Relevant bibliographies by topics / Rat carotid body cells

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Rat carotid body cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "Rat carotid body cells"

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Tse, Amy, Lei Yan, Andy K. Lee, and Frederick W. Tse. "Autocrine and paracrine actions of ATP in rat carotid body." Canadian Journal of Physiology and Pharmacology 90, no. 6 (June 2012): 705–11. http://dx.doi.org/10.1139/y2012-054.

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Carotid bodies are peripheral chemoreceptors that detect lowering of arterial blood O2 level. The carotid body comprises clusters of glomus (type I) cells surrounded by glial-like sustentacular (type II) cells. Hypoxia triggers depolarization and cytosolic [Ca2+] ([Ca2+]i) elevation in glomus cells, resulting in the release of multiple transmitters, including ATP. While ATP has been shown to be an important excitatory transmitter in the stimulation of carotid sinus nerve, there is considerable evidence that ATP exerts autocrine and paracrine actions in carotid body. ATP acting via P2Y1 receptors, causes hyperpolarization in glomus cells and inhibits the hypoxia-mediated [Ca2+]i rise. In contrast, adenosine (an ATP metabolite) triggers depolarization and [Ca2+]i rise in glomus cells via A2A receptors. We suggest that during prolonged hypoxia, the negative and positive feedback actions of ATP and adenosine may result in an oscillatory Ca2+ signal in glomus cells. Such mechanisms may allow cyclic release of transmitters from glomus cells during prolonged hypoxia without causing cellular damage from a persistent [Ca2+]i rise. ATP also stimulates intracellular Ca2+ release in sustentacular cells via P2Y2 receptors. The autocine and paracrine actions of ATP suggest that ATP has important roles in coordinating chemosensory transmission in the carotid body.
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Yamamoto, Y., and K. Taniguchi. "Expression of Tandem P Domain K+ Channel, TREK-1, in the Rat Carotid Body." Journal of Histochemistry & Cytochemistry 54, no. 4 (January 6, 2006): 467–72. http://dx.doi.org/10.1369/jhc.5a6755.2005.

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TREK-1 is one of the important potassium channels for regulating membrane excitability. To examine the distribution of TREK-1 in the rat carotid body, we performed RT-PCR for mRNA expression and in situ hybridization and immunohistochemistry for tissue distribution of TREK-1. RT-PCR detected mRNA expression of TREK-1 in the carotid body. Furthermore, in situ hybridization revealed the localization of TREK-1 mRNA in the glomus cells. TREK-1 immunoreactivity was mainly distributed in the glomus cells and nerve fibers in the carotid body. TREK-1 may modulate potassium current of glomus cells and/or afferent nerve endings in the rat carotid body.
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Pallot, D. J., K. W. Al Neamy, and N. Blakeman. "Quantitative Studies of Rat Carotid Body Type I Cells." Cells Tissues Organs 126, no. 3 (1986): 187–92. http://dx.doi.org/10.1159/000146213.

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Martinez, A., L. Saldise, MJ Ramirez, S. Belzunegui, E. Zudaire, MR Luquin, and F. Cuttitta. "Adrenomedullin expression and function in the rat carotid body." Journal of Endocrinology 176, no. 1 (January 1, 2003): 95–102. http://dx.doi.org/10.1677/joe.0.1760095.

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Adrenomedullin (AM) immunoreactivity has been found in granules of the glomus (type I) cells of the carotid bodies in rats. The identity of these cells was ascertained by colocalization of immunoreactivities for AM and tyrosine hydroxylase in their cytoplasm. Exposure of freshly isolated carotid bodies to synthetic AM resulted in a concentration- and time-dependent degranulation of glomus cells as measured by dopamine (DA) release. DA release reached a zenith 30 min after exposure to AM (94.2% over untreated controls). At this time-point, the response to AM was similar to the one elicited by 5 min of exposure to 100 mM K+. Nevertheless, injection of 1 micro l 60 nM AM/g body weight into the tail vein of the rats did not induce statistical differences in DA release from the carotid bodies. Exposure of the oxygen-sensitive cell line PC-12 to hypoxia elicited an increase in AM mRNA expression and peptide secretion into serum-free conditioned medium. Previous data have shown that elevation of AM expression under hypoxia is mediated through hypoxia-inducible factor-1, and that exposure of chromaffin cells to AM results in degranulation. All these data suggest that AM is an important autocrine regulator of carotid body function.
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Makarenko, Vladislav V., Ying-Jie Peng, Guoxiang Yuan, Aaron P. Fox, Ganesh K. Kumar, Jayasri Nanduri, and Nanduri R. Prabhakar. "CaV3.2 T-type Ca2+ channels in H2S-mediated hypoxic response of the carotid body." American Journal of Physiology-Cell Physiology 308, no. 2 (January 15, 2015): C146—C154. http://dx.doi.org/10.1152/ajpcell.00141.2014.

