Relevant bibliographies by topics / Α7 nicotinic receptor

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Academic literature on the topic 'Α7 nicotinic receptor'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "Α7 nicotinic receptor"

1

Lavezzi, Anna. "Toxic Effect of Cigarette Smoke on Brainstem Nicotinic Receptor Expression: Primary Cause of Sudden Unexplained Perinatal Death." Toxics 6, no. 4 (October 18, 2018): 63. http://dx.doi.org/10.3390/toxics6040063.

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Among the neurotoxicants contained in tobacco smoke, if absorbed during pregnancy, nicotine significantly affects α7-nicotinic acetylcholine receptors, which play essential roles in the development of the brainstem regions receiving cholinergic projections in perinatal life. Immunohistochemical procedures for analysing formalin-fixed and paraffin-embedded brainstem samples from 68 fetuses and early newborns, with smoking and non-smoking mothers, who died of known and unknown causes, were carried out in order to determine if nicotine had activated the α7-nicotinic acetylcholine receptors. High α7-nicotinic acetylcholine receptor expression levels were only observed in the victims with smoking mothers. Frequently, these findings were associated with the hypoplasia of the brainstem structures controlling vital functions. The results of this study indicate that the exposition to nicotine in pregnancy exerts a strong direct effect on α7-nicotinic acetylcholine receptor activity especially in perinatal life and may be one of the primary risk factors leading to the sudden unexplained death of fetuses and newborns.
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2

MANEU, VICTORIA, GUILLERMO GERONA, LAURA FERNÁNDEZ, NICOLÁS CUENCA, and PEDRO LAX. "Evidence of alpha 7 nicotinic acetylcholine receptor expression in retinal pigment epithelial cells." Visual Neuroscience 27, no. 5-6 (October 8, 2010): 139–47. http://dx.doi.org/10.1017/s0952523810000246.

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AbstractSome evidence suggests that retinal pigment epithelium (RPE) can express nicotinic acetylcholine receptors (nAChRs) as described for other epithelial cells, where nAChRs have been involved in processes such as cell development, cell death, cell migration, and angiogenesis. This study is designed to determine the expression and activity of α7 nAChRs in RPE cells. Reverse transcriptase (RT)-PCR was performed to test the expression of nicotinic α7 subunit in bovine RPE cells. Protein expression was determined by Western blot and by immunocytochemistry. Expression of nicotinic α7 subunits was also analyzed in cryostat sections of albino rat retina. Changes in protein expression were tested under hypoxic conditions. Functional nAChRs were studied by examining the Ca2+transients elicited by nicotine and acetylcholine stimulation in fura-2–loaded cells. Expression of endogenous modulators of nAChRs was analyzed by RT-PCR and Western blot in retina and RPE. Cultured bovine RPE cells expressed nicotinic receptors containing α7 subunit. RT-PCR amplified the expected specific α7 fragment. Western blotting showed expression at the protein level, with a specific band being found at 57 kDa in both cultured and freshly isolated RPE cells. Expression of nAChRs was confirmed for cultured cells by immunofluorescence. Immunohistochemistry confirmed α7 receptor expression in rat RPE retina. α7 receptor expression was down-regulated by long-term hypoxia. A small subpopulation of RPE cultured cells showed functional nAChRs, as evidenced by the selective response elicited by nicotine and acetylcholine stimulation. Expression of the endogenous nicotinic receptors’ modulator lynx1 was confirmed in bovine retina and RPE, and expression of lynx1 and other endogenous nicotinic receptor modulators (SLURP1 and RGD1308195) were also confirmed in rat retina. These results suggest that nAChRs could have a significant role in RPE, which may not be related to the traditional role in nerve transmission but could more likely be related to the nonneuronal cholinergic system in the eye.
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Beckel, Jonathan M., Anthony Kanai, Sun-Ju Lee, William C. de Groat, and Lori A. Birder. "Expression of functional nicotinic acetylcholine receptors in rat urinary bladder epithelial cells." American Journal of Physiology-Renal Physiology 290, no. 1 (January 2006): F103—F110. http://dx.doi.org/10.1152/ajprenal.00098.2005.

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Although nicotinic acetylcholine receptors in both the central and peripheral nervous systems play a prominent role in the control of urinary bladder function, little is known regarding expression or function of nicotinic receptors in the bladder epithelium, or urothelium. Nicotinic receptors have been described in epithelial cells lining the upper gastrointestinal tract, respiratory tract, and the skin. Thus the present study examined the expression and functionality of nicotinic receptors in the urothelium, as well as the effects of stimulation of nicotinic receptors on the micturition reflex. mRNA for the α3, α5, α7, β3, and β4 nicotinic subunits was identified in rat urothelial cells using RT-PCR. Western blotting also confirmed urothelial expression of the α3- and α7-subunits. Application of nicotine (50 nM) to cultured rat urothelial cells elicited an increase in intracellular Ca2+ concentration, indicating that at least some of the subunits form functional channels. These effects were blocked by the application of the nicotinic antagonist hexamethonium. During in vivo bladder cystometrograms in urethane-anesthetized rats, intravesical administration of nicotine, choline, or the antagonists methyllycaconitine citrate and hexamethonium elicited changes in voiding parameters. Intravesical nicotine (50 nM, 1 μM) increased the intercontraction interval. Intravesical choline (1–100 μM) also affected bladder reflexes similarly, suggesting that α7 nicotinic receptors mediate this effect. Intravesical administration of hexamethonium (1–100 μM) potentiated the nicotine-induced changes in bladder reflexes. Methyllycaconitine citrate, a specific α7-receptor antagonist, prevented nicotine-, choline-, and hexamethonium-induced bladder inhibition. These results are the first indication that stimulation of nonneuronal nicotinic receptors in the bladder can affect micturition.
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Wongtrakool, Cherry, Susanne Roser-Page, Hilda N. Rivera, and Jesse Roman. "Nicotine alters lung branching morphogenesis through the α7 nicotinic acetylcholine receptor." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 3 (September 2007): L611—L618. http://dx.doi.org/10.1152/ajplung.00038.2007.

