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1

Wu, Jie, Xiaoping Hong, Jinhao Deng, Hongyu Cui, Dajun Sun, and Shuang Xiao. "Iterative double-differential M-ary phase-shift keying direct-sequence spread-spectrum receiver in underwater acoustic channels." Journal of the Acoustical Society of America 157, no. 6 (2025): 3976–89. https://doi.org/10.1121/10.0036808.

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In the underwater acoustic channel, the conventional M-ary phase-shift keying (MPSK) direct-sequence spread-spectrum (DSSS) systems are sensitive to time-varying Doppler shifts. To address this issue, this paper proposes an iterative multi-channel double-differential MPSK DSSS receiver in which a per-survivor processing (PSP) method is incorporated in a soft-input/soft-output convolutional decoder to jointly estimate the data sequences and the time-varying Doppler shifts for each symbol. This PSP method embeds data-aided Doppler shift estimation within the structure of the Bahl-Cocke-Jelinek-Raviv algorithm, ensuring that the Doppler shift estimation is unaffected by the information bits. To estimate and track Doppler shifts, a symbol-by-symbol cross correlation method is employed, which is then used for dynamic phase compensation using a linear prediction model to enhance decoding performance in time-varying channels. Additionally, a multi-channel diversity combiner using soft information combines the branch metrics from each channel. Numerical simulation results demonstrate that the proposed receiver method exhibits superior performance in time-varying channels. Finally, the performance of the proposed receiver is validated through experiments conducted in shallow-water horizontal channels and deep-sea vertical channels.
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2

Holdengreber, E., M. Mizrahi, E. Glassner, Y. Koral, S. E. Schacham, and E. Farber. "Phase shift combiner for multi-channel VHF communication." International Journal of Microwave and Wireless Technologies 9, no. 1 (2015): 79–83. http://dx.doi.org/10.1017/s1759078715001464.

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The growing demand for communication systems requires multi-channel solutions. However, the number of antennas in communication systems is dictated by the number of channels in each system which is limited by the available space on a broadcasting platform and by the limited available resources. We have developed a Multi-Channel Phase Control coupler in the VHF frequency range enabling a reduction in the number of antennas to a third of the original setup. The system is based on a phase shifter in a meander stripline geometry connected to each channel individually. The channels are then phase matched simultaneously to a single antenna through a computer-controlled capacitor bank connected to each phase shifter. The system performance shows a low insertion loss of 0.5 dB and a low return loss of −15 dB for the multi-channel setup.
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3

Starmer, C. F., and K. R. Courtney. "Modeling ion channel blockade at guarded binding sites: application to tertiary drugs." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 4 (1986): H848—H856. http://dx.doi.org/10.1152/ajpheart.1986.251.4.h848.

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Excitable membranes exposed to sodium channel blocking agents (D; local anesthetics and antiarrhythmic drugs) show a progressive reduction of peak sodium current when repetitively depolarized (use dependence). Thus, with repetitive excitation, use dependence reflects a net rightward shift in the balance between unblocked channels (U) and blocked channels (B): U + D in equilibrium with B. The modulated receptor hypothesis (a 7-parameter model) has been proposed to account for this shift and is based on a channel lumen binding site whose affinity varies with channel state and where drug-complexed channels exhibit modified inactivation gate kinetics. Alternatively, we consider use-dependent binding as the result of transient access to a constant-affinity binding site. In this setting, the channel gate conformation is viewed as controlling the flux of drug as it diffuses between drug pools and the binding site. Apparent variation in binding rates is therefore considered the result of variations in the fraction of accessible sites. This guarded receptor hypothesis, with three fewer parameters, is able to predict apparent changes in channel binding and apparent shifts in channel inactivation without incorporating modified gating parameters in drug-complexed channels. Furthermore, with this model one is able to characterize both relaxation kinetics and channel blockade associated with tertiary amines as well as hydrophobic and hydrophilic agents. The pH dependence of repriming rates is utilized to estimate several of the important parameters associated with this simplified hypothesis.
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4

Yau, Michael C., Robin Y. Kim, Caroline K. Wang, et al. "One drug-sensitive subunit is sufficient for a near-maximal retigabine effect in KCNQ channels." Journal of General Physiology 150, no. 10 (2018): 1421–31. http://dx.doi.org/10.1085/jgp.201812013.

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Retigabine is an antiepileptic drug and the first voltage-gated potassium (Kv) channel opener to be approved for human therapeutic use. Retigabine is thought to interact with a conserved Trp side chain in the pore of KCNQ2–5 (Kv7.2–7.5) channels, causing a pronounced hyperpolarizing shift in the voltage dependence of activation. In this study, we investigate the functional stoichiometry of retigabine actions by manipulating the number of retigabine-sensitive subunits in concatenated KCNQ3 channel tetramers. We demonstrate that intermediate retigabine concentrations cause channels to exhibit biphasic conductance–voltage relationships rather than progressive concentration-dependent shifts. This suggests that retigabine can exert its effects in a nearly “all-or-none” manner, such that channels exhibit either fully shifted or unshifted behavior. Supporting this notion, concatenated channels containing only a single retigabine-sensitive subunit exhibit a nearly maximal retigabine effect. Also, rapid solution exchange experiments reveal delayed kinetics during channel closure, as retigabine dissociates from channels with multiple drug-sensitive subunits. Collectively, these data suggest that a single retigabine-sensitive subunit can generate a large shift of the KCNQ3 conductance–voltage relationship. In a companion study (Wang et al. 2018. J. Gen. Physiol. https://doi.org/10.1085/jgp.201812014), we contrast these findings with the stoichiometry of a voltage sensor-targeted KCNQ channel opener (ICA-069673), which requires four drug-sensitive subunits for maximal effect.
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5

Ye, Zhengmao. "Exploring Impact of Doppler Effect on Time-Varying Multipath Wireless Communication Channels via Model Based Characteristic Analysis." WSEAS TRANSACTIONS ON SIGNAL PROCESSING 20 (December 31, 2024): 145–52. https://doi.org/10.37394/232014.2024.20.15.

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In areas of outdoor wireless communication, the Doppler shift occurs due to the relative motion between the transmitter and receiver. To apply any baseband channel model for multipath propagation, some real-world phenomena must be taken into account, such as the Doppler effect, time dispersion, and multipath scattering. Time dispersion of the radio channel leads to the Intersymbol Interference (ISI) which degrades communication performance. Scattering at diverse angles gives rise to a range of Doppler frequency shifts referred to as the Doppler spectrum. The maximum Doppler shift arises whenever the scattering direction is opposite to the channel trajectory. The Rayleigh or Rician fading distributions of the communication channel are used to characterize the line-of-sight path (LOS) and non-line-of-sight (NLOS) path radio propagation, respectively. Multipath fading causes frequency-selectivity and Doppler shifting causes time-selectivity. Two popular modeling techniques for fading channels are the Filtered White Gaussian Noise and Sum-Of-Sinusoids schemes. The impact of the Doppler effect on wireless communication channel characteristics will be examined using the model based performance analysis.
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6

DIAZ-OTERO, FRANCISCO J., and PEDRO CHAMORRO-POSADA. "MULTICHANNEL SOLITON COLLISIONS IN STRONGLY DISPERSION MANAGED WDM TRANSMISSION SYSTEMS." Journal of Nonlinear Optical Physics & Materials 21, no. 03 (2012): 1250034. http://dx.doi.org/10.1142/s0218863512500348.

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We study the collision-induced timing jitter of optical solitons in dispersion managed wavelength-division multiplexed communication systems. The work presented here is an extension of previous analyzes of two-pulse interactions to the multiple channel case. The numerical study is based on a system of ordinary differential equations obtained using a variational approach that models the evolution of the main parameters of the propagating pulses. We explain the mechanism associated with inter-channel interactions and study the evolution of multiplexed soliton trains and the resulting frequency shift induced jitter as the map strength is varied. The results obtained indicate a strong dependence of the frequency shifts on the position of the channel within the multiplex and the existence of patterns for the frequency shifts that depend on the parity of the number of channels.
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7

Estacion, Mark, and Stephen G. Waxman. "Nonlinear effects of hyperpolarizing shifts in activation of mutant Nav1.7 channels on resting membrane potential." Journal of Neurophysiology 117, no. 4 (2017): 1702–12. http://dx.doi.org/10.1152/jn.00898.2016.

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The Nav1.7 sodium channel is preferentially expressed within dorsal root ganglion (DRG) and sympathetic ganglion neurons. Gain-of-function mutations that cause the painful disorder inherited erythromelalgia (IEM) shift channel activation in a hyperpolarizing direction. When expressed within DRG neurons, these mutations produce a depolarization of resting membrane potential (RMP). The biophysical basis for the depolarized RMP has to date not been established. To explore the effect on RMP of the shift in activation associated with a prototypical IEM mutation (L858H), we used dynamic-clamp models that represent graded shifts that fractionate the effect of the mutation on activation voltage dependence. Dynamic-clamp recording from DRG neurons using a before-and-after protocol for each cell made it possible, even in the presence of cell-to-cell variation in starting RMP, to assess the effects of these graded mutant models. Our results demonstrate a nonlinear, progressively larger effect on RMP as the shift in activation voltage dependence becomes more hyperpolarized. The observed differences in RMP were predicted by the “late” current of each mutant model. Since the depolarization of RMP imposed by IEM mutant channels is known, in itself, to produce hyperexcitability of DRG neurons, the development of pharmacological agents that normalize or partially normalize activation voltage dependence of IEM mutant channels merits further study. NEW & NOTEWORTHY Inherited erythromelalgia (IEM), the first human pain disorder linked to a sodium channel, is widely regarded as a genetic model of neuropathic pain. IEM is produced by Nav1.7 mutations that hyperpolarize activation. These mutations produce a depolarization of resting membrane potential (RMP) in dorsal root ganglion neurons. Using dynamic clamp to explore the effect on RMP of the shift in activation, we demonstrate a nonlinear effect on RMP as the shift in activation voltage dependence becomes more hyperpolarized.
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8

Wang, Laihe, Yueli Li, Wu Wang, and Daoxiang An. "Moving Target Indication for Dual-Channel Circular SAR/GMTI Systems." Sensors 20, no. 1 (2019): 158. http://dx.doi.org/10.3390/s20010158.

