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cAMP assay and measurement of expression of cAMP-regulated genes were conducted to determine the relationship between external glucose concentration and cAMP levels inside Escherichi coli. Results reveal that E. coli controls its cAMP levels through two or more transitions influenced by external glucose concentration and does not respond to decreasing saturation of glucose transport. Furthermore, results present implications for models of phosphotransferase-mediated regulation of adenylate cyclase.

Endogenous inducer synthesis under conditions of reduced nutrient availability represents a natural adaptation to increase the ability of Escherichia coli for scavenging glucose. Exogenous induction exhibits no influence on bacterial growth with limiting carbohydrates. Endogenous galactose and cyclic AMP pools are enough for high expression of mgl and gal genes. A functional galETK operon is essential for limitation-induced induction of mgl. Mgl/gal induction exhibits a better correlation with inducer availability than with cAMP concentrations. Internal inducer synthesis is minimum during oligotrophic conditions.

LamB protein is the general glycoporin in the Escherichia coli outer membrane. Contrary to an earlier finding, the LamB- phenotype exhibited reduced competitive abilities when cultured together with LamB+ bacteria in conditions with carbohydrate concentration as the limiting factor. Further, LamB was demonstrated to have a more extensive sugar transportfunction than mere maltosaccharide uptake.

Presents the results of a study which was conducted to determine the relationship between external glucose concentration and cAMP levels inside Escherichia coli. Outline of the hypothesis; Methods used to conduct the study; Study findings.

There exists a striking gender difference in atherosclerotic vascular disease. For decades, estrogen was considered atheroprotective; however, an alternative is that androgen exposure in early life may predispose men to earlier atherosclerosis. We recently demonstrated that the potent androgen, dihydrotestosterone (DHT), enhanced the binding of monocytes to the endothelium, a key early event in atherosclerosis, via increased expression of vascular cell adhesion molecule-1 (VCAM-1). We now show that DHT mediates its effects on VCAM-1 expression at the promoter level through a novel androgen receptor (AR)/nuclear factor-kappaB (NF-kappaB) mechanism. Human umbilical vein endothelial cells were exposed to 4-400 nm DHT. DHT increased VCAM-1 mRNA in a dose- and time-dependent manner. The DHT effect could be blocked by the AR antagonist, hydroxyflutamide. DHT increased VCAM-1 promoter activity via NF-kappaB activation without affecting VCAM-1 mRNA stability. Using 5' deletion analysis, it was determined that the NF-kappaB sites within the VCAM-1 promoter region were responsible for the DHT-mediated increase in VCAM-1 expression; however, coimmunoprecipitation studies suggested there is no direct interaction between AR and NF-kappaB. Instead, DHT treatment decreased the level of the NF-kappaB inhibitory protein. DHT did not affect VCAM-1 protein expression and monocyte adhesion when female endothelial cells were tested. AR expression was higher in male, relative to female, endothelial cells, associated with increased VCAM-1 levels. These findings highlight a novel AR/NF-kappaB mediated mechanism for VCAM-1 expression and monocyte adhesion operating in male endothelial cells that may represent an important unrecognized mechanism for the male predisposition to atherosclerosis.