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There is abundant epidemiological data linking prenatal environmental tobacco smoke with childhood asthma and wheezing, but the underlying molecular and physiological mechanisms that occur in utero to explain this link remain unelucidated. Several studies suggest that nicotine, which traverses the placenta, is a causative agent. Therefore, we studied the effects of nicotine on lung branching morphogenesis using embryonic murine lung explants. We found that the expression of α7 nicotinic acetylcholine receptors, which mediate many of the biological effects of nicotine, is highest in pseudoglandular stage lungs compared with lungs at later stages. We then studied the effects of nicotine in the explant model and found that nicotine stimulated lung branching in a dose-dependent fashion. α-Bungarotoxin, an antagonist of α7 nicotinic acetylcholine receptors, blocked the stimulatory effect of nicotine, whereas GTS-21, a specific agonist, stimulated branching, thereby mimicking the effects of nicotine. Explants deficient in α7 nicotinic acetylcholine receptors did not respond to nicotine. Nicotine also stimulated the growth of the explant. Altogether, these studies suggest that nicotine stimulates lung branching morphogenesis through α7 nicotinic acetylcholine receptors and may contribute to dysanaptic lung growth, which in turn may predispose the host to airway disease in the postnatal period.
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Dhar, S., F. Nagy, J. M. McIntosh, and H. N. Sapru. "Receptor subtypes mediating depressor responses to microinjections of nicotine into medial NTS of the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 1 (July 1, 2000): R132—R140. http://dx.doi.org/10.1152/ajpregu.2000.279.1.r132.

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Microinjections (50 nl) of nicotine (0.01–10 μM) into the nucleus of the solitary tract (NTS) of adult, urethan-anesthetized, artificially ventilated, male Wistar rats, elicited decreases in blood pressure and heart rate. Prior microinjections of α-bungarotoxin (α-BT) and α-conotoxin ImI (specific toxins for nicotinic receptors containing α7 subunits) elicited a 20–38% reduction in nicotine responses. Similarly, prior microinjections of hexamethonium, mecamylamine, and α-conotoxin AuIB (specific blockers or toxin for nicotinic receptors containing α3β4 subunits) elicited a 47–79% reduction in nicotine responses. Nicotine responses were completely blocked by prior sequential microinjections of α-BT and mecamylamine into the NTS. Complete blockade of excitatory amino acid receptors (EAARs) in the NTS did not attenuate the responses to nicotine. It was concluded that 1) the predominant type of nicotinic receptor in the NTS contains α3β4 subunits, 2) a smaller proportion contains α7 subunits, 3) the presynaptic nicotinic receptors in the NTS do not contribute to nicotine-induced responses, and 4) EAARs in the NTS are not involved in mediating responses to nicotine.
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Jones, Candace. "α7 Nicotinic Acetylcholine Receptor." Journal of Clinical Psychopharmacology 38, no. 3 (June 2018): 247–49. http://dx.doi.org/10.1097/jcp.0000000000000859.

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Pinheiro, Nathalia M., Rosana Banzato, Iolanda Tibério, Marco A. M. Prado, Vânia F. Prado, Ayman K. Hamouda, and Carla M. Prado. "Acute Lung Injury in Cholinergic-Deficient Mice Supports Anti-Inflammatory Role of α7 Nicotinic Acetylcholine Receptor." International Journal of Molecular Sciences 22, no. 14 (July 14, 2021): 7552. http://dx.doi.org/10.3390/ijms22147552.

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(1) Background: The lung cholinergic pathway is important for controlling pulmonary inflammation in acute lung injury, a condition that is characterized by a sudden onset and intense inflammation. This study investigated changes in the expression levels of nicotinic and muscarinic acetylcholine receptors (nAChR and mAChR) in the lung during acute lung injury. (2) Methods: acute lung injury (ALI) was induced in wild-type and cholinergic-deficient (VAChT-KDHOM) mice using intratracheal lipopolysaccharide (LPS) instillation with or without concurrent treatment with nicotinic ligands. Bronchoalveolar lavage fluid was collected to evaluate markers of inflammation, and then the lung was removed and processed for isolation of membrane fraction and determination of acetylcholine receptors level using radioligand binding assays. (3) Results: LPS-induced increase in lung inflammatory markers (e.g., neutrophils and IL-1β) was significantly higher in VAChT-KDHOM than wild-type mice. In contrast, LPS treatment resulted in a significant increase in lung’s α7 nicotinic receptor level in wild-type, but not in VAChT-KDHOM mice. However, treatment with PNU 282987, a selective α7 nicotinic receptor agonist, restored VAChT-KDHOM mice’s ability to increase α7 nicotinic receptor levels in response to LPS-induced acute lung injury and reduced lung inflammation. LPS also increased muscarinic receptors level in VAChT-KDHOM mice, and PNU 282987 treatment reduced this response. (4) Conclusions: Our data indicate that the anti-inflammatory effects of the lung cholinergic system involve an increase in the level of α7 nicotinic receptors. Pharmacological agents that increase the expression or the function of lung α7 nicotinic receptors have potential clinical uses for treating acute lung injury.
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Strang, Christianne E., Ye Long, Konstantin E. Gavrikov, Franklin R. Amthor, and Kent T. Keyser. "Nicotinic and muscarinic acetylcholine receptors shape ganglion cell response properties." Journal of Neurophysiology 113, no. 1 (January 1, 2015): 203–17. http://dx.doi.org/10.1152/jn.00405.2014.