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Arterial blood O2 levels are detected by specialized sensory organs called carotid bodies. Voltage-gated Ca2+ channels (VGCCs) are important for carotid body O2 sensing. Given that T-type VGCCs contribute to nociceptive sensation, we hypothesized that they participate in carotid body O2 sensing. The rat carotid body expresses high levels of mRNA encoding the α1H-subunit, and α1H protein is localized to glomus cells, the primary O2-sensing cells in the chemoreceptor tissue, suggesting that CaV3.2 is the major T-type VGCC isoform expressed in the carotid body. Mibefradil and TTA-A2, selective blockers of the T-type VGCC, markedly attenuated elevation of hypoxia-evoked intracellular Ca2+ concentration, secretion of catecholamines from glomus cells, and sensory excitation of the rat carotid body. Similar results were obtained in the carotid body and glomus cells from CaV3.2 knockout ( Cacna1h−/−) mice. Since cystathionine-γ-lyase (CSE)-derived H2S is a critical mediator of the carotid body response to hypoxia, the role of T-type VGCCs in H2S-mediated O2 sensing was examined. Like hypoxia, NaHS, a H2S donor, increased intracellular Ca2+ concentration and augmented carotid body sensory nerve activity in wild-type mice, and these effects were markedly attenuated in Cacna1h−/− mice. In wild-type mice, TTA-A2 markedly attenuated glomus cell and carotid body sensory nerve responses to hypoxia, and these effects were absent in CSE knockout mice. These results demonstrate that CaV3.2 T-type VGCCs contribute to the H2S-mediated carotid body response to hypoxia.
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Di Giulio, C., P. G. Data, and S. Lahiri. "Chronic cobalt causes hypertrophy of glomus cells in the rat carotid body." American Journal of Physiology-Cell Physiology 261, no. 1 (July 1, 1991): C102—C105. http://dx.doi.org/10.1152/ajpcell.1991.261.1.c102.

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We tested the hypothesis that chronic cobalt administration would induce carotid body cellular response along with polycythemia as found in chronic hypoxia if common oxygen-sensitive mechanisms were involved in the two instances. Morphometric studies were performed on carotid bodies in male rats that were chronically treated with cobalt chloride (0.17 mumol/kg, ip, daily for 6 wk) and in control rats that received blank saline injections. The rats were anesthetized, blood samples were collected for hematocrit, and the carotid bodies were surgically exposed and were perfused and superfused with the buffered fixative (3% glutaraldehyde plus 1% paraformaldehyde, pH 7.40, 330-340 mosM). The carotid bodies were processed, and ultrathin sections were cut for electron microscopy and morphometry of type I (glomus) and type II cells. Hematocrit increased from 44% in the control to 74% in the cobalt-treated rats, and the mean volume of type I cells increased from 424 to 1,061 microns 3. Type II cells did not show any significant change in size. The results suggest that cobalt stimulated oxygen-sensitive mechanism in the glomus cells of the carotid body and that the glomus cell is a site of oxygen chemosensing.
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Monti-Bloch, L., Vero´nica Abudara, and C. Eyzaguirre. "Electrical communication between glomus cells of the rat carotid body." Brain Research 622, no. 1-2 (September 1993): 119–31. http://dx.doi.org/10.1016/0006-8993(93)90810-a.

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Fung, Man-Lung, Siu-Yin Lam, Tung-Po Wong, Yung-Wui Tjong, and Po-Sing Leung. "Carotid Body AT4 Receptor Expression and its Upregulation in Chronic Hypoxia." Open Cardiovascular Medicine Journal 1, no. 1 (June 11, 2007): 1–7. http://dx.doi.org/10.2174/1874192400701010001.

