Journal articles on the topic 'Channel effects'
To see the other types of publications on this topic, follow the link: Channel effects.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Channel effects.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Thies, Jennifer, Vanessa Neutzler, Fidelma O'leary, and He Liu. "Differential Effects of TRPA and TRPV Channels on Behaviors of Caenorhabditis elegans." Journal of Experimental Neuroscience 10 (January 2016): JEN.S32837. http://dx.doi.org/10.4137/jen.s32837.
Full textAbstract:
TRPA and TRPV ion channels are members of the transient receptor potential (TRP) cation channel superfamily, which mediates various sensory transductions. In Caenorhabditis elegans, the TRPV channels are known to affect chemosensation, while the TRPA-1 channel is associated with thermosensation and mechanosensation. We examined thermosensation, chemosensation, and osmosensation in strains lacking TRPA-1 or TRPV channels. We found that TRPV channel knockout worms exhibited similar behavioral deficits associated with thermotaxis as the TRPA-1 channel knockout, suggesting a dual role for TRPV channels. In contrast, chemosensation responses, assessed by both avoidance reversal behavior and NaCl osmosensation, were dependent on TRPV channels but seemed independent of TRPA-1 channel. Our findings suggest that, in addition to TRPA-1 channel, TRPV channels are necessary for thermotaxis and may activate, or modulate, the function of TRPA-1 channels. In contrast, TRPA-1 channels do not have a dual responsibility, as they have no functional role in odorant avoidance or osmosensation.
2
Chalov, Sergey R., and Nikolay I. Alexeevsky. "Braided rivers: structure, types and hydrological effects." Hydrology Research 46, no. 2 (December 16, 2013): 258–75. http://dx.doi.org/10.2166/nh.2013.023.
Full textAbstract:
Braided rivers have been intensively analyzed mostly by geomorphologists. In the present study the approach to recognize braided channel types and effects with the special emphasis on flow partitioning has been applied. It is assumed that each braided channel represents the reach which is initiated with dividing of the single channel and completed below the confluence of the total multiplicity of channels. Proposed indices of braided channel structure and water discharges ratio which have been proposed and applied to 200 braided reaches of 40 rivers in Russia, China, and the USA enable the description of the origin and types of the observed rivers and further analysis of hydrological effects of braided channels. The latter represent physical, hydrochemical, and ecological conditions of stream along braided reaches caused by flow distribution among branches in relation to braiding intensity. Structure and braided channel pattern types impact on hydraulics, sediment transport, water temperatures, and stream communities are of primary interest in the present study.
3
Kellis, Douglas L., Amy J. Moll, and Donald G. Plumlee. "Effects of Silver Paste Application on Embedded Channels in Low Temperature Co-fired Ceramics." Journal of Microelectronics and Electronic Packaging 6, no. 1 (January 1, 2009): 54–58. http://dx.doi.org/10.4071/1551-4897-6.1.54.
Full textAbstract:
A monopropellant micropropulsion device is being developed in low-temperature cofired ceramics (LTCC). The device uses catalytic decomposition of hydrogen peroxide as a propellant: hence catalytic channels are embedded internally in these devices. Consistent construction of these channels depends on a wide range of variables both in the design and fabrication of the channel structures. The primary focus of this paper is the characterization of final channel geometry when silver paste is applied to the upper and lower surfaces of an embedded single layer channel. Application of silver paste to the upper and lower channel surfaces has been shown to alter the final shape of the channels within the test structure. Upper and lower surface deflection into the channel area is discussed and characterization of this phenomena is illustrated as a function of channel width. A design of experiment (DOE) method is used to explore how process parameters affect the channel geometry/integrity. Construction of the test structures includes the use of pressure sensitive adhesives and a sacrificial material to maintain the overall channel geometry/integrity. Lamination and firing profiles are modified in order to enhance this construction methodology. Techniques used to produce and characterize these channels are discussed as well as the methods used to maintain channel geometry/integrity.
4
Laghmach, R., H. El Hadfi, B. Maroufi, and M. Daoud. "Fisher and skew information for two-qubit Bell states under decoherence effects." International Journal of Quantum Information 18, no. 04 (June 2020): 2050018. http://dx.doi.org/10.1142/s0219749920500185.
Full textAbstract:
We give the explicit expressions of quantum Fisher information and skew information for a two-qubit Bell states. We investigate their dynamics under the decoherence effects: phase-damping channel, depolarizing channel and amplitude-damping channel. We also discuss the thermal entanglement quantified by Wootters concurrence for these three decoherence channels and we compare its dynamical behavior with the quantum Fisher information and skew information. We then use this comparison to investigate the influence of noisy channels on thermal entanglement and its role in boosting the performance of metrology protocols. It is shown that the correlations in two-qubit Bell states are more resistant to phase-damping channel and depolarizing channels.
5
Kang, Jun, Thomas Brashear-Alejandro, Anthony K. Asare, and Sixing Chen. "The effects of value appropriation strategies in channels on intangible firm value." Journal of Business & Industrial Marketing 33, no. 2 (March 5, 2018): 208–19. http://dx.doi.org/10.1108/jbim-10-2016-0234.
Full textAbstract:
Purpose This study aims to examine the role of channel strategies in value appropriation and their effects on firm value with the consideration of situational factors. Design/methodology/approach An empirical study with secondary data is conducted in the context of public franchised channels. The authors use Entrepreneur Franchise Top 500 (2012) as the sampling frame and merge the data from three sources to create the final data set. A set of models are built to test the hypotheses in a hierarchical manner. Findings Value appropriation provides a solid rationale to link marketing channel strategies to firm value. Channel integration is an effective strategy driving intangible firm value. The influence of channel compression on intangible firm value depends on its interaction with other marketing environmental variables. Research limitations/implications First, the sample size in this study is relatively small though these samples show high representativeness. Second, the empirical analysis in this study focuses on the franchised channels because of data availability. Practical implications Managers should consider the role of value appropriation when developing new channel strategies. A channel strategy deserves firm-level attention and resources because of its relevance to firm value. Managers should examine channel environment carefully and deploy internal resources to augment the potential of value appropriation strategies in channels. Originality/value This study is among the first to investigate the value relevance of marketing channel strategies from a value appropriation perspective. It identifies profit appropriation and resource appropriation as two mechanisms of value appropriation in marketing channels and uses these two processes to link channel integration and channel compression strategies with firm value.
6
Yatani, A., D. L. Kunze, and A. M. Brown. "Effects of dihydropyridine calcium channel modulators on cardiac sodium channels." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 1 (January 1, 1988): H140—H147. http://dx.doi.org/10.1152/ajpheart.1988.254.1.h140.
Full textAbstract:
To investigate whether cardiac sodium channels have dihydropyridine (DHP) receptors we studied the effects of the optically pure (greater than 95%) enantiomers of the DHPs PN200–110 and BAY-K 8644 and the racemic DHP nitrendipine (NTD). Whole cell and single-channel sodium currents were recorded from cultured ventricular cells of neonatal rats using the patch-clamp method. NTD reduced cardiac sodium currents in a voltage-dependent manner. Inhibitory effects were due to an increase in traces without activity. The unit conductance remained unchanged. At negative holding potentials, NTD transiently increased the probability of channel opening. Both (+) and (-) PN 200–110 blocked sodium channels, although the (-) isomer was about one order of magnitude less effective. The blocking effects were voltage dependent. (+) BAY-K 8644 had similar blocking effects. (-) BAY-K 8644 produced an increase in sodium currents due to an increased frequency of channel openings and a marked prolongation of open time without any significant change in unit conductance. The DHPs have effects on cardiac sodium whole cell and single-channel currents that appear identical to and are as stereospecific as their effects on cardiac calcium currents, although the concentrations required are larger. In contrast the inwardly rectifying potassium channel (IK1) is unaffected by these DHPs. We conclude that functionally equivalent DHP receptors are present in cardiac sodium and calcium channels but not potassium channels and take this as evidence of the homology between sodium and calcium channels.
7
Elinder, Fredrik, and Peter Århem. "Metal ion effects on ion channel gating." Quarterly Reviews of Biophysics 36, no. 4 (November 2003): 373–427. http://dx.doi.org/10.1017/s0033583504003932.