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In a dual-channel circular synthetic aperture radar (CSAR) and ground moving target indication (GMTI) system, the antenna baseline is not parallel with the flight path due to a yaw angle. The angle causes a varying group-phase shift between the dual-channel signals and therefore degrades the correlation between the image pair. Therefore, the group-phase shift needs to be removed before channel equalization. To resolve the problem, the interferometric phase term was deduced and analyzed based on the geometry of a dual-channel CSAR system. Then, the varying phase term with respect to the Doppler frequency and the varying group-phase shift over the range were compensated for in the channel registration. Furthermore, blind channel equalization, including two-dimensional calibration and amplitude equalization, was applied to eliminate the amplitude and residual phase differences between the channels. Finally, the amplitude image obtained using a displaced phase center antenna (DPCA) was multiplied by the phase image obtained with along-track interferometry (ATI) to detect moving targets. The experimental results verified the effectiveness of the method for both uniform and non-uniform clutter suppression.
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9

Vassilev, P. M., R. W. Hadley, K. S. Lee, and J. R. Hume. "Voltage-dependent action of tetrodotoxin in mammalian cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 2 (1986): H475—H480. http://dx.doi.org/10.1152/ajpheart.1986.251.2.h475.

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Single Na+ channel currents have been examined in isolated guinea pig ventricular myocytes using the patch-clamp technique. The effects of lidocaine, extracellular calcium [(Ca)o], and tetrodotoxin on patch Na+ channel availability were assessed using ensemble averages of Na+-channel openings during depolarizing test potential steps from 7 to 10 different patch-holding potentials in each cell-attached patch. In six control patches, the potential for 50% channel availability (Vh) was -15 mV (relative to an average resting membrane potential of -80 mV). Exposure of patches to either lidocaine or elevated (Ca)o produced the expected shifts in Vh [average -22 mV for lidocaine and +10 mV for 6 mM (Ca)o]. Exposure of patches to tetrodotoxin (0.5 microM or 1.0 microM) produced a dose-dependent hyperpolarizing shift of Vh (average -10 and -17 mV) compared with control patches. The hyperpolarizing shift by tetrodotoxin was observed with pulses applied at frequencies of 1.0 or 0.067 Hz. In agreement with earlier maximal upstroke velocity studies in the same preparation, we conclude that block of ventricular Na+ channels by tetrodotoxin exhibits genuine steady-state voltage dependence.
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10

Leipziger, Jens, Gordon G. MacGregor, Gordon J. Cooper, Jason Xu, Steven C. Hebert, and Gerhard Giebisch. "PKA site mutations of ROMK2 channels shift the pH dependence to more alkaline values." American Journal of Physiology-Renal Physiology 279, no. 5 (2000): F919—F926. http://dx.doi.org/10.1152/ajprenal.2000.279.5.f919.

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Close similarity between the rat native low-conductance K+ channel in the apical membrane of renal cortical collecting duct principal cells and the cloned rat ROMK channel strongly suggest that the two are identical. Prominent features of ROMK regulation are a steep pH dependence and activation by protein kinase A (PKA)-dependent phosphorylation. In this study, we investigated the pH dependence of cloned renal K+ channel (ROMK2), wild-type (R2-WT), and PKA site mutant channels (R2-S25A, R2-S200A, and R2-S294A). Ba2+-sensitive outward whole cell currents (holding voltage −50 mV) were measured in two-electrode voltage-clamp experiments in Xenopus laevisoocytes expressing either R2-WT or mutant channels. Intracellular pH (pHi) was measured with pH-sensitive microelectrodes in a different group of oocytes from the same batch on the same day. Resting pHi of R2-WT and PKA site mutants was the same: 7.32 ± 0.02 ( n = 22). The oocytes were acidified by adding 3 mM Na butyrate with external pH (pHo) adjusted to 7.4, 6.9, 6.4, or 5.4. At pHo 7.4, butyrate led to a rapid (τ: 163 ± 14 s, where τ means time constant, n= 4) and stable acidification of the oocytes (ΔpHi0.13 ± 0.02 pH units, where Δ means change, n = 12). Intracellular acidification reversibly inhibited ROMK2-dependent whole cell current. The effective acidic dissociation constant (p K a) value of R2-WT was 6.92 ± 0.03 ( n = 8). Similarly, the effective p K a value of the N-terminal PKA site mutant R2-S25A was 6.99 ± 0.02 ( n = 6). The effective p K a values of the two COOH-terminal PKA site mutant channels, however, were significantly shifted to alkaline values; i.e., 7.15 ± 0.06 ( n = 5) for R2-S200A and 7.16 ± 0.03 ( n = 8) for R2-S294A. The apparent ΔpH shift between the R2-WT and the R2-S294A mutant was 0.24 pH units. In excised inside-out patches, alkaline pH 8.5 activated R2-S294A channel current by 32 ± 6.7%, whereas in R2-WT channel patches alkalinzation only marginally increased current by 6.5 ± 1% ( n = 5). These results suggest that channel phosphorylation may substantially influence the pH sensitivity of ROMK2 channel. Our data are consistent with the hypothesis that in the native channel PKA activation involves a shift of the pKa value of ROMK channels to more acidic values, thus relieving a H+-mediated inhibition of ROMK channels.
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11

Yusuf, Yogi Muhamad, Vikry Abdullah Rahiem, Wawan Wartono, and Charisma Asri Fitrananda. "Representasi Busana Muslim Pemuda Hijrah di Channel Youtube Shift Media." Jurnal Komunikasi Global 10, no. 2 (2021): 294–311. http://dx.doi.org/10.24815/jkg.v10i2.23093.

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Busana secara simbolik merupakan bentuk komunikasi nonverbal yang dapat mengikat suatu komunitas. Pemuda hijrah dalam komunitas Shift di Y outube berusaha menyajikan keberagaman busana dan citra simbolis dalam video-video dakwah yang menampilkan Ustaz Hanan Attaki. Penelitian ini bertujuan untuk mengetahui bagaimana representasi busana muslim yang ditampilkan oleh Pemuda Hijrah di Channel Youtube Shift Media dalam rangka menarik perhatian generasi milenial. Metode penelitian yang digunakan adalah studi etnografi virtual, dengan pendekatan kualitatif yang bersifat deskriptif dan menggunakan teori interaksi simbolik. Hasil penelitian menunjukkan representasi busana muslim yang ditampilkan dalam video komunikasi dakwah Pemuda Hijrah di Channel Youtube Shift Media bertujuan untuk melakukan pembauran dengan jamaah anak muda. Dengan menentukan segmentasi khalayak, kreator Channel Youtube Shift Media mencoba untuk menggeser busana muslim menjadi busana kasual yang lebih dekat dengan milenial saat mendatangi kegiatan kajian dakwah. Proses kontruksi makna denotatif busana muslim ditandai oleh Ustaz Hanan Attaki yang kerap tampil dengan menggunakan kemeja, kaos atau sweater dan penutup kepala model reggae (topi kupluk).Symbolically, clothing is a form of nonverbal communication that can bind a community. Pemuda Hijrah in the Shift community on Youtube tries to present various clothing and symbolic images in da'wah videos featuring Ustaz Hanan Attaki. This study aims to find out how Pemuda Hijrah displays the representation of Muslim clothing on the Shift Media Youtube Channel to attract the attention of millennial generation. The research method used is a virtual ethnographic study, with a qualitative descriptive approach and using symbolic interaction theory. The results of the study show that the representation of Muslim clothing displayed in the communication video of Pemuda Hijrah propaganda on the Shift Media Youtube Channel aims to mingle with young congregations. By determining the segmentation of the audience, the creators of Channel Youtube Shift Media are trying to Shift Muslim clothing into casual clothing that is more suited to millennials when they come to da’wah activities. The process of constructing the denotative meaning of Muslim clothing was marked by Ustaz Hanan Attaki, who often appeared wearing a shirt, t-shirt or sweater and a reggae-style head covering.
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12

Qu, Y., J. C. Rogers, T. N. Tanada, W. A. Catterall, and T. Scheuer. "Phosphorylation of S1505 in the cardiac Na+ channel inactivation gate is required for modulation by protein kinase C." Journal of General Physiology 108, no. 5 (1996): 375–79. http://dx.doi.org/10.1085/jgp.108.5.375.

