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Volcanic ash deposits have been proposed to potentially liquefy and act as preferential failure planes during submarine landslides along active margins. However, particle angularity and surface roughness of volcanic material significantly influence its shear behavior and hence do not unambiguously support this contention. This manuscript challenges the hypothesis of preferential failure of ash layers by conducting drained and undrained monotonic and undrained cyclic triaxial shear experiments ( σ' < 1 MPa) on volcanic silts/sands and quartz sands as a reference material. Results attest the key role of particle geometry and particle strength in sediment stability. Decreased failure susceptibility of volcanic material compared to smoothed, rounded, and hard-grained quartz sand was attributed to roughness, angularity, and low crushability at low effective confining stresses in drained monotonic and undrained cyclic shear experiments. However, in undrained monotonic shear experiments on soft-grained and porous volcanic material, we observe major weakening due to crushability and excess pore pressure buildup related to particle internal water expulsion. In contrast, hard-grained angular volcanic particles are less susceptible to liquefaction than grain-size equivalent-rounded quartz sand, and may in fact be favorable for seismic strengthening, in which ground shaking causes enhanced settling rather than failure. Our data suggest that ash layers may not serve as preferential failure planes in the majority of earthquake-triggered submarine landslides along active margins. [ABSTRACT FROM AUTHOR]

In an experimental model of atherosclerosis we investigated whether rabbits fed an atherogenic diet (0.25% cholesterol, 3% coconut oil) develop endothelial dysfunction accompanied with increased infarct mass compared to normal fed rabbits and, whether hypercholesterolemia would interfere with the beneficial outcome of ischemic preconditioning observed in normal rabbits. After four weeks on either a normal or an atherogenic diet, New Zealand White rabbits (n=7 in each group) were subjected to 30 min of myocardial ischemia by occlusion of a branch of the left anterior descending coronary artery (LAD) followed by 2 hours of reperfusion (infarct studies). For ischemic preconditioning experiments, LAD was additionally occluded twice for 5 min followed by 10 min reperfusion before the long-lasting (30 min) ischemia. Infarct mass was evaluated by triphenyl-tetrazolium staining. Besides the assessment of aortic endothelium-dependent function and NO-release, aortic and cardiac vessels were inspected for atherosclerotic lesions. Total cholesterol serum levels in rabbits on an atherogenic diet were significantly higher (15.3±2.7 mmol/L) than those on a standard diet (0.65±0.08 mmol/L). The aortas and heart vessels were without any histological evidence of atherosclerosis, whereas endothelial dysfunction and significantly reduced calcium-ionophore stimulated endothelial NO-release were found in isolated aortic rings ofhypercholesterolemic animals. Rabbits on a standard diet showed an infarct mass (related to the area at risk) of 41±3%, which was reduced to 21±2% by ischemic preconditioning (49% decrease, p<0.05). In rabbits on an atherogenic diet, infarct mass was significantly increased to 63±3% (52% increase versus standard diet). Interestingly, hypercholesterolemia did not affect the beneficial influence of ischemic preconditioning; infarct mass (21±3%, p<0.05 vs hypercholesterolemia) was similar to rabbits on a standard diet... [ABSTRACT FROM AUTHOR]

A radioreceptor assay (RRA) for the assay of beta-adrenoceptor antagonists in native human plasma is described. The hydrophilic antagonistH-CGP 12177 was used as the radioligand. In contrast to the hydrophobic radioligandH-dihydroalprenolol, which was investigated in parallel, the beta-adrenoceptor binding ofH-CGP 12177 by rat reticulocyte membranes was found not to be affected by inclusion of increasing proportions (0-66% of incubation volume) of human plasma in the assay. Thus, solvent extraction of drug and/or active metabolites was not necessary to avoid binding of the radioligand tracer to plasma added in the RRA. The assay of unprocessed samples was possible. Drug concentrations in plasma after oral administration of propranolol (240 mg) or carteolol (30 mg) to 6 healthy volunteers were measured by the RRA and in parallel by a chemical method. The results from both methods agreed when the plasma concentration kinetics of propranolol were investigated (elimination half-life: 3.9 h). In contrast, plasma concentrations of carteolol were consistently higher according to the RRA after oral administration of the drug. Identical concentrations, however, were found by the RRA and chemical method using plasma samples spiked with carteolol. Plasma concentrations of carteolol detected by the chemical method decline monoexponentially (elimination half-life: 5.4 h). A similar half-life of elimination for parent drug was found by the RRA (5.9 h), but an additional term describing the appearance of an active metabolite was necessary to account for the biphasic drug elimination (elimination half-life of metabolite: 17.3 h). The latter result is in agreement with the appearance of 8-hydroxy-carteolol as an active metabolite, which shows similar affinity for beta-adrenoceptors as the parent drug. The active metabolite, with a 3-fold longer elimination half-life than the parent drug, will prolong the duration of the clinical effects of orally administered carteolol. In conclusion, the RRA permits the determination of beta-adrenoceptor antagonistic activity in native human plasma at concentrations as low as 0.1-fold the IC-value of the drug or an active metabolite. [ABSTRACT FROM AUTHOR]

