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Academic literature on the topic 'Arteriole'

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Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Arteriole"

1

Boegehold, M. A. "Effect of dietary salt on arteriolar nitric oxide in striated muscle of normotensive rats." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 6 (June 1, 1993): H1810—H1816. http://dx.doi.org/10.1152/ajpheart.1993.264.6.h1810.

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This study evaluated the influence of high dietary salt intake on nitric oxide (NO) activity in the arteriolar network of rats resistant to salt-induced hypertension. The spinotrapezius muscle microvasculature was studied in inbred Dahl salt-resistant (SR/Jr) rats fed low (0.45%)- or high (7%)-salt diets for 4–5 wk. Arterial pressures were not different between groups at any time during the study. NO synthesis inhibition with NG-nitro-L-arginine-methyl ester (L-NAME) constricted arcade arterioles in low-salt SR/Jr and dilated arcade arterioles in high-salt SR/Jr. Arcade arteriole dilation to acetylcholine (ACh), but not sodium nitroprusside (SNP), was impaired in high-salt SR/Jr. In contrast, transverse and distal arteriole responses to L-NAME, ACh, and SNP were identical in high- and low-salt SR/Jr. These findings indicate that high salt intake, in the absence of increased arterial pressure, suppresses the influence of basal and evoked NO on vascular tone in arcading arterioles, but not in smaller transverse and distal arterioles. Unaltered SNP responses in high-salt SR/Jr suggest that this effect does not involve a change in arteriolar smooth muscle responsiveness to NO.
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2

Hester, R. L. "Venular-arteriolar diffusion of adenosine in hamster cremaster microcirculation." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 6 (June 1, 1990): H1918—H1924. http://dx.doi.org/10.1152/ajpheart.1990.258.6.h1918.

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During increases in blood flow, both the terminal and the proximal arterioles dilate. The mechanism behind the dilation of the proximal arterioles is not known but may be the result of the diffusion of a vasoactive metabolite from adjacent venules. To determine whether an increase in venous adenosine (ADO) concentration could affect an adjacent arteriole, venules were perfused using a micropipette containing 10(-7)-10(-4) M ADO. During the venular perfusion, arteriolar diameter and red blood cell velocity were measured at a site 0.5 to 6 mm from the micropipette tip. The adjacent arteriole of the venular arteriolar pair dilated 29 +/- 3% with a 5-s 10(-4) M ADO perfusion, 32 +/- 4% with a 10-s 10(-4) M ADO perfusion, and 85 +/- 22% with a 60-s 10(-4) M ADO perfusion. One and 2-min perfusions with 10(-5) M ADO resulted in a 36 +/- 6% and 33 +/- 4% increase in diameter of the paired arteriole, respectively. The red blood cell velocity responses were variable, yet, on average, calculated blood flow increased in each group of experiments. Venular perfusions with saline resulted in a 2% change in arteriolar diameter. To rule out nondiffusional effects, venular perfusions were performed when the arteriole was not paired with the venule but crossed the venule. Venular perfusion with 10(-6) and 10(-7) M ADO resulted in a significant increase in diameter of the crossing arteriole of 19 +/- 3% and 6 +/- 2%, respectively. Therefore, the diffusion of a vasoactive metabolite from a venule to an arteriole may provide a mechanism by which the tissue can send a signal to cause a dilation of the more proximal arterioles.
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Cohen, Kenneth D., Bradley R. Berg, and Ingrid H. Sarelius. "Remote arteriolar dilations in response to muscle contraction under capillaries." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 6 (June 1, 2000): H1916—H1923. http://dx.doi.org/10.1152/ajpheart.2000.278.6.h1916.

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In hamster cremaster muscle, it has been shown previously that contraction of skeletal muscle fibers underlying small groups of capillaries (modules) induces dilations that are proportional to metabolic rate in the two arteriolar generations upstream of the stimulated capillaries (Berg BR, Cohen KD, and Sarelius IH. Am J Physiol Heart Circ Physiol 272: H2693–H2700, 1997). These remote dilations were hypothesized to be transmitted via gap junctions and not perivascular nerves. In the present study, halothane (0.07%) blocked dilation in the module inflow arteriole, and dilation in the second arteriolar generation upstream, the branch arteriole, was blocked by both 600 mosM sucrose and halothane but not tetrodotoxin (2 μM). Dilations in both arterioles were not blocked by the gap junction uncoupler 18-β-glycyrrhetinic acid (40 μM), and 80 mM KCl did not block dilation of the module inflow arteriole. These data implicate a gap junctional-mediated pathway insensitive to 18-β-glycyrrhetinic acid in dilating the two arterioles upstream of the capillary module during “remote” muscle contraction. Dilation in the branch arteriole, but not the module inflow arteriole, was attenuated by 100 μM N ω-nitro-l-arginine. Thus selective contraction of muscle fibers underneath capillaries results in dilations in the upstream arterioles that have characteristics consistent with a signal that is transmitted along the vessel wall through gap junctions, i.e., a conducted vasodilation. The observed insensitivities to 18-β-glycyrrhetinic acid, to KCl, and to N ω-nitro-l-arginine suggest, however, that there are multiple signaling pathways by which remote dilations can be initiated in these microvessels.
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Dawson, C. A., R. L. Capen, L. P. Latham, W. L. Hanson, S. E. Hofmeister, T. A. Bronikowski, D. A. Rickaby, and W. W. Wagner. "Pulmonary arterial transit times." Journal of Applied Physiology 63, no. 2 (August 1, 1987): 770–77. http://dx.doi.org/10.1152/jappl.1987.63.2.770.

