BackgroundIt is well documented that there is some correlation between poor oral health in the form of periodontal disease and coronary heart disease (CHD). It is unclear whether this correlation is due to a causal relationship or shared underlying disorder such as inflammation. A suitable integrated model of the CHD pathogenetic pathways relevant to periodontal disease may help to elucidate the association. Such a model is currently not available in literature.MethodsA previously developed integrated model of CHD was used to investigate potential pathogenetic pathways linking periodontal disease to CHD biomarkers.ResultsThe integrated model was created to provide insight into possible higher-order biological interactions underlying CHD and periodontal disease. In order to simplify these interactions a novel ‘connection graph’ was developed. It quantitatively illustrates the relationship between periodontal disease and various serological biomarkers of CHD. The pathogenesis of periodontitis shows various possible pathways which could link periodontitis to CHD pathogenesis.ConclusionAn integrated model of CHD was developed which provides a summary of the potential CHD effects of periodontal disease. Further research must refine and validate the model.

SummaryBackground:Moderate exercise is associated with a lower risk for coronary heart disease (CHD). A suitable integrated model of the CHD pathogenetic pathways relevant to moderate exercise may help to elucidate this association. Such a model is currently not available in the literature.Methods:An integrated model of CHD was developed and used to investigate pathogenetic pathways of importance between exercise and CHD. Using biomarker relative-risk data, the pathogenetic effects are representable as measurable effects based on changes in biomarkers.Results:The integrated model provides insight into higherorder interactions underlying the associations between CHD and moderate exercise. A novel ‘connection graph’ was developed, which simplifies these interactions. It quantitatively illustrates the relationship between moderate exercise and various serological biomarkers of CHD. The connection graph of moderate exercise elucidates all the possible integrated actions through which risk reduction may occur.Conclusion:An integrated model of CHD provides a summary of the effects of moderate exercise on CHD. It also shows the importance of each CHD pathway that moderate exercise influences. The CHD risk-reducing effects of exercise appear to be primarily driven by decreased inflammation and altered metabolism.

BackgroundDue to their high proliferative requirements, tumorigenic cells possess altered metabolic systems whereby cells utilize higher quantities of glutamine and glucose. These altered metabolic requirements make it of interest to investigate the effects of physiological non-tumorigenic concentrations of glucose and glutamine on tumorigenic cells since deprivation of either results in a canonical amino acid response in mammalian cell.MethodsThe influence of short-term exposure of tumorigenic cells to correlating decreasing glutamine- and glucose quantities were demonstrated in a highly glycolytic metastatic breast cell line and a cervical carcinoma cell line. Thereafter, cells were propagated in medium containing typical physiological concentrations of 1 mM glutamine and 6 mM glucose for 7 days. The effects on morphology were investigated by means of polarization-optical transmitted light differential interference contrast. Flow cytometry was used to demonstrate the effects of glutamine-and glucose starvation on cell cycle progression and apoptosis induction. Fluorometrics were also conducted to investigate the effects on intrinsic apoptosis induction (mitocapture), reactive oxygen species production (2,7-dichlorofluorescein diacetate) and acidic vesicle formation (acridine orange).ResultsMorphological data suggests that glutamine-and glucose deprivation resulted in reduced cell density and rounded cells. Glutamine-and glucose starvation also resulted in an increase in the G2M phase and a sub-G1 peak. Complete starvation of glutamine and glucose resulted in the reduction of the mitochondrial membrane potential in both cell lines with MDA-MB-231 cells more prominently affected when compared to HeLa cells. Further, starved cells could not be rescued sufficiently by propagating since cells possessed an increase in reactive oxygen species, acidic compartments and vacuole formation.ConclusionStarvation from glutamine and glucose for short periods resulted in decreased cell density, rounded cells and apoptosis induction by means of reactive oxygen species generation and mitochondrial dysfunction. In addition, the metastatic cell line reacted more prominently to glutamine-and glucose starvation due to their highly glycolytic nature. Satisfactory cellular rescue was not possible as cells demonstrated oxidative stress and depolarized mitochondrial membrane potential. This study contributes to the knowledge regarding the in vitro effects and signal transduction of glucose and/or l-glutamine deprivation in tumorigenic cell lines.

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The nature of the solid phase was determined by two methods. In the case of the hexahydrate, the moist residues in three instances were centrifuged, and the crystals analyzed. The values obtained were 6.16, 6.2 and 6.0 molecules of water per molecule of magnesium nitrate. The dihydrate and the anhydride were so hygroscopic that this method was not feasible.Here the "tie line'' method was used. The total residue was dissolved in a weighed amount of water, and its composition determined by analysis. The "tie lines" are plotted on Fig. 1, and indicate the existence of the solid phases mentioned above. SummaryThe equilibrium diagram for the ternary system magnesium nitratenitric acid-water at 25°has been established.The forms of magnesium nitrate in stable equilibrium with nitric acid at 25°are the hexahydrate, the dihydrate and the anhydride.