Journal articles: 'ICAL'

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Alvarez, J. L., and G. Vassort. "Properties of the low threshold Ca current in single frog atrial cardiomyocytes. A comparison with the high threshold Ca current." Journal of General Physiology 100, no. 3 (September 1, 1992): 519–45. http://dx.doi.org/10.1085/jgp.100.3.519.

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The properties of the low threshold Ca current (ICaT) in bullfrog (Rana catesbeiana) isolated atrial cardiomyocytes were studied using the whole-cell recording patch-clamp technique and compared with those of the high threshold Ca current (ICaL). In 91% of atrial cells we observed both ICaT and ICaL when collagenase and trypsin were used to dissociate the cells. But when pronase was used, only 30% of the cells exhibited ICaT. ICaT was never found in ventricular cells. ICaT could be investigated more easily when ICaL was inhibited by Cd ions (50 microM). Its kinetics were unchanged by substituting Ba for Ca, or in the presence of high concentrations of Ba. Both ICaT and ICaL exhibited reduced inactivation after high depolarizing prepulses. ICaT was found to be sensitive to dihydropyridines: 1 microM nifedipine decreased this current while 1 microM BAY K 8644 increased it; this occurred without significant variations in the steady-state inactivation curve. ICaT was more sensitive than ICaL to alpha 1-adrenergic and P2-purinergic stimulations, while ICaL was more sensitive to beta-adrenergic stimulation. Isoproterenol was still able to increase ICaT in the presence of high intracellular cAMP. Both currents were increased by 1 microM ouabain (although ICaL only transiently) and decreased by 10 microM ouabain. It is concluded that the two types of Ca channels can be observed in bullfrog atrial cells and that they are specifically altered by pharmacological agents and neuromediators. This may have implications for cardiac behavior.

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Béhé, P., J. A. DeSimone, P. Avenet, and B. Lindemann. "Membrane currents in taste cells of the rat fungiform papilla. Evidence for two types of Ca currents and inhibition of K currents by saccharin." Journal of General Physiology 96, no. 5 (November 1, 1990): 1061–84. http://dx.doi.org/10.1085/jgp.96.5.1061.

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Taste buds were isolated from the fungiform papilla of the rat tongue and the receptor cells (TRCs) were patch clamped. Seals were obtained on the basolateral membrane of 281 TRCs, protruding from the intact taste buds or isolated by micro-dissection. In whole-cell configuration 72% of the cells had a TTX blockable transient Na inward current (mean peak amplitude 0.74 nA). All cells had outward K currents. Their activation was slower than for the Na current and a slow inactivation was also noticeable. The K currents were blocked by tetraethylammonium, Ba, and 4-aminopyridine, and were absent when the pipette contained Cs instead of K. With 100 mM Ba or 100 mM Ca in the bath, two types of inward current were observed. An L-type Ca current (ICaL) activated at -20 mV had a mean peak amplitude of 440 pA and inactivated very slowly. At 3 mM Ca the activation threshold of ICaL was near -40 mV. A transient T-type current (ICaT) activated at -50 mV had an average peak amplitude of 53 pA and inactivated with a time constant of 36 ms at -30 mV. ICaL was blocked more efficiently by Cd and D600 than ICaT. ICaT was blocked by 0.2 mM Ni and half blocked by 200 microM amiloride. In whole-cell voltage clamp, Na-saccharin caused (in 34% of 55 cells tested) a decrease in outward K currents by 21%, which may be expected to depolarize the TRCs. Also, Na-saccharin caused some taste cells to fire action potentials (on-cell, 7 out of 24 cells; whole-cell, 2 out of 38 cells responding to saccharin) of amplitudes sufficient to activate ICaL. Thus the action potentials will cause Ca inflow, which may trigger release of transmitter.

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Vishnyakova, A. Yu, A. B. Berdalin, D. A. Golovin, S. E. Lelyuk, and V. G. Lelyuk. "Similarities and differences in ultrasound of extracranial brachiocephalic atherosclerotic lesions in patients with ischemic anterior and posterior circulation stroke." Cardiovascular Therapy and Prevention 20, no. 1 (February 19, 2021): 2437. http://dx.doi.org/10.15829/1728-8800-2021-2437.

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Aim. To establish similarities and differences in ultrasound of extracranial brachiocephalic atherosclerotic lesions in patients with ischemic anterior and posterior circulation stroke.Material and methods. The study involved 668 patients (men, 370; women, 298) with carotid territory IS aged 63±11 and 69±9 years, respectively, and 235 patients (men, 129; women, 106) with vertebrobasilar (VB) territory IS aged 59±12 and 63±10 years, respectively, who underwent duplex ultrasound.Results. Atherosclerotic plaques (ASP) in the internal carotid arteries (ICA) were diagnosed significantly more often (p<0,05) (right ICA (ICAr) — 44,0% of cases; left ICA (ICAl) — 48,4%) and the degree of stenosis of ICA mouths was significantly higher (p<0,05) (ICAr —53±23%, ICAl — 54±24%) in carotid territory IS than in VB territory IS (ICAr — 34,0% of cases; average degree of stenosis — 47±18%; ICAl — 33,6%, average degree of stenosis — 46±18%. There were no significant differences in the prevalence of ASP in vertebral arteries and related stenosis in IS in both territories. Also, there were no significant intergroup differences in the prevalence of homogeneous anechoic or hypoechoic and heterogeneous with hypoechoic predominance ASPs in the ICA mouths: in carotid territory IS, such ASPs were detected in each ICA in 33,5% of cases; in VB territory IS, in 29,6% of cases.Conclusion. In patients with carotid and VB territory IS, risky ASPs were recorded with the same frequency, while the overall prevalence of ASPs and the stenosis degree of ICA mouths was significantly higher in carotid IS.

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Avila, Guillermo, Irma M. Medina, Esperanza Jiménez, Guillermo Elizondo, and Citlalli I. Aguilar. "Transforming growth factor-β1 decreases cardiac muscle L-type Ca2+ current and charge movement by acting on the Cav1.2 mRNA." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 1 (January 2007): H622—H631. http://dx.doi.org/10.1152/ajpheart.00781.2006.

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Transforming growth factors-β (TGF-βs) are essential to the structural remodeling seen in cardiac disease and development; however, little is known about potential electrophysiological effects. We hypothesized that chronic exposure (6–48 h) of primary cultured neonatal rat cardiomyocytes to the type 1 TGF-β (TGF-β1, 5 ng/ml) may affect voltage-dependent Ca2+ channels. Thus we investigated T- ( ICaT) and L-type ( ICaL) Ca2+ currents, as well as dihydropyridine-sensitive charge movement using the whole cell patch-clamp technique and quantified CaV1.2 mRNA levels by real-time PCR assay. In ventricular myocytes, TGF-β1 did not exert significant electrophysiological effects. However, in atrial myocytes, TGF-β1 reduced both ICaL and charge movement (55% at 24–48 h) without significantly altering ICaT, cell membrane capacitance, or channel kinetics (voltage dependence of activation and inactivation, as well as the activation and inactivation rates). Reductions of ICaL and charge movement were explained by concomitant effects on the maximal values of L-channels conductance ( Gmax) and charge movement (Qmax). Thus TGF-β1 selectively reduces the number of functional L-channels on the surface of the plasma membrane in atrial but not ventricular myocytes. The TGF-β1-induced ICaL reduction was unaffected by supplementing intracellular recording solutions with okadaic acid (2 μM) or cAMP (100 μM), two compounds that promote L-channel phosphorylation. This suggests that the decreased number of functional L-channels cannot be explained by a possible regulation in the L-channels phosphorylation state. Instead, we found that TGF-β1 decreases the expression levels of atrial CaV1.2 mRNA (70%). Thus TGF-β1 downregulates atrial L-channel expression and may be therefore contributing to the in vivo cardiac electrical remodeling.

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Larochelle, Stéphane. "KRIT-ical interactions." Nature Structural & Molecular Biology 20, no. 2 (February 2013): 143. http://dx.doi.org/10.1038/nsmb.2513.

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Kousha, Jafar, and ali pourhasan sangari. "ical criminal law." Journal of Law Research 22, no. 87 (November 1, 2019): 101–26. http://dx.doi.org/10.29252/lawresearch.22.87.101.