Full textAbstract:
1. Introduction 3742. Metals in biology 3783. The targets: structure and function of ion channels 3804. General effects of metal ions on channels 3824.1 Three types of general effect 3824.2 The main regulators 3835. Effects on gating: mechanisms and models 3845.1 Screening surface charges (Mechanism A) 3875.1.1 The classical approach 3875.1.1.1 Applying the Grahame equation 3885.1.2 A one-site approach 3915.2 Binding and electrostatically modifying the voltage sensor (Mechanism B) 3915.2.1 The classical model 3915.2.1.1 The classical model as state diagram – introducing basic channel kinetics 3925.2.2 A one-site approach 3955.2.2.1 Explaining state-dependent binding – a simple electrostatic mechanism 3955.2.2.2 The relation between models assuming binding to smeared and to discrete charges 3965.2.2.3 The special case of Zn2+ – no binding in the open state 3965.2.2.4 Opposing effects of Cd2+ on hyperpolarization-activated channels 3985.3 Binding and interacting non-electrostatically with the voltage sensor (Mechanism C) 3985.3.1 Combining mechanical slowing of opening and closing with electrostatic modification of voltage sensor 4005.4 Binding to the pore – a special case of one-site binding models (Mechanism D) 4005.4.1 Voltage-dependent pore-block – adding extra gating 4015.4.2 Coupling pore block to gating 4025.4.2.1 The basic model again 4025.4.2.2 A special case – Ca2+ as necessary cofactor for closing 4035.4.2.3 Expanding the basic model – Ca2+ affecting a voltage-independent step 4045.5 Summing up 4056. Quantifying the action: comparing the metal ions 4076.1 Steady-state parameters are equally shifted 4076.2 Different metal ions cause different shifts 4086.3 Different metal ions slow gating differently 4106.4 Block of ion channels 4127. Locating the sites of action 4127.1 Fixed surface charges involved in screening 4137.2 Binding sites 4137.2.1 Group 2 ions 4147.2.2 Group 12 ions 4148. Conclusions and perspectives 4159. Appendix 41610. Acknowledgements 41811. References 418Metal ions affect ion channels either by blocking the current or by modifying the gating. In the present review we analyse the effects on the gating of voltage-gated channels. We show that the effects can be understood in terms of three main mechanisms. Mechanism A assumes screening of fixed surface charges. Mechanism B assumes binding to fixed charges and an associated electrostatic modification of the voltage sensor. Mechanism C assumes binding and an associated non-electrostatic modification of the gating. To quantify the non-electrostatic effect we introduced a slowing factor, A. A fourth mechanism (D) is binding to the pore with a consequent pore block, and could be a special case of Mechanisms B or C. A further classification considers whether the metal ion affects a single site or multiple sites. Analysing the properties of these mechanisms and the vast number of studies of metal ion effects on different voltage-gated ion channels we conclude that group 2 ions mainly affect channels by classical screening (a version of Mechanism A). The transition metals and the Zn group ions mainly bind to the channel and electrostatically modify the gating (Mechanism B), causing larger shifts of the steady-state parameters than the group 2 ions, but also different shifts of activation and deactivation curves. The lanthanides mainly bind to the channel and both electrostatically and non-electrostatically modify the gating (Mechanisms B and C). With the exception of the ether-à-go-go-like channels, most channel types show remarkably similar ion-specific sensitivities.
8
Coetzee, W. A., T. Y. Nakamura, and J. F. Faivre. "Effects of thiol-modifying agents on KATP channels in guinea pig ventricular cells." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 5 (November 1, 1995): H1625—H1633. http://dx.doi.org/10.1152/ajpheart.1995.269.5.h1625.
Full textAbstract:
ATP-sensitive K+ (KATP) channels are thought only to open during conditions of metabolic impairment (e.g., myocardial ischemia). However, the regulation of KATP channel opening during ischemia remains poorly understood. We tested whether thiol (SH) group oxidation, which is known to occur during ischemia, may be involved in KATP channel regulation. Inside-out membrane patches were voltage clamped at a constant potential (O mV) in asymmetrical K+ solutions. The effects of compounds that specifically modify SH groups [p-chloromercuri-phenylsulfonic acid (pCMPS), 5-5'-dithio-bis(2-nitrobenzoic acid) [DTNB], and thimerosal] were tested. The membrane-impermeable compound, pCMPS (> or = 5 microM), caused a quick and irreversible inhibition of KATP channel activity. The reducing agent, dl-dithiothreitol (DTT) (3 mM) was able to reverse this inhibition. DTNB (500 microM) caused a rapid, but spontaneously reversible, block of KATP channel activity. After DTNB, no change was observed in single channel conductance. Oxidized glutathione (GSSG, 3 mM) did not block KATP channel activity. Thimerosal (100-500 microM) induced a DTT-reversible block of partially rundown KATP channels, or channels that underwent complete rundown; these channels were reactivated with trypsin (1 mg/ml). Thimerosal did not block KATP channels that had a high degree of activity. However, the ATP sensitivity was decreased; the concentration of ATP needed to half-maximally inhibit the channel (Ki) was increased from 47 +/- 12 to 221 +/- 35 microM (n = 6, P < 0.05). This was not due to a spontaneous change with time.(ABSTRACT TRUNCATED AT 250 WORDS)
9
Garcia, M. L., H. G. Knaus, P. Munujos, R. S. Slaughter, and G. J. Kaczorowski. "Charybdotoxin and its effects on potassium channels." American Journal of Physiology-Cell Physiology 269, no. 1 (July 1, 1995): C1—C10. http://dx.doi.org/10.1152/ajpcell.1995.269.1.c1.
Full textAbstract:
Over the last few years, a considerable amount of information has been obtained regarding K+ channels. Different areas of research have contributed to knowledge in this field. Charybdotoxin (ChTX), a 37-amino acid peptide isolated from venom of the scorpion Leiurus quinquestriatus var. hebraeus, represents a remarkable tool for studying K+ channels. With its use, it has been possible to purify the high-conductance Ca(2+)-activated K+ (maxi-K) channel to homogeneity and determine the subunit composition of this channel. This has led to the discovery of an auxiliary beta-subunit that, when coexpressed with the pore-forming subunit, mSlo, alters the biophysical and pharmacological properties of this latter subunit. With the feasibility of producing large amounts of ChTX by recombinant techniques and the knowledge of the three-dimensional structure of the peptide, it has been possible to carry out site-directed mutagenesis studies and obtain a picture of the interaction surface of the toxin with two channels, maxi-K and Shaker, and to derive a picture of the complementary surface of the receptor in these two channels. Finally, ChTX, and the more selective K+ channel toxins that were subsequently discovered, have provided us with unique tools not only to determine the functional role that K+ channels play in target tissues but also to develop the molecular pharmacology of these channels.
10
Gillis, K. D., W. M. Gee, A. Hammoud, M. L. McDaniel, L. C. Falke, and S. Misler. "Effects of sulfonamides on a metabolite-regulated ATPi-sensitive K+ channel in rat pancreatic B-cells." American Journal of Physiology-Cell Physiology 257, no. 6 (December 1, 1989): C1119—C1127. http://dx.doi.org/10.1152/ajpcell.1989.257.6.c1119.
Full textAbstract:
Intracellular ATP (ATPi)-sensitive K+ [K+(ATP)] channels are now a recognized site of action of clinically useful hypoglycemic and hyperglycemic sulfonamides. We have further examined the action of these agents on single K+ channels in rat pancreatic B-cells 1) Tolbutamide and glyburide, two hypoglycemic sulfonylureas which decrease K+(ATP) channel activity in the cell-attached patch, affect the kinetics of K+(ATP) channel in a manner similar to glucose. They shorten the duration of the “burst,” or cluster of open channel events, while lengthening the intervals between bursts. 2) The hyperglycemic vasodilator diazoxide increases mean K+(ATP) channel activity in the cell-attached patch as well as in the inside-out excised patch exposed to ATPi. It appears to lengthen channel bursts and shorten the intervals between them. Two structurally similar diuretics, hydrochlorothiazide and furosemide, which have mild hyperglycemic effects, do not increase K+(ATP) channel activity even at clinically toxic concentrations. 3) Neither the sulfonylureas nor diazoxide directly affect the activity of single delayed rectifier K+ channels or single calcium and voltage-activated K+ channels in normal B-cells.
11
Rodriguez-Contreras, Adrian, Ping Lv, Jun Zhu, Hyo Jeong Kim, and Ebenezer N. Yamoah. "Effects of Strontium on the Permeation and Gating Phenotype of Calcium Channels in Hair Cells." Journal of Neurophysiology 100, no. 4 (October 2008): 2115–24. http://dx.doi.org/10.1152/jn.90473.2008.
Full textAbstract:
To minimize the effects of Ca2+ buffering and signaling, this study sought to examine single Ca2+ channel properties using Sr2+ ions, which substitute well for Ca2+ but bind weakly to intracellular Ca2+ buffers. Two single-channel fluctuations were distinguished by their sensitivity to dihydropyridine agonist (L-type) and insensitivity toward dihydropyridine antagonist (non-L-type). The L- and non-L-type single channels were observed with single-channel conductances of 16 and 19 pS at 70 mM Sr2+ and 11 and 13 pS at 5 mM Sr2+, respectively. We obtained KD estimates of 5.2 and 1.9 mM for Sr2+ for L- and non-L-type channels, respectively. At Ca2+ concentration of ∼2 mM, the single-channel conductances of Sr2+ for the L-type channel was ∼1.5 and 4.0 pS for the non-L-type channels. Thus the limits of single-channel microdomain at the membrane potential of a hair cell (e.g., −65 mV) for Sr2+ ranges from 800 to 2,000 ion/ms, assuming an ECa of 100 mV. The channels are ≥4-fold more sensitive at the physiological concentration ranges than at concentrations >10 mM. Additionally, the channels have the propensity to dwell in the closed state at high concentrations of Sr2+, which is reflected in the time constant of the first latency distributions. It is concluded that the concentration of the permeant ion modulates the gating of hair cell Ca2+ channels. Finally, the closed state/s that is/are altered by high concentrations of Sr2+ may represent divalent ion-dependent inactivation of the L-type channel.
12
Ghovanloo, Mohammad-Reza, Noah Gregory Shuart, Janette Mezeyova, Richard A. Dean, Peter C. Ruben, and Samuel J. Goodchild. "Inhibitory effects of cannabidiol on voltage-dependent sodium currents." Journal of Biological Chemistry 293, no. 43 (September 14, 2018): 16546–58. http://dx.doi.org/10.1074/jbc.ra118.004929.
