Several postmortem studies report
the presence of inflammatory markers in the brains of depressed or mood - disordered patients.
Not exact matches
Current projects are investigating: 1) the expression
of inflammatory genes during ischemia and reperfusion
of kidneys during urology transplantation and in mouse models; 2) the expression
of inflammatory genes and proteins in urine as
markers indicating the
presence of rejection in renal allografts; and 3) the role
of adhesion molecules and chemokines in directing leukocyte infiltration into organ allografts.
These syndromes include conditions in which autoimmunity is clearly implicated as causal, in light
of identification
of autoantibodies to relevant autoantigens; diseases suspected to be autoimmune because
of the
presence of autoantibodies, although the autoreactive response has not been proven to be pathogenic and could be a consequence or
marker of tissue damage; and other diseases often considered to be «autoimmune,» such as psoriasis or
inflammatory bowel disease, characterized by organ - targeted inflammation but without evidence
of a stimulating autoantigen.
These
markers can be used to differentiate between inflammation associated with Crohn's disease or ulcerative colitis (IBD —
inflammatory bowel disease), and less severe inflammation (IBS — irritable bowel syndrome) that can be associated with the
presence of bacteria or yeast overgrowth.
These
markers can be used to differentiate between inflammation associated with potentially life - threatening
inflammatory bowel disease (IBD), which requires lifelong treatment, and less severe inflammation that can be associated with irritable bowel syndrome (IBS) which is frequently due to the
presence of enteroinvasive pathogens.
These
markers can be used to differentiate between inflammation associated with potentially life threatening
inflammatory bowel disease (IBD), which requires life long treatment, and less severe inflammation that can be associated with the
presence of enteroinvasive pathogens.