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Treinys, Rimantas, Giedrius Kanaporis, Rodolphe Fischmeister, and Jonas Jurevičius. "Metabolic Inhibition Induces Transient Increase of L-type Ca2+ Current in Human and Rat Cardiac Myocytes." International Journal of Molecular Sciences 20, no. 6 (March 26, 2019): 1501. http://dx.doi.org/10.3390/ijms20061501.

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Metabolic inhibition is a common condition observed during ischemic heart disease and heart failure. It is usually accompanied by a reduction in L-type Ca2+ channel (LTCC) activity. In this study, however, we show that metabolic inhibition results in a biphasic effect on LTCC current (ICaL) in human and rat cardiac myocytes: an initial increase of ICaL is observed in the early phase of metabolic inhibition which is followed by the more classical and strong inhibition. We studied the mechanism of the initial increase of ICaL in cardiac myocytes during β-adrenergic stimulation by isoprenaline, a non-selective agonist of β-adrenergic receptors. The whole-cell patch–clamp technique was used to record the ICaL in single cardiac myocytes. The initial increase of ICaL was induced by a wide range of metabolic inhibitors (FCCP, 2,4-DNP, rotenone, antimycin A). In rat cardiomyocytes, the initial increase of ICaL was eliminated when the cells were pre-treated with thapsigargin leading to the depletion of Ca2+ from the sarcoplasmic reticulum (SR). Similar results were obtained when Ca2+ release from the SR was blocked with ryanodine. These data suggest that the increase of ICaL in the early phase of metabolic inhibition is due to a reduced calcium dependent inactivation (CDI) of LTCCs. This was further confirmed in human atrial myocytes where FCCP failed to induce the initial stimulation of ICaL when Ca2+ was replaced by Ba2+, eliminating CDI of LTCCs. We conclude that the initial increase in ICaL observed during the metabolic inhibition in human and rat cardiomyocytes is a consequence of an acute reduction of Ca2+ release from SR resulting in reduced CDI of LTCCs.

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Brette, Fabien, Alain Lacampagne, Laurent Sallé, Ian Findlay, and Jean-Yves Le Guennec. "Intracellular Cs+ activates the PKA pathway, revealing a fast, reversible, Ca2+-dependent inactivation of L-type Ca2+ current." American Journal of Physiology-Cell Physiology 285, no. 2 (August 2003): C310—C318. http://dx.doi.org/10.1152/ajpcell.00368.2002.

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Inactivation of the L-type Ca2+ current ( ICaL) was studied in isolated guinea pig ventricular myocytes with different ionic solutions. Under basal conditions, ICaL of 82% of cells infused with Cs+-based intracellular solutions showed enhanced amplitude with multiphasic decay and diastolic depolarization-induced facilitation. The characteristics of ICaL in this population of cells were not due to contamination by other currents or an artifact. These phenomena were reduced by ryanodine, caffeine, cyclopiazonic acid, the protein kinase A inhibitor H-89, and the cAMP-dependent protein kinase inhibitor. Forskolin and isoproterenol increased ICaL by only ∼60% in these cells. Cells infused with either N-methyl-d-glucamine or K+-based intracellular solutions did not show multiphasic decay or facilitation under basal conditions. Isoproterenol increased ICaL by ∼200% in these cells. In conclusion, we show that multiphasic inactivation of ICaL is due to Ca2+-dependent inactivation that is reversible on a time scale of tens of milliseconds. Cs+ seems to activate the cAMP-dependent protein kinase pathway when used as a substitute for K+ in the pipette solution.

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Ullrich, Nina D., Andree Krust, Peter Collins, and Kenneth T. MacLeod. "Genomic deletion of estrogen receptors ERα and ERβ does not alter estrogen-mediated inhibition of Ca2+ influx and contraction in murine cardiomyocytes." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 6 (June 2008): H2421—H2427. http://dx.doi.org/10.1152/ajpheart.01225.2007.

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Estrogens modify contraction of vascular smooth muscle and cardiomyocytes, but suggestions that they confer protective effects on the cardiovascular system remain controversial. The negative inotropic effects of estrogens are a consequence of L-type Ca2+ channel inhibition, but the underlying mechanisms remain elusive. We tested the hypothesis that membrane-associated estrogen receptors (ER)-α and -β are involved. We measured the effect of estrogens on Ca2+ current ( ICaL) in isolated ventricular cardiomyocytes of wild-type (WT), ERα knockout (ERαKO), and ERβKO mice using the whole cell patch-clamp technique at 37°C. No differences in current densities or inactivation profiles of ICaL were found under control conditions in WT, ERαKO, and ERβKO cardiomyocytes, suggesting that absence of either ER has no effect on functional properties of ICaL. In all groups, application of raloxifene (2 μM) or 17α- or 17β-estradiol (50 μM) reduced ICaL ( P < 0.001). Raloxifene decreased ICaL by 44 ± 9% (mean ± SE) in WT ( n = 5), 34 ± 5% in ERαKO ( n = 5), and 30 ± 5% in ERβKO mice ( n = 8). 17α-Estradiol reduced ICaL by 41 ± 10% in WT ( n = 4), 34 ± 12% in ERαKO ( n = 7), and 38 ± 8% in ERβKO mice ( n = 7). 17β-Estradiol inhibited ICaL by 31 ± 4% in WT ( n = 4), 28 ± 6% in ERαKO ( n = 3), and 42 ± 3% in ERβKO mice ( n = 5). Decreases in cell shortening occurred in parallel with these findings. Our results suggest that inhibition of ICaL and the decrease in contraction by estrogens do not depend on ERα or ERβ.

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Satyanarayana, B., S. R. Bharathi, Pandi Chinnappan, V. M. Datar, Mamta Jangra, Jim John, S. R. Joshi, et al. "Cosmic Muon Veto for the mini-ICAL detector at IICHEP, Madurai." Journal of Physics: Conference Series 2374, no. 1 (November 1, 2022): 012034. http://dx.doi.org/10.1088/1742-6596/2374/1/012034.

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A 51-kiloton magnetised Iron Calorimeter (ICAL) detector, using Resistive Plate Chambers (RPCs) as active detector elements, aims to study atmospheric neutrinos. A prototype - 1/600 of the weight of ICAL, called mini-ICAL was installed in the INO transit campus at Madurai. A modest proof-of-principle cosmic muon veto detector of about 1 m × 1 m × 0.3 m dimensions was setup a few years ago, using scintillator paddles. The measured cosmic muon veto efficiency of 99.98% and simulation studies of muon-induced background events in the ICAL detector surrounded by an efficient veto detector were promising. This led to the idea of constructing a bigger cosmic muon veto around the mini-ICAL detector. Details of the design and construction of the detector including the electronics, trigger and DAQ systems planned will be briefly presented.

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Chen, Xiongwen, Xiaoying Zhang, David M. Harris, Valentino Piacentino, Remus M. Berretta, Kenneth B. Margulies, and Steven R. Houser. "Reduced effects of BAY K 8644 on L-type Ca2+ current in failing human cardiac myocytes are related to abnormal adrenergic regulation." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 5 (May 2008): H2257—H2267. http://dx.doi.org/10.1152/ajpheart.01335.2007.

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Abnormal L-type Ca2+ channel (LTCC, also named Cav1.2) density and regulation are important contributors to depressed contractility in failing hearts. The LTCC agonist BAY K 8644 (BAY K) has reduced inotropic effects on failing myocardium. We hypothesized that BAY K effects on the LTCC current ( ICaL) in failing myocytes would be reduced because of increased basal activity. Since support of the failing heart with a left ventricular assist device (LVAD) improves contractility and adrenergic responses, we further hypothesized that BAY K effects on ICaL would be restored in LVAD-supported failing hearts. We tested our hypotheses in human ventricular myocytes (HVMs) isolated from nonfailing (NF), failing (F), and LVAD-supported failing hearts. We found that 1) BAY K had smaller effects on ICaL in F HVMs compared with NF HVMs; 2) BAY K had diminished effects on ICaL in NF HVM pretreated with isoproterenol (Iso) or dibutyryl cyclic AMP (DBcAMP); 3) BAY K effects on ICaL in F HVMs pretreated with acetylcholine (ACh) were normalized; 4) Iso had no effect on NF HVMs pretreated with BAY K; 5) BAY K effects on ICaL in LVAD HVMs were similar to those in NF HVMs; 6) BAY K effects were reduced in LVAD HVMs pretreated with Iso or DBcAMP; 7) Iso had no effect on ICaL in LVAD HVMs pretreated with BAY K. Collectively, these results suggest that the decreased BAY K effects on LTCC in F HVMs are caused by increased basal channel activity, which should contribute to abnormal contractility reserve.

