Given the combination of large blood pressure effects and increased rates of glucose intolerance resting on a basis of prevalent obesity before middle age, which is characteristic for Nigeria today, it is not surprising that disability and deaths from stroke and coronary heart disease are rapidly increasing. To adequately address this trend in non-communicable diseases on a community level requires a developed health care (+)-JQ1 infrastructure providing life-long treatment and follow-up. The increasing burden of chronic diseases therefore poses a massive challenge to the already crippled health care systems of sub-Saharan Africa. In summary, our study demonstrates a fetal-infant contribution to adult hypertension and glucose intolerance in an African cohort. It can be assumed that fetal and infant undernutrition is a significant contributor to the increasing prevalence of hypertension and glucose intolerance also in other parts of sub-Saharan Africa. Therefore, prevention of fetal and infant undernutrition should be given high priority in national health, education, and economic agendas to limit the increase of non-communicable diseases in many African countries. Given that the highest risk for hypertension was found in those undernourished in early life and then growing overweight, it is appropriate to consider that preventing excess growth in later childhood may be as important for reducing adult ill-health as supporting fetal-infant growth. It is expressed in endothelial and epithelial tight junctions, by mononuclear cells, neutrophils and thrombocytes. In endothelial and epithelial cells, JAMA contributes to the paracellular solute barrier by formation of JAM-A homodimers within the cell membrane, binding homodimers of neighbouring cells. Upon inflammatory stimulation of endothelial cells, JAM-A redistributes from tight junctions to the apical cell surface where it mediates immune cell adhesion in vitro under static and flow conditions. Chemokine-triggered leukocyte transmigration across cultured EC is also mediated by endothelial JAM-A, however without endothelial JAM-A redistribution as a prerequisite. T-cell and neutrophil adhesion and transmigration governed by endothelial JAM-A were found to be mediated by aLb2-integrin on leukocytes, a result that could not be confirmed by another group. Together these studies indicated a tissuespecific role of endothelial JAM-A in the regulation of leukocyte extravasation. A soluble form of JAM-A can be detected in the peripheral blood. Increased sJAM-A plasma or serum levels compared to healthy controls were described in patients with coronary artery disease, arterial hypertension, systemic sclerosis, and renal insufficiency undergoing hemodialysis.