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The purpose of this study was to evaluate the expression patterns of nicotinic and muscarinic ACh receptors (nAChRs and mAChRs, respectively) in relation to one another and to understand their effects on rabbit retinal ganglion cell response properties. Double-label immunohistochemistry revealed labeled inner-retinal cell bodies and complex patterns of nAChR and mAChR expression in the inner plexiform layer. Specifically, the expression patterns of m1, m4, and m5 muscarinic receptors overlapped with those of non-α7 and α7 nicotinic receptors in presumptive amacrine and ganglion cells. There was no apparent overlap in the expression patterns of m2 muscarinic receptors with α7 nicotinic receptors or of m3 with non-α7 nicotinic receptors. Patch-clamp recordings demonstrated cell type-specific effects of nicotinic and muscarinic receptor blockade. Muscarinic receptor blockade enhanced the center responses of brisk-sustained/G4 On and G4 Off ganglion cells, whereas nicotinic receptor blockade suppressed the center responses of G4 On-cells near the visual streak but enhanced the center responses of nonstreak G4 On-cells. Blockade of muscarinic or nicotinic receptors suppressed the center responses of brisk-sustained Off-cells and the center light responses of subsets of brisk-transient/G11 On- and Off-cells. Only nicotinic blockade affected the center responses of G10 On-cells and G5 Off-cells. These data indicate that physiologically and morphologically identified ganglion cell types have specific patterns of AChR expression. The cholinergic receptor signatures of these cells may have implications for understanding visual defects in disease states that result from decreased ACh availability.
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Ouchi, Yasuomi. "PET imaging of α7 nicotinic receptor." Folia Pharmacologica Japonica 145, no. 5 (2015): 266–67. http://dx.doi.org/10.1254/fpj.145.266.

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Liu, Qing-Song, and Darwin K. Berg. "Extracellular Calcium Regulates Responses of Both α3- and α7-Containing Nicotinic Receptors on Chick Ciliary Ganglion Neurons." Journal of Neurophysiology 82, no. 3 (September 1, 1999): 1124–32. http://dx.doi.org/10.1152/jn.1999.82.3.1124.

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Neuronal nicotinic receptors are generally both permeable to calcium and potentiated by it. We have examined acute calcium regulation of both native α7-containing and the less abundant α3-containing nicotinic receptors on chick ciliary ganglion neurons. Most of the receptors are concentrated on somatic spines tightly overlaid in situ by a large presynaptic calyx. Whole cell patch-clamp recording from dissociated neurons using perforated patch-clamp techniques indicates that the rapidly desensitizing nicotinic response of α7-containing receptors achieves maximum amplitude in 2 mM calcium; both lower and higher concentrations of calcium are less effective. Barium and strontium but not magnesium can substitute for calcium in potentiating the response. Neither calcium current through the receptors nor calcium action at intracellular sites is necessary. These latter conclusions are supported by current-voltage analysis of the nicotine-induced response, ion substitution experiments, and internal perfusion of the cells with 1,2-bis-(2-aminophenoxy)-ethane- N,N,N′,N′-tetraacetic acid (BAPTA) via a conventional patch pipette. Varying the agonist concentration indicates that some of the calcium-dependent enhancement may involve a shift in the dose-response curve for agonist binding, but much of the effect is also likely to involve increased receptor responsiveness. Blockade of α7-containing receptors with α-bungarotoxin showed that the heteromeric α3-containing nicotinic receptors also undergo calcium-dependent potentiation. Calcium did not have a major effect on the desensitization rate of either receptor class but did have a selective effect on the rise time of α7-containing receptors. Analysis of stably transfected cells expressing an α7 gene construct showed that the calcium potentiation observed for native receptors did not require neuron-specific modifications or components and that it could be seen with the natural agonist acetylcholine. Receptor dependence on extracellular calcium may provide a regulatory mechanism for constraining synaptic signaling, avoiding local depletion of external calcium, and limiting calcium buildup in postsynaptic compartments.
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Dissertations / Theses on the topic "Α7 nicotinic receptor"

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Brown, Jack. "α7 Nicotinic acetylcholine receptor-mediated calcium signalling in neuronal cells." Thesis, University of Bath, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.636524.