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Inactivation of both brain and cardiac Na+ channels is modulated by activation of protein kinase C (PKC) but in different ways. Previous experiments had shown that phosphorylation of serine 1506 in the highly conserved loop connecting homologous domains III and IV (LIII/IV) of the brain Na+ channel alpha subunit is necessary for all effects of PKC. Here we examine the importance of the analogous serine for the different modulation of the rH1 cardiac Na+ channel. Serine 1505 of rH1 was mutated to alanine to prevent its phosphorylation, and the resulting mutant channel was expressed in 1610 cells. Electrophysiological properties of these mutant channels were indistinguishable from those of wild-type (WT) rH1 channels. Activation of PKC with 1-oleoyl-2-acetyl-sn-glycerol (OAG) reduced WT Na+ current by 49.3 +/- 4.2% (P < 0.01) but S1505A mutant current was reduced by only 8.5 +/- 5.4% (P = 0.29) when the holding potential was -94 mV. PKC activation also caused a -17-mV shift in the voltage dependence of steady-state inactivation of the WT channel which was abolished in the mutant. Thus, phosphorylation of serine 1505 is required for both the negative shift in the inactivation curve and the reduction in Na+ current by PKC. Phosphorylation of S1505/1506 has common and divergent effects in brain and cardiac Na+ channels. In both brain and cardiac Na+ channels, phosphorylation of this site by PKC is required for reduction of peak Na+ current. However, phosphorylation of S1506 in brain Na+ channels slows and destabilizes inactivation of the open channel. Phosphorylation of S1505 in cardiac, but not S1506 in brain, Na+ channels causes a negative shift in the inactivation curve, indicating that it stabilizes inactivation from closed states. Since LIII/IV containing S1505/S1506 is completely conserved, interaction of the phosphorylated serine with other regions of the channel must differ in the two channel types.
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13

Zhong, Z. W., S. C. Lim, and A. Asundi. "Optical Fiber Shifts and Shear Stains in V-Groove Arrays for Optical MEMS Packaging." Journal of Electronic Packaging 127, no. 1 (2005): 25–28. http://dx.doi.org/10.1115/1.1846063.

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The objective of this study is to investigate optical fiber shifts and shear stains in V-groove arrays for optical microelectromechanical system packaging, when the arrays are subjected to temperature cycling. Thermally induced optical fiber shifts in the joints consisting of an optical fiber, epoxy adhesive, and silicon substrate were simulated using a finite element analysis (FEA) package ANSYS. Experiments using real-time Moire´ interferometry were also performed at temperatures of 25, 40, 60, 85 and 100°C for confirmation of the analysis results. The study revealed that thermally induced fiber shifts increased with the number of V-groove channels. The shear strains at the fiber and silicon interface in the fiber joints increased as the V-groove channel was further away from the neutral point of the fiber array packages. The optical coupling loss is the greatest during thermal loading for the outer fiber in the four channel V-groove array. Optical loss of 0.334 and 0.346 dB was calculated using the fiber shift values obtained from the FEA and experimental results, respectively. The effect of fiber shifts, especially the shift of the fiber that is positioned at the outermost V-groove in the array, cannot be ignored.
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14

Halder, Amit, Md Riyad Tanshen, Khandakar Ahammad Ali, Fauzia Khan Juthy, Md Younus Ali, and Nusrat Jahan. "Performance Analysis of 16-FSK Modulator and Demodulator Over Rician Fading Channel by Varying Channel Parameters." Asian Journal of Basic Science & Research 05, no. 02 (2023): 97–104. http://dx.doi.org/10.38177/ajbsr.2023.5209.

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This article presents a comprehensive analysis of a 16-FSK modulator and demodulator's performance over a Rician fading channel, which accurately models wireless communication channels with line-of-sight and non-line-of-sight components. The study investigates the impact of various parameters, including the Rician K-factor, Maximum Diffuse Doppler Shift, and Delay Vector, using the MATLAB Simulink communication blockset. The results indicate that increasing the K-factor and delay vector of the channel leads to an improvement in bit error rate. Additionally, it is observed that the maximum diffuse Doppler shift has minimal influence on the bit error rate. These findings provide valuable insights into optimizing the performance of 16-FSK modulation schemes in Rician fading channels, thereby enhancing the design and deployment of wireless communication systems.
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15

Almaamory, Aqiel N. "LDPC CODED MULTIUSER MC-CDMA PERFORMANCE OVERMULTIPATH RAYLEIGH FADING CHANNEL." Journal of Engineering 17, no. 04 (2011): 1039–46. http://dx.doi.org/10.31026/j.eng.2011.04.28.

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This work presents the simulation of a Low density Parity Check (LDPC) coding scheme withmultiuserMulti-Carrier Code Division Multiple Access (MC-CDMA) system over Additive WhiteGaussian Noise (AWGN) channel and multipath fading channels. The decoding technique used inthe simulation was iterative decoding since it gives maximum efficiency with ten iterations.Modulation schemes that used are Phase Shift Keying (BPSK, QPSK and 16 PSK), along with theOrthogonal Frequency Division Multiplexing (OFDM). A 12 pilot carrier were used in the estimatorto compensate channel effect. The channel model used is Long Term Evolution (LTE) channel withTechnical Specification TS 25.101v2.10 and 5 MHz bandwidth including the channels of indoorto outdoor/ pedestrian channel and Vehicular channel
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16

Пензин, Максим, Maksim Penzin, Николай Ильин, and Nikolay Ilyin. "Modeling of Doppler frequency shift in multipath radio channels." Solar-Terrestrial Physics 2, no. 2 (2016): 66–76. http://dx.doi.org/10.12737/21000.

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We discuss the modeling of propagation of a quasi-monochromatic radio signal, represented by a coherent pulse sequence, in a non-stationary multipath radio channel. In such a channel, signal propagation results in the observed frequency shift for each ray (Doppler effect). The modeling is based on the assumption that during propagation of a single pulse a channel can be considered stationary. A phase variation in the channel transfer function is shown to cause the observed frequency shift in the received signal. Thus, instead of measuring the Doppler frequency shift, we can measure the rate of variation in the mean phase of one pulse relative to another. The modeling is carried out within the framework of the method of normal waves. The method enables us to model the dynamics of the electromagnetic field at a given point with the required accuracy. The modeling reveals that a local change in ionospheric conditions more severely affects the rays whose reflection region is in the area where the changes occur.
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Berg, C., J. Boogaart, F. Sibbing, and J. Osse. "IMPLICATIONS OF GILL ARCH MOVEMENTS FOR FILTER-FEEDING: AN X-RAY CINEMATOGRAPHICAL STUDY OF FILTER-FEEDING WHITE BREAM (BLICCA BJOERKNA) AND COMMON BREAM (ABRAMIS BRAMA)." Journal of Experimental Biology 191, no. 1 (1994): 257–82. http://dx.doi.org/10.1242/jeb.191.1.257.

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Previous research shows that the reducible-channel model of filter-feeding can probably be applied to common bream, but not to white bream. According to this model, zooplankton are retained in the channels between the medial gill rakers; the mesh size of the sieve can be reduced by lowering the lateral rakers of the neighbouring gill arch into these channels. Gill arch movements may well disturb this mechanism; the depressed lateral gill rakers will move in and out of the medial channels and also shift out of their centre. We have quantified these disturbances by measuring the gill arch movements during filter-feeding in white bream and common bream, using dorsal X-ray films. In both species, the lateral rakers are long enough to bridge the gill slits. It was expected that common bream, which can reduce their channels, would have considerably less shift out of the channel centre than white bream, which cannot reduce their channels. However, the predicted shift is 40­50 % of the channel width in white bream and 75 % in common bream. A new, dynamic retention mechanism is proposed for common bream. According to this hypothesis, once a particle is trapped in a reduced channel, the channel walls release mucus and the particle becomes sticky. Hence, particles need to be retained mechanically only during part of the gulping cycle. According to the hypothesis, this is achieved by sideways rotation of the lateral rakers in combination with their tapering shape. Retention mechanisms with interdigitating rakers are expected chiefly in facultative filter-feeders, because such mechanisms are easily disturbed by gill arch movements.
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18

Chabala, L. D., B. W. Urban, L. B. Weiss, W. N. Green, and O. S. Andersen. "Steady-state gating of batrachotoxin-modified sodium channels. Variability and electrolyte-dependent modulation." Journal of General Physiology 98, no. 1 (1991): 197–224. http://dx.doi.org/10.1085/jgp.98.1.197.

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The steady-state gating of individual batrachotoxin-modified sodium channels in neutral phospholipid bilayers exhibits spontaneous, reversible changes in channel activation, such that the midpoint potential (Va) for the gating curves may change, by 30 mV or more, with or without a change in the apparent gating valence (za). Consequently, estimates for Va and, in particular, za from ensemble-averaged gating curves differ from the average values for Va and za from single-channel gating curves. In addition to these spontaneous variations, the average Va shifts systematically as a function of [NaCl] (being -109, -88, and -75 mV at 0.1, 0.5, and 1.0 M NaCl), with no systematic variation in the average za (approximately 3.7). The [NaCl]-dependent shifts in Va were interpreted in terms of screening of fixed charges near the channels' gating machinery. Estimates for the extracellular and intracellular apparent charge densities (sigma e = -0.7 and sigma i = -0.08 e/nm2) were obtained from experiments in symmetrical and asymmetrical NaCl solutions using the Gouy-Chapman theory. In 0.1 M NaCl the extracellular and intracellular surface potentials are estimated to be -94 and -17 mV, respectively. The intrinsic midpoint potential, corrected for the surface potentials, is thus about -30 mV, and the standard free energy of activation is approximately -12 kJ/mol. In symmetrical 0.1 M NaCl, addition of 0.005 M Ba2+ to the extracellular solution produced a 17-mV depolarizing shift in Va and a slight reduction in za. The shift is consistent with predictions using the Gouy-Chapman theory and the above estimate for sigma e. Subsequent addition of 0.005 M Ba2+ to the intracellular solution produced a approximately 5-mV hyperpolarizing shift in the ensemble-averaged gating curve and reduced za by approximately 1. This Ba(2+)-induced shift is threefold larger than predicted, which together with the reduction in za implies that Ba2+ may bind at the intracellular channel surface.
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19

Li, Guang, Juejin Wang, Ping Liao, et al. "Exclusion of alternative exon 33 of CaV1.2 calcium channels in heart is proarrhythmogenic." Proceedings of the National Academy of Sciences 114, no. 21 (2017): E4288—E4295. http://dx.doi.org/10.1073/pnas.1617205114.