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Hypoxia regulates the local expression of angiotensin-generating system in the rat carotid body and the me-tabolite angiotensin IV (Ang IV) may be involved in the modulation of carotid body function. We tested the hypothesis that Ang IV-binding angiotensin AT4 receptors play a role in the adaptive change of the carotid body in hypoxia. The expression and localization of Ang IV-binding sites and AT4 receptors in the rat carotid bodies were studied with histochemistry. Specific fluorescein-labeled Ang IV binding sites and positive staining of AT4 immunoreactivity were mainly found in lobules in the carotid body. Double-labeling study showed the AT4 receptor was localized in glomus cells containing tyrosine hydroxylase, suggesting the expression in the chemosensitive cells. Intriguingly, the Ang IV-binding and AT4 immunoreactivity were more intense in the carotid body of chronically hypoxic (CH) rats (breathing 10% oxygen for 4 weeks) than the normoxic (Nx) control. Also, the protein level of AT4 receptor was doubled in the CH comparing with the Nx group, supporting an upregulation of the expression in hypoxia. To examine if Ang IV induces intracellular Ca2+ response in the carotid body, cytosolic calcium ([Ca2+]i) was measured by spectrofluorimetry in fura-2-loaded glomus cells dissociated from CH and Nx carotid bodies. Exogenous Ang IV elevated [Ca2+]i in the glomus cells and the Ang IV response was significantly greater in the CH than the Nx group. Hence, hypoxia induces an upregulation of the expression of AT4 receptors in the glomus cells of the carotid body with an increase in the Ang IV-induced [Ca2+]i elevation. This may be an additional pathway enhancing the Ang II action for the activation of chemoreflex in the hypoxic response during chronic hypoxia.
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Otlyga, D. A., O. A. Junemann, E. G. Tsvetkova, K. R. Gorokhov, and S. V. Saveliev. "Immunohistochemical features of the human carotid body." CLINICAL AND EXPERIMENTAL MORPHOLOGY 9, no. 3 (September 23, 2020): 61–67. http://dx.doi.org/10.31088/cem2020.9.3.61-67.

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Introduction. The carotid body is a chemoreceptor organ and the initial link of the reflex regulation of car-diovascular and respiratory systems. However, molecular genetic and immunohistochemical characteristics of the human carotid body remains underinvestigated. Although there are numerous studies of the second half of the 20th century devoted to the classical light-optical histology of the human organ, the immunohis-tochemical investigations are very few. The aim of our study was to clarify immunohistochemical features of the human carotid body in comparison with those of the most commonly used laboratory animals. Materials and methods. The study was performed on 10 carotid bodies of the adult human of different ages of both sexes using immunoperoxidase labeling with antibodies to bIII-tubulin, tyrosine hydroxylase, syn-aptophysin, PGP9.5, neurofilaments 200kDa, S100, and GFAP. Results. Nerve fibers passing between the lobules, as well as entering them, were positive for bIII-tubulin, tyrosine hydroxylase, PGP9.5 and neurofilaments. Type I cells had cytoplasmic reaction for bIII-tubulin and synaptophysin as well as cytoplasmic and nuclear staining for PGP9.5. At the same time, they had weaker reaction for tyrosine hydroxylase. Type II cells were positive for GFAP and S100. Conclusion. Immunohistochemical characteristics of the human carotid body were similar to those of rats and mice. The human carotid body cells and nerve fibers showed the same distribution of PGP9.5, bIII-tubulin, synaptophysin, neurofilaments, GFAP and S100 as rat and mouse carotid body cells. However, human carotid body reaction for tyrosine hydroxylase was much lower, which may indicate a smaller amount of synthesized catecholamines compared to the carotid body in rats and mice. Keywords: human carotid body, immunohistochemistry, sympathoadrenal system, tyrosine hydroxylase
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Stea, A., and C. A. Nurse. "Chloride channels in cultured glomus cells of the rat carotid body." American Journal of Physiology-Cell Physiology 257, no. 2 (August 1, 1989): C174—C181. http://dx.doi.org/10.1152/ajpcell.1989.257.2.c174.

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As part of our investigations on the chemosensory mechanisms in the rat carotid body, we are studying the physiology of the parenchymal glomus cells by the patch-clamp technique. Here we characterize a large-conductance chloride channel (approximately 296 pS) with random open and closed kinetics in inside-out patches of cultured glomus cells. The open-state probability (Po; mean = 0.61) was hardly affected by membrane potential (-50 to +50 mV) and cytoplasmic calcium (0-1 mM). Similarly, the channel did not appear to be regulated by cytoplasmic nucleotides (1 mM) or pH (6.5-8). Ion-substitution experiments yielded the following selectivity sequence: chloride greater than bicarbonate greater than sulfate greater than glutamate approximately sodium. Single-channel currents were reversibly reduced or blocked by anthracene-9-carboxylic acid (5-10 mM) but were unaffected by stilbene derivatives (0.5-1 mM), by furosemide (1 mM), and by 5-nitro-2-(3-phenyl-propylamino)benzoic acid (0.01 mM). Because these cultured glomus cells have been shown to express carbonic anhydrase, it is inferred that the chloride channels may play an important role in the physiology of glomus cells by aiding in the regulation of pHi and the resting potential via bicarbonate and chloride permeability.
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Dissertations / Theses on the topic "Rat carotid body cells"

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O'Donnell, Jean. "Mechanism of excitation of carotid body chemoreceptor cells." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236119.

