Relevant bibliographies by topics / Voltage-clamp technique (Electrophysiology)

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Academic literature on the topic 'Voltage-clamp technique (Electrophysiology)'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 February 2022

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Journal articles on the topic "Voltage-clamp technique (Electrophysiology)"

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Annecchino, Luca A., and Simon R. Schultz. "Progress in automating patch clamp cellular physiology." Brain and Neuroscience Advances 2 (January 1, 2018): 239821281877656. http://dx.doi.org/10.1177/2398212818776561.

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Patch clamp electrophysiology has transformed research in the life sciences over the last few decades. Since their inception, automatic patch clamp platforms have evolved considerably, demonstrating the capability to address both voltage- and ligand-gated channels, and showing the potential to play a pivotal role in drug discovery and biomedical research. Unfortunately, the cell suspension assays to which early systems were limited cannot recreate biologically relevant cellular environments, or capture higher order aspects of synaptic physiology and network dynamics. In vivo patch clamp electrophysiology has the potential to yield more biologically complex information and be especially useful in reverse engineering the molecular and cellular mechanisms of single-cell and network neuronal computation, while capturing important aspects of human disease mechanisms and possible therapeutic strategies. Unfortunately, it is a difficult procedure with a steep learning curve, which has restricted dissemination of the technique. Luckily, in vivo patch clamp electrophysiology seems particularly amenable to robotic automation. In this review, we document the development of automated patch clamp technology, from early systems based on multi-well plates through to automated planar-array platforms, and modern robotic platforms capable of performing two-photon targeted whole-cell electrophysiological recordings in vivo.
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Harrison, Reid R., Ilya Kolb, Suhasa B. Kodandaramaiah, Alexander A. Chubykin, Aimei Yang, Mark F. Bear, Edward S. Boyden, and Craig R. Forest. "Microchip amplifier for in vitro, in vivo, and automated whole cell patch-clamp recording." Journal of Neurophysiology 113, no. 4 (February 15, 2015): 1275–82. http://dx.doi.org/10.1152/jn.00629.2014.

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Patch clamping is a gold-standard electrophysiology technique that has the temporal resolution and signal-to-noise ratio capable of reporting single ion channel currents, as well as electrical activity of excitable single cells. Despite its usefulness and decades of development, the amplifiers required for patch clamping are expensive and bulky. This has limited the scalability and throughput of patch clamping for single-ion channel and single-cell analyses. In this work, we have developed a custom patch-clamp amplifier microchip that can be fabricated using standard commercial silicon processes capable of performing both voltage- and current-clamp measurements. A key innovation is the use of nonlinear feedback elements in the voltage-clamp amplifier circuit to convert measured currents into logarithmically encoded voltages, thereby eliminating the need for large high-valued resistors, a factor that has limited previous attempts at integration. Benchtop characterization of the chip shows low levels of current noise [1.1 pA root mean square (rms) over 5 kHz] during voltage-clamp measurements and low levels of voltage noise (8.2 μV rms over 10 kHz) during current-clamp measurements. We demonstrate the ability of the chip to perform both current- and voltage-clamp measurement in vitro in HEK293FT cells and cultured neurons. We also demonstrate its ability to perform in vivo recordings as part of a robotic patch-clamping system. The performance of the patch-clamp amplifier microchip compares favorably with much larger commercial instrumentation, enabling benchtop commoditization, miniaturization, and scalable patch-clamp instrumentation.
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Ruknudin, A., M. J. Song, A. Auerbach, and F. Sachs. "The structure of patch-clamped membranes in high voltage Electron Microscopy." Proceedings, annual meeting, Electron Microscopy Society of America 47 (August 6, 1989): 936–37. http://dx.doi.org/10.1017/s0424820100156663.