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Alternative splicing changes the CaV1.2 calcium channel electrophysiological property, but the in vivo significance of such altered channel function is lacking. Structure–function studies of heterologously expressed CaV1.2 channels could not recapitulate channel function in the native milieu of the cardiomyocyte. To address this gap in knowledge, we investigated the role of alternative exon 33 of the CaV1.2 calcium channel in heart function. Exclusion of exon 33 in CaV1.2 channels has been reported to shift the activation potential −10.4 mV to the hyperpolarized direction, and increased expression of CaV1.2Δ33 channels was observed in rat myocardial infarcted hearts. However, how a change in CaV1.2 channel electrophysiological property, due to alternative splicing, might affect cardiac function in vivo is unknown. To address these questions, we generated mCacna1c exon 33−/−-null mice. These mice contained CaV1.2Δ33 channels with a gain-of-function that included conduction of larger currents that reflects a shift in voltage dependence and a modest increase in single-channel open probability. This altered channel property underscored the development of ventricular arrhythmia, which is reflected in significantly more deaths of exon 33−/− mice from β-adrenergic stimulation. In vivo telemetric recordings also confirmed increased frequencies in premature ventricular contractions, tachycardia, and lengthened QT interval. Taken together, the significant decrease or absence of exon 33-containing CaV1.2 channels is potentially proarrhythmic in the heart. Of clinical relevance, human ischemic and dilated cardiomyopathy hearts showed increased inclusion of exon 33. However, the possible role that inclusion of exon 33 in CaV1.2 channels may play in the pathogenesis of human heart failure remains unclear.
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20

Wang, Jun A., Wei Lin, Terence Morris, Umberto Banderali, Peter F. Juranka, and Catherine E. Morris. "Membrane trauma and Na+ leak from Nav1.6 channels." American Journal of Physiology-Cell Physiology 297, no. 4 (2009): C823—C834. http://dx.doi.org/10.1152/ajpcell.00505.2008.

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During brain trauma, white matter experiences shear and stretch forces that, without severing axons, nevertheless trigger their secondary degeneration. In central nervous system (CNS) trauma models, voltage-gated sodium channel (Nav) blockers are neuroprotective. This, plus the rapid tetrodotoxin-sensitive Ca2+ overload of stretch-traumatized axons, points to “leaky” Nav channels as a pivotal early lesion in brain trauma. Direct effects of mechanical trauma on neuronal Nav channels have not, however, been tested. Here, we monitor immediate responses of recombinant neuronal Nav channels to stretch, using patch-clamp and Na+-dye approaches. Trauma constituted either bleb-inducing aspiration of cell-attached oocyte patches or abrupt uniaxial stretch of cells on an extensible substrate. Nav1.6 channel transient current displayed irreversible hyperpolarizing shifts of steady-state inactivation [availability(V)] and of activation [ g(V)] and, thus, of window current. Left shift increased progressively with trauma intensity. For moderately intense patch trauma, a ∼20-mV hyperpolarizing shift was registered. Nav1.6 voltage sensors evidently see lower energy barriers posttrauma, probably because of the different bilayer mechanics of blebbed versus intact membrane. Na+ dye-loaded human embryonic kidney (HEK) cells stably transfected with αNav1.6 were subjected to traumatic brain injury-like stretch. Cytoplasmic Na+ levels abruptly increased and the trauma-induced influx had a significant tetrodotoxin-sensitive component. Nav1.6 channel responses to cell and membrane trauma are therefore consistent with the hypothesis that mechanically induced Nav channel leak is a primary lesion in traumatic brain injury. Nav1.6 is the CNS node of Ranvier Nav isoform. When, during head trauma, nodes experienced bleb-inducing membrane damage of varying intensities, nodal Nav1.6 channels should immediately “leak” over a broadly left-smeared window current range.
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Cukierman, S., W. C. Zinkand, R. J. French, and B. K. Krueger. "Effects of membrane surface charge and calcium on the gating of rat brain sodium channels in planar bilayers." Journal of General Physiology 92, no. 4 (1988): 431–47. http://dx.doi.org/10.1085/jgp.92.4.431.

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The voltage-dependent gating of single, batrachotoxin-activated Na channels from rat brain was studied in planar lipid bilayers composed of negatively charged or neutral phospholipids. The relationship between the probability of finding the Na channel in the open state and the membrane potential (Po vs. Vm) was determined in symmetrical NaCl, both in the absence of free Ca2+ and after the addition of Ca2+ to the extracellular side of the channel, the intracellular side, or both. In the absence of Ca2+, neither the midpoint (V0.5) of the Po vs. Vm relation, nor the steepness of the gating curve, was affected by the charge on the bilayer lipid. The addition of 7.5 mM Ca2+ to the external side caused a depolarizing shift in V0.5. This depolarizing shift was approximately 17 mV in neutral bilayers and approximately 25 mV in negatively charged bilayers. The addition of the same concentration of Ca2+ to only the intracellular side caused hyperpolarizing shifts in V0.5 of approximately 7 mV (neutral bilayers) and approximately 14 mV (negatively charged bilayers). The symmetrical addition of Ca2+ caused a small depolarizing shift in Po vs. Vm. We conclude that: (a) the Na channel protein possesses negatively charged groups on both its inner and outer surfaces. Charges on both surfaces affect channel gating but those on the outer surface exert a stronger influence. (b) Negative surface charges on the membrane phospholipid are close enough to the channel's gating machinery to substantially affect its operation. Charges on the inner and outer surfaces of the membrane lipid affect gating symmetrically. (c) Effects on steady-state Na channel activation are consistent with a simple superposition of contributions to the local electrostatic potential from charges on the channel protein and the membrane lipid.
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22

Stocker, Patrick J., and Eric S. Bennett. "Differential Sialylation Modulates Voltage-gated Na+ Channel Gating throughout the Developing Myocardium." Journal of General Physiology 127, no. 3 (2006): 253–65. http://dx.doi.org/10.1085/jgp.200509423.

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Voltage-gated sodium channel function from neonatal and adult rat cardiomyocytes was measured and compared. Channels from neonatal ventricles required an ∼10 mV greater depolarization for voltage-dependent gating events than did channels from neonatal atria and adult atria and ventricles. We questioned whether such gating shifts were due to developmental and/or chamber-dependent changes in channel-associated functional sialic acids. Thus, all gating characteristics for channels from neonatal atria and adult atria and ventricles shifted significantly to more depolarized potentials after removal of surface sialic acids. Desialylation of channels from neonatal ventricles did not affect channel gating. After removal of the complete surface N-glycosylation structures, gating of channels from neonatal atria and adult atria and ventricles shifted to depolarized potentials nearly identical to those measured for channels from neonatal ventricles. Gating of channels from neonatal ventricles were unaffected by such deglycosylation. Immunoblot gel shift analyses indicated that voltage-gated sodium channel α subunits from neonatal atria and adult atria and ventricles are more heavily sialylated than α subunits from neonatal ventricles. The data are consistent with approximately 15 more sialic acid residues attached to each α subunit from neonatal atria and adult atria and ventricles. The data indicate that differential sialylation of myocyte voltage-gated sodium channel α subunits is responsible for much of the developmental and chamber-specific remodeling of channel gating observed here. Further, cardiac excitability is likely impacted by these sialic acid–dependent gating effects, such as modulation of the rate of recovery from inactivation. A novel mechanism is described by which cardiac voltage-gated sodium channel gating and subsequently cardiac rhythms are modulated by changes in channel-associated sialic acids.
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23

Grigoriev, N. G., J. D. Spafford, W. J. Gallin, and A. N. Spencer. "Voltage sensing in jellyfish Shaker K+ channels." Journal of Experimental Biology 200, no. 22 (1997): 2919–26. http://dx.doi.org/10.1242/jeb.200.22.2919.

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The S4 segment of the jellyfish (Polyorchis penicillatus) Shaker channel jShak1 contains only six positively charged motifs. All other Shaker channels, including the jellyfish Shaker channel jShak2, have seven charges in this segment. Despite their charge differences, both these jellyfish channels produce currents with activation and inactivation curves shifted by approximately +40 mV relative to other Shaker currents. Adding charge without changing segment length by mutating the N-terminal side of jShak1 S4 does not have a pronounced effect on channel activation properties. Adding the positively charged motif RIF on the N-terminal side of K294 (the homologue of K374 in Drosophila Shaker, which is a structurally critical residue) produced a large positive shift in both activation and inactivation without altering the slope of the activation curve of the channel. When IFR was added to the other side of K294, there was a small negative shift in activation and fast inactivation of the channel was prevented. Our results demonstrate that K294 divides the S4 segment into functionally different regions and that the voltage threshold for activation and inactivation of the channel is not determined by the total charge on S4.
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24

Wang, Yuan, Zhou Mo Zeng, Yi Bo Li, Wen Zhang, and Hao Feng. "Research on Doppler and Channel Estimation for Multicarrier Spread Spectrum Underwater Acoustic Communication System." Advanced Materials Research 1079-1080 (December 2014): 752–56. http://dx.doi.org/10.4028/www.scientific.net/amr.1079-1080.752.