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Burlon, Drew C. "THE PRESYNAPTIC REGULATION OF ISOLATED NEONATAL RAT CAROTID BODY TYPE I CELLS BY HISTAMINE." Wright State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=wright1252943387.

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Ricker, Ellen M. "The inhibitory effects of opioids on voltage-gated calcium influx in neonatal rat carotid body type I cells." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1424262410.

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Dunn, Eric J. "Effect of Somatostatin on Voltage-Gated CalciumInflux in Isolated Neonatal Rat Carotid Body Type I Cells." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1432132454.

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Jackson, Adele. "Oxygen sensing, plasticity and catecholaminergic functions in cultured chromaffin cells of rat carotid body and adrenal medulla : modulation by chronic hypoxia and acetylcholine receptors /." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0018/NQ30096.pdf.

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Richmond, Patrick Henry. "The regulation of intracellular pH (pHi) and its role in chemoreception in the carotid body type-1 cell of the neonatal rat." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359506.

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Rakoczy, Ryan J. "Measuring the Effects of High-Fat Diet on Breathing and Oxygen-Sensitivity of the Carotid Body Type I Cell." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright1505728876488752.

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Arnold, Alexandre José Tavolari. "O papel do corpúsculo carotídeo na insuficiência cardíaca induzida pela doxorrubicina." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-05062018-121228/.

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A insuficiência cardíaca (IC) é o estágio final de diversas patologias cardíacas e apresenta alta morbimortalidade. Dentre as causas, estão os efeitos cardiotóxicos em pacientes tratados com doxorrubicina (Dox). A fisiopatologia da IC apresenta aumento da atividade barorreflexa e marcada hiperatividade simpática (HS), estado compensatório à redução do débito cardíaco. Porém, a HS prolongada culmina em alterações deletérias para o sistema cardiovascular (SC) com piora do quadro de sintomas. Atualmente muito se discute sobre o papel dos corpúsculos carotídeos (CC) na fisiopatologia da IC devido ao seu reflexo simpatotônico e a melhora de pacientes portadores de IC após a remoção dos CC. O nosso objetivo foi avaliar a influência do CC na evolução da IC induzida pela DOX. Para tal, 35 ratos Wistar machos foram dispostos em 4 grupos: controle Salina (CSAL; n=7) e Controle Dox (CDOX; n=12), Desnervado Salina (DSAL; n=4) e Desnervado Doxo (DDOX; n=12). A desnervação consistiu na ressecção do nervo sinusal bilateral prévia à administração de Dox; a indução da IC ocorreu através de 6 aplicações de Dox, na dose de 2.5mg/kg, pela via IP a cada 4 dias. Após 15 dias do término da indução, os animais foram avaliados pelo ecocardiograma e canulados para registro de pressão arterial invasiva e avaliação hemodinâmica, autonômica, barorreflexa e quimiorreflexa. A análise dos resultados mostra que o grupo CDOX apresentou redução do peso corporal, da sensibilidade baro e quimiorreflexa, hiperatividade simpática acompanhada de redução vagal, redução da morfologia cardíaca associada à disfunção diastólica e sistólica e redução do peso bruto cardíaco e ventricular. A desnervação não foi capaz de reverter os efeitos deletérios causados pela Dox, inclusive a desnervação acentuou a disfunção diastólica e sistólica induzida pela Dox. Concluiu-se que a desnervação carotídea não foi eficiente em melhorar a insuficiência cardíaca induzida pela Dox no modelo experimental proposto
Heart failure (HF) is the final stage of several cardiac pathologies and results in high morbimortality. Among the causes, we can mention the cardiotoxic effects in patients treated with doxorubicin (Dox). The pathophysiology of HF has increased baroreflex activity and marked sympathetic hyperactivity (HS), a compensatory state to the reduction of cardiac output. However, prolonged HS results in worsening of the symptoms. Currently, the role of carotid corpuscles (CC) in the pathophysiology of HF is discussed due improvement of sympathetic reflex presents in patients with HF after CC removal. The objective of this study was to evaluate the influence of CC on the evolution of HF induced by DOX for this method 35 Male Wistar rats arranged in 4 groups: Salina control (CSAL; n = 7) and Dox Control (CDOX; n = 12) Salina Denerved (DSAL; n = 4) and Dox Denerved (DDOX; n = 12). A denervation consisted of bilateral sinus nerve resection prior to Dox administration, induction of HF through 6 Dox applications at a dose of 2.5mg / kg, via IP every 4 days. After 15 days of the end of the induction, the animals were evaluated by echocardiogram and cannulated to record invasive blood pressure and hemodynamic, autonomic, baroreflex and chemorreflex evaluation. Our experiment demonstrated that the CDOX group had reduction of body weight, baro and chemoreflex sensitivity, sympathetic hyperactivity accompanied by vagal reduction, reduction of cardiac morphology associated with diastolic and systolic dysfunction and reduction of gross cardiac and ventricular weight. The denervation is not able to reverse the deleterious effects caused by Dox, including denervation accentuated by Dox-induced diastolic and systolic dysfunction. Based on our results on a carotid denervation it was not effective in improving heart failure induced by Dox
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Shaw, Karen. "Stimulus-secretion coupling in the rat carotid body." Thesis, University of Leicester, 1989. http://hdl.handle.net/2381/35148.