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To begin to characterize the pulmonary arterial transport function we rapidly injected a bolus containing a radiopaque dye and a fluorescence dye into the right atrium of anesthetized dogs. The concentrations of the dye indicators were measured in the main pulmonary artery (fluoroscopically) and in a subpleural pulmonary arteriole (by fluorescence microscopy). The resulting concentration vs. time curves were subjected to numerical deconvolution and moment analysis to determine how the bolus was dispersed as it traveled through the arteriole stream tube from the main pulmonary artery to the arteriole. The mean transit time and standard deviation of the transport function from the main pulmonary artery to the arterioles studied averaged 1.94 and 1.23 s, respectively, and the relative dispersion (ratio of standard deviation to mean transit time) was approximately 64%. This relative dispersion is at least as large as those reported for the whole dog lung, indicating that relative to their respective mean transit times the dispersion upstream from the arterioles is comparable to that taking place in capillaries and/or veins. The standard deviations of the transport functions were proportional to their mean transit times. Thus the relative dispersion from the main pulmonary artery to the various arterioles studied was fairly consistent. However, there were variations in mean transit time even between closely adjacent arterioles, suggesting that variations in mean transit times between arteriole stream tubes also contribute to the dispersion in the pulmonary arterial tree.
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Park, Sungmi, Benjamin J. Bivona, and Lisa M. Harrison-Bernard. "Lack of contribution of nitric oxide synthase to cholinergic vasodilation in murine renal afferent arterioles." American Journal of Physiology-Renal Physiology 314, no. 6 (June 1, 2018): F1197—F1204. http://dx.doi.org/10.1152/ajprenal.00433.2017.

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We have previously reported significant increases in neuronal nitric oxide synthase (NOS) immunostaining in renal arterioles of angiotensin type 1A receptor (AT1A) knockout mice, and in arterioles and macula densa cells of AT1A/AT1B knockout mice. The contribution of nitric oxide derived from endothelial and macula densa cells in the maintenance of afferent arteriolar tone and acetylcholine-induced vasodilation was functionally determined in kidneys of wild-type, AT1A, and AT1A/AT1B knockout mice. Acetylcholine-induced changes in arteriolar diameters of in vitro blood-perfused juxtamedullary nephrons were measured during control conditions, in the presence of the nonspecific NOS inhibitor, Nω-nitro-l-arginine methyl ester (NLA), or the highly selective neuronal NOS inhibitor, N5-(1-imino-3-butenyl)-l-ornithine (VNIO). Acetylcholine (0.1 mM) produced a significant vasoconstriction in afferent arterioles of AT1A/AT1B mice (−10.9 ± 5.1%) and no changes in afferent arteriolar diameters of AT1A knockout mice. NLA (0.01–1 mM) or VNIO (0.01–1 μM) induced significant dose-dependent vasoconstrictions (−19.8 ± 4.0% 1 mM NLA; −7.8 ± 3.5% 1 μM VNIO) in afferent arterioles of kidneys of wild-type mice. VNIO had no effect on afferent arteriole diameters of AT1A knockout or AT1A/AT1B knockout mice, suggesting nonfunctional neuronal nitric oxide synthase. These data indicate that acetylcholine produces a significant renal afferent arteriole vasodilation independently of nitric oxide synthases in wild-type mice. AT1A receptors are essential for the manifestation of renal afferent arteriole responses to neuronal nitric oxide synthase-mediated nitric oxide release.
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Baker, Wesley B., Ashwin B. Parthasarathy, Kimberly P. Gannon, Venkaiah C. Kavuri, David R. Busch, Kenneth Abramson, Lian He, et al. "Noninvasive optical monitoring of critical closing pressure and arteriole compliance in human subjects." Journal of Cerebral Blood Flow & Metabolism 37, no. 8 (May 25, 2017): 2691–705. http://dx.doi.org/10.1177/0271678x17709166.

