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We present a rigorous comparison between resistivity data and theoretical predictions involving the theory of Palasantzas [G. Palasantzas and J. Barnas, Phys. Rev. B 56, 7726 (1997)], and the modified Sheng, Xing, and Wang-fractal theory [R. C. Munoz et al., Phys. Rev. B 66, 205401 (2002)], regarding the resistivity arising from electron scattering by a self-affine fractal surface on gold films using no adjustable parameters. We find that both theories lead to an approximate description of the temperature dependence of the resistivity data. However, the description of charge transport based upon fractal scaling seems oversimplified, and the predicted increase in resistivity arising from electron-surface scattering seems at variance with other experimental results. If the samples are made up of grains such that the mean grain diameter D > ℓ0(300), the electronic mean free path in the bulk at 300 K, then the predicted increase in resistivity at 4 K is of the order of a few percent. This contradicts published measurements of magnetomorphic effects arising from size effects where electron-surface scattering is the dominant electron scattering mechanism at 4 K. On the contrary, if the samples are made out of grains such that D < ℓ0(300), then the dominant electron scattering mechanism controlling the resistivity is not electron-surface scattering but rather electron-grain boundary scattering, and the latter electron scattering mechanism is not included in either theory. [ABSTRACT FROM AUTHOR]

We report the Hall constant RH, drift mobility μD, and Hall mobility μH measured at 4 K in thin gold films deposited on mica substrates, where the dominant electron scattering mechanism is electron-surface scattering. RH increases with increasing film thickness and decreases with increasing magnetic field. For high magnetic fields B≥6 T, RH turns out to be approximately independent of magnetic field, and its value is close to that of the free electron model. We use the high magnetic field values of RH to determine film thickness. This nondestructive method leads to a determination of film thickness that agrees to within 10% with the thickness measured by other techniques. The theoretical predictions, based upon the theory of Fuchs-Sondheimer and the theory of Calecki, are at variance with experimental observations. [ABSTRACT FROM AUTHOR]

Renin is synthesized in the principal cells of the collecting duct (CD), and its production is increased via cAMP in angiotensin (ANG) II-dependent hypertension, despite suppression of juxtaglomerular (JG) renin. Vasopressin, one of the effector hormones of the reninangiotensin system (RAS) via the type 2-receptor (V2R), activates the cAMP/PKA/cAMP response element-binding protein (CREB) pathway and aquaporin-2 expression in principal cells of the CD. Accordingly, we hypothesized that activation of V2R increases renin synthesis via PKA/CREB, independently of ANG II type 1 (AT1) receptor activation in CD cells. Desmopressin (DDAVP; 10-6 M), a selective V2R agonist, increased renin mRNA (~3-fold), prorenin (~1.5-fold), and renin (~2-fold) in cell lysates and cell culture media in the M-1 CD cell line. Cotreatment with DDAVP+H89 (PKA inhibitor) or CREB short hairpin (sh) RNA prevented this response. H89 also blunted DDAVP-induced CREB phosphorylation and nuclear localization. In 48-h water-deprived (WD) mice, prorenin-renin protein levels were increased in the renal inner medulla (~1.4- and 1.8-fold). In WD mice treated with an ACE inhibitor plus AT1 receptor blockade, renin mRNA and prorenin protein levels were still higher than controls, while renin protein content was not changed. In M-1 cells, ANG II or DDAVP increased prorenin-renin protein levels; however, there were no further increases by combined treatment. These results indicate that in the CD the activation of the V2R stimulates renin synthesis via the PKA/CREB pathway independently of RAS, suggesting a critical role for vasopressin in the regulation of renin in the CD. [ABSTRACT FROM AUTHOR]

We report a new formula for the electrical conductivity of a thin wire of rectangular cross-section, obtained from an exact solution of the Boltzmann equation by assuming perfectly diffuse surface scattering and absence of grain boundaries. Also, we calculate the electrical conductivity of polycrystalline metallic wires, both for the case of rectangular and circular cross-sections and for arbitrary values of Fuchs' specularity parameter, by means of a seminumerical procedure that solves the Boltzmann equation by summing over classical trajectories in accordance with Chambers' method. Following Szczyrbowski and Schmalzbauer, the scattering by grain boundaries is represented by a peculiar specularity parameter and a boundary transmittance. The difference between one and the sum of these two probabilities measures the probability of diffuse scattering. We examine the dependence of the conductivity on the values of these parameters and the effects of disorder on the diameters of the grains. [ABSTRACT FROM AUTHOR]

Prenatal stress has been associated with alterations in weight and body size, as well as disturbances in the process of developing skeletal ossification, occurring during childbirth and the early stages of life. However, the effect evidence of prenatal stress on bone growth and development during the gestation period has been low; therefore, it is unknown whether these alterations are associated with potential for growth disorders Because of this, the study aims to determine the short-term effects of prenatal stress on the CF-1 mouse bone structure growth in your date of birth. The female mice were divided randomly in two groups: controlled (n=2) and stressed (n=3). The latter was put under stress by means of movement restriction during the last week of gestation. Second, an evaluation of their gestational development was made, obtaining measurements of their weight. Finally, diaphanization with KOH and staining with Alizarin red was used to measure the length of their appendicular bones and their flat pelvic bones, of 53 PO mice (25 control; 28 stressed during gestation). The stressed mice's body weight (p=0.02) and the length of their appendicular bones (radii, p=0.0011; ulnae, p= 0.0001; humeri, p=0.0001; femorae, p=0.0006; tibiae, p=0.0015) were affected significantly in contrast with the controlled group. On the other hand, there were no significant differences in maternal body weight and length of the mice pelvic bones (isquium, ilium; p>0.05). The prenatal stress by means of movement restriction alters the osseous appendicular morphology of the CF-1 mouse evaluated at birth. [ABSTRACT FROM AUTHOR]