Full textAbstract:
Cannabis sativa contains many related compounds known as phytocannabinoids. The main psychoactive and nonpsychoactive compounds are Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD), respectively. Much of the evidence for clinical efficacy of CBD-mediated antiepileptic effects has been from case reports or smaller surveys. The mechanisms for CBD's anticonvulsant effects are unclear and likely involve noncannabinoid receptor pathways. CBD is reported to modulate several ion channels, including sodium channels (Nav). Evaluating the therapeutic mechanisms and safety of CBD demands a richer understanding of its interactions with central nervous system targets. Here, we used voltage-clamp electrophysiology of HEK-293 cells and iPSC neurons to characterize the effects of CBD on Nav channels. Our results show that CBD inhibits hNav1.1–1.7 currents, with an IC50 of 1.9–3.8 μm, suggesting that this inhibition could occur at therapeutically relevant concentrations. A steep Hill slope of ∼3 suggested multiple interactions of CBD with Nav channels. CBD exhibited resting-state blockade, became more potent at depolarized potentials, and also slowed recovery from inactivation, supporting the idea that CBD binding preferentially stabilizes inactivated Nav channel states. We also found that CBD inhibits other voltage-dependent currents from diverse channels, including bacterial homomeric Nav channel (NaChBac) and voltage-gated potassium channel subunit Kv2.1. Lastly, the CBD block of Nav was temperature-dependent, with potency increasing at lower temperatures. We conclude that CBD's mode of action likely involves 1) compound partitioning in lipid membranes, which alters membrane fluidity affecting gating, and 2) undetermined direct interactions with sodium and potassium channels, whose combined effects are loss of channel excitability.
13
Mayorga-Wark, O., J. Costantin, W. P. Dubinsky, and S. G. Schultz. "Effects of a Shaker K+ channel peptide and trypsin on a K+ channel in Necturus enterocytes." American Journal of Physiology-Cell Physiology 265, no. 2 (August 1, 1993): C541—C547. http://dx.doi.org/10.1152/ajpcell.1993.265.2.c541.
Full textAbstract:
We have previously demonstrated that a synthetic peptide composed of the first 22 amino acids from the NH2-terminus of the Shaker B K+ channel protein deactivates a voltage-dependent K+ channel present in basolateral membrane of Necturus small intestinal epithelial cells reconstituted into planar lipid bilayers (Dubinsky et al. Proc. Natl. Acad. Sci. USA 89: 1770-1774, 1992). We now demonstrate that this peptide interacts with the inner surface of the Necturus channel only when it is in the open or conducting configuration and that this interaction is hindered by tetraethylammonium ion, a well-established blocker of this and other K+ channels. We conclude that this peptide is an open-pore blocker of the Necturus K+ channel as it appears to be in the case of the Shaker B K+ channel. We further demonstrate that trypsin, which abolishes the ability of this peptide to block both the Necturus and the Shaker K+ channels and inhibits spontaneous inactivation of the Shaker K+ channel, also impairs the voltage-gate of the Necturus K+ channel. These findings, and others to be reported in a companion paper, suggest structural homologies between the "inactivation peptide" of the Shaker B K+ channel and the voltage-gate of the Necturus K+ channel.
14
Nakamura, Akiyo, Shinji Kawahito, Takashi Kawano, Hossein Nazari, Akira Takahashi, Hiroshi Kitahata, Yutaka Nakaya, and Shuzo Oshita. "Differential Effects of Etomidate and Midazolam on Vascular Adenosine Triphosphate–sensitive Potassium Channels." Anesthesiology 106, no. 3 (March 1, 2007): 515–22. http://dx.doi.org/10.1097/00000542-200703000-00016.
Full textAbstract:
Background The aim of this study was to investigate the effects of two imidazoline-derived intravenous anesthetics, etomidate and midazolam, on vascular adenosine triphosphate-sensitive potassium (KATP) channel activity. Methods In isolated rat aorta, isometric tension was recorded to examine the anesthetic effects on vasodilator response to levcromakalim, a selective KATP channel opener. Using the patch clamp method, the anesthetic effects were also examined on the currents through (1) native vascular KATP channels, (2) recombinant KATP channels with different combinations of various types of inwardly rectifying potassium channel (Kir6.0 family: Kir6.1, 6.2) and sulfonylurea receptor (SUR1, 2A, 2B) subunits, (3) SUR-deficient channels derived from a truncated isoform of Kir6.2 subunit (Kir6.2DeltaC36 channels), and (4) mutant Kir6.2DeltaC36 channels with reduced sensitivity to adenosine triphosphate (Kir6.2DeltaC36-K185Q channels). Results Etomidate (> or = 10 m), but not midazolam (up to 10 m), inhibited the levcromakalim-induced vasodilation, which was sensitive to glibenclamide (IC50: 7.21 x 10 m; maximum inhibitory concentration: 1.22 x 10 m). Etomidate (> or = 3 x 10 m), but not midazolam (up to 10 m), inhibited the native KATP channel activity in both cell-attached and inside-out configurations with IC50 values of 1.68 x 10 m and 1.52 x 10 m, respectively. Etomidate (10 m) also inhibited the activity of various types of recombinant SUR/Kir6.0KATP channels, Kir6.2DeltaC36 channels, and Kir6.2DeltaC36-K185Q channels with equivalent potency. Conclusions Clinical concentrations of etomidate, but not midazolam, inhibit the KATP channel activity in vascular smooth muscle cells. The inhibition is presumably through its effects on the Kir6.0 subunit, but not on the SUR subunit, with the binding site different from adenosine triphosphate at the amino acid level.
15
Zaugg, Michael, Eliana Lucchinetti, Donat R. Spahn, Thomas Pasch, Carlos Garcia, and Marcus C. Schaub. "Differential Effects of Anesthetics on Mitochondrial KATPChannel Activity and Cardiomyocyte Protection." Anesthesiology 97, no. 1 (July 1, 2002): 15–23. http://dx.doi.org/10.1097/00000542-200207000-00004.
Full textAbstract:
Background Mitochondrial adenosine triphosphate-sensitive potassium (mitoK(ATP)) channels play a pivotal role in mediating cardiac preconditioning. The effects of intravenous anesthetics on this protective channel have not been investigated so far, but would be of importance with respect to experimental as well as clinical medicine. Methods Live cell microscopy was used to visualize and measure autofluorescence of flavoproteins, a direct reporter of mitoK(ATP) channel activity, in response to the direct and highly selective mitoK(ATP) channel opener diazoxide, or to diazoxide following exposure to various anesthetics commonly used in experimental and clinical medicine. A cellular model of ischemia with subsequent hypoosmolar trypan blue staining served to substantiate the effects of the anesthetics on mitoK(ATP) channels with respect to myocyte viability. Results Diazoxide-induced mitoK(ATP) channel opening was significantly inhibited by the anesthetics R-ketamine, and the barbiturates thiopental and pentobarbital. Conversely, urethane, 2,2,2-trichloroethanol (main metabolite of alpha-chloralose and chloral hydrate), and the opioid fentanyl potentiated the channel-opening effect of diazoxide, which was abrogated by coadministration of chelerythrine, a specific protein kinase C inhibitor. S-ketamine, propofol, xylazine, midazolam, and etomidate did not affect mitoK(ATP) channel activity. The significance of these modulatory effects of the anesthetics on mitoK(ATP) channel activity was substantiated in a cellular model of simulated ischemia, where diazoxide-induced cell protection was mitigated by R-ketamine and the barbiturates, while urethane, 2,2,2-trichloroethanol, and fentanyl potentiated myocyte protection. Conclusions These results suggest distinctive actions of individual anesthetics on mitoK(ATP) channels and provide evidence that the choice of background anesthesia may play a role in cardiac protection in both experimental and clinical medicine.
16
Song, Gimoon, and Heeil Park. "A Study on the Effects of Travel Product Distribution Channels Perception on Channel Satisfaction, Channel Reliability and Channel Loyalty." Journal of Tourism Management Research 23, no. 1 (January 31, 2019): 507–36. http://dx.doi.org/10.18604/tmro.2019.23.1.24.
Full text
17
Wang, Junjie, Meiyun Ma, Silviu Locovei, Robert W. Keane, and Gerhard Dahl. "Modulation of membrane channel currents by gap junction protein mimetic peptides: size matters." American Journal of Physiology-Cell Physiology 293, no. 3 (September 2007): C1112—C1119. http://dx.doi.org/10.1152/ajpcell.00097.2007.
Full textAbstract:
Connexin mimetic peptides are widely used to assess the contribution of nonjunctional connexin channels in several processes, including ATP release. These peptides are derived from various connexin sequences and have been shown to attenuate processes downstream of the putative channel activity. Yet so far, no documentation of effects of peptides on connexin channels has been presented. We tested several connexin and pannexin mimetic peptides and observed attenuation of channel currents that is not compatible with sequence specific actions of the peptides. Connexin mimetic peptides inhibited pannexin channel currents but not the currents of the channel formed by connexins from which the sequence was derived. Pannexin mimetic peptides did inhibit pannexin channel currents but also the channels formed by connexin 46. The same pattern of effects was observed for dye transfer, except that the inhibition levels were more pronounced than for the currents. The channel inhibition by peptides shares commonalities with channel effects of polyethylene glycol (PEG), suggesting a steric block as a mechanism. PEG accessibility is in the size range expected for the pore of innexin gap junction channels, consistent with a functional relatedness of innexin and pannexin channels.