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Spreadspectrum orthogonal frequency-division multiplexing (SS-OFDM), which appliesspread spectrum technique into OFDM, performs robustly in severely multipathfading underwater channels. However, this technology is sensitive to thefrequency shift. Furthermore, communication in underwater acoustic (UWA)channels is more vulnerable to Doppler effect than other wireless channels dueto the low speed of acoustic signal propagation. It presents challenges forcommunication between underwater mobile nodes. Therefore, accurate Dopplerfrequency shift estimation and compensation is important. Aself-designed receiver structure for SS-OFDM system including a novel Dopplerscale estimation method and channel estimation via compressed sensing method isproposed. The simulation and experimental results offer strong proofs for ourscheme to be a viable option for acoustic communication between underwatermobile nodes and compressed sensing method outperforms the conventionalleast-squares (LS) method in channel estimation.
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25

Cestèle, Sandrine, Todd Scheuer, Massimo Mantegazza, Hervé Rochat та William A. Catterall. "Neutralization of Gating Charges in Domain II of the Sodium Channel α Subunit Enhances Voltage-Sensor Trapping by a β-Scorpion Toxin". Journal of General Physiology 118, № 3 (2001): 291–302. http://dx.doi.org/10.1085/jgp.118.3.291.

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β-Scorpion toxins shift the voltage dependence of activation of sodium channels to more negative membrane potentials, but only after a strong depolarizing prepulse to fully activate the channels. Their receptor site includes the S3–S4 loop at the extracellular end of the S4 voltage sensor in domain II of the α subunit. Here, we probe the role of gating charges in the IIS4 segment in β-scorpion toxin action by mutagenesis and functional analysis of the resulting mutant sodium channels. Neutralization of the positively charged amino acid residues in the IIS4 segment by mutation to glutamine shifts the voltage dependence of channel activation to more positive membrane potentials and reduces the steepness of voltage-dependent gating, which is consistent with the presumed role of these residues as gating charges. Surprisingly, neutralization of the gating charges at the outer end of the IIS4 segment by the mutations R850Q, R850C, R853Q, and R853C markedly enhances β-scorpion toxin action, whereas mutations R856Q, K859Q, and K862Q have no effect. In contrast to wild-type, the β-scorpion toxin Css IV causes a negative shift of the voltage dependence of activation of mutants R853Q and R853C without a depolarizing prepulse at holding potentials from −80 to −140 mV. Reaction of mutant R853C with 2-aminoethyl methanethiosulfonate causes a positive shift of the voltage dependence of activation and restores the requirement for a depolarizing prepulse for Css IV action. Enhancement of sodium channel activation by Css IV causes large tail currents upon repolarization, indicating slowed deactivation of the IIS4 voltage sensor by the bound toxin. Our results are consistent with a voltage-sensor–trapping model in which the β-scorpion toxin traps the IIS4 voltage sensor in its activated position as it moves outward in response to depolarization and holds it there, slowing its inward movement on deactivation and enhancing subsequent channel activation. Evidently, neutralization of R850 and R853 removes kinetic barriers to binding of the IIS4 segment by Css IV, and thereby enhances toxin-induced channel activation.
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26

Vanishree Sah, P., D. Indira, and Gururajan Padmavathi. "Perception of Consumers towards Sustainable Omni-Channel Retailing." E3S Web of Conferences 552 (2024): 01083. http://dx.doi.org/10.1051/e3sconf/202455201083.

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The previous two decades have seen a considerable shift in the retailing paradigm due to information technology, going from a one way channel to online channel, multiple channel, and most recently, a sustainable omni-channel retailing. The innovations make it easier and more enjoyable for customers to purchase through numerous channels. Sustainable omni-channel system also makes it easier for merchants to identify different points of contact as well as strategies for meeting customer demands and boosting sales. The present study focuses on factors influencing consumer’s buying intention through sustainable omni-channel.
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27

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 (2015): 233–43. http://dx.doi.org/10.1085/jgp.201511458.

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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.
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28

Cornelisse, L. Niels, Wim J. J. M. Scheenen, Werner J. H. Koopman, Eric W. Roubos, and Stan C. A. M. Gielen. "Minimal Model for Intracellular Calcium Oscillations and Electrical Bursting in Melanotrope Cells of Xenopus Laevis." Neural Computation 13, no. 1 (2001): 113–37. http://dx.doi.org/10.1162/089976601300014655.

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A minimal model is presented to explain changes in frequency, shape, and amplitude of Ca2+ oscillations in the neuroendocrine melanotrope cell of Xenopus Laevis. It describes the cell as a plasma membrane oscillator with influx of extracellular Ca2+ via voltage-gated Ca2+ channels in the plasma membrane. The Ca2+ oscillations in the Xenopus melanotrope show specific features that cannot be explained by previous models for electrically bursting cells using one set of parameters. The model assumes a KCa-channel with slow Ca2+ -dependent gating kinetics that initiates and terminates the bursts. The slow kinetics of this channel cause an activation of the KCa-channel with a phase shift relative to the intracellular Ca2+ concentration. The phase shift, together with the presence of a Na+ channel that has a lower threshold than the Ca2+ channel, generate the characteristic features of the Ca2+ oscillations in the Xenopus melanotrope cell.
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29

Hu, Lei, Bina Santoro, Andrea Saponaro, Haiying Liu, Anna Moroni, and Steven Siegelbaum. "Binding of the auxiliary subunit TRIP8b to HCN channels shifts the mode of action of cAMP." Journal of General Physiology 142, no. 6 (2013): 599–612. http://dx.doi.org/10.1085/jgp.201311013.

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Hyperpolarization-activated cyclic nucleotide–regulated cation (HCN) channels generate the hyperpolarization-activated cation current Ih present in many neurons. These channels are directly regulated by the binding of cAMP, which both shifts the voltage dependence of HCN channel opening to more positive potentials and increases maximal Ih at extreme negative voltages where voltage gating is complete. Here we report that the HCN channel brain-specific auxiliary subunit TRIP8b produces opposing actions on these two effects of cAMP. In the first action, TRIP8b inhibits the effect of cAMP to shift voltage gating, decreasing both the sensitivity of the channel to cAMP (K1/2) and the efficacy of cAMP (maximal voltage shift); conversely, cAMP binding inhibits these actions of TRIP8b. These mutually antagonistic actions are well described by a cyclic allosteric mechanism in which TRIP8b binding reduces the affinity of the channel for cAMP, with the affinity of the open state for cAMP being reduced to a greater extent than the cAMP affinity of the closed state. In a second apparently independent action, TRIP8b enhances the action of cAMP to increase maximal Ih. This latter effect cannot be explained by the cyclic allosteric model but results from a previously uncharacterized action of TRIP8b to reduce maximal current through the channel in the absence of cAMP. Because the binding of cAMP also antagonizes this second effect of TRIP8b, application of cAMP produces a larger increase in maximal Ih in the presence of TRIP8b than in its absence. These findings may provide a mechanistic explanation for the wide variability in the effects of modulatory transmitters on the voltage gating and maximal amplitude of Ih reported for different neurons in the brain.
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30

Lundbæk, Jens A., Pia Birn, Anker J. Hansen, et al. "Regulation of Sodium Channel Function by Bilayer Elasticity." Journal of General Physiology 123, no. 5 (2004): 599–621. http://dx.doi.org/10.1085/jgp.200308996.

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Membrane proteins are regulated by the lipid bilayer composition. Specific lipid–protein interactions rarely are involved, which suggests that the regulation is due to changes in some general bilayer property (or properties). The hydrophobic coupling between a membrane-spanning protein and the surrounding bilayer means that protein conformational changes may be associated with a reversible, local bilayer deformation. Lipid bilayers are elastic bodies, and the energetic cost of the bilayer deformation contributes to the total energetic cost of the protein conformational change. The energetics and kinetics of the protein conformational changes therefore will be regulated by the bilayer elasticity, which is determined by the lipid composition. This hydrophobic coupling mechanism has been studied extensively in gramicidin channels, where the channel–bilayer hydrophobic interactions link a “conformational” change (the monomer↔dimer transition) to an elastic bilayer deformation. Gramicidin channels thus are regulated by the lipid bilayer elastic properties (thickness, monolayer equilibrium curvature, and compression and bending moduli). To investigate whether this hydrophobic coupling mechanism could be a general mechanism regulating membrane protein function, we examined whether voltage-dependent skeletal-muscle sodium channels, expressed in HEK293 cells, are regulated by bilayer elasticity, as monitored using gramicidin A (gA) channels. Nonphysiological amphiphiles (β-octyl-glucoside, Genapol X-100, Triton X-100, and reduced Triton X-100) that make lipid bilayers less “stiff”, as measured using gA channels, shift the voltage dependence of sodium channel inactivation toward more hyperpolarized potentials. At low amphiphile concentration, the magnitude of the shift is linearly correlated to the change in gA channel lifetime. Cholesterol-depletion, which also reduces bilayer stiffness, causes a similar shift in sodium channel inactivation. These results provide strong support for the notion that bilayer–protein hydrophobic coupling allows the bilayer elastic properties to regulate membrane protein function.
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31

Wang, Jixin, Joseph J. Salata, and Paul B. Bennett. "Saxitoxin Is a Gating Modifier of hERG K+ Channels." Journal of General Physiology 121, no. 6 (2003): 583–98. http://dx.doi.org/10.1085/jgp.200308812.

