.

Characterization of neuronal cell death induced by complement activation.

Recombinant C345C and factor I modules of complement components C5 and C7 inhibit C7 incorporation into the complement membrane attack complex.

Consequences of noggin expression by neural stem, glial, and neuronal precursor cells engrafted into the injured spinal cord.

Expression of hepatocyte growth factor and c-Met after spinal cord injury in rats.

Pathological CNS autoimmune disease triggered by traumatic spinal cord injury: implications for autoimmune vaccine therapy.

Upregulation of the HLH Id gene family in neural progenitors and glial cells of the rat spinal cord following contusion injury.