18
Buscarino, A., L. Fortuna, M. Frasca, G. Sciuto, and Mofeed Rashid. "Compensation of transmission channel effects in chaos synchronization." Iraqi Journal for Electrical and Electronic Engineering 7, no. 1 (June 1, 2011): 83–87. http://dx.doi.org/10.37917/ijeee.7.1.16.
Full textAbstract:
The synchronization of chaos is a well-known topic which attracted the attention of the scientific community in the last two decades. However, the robustness of the synchronous state has been not widely studied, especially considering real cases in which the effects introduced by the physical channel through which chaotic circuits interact, may deeply influence the quality of synchronization and even the onset of it. In this paper, the synchronization of two chaotic circuit coupled through a non–ideal channel is investigated. In particular, the effects of channels introducing a frequency–independent or frequency–dependent time–delay are investigated. Furthermore, two different design strategies to obtain a linear compensation block able to compensate the considered channel effects are presented and the recovery of the synchronous state is discussed.
19
Schoenfeld, N., J. Aelion, Y. Beigel, O. Epstein, and A. Atsmon. "The porphyrogenic effects of calcium channel blocking drugs." Clinical Science 69, no. 5 (November 1, 1985): 581–86. http://dx.doi.org/10.1042/cs0690581.
Full textAbstract:
1. Treatment of monolayers of chick embryo hepatocytes with the calcium channel blocking drugs nifedipine and verapamil resulted in a decrease in the activity of uroporphyrinogen decarboxylase, an increase in the activity of δ-aminolaevulinate synthase and accumulation of porphyrins with uroporphyrin and heptacarboxylic porphyrin predominating. 2. Diltiazem, another calcium channel blocking drug, did not affect uroporphyrinogen decarboxylase activity and had a slight effect only on the accumulation of porphyrins. 3. Experiments with nifedipine and verapamil in the presence of various concentrations of calcium indicate that the porphyrogenic effect is apparently not related to blocking of calcium channels.
20
Scheel, Olaf, Ulrich Seydel, and Rikard Blunck. "Effects of Hydrophobic Channel Modulators on Membrane Fluidity and Single Channel Kinetics of MaxiK Channels." Anesthesiology 96, Sup 2 (September 2002): A826. http://dx.doi.org/10.1097/00000542-200209002-00826.
Full text
21
Orio, Patricio, and Ramon Latorre. "Differential Effects of β1 and β2 Subunits on BK Channel Activity." Journal of General Physiology 125, no. 4 (March 14, 2005): 395–411. http://dx.doi.org/10.1085/jgp.200409236.
Full textAbstract:
High conductance, calcium- and voltage-activated potassium (BK) channels are widely expressed in mammals. In some tissues, the biophysical properties of BK channels are highly affected by coexpression of regulatory (β) subunits. β1 and β2 subunits increase apparent channel calcium sensitivity. The β1 subunit also decreases the voltage sensitivity of the channel and the β2 subunit produces an N-type inactivation of BK currents. We further characterized the effects of the β1 and β2 subunits on the calcium and voltage sensitivity of the channel, analyzing the data in the context of an allosteric model for BK channel activation by calcium and voltage (Horrigan and Aldrich, 2002). In this study, we used a β2 subunit without its N-type inactivation domain (β2IR). The results indicate that the β2IR subunit, like the β1 subunit, has a small effect on the calcium binding affinity of the channel. Unlike the β1 subunit, the β2IR subunit also has no effect on the voltage sensitivity of the channel. The limiting voltage dependence for steady-state channel activation, unrelated to voltage sensor movements, is unaffected by any of the studied β subunits. The same is observed for the limiting voltage dependence of the deactivation time constant. Thus, the β1 subunit must affect the voltage sensitivity by altering the function of the voltage sensors of the channel. Both β subunits reduce the intrinsic equilibrium constant for channel opening (L0). In the allosteric activation model, the reduction of the voltage dependence for the activation of the voltage sensors accounts for most of the macroscopic steady-state effects of the β1 subunit, including the increase of the apparent calcium sensitivity of the BK channel. All allosteric coupling factors need to be increased in order to explain the observed effects when the α subunit is coexpressed with the β2IR subunit.
22
Denson, Donald D., Xiaoping Wang, Roger T. Worrell, and Douglas C. Eaton. "Effects of fatty acids on BK channels in GH3cells." American Journal of Physiology-Cell Physiology 279, no. 4 (October 1, 2000): C1211—C1219. http://dx.doi.org/10.1152/ajpcell.2000.279.4.c1211.
Full textAbstract:
Ca2+-activated K+ (BK) channels in GH3 cells are activated by arachidonic acid (AA). Because cytosolic phospholipase A2 can produce other unsaturated free fatty acids (FFA), we examined the effects of FFA on BK channels in excised patches. Control recordings were made at several holding potentials. The desired FFA was added to the bath solution, and the voltage paradigm was repeated. AA increased the activity of BK channels by 3.6 ± 1.6-fold. The cis FFA, palmitoleic, oleic, linoleic, linolenic, eicosapentaenoic, and the triple bond analog of AA, eicosatetraynoic acid, all increased BK channel activity, whereas stearic (saturated) or the trans isomers elaidic, linolelaidic, and linolenelaidic had no effect. The cisunsaturated FFA shifted the open probability vs. voltage relationships to the left without a change in slope, suggesting no change in the sensitivity of the voltage sensor. Measurements of membrane fluidity showed no correlation between the change of membrane fluidity and the change in BK channel activation. In addition, AA effects on BK channels were unaffected in the presence of N-acetylcysteine. Arachidonyl-CoA, a membrane impermeable analog of AA, activates channels when applied to the cytosolic surface of excised patches, suggesting an effect of FFAs from the cytosolic surface of BK channels. Our data imply a direct interaction between cis FFA and the BK channel protein.
23
Kita, Masafumi, Takakazu Yunoki, Koichi Takimoto, Minoru Miyazato, Kaori Kita, William C. de Groat, Hidehiro Kakizaki, and Naoki Yoshimura. "Effects of bladder outlet obstruction on properties of Ca2+-activated K+ channels in rat bladder." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 5 (May 2010): R1310—R1319. http://dx.doi.org/10.1152/ajpregu.00523.2009.
Full textAbstract:
In this study, we investigated the effects of bladder outlet obstruction (BOO) on the expression and function of large conductance (BK) and small conductance (SK) Ca2+-activated K+ channels in detrusor smooth muscle. The bladder from adult female Sprague-Dawley rats with 6-wk BOO were used. The mRNA expression of the BK channel α-subunit, β1-, β2-, and β4-subunits and SK1, SK2, and SK3 channels were investigated using real-time RT-PCR. All subunits except for the BK-β2, SK2, and SK3 channels were predominantly expressed in the detrusor smooth muscle rather than in the mucosa. The mRNA expression of the BK channel α-subunit was not significantly changed in obstructed bladders. However, the expression of the BK channel β1-subunit and the SK3 channel was remarkably increased in obstructed bladders. On the other hand, the expression of the BK channel β4-subunit was decreased as the severity of BOO-induced bladder overactivity progressed. In detrusor smooth muscle strips from obstructed bladders, blockade of BK channels by iberiotoxin (IbTx) or charybdotoxin (CTx) and blockade of SK channels by apamin increased the amplitude of spontaneous contractions. These blockers also increased the contractility and affinity of these strips for carbachol during cumulative applications. The facilitatory effects elicited by these K+ channel blockers were larger in the strips from obstructed bladders compared with control bladders. These results suggest that long-term exposure to BOO for 6 wk enhances the function of both BK and SK types of Ca2+-activated K+ channels in the detrusor smooth muscle to induce an inhibition of bladder contractility, which might be a compensatory mechanism to reduce BOO-induced bladder overactivity.
24
Wang, Xuefang, Xianshan Dong, Junfeng Xiao, YuYu Zhang, Jianfeng Xu, Sheng Liu, and Liang Gao. "Quantum effects of gas flow in nanochannels." Nanotechnology Reviews 10, no. 1 (January 1, 2021): 254–63. http://dx.doi.org/10.1515/ntrev-2021-0022.
Full textAbstract:
Abstract Based on the thermal theory of Newtonian mechanics, the pressure difference in the macro channels will drive the gas flow until the pressure difference inside is zero. However, the 12-year vacuum packaging experiments in our laboratory showed that when the macroscopic channel is reduced to a critical size and reaches the nanometer level, the gas flow inside the channel is hindered, that is, the differential pressure cannot become zero. To explain this paradoxical phenomenon, this study analyzes the flow of air molecules in the channel by using the De Broglie’s matter waves and Heisenberg’s uncertainty principle. Based on the law of quantum mechanics, when the diameter of the nanochannel is reduced to a certain size, it has a localized high pressure in the channel, which impedes the gas flow. This article introduces quantum mechanics into nanochannel’s gas fluid dynamics for the first time, expanding the new direction of fluid mechanics.
25
WU, F. Q., and B. S. ZOU. "COUPLED CHANNEL EFFECTS IN ππ S-WAVE INTERACTION." International Journal of Modern Physics A 20, no. 08n09 (April 10, 2005): 1905–9. http://dx.doi.org/10.1142/s0217751x05023608.