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α7 nicotinic acetylcholine receptors (nAChR) are highly permeable to Ca2+ and are clinical targets for Alzheimer’s disease and schizophrenia. The aim of this work was to examine α7 nAChR-mediated Ca2+ signalling in neuronal cells using three different methods, and to evaluate the effects of the desensitizing agonist and prototypical smoking-cessation drug sazetidine-A on α7 nAChRs. Initial studies used 96-well plate assays with SH-SY5Y cells to characterize responses evoked by the α7 nAChR-selective agonist PNU-282987 and positive allosteric modulator PNU-120596. This was complemented by live-imaging of cortical cultures, where the compounds evoked robust Ca2+ responses from 12 % of cells. Co- application with Cd2+, ryanodine and xestospongin-C significantly inhibited these responses, suggesting the involvement of voltage-gated Ca2+ channels and Ca2+- induced Ca2+-release. CNQX and MK801 also significantly inhibited α7 nAChR mediated Ca2+ elevations, indicating a role for glutamate release. A high-content screening assay was developed to further examine these phenomena. Exploratory experiments using KCl, AMPA and NMDA validated a protocol that could be used to image Ca2+ elevations in large cell populations. Inconsistent responses to PNU-120596 and PNU2-282987 were also observed, reflecting the scarcity of α7 nAChRs in cortical cultures and the need for assay optimization. Combination with immunofluorescent labelling revealed α7 nAChR mediated Ca2+ elevations in a subpopulation of astrocytes and neurons, some of which were GABAergic. PNU-120596 potentiated the effects of sazetidine-A in SH-SY5Y cells (EC50 0.4 μM) eliciting responses in 14 % of cells in cortical cultures in a methyllycaconitine- sensitive manner, consistent with α7 nAChR activation. Pre-incubation with sazetidine-A concentration-dependently attenuated subsequent α7 nAChR-mediated responses in SH-SY5Y cells (IC50 476 nM) and cortical cultures, suggesting that α7 nAChRs could play a role in the behavioural effects of sazetidine-A. These comparative experiments enhance our understanding of α7 nAChR signalling and provide a new method to study them further.
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Young, Jared W. "Nicotine induced improvements in cognition : a possible role for the α7 nicotinic acetylcholine receptor." Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/27731.

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Assessment of sustained attention in rodents can be performed using the 5-choice serial reaction-time (5-CSR) task; analogous to the continuous performance test used in man. A 5-CSR protocol was established which allowed the demonstration of nicotine-induced improvements in sustained attention in mice. In this task α7 nAChR knockout (KO) mice exhibited impaired acquisition and performance, providing additional evidence that this receptor may be a valid therapeutic target for cognitive enhancement. In order to investigate the role of nAChR manipulation on working memory, the odour span task, a test of olfactory working memory capacity, was established in mice. Nicotine administration did not improve performance of C57B1/6J mice probably as a consequence of ceiling effects. Transgenic mice over-expressing human caspase-3 (hc-3) displayed a robust impairment in the task that was attenuated by nicotine administration. Moreover α7 nAChR KO mice exhibited impaired acquisition and performance in the task but in a different pattern to that of the hc-3 mice. This pattern may reflect an impaired ability to attend to the task as opposed to a working memory deficit alone. These demonstrations provide further support for a role of the α7 nAChR in cognition. Tg2576 mice represent the best well characterised transgenic model of AD, however there remains a dearth of information on their attentional and olfactory capabilities. The mice exhibited a deficit in sustained attention in the 5-CSR task, as well as an age-related impairment in the odour span task. In conclusion the development of the 5-CSR task for mice was used to identify a nicotine-induced improvement in normal mice and impaired performance in α7 KO and Tg2576 mice. In summary these data provide some evidence for a role of the α7 nAChR in nicotine-induced improvement in cognition, and with the tasks developed provide new tools for the assessment of putative cognitive enhancing compounds.
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Chandley, Michelle Johnson. "Elucidating the Role of the α7 Nicotinic Receptor in the Etiology of Schizophrenia." Digital Commons @ East Tennessee State University, 2008. https://dc.etsu.edu/etd/1995.

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The α7 subunit of the nicotinic receptor, a ligand gated ion channel with an affinity for nicotine, has long been implicated in the pathophysiology of schizophrenia due to the extremely high rate of smoking within the patient population. However, the exact role of the receptor has never fully been determined. In the following studies, various functions the receptor may assume in disease state are evaluated. There is a strong relationship between the immune system and schizophrenia, with the α7 subunit possibly serving as the link between the two. One of the following studies looks at the possibility of the receptor functioning as antigen in an autoimmune response. Blood sera of schizophrenic patients, as well as controls, were analyzed for the presence of antibodies to the α7 subunit of the nicotinic receptor. A sensitive ligand-based assay revealed schizophrenic patients could possess a pathogenic level of antibody that may exacerbate the degenerative nature of the disease, allowing for the possibility that receptor antibodies may serve as a contributing factor in the etiology of the disorder in at least a subset of patients. In other studies, the expression of the α7 receptor was investigated. Recombinant α7 receptor production has eluded researchers in non-mammalian species and this was the focus of our initial studies. In general, the lack of sufficient molecular recombinant techniques utilizing the receptor makes characterization of the α7 receptor and it's specific protein interactions difficult to evaluate. The regulatory mechanisms of the nicotinic receptor α7 subunit production and receptor formation have yet to be completely elucidated. Results in this investigation found a relationship between a functional CRE-element in the promoter region.
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Nishio, Takahiro. "Hepatic vagus nerve regulates Kupffer cell activation via α7 nicotinic acetylcholine receptor in nonalcoholic steatohepatitis." Kyoto University, 2017. http://hdl.handle.net/2433/225984.