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The critical closing pressure ( CrCP) of the cerebral circulation depends on both tissue intracranial pressure and vasomotor tone. CrCP defines the arterial blood pressure ( ABP) at which cerebral blood flow approaches zero, and their difference ( ABP − CrCP) is an accurate estimate of cerebral perfusion pressure. Here we demonstrate a novel non-invasive technique for continuous monitoring of CrCP at the bedside. The methodology combines optical diffuse correlation spectroscopy (DCS) measurements of pulsatile cerebral blood flow in arterioles with concurrent ABP data during the cardiac cycle. Together, the two waveforms permit calculation of CrCP via the two-compartment Windkessel model for flow in the cerebral arterioles. Measurements of CrCP by optics (DCS) and transcranial Doppler ultrasound (TCD) were carried out in 18 healthy adults; they demonstrated good agreement (R = 0.66, slope = 1.14 ± 0.23) with means of 11.1 ± 5.0 and 13.0 ± 7.5 mmHg, respectively. Additionally, a potentially useful and rarely measured arteriole compliance parameter was derived from the phase difference between ABP and DCS arteriole blood flow waveforms. The measurements provide evidence that DCS signals originate predominantly from arteriole blood flow and are well suited for long-term continuous monitoring of CrCP and assessment of arteriole compliance in the clinic.
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Nurkiewicz, Timothy R., and Matthew A. Boegehold. "High dietary salt alters arteriolar myogenic responsiveness in normotensive and hypertensive rats." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 6 (December 1, 1998): H2095—H2104. http://dx.doi.org/10.1152/ajpheart.1998.275.6.h2095.

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We evaluated arteriolar myogenic responsiveness in normotensive, salt-loaded and hypertensive rats and investigated the potential influence of luminal blood flow or shear stress on myogenic responses under each of these conditions. Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) fed low-salt (0.45%, LS) or high-salt (7%, HS) diets were enclosed in a ventilated airtight box with the spinotrapezius muscle exteriorized for intravital microscopy. Dietary salt did not affect mean arterial pressure (MAP) in WKY, whereas MAP in SHR was significantly higher and augmented by dietary salt. In all groups, box pressurization caused similar increases in MAP that were completely transmitted to the arterioles. After these pressure increases, large arteriole diameters decreased by 0–30% and intermediate arteriole diameters decreased by 21–27%. Arteriolar myogenic responsiveness was not different between WKY-LS and SHR-LS. Large arterioles in WKY-HS displayed an attenuated pressure-diameter relationship compared with that in WKY-LS. Large arterioles in SHR-HS displayed an augmented pressure-diameter relationship compared with that in SHR-LS. There were no correlations between resting flow or wall shear rate and the magnitude of initial myogenic constriction in any group or vessel type. The capacity for sustained myogenic constriction was unrelated to secondary decreases in flow (14–41%) or increases in wall shear rate (21–88%) in each group. We conclude that 1) dietary salt impairs the myogenic responsiveness of large arterioles in normotensive rats and augments the myogenic responsiveness of large arterioles in hypertensive rats, 2) hypertension does not alter arteriolar myogenic responsiveness in this vascular bed, and 3) flow- or shear-dependent mechanisms do not attenuate myogenic responses in the intact arteriolar network of normal, salt-loaded, or hypertensive rats.
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Kavdia, Mahendra, and Aleksander S. Popel. "Venular endothelium-derived NO can affect paired arteriole: a computational model." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 2 (February 2006): H716—H723. http://dx.doi.org/10.1152/ajpheart.00776.2005.

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Venular endothelial cells can release nitric oxide (NO) in response to intraluminal flow both in isolated venules and in vivo. Experimental studies suggest that venular endothelium-released NO causes dilation of the adjacent paired arteriole. In the vascular wall, NO stimulates its target hemoprotein, soluble guanylate cyclase (sGC), which relaxes smooth muscle cells. In this study, a computational model of NO transport for an arteriole and venule pair was developed to determine the importance of the venular endothelium-released NO and its transport to the adjacent arteriole in the tissue. The model predicts that the tissue NO levels are affected within a wide range of parameters, including NO-red blood cell reaction rate and NO production rate in the arteriole and venule. The results predict that changes in the venular NO production affected not only venular endothelial and smooth muscle NO concentration but also endothelial and smooth muscle NO concentration in the adjacent arteriole. This suggests that the anatomy of microvascular tissue can permit the transport of NO from arteriolar to venular side, and vice versa, and may provide a mechanism for dilation of proximal arterioles by venules. These results will have significant implications for our understanding of tissue NO levels in both physiological and pathophysiological conditions.
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Mitrophanov, Alexander Y., Glenn Merrill-Skoloff, Steven P. Grover, Vijay Govindarajan, Arun Kolanjiyil, Daniel S. Hariprasad, Ginu Unnikrishnan, Robert Flaumenhaft, and Jaques Reifman. "Injury Length and Arteriole Constriction Shape Clot Growth and Blood-Flow Acceleration in a Mouse Model of Thrombosis." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 9 (September 2020): 2114–26. http://dx.doi.org/10.1161/atvbaha.120.314786.