Full textAbstract:
We study coupled channel effects upon isospin I=2 and I=0 ππ S-wave interaction. With introduction of the ππ→ρρ→ππ coupled channel box diagram contribution into ππ amplitude in addition to ρ and f2(1270) exchange, we reproduce the ππ I =2 S-wave and D-wave scattering phase shifts and inelasticities up to 2 GeV quite well in a K-matrix formalism. For I=0 case, the same ππ→ρρ→ππ box diagram is found to give the largest contribution for the inelasticity among all possible coupled channels including ππ→ωω→ππ, [Formula: see text]. We also show why the broad σ appears narrower in production processes than in ππ scattering process.
26
Hoang, Q. V., P. Zhao, S. Nakajima, and Y. Nakajima. "Orexin (Hypocretin) Effects on Constitutively Active Inward Rectifier K+ Channels in Cultured Nucleus Basalis Neurons." Journal of Neurophysiology 92, no. 6 (December 2004): 3183–91. http://dx.doi.org/10.1152/jn.01222.2003.
Full textAbstract:
Orexins are excitatory transmitters implicated in sleep disorders. Because orexins were discovered only recently, their ionic and signal transduction mechanisms have not been well clarified. We recently reported that orexin A (OXA) inhibits G protein–coupled inward rectifier K+ (GIRK) channels in cultured locus coeruleus and nucleus tuberomammillaris neurons. Other work in our laboratory revealed the existence of a novel inward rectifier K+ channel (KirNB), which is located in cholinergic neurons of the nucleus basalis (NB) and possesses unique single-channel characteristics. The mean open time is considerably shorter in KirNB than in Kir2.0 channels. Constitutive activity and a smaller unitary conductance set KirNB apart from cloned Kir3.0 channels. Previously, we found that substance P excites NB neurons by inhibiting KirNB channels. Here we show that orexins suppress KirNB channel activity, likely leading to neuronal excitation. Electrophysiological studies were performed on cultured NB neurons from the basal forebrain. OXA application decreased whole cell conductance through a pertussis toxin (PTX)-insensitive G protein. The OXA-suppressed current was inwardly rectifying with a reversal potential around EK. Single-channel recordings of NB neurons revealed that constitutively active KirNB channels were transiently inhibited by OXA. Okadaic acid pretreatment abolished the recovery. The results suggest that OXA inhibition of KirNB is mediated by a PTX-insensitive G protein (i.e., Gq/11), which eventually results in channel phosphorylation. Recovery from this inhibition is by dephosphorylation. These results, taken together with our previous study, suggest that orexin receptors can elicit neuronal excitation through at least two families of inward rectifier K+ channels: GIRK and KirNB channels.
27
Li, Chen-Hong, Qi Zhang, Bunyen Teng, S. Jamal Mustafa, Jian-Ying Huang, and Han-Gang Yu. "Src tyrosine kinase alters gating of hyperpolarization-activated HCN4 pacemaker channel through Tyr531." American Journal of Physiology-Cell Physiology 294, no. 1 (January 2008): C355—C362. http://dx.doi.org/10.1152/ajpcell.00236.2007.
Full textAbstract:
We recently discovered that the constitutively active Src tyrosine kinase can enhance hyperpolarization-activated, cyclic nucleotide-gated (HCN) 4 channel activity by binding to the channel protein. To investigate the mechanism of modulation by Src of HCN channels, we studied the effects of a selective inhibitor of Src tyrosine kinase, 4-amino-5-(4-chlorophenyl)-7-( t-butyl)pyrazolo[3,4-d]pyrimidine (PP2), on HCN4 and its mutant channels expressed in HEK 293 cells by using a whole cell patch-clamp technique. We found that PP2 can inhibit HCN4 currents by negatively shifting the voltage dependence of channel activation, decreasing the whole cell channel conductance, and slowing activation and deactivation kinetics. Screening putative tyrosine residues subject to phosphorylation yielded two candidates: Tyr531 and Tyr554. Substituting HCN4-Tyr531 with phenylalanine largely abolished the effects of PP2 on HCN4 channels. Replacing HCN4-Tyr554 with phenylalanine did not abolish the effects of PP2 on voltage-dependent activation but did eliminate PP2-induced slowing of channel kinetics. The inhibitory effects of HCN channels associated with reduced Src tyrosine activity is confirmed in HL-1 cardiomyocytes. Finally, we found that PP2 can decrease the heart rate in a mouse model. These results demonstrate that Src tyrosine kinase enhances HCN4 currents by shifting their activation to more positive potentials and increasing the whole cell channel conductance as well as speeding the channel kinetics. The tyrosine residue that mediates most of Src's actions on HCN4 channels is Tyr531.
28
Shi, Jingyi, and Jianmin Cui. "Intracellular Mg2+ Enhances the Function of Bk-Type Ca2+-Activated K+ Channels." Journal of General Physiology 118, no. 5 (November 1, 2001): 589–606. http://dx.doi.org/10.1085/jgp.118.5.589.
Full textAbstract:
BK channels modulate neurotransmitter release due to their activation by voltage and Ca2+. Intracellular Mg2+ also modulates BK channels in multiple ways with opposite effects on channel function. Previous single-channel studies have shown that Mg2+ blocks the pore of BK channels in a voltage-dependent manner. We have confirmed this result by studying macroscopic currents of the mslo1 channel. We find that Mg2+ activates mslo1 BK channels independently of Ca2+ and voltage by preferentially binding to their open conformation. The mslo3 channel, which lacks Ca2+ binding sites in the tail, is not activated by Mg2+. However, coexpression of the mslo1 core and mslo3 tail produces channels with Mg2+ sensitivity similar to mslo1 channels, indicating that Mg2+ sites differ from Ca2+ sites. We discovered that Mg2+ also binds to Ca2+ sites and competitively inhibits Ca2+-dependent activation. Quantitative computation of these effects reveals that the overall effect of Mg2+ under physiological conditions is to enhance BK channel function.
29
Hansen, Henrik Enggaard, Metodi P. Yankov, Leif Katsuo Oxenløwe, and Søren Forchhammer. "Optimization of Probabilistic Shaping for Nonlinear Fiber Channels with Non-Gaussian Noise." Entropy 22, no. 8 (August 8, 2020): 872. http://dx.doi.org/10.3390/e22080872.
Full textAbstract:
Probabilistic constellation shaping is investigated in the context of nonlinear fiber optic communication channels. Based on a general framework, different link types are considered—1. dispersion-managed channels, 2. unrepeatered transmission channels and 3. ideal distributed Raman amplified channels. These channels exhibit nonlinear effects to a degree that conventional probabilistic constellation shaping strategies for the additive white Gaussian (AWGN) noise channel are suboptimal. A channel-agnostic optimization strategy is used to optimize the constellation probability mass functions (PMFs) for the channels in use. Optimized PMFs are obtained, which balance the effects of additive amplified spontaneous emission noise and nonlinear interference. The obtained PMFs cannot be modeled by the conventional Maxwell-Boltzmann PMFs and outperform optimal choices of these in all the investigated channels. Suboptimal choices of constellation shapes are associated with increased nonlinear effects in the form of non-Gaussian noise. For dispersion-managed channels, a reach gain in 2 spans is seen and across the three channel types, gains of >0.1 bits/symbol over unshaped quadrature-amplitude modulation (QAM) are seen using channel-optimized probablistic shaping.
30
Mercer, Aaron J., Robert J. Szalewski, Skyler L. Jackman, Matthew J. Van Hook, and Wallace B. Thoreson. "Regulation of presynaptic strength by controlling Ca2+ channel mobility: effects of cholesterol depletion on release at the cone ribbon synapse." Journal of Neurophysiology 107, no. 12 (June 15, 2012): 3468–78. http://dx.doi.org/10.1152/jn.00779.2011.
Full textAbstract:
Synaptic communication requires proper coupling between voltage-gated Ca2+ (CaV) channels and synaptic vesicles. In photoreceptors, L-type CaV channels are clustered close to synaptic ribbon release sites. Although clustered, CaV channels move continuously within a confined domain slightly larger than the base of the ribbon. We hypothesized that expanding CaV channel confinement domains should increase the number of channel openings needed to trigger vesicle release. Using single-particle tracking techniques, we measured the expansion of CaV channel confinement domains caused by depletion of membrane cholesterol with cholesterol oxidase or methyl-β-cyclodextrin. With paired whole cell recordings from cones and horizontal cells, we then determined the number of CaV channel openings contributing to cone CaV currents ( ICa) and the number of vesicle fusion events contributing to horizontal cell excitatory postsynaptic currents (EPSCs) following cholesterol depletion. Expansion of CaV channel confinement domains reduced the peak efficiency of release, decreasing the number of vesicle fusion events accompanying opening of each CaV channel. Cholesterol depletion also inhibited exocytotic capacitance increases evoked by brief depolarizing steps. Changes in efficiency were not due to changes in ICa amplitude or glutamate receptor properties. Replenishing cholesterol restored CaV channel domain size and release efficiency to control levels. These results indicate that cholesterol is important for organizing the cone active zone. Furthermore, the finding that cholesterol depletion impairs coupling between channel opening and vesicle release by allowing CaV channels to move further from release sites shows that changes in presynaptic CaV channel mobility can be a mechanism for adjusting synaptic strength.
31
Bychkov, R., M. Gollasch, C. Ried, F. C. Luft, and H. Haller. "Effects of pinacidil on K+ channels in human coronary artery vascular smooth muscle cells." American Journal of Physiology-Cell Physiology 273, no. 1 (July 1, 1997): C161—C171. http://dx.doi.org/10.1152/ajpcell.1997.273.1.c161.