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The effects of a variety of agents known to stimulate chemoafferent activity were employed to define in greater detail the stimulus-secretion coupling mechanism in the rat carotid body superfused in vitro. Hypoxia, carbachol and sodium cyanide were independently able to elicit amine release. Hypoxia-evoked release was calcium dependent and was reduced by nitrendipine suggesting the involvement of voltage-dependent calcium channels in the secretory response. The effect of carbachol on catecholamine release was abolished by atropine indicating the presence of muscarinic cholinergic receptors on the Type I cells. Hypoxia-induced catecholamine release was partially blocked by atropine suggesting a possible role for muscarinic receptors in the secretory response. Hypoxia, carbachol and cyanide stimulated the release of 4 5Ca from carotid bodies pre-loaded with 4 5Ca, and the release of 4 5Ca by hypoxia or carbachol could be reduced by atropine and nitrendipine. These results suggest that the mobilization of intracellular calcium pools may also contribute to the secretory response. Carbachol was able to stimulate the efflux of [3H] inositol from pre-loaded carotid bodies and the response was abolished in the presence of atropine or lithium. Cytoplasmic concentrations of IP3 and IP3 significantly increased following stimulation with carbachol and the effect was abolished with atropine. In comparison, hypoxia was unable to induce [3H] inositol efflux and only had a moderate effect on inositol phosphate accumulation. These results suggest that carbachol may control cytosolic calcium via the formation of inositol phosphate second messengers. It is suggested that carbachol and hypoxia stimulate catecholamine secretion by altering the intracellular free calcium concentration in the Type I cells. The major effect of hypoxia was to stimulate the entry of extracellular calcium via the voltage-dependent calcium channels whereas mobilization of intracellular calcium stores was a more important event during carbachol-induced catecholamine secretion.
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Paulet, Julia. "MATURATION OF THE CAROTID BODY OXYGEN-SENSOR DURING RAT DEVELOPMENT." Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1337703804.

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Books on the topic "Rat carotid body cells"

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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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Constancio, Gonzalez, ed. The carotid body chemoreceptors. Austin: Landes Bioscience, 1997.

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Arterial Chemoreception Advances in Experimental Medicine and Biology. Springer, 2012.

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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.

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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.

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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.

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Phenylephrine-induced electrophysiological changes in cultured neonatal rat ventricular myocytes. 1995.

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Studies on calcitonin in the carotid body chief cells during development and in SIDS: Immunohistochemical localization, quantitative analysis and detection of calcitonin mRNA by in situ hybridization. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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G, O'Regan R., and International Symposium on Arterial Chemoreceptors (12th : 1993 : Dublin, Ireland), eds. Arterial chemoreceptors: Cell to system. New York: Plenum Press, 1994.

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Book chapters on the topic "Rat carotid body cells"

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Powell, Frank L., Tatsumi Kusakabe, and Mark H. Ellisman. "Effects of Chronic Hypoxia on Rat Carotid Body and Toad Carotid Labyrinth Glomus Cells." In Advances in Experimental Medicine and Biology, 365–67. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2572-1_68.

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Zhong, Huijun, and Colin Nurse. "Co-Cultures of Rat Petrosal Neurons and Carotid Body Type 1 Cells." In Frontiers in Arterial Chemoreception, 189–93. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5891-0_27.

