Does anybody publish work in stress and inflammation biomarkers?

Thanks for your prompt reply. I meant to find a collaborator in the US to pursue a NIH grant in caregiving stress induced coronary heart disease risk. My targeting biomarkers will be 12-hour urine catecholamin, blood cholesterol and carbohydrate metabolism (total cholesterol, HDL, HbA1c), DHE-S, hsCRP, MCP-1, IL-6 etc.

Hsueh-Fen Sabrina Kao

Thanks for your reply. I meant to find a collaborator in the US to pursue a NIH grant in caregiving stress induced coronary heart disease risk in community-based population. My targeting biomarkers will be 12-hour urine catecholamin, blood cholesterol and carbohydrate metabolism (total cholesterol, HDL, HbA1c), DHE-S, hsCRP, MCP-1, IL-6 etc.

Ilya B. Tsyrlov

Hi Hsueh-Fen,

As regards inflammation biomarkers like MCP-1 and IL-6, which could be trans-activated with low concentrations of bodily xenobiotics, please read our paper, entitled: REGULATORY REGION OF HUMAN GENES ENCODING MACROPHAGEAL TRANSCRIPTION FACTORS POSSESS MULTIPLE POTENTIAL DIOXIN RESPONSE ELEMENTS. Article in Organohalogen Compounds, volume 70, 1467-1472 (2008), by E. Oshchepkova, D. Furman, Dmitry Oshchepkov, and Ilya Tsyrlov

Abstract

Here, we propose with regard to pro-inflammatory and pre-malignancy cytokines that their AhR-mediated regulation by TCDD in macrophages might be executed by a dual mechanism: direct interaction of TCDD (at nanomolar concentrations) with promoter DRE of ultimate cytokine gene, and throughout a cascade of interrelated genes. The latter is epitomized by TCDD up-regulation of macrophageal transcription factors genes. Such genes, like RelA, possess multiple highly potential DREs, and therefore might be very susceptible to TCDD at low picomolar concentrations. Consequently, products of transcriptional factor gene expression could activate ultimate cytokine’s gene which itself is tolerant to the direct activation by low-dose TCDD treatment.

Best wishes,

Ilya

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