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Objective: Quantitative relationships between the extent of injury and thrombus formation in vivo are not well understood. Moreover, it has not been investigated how increased injury severity translates to blood-flow modulation. Here, we investigated interconnections between injury length, clot growth, and blood flow in a mouse model of laser-induced thrombosis. Approach and Results: Using intravital microscopy, we analyzed 59 clotting events collected from the cremaster arteriole of 14 adult mice. We regarded injury length as a measure of injury severity. The injury caused transient constriction upstream and downstream of the injury site resulting in a 50% reduction in arteriole diameter. The amount of platelet accumulation and fibrin formation did not depend on arteriole diameter or deformation but displayed an exponentially increasing dependence on injury length. The height of the platelet clot depended linearly on injury length and the arteriole diameter. Upstream arteriolar constriction correlated with delayed upstream velocity increase, which, in turn, determined downstream velocity. Before clot formation, flow velocity positively correlated with the arteriole diameter. After the onset of thrombus growth, flow velocity at the injury site negatively correlated with the arteriole diameter and with the size of the above-clot lumen. Conclusions: Injury severity increased platelet accumulation and fibrin formation in a persistently steep fashion and, together with arteriole diameter, defined clot height. Arterial constriction and clot formation were characterized by a dynamic change in the blood flow, associated with increased flow velocity.
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Kimura, K., Y. Hirata, S. Nanba, A. Tojo, H. Matsuoka, and T. Sugimoto. "Effects of atrial natriuretic peptide on renal arterioles: morphometric analysis using microvascular casts." American Journal of Physiology-Renal Physiology 259, no. 6 (December 1, 1990): F936—F944. http://dx.doi.org/10.1152/ajprenal.1990.259.6.f936.

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In normal rat kidneys, the effect of atrial natriuretic peptide (ANP) on the diameter of the arterioles was evaluated by scanning electron microscopy of vascular casts. Acryl resin was infused into rat kidneys during the administration of ANP, either alone or with norepinephrine (NE). ANP infusion constricted the proximal efferent arteriole in the superficial cortex. Although NE constricted the proximal and distal segments of the afferent arteriole in the superficial cortex, the addition of ANP reversed the constriction and further constricted the efferent arteriole. In the deep cortex, only the proximal segment of the afferent arteriole was dilated by ANP when infused with NE. In a separate set of experiments, ANP increased both the glomerular filtration rate (GFR) and urinary sodium excretion (UNaV), and NE decreased the renal blood flow (RBF). However, administration of ANP after NE recovered RBF and increased GFR as well as UNaV. Results indicate that ANP increases GFR and natriuresis by constricting the efferent arteriole. NE appears to decrease RBF by constricting the afferent arteriole. ANP antagonizes the renal effects of NE primarily by dilating afferent arterioles.
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Dissertations / Theses on the topic "Arteriole"

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Zale, Kathryn. "Utilizing Doppler ultrasound to detect arteriole blood flow within the median nerve sheath." Connect to resource, 2010. http://hdl.handle.net/1811/45325.

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Kornfeld, Mark. "Calcium responses in the renal afferent arteriole to angiotensin II and norepinephrine stimulation." Lund : Dept. of Physiology and Neuroscience, Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/39750494.html.

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Leichtle, Anke. "Molekulare Charakterisierung von einwärtsgleichrichtenden Kaliumkanälen (Kir) in reninsezernierenden Zellen in der afferenten Arteriole der Rattenniere." [S.l. : s.n.], 2005. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB12168217.

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Guo, Hong. "Effects of biaxial stretch on arteriolar function in vitro." Thesis, [College Station, Tex. : Texas A&M University, 2006. http://hdl.handle.net/1969.1/ETD-TAMU-1739.

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Gao, Xiang. "Local Purinergic Control of Arteriolar Reactivity in Pancreatic Islets and Renal Glomeruli." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-230770.

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Local control of regional blood flow is exerted mainly through the arterioles. An adequate minute-to-minute regulation of blood perfusion of the kidney and the pancreas is obtained by the modulation of arteriolar reactivity, which will influence the organ function. The importance of purinergic signaling in this concept has been addressed, with special emphasis on the role of the adenosine A1 receptor. The effects of adenosine on two specialized vascular beds, namely the renal glomerulus and the pancreatic islets, have been examined. Characteristic for these regional circulations is their very high basal blood flow, but with somewhat different responses to vasoconstrictor and vasodilator stimuli. By adapting a unique microperfusion technique it was possible to separately perfuse isolated single mouse arterioles with attached glomeruli or pancreatic islets ex vivo. Microvascular responses were investigated following different additions to the perfusion fluid to directly examine the degree of dilation or constriction of the arterioles. This has been performed on transgenic animals in this thesis, e.g. A1 receptor knockout mice. Also effects of P2Y receptors on islet arterioles were examined in both normoglycemic and type 2 diabetic rats. Furthermore, interference with adenosine transport in glomerular arterioles were examined.. Our studies demonstrate important, yet complex, effects of adenosine and nucleotide signaling on renal and islet microvascular function, which in turn may influence both cardiovascular and metabolic regulations. They highlight the need for further studies of other purinergic receptors in this context, studies that are at currently being investigated.
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Vargel, Michelland Murielle. "Influence de la température sur la vasomotricité artériolaire : du vaisseau isolé au phénomène de Raynaud." Université Joseph Fourier (Grenoble), 1998. http://www.theses.fr/1998GRE10260.

