Renal tubular dysgenesis, a not uncommon autosomal recessive disorder leading to oligohydramnios: Role of the Renin-Angiotensin system.

Renal tubular dysgenesis is a clinical disorder that is observed in fetuses and characterized by the absence or poor development of proximal tubules, early onset and persistent oligohydramnios that leads to the Potter sequence, and skull ossification defects. It may be acquired during fetal development or inherited as an autosomal recessive disease. It was shown recently that autosomal recessive renal tubular dysgenesis is genetically heterogeneous and linked to mutations in the genes that encode components of the renin-angiotensin system.

Characterization of a plasma membrane-resident albumin-binding protein associated with the proliferation of estrogen-target, serum-sensitive cells.

Estrogens control the proliferation of their target cells through a receptor-mediated pathway. Recently presented evidence suggests that estradiol cancels the proliferative inhibition exerted by human albumin (HA) and recombinant human albumin (rHA) on estrogen-target serum-sensitive cells (indirect-negative hypothesis). We postulate that this mechanism requires the presence of a plasma membrane estrogen receptor (mER) and a plasma membrane albumin-binding protein (mABP).

Chronic pain induces a paradoxical increase in growth hormone secretion without affecting other hormones related to acute stress in the rat.

In several diseases chronic pain is associated with long-lasting pathophysiological responses which differ strongly from those observed in acute situations. When persisting, acute pain often results in physical and psychological stress which may in turn aggravate the initial pathological state. In the present work we examined the secretory patterns of pituitary hormones related to acute stress (growth hormone (GH), prolactin (PRL) and beta-endorphin (beta-END)) in rats during the phase of Freund adjuvant-induced arthritis (AIA, a model used for chronic pain studies) when chronic pain is maximum (14 and 21 days, postinoculation (PI)).