The articles in German and French were assembled in a four-volume book entitled “Moritz Schiff’s Gesammelte Beiträge Zur Physiologie” (Lausanne, 1894–1898). In volume 1, Schiff himself rearranged some of his articles on centers in the nervous system that are related to respiration. Immediately after his death, the British Medical Journal published a highly praising obituary but, Inhibitors,research,lifescience,medical in the last century, there were only a few attempts

1,5,13,18,20–22 to recognize Schiff’s contributions to signaling pathway nearly all fields of physiology, at a period when experimental physiology was still taking its formative steps. Schiff should also be regarded as a person who paid dearly for his adherence to the ideas of freedom and liberalism and to genuine physiological research. His Inhibitors,research,lifescience,medical personality, contributions, and impact deserve a thorough biography. Footnotes Conflict of interest: No potential conflict of interest relevant to this article was reported.
In 1988, Brenner, Anderson, and Garcia suggested that a low nephron number, acquired in

utero, may be a common denominator in populations with high susceptibility to hypertension and renal disease.1 Such a kidney with fewer nephrons, and hence a low filtration surface area, would Inhibitors,research,lifescience,medical have a reduced capacity to excrete sodium, inducing a hypervolemic state, thereby contributing to the development of hypertension (Figure 1). Animal experiments and epidemiological data have accumulated in support of this “nephron Inhibitors,research,lifescience,medical number” hypothesis.2–8 Nephron number varies surprisingly widely among individuals, more, for example, than height or weight, with a variability of up to 10-fold within select populations.5,6,9–17 An individual’s nephron number is the result of a complex interplay between genetics and environment that plays out through their Inhibitors,research,lifescience,medical lifetime, carrying the imprint of their past, being reflected in their present renal function, and impacting their future risk of hypertension and kidney disease. Figure

1 Known causes of low nephron number. Linifanib (ABT-869) DETERMINANTS OF NEPHRON NUMBER Prenatal Life and Birth Weight Kidney development in humans begins in the 9th week and ends around the 36th week of gestation.5 There is no evidence for postnatal nephrogenesis in humans, except in extremely preterm infants in whom abnormal nephrogenesis was observed until day 40 after birth.16,18 Similarly, in preterm baboons followed for 21 days after birth, nephrogenesis did continue, but the proportion of immature, poorly vascularized and abnormal glomeruli was increased compared to gestational controls.19 In young adult rats exposed to a low protein diet in utero, glomerulogenesis was retarded with a higher proportion of immature nephrons, associated with abnormalities in the glomerular basement membrane and podocyte structure.