Full textAbstract:
We investigated pinacidil-activated K+ currents in vascular smooth muscle cells (VSMC) from human coronary arteries with the patch-clamp method. In 19 of 54 VSMC, pinacidil (1 and 20 microM) induced a large, nonrectifying, outward current [IK(ATP)] and increased voltage-dependent outward K+ currents [IK(Ca)] positive to voltages of -25 mV. The pinacidil-induced (1 microM) IK(ATP) was blocked by glibenclamide (3 microM) but was not affected by iberiotoxin (100-300 nM). Pinacidil activated up to 150 functionally active ATP-dependent K+ channels (KATP channels) per cell with a single-channel conductance of approximately 17 pS at physiological membrane potentials (between -80 and -30 mV) and K+ gradients (6 mM/130 mM). In 26 of 54 VSMC, on the other hand, pinacidil (1-20 microM) failed to induce IK(ATP) but increased IK(Ca). This current was completely blocked by iberiotoxin (100-300 nM) and tetraethylammonium (1 mM) but not by glibenclamide (3 microM). The single-channel conductance of the channel underlying IK(Ca) was approximately 150 +/- 16 pS between -10 and +30 mV, consistent with large-conductance, maxi Ca(2+)-activated, K+ channels (BKCa channels). We conclude that pinacidil is a nonselective K+ channel opener targeting KATP and BKCa channels. Furthermore, the conductance of KATP channels in human coronary arteries is likely to be small under physiological conditions.
32
Webb, Kevin L., and John E. Hogan. "Hybrid channel conflict: causes and effects on channel performance." Journal of Business & Industrial Marketing 17, no. 5 (September 2002): 338–56. http://dx.doi.org/10.1108/08858620210439031.
Full text
33
Zhao, Yonghui, Zongyun Chen, Zhijian Cao, Wenxin Li, and Yingliang Wu. "Diverse Structural Features of Potassium Channels Characterized by Scorpion Toxins as Molecular Probes." Molecules 24, no. 11 (May 29, 2019): 2045. http://dx.doi.org/10.3390/molecules24112045.
Full textAbstract:
Scorpion toxins are well-known as the largest potassium channel peptide blocker family. They have been successfully proven to be valuable molecular probes for structural research on diverse potassium channels. The potassium channel pore region, including the turret and filter regions, is the binding interface for scorpion toxins, and structural features from different potassium channels have been identified using different scorpion toxins. According to the spatial orientation of channel turrets with differential sequence lengths and identities, conformational changes and molecular surface properties, the potassium channel turrets can be divided into the following three states: open state with less hindering effects on toxin binding, half-open state or half-closed state with certain effects on toxin binding, and closed state with remarkable effects on toxin binding. In this review, we summarized the diverse structural features of potassium channels explored using scorpion toxin tools and discuss future work in the field of scorpion toxin-potassium channel interactions.
34
Kim, Yunjeong, and Yuri Lee. "Cross-channel spillover effect of price promotion in fashion." International Journal of Retail & Distribution Management 48, no. 10 (June 29, 2020): 1139–54. http://dx.doi.org/10.1108/ijrdm-12-2019-0393.
Full textAbstract:
PurposeThe purpose of this study was to investigate whether consumers differ in their online or offline purchase intention, depending on which channel with price promotion information they are first exposed to, and to analyse the moderating role of brand trust.Design/methodology/approachOverall, 174 responses were obtained via an online survey using two contact channels (online/offline) by two levels of brand trust (high/low) between-subject designs.FindingsSpillover effects were found across channels when a consistent price promotion is executed in both online and offline channels, purchase intentions for cross-channel and contact channel increase simultaneously. Although there was a similar effect in the discrepancy of purchase intentions towards the cross-channel according to contact channels, it varied depending on brand trust. When brand trust is high, having contact with offline price-discount information has a large online spillover effect. When brand trust is low, the spillover effect from online to offline is large.Research limitations/implicationsThis study expands the multi-channel research by proving the spillover effects between channels and confirming the difference according to brand trust.Practical implicationsIncreasing promotion information for online contact is effective in driving offline visits for new brands, and the effective use of promotion information at offline stores can have a positive impact on online channels for well-known brands.Originality/valueThis study explores the cross-channel spillover effect of price promotion and proves that these effects depend on brand trust.
35
Zhou, Cheng, Bowen Ke, Yi Zhao, Peng Liang, Daqing Liao, Tao Li, Jin Liu, and Xiangdong Chen. "Hyperpolarization-activated Cyclic Nucleotide-gated Channels May Contribute to Regional Anesthetic Effects of Lidocaine." Anesthesiology 122, no. 3 (March 1, 2015): 606–18. http://dx.doi.org/10.1097/aln.0000000000000557.
Full textAbstract:
Abstract Background: Local anesthetics (e.g., lidocaine) have been found to inhibit hyperpolarization-activated cyclic nucleotide-gated (HCN) channels besides sodium channels. However, the exact role of HCN channels in regional anesthesia in vivo is still elusive. Methods: Sciatic nerve block and intrathecal anesthesia were performed using lidocaine in wild-type and HCN1 channel knockout (HCN1−/−) mice. EC50 of lidocaine and durations of 1% lidocaine were determined. In electrophysiologic recordings, effects of lidocaine on HCN channel currents, voltage-gated sodium channel currents, and neural membrane properties were recorded on dorsal root ganglia neurons. Results: In both sciatic nerve block and intrathecal anesthesia, EC50 of lidocaine for tactile sensory blockade (2 g von Frey fiber) was significantly increased in HCN1−/− mice, whereas EC50 of lidocaine for pinprick blockade was unaffected. Durations of 1% lidocaine were significantly shorter in HCN1−/− mice for both sciatic nerve block and intrathecal anesthesia (n = 10). ZD7288 (HCN blocker) could significantly prolong durations of 1% lidocaine including pinprick blockade in sciatic nerve block (n = 10). Forskolin (raising cyclic adenosine monophosphate to enhance HCN2) could significantly shorten duration of pinprick blockade of 1% lidocaine in sciatic nerve block (n = 10). In electrophysiologic recordings, lidocaine could nonselectively inhibit HCN channel and sodium channel currents both in large and in small dorsal root ganglia neurons (n = 5 to 6). Meanwhile, lidocaine caused neural membrane hyperpolarization and increased input resistance of dorsal root ganglia neurons but not in large dorsal root ganglia neurons from HCN1−/− mice (n = 5–7). Conclusions: These data indicate that HCN channels may contribute to regional anesthetic effects of lidocaine. By inhibiting HCN channels, lidocaine could alter membrane properties of neurons.
36
Middendorf, Thomas R., and Richard W. Aldrich. "Effects of Ultraviolet Modification on the Gating Energetics of Cyclic Nucleotide–Gated Channels." Journal of General Physiology 116, no. 2 (July 31, 2000): 253–82. http://dx.doi.org/10.1085/jgp.116.2.253.
Full textAbstract:
Middendorf et al. (Middendorf, T.R., R.W. Aldrich, and D.A. Baylor. 2000. J. Gen. Physiol. 116:227–252) showed that ultraviolet light decreases the current through cloned cyclic nucleotide–gated channels from bovine retina activated by high concentrations of cGMP. Here we probe the mechanism of the current reduction. The channels' open probability before irradiation, Po(0), determined the sign of the change in current amplitude that occurred upon irradiation. UV always decreased the current through channels with high initial open probabilities [Po(0) > 0.3]. Manipulations that promoted channel opening antagonized the current reduction by UV. In contrast, UV always increased the current through channels with low initial open probabilities [Po(0) ≤ 0.02], and the magnitude of the current increase varied inversely with Po(0). The dual effects of UV on channel currents and the correlation of both effects with Po(0) suggest that the channels contain two distinct classes of UV target residues whose photochemical modification exerts opposing effects on channel gating. We present a simple model based on this idea that accounts quantitatively for the UV effects on the currents and provides estimates for the photochemical quantum yields and free energy costs of modifying the UV targets. Simulations indicate that UV modification may be used to produce and quantify large changes in channel gating energetics in regimes where the associated changes in open probability are not measurable by existing techniques.
37
Pappone, P. A., and G. L. Barchfeld. "Modifications of single acetylcholine-activated channels in BC3H-1 cells. Effects of trimethyloxonium and pH." Journal of General Physiology 96, no. 1 (July 1, 1990): 1–22. http://dx.doi.org/10.1085/jgp.96.1.1.
Full textAbstract:
We have examined the effects of chemical modification with trimethyloxonium (TMO) and changes in external pH on the properties of acetylcholine (ACh)-activated channels in BC3H-1 cells, a clonal muscle cell line. TMO reacts covalently and specifically with carboxylic acid moieties in proteins to convert them to neutral methyl esters. In BC3H-1 cells TMO modification reduces the whole-cell response to ACh measured at negative membrane potentials by approximately 60%. G omega seal patch-clamp recordings of single ACh channel currents showed that the reduction in ACh sensitivity is due to alterations in both the current-carrying and the kinetic properties of the channels. Under all our experimental conditions, i.e., in external solutions of normal or low ionic strength, with or without external divalent cations, and at external pHs between 5.5 and 8.1, TMO treatment reduced ACh single-channel conductance to 70-90% of normal. The effects of TMO on channel kinetics were dependent on the ionic conditions. In normal ionic strength solutions containing both calcium and magnesium ions TMO modification reduced the channel average open time by approximately 25%. A similar reduction in open time was seen in calcium-free solution, but was not present when both calcium and magnesium ions were absent from the external solution. Lowering the ionic strength of the solution increased the mean open time in normal channels by about threefold, but did not affect the kinetics of modified channels. In low ionic strength solutions normal ACh channel open times were maximal at approximately pH 6.7 and decreased by three- to fourfold at both acid and alkaline pH. TMO modification removed the pH dependence of channel kinetics, and average open times were short at all pHs between 5.5 and 8.1. We suggest that TMO modifies normally titratable groups on the external surface of ACh channels that help to determine both the gating and permeability properties of ACh channels.