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Potassium (K+) channels mediate numerous electrical events in excitable cells, including cellular membrane potential repolarization. The hERG K+ channel plays an important role in myocardial repolarization, and inhibition of these K+ channels is associated with long QT syndromes that can cause fatal cardiac arrhythmias. In this study, we identify saxitoxin (STX) as a hERG channel modifier and investigate the mechanism using heterologous expression of the recombinant channel in HEK293 cells. In the presence of STX, channels opened slower during strong depolarizations, and they closed much faster upon repolarization, suggesting that toxin-bound channels can still open but are modified, and that STX does not simply block the ion conduction pore. STX decreased hERG K+ currents by stabilizing closed channel states visualized as shifts in the voltage dependence of channel opening to more depolarized membrane potentials. The concentration dependence for steady-state modification as well as the kinetics of onset and recovery indicate that multiple STX molecules bind to the channel. Rapid application of STX revealed an apparent “agonist-like” effect in which K+ currents were transiently increased. The mechanism of this effect was found to be an effect on the channel voltage-inactivation relationship. Because the kinetics of inactivation are rapid relative to activation for this channel, the increase in K+ current appeared quickly and could be subverted by a decrease in K+ currents due to the shift in the voltage-activation relationship at some membrane potentials. The results are consistent with a simple model in which STX binds to the hERG K+ channel at multiple sites and alters the energetics of channel gating by shifting both the voltage-inactivation and voltage-activation processes. The results suggest a novel extracellular mechanism for pharmacological manipulation of this channel through allosteric coupling to channel gating.
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32

Lee, Ming-Jen, Pi-Chen Lin, Ming-Hong Lin, Hsin-Ying Clair Chiou, Kai Wang, and Chiung-Wei Huang. "Kinetic Alterations in Resurgent Sodium Currents of Mutant Nav1.4 Channel in Two Patients Affected by Paramyotonia Congenita." Biology 11, no. 4 (2022): 613. http://dx.doi.org/10.3390/biology11040613.

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Paramyotonia congenita (PMC) is a rare skeletal muscle disorder characterized by muscle stiffness upon repetitive exercise and cold exposure. PMC was reported to be caused by dominant mutations in the SCN4A gene encoding the α subunit of the Nav1.4 channel. Recently, we identified two missense mutations of the SCN4A gene, p.V781I and p.A1737T, in two PMC families. To evaluate the changes in electrophysiological properties caused by the mutations, both mutant and wild-type (WT) SCN4A genes were expressed in CHO-K1 and HEK-293T cells. Then, whole-cell patch-clamp recording was employed to study the altered gating of mutant channels. The activation curve of transient current showed a hyperpolarizing shift in both mutant Nav1.4 channels as compared to the WT channel, whereas there was a depolarizing shift in the fast inactivation curve. These changes confer to an increase in window current in the mutant channels. Further investigations demonstrated that the mutated channel proteins generate significantly larger resurgent currents as compared to the WT channel and take longer to attain the peak of resurgent current than the WT channel. In conclusion, the current study demonstrates that p.V781I and p.A1737T mutations in the Nav1.4 channel increase both the sustained and the resurgent Na+ current, leading to membrane hyperexcitability with a lower firing threshold, which may influence the clinical phenotype.
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33

Savalli, Nicoletta, Andrei Kondratiev, Sarah Buxton de Quintana, Ligia Toro та Riccardo Olcese. "Modes of Operation of the BKCa Channel β2 Subunit". Journal of General Physiology 130, № 1 (2007): 117–31. http://dx.doi.org/10.1085/jgp.200709803.

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The β2 subunit of the large conductance Ca2+- and voltage-activated K+ channel (BKCa) modulates a number of channel functions, such as the apparent Ca2+/voltage sensitivity, pharmacological and kinetic properties of the channel. In addition, the N terminus of the β2 subunit acts as an inactivating particle that produces a relatively fast inactivation of the ionic conductance. Applying voltage clamp fluorometry to fluorescently labeled human BKCa channels (hSlo), we have investigated the mechanisms of operation of the β2 subunit. We found that the leftward shift on the voltage axis of channel activation curves (G(V)) produced by coexpression with β2 subunits is associated with a shift in the same direction of the fluorescence vs. voltage curves (F(V)), which are reporting the voltage dependence of the main voltage-sensing region of hSlo (S4-transmembrane domain). In addition, we investigated the inactivating mechanism of the β2 subunits by comparing its properties with the ones of the typical N-type inactivation process of Shaker channel. While fluorescence recordings from the inactivated Shaker channels revealed the immobilization of the S4 segments in the active conformation, we did not observe a similar feature in BKCa channels coexpressed with the β2 subunit. The experimental observations are consistent with the view that the β2 subunit of BKCa channels facilitates channel activation by changing the voltage sensor equilibrium and that the β2-induced inactivation process does not follow a typical N-type mechanism.
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34

Gómez-Déniz, E., L. Gómez, and H. W. Gómez. "The Slashed-Rayleigh Fading Channel Distribution." Mathematical Problems in Engineering 2019 (February 11, 2019): 1–14. http://dx.doi.org/10.1155/2019/2719849.

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We propose an alternative distribution for modelling fading-shadowing wireless channels. This distribution presents certain advantages over the Rayleigh-lognormal distribution and the K distribution and has proved useful in the setting described. We obtain closed-form expressions for the average channel capacity and for the average bit error rate of differential phase-shift keying and of minimum shift keying when the new distribution is used. This distribution can be obtained exactly as the sum of mutual independent Gaussian stochastic processes, because it must represent the simulation of the fading channel; that is, it simulates the signal envelope. Finally, we describe practical applications of this distribution, comparing it with the Rayleigh-lognormal and K distributions.
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35

Matteson, D. R., and R. P. Swenson. "External monovalent cations that impede the closing of K channels." Journal of General Physiology 87, no. 5 (1986): 795–816. http://dx.doi.org/10.1085/jgp.87.5.795.

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We have examined the effects of a variety of monovalent cations on K channel gating in squid giant axons. The addition of the permeant cations K, Rb, or Cs to the external medium decreases the channel closing rate and causes a negative shift of the conductance-voltage relationship. Both of these effects are larger in Rb than in K. The opening kinetics of the K channel are, on the other hand, unaffected by these monovalent cations. Other permeant species, like NH4 and Tl, slightly increase the closing rate, whereas the relatively impermeant cations Na, Li, and Tris have little or no effect on K channel gating. The permeant cations have different effects on the reversal potential and the shape of the instantaneous current-voltage relationship. These effects give information about entry and binding of the cations in K channels. Rb, for example, enters the pore readily (large shift of the reversal potential), but binds tightly to the channel interior, inhibiting current flow. We find a correlation between the occupancy of the channel by a monovalent cation and the closing rate, and conclude that the presence of a monovalent cation in the pore inhibits channel closing, and thereby causes a leftward shift in the activation-voltage curve. In causing these effects, the cations appear to bind near the inner surface of the membrane.
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36

Chen, Jinhao, Zixin Chen, and Jianlin Pan. "Cross-subject EEG Emotion Classification on Datasets with Limited Channels." Theoretical and Natural Science 109, no. 1 (2025): 150–56. https://doi.org/10.54254/2753-8818/2025.gl24062.

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To solve the challenge of achieving strong and accurate EEG datasets, while solving the domain shift problem, this research focused on integrating the Few-Label Adversarial Domain Adaptation (FLADA) method with attention mechanism to see if the addition of the attention mechanism improves the performance over FLADA alone on EEG datasets with a small number of channels (specifically, 14 channels). We first apply the FLADA method to the research by solving the "domain shift" problem. Next, we added channel-wise-attention in an attempt to improve the algorithm. However, we found that the addition of channel-wise-attention failed to improve accuracy over the FLADA method alone, and in some cases made it even worse.
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37

Wells, Mathew, and Remo Cossu. "The possible role of Coriolis forces in structuring large-scale sinuous patterns of submarine channel–levee systems." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 371, no. 2004 (2013): 20120366. http://dx.doi.org/10.1098/rsta.2012.0366.

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Submarine channel–levee systems are among the largest sedimentary structures on the ocean floor. These channels have a sinuous pattern and are the main conduits for turbidity currents to transport sediment to the deep ocean. Recent observations have shown that their sinuosity decreases strongly with latitude, with high-latitude channels being much straighter than similar channels near the Equator. One possible explanation is that Coriolis forces laterally deflect turbidity currents so that at high Northern latitudes both the density interface and the downstream velocity maximum are deflected to the right-hand side of the channel (looking downstream). The shift in the velocity field can change the locations of erosion and deposition and introduce an asymmetry between left- and right-turning bends. The importance of Coriolis forces is defined by two Rossby numbers, Ro W = U / Wf and Ro R = U / Rf , where U is the mean downstream velocity, W is the width of the channel, R is the radius of curvature and f is the Coriolis parameter. In a bending channel, the density interface is flat when Ro R ∼−1, and Coriolis forces start to shift the velocity maximum when | Ro W |<5. We review recent experimental and field observations and describe how Coriolis forces could lead to straighter channels at high latitudes.
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38

Cao, Xinran, and Lijun Xu. "Joint channel and Doppler shift estimation for underwater acoustic single carrier system." Journal of the Acoustical Society of America 154, no. 4_supplement (2023): A212. http://dx.doi.org/10.1121/10.0023314.