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Peterson, Daniel J., Jim Wherry, Elizabeth D. Cummins, Don Hoover, and Russell W. Brown. "The Role of the Α7 and Α4β2 Nicotinic Receptors in Nicotine Sensitization and Neural Plasticity of Adolescent Rats Neonatally Treated with Quinpirole: Effects on Mtor and Nicotinic Receptor Density." Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/etsu-works/2769.

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Aims: (1) Analyze the roles of α7 and α4β2 nicotinic receptors (nAChRs) in nicotine sensitization in adolescent male and female rats neonatally treated with quinpirole as well as their effects on brain-derived neurotrophic factor (BDNF) and mammalian target of rapamycin (mTOR) 1 h and 24 h post drug treatment. (2) Analyze the effects of behavioral sensitization to nicotine on α7 and α4β2 nAChR density in the nucleus accumbens and dorsal striatum. Methods: Animals were neonatally treated with quinpirole (1 mg/kg) or saline from postnatal days (P)1-21. Beginning on P33, animals were ip injected with nicotine (0.5 mg/kg free base) or saline and tested every second day from P33-49. Approximately 30 min before injection, animals were ip injected with either the α7 nicotinic receptor (nAChR) antagonist methllycacontine (MLA; 2 or 4 mg/kg) or the α4β2 nAChR antagonist dihyro-β-erythrodine (DhβE; 1 or 3 mg/kg). Brain tissue was taken either 1 h or 24 h after the last day of testing. In a second experiment, animals were identically treated and brain tissue analyzed for nAChR density using the autoradiographic technique. Results: Neonatal quinpirole enhanced nicotine sensitization and the 3 mg/kg dose DhβE effectively blocked nicotine sensitization on Day 9 but enhanced the hypoactive response to nicotine on Day 1. MLA appears more important in the acute response to nicotine. Neonatal quinpirole sensitized the accumbal BDNF response to nicotine, but resulted in a decrease of accumbal mTOR. The nAChR density data will be presented. Conclusions: The α4β2 receptor played a critical role in the development of adolescent nicotine sensitization, and both nAChRs appear to be important in accumbal BDNF and in the mTOR response, demonstrating their important role in synaptic strength.
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Davy, Robert Carlos Barton. "Development of a transient expression system for the α7 neuronal nicotinic acetylcholine receptor in mammalian cells." Thesis, University of Bath, 1995. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295445.

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Peterson, Daniel J., Wesley Drew Gill, John M. Dose, Donald B. Hoover, James R. Pauly, Elizabeth D. Cummins, Katherine C. Burgess, and Russell W. Brown. "The Effects of Nicotine in the Neonatal Quinpirole Rodent Model of Psychosis: Neural Plasticity Mechanisms and Nicotinic Receptor Changes." Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/etsu-works/942.

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Neonatal quinpirole (NQ) treatment to rats increases dopamine D2 receptor sensitivity persistent throughout the animal’s lifetime. In Experiment 1, we analyzed the role of α7 and α4β2 nicotinic receptors (nAChRs) in nicotine behavioral sensitization and on the brain-derived neurotrophic factor (BDNF) response to nicotine in NQ- and neonatally saline (NS)-treated rats. In Experiment 2, we analyzed changes in α7 and α4β2 nAChR density in the nucleus accumbens (NAcc) and dorsal striatum in NQ and NS animals sensitized to nicotine. Male and female Sprague-Dawley rats were neonatally treated with quinpirole (1mg/kg) or saline from postnatal days (P)1-21. Animals were given ip injections of either saline or nicotine (0.5mg/kg free base) every second day from P33 to P49 and tested on behavioral sensitization. Before each injection, animals were ip administered the α7 nAChR antagonist methyllycaconitine (MLA; 2 or 4mg/kg) or the α4β2 nAChR antagonist dihydro beta erythroidine (DhβE; 1 or 3mg/kg). Results revealed NQ enhanced nicotine sensitization that was blocked by DhβE. MLA blocked the enhanced nicotine sensitization in NQ animals, but did not block nicotine sensitization. NQ enhanced the NAcc BDNF response to nicotine which was blocked by both antagonists. In Experiment 2, NQ enhanced nicotine sensitization and enhanced α4β2, but not α7, nAChR upregulation in the NAcc. These results suggest a relationship between accumbal BDNF and α4β2 nAChRs and their role in the behavioral response to nicotine in the NQ model which has relevance to schizophrenia, a behavioral disorder with high rates of tobacco smoking.
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Vetel, Steven. "Neuroinflammation et neuroprotection dans un modèle de maladie de Parkinson précoce (lésion à la 6-hydroxydopamine chez le rat)." Thesis, Tours, 2018. http://www.theses.fr/2018TOUR3309/document.