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Khindri, Honey, B. Satyanarayana, R. Shinde, V. M. Datar, D. Indumathi, Ram K. V. Thulasi, N. Dalal, et al. "Magnetic field measurements on the mini-ICAL detector using Hall probes." Journal of Instrumentation 17, no. 10 (October 1, 2022): T10006. http://dx.doi.org/10.1088/1748-0221/17/10/t10006.

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Abstract The magnetised 51 kton Iron Calorimeter (ICAL) detector proposed to be built at INO is designed with a focus on detecting 1–20 GeV muons. The magnetic field will enable the measurement of the momentum of the μ - and μ + generated from the charge current interactions of atmospheric νμ and ν̅μ separately within iron in the detector, thus permitting the determination of the neutrino mass ordering/hierarchy, among other important goals of ICAL. Hence it is important to determine the magnetic field as accurately as possible. The mini-ICAL detector is an 85-ton prototype of ICAL, which is operational at Madurai in South India. We describe here the first measurement of the magnetic field in mini-ICAL using Hall sensors. A set-up was developed to calibrate the Hall probe sensors using an electromagnet. The readout system has been designed using an Arduino Nano board for selection of channels of Hall probes mounted on the PCB and the output voltage was measured. The magnetic field has been measured in the small gaps (provided for the purpose) between iron plates in the top layer of mini-ICAL as well as in the air just outside the detector. A precision of better than 3% was obtained, with a sensitivity down to about 3 mT when measuring the small fringe fields outside the detector.

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Farrugia, G., M. J. Macielag, T. L. Peeters, M. G. Sarr, A. Galdes, and J. H. Szurszewski. "Motilin and OHM-11526 activate a calcium current in human and canine jejunal circular smooth muscle." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 2 (August 1, 1997): G404—G412. http://dx.doi.org/10.1152/ajpgi.1997.273.2.g404.

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Motilin is a potent agonist for gastrointestinal smooth muscle contraction and has been proposed to regulate the onset of phase III of the migrating motor complex in dogs and humans. The effects of motilin and OHM-11526, a motilin antagonist in rabbit smooth muscle strips, were examined in isolated canine and human jejunal circular smooth muscle cells using whole cell patch-clamp techniques with Ba2+ as the charge carrier. Effects of both drugs on inward current through L-type Ca2+ channels (ICaL) in both canine and human cells were first observed at 10(-3) M. At 10(-6) M, motilin increased ICaL in canine and human jejunal circular smooth muscle cells by 43 +/- 20 and 45 +/- 11%, respectively, and OHM-11526 increased ICaL by 54 +/- 8 and 54 +/- 14%, respectively. The increase in inward current was blocked by nifedipine and by guanosine 5'-O-(2-thiodiphosphate) but not by pertussis toxin. Washout of both drugs resulted in a further increase in ICaL. These data suggest that both motilin and OHM-11526 activate and ICaL in human and canine jejunal circular smooth muscle cells through a G protein-coupled mechanism.

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Skeberdis, Vytenis, Vida Gendvilienė, Danguolė Zablockaitė, Irma Martišienė, and Antanas Stankevičius. "inhibitor 2-[(4-methylphenyl)sulfonylcarbamido]-1-(4-nitrobenzyl)pyridinium bromide (2-AP27) is a muscarinic M2 receptor antagonist." Medicina 45, no. 7 (July 8, 2009): 516. http://dx.doi.org/10.3390/medicina45070068.

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Aminopyridines are known to inhibit acetylcholine-activated K+ current (IKACh) in cardiac myocytes. The aim of this study was to examine the effect of 2-aminopyridine sulfonylcarbamide derivative 2-AP27 on isoprenaline-stimulated L-type Ca2+ current (ICaL) and to identify whether 2-AP27 acts via blocking of muscarinic M2-receptors in frog cardiomyocytes. The whole-cell configuration of the patch-clamp technique was used to record ICaL in enzymatically isolated cardiac myocytes. Isoprenaline (0.1 μM), an agonist of β1-β2-adrenoreceptors, stimulated the ICaL up to 475±61% (n=4) (P<0.05) vs. control. Then, in the first series of experiments, carbachol (0.01 μM), an agonist of M2 muscarinic receptors, reduced the stimulatory effect of isoprenaline to 42±15% vs. isoprenaline alone. 2- AP27 (100 μM) alone completely abolished the inhibitory effect of carbachol on isoprenaline-stimulated ICaL, which recovered to 95±5.8% of the effect of isoprenaline. In the second series of experiments, adenosine (1 μM), an agonist of A1-adenosine receptors, reduced the stimulatory effect of isoprenaline on ICaL to 56±10% (n=3) (P<0.05). Then 2-AP27 (100 μM) applied in the presence of adenosine, had no effect on ICaL, which remained at 51±7.9% (n=3) (P<0.05) of the effect of isoprenaline. These results suggest that 2-AP27, a new derivative of 2-AP, containing 4-toluolsulfonylcarbamide instead of amino group and quaternizated nitrogen by 4-nitrobenzylbromide in pyridine ring, is acting as an antagonist of muscarinic M2 receptors in frog ventricular myocytes.

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Karpushev, Alexey V., Valeria B. Mikhailova, Ekaterina S. Klimenko, Alexander N. Kulikov, Dmitry Yu Ivkin, Elena Kaschina, and Sergey V. Okovityi. "SGLT2 Inhibitor Empagliflozin Modulates Ion Channels in Adult Zebrafish Heart." International Journal of Molecular Sciences 23, no. 17 (August 23, 2022): 9559. http://dx.doi.org/10.3390/ijms23179559.

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Empagliflozin, an inhibitor of sodium-glucose co-transporter 2 (iSGLT2), improves cardiovascular outcomes in patients with and without diabetes and possesses an antiarrhythmic activity. However, the mechanisms of these protective effects have not been fully elucidated. This study aimed to explore the impact of empagliflozin on ion channel activity and electrophysiological characteristics in the ventricular myocardium. The main cardiac ionic currents (INa, ICaL, ICaT, IKr, IKs) and action potentials (APs) were studied in zebrafish. Whole-cell currents were measured using the patch clamp method in the isolated ventricular cardiomyocytes. The conventional sharp glass microelectrode technique was applied for the recording of APs from the ventricular myocardium of the excised heart. Empagliflozin pretreatment compared to the control group enhanced potassium IKr step current density in the range of testing potentials from 0 to +30 mV, IKr tail current density in the range of testing potentials from +10 to +70 mV, and IKs current density in the range of testing potentials from −10 to +20 mV. Moreover, in the ventricular myocardium, empagliflozin pretreatment shortened AP duration APD as shown by reduced APD50 and APD90. Empagliflozin had no influence on sodium (INa) and L- and T-type calcium currents (ICaL and ICaT) in zebrafish ventricular cardiomyocytes. Thus, we conclude that empagliflozin increases the rapid and slow components of delayed rectifier K+ current (IKr and IKs). This mechanism could be favorable for cardiac protection.

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Ross, Nigel J. "The -ic and -ical pickle." English Today 14, no. 2 (April 1998): 40–44. http://dx.doi.org/10.1017/s026607840001018x.

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English – like all languages – has a predilection for ‘rules’, as grammatical patterns are often called. Generally the patterns are fairly straight-forward, though sometimes they become rather complex, perhaps with numerous exceptions or irregular features. To further obscure the picture, language patterns do not stay still, variations occurring in place and time. At first sight, English word-building elements – such as prefixes and suffixes – would appear to be fairly regular, presenting clear morphological patterns with few exceptions. But first appearances can be deceptive.

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EVTEKHOVA, A. V., E. A. BOREIKO, V. D. Evtekhov, and E. P. GEORGIEVA. "Mineralog-ical Museum. E.K. Fuchs." Geology and mineralogy bulletin of Kryvyi Rih National University 45-46, no. 1-2 (January 21, 2022): 5–13. http://dx.doi.org/10.31721/2306-5443-2021-45-46-1-2-5-13.

