Therefore, the link between hypoxia and STOX1 exists, but probably in a subtle form. In conclusion, our study indicates that STOX1 deserves further investigation for its role in the aetiology of preeclampsia. The detection of Streptococcus oralis is in agreement with a 21% prevalence of Streptococcus spp. at endodontical of previously treated teeth. Bacterial migration between endodontium and periodontium has been previously established. Our results validated our postulate that it is possible to retrieve bacterial DNA in the dental pulp during a bacteremia. The procedure we developed provides a new tool for the retrospective diagnostic of bacteremia in patients who benefited dental extraction since the dental pulp is equivalent to a small blood culture. It would allow to broader the spectrum of bacteremic organisms detectable in the dental pulp, beyond the scope of Y. pestis, B. quintana in humans and B. henselae in cats. It may help resolve the aetiology of historical epidemics of unknown aetiology such as the 15�C17th century episodes known as the London plague. Later episodes were investigated without success, no evidence of Y. pestis was found so that the cause of these episodes remains uncertain. The metabolic basis of type 2 diabetes mellitus has traditionally had hyperglycemia as its sine qua non, despite generally being accompanied by a long prior history of obesity together with relative physical Apoptosis Activator 2 inactivity. Evidence suggests that blood vessel dysfunction, either overt or inducible, is detectable prior to rises in blood glucose, as Equol occurs in the disease itself. Debate over whether glucose is the direct cause of the blood vessel damage has not yet been resolved. Many lines of evidence suggest that hyperglycemia may not be the earliest metabolic change in the complications of T2DM. One, based on current treatment results in clinical trials, is that complications are not prevented by glycemic control, intensive or not, confirmed by the latest very large trials of dipeptidyl peptidase-4 inhibitors. Earlier evidence suggested that microvascular components were delayed more by lowered blood pressure than by tight blood glucose control.