Search

Neutrophil to lymphocyte ratio (NLR) in peripheral blood is established to correlate with the morbidity and mortality of heart disease patients. We aimed to define the severity of inflammation (NLR) by observing the association of NLR with cardiac functions or myocardial damage parameters in patients with acute myocardial infarction.

Angiotensin II (Ang II)-induces vasoconstriction, in vivo perfusion has been shown to induce preeclampsia (PE) in pregnant rats. In this study, we aimed to examine the protein and mRNA expressions of endothelial and neuronal NOS (eNOS, nNOS) as well as angiotensin II type 2 receptor (AT2R) in normal pregnant and Ang II-induced PE rats.Pregnant (8 weeks) and non-pregnant SD rats (8 weeks, GD-8) were infused with Ang II via an osmotic minipump (1 ug/kg/min), and the rats (GD-21) were sacrificed 13 days later. Pregnant and non-pregnant rats without Ang II were taken as sham controls. The fetal weight, crown-rump length and placental weight of PE rats were significantly lower compared to those without Ang II infusion. Immunohistochemistry results showed an approximately 30% increase in glomerular volume, suggesting morphological changes in the kidney and Ang II infusion exhibits a PE phenotype. Ang II infusion did not affect AT2R, AT1R and nNOS protein or mRNA expression in the uterus of non-pregnant or pregnant rats. However, eNOS mRNA expression was reduced in PE rats (p < 0.0001) although protein expression was not affected by Ang II infusion. However, in the placenta, AT1R and AT2R protein expression were not different in PE, but AT2R mRNA was decreased (p < 0.0001). eNOS protein was only expressed in fetal vascular endothelial cells, and eNOS protein expression was higher in PE rats (P = 0.001) but eNOS mRNA was decreased (p = 0.0096). Notably, strong nNOS expression was observed in placental trophoblast cell groups of sham and PE rats, and both mRNA and protein expression of nNOS was decreased in placental lysates of Ang II rats (respectively p = 0.0287 and p < 0.0001).These results demonstrate that we have recapitulated the PE model of Ang II infusion in rats. The expression of nNOS was reduced, and the localization of nNOS in the trophoblast suggested a new functional remodeling in the fetal vasculature.In the placenta, decreased expression of AT2R and nNOS may be a novel mechanism of impaired fetal development.

•Interpretable hybrid model for patient-wise electrocardiogram (ECG) categorization as normotensive and hypertensive is proposed.•Proposed architecture consists of convolutional neural network (CNN) and support vector machine (SVM) classifier as hybrid model.•In addition, an automated digitization algorithm is proposed for converting paper-ECG to 1D digital signal.•Achieved highest accuracy of 93.33%, sensitivity of 100% and specificity of 87.5% in patient-wise classification.

The sulfate corrosion resistance of concrete admixed with fly ash was tested. Specimens were completely immersed in sulfate solution which was aimed at simulating the real corrosion environment. The compressive strength of fresh concrete specimens and precast concrete specimens in different corrosion age and corrosion environment was measured when the mixing amount of fly ash is 0%, 20% and 40%. The evaluation index is corrosion resistance coefficient of compressive strength Kf . The test results indicate that the sulfate corrosion resistance of fresh concrete is better than that of precast concrete during experimental period of 270 days; the sulfate corrosion resistance of fresh concrete can be improved by mixing a certain amount of fly ash.

Transient receptor potential vanilloid 1 (TRPV1) is a Ca2+-permeable cation channel activated by a variety of physicochemical stimuli. The effect of hypoxia (, 3%) on rat TRPV1 overexpressed in HEK293T has been studied. The basal TRPV1 current (ITRPV1) was partly activated by hypoxia, whereas capsaicin-induced TRPV1 (ITRPV1,Cap) was attenuated. Such changes were also suggested from hypoxia- and capsaicin-induced Ca2+signals in TRPV1-expressing cells. Regarding plausible changes of reactive oxygen species (ROS) under hypoxia, the effects of antioxidants, vitamin C and tiron, as membrane-impermeable and -permeable, respectively, were tested. Both ITRPV1and ITRPV1,Capwere increased by vitamin C, while only ITRPV1was slightly increased by tiron. The hypoxic inhibition of ITRPV1,Capwas still persistent under hypoxia/vitamin C. Interestingly, hypoxia/tiron strongly inhibited both ITRPV1and ITRPV1,Cap. Also, with vitamin C applied through a pipette solution, hypoxia inhibited ITRPV1and ITRPV1,Cap. In contrast, hypoxia and hypoxia/tiron had no effect on the ITRPV1induced by acid (pH 6.2, ITRPV1,Acid). Taken together, hypoxia partly activated TRPV1 while it decreased their sensitivity to capsaicin. Putative changes of ROS under hypoxia might underlie the side-specific effects of ROS on TRPV1: inhibitory at the extracellular and stimulatory at the intracellular side, respectively. The differential effects of hypoxia on ITRPV1,Capand ITRPV1,Acidsuggested that the intracellular ROS increase might attenuate the pharmacological potency of capsaicin.

1Stretch‐activated channels (SACs) were studied in isolated rat atrial myocytes using the whole‐cell and single‐channel patch clamp techniques. Longitudinal stretch was applied by using two patch electrodes.2In current clamp configuration, mechanical stretch of 20 % of resting cell length depolarised the resting membrane potential (RMP) from ‐63·6 ± 0·58 mV (n= 19) to ‐54·6 ± 2·4 mV (n= 13) and prolonged the action potential duration (APD) by 32·2 ± 8·8 ms (n= 7). Depolarisation, if strong enough, triggered spontaneous APs. In the voltage clamp configuration, stretch increased membrane conductance in a progressive manner. The current‐voltage (I–V) relationship of the stretch‐activated current (ISAC) was linear and reversed at ‐6·1 ± 3·7 mV (n= 7).3The inward component of ISACwas abolished by the replacement of Na+with NMDG+, but ISACwas hardly altered by the Cl−channel blocker DIDS or removal of external Cl−. The permeability ratio for various cations (PCs:PNa:PLi= 1·05:1:0·98) indicated that the SAC current was a non‐selective cation current (ISAC,NC). The background current was also found to be non‐selective to cations (INSC,b); the permeability ratio (PCs:PNa:PLi= 1·49:1:0·70) was different from that of ISAC,NC.4Gadolinium (Gd3+) acted on INSC,band ISAC,NCdifferently. Gd3+inhibited INSC,bin a concentration‐dependent manner with an IC50value of 46·2 ± 0·8 μM (n= 5). Consistent with this effect, Gd3+hyperpolarised the resting membrane potential (‐71·1 ± 0·26 mV, n= 9). In the presence of Gd3+(0·1 mM), stretch still induced ISAC,NCand diastolic depolarisation.5Single‐channel activities were recorded in isotonic Na+and Cs+solutions using the inside‐out configuration. In NMDG+solution, outward currents were abolished. Gd3+(100 μM) strongly inhibited channel opening both from the inside and outside. In the presence of Gd3+(100 μM) in the pipette solution, an increase in pipette pressure induced an increase in channel opening (21·27 ± 0·24 pS; n= 7), which was distinct from background activity.6We concluded from the above results that longitudinal stretch in rat atrial myocytes induces the activation of non‐selective cation channels that can be distinguished from background channels by their different electrophysiology and pharmacology.