Multilayer Film Elements for Clinical Analysis: General Concepts

Curme, H.G.; Columbus, Richard S; Dappen, Glenn M; Eder, Thomas W; Fellows, Williams D; Figueras, John; Glover, Clyde P; Goffe, C A; Hill, D. E.; Lawton, William H.; Muka, Edward; Pinney, J. E.; Rand, R N; Sandford, Kari J; Wu, Tal W

doi:10.1093/clinchem/24.12.2202

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“…Glucose Determination. Levels of glucose in serum samples were measured using glucose oxidase reagent kit (KODAK Ektachem Clinical Chemistry Slide) as described elsewhere (20). In this assay, hydrogen peroxide is detected based on its oxidant activity in a peroxidase-catalyzed oxidative-coupling reaction in the presence of chromogen to form a dye.…”

Section: Measurements Of Acth In Plasmamentioning

confidence: 99%

Role of interleukin 6 (IL-6) in protection from lethal irradiation and in endocrine responses to IL-1 and tumor necrosis factor.

Neta¹,

Perlstein²,

Vogel³

et al. 1992

The Journal of Experimental Medicine

118

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Primary responsibility for the induction of various acute phase reactions has been ascribed to interleukin 1 (IL-1), tumor necrosis factor (TNF), or IL-6, suggesting that these cytokines may have many overlapping activities. Thus, it is difficult to identify the cytokine primarily responsible for a particular biologic effect, since IL-1 and TNF stimulate one another, and both IL-1 and TNF stimulate IL-6. In this work, the contribution of IL-6 in radioprotection, induction of adrenocorticotropic hormone (ACTH), and induction of hypoglycemia was assessed by blocking IL-6 activity. Administration of anti-IL-6 antibody to otherwise untreated mice greatly enhanced the incidence of radiation-induced mortality, indicating that like IL-1 and TNF, IL-6 also contributes to innate resistance to radiation. Anti-IL-6 antibody given to IL-1-treated or TNF-treated mice reduced survival from lethal irradiation, demonstrating that IL-6 is also an important mediator of both IL-1- and TNF-induced hemopoietic recovery. A similar IL-1/IL-6 interaction was observed in the case of ACTH induction. Anti-IL-6 antibody blocked the IL-1-induced increase in plasma ACTH, whereas recombinant IL-6 by itself did not induce such an increase. Anti-IL-6 antibody also mitigated TNF-induced hypoglycemia, but did not reverse IL-1-induced hypoglycemia. It is, therefore, likely that TNF and IL-1 differ in their mode of induction of hypoglycemia. Our results suggest that an interaction of IL-6 with IL-1 and TNF is a prerequisite for protection from radiation lethality, and its interaction with IL-1 for induction of ACTH.

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Section: Measurements Of Acth In Plasmamentioning

confidence: 99%