Streptozotocin-induced renal fibrosis, PAI-1 expression, TGF-beta1 expression, and macrophage infiltration occur via mineralocorticoid receptor, and spironolactone ameliorates renal fibrosis presumably via the inhibition of macrophage infiltration, PAI-1 expression, and TGF-beta1 expression in streptozotocin-induced early diabetic injury.

In this study, subjects with glaucoma who had the OPTN E50K mutation were found to have NTG that appeared to be more severe than that in a control group of subjects with NTG without this mutation. The findings emphasize the importance of early detection and treatment of glaucoma in such individuals, to minimize visual loss.

The short-term effect of ALDO on NHE activity is not mediated through either MR or GR, occurs independent of gene transcription and protein synthesis, and occurs through a mechanism involving the structural elements of cytoskeleton. The long-term effect of ALDO on NHE activity occurs through both MR and GR and requires gene transcription and protein synthesis. Both short- and long-term effects of ALDO are mediated through PKC activation. Therefore, ALDO activates NHE by nongenomic and genomic mechanisms in VSMCs.

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This paper shows that nonperfect secret sharing schemes (NSS) have matroid structures and presents a direct link between the secret sharing matroids and entropy for both perfect and nonperfect schemes. W e define natural classes of NSS and derive a lower bound of Iv,l for those ClaSSeS. "Ideal" nonperfect schemes are defined based on this lower bound. We prove that every such ideal secret sharing scheme has a matroid structure. The rank function of the matroid is given by the entropy divided by some constant. It satisfies a simple equation which represents the access level of each subset of participants.

Abstract-Long-term exposure of uninephrectomized rats to desoxycorticosterone acetate (DOCA)/salt induces cardiac fibrosis and hypertrophy through mineralocorticoid receptors (MRs). However, the underlying cellular mechanisms remain unclear. To determine whether Na/H exchange isoform 1 (NHE1) is involved in the cellular mechanisms, we examined the effects of a specific NHE1 inhibitor, cariporide, and an MR antagonist, spironolactone, on DOCA/saltinduced cardiac fibrosis and hypertrophy. Uninephrectomized rats were given 20 mg of DOCA (single subcutaneous injection) plus 0.9% NaCl/0.3% KCl to drink and were killed at 8 days. Two groups of rats given DOCA/salt were treated with either spironolactone (50 mg/kg per day SC) or cariporide (30 mg/kg per day PO) for 8 days. Control rats were treated with only high salt after the operation. The DOCA/salt-induced perivascular collagen deposition was completely abolished by cariporide and spironolactone. DOCA/salt-induced interstitial collagen deposition was partially and completely suppressed by spironolactone and cariporide, respectively. The rats exposed to DOCA/salt had cardiocyte hypertrophy in the subendocardial and subepicardial regions, a finding that was completely inhibited by cariporide but not by spironolactone. In rats given DOCA/salt, NHE1 protein expression was markedly increased. This was partially and completely reversed by spironolactone and cariporide, respectively. We concluded that cardiac NHE1 contributes to DOCA/salt-induced cardiac fibrosis and hypertrophy and that the NHE1 inhibitor cariporide completely prevents the detrimental effects of DOCA/salt on the heart. We also demonstrated that DOCA/salt-induced cardiac injury through the MRs partly occurs through NHE1 activation.

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Elevated levels of plasma arginine vasopressin (AVP) have been suggested to impair water excretion in congestive heart failure. In the present study, to determine a role for AVP in the impaired water excretion in rats with the inferior vena cava constriction (IVC), two AVP antagonists were used in the IVC rats at the proximal portion of the hepatic vein under the diaphragm and in sham-operated (control) rats. After surgery, 48 hrs were allowed before the experiments were started. A mean cardiac index of 260.0 +/- 12.3 ml/min/kg in the IVC rats was significantly lower than that in the control rats, 323.6 +/- 13.2 ml/min/kg (P less than 0.01). The rats were given an antidiuretic antagonist, [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid), 2-(O-ethyl)-D-tyrosine, 4-valine] AVP (30 micrograms/kg) or the antagonist vehicle, i.p., and 20 min later they were administered 30 ml/kg of water orally. Minimal urinary osmolality (Uosm) in the IVC rats receiving the vehicle was significantly greater than the control rats (292.7 +/- 53.1 vs. 97.8 +/- 10.6 mOsm/kg H2O, P less than 0.01). The administration of the antidiuretic antagonist in the IVC rats decreased minimal Uosm to 90.0 +/- 3.6 mOsm/kg H2O. This value was significantly lower than the vehicle rats (P less than 0.01), and was a comparable level to minimal Uosm of 82.1 +/- 3.7 mOsm/kg H2O in the control rats receiving the antidiuretic antagonist. The IVC rats excreted 51.4 +/- 5.9% of the water load in three hr, a value significantly less than that excreted by the control rats, 95.1 +/- 6.0% (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)