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Gauda, Estelle B., Reed Cooper, and Shereé M. Johnson. "Autonomic Ganglion Cells : Likely Source of Acetylcholine in the Rat Carotid Body." In Advances in Experimental Medicine and Biology, 505–15. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9280-2_64.

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Böck, P. "Localization of Lysosomal Enzymes in Chromaffin Cells of the Rat Carotid Body." In Histochemistry and Cell Biology of Autonomic Neurons and Paraganglia, 125–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72749-8_22.

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Murali, Sindhubarathi, Min Zhang, and Colin A. Nurse. "Paracrine Signaling in Glial-Like Type II Cells of the Rat Carotid Body." In Advances in Experimental Medicine and Biology, 41–47. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-18440-1_5.

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Buckler, K. J. "Role of Potassium Channels in Hypoxic Chemoreception in Rat Carotid Body Type-I Cells." In Frontiers in Arterial Chemoreception, 83–87. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5891-0_11.

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Vaughan-Jones, R. D., K. J. Buckler, C. Peers, and P. C. G. Nye. "Regulation of Intracellular pH in Type I Cells of the Neonatal Rat Carotid Body." In Advances in Experimental Medicine and Biology, 251–56. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2966-8_35.

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Mokashi, A., A. Roy, C. Rozanov, P. Daudu, and S. Lahiri. "Effect of Barium on Rat Carotid Body Glomus Cell [Ca2+]i and Carotid Chemosensory Response." In Oxygen Sensing, 715–22. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/0-306-46825-5_71.

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Peers, Chris, Christopher N. Wyatt, and Keith J. Buckler. "Actions of Nicotinic Agonists on Isolated Type I Cells of the Neonatal Rat Carotid Body." In Advances in Experimental Medicine and Biology, 155–57. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2572-1_17.

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Wyatt, Christopher N., and Chris Peers. "Ca2+-Activated K+-Channels from Isolated Type I Carotid Body Cells of the Neonatal Rat." In Advances in Experimental Medicine and Biology, 159–61. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2572-1_18.

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Conference papers on the topic "Rat carotid body cells"

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Agarwal, Amit, Dong Yang, Insook Kim, and John L. Carroll. "Purinergic Modulation Of Carotid Body Glomus Cell Hypoxia Response During Postnatal Development In Rats." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4187.

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2

Attaluri, Anilchandra, Liang Zhu, and Zhongping Huang. "Targeted Brain Hypothermia Induced by an Interstitial Cooling Device in Human Neck: An Experimental Study." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205558.

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In recent years, mild or moderate hypothermia during which brain temperature is reduced to 30–35°C, has been proposed for clinical use as an adjunct for achieving protection from cerebral ischemia during cardiac bypass injury [Nussmeier 2002], carotid endarterectomy [Jamieson et al., 2003] and resection of extra-cranial aneurysm [Wagner and Zuccarello 2005], as well as stroke and traumatic brain injury [Marion et al., 1996; Marion 1997]. It has been shown that a reduction in brain temperature as small as 2°C substantially reduced ischemic cell damage [Clark et al., 1996], or improved significantly post-ischemic regional histopathology [Wass et al., 1995]. Most of the currently used clinical studies have examined only systemic hypothermia by whole body cooling. The major methodological drawback of this approach is slow cooling rate (∼0.5°/hour) due to the large volume of the human body and arteriovenous shunt vasoconstriction [Krieger et al., 2001; Marion et al., 1997; Schwab et al., 1998]. Whole body cooling does induce systemic complications. The systemic risks may outweigh the beneficial effects of neuro-hypothermia in the current clinical practice. Selective brain cooling which keeps the rest of body at normal temperature, on the other hand, can be used to maximize the neuroprotection of hypothermia.
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3

Dryjski, Maciej, Eileen Mikat, and Thorir D. Bjornsson. "IN VIVO POTENCY OF HEPARIN AND HEPARINOIDS TO INHIBIT RAT SMOOTH MUSCLE CELL PROLIFERATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644604.