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Underwater acoustic channel is a time-varying, strong multipath channel. Due to the low velocity of sound (about 1500 m/s), Doppler shift, occurred by the relative motion between transmitter and receiver, restricts the performance of communication. In order to transmit data in underwater acoustic single carrier communication system with strong stability and high reliability, especially in high mobility scenarios, a joint channel and Doppler shift estimation method is proposed in this paper. We propose a novel data frame structure based on a Gold sequence, so the channel and Doppler shift can be estimated. For different underwater scenarios, we design Gold sequence templates with different Doppler factors. When the Gold sequence from the received data frame is extracted, with good correlation characteristics of the Gold sequence, the maximum correlation value can be calculated, and the Doppler shift corresponding to the maximum is the estimation of Doppler shift. Then Doppler shift will be compensated by resampling the communication data. For channel estimation, the Gold sequence is also used to estimate the time-domain channel impulse response (CIR). Simulation results show that the proposed method can effectively estimate channel and Doppler shift in an environment with multipath and Doppler.
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39

Wang, Yue, Li Liu, Xian-Li Zhou, and Ming-Yu Wu. "Lysosome-Targeted Single Fluorescence Probe for Two-Channel Imaging Intracellular SO2 and Biothiols." Molecules 24, no. 3 (2019): 618. http://dx.doi.org/10.3390/molecules24030618.

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As the members of reactive sulfur species, SO2 and biothiols play a significant role in physiological and pathological processes and directly influence numerous diseases. Furthermore, SO2 and biothiols can provide a reductive environment for lysosomes to carry out their optimal functionality. To this end, the development of single fluorescent probes for imaging SO2 and biothiols from different emission channels is highly desirable for understanding their physiological nature. Here, a lysosome-targeted fluorescent probe (BPO-DNSP) with a dual reaction site for SO2 and biothiols was presented. BPO-DNSP can sensitively and selectively respond to SO2 in the green channel with a large Stokes shift over 105 nm, and to biothiols in the near-infrared emission channel with a large Stokes shift over 109 nm. The emission shift for the two channels was as high as 170 nm. Colocalization experiments verified that BPO-DNSP can selectively enrich lysosomes. Notably, BPO-DNSP can not only be used to image intracellular SO2 and biothiols from two different channels, but also to monitor the conversion of biothiols to SO2 without adding exogenous enzymes in living HeLa cells.
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40

Wang, Zhigang, Zihao Wang, Fusheng Zhu, Zezhou Luo, Fang Li, and Haopeng Liu. "Joint Doppler Shift and Channel Estimation for High-Speed Railway Wireless Communications in Tunnel Scenarios." Wireless Communications and Mobile Computing 2022 (January 31, 2022): 1–6. http://dx.doi.org/10.1155/2022/6804412.

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In this work, we study the problem of Doppler shift and channel estimation for wireless communication systems on high-speed railways (HSRs). We focus on tunnel scenario, one of the classical scenarios of HSRs. We first build up the mathematical system model, design a joint Doppler shift and channel estimator, and compare its performance with the typical Moose algorithm. We show that our estimator outperforms the Moose algorithm in Doppler estimation. Besides, since wireless channels in tunnel scenarios often contain several or multiple taps, we suggest an adaptive frame structure to improve transmission efficiency. Simulations are then provided to corroborate our proposed studies.
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41

Qin, Yongpeng, Tiago M. Alves, José Antonio Constantine, Davide Gamboa, and Shiguo Wu. "Effect of channel tributaries on the evolution of submarine channel confluences (Espírito Santo Basin, SE Brazil)." GSA Bulletin 132, no. 1-2 (2019): 263–72. http://dx.doi.org/10.1130/b35082.1.

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AbstractConfluences are geomorphologic features fed by distinct channel tributaries that record the contribution of multiple sediment sources. They are key features of both fluvial and submarine channels in geomorphologic and sedimentologic terms. Here, we use high-quality three-dimensional seismic data from SE Brazil to document the response of a submarine channel confluence to turbidity currents originating from a tributary. The studied channel system consists of a west tributary, an east tributary, and a postconfluence channel, with the last two comprising the main channel at present. Downstream from the confluence, changes in planform morphology and architecture were found due to the effect of turbidity currents sourced from the west tributary channel. A channel bend in the main channel curved toward the west when it was first formed but later curved toward the east, and so remains until the present day. This process led to the migration of the confluence point ∼500 m to the east, and changed the bed morphology from discordant (where the beds of tributaries and main channels meet at an unequal depth) to concordant (where the beds of tributaries and main channels meet at approximately the same depth). In addition to the channel bend near the confluence, two other bends further downstream recorded significant changes with time, increasing channel sinuosity from 1.11 to 1.72. These three channel bends near the confluence accumulated a large volume of sediment at their inner banks, generating depositional bars. Multiple channel forms within the depositional bars indicate the occurrence of large-scale lateral migration near the confluence. Hence, turbidity currents from the west tributary are shown to influence the submarine channel by promoting lateral channel migration, confluence migration, increases in channel sinuosity, and the formation of large depositional bars. These variations near the confluence reveal a change in tributary activity and a shift in sediment sources from east to west on the continental shelf. Such a shift suggests variations in sedimentary processes on the continental shelf probably due to avulsions on Doce River Delta.
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Eid, Mahmoud M. A., Ashraf S. Seliem, Ahmed Nabih Zaki Rashed, Abd El-Naser A. Mohammed, Mohamed Yassin Ali, and Shaimaa S. Abaza. "High modulated soliton power propagation interaction with optical fiber and optical wireless communication channels." Indonesian Journal of Electrical Engineering and Computer Science 21, no. 3 (2021): 1575–83. https://doi.org/10.11591/ijeecs.v21.i3.pp1575-1583.

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This paper has presented high modulated soliton power transmission interaction with optical fiber and optical wireless communication channels at flow rate of 40 Gbps and 20 km link range. The proposed modulation schemes are continuous phase frequency shift keying (CPFSK), Quadrature amplitude modulation (QAM), differential phase shift keying (DPSK), frequency shift keying (FSK), pulse amplitude modulation (PAM), minimum shift keying (MSK), and optical quadrature phase shift keying (OQPSK). CPFSK has presented better performance than other proposed modulation schemes for both optical fiber and optical wireless communication channels. The enhancement of optical signal/noise ratio at fiber/wireless channel, received electrical power and signal/noise ratio at optical receiver with increase of bits per symbol for different proposed modulation schemes except for CPFSK scheme. Therefore it is evident that CPFSK modulation scheme is more efficient and better performance than other modulation schemes for different communication channels. The obtained results are simulated with optisystem program version 13.
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43

Park, Taeho, Kyoungah Cho, and Sangsig Kim. "Temperature-Dependent Feedback Operations of Triple-Gate Field-Effect Transistors." Nanomaterials 14, no. 6 (2024): 493. http://dx.doi.org/10.3390/nano14060493.

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In this study, we examine the electrical characteristics of triple-gate feedback field-effect transistors (TG FBFETs) over a temperature range of −200 °C to 280 °C. With increasing temperature from 25 °C to 280 °C, the thermally generated charge carriers increase in the channel regions such that a positive feedback loop forms rapidly. Thus, the latch-up voltage shifts from −1.01 V (1.34 V) to −11.01 V (10.45 V) in the n-channel (p-channel) mode. In contrast, with decreasing temperature from 25 °C to −200 °C, the thermally generated charge carriers decrease, causing a shift in the latch-up voltage in the opposite direction to that of the increasing temperature case. Despite the shift in the latch-up voltage, the TG FBFETs exhibit ideal switching characteristics, with subthreshold swings of 6.6 mV/dec and 7.2 mV/dec for the n-channel and p-channel modes, respectively. Moreover, the memory window widens with increasing temperature. Specifically, at temperatures above 85 °C, the memory windows are wider than 3.05 V and 1.42 V for the n-channel and p-channel modes, respectively.
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44

Reeve, Helen L., E. Kenneth Weir, Stephen L. Archer, and David N. Cornfield. "A maturational shift in pulmonary K+ channels, from Ca2+ sensitive to voltage dependent." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 6 (1998): L1019—L1025. http://dx.doi.org/10.1152/ajplung.1998.275.6.l1019.