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Les stratégies thérapeutiques mises en place dans la maladie de Parkinson sont symptomatiques et ne permettent pas de ralentir la progression de la maladie, nécessitant le développement de nouvelles approches neuroprotectrices. La neuroinflammation joue un rôle majeur dans le processus neurodégénératif où elle se manifeste précocement par l’activation de cellules gliales (microglie et astrocytes). En s’appuyant sur l’utilisation de modèles animaux mimant les stades précoces de la maladie, l’élaboration de stratégies thérapeutiques à visée anti-inflammatoire constitue donc une approche thérapeutique prometteuse. Ce travail de thèse a consisté à mettre au point et à caractériser un modèle de lésion partielle à la 6-hydroxydopamine chez le rat afin d’évaluer les effets d’une stratégie thérapeutique originale basée sur l’utilisation en combinaison d’un agoniste des récepteurs nicotiniques α7 et d’un agoniste des récepteurs σ1. En utilisant différentes approches expérimentales, nous avons tout d’abord évalué le processus neurodégénératif et la neuroinflammation dans le modèle que nous avons mis en place. Nos résultats ont montré une dégénérescence partielle et reproductible des neurones dopaminergiques nigro-striataux associée à une importante neuroinflammation. Nos analyses métabolomiques ont également révélé plusieurs altérations spécifiques, apportant ainsi de nouvelles informations sur les mécanismes intervenant dans le processus neurodégénératif. En s’appuyant sur l’utilisation de la tomographie par émission de positrons, nous avons ensuite évalué longitudinalement le profil d’expression des récepteurs nicotiniques α7 dans les structures clés de la voie nigrostriée. Nos résultats ont montré des modifications transitoires de la densité de ces récepteurs pouvant être liées à des réponses microgliales biphasiques en association avec la cinétique de la dégénérescence neuronale. Ainsi, ces résultats renforcent l’idée de cibler spécifiquement les récepteurs nicotiniques α7 dans l’atténuation des processus neuroinflammatoires. Nous avons enfin évalué les effets de notre stratégie thérapeutique dans le modèle et nos résultats ont permis de montrer que ce type de combinaison préserve partiellement l’intégrité des neurones dopaminergiques nigro-striataux et réduit les réactions gliales chez les animaux lésés. Bien qu’il sera nécessaire de confirmer et de compléter ces résultats avec d’autres analyses, ce type de combinaison pourrait constituer une nouvelle entité biochimique prometteuse dans le traitement de la maladie de Parkinson
Currently, therapeutic strategies in Parkinson’s disease are symptomatic and the progression of the disease is uncontrolled, requiring the development of new neuroprotective approaches. Neuroinflammation plays a major role in the neurodegenerative process where it occurs early through the activation of glial cells (microglia and astrocytes). Based on the use of animal models mimicking the early stages of the disease, the development of anti-inflammatory strategies is therefore a promising therapeutic approach. This thesis work consisted in the development and the characterisation of a partial 6-hydroxydopamine lesion model in rats in order to evaluate the effects of an original therapeutic strategy based on the combined use of a α7 nicotinic receptors agonist and a σ1 receptors agonist. Using different experimental approaches, we first evaluated the neurodegenerative and neuroinflammation processes in the model that we developped. Our results showed a partial and reproductible degeneration of nigro-striatal dopaminergic neurons associated with a marked neuroinflammation. Our metabolic analyses have also revealed several specific alterations, providing new insight on the mechanisms involved in the neurodegenerative process. Using positron emission tomography imaging, we then evaluated longitudinally the expression profile of α7 nicotinic receptors in the key structures of the nigro-striatal pathway. Our results showed transient changes in the density of these receptors that may be linked to biphasic microglial responses in association with the kinetics of neuronal degeneration. Thus, these results reinforce the hypothesis of specifically targeting α7 nicotinic receptors in order to reduce the neuroinflammatory processes. Finally, we evaluated the effects of our therapeutic strategy in the model and our results showed that this type of combination partially preserves the integrity of nigro-striatal dopaminergic neurons and reduces glial reactions in lesioned animals. Although it is necessary to confirm and extend these results, this type of combination could represent a promising new pharmacological approach in the treatment of Parkinson’s disease
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Jackson, Asti. "Investigating the Modulation and Mechanisms of α7 Nicotinic Acetylcholine Receptors in Nicotine Dependence." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4851.