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У статті відображено історію створення мінералогічного музею імені Е.К. Фукса, який розташований в одному із приміщень Криворізького національного університету. Перераховано основні експозиції музею та наведено їх склад.

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Tanrasula, Muhammad Agung Tirtayasa Gemuruh Tanrasula, and Muh Akbar. "Sewindu Dramaturgi Komunikasi Politik Deng Ical (Tahun 2013-2021)." Journals of Social, Science, and Engineering 1, no. 1 (May 12, 2022): 32–38. http://dx.doi.org/10.47354/jsse.v1i1.328.

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Saat pilkada, masyarakat akan memilih pemimpinnya, oleh karena itu politisi perlu membangun citra melalui komunikasi politik yang baik agar mendapat kepercayaan masyarakat sehingga dapat dipilih. Penelitian ini mengkaji komunikasi politik yang dilakukan Deng Ical dalam mengelola hubungan dengan masyarakat Makassar dilihat dari perspektif teori dramaturgi Erving Goffman. Metode penelitian menggunakan pendekatan kualitatif. Hasil penelitian ini menjelaskan komunikasi politik dilakukan Deng Ical saat berada di panggung depan dan panggung belakang, bagaimana melakukan kontrol terhadap informasi, dan manejemen impresi. Secara keseluruhan dapat disimpulkan bahwa Deng Ical mampu membangun citra yang baik di mata masyarakat, bahkan dikenal sebagai pemimpin yang merakyat.

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Sahoo, Sadashiv, Anil Kumar, and Sanjib Kumar Agarwalla. "Exploring the Violation of Lorentz Invariance using Atmospheric Neutrinos at INO-ICAL." Journal of Physics: Conference Series 2156, no. 1 (December 1, 2021): 012238. http://dx.doi.org/10.1088/1742-6596/2156/1/012238.

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Abstract We explore the signature of Lorentz Invariance Violation (LIV) in the Standard Model Extension framework by observing the atmospheric neutrinos and antineutrinos separately with the help of magnetized Iron Calorimeter (ICAL) detector at the proposed India-based Neutrino Observatory (INO). Using 500 kt-yr exposure of ICAL, we place stringent bounds on the CPT-violating LIV parameters α μτ , α ॉμ , and aeT (one-at-a-time) at 95% C.L. (1 d.o.f). We demonstrate the advantages of charge identification capability and hadron energy information at ICAL while constraining these LIV parameters. We also explore interesting correlations among various LIV parameters.

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Singh, Jaydip, and Jyotsna Singh. "Atmospheric Muon Charge Ratio Analysis at the INO-ICAL Detector." Advances in High Energy Physics 2019 (July 1, 2019): 1–13. http://dx.doi.org/10.1155/2019/9585234.

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The proposed Iron Calorimeter (ICAL) detector at Indian Neutrino Observatory (INO) will be a large (50 kt) magnetized detector located 1270 m underground at Bodi West Hills in Tamilnadu. ICAL is capable of identifying the charge of the particles. In this paper its potential for the measurement of the muon charge ratio is explored by means of a detailed simulation-based study, first using the CORSIKA code and then comparing it with an analytical model (the pika model). The simulated muon charge ratio is in agreement with the existing experimental observations; its measure can be extended by INO-ICAL up to 10.50 TeV and up to 60 degrees.

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Brette, Fabien, Jean-Yves Le Guennec, and Ian Findlay. "Low-voltage triggering of Ca2+ release from the sarcoplasmic reticulum in cardiac muscle cells." American Journal of Physiology-Cell Physiology 285, no. 6 (December 2003): C1544—C1552. http://dx.doi.org/10.1152/ajpcell.00145.2003.

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This study investigated the interaction between L-type Ca2+ current (ICaL) and Ca2+ release from the sarcoplasmic reticulum (SRCR) in whole cell voltage-clamped guinea pig ventricular myocytes. Quasiphysiological cation solutions (Nao+:KI+) were used for most experiments. In control conditions, there was no obvious interaction between ICaL and SRCR. In isoproterenol, activation of ICaL from voltages between -70 and -50 mV reduced the amplitude and accelerated the decay of the current. Short (50 ms), small-amplitude voltage steps applied 60 or 510 ms before stimulating ICaL inhibited and facilitated the current, respectively. These changes were blocked by ryanodine. Low-voltage activated currents such as T-type Ca2+ current, TTX-sensitive ICa (ICaTTX), or “slip mode” Ca2+ conductance via INa+ were not responsible for low-voltage SRCR. However, L-type Ca2+ currents could be distinguished at voltages as negative as -45 mV. It is concluded that in the presence of isoproterenol, Ca2+ release from the SR at negative potentials is due to activation of L-type Ca2+ channels.

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Sun, Hui, Diego Varela, Denis Chartier, Peter C. Ruben, Stanley Nattel, Gerald W. Zamponi, and Normand Leblanc. "Differential Interactions of Na+ Channel Toxins with T-type Ca2+ Channels." Journal of General Physiology 132, no. 1 (June 30, 2008): 101–13. http://dx.doi.org/10.1085/jgp.200709883.

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Two types of voltage-dependent Ca2+ channels have been identified in heart: high (ICaL) and low (ICaT) voltage-activated Ca2+ channels. In guinea pig ventricular myocytes, low voltage–activated inward current consists of ICaT and a tetrodotoxin (TTX)-sensitive ICa component (ICa(TTX)). In this study, we reexamined the nature of low-threshold ICa in dog atrium, as well as whether it is affected by Na+ channel toxins. Ca2+ currents were recorded using the whole-cell patch clamp technique. In the absence of external Na+, a transient inward current activated near −50 mV, peaked at −30 mV, and reversed around +40 mV (HP = −90 mV). It was unaffected by 30 μM TTX or micromolar concentrations of external Na+, but was inhibited by 50 μM Ni2+ (by ∼90%) or 5 μM mibefradil (by ∼50%), consistent with the reported properties of ICaT. Addition of 30 μM TTX in the presence of Ni2+ increased the current approximately fourfold (41% of control), and shifted the dose–response curve of Ni2+ block to the right (IC50 from 7.6 to 30 μM). Saxitoxin (STX) at 1 μM abolished the current left in 50 μM Ni2+. In the absence of Ni2+, STX potently blocked ICaT (EC50 = 185 nM) and modestly reduced ICaL (EC50 = 1.6 μM). While TTX produced no direct effect on ICaT elicited by expression of hCaV3.1 and hCaV3.2 in HEK-293 cells, it significantly attenuated the block of this current by Ni2+ (IC50 increased to 550 μM Ni2+ for CaV3.1 and 15 μM Ni2+ for CaV3.2); in contrast, 30 μM TTX directly inhibited hCaV3.3-induced ICaT and the addition of 750 μM Ni2+ to the TTX-containing medium led to greater block of the current that was not significantly different than that produced by Ni2+ alone. 1 μM STX directly inhibited CaV3.1-, CaV3.2-, and CaV3.3-mediated ICaT but did not enhance the ability of Ni2+ to block these currents. These findings provide important new implications for our understanding of structure–function relationships of ICaT in heart, and further extend the hypothesis of a parallel evolution of Na+ and Ca2+ channels from an ancestor with common structural motifs.

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Ying, Xiao, Long Weiqing, Lu Guihua, Zhang Juhong, and Zhibin Huang. "Effect of Valsartan on Sarcoplasmic Reticulum Ca2+-ATPase Pump of the Left Ventricular Myocardium in Rats with Heart Failure with Preserved Ejection Fraction." Biomedicine Hub 1, no. 2 (July 30, 2016): 1–9. http://dx.doi.org/10.1159/000448132.

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Objectives: The aim was to investigate the effects of valsartan on the sarcoplasmic reticulum Ca2+-ATPase pump (SERCA) and L-type Ca2+ channel current (ICaL) of the left ventricular myocardium in rats with heart failure with preserved ejection fraction. Methods: The 30-week-old male spontaneously hypertensive rats (SHRs) are randomly divided into the non-Valsartan and Valsartan groups, and the 30-week-old male Wistar-Kyoto rats served as control rats. The expression of SERCA is measured by Western blot. The ICaL is measured by whole-cell patch clamp. The left ventricular end-diastolic pressure and left ventricular relaxation time constant quantity are measured at the same time. Results: The left ventricular end-diastolic pressure is much higher in SHRs compared with that in control rats (p < 0.01). The left ventricular relaxation time constant quantity is markedly extended in SHRs compared with control rats (p < 0.01). Valsartan cannot increase the expression of SERCA nor decrease the density of ICaL compared with the non-Valsartan group (p > 0.05). Conclusions: Valsartan has no effect on SERCA and ICaL of the left ventricular myocardium in rats with heart failure with preserved ejection fraction.

