Relevant bibliographies by topics / Neurokinin

Academic literature on the topic 'Neurokinin'

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Published: 4 June 2021
Last updated: 27 January 2023

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Journal articles on the topic "Neurokinin"

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Dobbins, David E. "Neuropeptide modulation of lymphatic smooth muscle tone in the canine forelimb." Mediators of Inflammation 1, no. 4 (1992): 241–46. http://dx.doi.org/10.1155/s096293519200036x.

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Neurokinin A and B are putative inflammatory mediators. We assessed their ability to alter prenodal lymphatic resistance. Intralymphatic neurokinin A (3.0 × 10−6, 3.0 × 10−5and 3.0 × 10−4mol l−1) significantly constricted lymphatics at the two highest doses. Preliminary experiments suggested that neurokinin B might dilate lymphatics. To test this, lymphatic pressure was increased by norepinephrine (3.1 × 10−6mol l−1). Neurokinin B (2.7 × 10−4mol l−1) was then infused intralymphatically during norepinephrine infusion. Norepinephrine increased perfusion pressure from 5.6 ± 0.6 mmHg to 12.1 ± 1.4 mmHg. Subsequent infusion of neurokinin B significantly decreased lymphatic perfusion pressure from 11.9 ± 1.3 mmHg to 9.9 ± 1.1 mmHg. These data indicate that neurokinin A and B can alter lymphatic resistance and are consistent with the hypothesis that lymph vessel function may be subject to modulation by neurokinins.
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Lundberg, Jan M. "Tachykinins, sensory nerves, and asthma—an overview." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 1995): 908–14. http://dx.doi.org/10.1139/y95-125.

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Tachykinin peptides, substance P (SP) and neurokinin A (NKA), are released from airway sensory nerves upon exposure to irritant chemicals and endogenous agents including bradykinin, prostaglandins, histamine, and protons. The released neuropeptides are potent inducers of a cascade of responses, including vasodilatation, mucus secretion, plasma protein extravasation, leukocyte adhesion–activation, and bronchoconstriction. Neurokinin 1 receptors (preferably activated by SP) seem to be most important for inflammatory actions, while neurokinin 2 receptors (preferably activated by NKA) mediate bronchoconstriction. Species differences exist whereby rat and guinea-pig have a more developed neurogenic inflammation response than normal human airways. However, disease states such as inflammation or viral infections lead to enhanced peptide synthesis and (or) increased sensory nerve excitability. Together with increased neurokinin 1 receptor synthesis and loss of major tachykinin-degrading enzymes such as neutral endopeptidase in airway inflammation, this suggests that recently developed, orally active nonpeptide neurokinin receptor antagonists could have a therapeutic potential in asthmatic patients.Key words: neurokinins, sensory nerves, inflammation, bronchoconstriction, receptors.
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Kimball, E. S., F. J. Persico, and J. L. Vaught. "Substance P, neurokinin A, and neurokinin B induce generation of IL-1-like activity in P388D1 cells. Possible relevance to arthritic disease." Journal of Immunology 141, no. 10 (November 15, 1988): 3564–69. http://dx.doi.org/10.4049/jimmunol.141.10.3564.

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Abstract Near nanomolar concentrations of substance P induce production of IL-1 or an IL-1-like activity in the mouse macrophage cell line P388D1. Moreover, this could be accomplished with the carboxyl-terminal octapeptide substance P4-11, and could be inhibited with the substance P antagonist [D-Pro2, D-Trp7,9]-substance P. Two other mammalian neurokinins, neurokinin A and neurokinin B, were also found to induce secretion of IL-1-like activity in P388D1 cells. These findings suggest that activation of immune cells by neuromodulators can contribute to the maintenance of the chronic inflammatory state and the immunopathology observed in arthritic disease mediated by IL-1. The results also suggest that one approach to the treatment of rheumatoid arthritis might be to attempt to inhibit the local effects of immuno-modulatory neuropeptides, specifically the neurokinins, in affected joints.
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Edvinsson, Jacob CA, Philip V. Reducha, Majid Sheykhzade, Karin Warfvinge, Kristian A. Haanes, and Lars Edvinsson. "Neurokinins and their receptors in the rat trigeminal system: Differential localization and release with implications for migraine pain." Molecular Pain 17 (January 2021): 174480692110594. http://dx.doi.org/10.1177/17448069211059400.

