The Rheometric Analysis of the Polymer Modifier’s Properties in the Environment of Hydrated Cement

This paper investigates the effect of polymer modifiers (re-dispersible powder, multifunctional additives, methylhydroxyethylcellulose) on the rheological behavior of emulsions, saturated of calcium hydrosilicates to simulate a hydrating cement structure. The subjects of the study were modified emulsions which had varied concentrations of each additive and they were examined comparatively to a base emulsion. Tests were performed with a CR-rheometer (“Himpribor-1”, Tula, Russia) applying the Searle measuring principle at various shear rates to characterize viscosity properties. The performance of modified mixtures within the operating period was analyzed by using two parameters—effective viscosity (η) and the proportion of structural failure (|m|). The test results showed that the most important factor influencing rheological characteristics is the addition of methylhydroxyethylcellulose additive—the higher additive amount in the emulsion, the higher the viscosity. Furthermore it was noted in the work that adding olefin sulfonate sodium salt causes reduced viscosities as well as lower shear moduli. If ethylhydroxyethylcellulose and ethylene vinyl acetate additives are used in the same mixture together, the rate of structural failure |m| can be relatively similar and low regardless of whether the mixture has large or small viscosity values.     

The Impact of Water and Road Salt with Anti-Caking Agent on the Stiffness of Select Mixes Used for the Road Surface

An original experimental method was used to investigate the influence of water and road salt with anti-caking agent on the material used in pavement construction layers. This method allowed for monitoring material changes resulting from the influence of water and road salt with anti-caking agent over time. The experiment used five different mineral road mixes, which were soaked separately in water and brine for two time intervals (2 days and 21 days). Then, each sample of the mix was subjected to tests of the complex module using the four-point bending (4PB-PR) method. The increase in mass of the soaked samples and the change in value of the stiffness modulus were analyzed. Exemplary tomographic (X-ray) imaging was performed to confirm the reaction of the road salt and anti-caking agent (lead agent) with the material. Based on measurements of the stiffness modulus and absorption, the correlations of the mass change and the value of the stiffness modulus were determined, which may be useful in estimating the sensitivity of mixes to the use of winter maintenance agents—e.g., road salt with anti-caking agent (sodium chloride). It was found that the greatest changes occur for mixes intended for base course layers (mineral cement mix with foamed asphalt (MCAS) and mineral-cement-emulsion mixes (MCE)) and that the smallest changes occur for mixes containing highly modified asphalt (HIMA).     

Effect of sodium mercaptoacetic acid on different antimicrobial disks in the sodium mercaptoacetic acid double disk synergy test for detection of IMP-1 metallo-β-lactamase-producing Pseudomonas aeruginosa isolates in Japan

We determined the optimal antimicrobial in the sodium mercaptoacetic acid double disk synergy test (SMA-DDST) for the detection of IMP-1-producing Pseudomonas aeruginosa isolates in Japan and evaluated the performance of the test.Fifty-four P. aeruginosa clinical isolates were tested, including 39 IMP-1 producers and 15 non-metallo-β-lactamase (MBL)-producing carbapenem- and ceftazidime (CAZ)-resistant isolates. The SMA-DDST was performed with CAZ, cefepime (CFPM), imipenem (IPM), meropenem (MEPM), doripenem (DRPM), or biapenem (BIPM)-containing disks. The sensitivity of the SMA-DDST with CAZ, CFPM, IPM, MEPM, DRPM, and BIPM was 39/39 (100%), 36/39 (92%), 18/39 (46%), 8/39 (21%), 19/39 (49%), and 36/39 (92%), respectively. The specificity was 15/15 (100%) for all SMA-DDSTs. This suggests that the isolates may have a resistance mechanism other than MBL production for IPM, MEPM, or DRPM. Since the CAZ resistance mechanism in P. aeruginosa is the same as that of CFPM, but differs from that of carbapenems, we conclude that combining CAZ with BIPM SMA-DDSTs can prevent any failure in the detection of IMP-1-producing P. aeruginosa.     