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Ce travail a pour but de determiner le role du froid dans la survenue du vasospasme rencontre dans le phenomene de raynaud. Le phenomene de raynaud, acrosyndrome decrit en 1862 par m. Raynaud, s'affirme comme le plus frequent des troubles vasomoteurs des extremites. Le froid est toujours decrit comme un des facteurs declenchant du vasospasme. Dans une premiere partie de ce travail, l'influence de la temperature sur la reactivite noradrenergique vasculaire est observee in vitro, sur des arteres isolees de rat et, in vivo, sur des arterioles cutanees dans la chambre cutanee dorsale du hamster. Puis une seconde partie experimentale chez l'homme permet de mesurer avec un laser doppler imageur l'effet du froid sur la microcirculation cutanee digitale dans 3 populations (temoins sains, phenomene de raynaud primaire et phenomene de raynaud secondaire). Puis l'influence des facteurs climatiques sur la frequence et l'intensite du vasopasme dans la population generale sujette au phenomene de raynaud est evaluee par une etude epidemiologique. Sur le modele des vaisseaux isoles, la temperature de 25c induit une reaction opposee pour les vaisseaux profonds et les vaisseaux cutanes. Ce refroidissement n'a pas d'effet mesurable sur le diametre des arterioles dans la chambre cutanee dorsale du hamster. A l'inverse, sur les deux modeles animaux, le froid potentialise la reponse vasculaire lors d'une stimulation noradrenergique. La mesure du flux realisee a partir des cartographies de flux suit un profil de variation identiques dans les trois groupes de personnes etudies. C'est la valeur basale du flux qui differe entre temoins sains et patients. Il ressort une sensibilite particuliere au froid sur l'echantillon de population etudie. Ces resultats suggerent que le froid seul ne suffit pas a expliquer la survenue du vasospasme chez des patients souffrant d'un phenomene de raynaud. Neanmoins, les resultats sur les modeles animaux montrent l'effet amplificateur, peut etre catalyseur, d'un refroidissement sur la reponse vasculaire a une stimulation noradrenergique. Chez des patients atteint d'un phenomene de raynaud, le froid viendrait s'associer a un etat basal perturbe pour amplifier la reponse vasoconstrictrice.
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Li, Yao. "Contributions of TRPM4 and Rho Kinase to Myogenic Tone Development in Cerebral Parenchymal Arterioles." ScholarWorks @ UVM, 2016. http://scholarworks.uvm.edu/graddis/464.

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Cerebral parenchymal arterioles (PAs) play a critical role in assuring appropriate blood flow and perfusion pressure within the brain. PAs are unique in contrast to upstream pial arteries, as defined by their critical roles in neurovascular coupling, distinct sensitivities to vasoconstrictors, and enhanced myogenic responsiveness. Dysfunction of these blood vessels is implicated in numerous cardiovascular diseases. However, treatments are limited due to incomplete understanding of the fundamental control mechanisms at this level of the circulation. One of the key elements within most vascular networks, including the cerebral circulation, is the presence of myogenic tone, an intrinsic process whereby resistance arteries constrict and reduce their diameter in response to elevated arterial pressure. This process is centrally involved in the ability of the brain to maintain nearly constant blood flow over a broad range of systemic blood pressures. The overall goal of this dissertation was to investigate the unique mechanisms of myogenic tone regulation in the cerebral microcirculation. To reveal the contributions of various signaling factors in this process, measurements of diameter, intracellular Ca2+ concentration ([Ca2+]i), membrane potential and ion channel activity were performed. Initial work determined that two purinergic G protein-coupled receptors, P2Y4 and P2Y6 receptors, play a unique role in mediating pressure-induced vasoconstriction of PAs in a ligand-independent manner. Moreover, a particular transient receptor potential (TRP) channel in the melastatin subfamily, i.e. TRPM4, was also identified as a mediator of PA myogenic responses. Notably, the observations that inhibiting TRPM4 channels substantially reduces P2Y receptor-mediated depolarization and vasoconstriction, and that P2Y receptor ligands markedly activate TRPM4 currents provide definitive evidence that this ion channel functions as an important link between mechano-sensitive P2Y receptor activation and the myogenic response in PAs. Next, the signaling cascades that mediate stretch-induced TRPM4 activation in PA myocytes were explored. Interestingly, these experiments determined that the RhoA/Rho kinase signaling pathway is involved in this mechanism by facilitating pressure-induced, P2Y receptor-mediated stimulation of TRPM4 channels, leading to subsequent smooth muscle depolarization, [Ca2+]i increase and contraction. Since Rho kinase is generally accepted as a 'Ca2+-sensitization' mediator, the present, contrasting observations point to an underappreciated role of RhoA/Rho kinase signaling in the excitation-contraction mechanisms within the cerebral microcirculation. Overall, this dissertation provides evidence that myogenic regulation of cerebral PAs is mediated by mechano-sensitive P2Y receptors, which initiate the RhoA/Rho kinase signaling pathway, subsequent TRPM4 channel opening, and concomitant depolarization and contraction of arteriolar smooth muscle cells. Revealing the unique mechanochemical coupling mechanisms in the cerebral microcirculation may lead to development of innovative therapeutic strategies for prevention and treatment of microvascular pathologies in the brain.
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Leichtle, Anke [Verfasser], and U. [Akademischer Betreuer] Quast. "Molekulare Charakterisierung von einwärtsgleichrichtenden Kaliumkanälen (Kir) in reninsezernierenden Zellen in der afferenten Arteriole der Rattenniere / Anke Leichtle ; Betreuer: U. Quast." Tübingen : Universitätsbibliothek Tübingen, 2005. http://d-nb.info/1160754276/34.