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Seth, S., A. Bhatt, G. Majumder, and A. Mishra. "Update of INO-ICAL reconstruction algorithm." Journal of Instrumentation 13, no. 09 (September 18, 2018): P09015. http://dx.doi.org/10.1088/1748-0221/13/09/p09015.

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Ajmi, A., and S. U. Sankar. "Muonless events in ICAL at INO." Journal of Instrumentation 10, no. 04 (April 20, 2015): P04006. http://dx.doi.org/10.1088/1748-0221/10/04/p04006.

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Fauconnier, Jérémy, Alain Lacampagne, Jean-Michel Rauzier, Pierre Fontanaud, Jean-Marc Frapier, Ole M. Sejersted, Guy Vassort, and Sylvain Richard. "Frequency-dependent and proarrhythmogenic effects of FK-506 in rat ventricular cells." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 2 (February 2005): H778—H786. http://dx.doi.org/10.1152/ajpheart.00542.2004.

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FK-506, a widely used immunosuppressant, has caused a few clinical cases with QT prolongation and torsades de pointe at high blood concentration. The proarrhytmogenic potential of FK-506 was investigated in single rat ventricular cells using the whole cell clamp method to record action potentials (APs) and ionic currents. Fluorescence measurements of Ca2+ transients were performed with indo-1 AM using a multiphotonic microscope. FK-506 (25 μmol/l) hyperpolarized the resting membrane potential (RMP; −3 mV) and prolonged APs (AP duration at 90% repolarization increased by 21%) at 0.1 Hz. Prolongation was enhanced by threefold at 3.3 Hz, and early afterdepolarizations (EADs) occurred in 59% of cells. EADs were prevented by stronger intracellular Ca2+ buffering (EGTA: 10 vs. 0.5 mmol/l in the patch pipette) or replacement of extracellular Na+ by Li+, which abolishes Na+/Ca2+ exchange [Na+/Ca2+ exchanger current ( INaCa)]. In indo-1-loaded cells, FK-506 generated doublets of Ca2+ transients associated with increased diastolic Ca2+ in one-half of the cells. FK-506 reversibly decreased the L-type Ca2+ current ( ICaL) by 25%, although high-frequency-dependent facilitation of ICaL persisted, and decreased three distinct K+ currents: delayed rectifier K+ current ( IK; >80%), transient outward K+ current (<20%), and inward rectifier K+ current ( IK1; >40%). A shift in the reversal potential of IK1 (−5 mV) accounted for RMP hyperpolarization. Numerical simulations, reproducing all experimental effects of FK-506, and the use of nifedipine showed that frequency-dependent facilitation of ICaL plays a role in the occurrence of EADs. In conclusion, the effects of FK-506 on the cardiac AP are more complex than previously reported and include inhibitions of IK1 and ICaL. Alterations in Ca2+ release and INaCa may contribute to FK-506-induced AP prolongation and EADs in addition to the permissive role of ICaL facilitation at high rates of stimulation.

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Pachajoa, Diana C., Catalina Tobón, Juan P. Ugarte, and Javier Saiz. "CO, Pb++ and SO2 effects on L-type calcium channel and action potential in human atrial myocytes. In silico study." TecnoLógicas 20, no. 40 (September 4, 2017): 113–23. http://dx.doi.org/10.22430/22565337.718.

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Exposure to air pollutants like carbon monoxide (CO), lead (Pb++) and sulfur dioxide (SO2) promotes the occurrence of cardiovascular diseases. Experimental studies have shown that CO, Pb++ and SO2 block L-type calcium channels, reducing the calcium current (ICaL) and the action potential duration (APD), which favors the initiation of atrial arrhythmias. The goal is to study the effects of CO, Pb++ and SO2 at different concentrations on ICaL and action potential using computational simulation. For this purpose, models of the effects of the air pollutants on the atrial L-type calcium channel were developed and were incorporated into a mathematical model of a human atrial cell. The results suggest that CO, Pb++ and SO2 block the ICaL current in a fraction that increases along with the concentration, generating an APD shortening. These results are consistent with experimental studies. The combined effect of the three air pollutants produced an APD shortening, which is considered to be a pro-arrhythmic effect.

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Kurata, Yasutaka, Kunichika Tsumoto, Kenshi Hayashi, Ichiro Hisatome, Mamoru Tanida, Yuhichi Kuda, and Toshishige Shibamoto. "Dynamical mechanisms of phase-2 early afterdepolarizations in human ventricular myocytes: insights from bifurcation analyses of two mathematical models." American Journal of Physiology-Heart and Circulatory Physiology 312, no. 1 (January 1, 2017): H106—H127. http://dx.doi.org/10.1152/ajpheart.00115.2016.

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Early afterdepolarization (EAD) is known as a cause of ventricular arrhythmias in long QT syndromes. We theoretically investigated how the rapid ( IKr) and slow ( IKs) components of delayed-rectifier K+ channel currents, L-type Ca2+ channel current ( ICaL), Na+/Ca2+ exchanger current ( INCX), Na+-K+ pump current ( INaK), intracellular Ca2+ (Cai) handling via sarcoplasmic reticulum (SR), and intracellular Na+ concentration (Nai) contribute to initiation, termination, and modulation of phase-2 EADs, using two human ventricular myocyte models. Bifurcation structures of dynamical behaviors in model cells were explored by calculating equilibrium points, limit cycles (LCs), and bifurcation points as functions of parameters. EADs were reproduced by numerical simulations. The results are summarized as follows: 1) decreasing IKs and/or IKr or increasing ICaL led to EAD generation, to which mid-myocardial cell models were especially susceptible; the parameter regions of EADs overlapped the regions of stable LCs. 2) Two types of EADs (termination mechanisms), IKs activation–dependent and ICaL inactivation–dependent EADs, were detected; IKs was not necessarily required for EAD formation. 3) Inhibiting INCX suppressed EADs via facilitating Ca2+-dependent ICaL inactivation. 4) Cai dynamics (SR Ca2+ handling) and Nai strongly affected bifurcations and EAD generation in model cells via modulating ICaL, INCX, and INaK. Parameter regions of EADs, often overlapping those of stable LCs, shifted depending on Cai and Nai in stationary and dynamic states. 5) Bradycardia-related induction of EADs was mainly due to decreases in Nai at lower pacing rates. This study demonstrates that bifurcation analysis allows us to understand the dynamical mechanisms of EAD formation more profoundly. NEW & NOTEWORTHY We investigated mechanisms of phase-2 early afterdepolarization (EAD) by bifurcation analyses of human ventricular myocyte (HVM) models. EAD formation in paced HVMs basically depended on bifurcation phenomena in non-paced HVMs, but was strongly affected by intracellular ion concentrations in stationary and dynamic states. EAD generation did not necessarily require IKs.

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Ballah, Fatimah Muhammad, Md Saiful Islam, Md Liton Rana, Farhana Binte Ferdous, Rokeya Ahmed, Pritom Kumar Pramanik, Jarna Karmoker, et al. "Phenotypic and Genotypic Detection of Biofilm-Forming Staphylococcus aureus from Different Food Sources in Bangladesh." Biology 11, no. 7 (June 22, 2022): 949. http://dx.doi.org/10.3390/biology11070949.