Endogenous adenosine differentially modulates 5-hydroxytryptamine release from a human enterochromaffin cell model

BACKGROUND & AIMS: The aim was to determine whether adenosine receptors modulate cAMP, intracellular free calcium ([Ca(2+)](i)), and 5-hydroxytryptamine (5-HT) release in human carcinoid BON cells. METHODS: Adenosine receptor (R) mRNA, proteins, and function were identified by Western blots, immunofluorescent labeling, Fluo-4/AM [Ca(2+)](i) imaging, and pharmacologic/physiologic techniques. RESULTS: A1, A2, and A3Rs were present in BON cells and carcinoid tumors. Baseline 5-HT levels increased with adenosine deaminase, activation of A2Rs, and inhibition of A3Rs, whereas A3R activation decreased 5-HT. A2R antagonists or blockade of adenosine reuptake that elevates extracellular adenosine reduced mechanically evoked 5-HT release. In single BON cells, touch elevated [Ca(2+)](i) responses were augmented by adenosine deaminase, A1, and A3R antagonists. CONCLUSIONS: Tonic or mechanically evoked release of endogenous adenosine is a critical determinant of differential activation of adenosine receptors and may have important implications for gut mechanosensory reflexes.     

Myocardial Ischemic Tolerance Following Heat Stress Is Abolished by ATP-Sensitive Potassium Channel Blockade

Heat stress is known to confer protection against ischemia, but the mechanisms involved are yet to be elucidated. Opening of ATP-sensitive potassium (K_ATP) channels has been demonstrated to be involved in other endogenous forms of cardioprotection, in particular“classic” ischemic preconditioning and delayed preconditioning following treatment with the endotoxin derivative, monophosphoryl lipid A. We therefore speculated that there may be a role for K_ATPchannels in delayed heat stress–induced cardioprotection. This hypothesis was investigated in an in vivo rabbit model of acute myocardial infarction using two structurally dissimilar K_ATP channel blockers, glibenclamide and sodium 5-hydroxydecanoate. Sodium pentobarbitone–anesthetized rabbits were subjected to either transient heat stress at 42 ± 0.2°C for 15 minutes or sham anesthesia. Twenty-four hours later, animals were reanesthetized (“Hypnorm” and sodium pentobarbitone) and a midline sternotomy and pericardiotomy were performed. An anterolateral branch of the circumflex coronary artery was occluded for 30 minutes and reperfused for 2 hours. The infarct-to-risk ratio was significantly limited in vehicle-treated rabbits from 41.3 ± 4.0% in controls (n = 10) to 24.1 ± 5.0% (n = 9; P = 0.014 by one-factor ANOVA) in heat-stressed hearts. This limitation in infarct size was abolished by 0.3 mg/kg iv glibenclamide or 5 mg/kg iv5-hydroxydecanoate when administered 10 minutes prior to coronary occlusion (45.2 ± 6.4%; n = 9 and 41.5 ± 5.0%; n = 5, respectively.) The same doses of glibenclamide and 5-hydroxydecanoate in sham-anesthetized hearts had no effect (42.3 ±5.1%; n = 10 and 51.9 ± 2.2%; n = 6, respectively). The adequacy of the heat stress protocol was confirmed by Western blot analysis of the inducible 72-kD heat stress protein. It is concluded, therefore, that K_ATP channels appear to play a role in the heat stress response. The underlying mechanisms involved are, however, unclear. This revised version was published online in July 2006 with corrections to the Cover Date.     

Epidermal growth factor partially restores colonic ion transport responses in mouse models of chronic colitis