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The mechanism responsible for the abrupt decrease in resistance of the pulmonary circulation at birth may include changes in the activity of O2-sensitive K+ channels. We characterized the electrophysiological properties of fetal and adult ovine pulmonary arterial (PA) smooth muscle cells (SMCs) using conventional and amphotericin B-perforated patch-clamp techniques. Whole cell K+ currents of fetal PASMCs in hypoxia were small and characteristic of spontaneously transient outward currents. The average resting membrane potential (RMP) was −36 ± 3 mV and could be depolarized by charybdotoxin (100 nM) or tetraethylammonium chloride (5 mM; both blockers of Ca2+-dependent K+ channels) but not by 4-aminopyridine (4-AP; 1 mM; blocker of voltage-gated K+ channels) or glibenclamide (10 μM; blocker of ATP-dependent K+channels). In hypoxia, chelation of intracellular Ca2+ by 5 mM 1,2-bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid further reduced the amplitude of the whole cell K+ current and prevented spontaneously transient outward current activity. Under these conditions, the remaining current was partially inhibited by 1 mM 4-AP. K+ currents of fetal PASMCs maintained in normoxia were not significantly reduced by acute hypoxia. In normoxic adult PASMCs, whole cell K+ currents were large and RMP was −49 ± 3 mV. These 4-AP-sensitive K+ currents were partially inhibited by exposure to acute hypoxia. We conclude that the K+ channel regulating RMP in the ovine pulmonary circulation changes after birth from a Ca2+-dependent K+ channel to a voltage-dependent K+ channel. The maturational-dependent differences in the mechanism of the response to acute hypoxia may be due to this difference in K+ channels.
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45

Tan, Peter S., Matthew D. Perry, Chai Ann Ng, Jamie I. Vandenberg, and Adam P. Hill. "Voltage-sensing domain mode shift is coupled to the activation gate by the N-terminal tail of hERG channels." Journal of General Physiology 140, no. 3 (2012): 293–306. http://dx.doi.org/10.1085/jgp.201110761.

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Human ether-a-go-go–related gene (hERG) potassium channels exhibit unique gating kinetics characterized by unusually slow activation and deactivation. The N terminus of the channel, which contains an amphipathic helix and an unstructured tail, has been shown to be involved in regulation of this slow deactivation. However, the mechanism of how this occurs and the connection between voltage-sensing domain (VSD) return and closing of the gate are unclear. To examine this relationship, we have used voltage-clamp fluorometry to simultaneously measure VSD motion and gate closure in N-terminally truncated constructs. We report that mode shifting of the hERG VSD results in a corresponding shift in the voltage-dependent equilibrium of channel closing and that at negative potentials, coupling of the mode-shifted VSD to the gate defines the rate of channel closure. Deletion of the first 25 aa from the N terminus of hERG does not alter mode shifting of the VSD but uncouples the shift from closure of the cytoplasmic gate. Based on these observations, we propose the N-terminal tail as an adaptor that couples voltage sensor return to gate closure to define slow deactivation gating in hERG channels. Furthermore, because the mode shift occurs on a time scale relevant to the cardiac action potential, we suggest a physiological role for this phenomenon in maximizing current flow through hERG channels during repolarization.
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46

Armstrong, C. M., and G. Cota. "Modification of sodium channel gating by lanthanum. Some effects that cannot be explained by surface charge theory." Journal of General Physiology 96, no. 6 (1990): 1129–40. http://dx.doi.org/10.1085/jgp.96.6.1129.

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In clonal pituitary (GH3) cells we studied the changes in sodium channel gating caused by substitution of La3+ for Ca2+ ion. Gating of sodium channels was simplified by using intracellular papain to remove inactivation. To quantify La effects, we empirically fitted closing and the late phase of opening of the channels with single exponentials, determined the opening (a) and closing (b) rate, and plotted these rates as a function of Vm (membrane voltage). The midpoint of the fraction open-Vm curve was also determined. Changing from Ca to La shifted the curves for these three measures of Na channel gating along the voltage axis and changed their shape somewhat. Surface charge theory, in the form usually presented, predicts equal shifts of all three curves, with no change in shape. We found, however, that the shift for each of the measurements was different. 2 mM La, for example, shifted opening kinetics by +52 mV (i.e., 52 mV must be added to the depolarization to make activation in 2 mM La as fast as in 2 mM Ca), the fraction open voltage curve by +42.5 mV, and the closing rate curve by +28 mV. The shift was an almost linear function of log [La] for each of the measures. The main finding is that changing from 2 mM Ca to 10 microM La causes a positive shift of the opening rate and fraction open curves, but a negative shift of the closing rate curve. The opposite signs of the two effects cannot be explained in terms of surface charge theory. We briefly discuss some alternatives to this theory.
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47

Lu, Qing, and Peter A. Johnson. "Characterizing New Channels of Communication: A Case Study of Municipal 311 Requests in Edmonton, Canada." Urban Planning 1, no. 2 (2016): 18–31. http://dx.doi.org/10.17645/up.v1i2.621.

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City governments around the world are developing and expanding how they connect to citizens. Technologies play an important role in making this connection, and one frequent way that cities connect with citizens is through 311-style request systems. 311 is a non-emergency municipal notification system that uses telephone, email, web forms, and increasingly, mobile applications to allow citizens to notify government of infrastructure issues and make requests for municipal services. In many ways, this process of citizen contribution mirrors the provision of volunteered geographic information, that is spatially-referenced user generated content. This research presents a case study of the city of Edmonton, Canada, an early adopter of multi-channel 311 service request systems, including telephone, email, web form, and mobile app 311 request channels. Three methods of analysis are used to characterize and compare these different channels over three years of request data; a comparison of relative request share for each channel, a spatial hot spot analysis, and regression models to compare channel usage with sociodemographic variables. The results of this study indicate a shift in channel usage from traditional to Internet-enabled, that this shift is mirrored in the hotspots of request activity, and that specific digital inequalities exist that reinforce this distinction between traditional and Internet-enabled reporting channels.
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48

Seo, Jong-Hyeon, Ichiro Tsuda, Young Ju Lee, et al. "Pattern Recognition in Epileptic EEG Signals via Dynamic Mode Decomposition." Mathematics 8, no. 4 (2020): 481. http://dx.doi.org/10.3390/math8040481.

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In this paper, we propose a new method based on the dynamic mode decomposition (DMD) to find a distinctive contrast between the ictal and interictal patterns in epileptic electroencephalography (EEG) data. The features extracted from the method of DMD clearly capture the phase transition of a specific frequency among the channels corresponding to the ictal state and the channel corresponding to the interictal state, such as direct current shift (DC-shift or ictal slow shifts) and high-frequency oscillation (HFO). By performing classification tests with Electrocorticography (ECoG) recordings of one patient measured at different timings, it is shown that the captured phenomenon is the unique pattern that occurs in the ictal onset zone of the patient. We eventually explain how advantageously the DMD captures some specific characteristics to distinguish the ictal state and the interictal state. The method presented in this study allows simultaneous interpretation of changes in the channel correlation and particular information for activity related to an epileptic seizure so that it can be applied to identification and prediction of the ictal state and analysis of the mechanism on its dynamics.
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49

Zeng, Haoyu, Thomas M. Weiger, Hong Fei, and Irwin B. Levitan. "Mechanisms of Two Modulatory Actions of the Channel-binding Protein Slob on the Drosophila Slowpoke Calcium-dependent Potassium Channel." Journal of General Physiology 128, no. 5 (2006): 583–91. http://dx.doi.org/10.1085/jgp.200609653.

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Slob57 is an ion channel auxiliary protein that binds to and modulates the Drosophila Slowpoke calcium-dependent potassium channel (dSlo). We reported recently that residues 1–39 of Slob57 comprise the key domain that both causes dSlo inactivation and shifts its voltage dependence of activation to more depolarized voltages. In the present study we show that removal of residues 2–6 from Slob57 abolishes the inactivation, but the ability of Slob57 to rightward shift the voltage dependence of activation of dSlo remains. A synthetic peptide corresponding in sequence to residues 1–6 of Slob57 blocks dSlo in a voltage- and dose-dependent manner. Two Phe residues and at least one Lys residue in this peptide are required for the blocking action. These data indicate that the amino terminus of Slob57 directly blocks dSlo, thereby leading to channel inactivation. Further truncation to residue Arg16 eliminates the modulation of voltage dependence of activation. Thus these two modulatory actions of Slob57 are independent. Mutation within the calcium bowl of dSlo greatly reduces its calcium sensitivity (Bian, S., I. Favre, and E. Moczydlowski. 2001. Proc. Natl. Acad. Sci. USA. 98:4776–4781). We found that Slob57 still causes inactivation of this mutant channel, but does not shift its voltage dependence of activation. This result confirms further the independence of the inactivation and the voltage shift produced by Slob57. It also suggests that the voltage shift requires high affinity Ca2+ binding to an intact calcium bowl. Furthermore, Slob57 inhibits the shift in the voltage dependence of activation of dSlo evoked by Ca2+, and this inhibition by Slob57 is greater at higher free Ca2+ concentrations. These results implicate distinct calcium-dependent and -independent mechanisms in the modulation of dSlo by Slob.
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50

Tanggara, Andrew, Ranjith Nair, Syed Assad, et al. "Quantum-optimal information encoding using noisy passive linear optics." Quantum 8 (January 4, 2024): 1218. http://dx.doi.org/10.22331/q-2024-01-04-1218.

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The amount of information that a noisy channel can transmit has been one of the primary subjects of interest in information theory. In this work we consider a practically-motivated family of optical quantum channels that can be implemented without an external energy source. We optimize the Holevo information over procedures that encode information in attenuations and phase-shifts applied by these channels on a resource state of finite energy. It is shown that for any given input state and environment temperature, the maximum Holevo information can be achieved by an encoding procedure that uniformly distributes the channel's phase-shift parameter. Moreover for large families of input states, any maximizing encoding scheme has a finite number of channel attenuation values, simplifying the codewords to a finite number of rings around the origin in the output phase space. The above results and numerical evidence suggests that this property holds for all resource states. Our results are directly applicable to the quantum reading of an optical memory in the presence of environmental thermal noise.
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