38
Golowasch, J., A. Kirkwood, and C. Miller. "Allosteric effects of Mg2+ on the gating of Ca2+-activated K+ channels from mammalian skeletal muscle." Journal of Experimental Biology 124, no. 1 (September 1, 1986): 5–13. http://dx.doi.org/10.1242/jeb.124.1.5.
Full textAbstract:
Ca2+-activated K+ channels from rat muscle transverse tubule membranes were inserted into planar phospholipid bilayers, and the activation of these channels by Ca2+ was studied. On the cytoplasmic side of the channel, calcium ions (in the range 10–100 mumol l-1) increase the opening probability of the channel in a graded way. This ‘activation curve’ is sigmoid, with an average Hill coefficient of about 2. Magnesium ions, in the range 1–10 mmol l-1, increase the apparent affinity of the channel for Ca2+ and greatly enhance the sigmoidicity of the Ca2+ activation curve. In the presence of 10 mmol l-1 Mg2+, the Hill coefficient for Ca2+ activation is about 4.5. This effect depends upon Mg2+ concentration but not upon applied voltage. Mg2+ is effective only when added to the cytoplasmic side of the channel. The results argue that this high-conductance, Ca2+-activated K+ channel contains at least six Ca2+-binding sites involved in the activation process.
39
Hanck, D. A., J. C. Makielski, and M. F. Sheets. "Kinetic effects of quaternary lidocaine block of cardiac sodium channels: a gating current study." Journal of General Physiology 103, no. 1 (January 1, 1994): 19–43. http://dx.doi.org/10.1085/jgp.103.1.19.
Full textAbstract:
The interaction of antiarrhythmic drugs with ion channels is often described within the context of the modulated receptor hypothesis, which explains the action of drugs by proposing that the binding site has a variable affinity for drugs, depending upon whether the channel is closed, open, or inactivated. Lack of direct evidence for altered gating of cardiac Na channels allowed for the suggestion of an alternative model for drug interaction with cardiac channels, which postulated a fixed affinity receptor with access limited by the conformation of the channel (guarded receptor hypothesis). We report measurement of the gating currents of Na channels in canine cardiac Purkinje cells in the absence and presence of QX-222, a quaternary derivative of lidocaine, applied intracellularly, and benzocaine, a neutral local anesthetic. These data demonstrate that the cardiac Na channel behaves as a modulated rather than a guarded receptor in that drug-bound channels gate with altered kinetics. In addition, the results suggest a new interpretation of the modulated receptor hypothesis whereby drug occupancy reduces the overall voltage-dependence of gating, preventing full movement of the voltage sensor.
40
Krzemień, Kazimierz, Elżbieta Gorczyca, Mateusz Sobucki, Maciej Liro, and Michał Łyp. "Effects of environmental changes and human impact on the functioning of mountain river channels, Carpathians, southern Poland." Annals of Warsaw University of Life Sciences, Land Reclamation 47, no. 3 (September 1, 2015): 249–60. http://dx.doi.org/10.1515/sggw-2015-0029.
Full textAbstract:
Abstract In the northern slope of the Carpathian Mountains and in their foreland, river and stream channels have been significantly transformed by human impact. These transformations result from changing land use in river basins and direct interference with river channels (alluvia extraction, engineering infrastructure, channel straightening). Anthropogenic impacts cause significant changes in the channel system patterns leading to increased impact of erosion. This mainly leads to the channelling of the fluvial system. This article reviews studies of structure and dynamics of Carpathian river channels conducted based on the methodology of collection of data on channel systems, developed in the Department of Geomorphology of the Institute of Geography and Spatial Management, Jagiellonian University.
41
PANG, H. R., J. L. PING, and L. Z. CHENG. "HIDDEN COLOR CHANNEL EFFECTS TO THE NONSTRANGE SIX-QUARK SYSTEMS." Modern Physics Letters A 24, no. 02 (January 20, 2009): 151–63. http://dx.doi.org/10.1142/s021773230902667x.
Full textAbstract:
A transformation table between physical bases including hidden color channels and symmetry bases for nonstrange six-quark systems is provided by using fractional parentage expansion method. By solving a coupled-channel equation, in the framework of the resonating group method (RGM), the effect of hidden color channels to all nonstrange six-quark systems is examined. It is shown that the overall effects from hidden color channels would reduce the energies of systems. For ΔΔ systems, the greatest decrease is about 20 MeV. Effects of hidden color on the masses of NN systems have been found to be about 1 MeV. However, we should emphasize that such a minor change for NN system is not negligible. We also give the most favorable hidden color channels for NN system.
42
Ratnakumari, Lingamaneni, and Hugh C. Hemmings. "Inhibition of Presynaptic Sodium Channels by Halothane." Anesthesiology 88, no. 4 (April 1, 1998): 1043–54. http://dx.doi.org/10.1097/00000542-199804000-00025.
Full textAbstract:
Background Recent electrophysiologic studies indicate that clinical concentrations of volatile general anesthetic agents inhibit central nervous system sodium (Na+) channels. In this study, the biochemical effects of halothane on Na+ channel function were determined using rat brain synaptosomes (pinched-off nerve terminals) to assess the role of presynaptic Na+ channels in anesthetic effects. Methods Synaptosomes from adult rat cerebral cortex were used to determine the effects of halothane on veratridine-evoked Na+ channel-dependent Na+ influx (using 22Na+), changes in intrasynaptosomal [Na+] (using ion-specific spectrofluorometry), and neurotoxin interactions with specific receptor sites of the Na+ channel (by radioligand binding). The potential physiologic and functional significance of these effects was determined by measuring the effects of halothane on veratridine-evoked Na+ channel-dependent glutamate release (using enzyme-coupled spectrofluorometry). Results Halothane inhibited veratridine-evoked 22Na+ influx (IC50 = 1.1 mM) and changes in intrasynaptosomal [Na+] (concentration for 50% inhibition [IC50] = 0.97 mM), and it specifically antagonized [3H]batrachotoxinin-A 20-alpha-benzoate binding to receptor site two of the Na+ channel (IC50 = 0.53 mM). Scatchard and kinetic analysis revealed an allosteric competitive mechanism for inhibition of toxin binding. Halothane inhibited veratridine-evoked glutamate release from synaptosomes with comparable potency (IC50 = 0.67 mM). Conclusions Halothane significantly inhibited Na+ channel-mediated Na influx, increases in intrasynaptosomal [Na+] and glutamate release, and competed with neurotoxin binding to site two of the Na+ channel in synaptosomes at concentrations within its clinical range (minimum alveolar concentration, 1-2). These findings support a role for presynaptic Na+ channels as a molecular target for general anesthetic effects.
43
Tian, Yutao, Florian Ullrich, Rong Xu, Stefan H. Heinemann, Shangwei Hou, and Toshinori Hoshi. "Two distinct effects of PIP2 underlie auxiliary subunit-dependent modulation of Slo1 BK channels." Journal of General Physiology 145, no. 4 (March 30, 2015): 331–43. http://dx.doi.org/10.1085/jgp.201511363.
Full textAbstract:
Phosphatidylinositol 4,5-bisphosphate (PIP2) plays a critical role in modulating the function of numerous ion channels, including large-conductance Ca2+- and voltage-dependent K+ (BK, Slo1) channels. Slo1 BK channel complexes include four pore-forming Slo1 (α) subunits as well as various regulatory auxiliary subunits (β and γ) that are expressed in different tissues. We examined the molecular and biophysical mechanisms underlying the effects of brain-derived PIP2 on human Slo1 BK channel complexes with different subunit compositions that were heterologously expressed in human embryonic kidney cells. PIP2 inhibited macroscopic currents through Slo1 channels without auxiliary subunits and through Slo1 + γ1 complexes. In contrast, PIP2 markedly increased macroscopic currents through Slo1 + β1 and Slo1 + β4 channel complexes and failed to alter macroscopic currents through Slo1 + β2 and Slo1 + β2 Δ2–19 channel complexes. Results obtained at various membrane potentials and divalent cation concentrations suggest that PIP2 promotes opening of the ion conduction gate in all channel types, regardless of the specific subunit composition. However, in the absence of β subunits positioned near the voltage-sensor domains (VSDs), as in Slo1 and probably Slo1 + γ1, PIP2 augments the negative surface charge on the cytoplasmic side of the membrane, thereby shifting the voltage dependence of VSD-mediated activation in the positive direction. When β1 or β4 subunits occupy the space surrounding the VSDs, only the stimulatory effect of PIP2 is evident. The subunit compositions of native Slo1 BK channels differ in various cell types; thus, PIP2 may exert distinct tissue- and divalent cation–dependent modulatory influences.