BACKGROUND & AIMS: Epidermal growth factor receptor (EGFR) activation, which plays an important role in regulating intestinal ion transport, can alleviate clinical symptoms such as diarrhea in patients with ulcerative colitis and promote mucosal restitution in animal models of colitis. Here, we investigate whether EGFR can regulate colonic ion transport in the setting of colitis. METHODS: Distal colon from control mice and mice with colitis was retained for immunohistochemistry or mounted in Ussing chambers. Ion transport responses across the tissues to the calcium agonist carbachol and the adenosine 3',5'-cyclic monophosphate agonist forskolin were measured with or without epidermal growth factor (EGF) pretreatment. RESULTS: EGF pretreatment of normal colonic mucosa inhibited ion transport responses to carbachol and forskolin but potentiated the reduced ion transport responses seen in dextran sulfate sodium (DSS)-treated and mdr1a knockout mouse colon. Ion substitution studies and the sodium transport inhibitor amiloride showed that sodium movement primarily accounted for the potentiating effect of EGF in DSS-treated tissues, despite decreased sodium channel expression. EGF potentiation of transport responses in DSS-treated colon was completely blocked by the cytoskeletal disruptor cytochalasin D and the phosphatidylinositol 3-kinase inhibitor wortmannin, whereas the novel and conventional protein kinase C isoform inhibitor G?6850 and the extracellular signal-regulated kinase inhibitor PD98059 partially reduced EGF effects. EGFR epithelial distribution and transforming growth factor alpha expression were also altered in DSS-treated tissues. CONCLUSIONS: Chronic inflammation uncovers a potentiating effect of EGFR activation on epithelial electrogenic sodium absorption that would be expected to ameliorate diarrheal symptoms associated with colitis.     

Activation of natriuretic peptide receptor-C attenuates the enhanced oxidative stress in vascular smooth muscle cells from spontaneously hypertensive rats: implication of Gialpha protein

We have recently shown that vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) exhibit enhanced expression of Giα proteins, which was attributed to the enhanced oxidative stress. Since C-ANP_4-23 that specifically interacts with natriuretic peptide C (NPR-C) receptor has been shown to decrease the expression of Giα protein in VSMC, the present study was undertaken to examine if C-ANP_4-23 can also decrease the enhanced expression of Giα protein in VSMC from SHR and whether it is attributed to its ability to attenuate the enhanced oxidative stress. Aortic VSMC from 12-week-old SHR and their age-matched Wistar-Kyoto (WKY) rats were used for the present studies. VSMC from SHR exhibited enhanced expression of Giα-2 and Giα-3 proteins, different subunits of NADPH oxidase such as Nox⁴ and p^47phox proteins but not of p^22phox, enhanced production of superoxide anion as well as NADPH oxidase activity as compared to age-matched WKY rats. Treatment of VSMC from SHR with C-ANP_4-23 decreased towards control levels the enhanced expression of Giα proteins, enhanced superoxide anion production and enhanced NADPH oxidase activity as well as the enhanced expression of Nox⁴ and p^47phox. However, C-ANP_4-23-induced attenuation of the enhanced level of O₂⁻ and NADPH oxidase activity occurs at 4 h before the decrease in the enhanced expression of p^47phox that occurs at 16 h of C-ANP_4-23 treatment. The decreased expression of NADPH oxidase in SHR was also associated with further decrease in O₂⁻ and NADPH oxidase activity. Furthermore, treatment of VSMC from SHR with pertussis toxin (PT) decreased the enhanced levels of superoxide anion as well as NADPH oxidase activity; however, the enhanced levels of different subunits of NADPH oxidase were not attenuated by PT treatment. These results suggest that C-ANP_4-23 decreases the enhanced oxidative stress in SHR by attenuating the enhanced expression of Giα proteins and also the enhanced levels of NADPH oxidase.     

Changes of systemic prostacyclin and thromboxane A2 in sodium taurocholate-and cerulein-induced acute pancreatitis in rats

Systemic prostacyclin and thromboxane A₂ production in rat experimental acute pancreatitis has been evaluated by measuring the urinary excretion of the 2,3-dinor 6-keto prostaglandin F₁ and 2,3-dinor thromboxane B₂, respectively. Acute pancreatitis was induced by intraductal administration of 4.5% sodium taurocholate (0.1 ml/100 mg body weight) and intravenous cerulein perfusion (5 g/kg/hr) for 6 hr, respectively. Urinary excretion of 2,3-dinor 6-keto prostaglandin F₁ and 2,3-dinor thromboxane B₂ were much more important in sodium taurocholate- than in cerulein-induced acute pancreatitis. These data confirm an altered prostacyclin and thromboxane metabolism occurring in experimental acute pancreatitis. Phospholipase A₂ activity and the effect of gabexate mesilate on the arachidonate metabolism were also evaluated.This work was supported by the Fondo de Investigación Sanitaria (89/386).