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Lai, Enyin. "Interaction between Adenosine and Angiotensin II in Renal Afferent Arterioles of Mice." Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7702.

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Renal arterioles represent the most important effecter site in the control of renal perfusion and filtration. Adenosine (Ado), angiotensin II (Ang II) and nitric oxide (NO) interact in modulating arteriolar tone. The present work investigates the mechanism of this interaction. We tested the hypothesis that AT1 receptor (AT1AR) mediated NO release in isolated perfused afferent arterioles. Further, special attention was given to mechanisms of Ado-Ang II -interactions.

We found (I) that Ang II specifically induces NO release via AT1AR in arterioles. The effect is important in view of high renin and Ang II concentrations in these vessels. (II) Ado modulates the Ang II response by acting on vasoconstrictor A1AR and vasodilator A2AR. Vice versa, Ang II critically enhances the constriction to Ado, which supports the assumption of its modulating action in the tubuloglomerular feedback (TGF). (III) The synergistic effect of Ang II and Ado on arteriolar contraction is concurrent with an increase in the cytosolic calcium. Further, (IV) Ado increases the calcium sensitivity of the contractile machinery in arteriolar smooth muscle cells most probably by enhancement of the phosphorylation of the myosin light chain regulatory unit. RhoA kinase, protein kinase C and p38 MAP are involved in the Ado effect, which is not receptor mediated and depends on the Ado uptake into vascular cells. Remarkably, the enhancing action of Ado is most likely limited to Ang II; since Ado does not influence endothelin-1 and norepinephrine induced contractions.

These novel results extend our knowledge about the synergistic action of Ang II and Ado in the control of renal filtration. Ado, the key factor in mediation of the TGF, develops a significant vasoconstrictor action only in the presence of Ang II. On the other hand, the Ang II induced vasoconstriction is modulated by Ado via receptor and non-receptor mediated intracellular signaling pathways.

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Brickler, Thomas Read. "The Role of Age and Model Severity on Cortical Vascular Response Following Traumatic Brain Injury." Diss., Virginia Tech, 2017. http://hdl.handle.net/10919/85566.

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Traumatic brain injury (TBI) is a growing health concern worldwide that affects a broad range of the population. As TBI is the leading cause of disability and mortality in children, several pre-clinical models have been developed using rodents at a variety of different ages; however, key brain maturation events are overlooked that leave some age groups more or less vulnerable to injury. Thus, there has been a large emphasis on producing relevant animal models to elucidate molecular pathways that could be of therapeutic potential to help limit neuronal injury and improve behavioral outcome. TBI involves a host of different biochemical events, including disruption of the cerebral vasculature and breakdown of the blood brain barrier (BBB) that exacerbate secondary injuries. A better of understanding of the mechanism(s) underlying cerebral vascular regulation will aid in establishing more effective treatment strategies aimed at improving cerebral blood flow restoration and preventing further neuronal loss. Our studies reveal an age-at- injury dependence on the Angiopoetin-Tie2 axis, which mediates neuroprotection in a model of juvenile TBI following cortical controlled impact (CCI) that is not seen in adult mice. The protection observed was mediated, in part, by the microvascular response to CCI injury and prompted further detailed analysis of the larger arteriole network across several mouse strains and models of TBI. Our second study revealed both a model and species dependent effect on a specialized network of arteriole vessels, called collaterals after trauma. We demonstrated that a repetitive mild TBI (rmTBI) can induce collateral remodeling in C57BL/6 but not CD1 mice; however, CCI injury had no effect on collateral changes in either strain. Together, these findings demonstrate an age-dependent and species/model dependent effect on vascular remodeling that highlights the importance of individualized therapeutics to TBI.
Ph. D.
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Books on the topic "Arteriole"

1

Singer, Jeremiah P. Travel time on arterials and rural highways: State-of-the-practice synthesis on arterial data collection technology ; arterial data collection technology. Washington, DC: U.S. Department of Transportation, Federal Highway Administration, 2013.

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D, Lambris John, Peers Chris, Cohen Irun R, Nurse Colin A, Gonzalez Constancio, Paoletti Rodolfo, Lajtha Abel, and SpringerLink (Online service), eds. Arterial Chemoreceptors: Arterial Chemoreceptors. Dordrecht: Springer Netherlands, 2009.

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Rosenthal, J., and R. Kolloch. Arterielle Hypertonie. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18507-6.

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Stimpel, Michael. Arterielle Hypertonie. Heidelberg: Steinkopff, 2001. http://dx.doi.org/10.1007/978-3-642-57617-1.