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Substance P (SP) and calcitonin gene-related peptide (CGRP) have both been considered potential drug candidates in migraine therapy. In recent years, CGRP receptor inhibition has been established as an effective treatment, in particular as a prophylactic for chronic migraine. Curiously, inhibition of neurokinin receptor 1 (NK1R) failed to alleviate acute migraine attacks in clinical trials, and the neurokinins were consequently abandoned as potential antimigraine candidates. The reason behind this has remained enigmatic. Utilizing immunohistochemistry and semi-quantitative cell counts the expression of neurokinins and their associated receptors was examined in the rat trigeminal ganglion. Immunohistochemistry results revealed SP co-localization in CGRP positive neurons and C-fibres, where it mainly concentrated at boutons. Neurokinin A (NKA) was observed in a population of C-fibres and small neurons where it could co-localize with SP. In contrast, neurokinin B (NKB) did not co-localize with SP and was observed in large/medium sized neurons and Aδ-fibres. All neurokinin receptors (NK1-3R) were found to be expressed in a majority of trigeminal ganglion neurons and A-fibres. The functional release of SP and CGRP in the trigeminovascular system was stimulated with either 60 mM K+ or 100 nM capsaicin and measured with an enzyme-linked immunosorbent assay (ELISA). ELISA results established that SP can be released locally from trigeminovascular system. The released SP was comparatively minor compared to the CGRP release from stimulated dura mater, trigeminal ganglion neurons and fibres. We hypothesize that SP and CGRP signalling pathways may work in tandem to exacerbate painful stimuli in the TGV system.
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Gleason, Neil R., George Gallos, Yi Zhang, and Charles W. Emala. "Propofol Preferentially Relaxes Neurokinin Receptor-2-induced Airway Smooth Muscle Contraction in Guinea Pig Trachea." Anesthesiology 112, no. 6 (June 1, 2010): 1335–44. http://dx.doi.org/10.1097/aln.0b013e3181d3d7f6.

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Background Propofol is the anesthetic of choice for patients with reactive airway disease and is thought to reduce intubation- or irritant-induced bronchoconstriction by decreasing the cholinergic component of vagal nerve activation. However, additional neurotransmitters, including neurokinins, play a role in irritant-induced bronchoconstriction. We questioned the mechanistic assumption that the clinically recognized protective effect of propofol against irritant-induced bronchoconstriction during intubation was due to attenuation of airway cholinergic reflexes. Methods Muscle force was continuously recorded from isolated guinea pig tracheal rings in organ baths. Rings were subjected to exogenous contractile agonists (acetylcholine, histamine, endothelin-1, substance P, acetyl-substance P, and neurokinin A) or to electrical field stimulation (EFS) to differentiate cholinergic or nonadrenergic, noncholinergic nerve-mediated contraction with or without cumulatively increasing concentrations of propofol, thiopental, etomidate, or ketamine. Results Propofol did not attenuate the cholinergic component of EFS-induced contraction at clinically relevant concentrations. In contrast, propofol relaxed nonadrenergic, noncholinergic-mediated EFS contraction at concentrations within the clinical range (20-100 mum, n = 9; P < 0.05), and propofol was more potent against an exogenous selective neurokinin-2 receptor versus neurokinin-1 receptor agonist contraction (n = 6, P < 0.001). Conclusions Propofol, at clinically relevant concentrations, relaxes airway smooth muscle contracted by nonadrenergic, noncholinergic-mediated EFS and exogenous neurokinins but not contractions elicited by the cholinergic component of EFS. These findings suggest that the mechanism of protective effects of propofol against irritant-induced bronchoconstriction involves attenuation of tachykinins released from nonadrenergic, noncholinergic nerves acting at neurokinin-2 receptors on airway smooth muscle.
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Ellis, James L. "Neurokinin receptors subserving bronchoconstriction." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 1995): 923–26. http://dx.doi.org/10.1139/y95-127.