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Inhibition of the angiotensin converting enzyme (ACE) with ramipril was studied in male Wistar rats during long-term inhibition of nitric oxide (NO) synthase by N-nitro- l-arginine methyl ester ( l-NAME). Chronic treatment with l-NAME in a dose of 25 mg/kg per day over 6 weeks caused myocardial hypertrophy and a significant increase in systolic blood pressure (245 ± 16 mmHg) as compared to controls (155+4 mmHg). Animals receiving simultaneously l-NAME and ramipril were protected against blood pressure increase and partially against myocardial hypertrophy. L-NAME caused a significant reduction in glomerular filtration rate (GFR: 2.56+0.73 ml·kg·min) and renal plasma flow (RPF: 6.93±1.70ml·kg·min) as compared to control (GFR: 7.29±0.69, RPF: 21.36±2.33ml·kg·min). Addition of ramipril prevented l-NAME-induced reduction in GFR and renal plasma flow. l-NAME produced an elevation in urinary protein excretion and serum creatinine and a decrease in potassium excretion which was antagonised by ramipril. L-NAME-induced increase in plasma renin activity (PRA) was further elevated with ramipril treatment. Isolated hearts from rats treated with l-NAME showed increased post-ischaemic reperfusion injuries. Compared to controls duration of ventricular fibrillation was increased and coronary flow reduced. During ischaemia the cytosolic enzymes lactate dehydrogenase and creatine kinase, as well as lactate in the venous effluent were increased. Myocardial tissue values of glycogen, ATP, and creatine phosphate were decreased, whereas lactate was increased. Coadministration of ramipril reversed these effects. l-NAME treatment reduced the cyclic GMP content in urine and renal arteries, and was not changed by additional ramipril-treatment. In the kidney hyalinosis of arterioles and of glomerular capillaries, as well as mesangial expansion and tubular atrophies seen after long-term inhibition of NO synthase were reduced by coadministration of ramipril. In conclusion, long-term ACE inhibition by ramipril prevented l-NAME-induced hypertension and cardiac hypertrophy, and attenuated functional and morphological changes in the kidneys. In addition, cardiac-dynamic and -metabolic deterioration induced by L-NAME was normalised by co-treatment with ramipril. [ABSTRACT FROM AUTHOR]

In reticulocyte-rich suspensions of red blood cells from rats extrusion of cAMP as a regulatory mechanism of intracellular cAMP was investigated. In response to isoprenaline and/or the phosphodiesterase inhibitors Ro 20-1724 and rolipram extrusion of cAMP increases dependent on the concentration of the drugs and time of exposure. However, these drugs exert their effects on the extrusion of cAMP only indirectly, i.e. via increased intracellular levels of cAMP, since the respective EC-values of the drugs for intracellular accumulation and extrusion of cAMP are identical (isoprenaline: ∼50 nM; rolipram: ∼1 μM; Ro 20-1724: 15 μM). The dependence of the rate of extrusion on intracellular levels of cAMP is characterized by a typical concentration-effect relationship from which a maximal capacity of cAMP extrusion of 3-6 nmol/10 min/10 cells and a half maximal effective intracellular cAMP concentration of 40-50 nmol/10 cells can be derived. This relationship has been inferred from either kinetic or steady-state approaches. At rapidly changing intracellular levels of cAMP an apparent time lag of extracellular cAMP accumulation is obligatorily conditioned by this relationship. Vasodilating drugs which lower the ATP content of the cells as well as the uncoupler of oxidative phosphorylation, FCCP, inhibit the extrusive process (papaverine > FCCP > dipyridamole > dilazep ≫ hexobendine ≥ carbocromene) leading to a 3-5-fold increase of the intrato extracellular concentration gradient of cAMP. It is concluded that extrusion of cAMP is a saturable and energy-dependent process which regulates the intracellular cAMP concentration independent of the activities of adenylate cyclase and phosphodiesterase. [ABSTRACT FROM AUTHOR]