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Andrés, Purroy Unanua, and Universidad de Navarra. Clínica Universitaria, eds. Hipertensión arterial. León [Spain]: Editorial Everest, 2002.

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Gauda, Estelle B., Maria Emilia Monteiro, Nanduri Prabhakar, Christopher Wyatt, and Harold D. Schultz, eds. Arterial Chemoreceptors. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91137-3.

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Fleenor, Bradley S., and Adam J. Berrones. Arterial Stiffness. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-24844-8.

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Gonzalez, Constancio, Colin A. Nurse, and Chris Peers, eds. Arterial Chemoreceptors. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2259-2.

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Eyzaguirre, Carlos, Sal J. Fidone, Robert S. Fitzgerald, Sukhamay Lahiri, and Donald M. McDonald, eds. Arterial Chemoreception. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3388-6.

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Berbari, Adel, and Giuseppe Mancia, eds. Arterial Disorders. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14556-3.

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Book chapters on the topic "Arteriole"

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Bährle-Rapp, Marina. "Arteriole, auch: Arteriola." In Springer Lexikon Kosmetik und Körperpflege, 48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_821.

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Moore, Leon C., and Daniel Casellas. "The Afferent Arteriole in Tubuloglomerular Feedback and Autoregulation." In Nephrology, 356–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-35158-1_30.

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Layton, Anita T., and Aurélie Edwards. "Vasomotion and Myogenic Response of the Afferent Arteriole." In Lecture Notes on Mathematical Modelling in the Life Sciences, 141–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27367-4_7.

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Ciocanel, Maria-Veronica, Tracy L. Stepien, Aurélie Edwards, and Anita T. Layton. "Modeling Autoregulation of the Afferent Arteriole of the Rat Kidney." In Association for Women in Mathematics Series, 75–100. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60304-9_5.

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Veera Krishna, M., B. V. Swarnalathamma, and J. Prakash. "Heat and Mass Transfer on Unsteady MHD Oscillatory Flow of Blood Through Porous Arteriole." In Lecture Notes in Mechanical Engineering, 207–24. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-5329-0_14.

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Xu, Xiayu, Tao Tan, and Feng Xu. "An Improved U-Net Architecture for Simultaneous Arteriole and Venule Segmentation in Fundus Image." In Communications in Computer and Information Science, 333–40. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95921-4_31.

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van Nugteren, Koos. "Arteriële claudicatio intermittens (perifeer arterieel vaatlijden)." In Hardloopblessures, 29–35. Houten: Bohn Stafleu van Loghum, 2020. http://dx.doi.org/10.1007/978-90-368-2584-9_6.

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Bährle-Rapp, Marina. "Arterie, auch Arteria, Plur.: Arteriae." In Springer Lexikon Kosmetik und Körperpflege, 47–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_818.

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Yuzawa, Izumi, Masaru Yamada, Ryusui Tanaka, and Kiyotaka Fujii. "Moderate Hypothermia Attenuates the Endothelium-Dependent Pial Arteriole Dilatation but Not the Endothelium-Independent Response in Rats." In Hypothermia for Acute Brain Damage, 135–40. Tokyo: Springer Japan, 2004. http://dx.doi.org/10.1007/978-4-431-53961-2_19.

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Champion, Howard R., Nova L. Panebianco, Jan J. De Waele, Lewis J. Kaplan, Manu L. N. G. Malbrain, Annie L. Slaughter, Walter L. Biffl, et al. "Arterioles." In Encyclopedia of Intensive Care Medicine, 266. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1157.

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Conference papers on the topic "Arteriole"

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Nakano, Takuma, Keisuke Yoshida, Seiichi Ikeda, Hiroyuki Oura, Toshio Fukuda, Takehisa Matsuda, Makoto Negoro, and Fumihito Arai. "Fabrication of Transparent Arteriole Membrane Models." In 2008 International Symposium on Micro-NanoMechatronics and Human Science. IEEE, 2008. http://dx.doi.org/10.1109/mhs.2008.4752496.

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NAKANO, TAKUMA, SEIICHI IKEDA, TOSHIO FUKUDA, TAKEHISA MATSUDA, MAKOTO NEGORO, and FUMIHITO ARAI. "FABRICATION OF TRANSPARENT ARTERIOLE MEMBRANE MODELS." In Proceedings of the Tohoku University Global Centre of Excellence Programme. PUBLISHED BY IMPERIAL COLLEGE PRESS AND DISTRIBUTED BY WORLD SCIENTIFIC PUBLISHING CO., 2009. http://dx.doi.org/10.1142/9781848163539_0047.

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Chung, Hansol, David Bahk, Edward Hong, and Richard Kyung. "Pressure analysis of the blood flow in the arteriole." In 2012 38th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2012. http://dx.doi.org/10.1109/nebc.2012.6207087.

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Oshima, Marie, Masamichi Oishi, Haruyuki Kinoshita, and Teruo Fujii. "Visualization and Measurement of Flow-Induced Dynamic Motion of Red Blood Cells Using Tracking Confocal Micro-PIV System." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80516.