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Tobacco dependence dramatically increases health burdens and financial costs. Limitations of current smoking cessation therapies indicate the need for improved molecular targets. Nicotine, the main addictive component of tobacco, exerts its dependency effects via nicotinic acetylcholine receptors (nAChRs). The homomeric α7 nAChR is one of the most abundant receptors found in the brain and has unique features in comparison to other nAChR subtypes such as high calcium permeability, low probability of channel opening, and a rapid desensitization rate. α7 nAChR agonists reduce nicotine's rewarding properties in the conditioned place preference (CPP) test and i.v. self-administration. Recently, the peroxisome proliferator-activated receptor type-α (PPARα) has been implicated as a downstream signaling target of the α7 nAChR in ventral tegmental area dopamine cells. It is unknown whether the intrinsic characteristics of the α7 nAChR and PPARα are involved in its attenuation of nicotine reward. Therefore, this dissertation sought to investigate the role of α7 nAChRs in a mouse model of nicotine CPP and nicotine withdrawal by 1) investigating the impact of pharmacological modulation of α7 nAChR function in nicotine dependence and 2) evaluating a possible role for PPARα as a downstream mediator of α7 nAChRs in nicotine dependence. Positive allosteric modulators (PAMs) and a silent agonist were used to investigate the role of α7 nAChR conformations. The utilization of the α7 nAChR Type I PAM NS1738, Type II PAM PNU120596, and silent agonist NS6740 provided insight about the probability of channel opening (NS1738, PNU120596), desensitization (PNU120596, NS6740), and modulation of the endogenous acetylcholine/ choline tone (NS1738, PNU120596) as it relates to the α7 nAChR in nicotine CPP and withdrawal. In addition, this dissertation sought to elucidate the role of the α7 nAChR and PPARα in nicotine dependence using pharmacological interventions. The results suggest that the role of the α7 nAChR in nicotine dependence is conformation-dependent and PPARα-mediated. This dissertation is the first to report PPARα-mediation of the effects of α7 nAChR in nicotine reward and attenuation of nicotine withdrawal signs by PPARα activation. This data supports the development of α7 nAChR agonists and PPARα activators as possible smoking cessation aids.
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Hammond, Victoria. "α7 nicotinic acetylcholine receptors at the glutamatergic synapse." Thesis, University of Bath, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633163.

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Nicotinic acetylcholine receptor (nAChR) activation is neuroprotective and nicotine is a cognitive enhancer. Loss of nAChRs, deposition of tau neurofibrillary tangles, cleavage of amyloid precursor protein (APP) and inflammation are well documented in the pathogenesis of Alzheimer’s disease (AD). Sequential cleavage of APP by β- and γ-secretase enzymes generates soluble Aβ peptides, with oligomeric forms of Aβ implicated in both the control of synaptic excitability and dysregulation of synaptic transmission and induction of neuronal death in AD. Aβ production is inhibited by calcium-dependent recruitment of α-secretase, as exemplified by activation of N-methyl-D-aspartate receptors (NMDAR). All neurodegenerative diseases are associated with inflammation, arising from altered homeostasis of the innate immune system, resulting in heightened activation of immune cells and induction of a pro-inflammatory environment. Stimulation of the α7 subtype of nAChR is anti-inflammatory and also enhances cognition and promotes neuronal survival. This work addressed the hypotheses that stimulation of highly calcium-permeable α7nAChR inhibits Aβ production by promoting α-secretase-mediated processing of APP and also modulates inflammatory cellular behaviour of microglia. Thus, this study assessed the role of α7nAChR at glutamatergic synapses, through probing effects on APP processing and phagocytosis in primary cortical neurons and microglia, respectively. Primary cortical neurons expressed functional α7nAChR and glutamate receptors, and through a number of experimental approaches, including immunoblotting and a cleavage reporter assay, results indicated α7nAChR activation with the α7nAChR-selective agonist PNU-282987 and positive allosteric modulator PNU-120596 had no effect on APP and Tau, in contrast to NMDAR activation that significantly modulated these proteins. Data suggest low expression of α7nAChR, coupled with distinct localisation of presynaptic α7nAChR and postsynaptic APP could explain the lack of effect. In addition, primary microglia were highly responsive to lipopolysaccharide and possessed functional α7nAChR that coupled to ERK phosphorylation. Microglial α7nAChR activation promoted neuroprotective phagocytic behaviour, in agreement with the ‘cholinergic anti-inflammatory pathway’. This study supports the hypothesis that α7nAChR are modulators of anti-inflammatory behaviour, thus α7nAChR-selective ligands are viable candidates for the treatment of AD and promoting cognitive enhancement.
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Book chapters on the topic "Α7 nicotinic receptor"

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Oz, Murat, Georg Petroianu, and Dietrich E. Lorke. "α7-Nicotinic Acetylcholine Receptors: New Therapeutic Avenues in Alzheimer’s Disease." In Nicotinic Acetylcholine Receptor Technologies, 149–69. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3768-4_9.

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Lorke, Dietrich E., Georg Petroianu, and Murat Oz. "α7-Nicotinic Acetylcholine Receptors and β-Amyloid Peptides in Alzheimer’s Disease." In Nicotinic Acetylcholine Receptor Technologies, 171–205. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3768-4_10.

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Li, Ming D. "Nicotine Modulates Innate Immune Pathways via α7 Nicotinic Acetylcholine Receptor." In Tobacco Smoking Addiction: Epidemiology, Genetics, Mechanisms, and Treatment, 287–302. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7530-8_16.

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Helekar, Santosh A., Lorna Colquhoun, Hong Dang, Danong Chen, Finn Goldner, and Jim Patrick. "A Cyclophilin-Dependent Mechanism for α7 Neuronal Nicotinic Acetylcholine Receptor Maturation." In Effects of Nicotine on Biological Systems II, 29–35. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7445-8_4.

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Olincy, Ann, and Robert Freedman. "Nicotinic Mechanisms in the Treatment of Psychotic Disorders: A Focus on the α7 Nicotinic Receptor." In Novel Antischizophrenia Treatments, 211–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-25758-2_8.

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Deutsch, Stephen I., and Jessica A. Burket. "An Evolving Therapeutic Rationale for Targeting the α7 Nicotinic Acetylcholine Receptor in Autism Spectrum Disorder." In Behavioral Pharmacology of the Cholinergic System, 167–208. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/7854_2020_136.