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Staphylococcus aureus is a major foodborne pathogen. The ability of S. aureus to produce biofilm is a significant virulence factor, triggering its persistence in hostile environments. In this study, we screened a total of 420 different food samples and human hand swabs to detect S. aureus and to determine their biofilm formation ability. Samples analyzed were meat, milk, eggs, fish, fast foods, and hand swabs. S. aureus were detected by culturing, staining, biochemical, and PCR. Biofilm formation ability was determined by Congo Red Agar (CRA) plate and Crystal Violet Microtiter Plate (CVMP) tests. The icaA, icaB, icaC, icaD, and bap genes involved in the synthesis of biofilm-forming intracellular adhesion compounds were detected by PCR. About 23.81% (100/420; 95% CI: 14.17–29.98%) of the samples harbored S. aureus, as revealed by detection of the nuc gene. The CRA plate test revealed 20% of S. aureus isolates as strong biofilm producers and 69% and 11% as intermediate and non-biofilm producers, respectively. By the CVMP staining method, 20%, 77%, and 3% of the isolates were found to be strong, intermediate, and non-biofilm producers. Furthermore, 21% of S. aureus isolates carried at least one biofilm-forming gene, where icaA, icaB, icaC, icaD, and bap genes were detected in 15%, 20%, 7%, 20%, and 10% of the S. aureus isolates, respectively. Bivariate analysis showed highly significant correlations (p < 0.001) between any of the two adhesion genes of S. aureus isolates. To the best of our knowledge, this is the first study in Bangladesh describing the detection of biofilm-forming S. aureus from foods and hand swabs using molecular-based evidence. Our findings suggest that food samples should be deemed a potential reservoir of biofilm-forming S. aureus, which indicates a potential public health significance.

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Mello, Priscila Luiza, Danilo Flávio Moraes Riboli, Lisiane de Almeida Martins, Maria Aparecida Vasconcelos Paiva Brito, Cassiano Victória, Letícia Calixto Romero, and Maria de Lourdes Ribeiro de Souza da Cunha. "Staphylococcus spp. Isolated from Bovine Subclinical Mastitis in Different Regions of Brazil: Molecular Typing and Biofilm Gene Expression Analysis by RT-qPCR." Antibiotics 9, no. 12 (December 10, 2020): 888. http://dx.doi.org/10.3390/antibiotics9120888.

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Bovine mastitis is mainly caused by bacteria of the genus Staphylococcus spp., which possess different virulence factors, including the capacity for biofilm formation that provides enhanced protection against the action of immune system components and serves as a barrier against the penetration of antimicrobial agents. This study aimed to characterize 181 Staphylococcus spp. Strains—including Staphylococcusaureus and coagulase-negative staphylococci (CoNS) isolated from bovine subclinical mastitis in six Brazilian states—by molecular methods. RT-qPCR was used to verify the expression of genes of the ica operon—mainly responsible for biofilm formation—as well as bap and bhp. Chromosome similarity among the isolates was investigated by pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST). The icaA gene was detected in 79 (43.6%) isolates, icaB in 24 (13.2%), icaC in 57 (31.4%), and icaD in 127 (70.1%). The bap gene was identified in 66 (36.4%) isolates, while the bhp gene was found in nine (4.9%). RT-qPCR confirmed the expression of the icaA gene in 60 (75.9%) isolates, of icaB in six (25%), of icaC in 26 (45.6%), and of icaD in 80 (63%). Clonal typing of the isolates by PFGE permitted the identification of eight Staphylococcusaureus clusters that simultaneously included ≥3 strains, with a similarity of ≥80%. Regarding the other species studied, three clusters were observed for Staphylococcuschromogenes and four clusters for Staphylococcusepidermidis. Only one cluster each was identified for Staphylococcussaprophyticus and Staphylococcussimulans, while the other species did not form any cluster. With respect to MLST, ST126 and ST1 were the prevalent sequence types in S. aureus, while in S.epidermidis all sequence types were different. These results reveal strains with the same evolutionary origin as other isolates, which might cause infections in humans and animals, suggesting their ability to spread between these species.

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Chung, Hye-yoon. "Contemporary Analytic Philosophy on Mus ical Expressiveness." Journal of The Society of philosophical studies 132 (March 31, 2021): 173–98. http://dx.doi.org/10.23908/jsps.2021.3.132.173.

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Sullivan, Meghan R., and Kara A. Bernstein. "RAD-ical New Insights into RAD51 Regulation." Genes 9, no. 12 (December 13, 2018): 629. http://dx.doi.org/10.3390/genes9120629.

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The accurate repair of DNA is critical for genome stability and cancer prevention. DNA double-strand breaks are one of the most toxic lesions; however, they can be repaired using homologous recombination. Homologous recombination is a high-fidelity DNA repair pathway that uses a homologous template for repair. One central HR step is RAD51 nucleoprotein filament formation on the single-stranded DNA ends, which is a step required for the homology search and strand invasion steps of HR. RAD51 filament formation is tightly controlled by many positive and negative regulators, which are collectively termed the RAD51 mediators. The RAD51 mediators function to nucleate, elongate, stabilize, and disassemble RAD51 during repair. In model organisms, RAD51 paralogs are RAD51 mediator proteins that structurally resemble RAD51 and promote its HR activity. New functions for the RAD51 paralogs during replication and in RAD51 filament flexibility have recently been uncovered. Mutations in the human RAD51 paralogs (RAD51B, RAD51C, RAD51D, XRCC2, XRCC3, and SWSAP1) are found in a subset of breast and ovarian cancers. Despite their discovery three decades ago, few advances have been made in understanding the function of the human RAD51 paralogs. Here, we discuss the current perspective on the in vivo and in vitro function of the RAD51 paralogs, and their relationship with cancer in vertebrate models.

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Risin, I. E., and I. N. Petrykina. "VORONEZH REGION SOCIOECONOM ICAL POLICY BASIC COMPONENTS." Region:systems,economics,management 38, no. 3 (2017): 48–51. http://dx.doi.org/10.22394/1997-4469-2017-38-3-48-51.

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Kissa, Jamila, Wafa El Kholti, Khadija Sekak, and Sihame Chemlali. "Multidisciplinary Approach to Cover an Apex-Exposed Tooth: A Case Report after 6-Year Follow-Up." Case Reports in Dentistry 2019 (April 7, 2019): 1–5. http://dx.doi.org/10.1155/2019/8020747.

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Introduction. The prognosis for a successful treatment of gingival recessions (GRs) is one of the main criteria for deciding whether or not and how to perform root coverage surgery. The defect-related factors are the most important to predict root coverage outcomes. Thus, severe GR could make the root coverage (RC) challenging especially in cases with advanced interdental clinical attachment loss (ICAL). Case Presentation. This case report demonstrates a challenging management of a deep localized Miller Class III GR with root apex exposure associated with ICAL. After initial therapy, the treatment had consisted of a multidisciplinary approach involving endodontic treatment, periodontal plastic surgery including a laterally positioned flap, and orthodontic treatment. The 6-year follow-up showed improvement in clinical outcomes (recession reduction (RR) and keratinized tissue (KT) augmentation) and a higher patient satisfaction. Conclusions. This case report demonstrates the role of the multidisciplinary approach in the management of deep GRs associated with ICAL. A rational choice of the RC technique was critical to achieve good clinical outcomes.

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Evdokimovskii, Edward V., Ryounghoon Jeon, Sungjo Park, Oleg Y. Pimenov, and Alexey E. Alekseev. "Role of α2-Adrenoceptor Subtypes in Suppression of L-Type Ca2+ Current in Mouse Cardiac Myocytes." International Journal of Molecular Sciences 22, no. 8 (April 16, 2021): 4135. http://dx.doi.org/10.3390/ijms22084135.

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Sarcolemmal α2 adrenoceptors (α2-AR), represented by α2A, α2B and α2C isoforms, can safeguard cardiac muscle under sympathoadrenergic surge by governing Ca2+ handling and contractility of cardiomyocytes. Cardiomyocyte-specific targeting of α2-AR would provide cardiac muscle-delimited stress control and enhance the efficacy of cardiac malfunction treatments. However, little is known about the specific contribution of the α2-AR subtypes in modulating cardiomyocyte functions. Herein, we analyzed the expression profile of α2A, α2B and α2C subtypes in mouse ventricle and conducted electrophysiological antagonist assay evaluating the contribution of these isoforms to the suppression of L-type Ca2+ current (ICaL). Patch-clamp electro-pharmacological studies revealed that the α2-agonist-induced suppression of ICaL involves mainly the α2C, to a lesser extent the α2B, and not the α2A isoforms. RT-qPCR evaluation revealed the presence of adra2b and adra2c (α2B and α2C isoform genes, respectively), but was unable to identify the expression of adra2a (α2A isoform gene) in the mouse left ventricle. Immunoblotting confirmed the presence only of the α2B and the α2C proteins in this tissue. The identified α2-AR isoform-linked regulation of ICaL in the mouse ventricle provides an important molecular substrate for the cardioprotective targeting.

