Development of Mortars That Use Recycled Aggregates from a Sodium Silicate Process and the Influence of Graphene Oxide as a Nano-Addition.

This research analyses how different cement mortars behave in terms of their physical and mechanical properties. Several components were necessary to make seven mixes of mortars, such as Portland cement, standard sand, and solid waste from a factory of sodium silicate, in addition to graphene oxide. Furthermore, graphene oxide (GO) was selected to reduce the micropores and increase the nanopores in the cement mortar. Hence, some tests were carried out to determine their density, humidity content, water absorption capacity, open void porosity, the alkali-silica reaction, as well as flexural and mechanical strength and acid resistance. Thus, standard-sand-manufactured mortars' mechanical properties were proved to be slightly better than those manufactured with recycled waste; the mortars with this recycled aggregate presented problems of alkali-silica reaction. In addition, GO (in a ratio GO/cement = 0.0003) performed as a filler, improving the mechanical properties (30%), alkali-silica (80%), and acid resistance.

Steric Interference in Bilayer Graphene with Point Dislocations.

We present evidence of strong steric interference in bilayer graphene containing offset point dislocations. Calculations are carried out with Large-scale Atomic/Molecular Massively Parallel Simulator (LAMMPS) using the Long-Range Carbon Bond-Order Potential (LCBOP) potential of Los et al.. We start by validating the potential in the harmonic response by comparing the predicted phonon dispersion curves to experimental data and other potentials. The requisite force constants are derived by linearization of the potential and are presented in full form. We then continue to validate the potential in applications involving the formation of dislocation dipoles and quadrupoles in monolayer configurations. Finally, we evaluate a number of dislocation quadrupole configurations in monolayer and bilayer graphene and document strong steric interactions due to out-of-plane displacements when the dislocations on the individual layers are sufficiently offset with respect to each other.

Renal denervation causes chronic hypotension in rats: role of beta1-adrenoceptor activity.

1. Renal denervation (RDNX) chronically lowers mean arterial pressure (MAP) in normal rats but mechanisms leading to this hypotensive response remain unknown. 2. We hypothesized that this sustained decrease in arterial pressure was because of a loss of beta1-adrenoceptor mediated renin secretion. Male Sprague-Dawley rats were assigned to sham (SHAM; n = 9), unilateral (UniRDNX; n = 9), or bilateral (RDNX; n = 10) renal denervation groups and instrumented for telemetric MAP measurements, plasma renin concentration (PRC) measurements and intravenous infusion. Twenty-four h MAP, heart rate, sodium and water balances were recorded 5 days before, 3 days during and 3 days after 1-adrenoceptor blockade with atenolol. 3. The 5-day control MAP was significantly lower in RDNX (97 +/- 1 mmHg) compared to SHAM (105 +/- 2 mmHg) and UniRDNX (102 +/- 2 mmHg) rats. No significant differences in basal PRC were observed between RDNX (2.2 +/- 0.3 ngAng1/mL per h), UniRDNX (2.6 +/- 0.4 ng/Ang1/mL per h) and SHAM (2.6 +/- 0.4 ngAng1/mL per h) rats. By day 1 of atenolol, PRC was significantly lower in UniRDNX rats (1.8 +/- 0.2 ngAg1/mL per h) compared to control values, but was unchanged during atenolol infusion in the other groups. By day 3 of atenolol, MAP was significantly decreased in all groups, but the absolute levels of MAP remained statistically different between RDNX (87 +/- 1 mmHg) and SHAM (91 +/- 1 mmHg) groups. 4. We conclude that the arterial pressure lowering effect of RDNX is not solely dependent on the loss of neural control of renin release.

Renal denervation chronically lowers arterial pressure independent of dietary sodium intake in normal rats.

The present study was designed to test the hypothesis that renal nerves chronically modulate arterial pressure (AP) under basal conditions and during changes in dietary salt intake. To test this hypothesis, continuous telemetric recording of AP in intact (sham) and renal denervated (RDNX) Sprague-Dawley rats was performed and the effect of increasing and decreasing dietary salt intake on AP was determined. In protocol 1, 24-h AP, sodium, and water balances were measured in RDNX (n = 11) and sham (n = 9) rats during 5 days of normal (0.4% NaCl) and 10 days of high (4.0% NaCl) salt intake, followed by a 3-day recovery period (0.4% NaCl). Protocol 2 was similar with the exception that salt intake was decreased to 0.04% NaCl for 10 days after the 5-day period of normal salt (0.04% NaCl) intake (RDNX; n = 6, sham; n = 5). In protocol 1, AP was lower in RDNX (91 +/- 1 mmHg) compared with sham (101 +/- 2 mmHg) rats during the 5-day 0.4% NaCl control period. During the 10 days of high salt intake, AP increased <5 mmHg in both groups so that the difference between sham and RDNX rats remained constant. In protocol 2, AP was also lower in RDNX (93 +/- 2 mmHg) compared with sham (105 +/- 4 mmHg) rats during the 5-day 0.4% NaCl control period, and AP did not change in response to 10 days of a low-salt diet in either group. Overall, there were no between-group differences in sodium or water balance in either protocol. We conclude that renal nerves support basal levels of AP, irrespective of dietary sodium intake in normal rats.