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RBC(Red Blood Cell)s have a biconcave shape with diameters of about 8 μm and thicknesses of about 2 μm like a capsule structure with highly deformable membrane. In arterioles having diameters of less than 100μm, the effect of RBCs becomes pronounced because the scales of the flow and the RBCs become similar. RBCs exhibit the axial migration [1] toward the center of blood vessel. The axial migration leads to non-Newtonian flow behavior such as decrease in flow resistance. The tank-tread motion [2] makes an important role for the axial migration and it is dependent on the shear rate of the surrounding flow, which ranges up to 500 s−1 in arteriole.
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Yang, Jason, Alexander Ruesch, and Jana M. Kainerstorfer. "Optical Methods for Non-Invasive Assessment of Arteriole Flow Impedance." In Optical Tomography and Spectroscopy. Washington, D.C.: OSA, 2020. http://dx.doi.org/10.1364/ots.2020.sw2d.5.

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Lapi, D., M. Varanini, R. Scuri, and A. Colantuoni. "Effects of Catechin on cerebral arteriole vasomotion in spontaneously hypertensive rats." In 2020 11th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2020. http://dx.doi.org/10.1109/esgco49734.2020.9158049.

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Ahmad, Faiza, and Zia Hameed. "Automatic Arteriole/Venule Segregation from Fundus Eye Image using Supervised Classifiers." In 2020 International Conference on Computing and Information Technology (ICCIT-1441). IEEE, 2020. http://dx.doi.org/10.1109/iccit-144147971.2020.9213740.

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"Automated Arteriole and Venule Recognition in Retinal Images using Ensemble Classification." In International Conference on Computer Vision Theory and Applications. SCITEPRESS - Science and and Technology Publications, 2014. http://dx.doi.org/10.5220/0004733701940202.

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Yang, Jason, Alexander Ruesch, and Jana M. Kainerstorfer. "Optical methods for non-invasive assessment of arteriole flow impedance (Conference Presentation)." In Neural Imaging and Sensing 2020, edited by Qingming Luo, Jun Ding, and Ling Fu. SPIE, 2020. http://dx.doi.org/10.1117/12.2547639.

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Reasor, Daniel A., Jonathan R. Clausen, and Cyrus K. Aidun. "Direct Numerical Simulation of Cellular Blood Flow Through a Model Arteriole Bifurcation." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19061.

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Blood is composed of a suspension of red blood cells (RBCs) suspended in plasma, and the presence of the RBCs substantially changes the flow characteristics and rheology of these suspensions. The viscosity of blood varies with the hematocrit (volume fraction of RBCs), which is a result not seen in Newtonian fluids. Additionally, RBCs are deformable, which can alter suspension dynamics. Understanding the physics in these flows requires accurately simulating the suspended phase to recover the microscale, and a subsequent analysis of the rheology to ascertain the continuum-level effects caused by the changes at the particle level. The direct numerical simulation of blood flow including RBC migration effects has the capability to resolve the Fåhraeus effect of observing low hematocrit values near walls, the subsequent cell-depleted layer, and the presence of velocity profile blunting due to the distribution of RBCs.
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Reports on the topic "Arteriole"

1

Singer, Robert, Brandon Root, and Peter Morone. Arterial Line. Touch Surgery Simulations, June 2015. http://dx.doi.org/10.18556/touchsurgery/2015.s0047.

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Cordis. Carotid Arterial Stenting. Touch Surgery Simulations, 2017. http://dx.doi.org/10.18556/touchsurgery/2017.s0095.

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Young, Stanley, and Dennis So Ting Fong. Arterial Trip Length Characteristics. Purdue University, December 2017. http://dx.doi.org/10.5703/1288284316560.

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Young, Stanley, and Dennis So Ting Fong. Arterial Performance Measures Software. Purdue University, December 2017. http://dx.doi.org/10.5703/1288284316567.

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Young, Stanley, and Dennis So Ting Fong. Arterial Performance Management System Lexicon. Purdue University, December 2017. http://dx.doi.org/10.5703/1288284316565.

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Young, Stanley, and Dennis So Ting Fong. Arterial Trip Length Characteristics Software. Purdue University, December 2017. http://dx.doi.org/10.5703/1288284316569.

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Young, Stanley, and Dennis So Ting Fong. Arterial Network Performance Measures Software. Purdue University, December 2017. http://dx.doi.org/10.5703/1288284316570.

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8

Kao, Peter N. Lineage Analysis in Pulmonary Arterial Hypertension. Fort Belvoir, VA: Defense Technical Information Center, June 2010. http://dx.doi.org/10.21236/ada541337.

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Kao, Peter N. Lineage Analysis in Pulmonary Arterial Hypertension. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ada599248.

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Kao, Peter. Lineage Analysis in Pulmonary Arterial Hypertension. Fort Belvoir, VA: Defense Technical Information Center, June 2011. http://dx.doi.org/10.21236/ada555153.

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