44
Fu, Wen-Lung, Lesley M. Wright, and Je-Chin Han. "Rotational Buoyancy Effects on Heat Transfer in Five Different Aspect-Ratio Rectangular Channels With Smooth Walls and 45Degree Ribbed Walls." Journal of Heat Transfer 128, no. 11 (April 6, 2006): 1130–41. http://dx.doi.org/10.1115/1.2352782.
Full textAbstract:
This paper experimentally studies the effects of the buoyancy force and channel aspect ratio (W:H) on heat transfer in two-pass rotating rectangular channels with smooth walls and 45deg ribbed walls. The channel aspect ratios include 4:1, 2:1, 1:1, 1:2, and 1:4. Four Reynolds numbers are studied: 5000, 10,000, 25,000, and 40,000. The rotation speed is fixed at 550rpm for all tests, and for each channel, two channel orientations are studied: 90deg and 45 or 135deg, with respect to the plane of rotation. The maximum inlet coolant-to-wall density ratio (Δρ∕ρ)inlet is maintained around 0.12. Rib turbulators are placed on the leading and trailing walls of the channels at an angle of 45deg to the flow direction. The ribs have a 1.59 by 1.59mm square cross section, and the rib pitch-to-height ratio (P∕e) is 10 for all tests. Under the fixed rotation speed (550rpm) and fixed inlet coolant-to-wall density ratio (0.12), the local buoyancy parameter is varied with different Reynolds numbers, local rotating radius, local coolant-to-wall density ratio, and channel hydraulic diameter. The effects of the local buoyancy parameter and channel aspect ratio on the regional Nusselt number ratio are presented. The results show that increasing the local buoyancy parameter increases the Nusselt number ratio on the trailing surface and decreases the Nusselt number ratio on the leading surface in the first pass for all channels. However, the trend of the Nusselt number ratio in the second pass is more complicated due to the strong effect of the 180deg turn. Results are also presented for this critical turn region of the two-pass channels. In addition to these regions, the channel averaged heat transfer, friction factor, and thermal performance are determined for each channel. With the channels having comparable Nusselt number ratios, the 1:4 channel has the superior thermal performance because it incurs the least pressure penalty.
45
Auclert, Adrien. "Monetary Policy and the Redistribution Channel." American Economic Review 109, no. 6 (June 1, 2019): 2333–67. http://dx.doi.org/10.1257/aer.20160137.
Full textAbstract:
This paper evaluates the role of redistribution in the transmission mechanism of monetary policy to consumption. Three channels affect aggregate spending when winners and losers have different marginal propensities to consume: an earnings heterogeneity channel from unequal income gains, a Fisher channel from unexpected inflation, and an interest rate exposure channel from real interest rate changes. Sufficient statistics from Italian and US data suggest that all three channels are likely to amplify the effects of monetary policy. (JEL E21, E31, E43, E52)
46
Sun, Hui Yong, and Peng Cao. "Researches on Channel Mismatch Effects in Time-Interleaved ADC System." Advanced Materials Research 655-657 (January 2013): 978–83. http://dx.doi.org/10.4028/www.scientific.net/amr.655-657.978.
Full textAbstract:
The Time-Interleaved ADC（TIADC) is an effective method for implement ultra high-speed data acquisition. However, the errors of channel mismatch are seriously degrade the signal-to-noise ratio of the system, such as Time-skew error, Gain error and Offset error. This paper have done some researches and analysis, and given the modeling of the three channels mismatch. What's more, it also given a detailed analysis of error and the method of measure it, derived the formula of signal to noise and distortion ratio(SINAD) and spurious free dynamic range(SFDR). All of them provide a reference for the tolerance range of TIADC channel mismatch error. Meanwhile, the result of this paper has provided a theoretical basis for eliminating TIADC channel mismatch error.
47
Ratnakumari, L., and H. C. Hemmings. "Effects of Propofol on Sodium Channel-dependent Sodium Influx and Glutamate Release in Rat Cerebrocortical Synaptosomes." Anesthesiology 86, no. 2 (February 1, 1997): 428–39. http://dx.doi.org/10.1097/00000542-199702000-00018.
Full textAbstract:
Background Previous electrophysiologic studies have implicated voltage-dependent Na+ channels as a molecular site of action for propofol. This study considered the effects of propofol on Na+ channel-mediated Na+ influx and neurotransmitter release in rat brain synaptosomes (isolated presynaptic nerve terminals). Methods Purified cerebrocortical synaptosomes from adult rats were used to determine the effects of propofol on Na+ influx through voltage-dependent Na+ channels (measured using 22Na+) and intracellular [Na+] (measured by ion-specific spectrofluorimetry). For comparison, the effects of propofol on synaptosomal glutamate release evoked by 4-aminopyridine (Na+ channel dependent), veratridine (Na+ channel dependent), KCi (Na+ channel independent) were studied using enzyme-coupled fluorimetry. Results Propofol inhibited veratridine-evoked 22Na+ influx (inhibitory concentration of 50% [IC50] = 46 microM; 8.9 microM free) and changes in intracellular [Na+] (IC50 = 13 microM; 6.3 microM free) in synaptosomes in a dose-dependent manner. Propofol also inhibited 4-aminopyridine-evoked (IC50 = 39 microM; 19 microM free) and veratridine (20 microM)-evoked (IC50 = 30 microM; 14 microM free), but not KCi-evoked (up to 100 microM) glutamate release from synaptosomes. Conclusions Inhibition of Na+ channel-mediated Na+ influx, increased in intracellular [Na+], and glutamate release occurred in synaptosomes at concentrations of propofol achieved clinically. These results support a role for neuronal voltage-dependent Na+ channels as a molecular target for presynaptic general anesthetic effects.
48
Beurg, Maryline, Adam C. Goldring, and Robert Fettiplace. "The effects of Tmc1 Beethoven mutation on mechanotransducer channel function in cochlear hair cells." Journal of General Physiology 146, no. 3 (August 31, 2015): 233–43. http://dx.doi.org/10.1085/jgp.201511458.
Full textAbstract:
Sound stimuli are converted into electrical signals via gating of mechano-electrical transducer (MT) channels in the hair cell stereociliary bundle. The molecular composition of the MT channel is still not fully established, although transmembrane channel–like protein isoform 1 (TMC1) may be one component. We found that in outer hair cells of Beethoven mice containing a M412K point mutation in TMC1, MT channels had a similar unitary conductance to that of wild-type channels but a reduced selectivity for Ca2+. The Ca2+-dependent adaptation that adjusts the operating range of the channel was also impaired in Beethoven mutants, with reduced shifts in the relationship between MT current and hair bundle displacement for adapting steps or after lowering extracellular Ca2+; these effects may be attributed to the channel’s reduced Ca2+ permeability. Moreover, the density of stereociliary CaATPase pumps for Ca2+ extrusion was decreased in the mutant. The results suggest that a major component of channel adaptation is regulated by changes in intracellular Ca2+. Consistent with this idea, the adaptive shift in the current–displacement relationship when hair bundles were bathed in endolymph-like Ca2+ saline was usually abolished by raising the intracellular Ca2+ concentration.
49
Phillips, Matthew B., Aparna Nigam, and Jon W. Johnson. "Interplay between Gating and Block of Ligand-Gated Ion Channels." Brain Sciences 10, no. 12 (December 1, 2020): 928. http://dx.doi.org/10.3390/brainsci10120928.
Full textAbstract:
Drugs that inhibit ion channel function by binding in the channel and preventing current flow, known as channel blockers, can be used as powerful tools for analysis of channel properties. Channel blockers are used to probe both the sophisticated structure and basic biophysical properties of ion channels. Gating, the mechanism that controls the opening and closing of ion channels, can be profoundly influenced by channel blocking drugs. Channel block and gating are reciprocally connected; gating controls access of channel blockers to their binding sites, and channel-blocking drugs can have profound and diverse effects on the rates of gating transitions and on the stability of channel open and closed states. This review synthesizes knowledge of the inherent intertwining of block and gating of excitatory ligand-gated ion channels, with a focus on the utility of channel blockers as analytic probes of ionotropic glutamate receptor channel function.
50
McFarlane, Matthew B., and William F. Gilly. "State-Dependent Nickel Block of a High-Voltage–Activated Neuronal Calcium Channel." Journal of Neurophysiology 80, no. 4 (October 1, 1998): 1678–85. http://dx.doi.org/10.1152/jn.1998.80.4.1678.
Full textAbstract:
McFarlane, Matthew B. and William F. Gilly. State-dependent nickel block of a high-voltage–activated neuronal calcium channel. J. Neurophysiol. 80: 1678–1685, 1998. Effects of nickel ions (Ni2+) on noninactivating calcium channels in squid giant fiber lobe (GFL) neurons were investigated with whole cell voltage clamp. Three different effects of Ni2+ were observed to be associated with distinct Ca2+ channel activation states. 1) Nickel ions appear to stabilize closed channel states and, as a result, slow activation kinetics. 2) Nickel ions block open channels with little voltage dependence over a wide range of potentials. 3) Block of open channels by Ni2+ becomes more effective during an extended strong depolarization, and this effect is voltage dependent. Recovery from this additional inhibition occurs at intermediate voltages, consistent with the presence of two distinct types of Ni2+ block that we propose correspond to two previously identified open states of the calcium channel. These results, taken together with earlier evidence of state-dependent block by ω-agatoxin IVA, suggest that Ni2+ generates these unique effects in part by interacting differently with the external surface of the GFL calcium channel complex in ways that depend on channel activation state.