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The study of single ion channel kinetics in cell electrophysiology has been made possible by the introduction of patch-clamp techniques. Recordings can be made from a patch of membrane either attached to the cell or excised into controlled solutions. Though this technique has been widely used for more than a decade, the structure of the membrane patch and its associated cytoplasmic elements are not known except for recent work done in this laboratory . We have improved this technique to visualize membrane patches using high voltage electron microscope and also identified one class of channels in the patch by immunocytochemistry.The procedure for preserving biological structure in a glass patch pipette is basically same as described earlier as “dry mounting technique” . Briefly, after making a patch, the pipette is removed from the bath and the tip is freeze-fixed in liquid propane. A slight negative pressure is applied to the pipette while freeze-fixing in order to stretch the shape of the patch. Once fixed, the tip is not exposed to temperatures higher than-126° C. A 0.5 cm bit of the pipette tip is broken off, stored in IN2, and then freeze dried between -126° to -80° C under high vaccum (10-6 Torr).
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Rubi, Lena, Vaibhavkumar S. Gawali, Helmut Kubista, Hannes Todt, Karlheinz Hilber, and Xaver Koenig. "Proper Voltage-Dependent Ion Channel Function in Dysferlin-Deficient Cardiomyocytes." Cellular Physiology and Biochemistry 36, no. 3 (2015): 1049–58. http://dx.doi.org/10.1159/000430278.

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Background/Aims: Dysferlin plays a decisive role in calcium-dependent membrane repair in myocytes. Mutations in the encoding DYSF gene cause a number of myopathies, e.g. limb-girdle muscular dystrophy type 2B (LGMD2B). Besides skeletal muscle degenerative processes, dysferlin deficiency is also associated with cardiac complications. Thus, both LGMD2B patients and dysferlin-deficient mice develop a dilated cardiomyopathy. We and others have recently reported that dystrophin-deficient ventricular cardiomyocytes from mouse models of Duchenne muscular dystrophy show significant abnormalities in voltage-dependent ion channels, which may contribute to the pathophysiology in dystrophic cardiomyopathy. The aim of the present study was to investigate if dysferlin, like dystrophin, is a regulator of cardiac ion channels. Methods and Results: By using the whole cell patch-clamp technique, we compared the properties of voltage-dependent calcium and sodium channels, as well as action potentials in ventricular cardiomyocytes isolated from the hearts of normal and dysferlin-deficient (dysf) mice. In contrast to dystrophin deficiency, the lack of dysferlin did not impair the ion channel properties and left action potential parameters unaltered. In connection with normal ECGs in dysf mice these results suggest that dysferlin deficiency does not perturb cardiac electrophysiology. Conclusion: Our study demonstrates that dysferlin does not regulate cardiac voltage-dependent ion channels, and implies that abnormalities in cardiac ion channels are not a universal characteristic of all muscular dystrophy types.
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Sun, Qiang, Wei-Jin Zang, and Chen Chen. "Growth Hormone Secretagogues Reduce Transient Outward K+ Current via Phospholipase C/Protein Kinase C Signaling Pathway in Rat Ventricular Myocytes." Endocrinology 151, no. 3 (January 7, 2010): 1228–35. http://dx.doi.org/10.1210/en.2009-0877.

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Endogenous ghrelin and its synthetic counterpart hexarelin are peptide GH secretagogues (GHS) that exert a positive ionotropic effect in the cardiovascular system. The mechanism by which GHS modulate cardiac electrophysiology properties to alter myocyte contraction is poorly understood. In the present study, we examined whether GHS regulates the transient outward potassium current (Ito) as well as the putative intracellular signaling cascade responsible for such regulation. GHS and experimental agents were applied locally onto freshly isolated adult Sprague-Dawley rat ventricular myocytes and action potential morphology and Ito was recorded using nystatin-perforated whole-cell patch-clamp recording technique. Under current clamp, ghrelin and hexarelin (10 nm) significantly prolonged action potential duration. Under voltage clamp, hexarelin and ghrelin inhibited Ito in a concentration-dependent manner. This inhibition was abolished in the presence of the GHS receptor (GHS-R) antagonist [d-Lys3]GH-releasing peptide-6 (10 μm) and GHS-R1a-specific antagonist BIM28163 (1 μm). GHS-induced Ito inhibition was totally reversed by the phospholipase C inhibitor U73122 (5 μm) and protein kinase C inhibitors GÖ6983 (1 μm) and calphostin C (0.1 μm) but not by the cAMP antagonist Rp-cAMP (100 μm) or the PKA inhibitor H89 (1 μm). We conclude that hexarelin and ghrelin activate phospholipase C and protein kinase C signaling cascade through the stimulation of the GHS-R, resulting in a decrease in the Ito current and subsequent prolongation of action potential duration.
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Cinquetti, Raffaella, Francesca Guia Imperiali, Salvatore Bozzaro, Daniele Zanella, Francesca Vacca, Cristina Roseti, Barbara Peracino, Michela Castagna, and Elena Bossi. "Characterization of Transport Activity of SLC11 Transporters in Xenopus laevis Oocytes by Fluorophore Quenching." SLAS DISCOVERY: Advancing the Science of Drug Discovery 26, no. 6 (April 7, 2021): 798–810. http://dx.doi.org/10.1177/24725552211004123.