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Hui, Le, Xiang Li, Chen Gong, Meng Fang, Joey Tianyi Zhou, and Jian Yang. "Inter-Class Angular Loss for Convolutional Neural Networks." Proceedings of the AAAI Conference on Artificial Intelligence 33 (July 17, 2019): 3894–901. http://dx.doi.org/10.1609/aaai.v33i01.33013894.

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Convolutional Neural Networks (CNNs) have shown great power in various classification tasks and have achieved remarkable results in practical applications. However, the distinct learning difficulties in discriminating different pairs of classes are largely ignored by the existing networks. For instance, in CIFAR-10 dataset, distinguishing cats from dogs is usually harder than distinguishing horses from ships. By carefully studying the behavior of CNN models in the training process, we observe that the confusion level of two classes is strongly correlated with their angular separability in the feature space. That is, the larger the inter-class angle is, the lower the confusion will be. Based on this observation, we propose a novel loss function dubbed “Inter-Class Angular Loss” (ICAL), which explicitly models the class correlation and can be directly applied to many existing deep networks. By minimizing the proposed ICAL, the networks can effectively discriminate the examples in similar classes by enlarging the angle between their corresponding class vectors. Thorough experimental results on a series of vision and nonvision datasets confirm that ICAL critically improves the discriminative ability of various representative deep neural networks and generates superior performance to the original networks with conventional softmax loss.

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Lebed’, Е. "Traditions of domest ic folklore and class ical mus ical art As a source of Composer Anatoly Krivoshey’s creativity." Bulletin of the South Ural State University Series «Social Sciences and the Humanities» 20, no. 02 (2020): 113–16. http://dx.doi.org/10.14529/ssh200215.

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Verkerk, Arie O., Illés J. Doszpod, Isabella Mengarelli, Tibor Magyar, Alexandra Polyák, Bence Pászti, Igor R. Efimov, Ronald Wilders, and István Koncz. "Acetylcholine Reduces L-Type Calcium Current without Major Changes in Repolarization of Canine and Human Purkinje and Ventricular Tissue." Biomedicines 10, no. 11 (November 21, 2022): 2987. http://dx.doi.org/10.3390/biomedicines10112987.

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Vagal nerve stimulation (VNS) holds a strong basis as a potentially effective treatment modality for chronic heart failure, which explains why a multicenter VNS study in heart failure with reduced ejection fraction is ongoing. However, more detailed information is required on the effect of acetylcholine (ACh) on repolarization in Purkinje and ventricular cardiac preparations to identify the advantages, risks, and underlying cellular mechanisms of VNS. Here, we studied the effect of ACh on the action potential (AP) of canine Purkinje fibers (PFs) and several human ventricular preparations. In addition, we characterized the effects of ACh on the L-type Ca2+ current (ICaL) and AP of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and performed computer simulations to explain the observed effects. Using microelectrode recordings, we found a small but significant AP prolongation in canine PFs. In the human myocardium, ACh slightly prolonged the AP in the midmyocardium but resulted in minor AP shortening in subepicardial tissue. Perforated patch-clamp experiments on hiPSC-CMs demonstrated that 5 µM ACh caused an ≈15% decrease in ICaL density without changes in gating properties. Using dynamic clamp, we found that under blocked K+ currents, 5 µM ACh resulted in an ≈23% decrease in AP duration at 90% of repolarization in hiPSC-CMs. Computer simulations using the O’Hara–Rudy human ventricular cell model revealed that the overall effect of ACh on AP duration is a tight interplay between the ACh-induced reduction in ICaL and ACh-induced changes in K+ currents. In conclusion, ACh results in minor changes in AP repolarization and duration of canine PFs and human ventricular myocardium due to the concomitant inhibition of inward ICaL and outward K+ currents, which limits changes in net repolarizing current and thus prevents major changes in AP repolarization.

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Haworth, Thomas Eliot, Jaakko Haverinen, Holly A. Shiels, and Matti Vornanen. "Electrical excitability of the heart in a Chondrostei fish, the Siberian sturgeon (Acipenser baerii)." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 9 (November 1, 2014): R1157—R1166. http://dx.doi.org/10.1152/ajpregu.00253.2014.

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Sturgeon (family Acipenseridae) are regarded as living fossils due to their ancient origin and exceptionally slow evolution. To extend our knowledge of fish cardiac excitability to a Chondrostei fish, we examined electrophysiological phenotype of the Siberian sturgeon ( Acipenser baerii) heart with recordings of epicardial ECG, intracellular action potentials (APs), and sarcolemmal ion currents. Epicardial ECG of A. baerii had the typical waveform of the vertebrate ECG with Q-T interval (average duration of ventricular AP) of 650 ± 30 ms and an intrinsic heart rate of 45.5 ± 5 beats min−1 at 20°C. Similar to other fish species, atrial AP was shorter in duration (402 ± 33 ms) than ventricular AP (585 ± 40) ( P < 0.05) at 20°C. Densities of atrial and ventricular Na+ currents were similar (−47.6 ± 4.5 and −53.2 ± 5.1 pA/pF, respectively) and close to the typical values of teleost hearts. Two major K+ currents, the inward rectifier K+ current ( IK1), and the delayed rectifier K+ current ( IKr) were found under basal conditions in sturgeon cardiomyocytes. The atrial IKr (3.3 ± 0.2 pA/pF) was about twice as large as the ventricular IKr (1.3 ± 0.4 pA/pF) ( P < 0.05) conforming to the typical pattern of teleost cardiac IKr. Divergent from other fishes, the ventricular IK1 was remarkably small (−2.5 ± 0.07 pA/pF) and not different from that of the atrial myocytes (−1.9 ± 0.06 pA/pF) ( P > 0.05). Two ligand-gated K+ currents were also found: ACh-activated inward rectifier ( IKACh) was present only in atrial cells, while ATP-sensitive K+ current ( IKATP) was activated by a mitochondrial blocker, CCCP, in both atrial and ventricular cells. The most striking difference to other fishes appeared in Ca2+ currents ( ICa). In atrial myocytes, ICa was predominated by nickel-sensitive and nifedipine-resistant T-type ICa, while ventricular myocytes had mainly nifedipine-sensitive and nickel-resistant L-type ICa. ICaT/ ICaL ratio of the sturgeon atrial myocytes (2.42) is the highest value ever measured for a vertebrate species. In ventricular myocytes, ICaT/ ICaL ratio was 0.09. With the exception of the large atrial ICaT and small ventricular IK1, electrical excitability of A. baerii heart is similar to that of teleost hearts.

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Mahdavi, Fatemeh Soghra, Rabieh Izadi Amoli, and Roghaye Oskooeian. "Molecular Identification of icaA, icaB, icaC and icaD Genes in Staphylococcus aureus Clinical Isolates Resistant to Methicillin." Alborz University Medical Journal 8, no. 3 (August 1, 2019): 245–52. http://dx.doi.org/10.29252/aums.8.3.245.

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Ahmad, Pishtiwan. "PHENOTYPIC AND MOLECULAR DETECTION OF BIOFILM FORMATION IN METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS ISOLATED FROM DIFFERENT CLINICAL SOURCE IN ERBIL CITY." Mediterranean Journal of Hematology and Infectious Diseases 15, no. 1 (February 28, 2023): e2023016. http://dx.doi.org/10.4084/mjhid.2023.016.

