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Inflammatory phase

Employ during the acute inflammatory phase, 1-5 days after injury. Prevent further injury... [Pg.903]

Lloyd CM, Minto AW, Dorf ME, et al. RANTES and monocyte chemoattractant protein-1 (MCP-1) play an important role in the inflammatory phase of crescentic nephritis, but only MCP-1 is involved in crescent formation and interstitial fibrosis. J Exp Med 1997 185(7) 1371-1380. [Pg.316]

Silybin (119) Flavonolignoid IdB 1016 (Silipide Silybin and phosphatidylcholine complex Silophos ) Oncology Antioxidant and anti-inflammatory Phase II (cancer chemo-prevention) American College of Gastroenterology/ Indena 714-719... [Pg.70]

Recent studies revealed that resveratrol protects from inflammation by acting at different phases of inflammation. Protection at the pro-inflammatory phase appears to be very important for reducing inflammation effectively and promptly. A recent study [Ge et al., 2006] showed that resveratrol inhibits macrophage expression of EMMPRIN by activating PPAR-y. In another similar study, Ma et al., [2006] showed a similar observation, but additionally found a role of nuclear transcription factor kB (NF-kB) in macrophage inhibition. Numerous studies confirmed that resveratrol suppresses the TNF-a... [Pg.311]

While inflammation is associated negatively with vasculitis and autoimmune disease, it is also necessary to protect normal cells from viral and bacterial infection. Many of the therapies that act positively as immunosuppressants have an initial inflammatory response. While lENp is an effective therapy in the inflammatory phases of MS, the initial response to each injection is an increase in inflammatory cytokines, IL-2 and lENy (Elliott et al., 2001). Conversely, natalizumab a therapy that show ed great potential in phase EE trials for aggressive MS by blocking activated lymphocyte trafficking into the CNS was withdrawn because of deaths due to progressive multifocal leukoencephalopathy. [Pg.286]

Both inflammatory andneurodegenerative components may contribute to the clinical profile of MS. Inflammation appears to be caused by overactive pro-inflammatory T helper 1 cells, initiating the inflammatory cascade. Current IFNp and glat-iramer acetate are most effective in this inflammatory phase of MS. Recent evidence also show s that inflammation may not only be destructive but may also play a part in tissue repair (Grigoriadis et al., 2006). [Pg.292]

Jose PJ, Moss IK, Maini RN, Williams TJ (1990) Measurement of the chemotactic complement fragment C5a in rheumatoid synovial fluids by radioimmunoassay Role of C5a in the acute inflammatory phase. Ann Rheum Dis 49 747-752. [Pg.688]

The absorption of excess exudate not only avoids tissue maceration but also removes exotoxins or cell debris that may retard growth or extend the inflammatory phase of the healing process. The balance between humidity and absorption is critical and excessive wick-ing must be avoided to prevent drying and necrosis. [Pg.1024]

Bacterial impermeability has a dual role. The wound will not heal if it is heavily infected. The inflammatory phase will be extended, and, unless topical or systemic antibacterial agents are used, a more general infection could result. However, a limited number of microorganisms are tolerated by most wounds, and the destructive or cleansing phase produced by phagocytic activity should result in a self-sterilized environment. The wound should be protected from secondary infection or, if still contaminated, be prevented from transmitting the infective organisms. [Pg.1024]

Inflammatory phase This phase lasts 1 or 2 days and consists of marked fibroblastic proliferation. In this stage, perforations may occur. [Pg.1226]

Alveolar lining fluid contains higher concentrations of glutathione (GSH) than found in most extracellular fluids (151). The concentration of GSH in BALF from patients with IPF is 23% of normal (152). Depletion of GSH may place the alveolar space at increased risk of additional injury caused by ROS generated by the influx of inflammatory cells during the inflammatory phase of the development... [Pg.85]

A more recent model of inflammation is the killed Mycobacterium adjuvant arthritis test. Besides an acute inflammatory phase, it produces a secondary phase characterized by induction of an inflammatory lesion at sites distant from the initial lesion and also by the development of biochemical alterations measured by changes in blood fibrinogen, mucopolysaccharides and a-globulin. These distant changes may be mediated by the kinin systems, such as bradykinin. This new model is affected by most drugs active in the human arthritis and promises better predictive value than earlier models, which measured primarily the acute phases. It permits measuring in man and animals such biochemical parameters as inflammation units related to the a-globulins. Such measurements may... [Pg.176]

The inflammatory phase, which occurs immediately after injury to tissue and during which swelling takes place ... [Pg.111]

Intestinal tuberculosis is a chronic inflammation of the bowel caused by Mycobacterium tuberculosis. The ileocecal area is the most common site. The classic radiographic appearance of ileocecal tuberculosis on barium enema has been described as a conical, shrunken, retracted cecum associated with a narrow ulcerated terminal ileum (Reeder and Palmer 1989). This cecal deformity is the result of spasm early in the disease and transmural infiltration with fibrosis in advanced phases. Narrowing of the terminal ileum may be caused by persistent irritability with rapid emptying of the narrowed segment, corresponding to the acute inflammatory phase, or it may be the result of stricture with thickening and ulceration. [Pg.109]

During the course of the inflammatory phase of tissue healing, various signaling factors orchestrate the functional behaviors of immune cells. Thus, the extent of immune response can be modulated locally by incorporating appropriate bioactive signaling molecules into the biomaterial scaffold. These biochemical factors can direct cellular adhesion, chemotactic migration, or functional phenotypes. [Pg.168]


See other pages where Inflammatory phase is mentioned: [Pg.348]    [Pg.902]    [Pg.301]    [Pg.305]    [Pg.358]    [Pg.264]    [Pg.272]    [Pg.272]    [Pg.252]    [Pg.317]    [Pg.589]    [Pg.591]    [Pg.589]    [Pg.591]    [Pg.1033]    [Pg.209]    [Pg.212]    [Pg.74]    [Pg.434]    [Pg.120]    [Pg.225]    [Pg.446]    [Pg.192]    [Pg.74]    [Pg.157]    [Pg.159]    [Pg.160]    [Pg.238]    [Pg.32]    [Pg.102]    [Pg.63]   


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