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Membrane proteins are involved in different physiological functions and are the target of pharmaceutical and abuse drugs. Xenopus laevis oocytes provide a powerful heterologous expression system for functional studies of these proteins. Typical experiments investigate transport using electrophysiology and radiolabeled uptake. A two-electrode voltage clamp is suitable only for electrogenic proteins, and uptake measurements require the existence of radiolabeled substrates and adequate laboratory facilities. Recently, Dictyostelium discoideum Nramp1 and NrampB were characterized using multidisciplinary approaches. NrampB showed no measurable electrogenic activity, and it was investigated in Xenopus oocytes by acquiring confocal images of the quenching of injected fluorophore calcein. This method is adequate to measure the variation in emitted fluorescence, and thus transporter activity indirectly, but requires long experimental procedures to collect statistically consistent data. Considering that optimal expression of heterologous proteins lasts for 48–72 h, a slow acquiring process requires the use of more than one batch of oocytes to complete the experiments. Here, a novel approach to measure substrate uptake is reported. Upon injection of a fluorophore, oocytes were incubated with the substrate and the transport activity measured, evaluating fluorescence quenching in a microplate reader. The technique permits the testing of tens of oocytes in different experimental conditions simultaneously, and thus the collection of significant statistical data for each batch, saving time and animals. The method was tested with different metal transporters (SLC11), DMT1, DdNramp1, and DdNrampB, and verified with the peptide transporter PepT1 (SLC15). Comparison with traditional methods (uptake, two-electrode voltage clamp) and with quenching images acquired by fluorescence microscopy confirmed its efficacy.
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Suzuki, Akihiro, Kei Aizawa, Susanne Gassmayr, Zeljko J. Bosnjak, and Wai-Meng Kwok. "Biphasic Effects of Isoflurane on the Cardiac Action Potential." Anesthesiology 97, no. 5 (November 1, 2002): 1209–17. http://dx.doi.org/10.1097/00000542-200211000-00026.

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Background The mechanism underlying isoflurane modulation of cardiac electrophysiology is not well understood. In the present study, the authors investigated the effects of isoflurane on the cardiac action potential (AP) characteristics. The results were correlated to modulation of the L-type calcium (I(Ca,L)), the delayed-rectifier potassium (I(Kdr)), and the inward-rectifier potassium (I(Kir)) currents. Methods Single ventricular myocytes were enzymatically isolated from guinea pig hearts. The current clamp and whole cell voltage clamp configurations of the patch clamp technique were used to monitor the cardiac AP and ionic currents, respectively. A dynamic AP voltage protocol that mimicked changes in membrane potential during an AP was used to monitor the I(Ca,L), I(Kdr) and I(Kir). Results Isoflurane produced a concentration-dependent, biphasic effect on the AP duration (APD). At 0.6 mm (1.26 vol%), isoflurane significantly increased APD50 and APD90 by 50.0 +/- 7.6% and 48.9 +/- 7.2%, respectively (P < 0.05; n = 6). At 1.0 mm (2.09 vol%), isoflurane had no significant effect on APD (n = 6). In contrast, at 1.8 mm (3.77 vol%), isoflurane decreased APD50 and APD90 by 38.3 +/- 5.4% and 32.2 +/- 5.5%, respectively (P < 0.05; n = 7). The inhibitory effects of isoflurane on I(Kdr) chord conductance were greater than those on I(Ca,L) (P < 0.05; n = 6/group). Both I(Ca,L) inactivation and I(Kdr) activation kinetics were accelerated by isoflurane. Isoflurane had no significant effects on I(Kir) chord conductance (n = 6). Conclusion At the lower anesthetic concentration, the prolongation of the APD may be the result of the dominant inhibitory effects of isoflurane on I(Kdr). At the higher concentration, the shortening of the APD may be caused by the inhibitory effects on I (Ca,L) combined with the isoflurane-induced acceleration of I(Ca,L) inactivation kinetics. Because I(Kdr) is significantly inhibited by isoflurane, I(Kir) appears to be the major repolarizing current, which is minimally affected by isoflurane.
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8

Coulter, D. A., S. Sombati, and R. J. DeLorenzo. "Electrophysiology of glutamate neurotoxicity in vitro: induction of a calcium-dependent extended neuronal depolarization." Journal of Neurophysiology 68, no. 2 (August 1, 1992): 362–73. http://dx.doi.org/10.1152/jn.1992.68.2.362.