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The final response of endothelial cell injury in the arterial wall is characterized by proliferation of smooth muscle cells (SMC) in the intima to form a fibro-musculo-elastic plaque. Recent in vivo and in vitro studies have shown that heparin can inhibit proliferation of SMC. These studies, however, have not elucidated the relationships between heparin dose or concentration and its in vivo antiproliferative response. In the present study, we investigated the potency of standard heparin (SH), low molecular weight heparin (LMWH) and a mixture of sulfated glycosaminoglycans (Organon 10172) with respect to the in vivo inhibition of SMC proliferation after endothelial cell injury. The injury was achieved by a short infusion of air into an isolated segment of the rat carotid artery. The drugs were administered by the AlzetR miniosmotic pumps for two weeks, at which time the animals were sacrificed and both carotid arteries were fixed in situ for light and transmission electron microscopy. The index of the intimal SMC proliferation was the maximum intima to media area (I/M) ratio. The control animals developed a marked intimal thickening (I/M: 0.97). The animals treated with 50 units/kg/hr of SH exhibited significantly less intimal hyperplasia (I/M: 0.10). With decreasing SH doses, there were increases in the I/M ratio (5 units/kg/hr, I/M: 0.44; 0.5 units/kg/hr, I/M: 0.75, and 0.05 units/kg/hr, I/M: 0.84). LMWH in doses of 50 units/kg/hr inhibited SMC proliferation as effectively as SH (I/M: 0.10), however, at doses of 15 units/kg/hr the I/M ratio was 0.55. The effect of Organon 10172 was significant at doses of 50 units/kg/hr (I/M: 0.04), but limited at doses of 15 units/kg/hr (I/M: 0.61). The APTT and anti-Xa levels were only slightly increased in the animals treated with 50 units/kg/hr of LMWH and Organon 10172, but unchanged in the animals receiving SH and the lower doses of LMWH and Organon 10172. It is concluded that SH, LMWH and Organon 10172 have significant antiproliferative effects upon SMC. The differences in the dose-response curves suggests more than one mechanism of action.
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4

Liu, Honghai, Julie X. Yun, Russel K. Pirlo, Delpine Dean, Hai Yao, Martine Laberge, and Bruce Z. Gao. "The Dependence of Mechanical Properties of Adult Rat Myocytes on Cell Alignment." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193024.

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In response to damage, stress and cell death cardiac muscle undergoes remodeling in which cardiomyocytes de-differentiate and re-differentiate. An understanding of the mechanisms involved in this process may lead to therapies to promote and enhance the repair of damaged cardiac tissue. However, due to the complexity of native environments, it is hard to investigate this remodeling process directly on tissues isolated from the body. Therefore, it is important to construct a cell-culture model that will replicate the most relevant characteristics of that tissue in controlled environments with greater capability to be assessed. Native cardiac myocytes have an aligned arrangement in which neighboring cardiomyocytes are electrically and mechanical coupled through contact junctions. When adult cardiomyocytes are placed into a culture dish, the cells will be randomly oriented and lose their native phenotypes gradually due to the lack of proper aligned cell-cell connections. To address this issue, we have implemented our laser cell micropatterning system to create an adult cardiomyocyte culturing model with aligned rows of cells connected end to end. In this abstract, we describe the experimental procedure to achieve the laser alignment of adult cardiomyocytes and the results of mechanical property testing of the myocytes investigated using Multimode Picoforce Nanoscope Atomic Force Microscope (AFM) (Veeco).
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Lieber, Samuel C., Nadine Aubry, Jayashree Pain, Gissela Diaz, Song-Jung Kim, and Stephen S. Vatner. "Measurement of the Transverse Apparent Elastic Modulus in Mammalian Cardiac Myocytes." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-41469.

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Transverse mechanical properties of mammalian cardiac myocytes, was determined by using atomic force microscopy (AFM). The AFM can be used as a nano-indentation device allowing transverse stiffness measurements to be conducted on biological cells in a physiological environment. This enables real-time biomechanical and physiological processes to be monitored with nano-scale resolution. Cellular mechanical properties were determined by indenting the cell’s body, and analyzing the indentation data with classical infinitesimal strain theory (CIST). This calculation was accomplished by modeling the AFM probe as a blunted cone. The blunted cone geometry fits the AFM force indentation data well and was used to calculate the apparent elastic modulus of the cardiac myocyte body. The mechanical properties of male 344 x Brown Norway F1 hybrid (F344×BN) rat cells was measured and an apparent elastic modulus of 35.1 ± 0.7 kPa (n = 53) was calculated. Further studies are being conducted on myocytes isolated from aged hearts to determine whether age effects cardiac mechanical properties at the level of the single myocyte.
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6

De Clerck, F., R. Van de Wiele, B. Xhonneux, L. Van Gorp, Y. Somers, W. Loots, J. Beetens, J. Van Wauwe, E. Freyne, and P. A. J. Janssen. "PLATELET TXA2 SYNTHETASE INHIBITION AND TXA2/PROSTAGLANDIN ENDOPEROXIDE RECEPTOR BLOCKADE COMBINED IN ONE MOLECULE (R 68070)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643465.

