Interferon-gamma impedes reverse cholesterol transport and promotes foam cell transformation in THP-1 human monocytes/macrophages.

Background: Cholesterol 27-hydroxylase, an enzyme expressed at high levels by human monocytes/macrophages, provides a first line of defense against the development of atherosclerosis. Prior studies have suggested that the cytokine interferon-gamma (IFN-gamma) promotes atherosclerosis. We therefore examined the effect of IFN-g on macrophage foam cell formation and on expression of the anti-atherogenic 27-hydroxylase in THP-1 human monocytes/macrophages.

Thermo-osmoregulation of heat-labile enterotoxin expression by Escherichia coli.

Enterotoxigenic Escherichia coli causes diarrhea by producing several virulence factors including heat-labile enterotoxin (LT). LT is maximally expressed at 37 degrees C. The histone-like nucleoid structuring protein (H-NS) appears to inhibit LT expression by binding to a downstream regulatory element (DRE) at low temperatures.

Role of estradiol metabolism and CYP1A1 polymorphisms in breast cancer risk.

The endogenous metabolism of estrogens is primarily oxidative and involves hydroxylation of the steroid at either C2 (2-OHE1) or C16 (16-OHE1). While the 2-OHE1 metabolites are essentially devoid of peripheral biological activity, 16-OHE1 is an estrogen agonist. There is evidence of an association between the 2-OHE1/16-OHE1 metabolites ratio and breast cancer risk.

Temperature regulation of heat-labile enterotoxin (LT) synthesis in Escherichia coli is mediated by an interaction of H-NS protein with the LT A-subunit DNA.

Protein and mRNA levels of heat-labile enterotoxin (LT) of Escherichia coli are highest at 37 degrees C, and they decrease gradually as temperature is decreased. This temperature effect is eliminated in an Hns- mutant. Deletion of portions of DNA coding for the LT A subunit also results in an increase in LT expression at low temperatures, suggesting that the H-NS protein causes inhibition of transcription at low temperatures by interacting with the LT A-subunit DNA.

Lung cancer risk and CYP1A1 genotype in African Americans.

The role of CYP1A1 genotype in lung cancer risk was assessed in African Americans through a case control study. The complete CYP1A1 genotype, including the frequency of all three polymorphisms (Msp1 [CYP1A1*2], exon 7 [CYP1A1*3] and African American specific [CYP1A1*4]) was determined by PCR on 307 controls and 105 cases of lung cancer among African Americans. We have confirmed our earlier observation of a significant increased risk (odds ratio = 2.