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Hajós, Mihály, and Bruce N. Rogers. "α7 Nicotinic Acetylcholine Receptors in the Treatment of Schizophrenia." In Targets and Emerging Therapies for Schizophrenia, 319–54. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118309421.ch12.

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Berg, Darwin K., Zhong-wei Zhang, William G. Conroy, Phyllis C. Pugh, Roderick A. Corriveau, Suzanne J. Romano, Margaret M. Rathouz, Bo Huang, and Sukumar Vijayaraghavan. "Expression, Function, and Regulation of Neuronal Acetylcholine Receptors Containing the α7 Gene Product." In Effects of Nicotine on Biological Systems II, 61–68. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7445-8_8.

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Uteshev, Victor V. "α7 Nicotinic ACh Receptors as a Ligand-Gated Source of Ca2+ Ions: The Search for a Ca2+ Optimum." In Advances in Experimental Medicine and Biology, 603–38. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2888-2_27.

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Martin, Laura F., and Robert Freedman. "Schizophrenia and the α7 Nicotinic Acetylcholine Receptor." In International Review of Neurobiology, 225–46. Elsevier, 2007. http://dx.doi.org/10.1016/s0074-7742(06)78008-4.

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Conference papers on the topic "Α7 nicotinic receptor"

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Dicpinigaitis, Peter, Brendan Canning, Robert DeVita, Michael Perelman, Qi Liu, Douglas Hay, and Jing Liang. "The antitussive effects of alpha7 (α7) nicotinic receptor agonists." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa4409.

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Batista, Victor de Sousa, Lourival Rodrigues de Sousa Neto, Roberto Ribeiro Faria, Keli Cristina Barbosa dos Reis, and Nailton Monteiro do Nascimento Júnior. "Post-processing of docking results through docking-based comparative intermolecular contacts analysis (dbCICA) of the α4β2 and α7 nicotinic acetylcholine receptors (nAChRs)." In VIII Simpósio de Estrutura Eletrônica e Dinâmica Molecular. Universidade de Brasília, 2020. http://dx.doi.org/10.21826/viiiseedmol2020146.

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The nAChRs are pentameric ligand-gated ionic channels that respond to the endogenous neurotransmitter acetylcholine, with the α4β2 and α7 subtypes being highly expressed in human brain. Those receptors are involved in many neurologic disorders such as Alzheimer’s disease and Schizophrenia, as well as in nicotine addiction. In this context, molecular modelling is a powerful tool for designing novel ligands targeting those receptors. In the present work, we applied dbCICA1 to identify optimal docking conditions for these two receptors. The methodology and results are summarized bellow. Briefly, bioactive compounds acting on each receptor where docked into the crystal structures obtained from PDB (5KXI2 for α4β2 and 5AFH3 for α7) using GOLD4 and the results were post-processed through dbCICA, a genetic algorithm based approach.
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Wongtrakool, C., HN Rivera, S. Roser-Page, and J. Roman. "Nicotine Induced Nerve Growth Factor Expression Is through α7 Nicotinic Acetylcholine Receptor Mediated Signals." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2429.

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Hong, Huixiao, Carmine Leggett, and Suguna Sakkiah. "Development of Nicotinic Acetylcholine Receptor nAChR α7 Binding Activity Prediction Model." In BCB '17: 8th ACM International Conference on Bioinformatics, Computational Biology, and Health Informatics. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3107411.3108191.

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McLoughlin, Wesley KX, Christophe Lucatelli, Dan Peters, Andrew H. Baker, David E. Newby, Patrick Hadoke, Adriana AS Tavares, and Mark G. MacAskill. "P3 α7 nicotinic acetylcholine receptor expression in vascular cells during normoxia and hypoxia." In The Scottish Cardiovascular Forum 2019, Saturday 2nd February 2019, The Centre for Health Science, Old Perth Road, Inverness, Scotland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-scf.11.

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Ma, J. D., Y. S. Mou, T. Yan, J. Jing, Y. Q. Mo, Y. L. Chen, and L. Dai. "SAT0036 Nicotine promotes mmp-3 and rankl secretion through overexpressed nicotinic acetylcholine receptor Α7 in rheumatoid arthritis fibroblast-like synoviocytes." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5115.

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Yilmazer, Selma. "Inhibition of nicotinic acetylcholine receptor nAChR α7 effects expression of BDNF in olfactory bulb organotypic slice cultures." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.400.

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Wang, Q., J. Lucas, I. K. Sundar, and I. Rahman. "Electronic-Cigarette Induces Dysregulated Repair Response and Extracellular Matrix Remodeling in Mouse Lung Via α7 Nicotinic Acetylcholine Receptor." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6240.

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Sobus, Samantha L., Michelle A. Romano, and Graham W. Warren. "Abstract 3948: The role of α7 nicotinic acetylcholine receptor activation and pharmacologic tobacco cessation agents on response to radiotherapy." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3948.

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Kyte, S. Lauren, Wisam Toma, Ganeshsingh Thakur, M. Imad Damaj, and David A. Gewirtz. "Abstract 602: The α7 nicotinic acetylcholine receptor silent agonist R-47 prevents and reverses paclitaxel-induced peripheral neuropathy without enhancing the proliferation of lung cancer cells or interfering with paclitaxel-induced antitumor activity." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-602.

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