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Abstract. Background: Staphylococcus aureus is an important causative pathogen. The production of biofilms is an important factor and makes these bacteria resistant to antimicrobial therapy. Objectives: the current study aimed to assess the prevalence of resistance to antibacterial agents and to evaluate the phenotypic and genotypic characterization of biofilm formation among S. aureus strains. Methods: In this study, 50 isolates of Methicillin-resistant S. aureus (MRSA) and Methicillin-Susceptible S. aureus (MSSA) were included. S. aureus was identified by molecular and conventional methods. Antimicrobial resistance was tested with a disc diffusion method. The biofilm formation was performed through Microtiter plate method. Strains were subjected to PCR to determine the presence of nuc, mecA, icaA, icaB, icaC, and icaD gene. Results: Of the total 50 S. aureus isolates, 32(64%) and 18(36%) were MRSA and MSSA respectively. A large number of MRSA and MSSA isolates showed resistance to Penicillin and Azithromycin and a lower number of MRSA and MSSA isolates showed resistance to Amikacin Gentamicin and none of the isolates was resistant to Vancomycin. The MRSA strains had significantly higher resistance against antibiotics than MSSA strains (P = 0.0154). All isolates (MRSA and MSSA) were able to produce biofilm with levels ranging from strong (31.25 %), (16.6%) to moderate (53.12%), (50%) to weak (15.6 %), (33.3% %) respectively. The MRSA strains had significantly higher ability of biofilm formation than MSSA strains (P = 0.0079). The biofilm encoding genes were detected among isolates with different frequencies. The majority of S. aureus isolates 42 (84%), were found to be positive for the icaA. The prevalence rates of the icaB, icaC, and icaD genes were found to be 37 (74%), 40 (80%) and 41 (82%) respectively. Conclusions: The prevalence of biofilm encoding genes, which are associated with multidrug resistance in S. aureus strains, is high. Therefore, identification of epidemiology, molecular characteristics, and biofilm management of S. aureus infection would be helpful.

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Malcolm Ross. "10-ICAL historical-comparative papers (review)." Oceanic Linguistics 48, no. 1 (2009): 274–86. http://dx.doi.org/10.1353/ol.0.0031.

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Ito, Akio, and Yoshifumi Takahashi. "Ecolog ical Footprint Analysis using Input-Output Table." Input-Output Analysis 14, no. 1 (2006): 27–34. http://dx.doi.org/10.11107/papaios.14.27.

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Phogat, Aman, Ankit Gaur, Moh Rafik, Ashok Kumar, and Md Naimuddin. "New front-end electronics for INO-ICAL experiment." Nuclear Instruments and Methods in Physics Research Section A: Accelerators, Spectrometers, Detectors and Associated Equipment 905 (October 2018): 193–98. http://dx.doi.org/10.1016/j.nima.2018.07.070.

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Yazdanbakhsh, Karina. "FcγR and SCD alloimmunization: a nonclass(ical) act." Blood 130, no. 19 (November 9, 2017): 2051–52. http://dx.doi.org/10.1182/blood-2017-09-807198.

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James, Casie, Randall Craver, and Isa Ashoor. "An A-Tip-ical Side Effect of Lithium." Pediatrics 147, no. 3_MeetingAbstract (March 1, 2021): 847–48. http://dx.doi.org/10.1542/peds.147.3ma9.847.

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Pirotte, Benoît, Boris Krischek, Marc Levivier, Serge Bolyn, Jean-Marie Brucher, and Jacques Brotchi. "Diagnostic and microsurgical presentation of intracranial angiolipomas." Journal of Neurosurgery 88, no. 1 (January 1998): 129–32. http://dx.doi.org/10.3171/jns.1998.88.1.0129.

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✓ Angiolipomas (ALs) are hamartomas composed of abnormally differentiated vessels and mature adipose tissue. Although they are most commonly found in peripheral tissues, ALs sometimes grow in the spinal epidural space. Intracranial ALs (ICALs) are rare: only seven cases have been reported in the literature. The authors describe the case of a 70-year-old woman who presented with ocular symptoms from a clinically and radiologically progressing parasellar ICAL. The radiological as well as the microsurgical findings are illustrated and compared with the seven previously published cases. The most frequent location of ALs is the skull base, especially the parasellar region. Other ICALs were diagnosed as components of cerebral arteriovenous malformations and were not symptomatic by themselves. Neuroradiological studies of ICALs usually demonstrate the characteristics of both adipose and vascular tissues. However, a review of the literature shows that the diagnosis had not been suspected preoperatively in any of the cases. Operative descriptions emphasize that most neurosurgeons were caught off guard by the profuse bleeding and the unusual relationship of this unexpected lesion to the cavernous sinus, so that removal was rarely complete. The authors conclude that preoperative diagnosis of ICALs is achievable based on magnetic resonance analysis, which should help optimize the microsurgical management of these lesions.

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SAMANTA, ABHIJIT, SUDEB BHATTACHARYA, AMBAR GHOSAL, KAMALES KAR, DEBASISH MAJUMDAR, and AMITAVA RAYCHAUDHURI. "A GEANT-BASED STUDY OF ATMOSPHERIC NEUTRINO OSCILLATION PARAMETERS AT INO." International Journal of Modern Physics A 23, no. 02 (January 20, 2008): 233–45. http://dx.doi.org/10.1142/s0217751x08037968.

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We have studied the dependence of the allowed space of the atmospheric neutrino oscillation parameters on the time of exposure for a magnetized Iron CALorimeter (ICAL) detector at the India-based Neutrino Observatory (INO). We have performed a Monte Carlo simulation for a 50 kTon ICAL detector generating events by the neutrino generator NUANCE and simulating the detector response by GEANT. A chi-square analysis for the ratio of the up-going and down-going neutrinos as a function of L/E is performed and the allowed regions at 90% and 99% CL are displayed. These results are found to be better than the current experimental results of MINOS and Super-K. The possibilities of further improvement have also been discussed.

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Datyner, N. B., and I. S. Cohen. "Slow inactivation of L-type calcium current distorts the measurement of L- and T-type calcium current in Purkinje myocytes." Journal of General Physiology 102, no. 5 (November 1, 1993): 859–69. http://dx.doi.org/10.1085/jgp.102.5.859.

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We have examined slow inactivation of L-type calcium current in canine Purkinje myocytes with the whole cell patch clamp technique. Slow inactivation is voltage dependent. It is negligible at -50 mV but can inactivate more than half of available iCaL at -10 mV. There are two major consequences of this slow inactivation. First, standard protocols for the measurement of T-type current can dramatically overestimate its contribution to total calcium current, and second, the position and steepness of the inactivation versus voltage curve for iCaL will depend on the method of measurement. Given the widespread attempts to identify calcium current components and characterize them biophysically, an important first step should be to determine the extent of slow inactivation of calcium current in each preparation.

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Lin, Yen-Chang, Jianying Huang, Hong Kan, Vincent Castranova, Jefferson C. Frisbee, and Han-Gang Yu. "Defective calcium inactivation causes long QT in obese insulin-resistant rat." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 4 (February 15, 2012): H1013—H1022. http://dx.doi.org/10.1152/ajpheart.00837.2011.

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The majority of diabetic patients who are overweight or obese die of heart disease. We suspect that the obesity-induced insulin resistance may lead to abnormal cardiac electrophysiology. We tested this hypothesis by studying an obese insulin-resistant rat model, the obese Zucker rat (OZR). Compared with the age-matched control, lean Zucker rat (LZR), OZR of 16–17 wk old exhibited an increase in QTc interval, action potential duration, and cell capacitance. Furthermore, the L-type calcium current ( ICaL) in OZR exhibited defective inactivation and lost the complete inactivation back to the closed state, leading to increased Ca2+ influx. The current density of ICaL was reduced in OZR, whereas the threshold activation and the current-voltage relationship of ICaL were not significantly altered. L-type Ba2+ current ( IBaL) in OZR also exhibited defective inactivation, and steady-state inactivation was not significantly altered. However, the current-voltage relationship and activation threshold of IBaL in OZR exhibited a depolarized shift compared with LZR. The total and membrane protein expression levels of Cav1.2 [pore-forming subunit of L-type calcium channels (LTCC)], but not the insulin receptors, were decreased in OZR. The insulin receptor was found to be associated with the Cav1.2, which was weakened in OZR. The total protein expression of calmodulin was reduced, but that of Cavβ2 subunit was not altered in OZR. Together, these results suggested that the 16- to 17-wk-old OZR has 1) developed cardiac hypertrophy, 2) exhibited altered electrophysiology manifested by the prolonged QTc interval, 3) increased duration of action potential in isolated ventricular myocytes, 4) defective inactivation of ICaL and IBaL, 5) weakened the association of LTCC with the insulin receptor, and 6) decreased protein expression of Cav1.2 and calmodulin. These results also provided mechanistic insights into a remodeled cardiac electrophysiology under the condition of insulin resistance, enhancing our understanding of long QT associated with obese type 2 diabetic patients.

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Journal articles on the topic 'ICAL'

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