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1. Physiological responses of hippocampal pyramidal neurons in primary culture to prolonged glutamate (GLU) exposure (500 microM in all experiments) were studied with the use of patch electrodes and whole-cell current-clamp recording techniques. In some experiments, perforated patch recordings were employed with electrodes containing the pore-forming antibiotic nystatin. 2. After washout of GLU after a 10-min exposure, pyramidal neurons remained depolarized by greater than or equal to 20 mV from rest for the duration of the recording (30 min to less than 4 h). This depolarization was accompanied by a 57.8% increase in membrane conductance and was termed an extended neuronal depolarization (END). The percentage of neurons in which END was induced varied with the duration of GLU exposure, with a 4-, 6-, 8-, 10-, and 20-min GLU exposure eliciting END in 12.5, 41.7, 81.8, 100, and 100% of neurons. END induction appeared to be an all-or-none phenomenon, because END levels did not differ when compared across GLU exposure times. 3. During the END, cells retained both the ability to fire action potentials and the ability to respond to GLU, appeared viable when examined anatomically, and still excluded vital dyes. This supports the conclusion that END is not a nonspecific consequence of cell death. Rather, END is a discrete physiological process triggered by prolonged GLU exposure. The results raise questions concerning the reversibility of END induction, i.e., can neurons be "rescued" once END is induced, or will these cells inevitably go on to die? 4. END induction was dependent on a rise in intracellular free calcium ([Ca]i). END was prevented by strong buffering of [Ca]i or by substitution of external Ba2+ for Ca2+. However, substitution of Mn2+ for Ca2+ still permitted END induction. In cells recorded with the perforated-patch technique, maintaining normal [Ca]i levels, END could be induced, but less readily than under unbuffered [Ca]i conditions. 5. END could not be induced by a 10- to 20-min current-clamp depolarization to 0 mV, nor by 10-min GLU application while the membrane potential was voltage clamped at rest in a solution containing 1 mM Mg2+. In addition, END induction by GLU could be blocked by application of MK-801 (10-30 microM) but not 6-cyano-7-nitroquinoxaline-2,3-dione [CNQX (100-200 microM)]. 6. The dependence of both delayed neuronal cell death and END induction on GLU exposure duration were similar.(ABSTRACT TRUNCATED AT 400 WORDS)
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Galli, Gina L. J., Edwin W. Taylor, and Holly A. Shiels. "Calcium flux in turtle ventricular myocytes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 6 (December 2006): R1781—R1789. http://dx.doi.org/10.1152/ajpregu.00421.2006.

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The relative contribution of the sarcoplasmic reticulum (SR), the L-type Ca2+ channel and the Na+/Ca2+ exchanger (NCX) were assessed in turtle ventricular myocytes using epifluorescent microscopy and electrophysiology. Confocal microscopy images of turtle myocytes revealed spindle-shaped cells, which lacked T-tubules and had a large surface area-to-volume ratio. Myocytes loaded with the fluorescent Ca2+-sensitive dye Fura-2 elicited Ca2+ transients, which were insensitive to ryanodine and thapsigargin, indicating the SR plays a small role in the regulation of contraction and relaxation in the turtle ventricle. Sarcolemmal Ca2+ currents were measured using the perforated-patch voltage-clamp technique. Depolarizing voltage steps to 0 mV elicited an inward current that could be blocked by nifedipine, indicating the presence of Ca2+ currents originating from L-type Ca2+ channels (ICa). The density of ICa was 3.2 ± 0.5 pA/pF, which led to an overall total Ca2+ influx of 64.1 ± 9.3 μM/l. NCX activity was measured as the Ni+-sensitive current at two concentrations of intracellular Na+ (7 and 14 mM). Total Ca2+ influx through the NCX during depolarizing voltage steps to 0 mV was 58.5 ± 7.7 μmol/l and 26.7 ± 3.2 μmol/l at 14 and 7 mM intracellular Na+, respectively. In the absence of the SR and L-type Ca2+ channels, the NCX is able to support myocyte contraction independently. Our results indicate turtle ventricular myocytes are primed for sarcolemmal Ca2+ transport, and most of the Ca2+ used for contraction originates from the L-type Ca2+ channel.
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Pan, Zhenwei, Tomohiko Ai, Po-Cheng Chang, Ying Liu, Jijia Liu, Mitsunori Maruyama, Mohamed Homsi, et al. "Atrial fibrillation and electrophysiology in transgenic mice with cardiac-restricted overexpression of FKBP12." American Journal of Physiology-Heart and Circulatory Physiology 316, no. 2 (February 1, 2019): H371—H379. http://dx.doi.org/10.1152/ajpheart.00486.2018.