To study the fundamental differences between agonist and antagonist interaction with the β-adrenoceptor of the rat reticulocyte the radiolabeled agonistH hydroxybenzylisoprenaline (H HBI) and the radiolabeled antagonistH dihydroalprenolol (H DHA) were used. Equilibrium binding experiments withH HBI revealed all characteristics expected to a β-adrenoceptor site, i. e. high affinity binding ( K=7.4±0.9×10 M), saturability ( B=230±24 fmoles/mg protein), and stereoselectivity. The rank order of potency for competing agonists was isoprenaline > adrenaline > noradrenaline > dopamine.H HBI high affinity binding sites amounted to about 25% of β-adrenoceptor sites detectable withH DHA. In competition experiments withH HBI and (-)isoprenaline[(-)Ipn]a K-value for (-)Ipn of 3.1±0.6×10M was obtained corresponding to the K-value of (-)Ipn obtained from competition experiments usingH DHA. For (-)propranolol K-values of 0.9±0.5×10 M and 1.0 ±1.0×10 M were measured usingH HBI andH DHA respectively. Agonist affinity derived from competition experiments with (-)Ipn versusH DHA was not affected by temperature changes. Guanylyl-imidodiphosphate [Gpp(NH)p] decreased concentration dependently the number of high affinity binding sites ofH HBI not affecting the respective K-value. Similar effects were observed after omission of Mg from the binding assay or inclusion of Na in the Mg-free incubation mixture. The association reaction ofH HBI at the β-adrenoceptor revealed two different velocities. The slower phase of the association reaction which represents high affinity binding (80% of equilibrium binding) is not observed in the presence of Gpp(NH)p. A biphasic dissociation ofH HBI binding was induced by 10 M (±)propranolol: 25% dissociated with a t of 1.3 min whereas the high affinity binding was reversed with a t of 150 min. This slowly reversible binding ofH HBI however was rapidly reversed by Gpp(NH)p ( t<1 min). It is concluded that the agonist ligandH HBI permits a direct qualitative and quantitative characterization of the agonist induced high affinity state of the β-adrenoceptor. In particular, the kinetic studies strongly support a two step binding model for the agonist-β-adrenoceptor interaction. [ABSTRACT FROM AUTHOR]

Rats pretreated with 1-acetyl-2-phenylhydrazide, to induce reticulocytosis, were treated with (±)isoprenaline (4×30 mg/kg in 6 h intervals within 24 h before blood sampling) in order to desensitize the β-adrenoceptor-adenylate cyclase-system of circulating red cells. [ABSTRACT FROM AUTHOR]

For the direct characterization of β-adrenoceptors in membrane preparations from the reticulocyte rich blood of rats treated with acetyl phenylhydrazide the β-adrenergic antagonist ligand (H)(−)dihydroalprenolol (DHAP) was used. [ABSTRACT FROM AUTHOR]

The degree of stimulation of adenylcyclase activity, in membranes from immature red blood cells from rats, brought about by isoprenaline, guanylyl-imidodiphosphate and sodium fluoride is strongly dependent on the basal activity of the enzyme. The inversal relationship between basal activity and the maximal degree of stimulation by (−) isoprenaline, shows an apparent seasonal dependence. [ABSTRACT FROM AUTHOR]

During the maturation of red blood cells from rats after stress erythropoiesis, adenyl cyclase activity and β-adrenoceptor density (pmoles/mg protein) decrease at distinctly different rates suggesting a different turnover of these membrane units. [ABSTRACT FROM AUTHOR]

The giant 2011 Tohoku-oki earthquake has been inferred to remobilise fine-grained, young surface sediment enriched in organic matter from the slope into the >7 km deep Japan Trench. Yet, this hypothesis and assessment of its significance for the carbon cycle has been hindered by limited data density and resolution in the hadal zone. Here we combine new high-resolution bathymetry data with sub-bottom profiler images and sediment cores taken during 2012-2016 in order to map for the first time the spatial extent of the earthquake-triggered event deposit along the hadal Japan Trench. We quantify a sediment volume of ~0.2 km3 deposited from spatially-widespread remobilisation of young surficial seafloor slope sediments triggered by the 2011 earthquake and its aftershock sequence. The mapped volume and organic carbon content in sediment cores encompassing the 2011 event reveals that this single tectonic event delivered >1 Tg of organic carbon to the hadal trench. This carbon supply is comparable to high carbon fluxes described for other Earth system processes, shedding new light on the impact of large earthquakes on long-term carbon cycling in the deep-sea. [ABSTRACT FROM AUTHOR]

The article presents that the insecticide, an organophosphate is used as a contact insecticide, acting as a cholinesterase inhibitor. It is effective against a wide range of insect pests of many crops. The insecticide is made from 2,2,2,2-tetrachloroacetophenone (TCAP) and triethyl phosphate. TCAP is made from dichloroacetophenone and chlorine. Patch tests were performed with the European standard series, the insecticide. Strong positive reactions were seen to both tests with TCAP. Tests to the other chemicals were negative. Sensitization to TCAP in humans has reported such as rashes developed on the patient's face as a result of walking through the insecticide plant.

The article focuses on a case study dealing with sensitization to DD-95, which is a soil fumigant that is used prior to crop cultivation. An active component of DD-95 is 1, 3-dichloropropene, which accounts for approximately 95 percent of the product. Sensitization to DD has been described twice. DD-95 is not only toxic but also a potent sensitizing agent, farmers and operators employed at pesticide plants who have dermatitis should be patch tested not only with the standard series but also with DD-95.

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