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F 68070, an oxime-alkane carboxylic acid derivative (Janssen Pharmaceutica), is a potent inhibitor of thromboxane A2 (TXA2) synthetase activity (IC50 in vitro against thrombin-stimulated human platelets in plasma : R 68070 : 2.9 x 10-8 M; CGS 13080 : 6 x 10-8 M; OKY-1581 : 8.2 x 10-8 M; dazmegrel : 2.6 x 10-8 M; dazoxiben : 2.3 x 10-8 M).The compound specifically inhibits platelet TXA2 synthetase activity (14C-arachidonic acid metabolism by washed human platelets) without effect on the cyclo-oxygenase, lipoxygenase (platelets, RBL cells) or prostacyclin synthetase activities (rat aortic rings).The inhibitory effect of R 68070 against human platelet TXA2 synthetase activity increases upon prolongation of the contact time (ICsg at 0.5 min of contact : 5.2 x 10-7 M; at 5 min : 8.3 x 10-8 M; at 30 min : 2.5 x 10-8 M) and is reversed by washing of the platelets.In vivo, the compound has a comparatively strong inhibitory effect on platelet TXA2 synthetase activity after oral administration to rats (ED50 - 2 h : R 68070 0.013 mg/kg; CGS-13080 : 0.8 mg/kg; OKY-1581 : 0.61 mg/kg; dazmegrel : 1 mg/kg; dazoxiben : 4.1 mg/kg) and a protracted duration of action in rats and dogs (inhibition 8 h after 1.25 mg/kg orally > 80 %).In vitro, R 68070 inhibits the aggregation of human platelets in plasma stimulated with collagen (IC50 : 4 x 10-6 M), but also with U 46619 (IC50 : 3.8 x 10-6 M) without affecting the primary aggregation reaction elicited by ADP, 5-HT or adrenaline. The compound thus also produces platelet TXA2/prostaglandin endoperoxide receptor blockade.In rats and in dogs R 68070 (1.25 mg/kg I.V.) potently prevents thrombus formation in carotid and coronary arteries damaged by electrical stimulation.The combination of platelet TXA2 synthetase inhibition with TXA2/prostaglandin endoperoxide blockade in one molecule thus might offer an improved anti-thrombotic effectiveness.
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7

Zhang, Qingwei, Wei Zhang, Donggang Yao, Peter I. Lelkes, and Jack G. Zhou. "The Co-Continuous Micro-Porous PLLA Scaffolds and Their Application for ACL Reconstruction." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-38291.

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Anterior cruciate ligament (ACL) reconstructive surgery is a major health concern world-wide because of a large aging population and increased occurrence of sport-related damage. Tissue engineering is a rapidly growing interdisciplinary field that offers a promising new approach for ACL repair. In order to overcome the shortages of current existing surgical fixation devices, we are combining gradient cellular structure (GCS) injection molding technique and biomedical engineering to develop novel surgical fixation devices (screw, anchor, plate, pin, staple, etc.) that not only incorporate bioactive materials such as growth factors, healing drugs and cells, but have natural bone GCS structure, intended to mimic the natural bone and promote bone tissue growth and eventually eliminate the defects associated with existing surgical fixation devices. In this work, a series of novel poly-L-lactic acid (PLLA) scaffolds with micro-porous structure were prepared by injection molding an immiscible polymer blend, with spatially controlled thermal conditioning to adjust the phase size from core to surface. The produced scaffolds were observed under SEM, which shows a co-continuous structure was created successfully through our method. The biocompatibility and the feasibility of produced micro-porous structural PLLA and PLLA/HA scaffolds as a matrix supporting cell growth tested by culturing murine osteoblasts cell line (7F2) for up to 9 days were assessed by Alamar Blue™ assay, which showed that the manufacturing process had no negative effects on cell proliferation. The cell attachment, spreading, migration and proliferation to confluence were assessed by fluorescent nuclear staining with Hoechst 33258. In order to evaluate the functional and cell biological applicability of the micro-porous structural PLLA scaffolds, a subcutaneous biodegradation test was performed through rat model for 1 week and 1 month time period, respectively. Our results showed that the micro-porous structural PLLA scaffolds are non-toxic, and they showed a mild foreign body reaction and complete fibrous encapsulation after implantation. Well created interconnected porous structure and biocompatibility suggest great potential of the micro-porous PLLA scaffolds in application for ACL reconstruction.
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