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Cardiomyocyte-restricted overexpression of FK506-binding protein 12 transgenic (αMyHC-FKBP12) mice develop spontaneous atrial fibrillation (AF). The aim of the present study is to explore the mechanisms underlying the occurrence of AF in αMyHC-FKBP12 mice. Spontaneous AF was documented by telemetry in vivo and Langendorff-perfused hearts of αMyHC-FKBP12 and littermate control mice in vitro. Atrial conduction velocity was evaluated by optical mapping. The patch-clamp technique was applied to determine the potentially altered electrophysiology in atrial myocytes. Channel protein expression levels were evaluated by Western blot analyses. Spontaneous AF was recorded in four of seven αMyHC-FKBP12 mice but in none of eight nontransgenic (NTG) controls. Atrial conduction velocity was significantly reduced in αMyHC-FKBP12 hearts compared with NTG hearts. Interestingly, the mean action potential duration at 50% but not 90% was significantly prolonged in αMyHC-FKBP12 atrial myocytes compared with their NTG counterparts. Consistent with decreased conduction velocity, average peak Na+ current ( INa) density was dramatically reduced and the INa inactivation curve was shifted by approximately +7 mV in αMyHC-FKBP12 atrial myocytes, whereas the activation and recovery curves were unaltered. The Nav1.5 expression level was significantly reduced in αMyHC-FKBP12 atria. Furthermore, we found increases in atrial Cav1.2 protein levels and peak L-type Ca2+ current density and increased levels of fibrosis in αMyHC-FKBP12 atria. In summary, cardiomyocyte-restricted overexpression of FKBP12 reduces the atrial Nav1.5 expression level and mean peak INa, which is associated with increased peak L-type Ca2+ current and interstitial fibrosis in atria. The combined electrophysiological and structural changes facilitated the development of local conduction block and altered action potential duration and spontaneous AF. NEW & NOTEWORTHY This study addresses a long-standing riddle regarding the role of FK506-binding protein 12 in cardiac physiology. The work provides further evidence that FK506-binding protein 12 is a critical component for regulating voltage-gated sodium current and in so doing has an important role in arrhythmogenic physiology, such as atrial fibrillation.
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Dissertations / Theses on the topic "Voltage-clamp technique (Electrophysiology)"

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Zhou, Yun. "STUDY OF SINGLE CELL SONOPORATION IN REAL TIME USING ELECTROPHYSIOLOGY TECHNIQUES." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1207251863.

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Wu, Jiang. "Instrumentation of the universal clamp and modeling in biochemistry /." View online ; access limited to URI, 2004. http://wwwlib.umi.com.helin.uri.edu/dissertations/dlnow/3160040.

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Steiger, DeAnna Lee Borchardt. "Optimization and use of a voltage clamp assay with insect midgut tissues." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file 0.38 Mb., 53 p, 2006. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:1435810.

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Lin, Kun-Han. "Functional properties and Ca2+-dependent feedback modulation of voltage-gated Ca2+ channels in glutamatergic nerve terminals of the mammalian auditory brainstem." Doctoral thesis, 2011. http://hdl.handle.net/11858/00-1735-0000-0006-AE4C-9.

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Books on the topic "Voltage-clamp technique (Electrophysiology)"

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1931-, Smith T. G., ed. Voltage and patch clamping with microelectrodes. Bethesda, Md: American Physiological Society, 1985.

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Graves, Smith Thomas, ed. Voltage and patch clamping with microelectrodes. Bethesda, Md: American Physiological Society, 1985.

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(Editor), John N. Abelson, Melvin I. Simon (Editor), Bernardo Rudy (Editor), and Linda E. Iverson (Editor), eds. Ion Channels, Volume 207 (Methods in Enzymology). Academic Press, 1992.

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1953-, Iverson Linda E., Conn P. Michael, and Rudy Bernardo, eds. Ion channels. San Diego: Academic Press, 1992.

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