Sex steroid ablation enhances lymphoid recovery following autologous hematopoietic stem cell transplantation.

Background: Autologous hematopoietic stem cell transplantation (auto-HSCT) patients experience long-term immunosuppression, which increases susceptibility to infection and relapse rates due to minimal residual disease (MRD). Sex steroid (SS) ablation is known to reverse age-related thymic atrophy and decline in B-cell production

Methods: This study used a congenic HSCT mouse model to analyze the effects of SS ablation (through surgical castration) on immune reconstitution and growth factor production following auto-HSCT. Bone marrow (BM) and thymic stromal cell (TSCs) populations were analyzed using RT-PCR and were tested for the production of growth factors previously implicated in immune reconstitution or age-relate immune degeneration

Results: Castration increased bone marrow (BM), thymic, and splenic cellularity following auto-HSCT.

Hypertonic NaCl enhances adenosine release and hormonal cAMP production in mouse thick ascending limb.

Adenosine 3',5'-cyclic monophosphate (cAMP), accumulated in the presence of adenosine, was measured in medullary portions of mouse thick ascending limbs of Henle's loop, suspended either in classic extracellular buffer or in the presence of added NaCl. Under control conditions (140 mmol/l NaCl), adenosine (< 10(-5) mol/l) and N6-cyclohexyladenosine, an A1 adenosine receptor agonist, inhibit the cAMP accumulation induced by arginine vasopressin (AVP). On the other hand, high concentrations of adenosine and CGS-21680, an A2 adenosine receptor agonist, stimulate cAMP formation.

Ontogeny of renal mineralocorticoid receptors and urinary electrolyte responses in the rat.

We examined the ontogeny of cytosol mineralocorticoid receptors in renal inner medulla-papilla (IM-PAP) and outer medulla-cortex (OM-CX) and of a biological response to administered corticosteroids (urinary K+/Na+ ratio). Rats at early (7-9 days), intermediate (13-15 days), and late (23-30 days) stages of maturation were used. Young rats were found to be essentially insensitive to aldosterone, in contrast to rats aged 13-15 days and older.