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Tachykinin receptor subtypes were initially defined using agonist potency ratios for the endogenous ligands substance P (SP), neurokinin (NK) A, and NKB. On this basis it was suggested that there are three tachykinin receptor subtypes. These subtypes were designated NK1, NK2, and NK3, where SP is most potent at NK1 receptors, NKA is most potent at NK2 receptors, and NKB is most potent at NK3 receptors. Recently analogs of the endogenous ligands that show greater selectivity (about 1000-fold) for the different receptor subtypes have been developed. In addition selective antagonists, which are either nonpeptides or modified peptides, for the receptor subtypes have been developed. This minireview concentrates on the wealth of new knowledge concerning the tachykinin receptor subtypes subserving bronchoconstriction in several mammalian species, including man, provided by the use of these selective agonists and antagonists.Key words: neurokinins, bronchoconstriction, substance P, neurokinin A, receptor subtypes.
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Dornan, Wayne A., Krista L. Vink, Peter Malen, Kevin Short, William Struthers, and Christopher Barrett. "Site-specific effects of intracerebral injections of three neurokinins (neurokinin A, neurokinin K, and neurokinin γ) on the expression of male rat sexual behavior." Physiology & Behavior 54, no. 2 (August 1993): 249–58. http://dx.doi.org/10.1016/0031-9384(93)90107-q.

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Eistetter, H. R., D. J. Church, A. Mills, P. P. Godfrey, A. M. Capponi, R. Brewster, M. F. Schulz, E. Kawashima, and S. J. Arkinstall. "Recombinant bovine neurokinin-2 receptor stably expressed in Chinese hamster ovary cells couples to multiple signal transduction pathways." Cell Regulation 2, no. 10 (October 1991): 767–79. http://dx.doi.org/10.1091/mbc.2.10.767.

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Neurokinins are a family of neuropeptides with widespread distribution mediating a broad spectrum of physiological actions through three distinct receptor subtypes: NK-1, NK-2, and NK-3. We investigated some of the second messenger and cellular processes under control by the recombinant bovine NK-2 receptor stably expressed in Chinese hamster ovary cells. In this system the NK-2 receptor displays its expected pharmacological characteristics, and the physiological agonist neurokinin A stimulates several cellular responses. These include 1) transient inositol 1,4,5-trisphosphate (IP3) formation and Ca2+ mobilization, 2) increased out put of arachidonic acid and prostaglandin E2 (PGE2), 3) enhanced cyclic AMP (cAMP) generation, 4) increased de novo DNA synthesis, and 5) an induction of the "immediate early" genes c-fos and c-jun. Although NK-2 receptor-mediated IP3 formation involves activation of a pertussis toxin-insensitive G-protein, increased cAMP production is largely a secondary response and can be at least partially attributed to autocrine stimulation by endogenously generated eicosanoids, particularly PGE2. This is the first demonstration that a single recombinant neurokinin receptor subtype can regulate, either directly or indirectly, multiple signal transduction pathways and suggests several potential important mediators of neurokinin actions under physiological conditions.
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Koelbel, C. B., E. A. Mayer, J. R. Reeve, W. J. Snape, A. Patel, and F. J. Ho. "Involvement of substance P in noncholinergic excitation of rabbit colonic muscle." American Journal of Physiology-Gastrointestinal and Liver Physiology 256, no. 1 (January 1, 1989): G246—G253. http://dx.doi.org/10.1152/ajpgi.1989.256.1.g246.

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Neurokinins have been implicated as noncholinergic excitatory neurotransmitters in the mammalian gastrointestinal tract. To characterize the myogenic and neurogenic response of colonic muscle to neurokinins we studied the mechanical response of muscle strips from proximal and distal colon and the release of [3H]acetylcholine in response to substance P (SP), neurokinin A (NKA) and neurokinin B (NKB). All neurokinins caused a dose-dependent inotropic response. SP was 80 times more potent in distal compared with proximal longitudinal muscle. The rank order of potencies in proximal longitudinal muscle was NKA greater than SP = NKB and in distal muscle NKA = SP = NKB. Desensitization to SP or pretreatment with a SP antagonist inhibited the mechanical response to SP and the atropine-resistant inotropic off response to electrical stimulation. Only longitudinal muscle from distal colon had an atropine- and hexamethonium-sensitive inotropic component to SP. In contrast, all three peptides were equipotent in releasing [3H]acetylcholine from longitudinal muscle strips preincubated with [3H]choline. These results suggest the following: 1) SP is a potent agonist of rabbit colon with a proximal distal gradient in biological potency; 2) the myogenic response of the distal colon appears to be mediated through a NK-1 receptor; and 3) SP is a major mediator of the noncholinergic component of the off response in distal longitudinal muscle.
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Canning, Brendan J., Sandra M. Reynolds, Linus U. Anukwu, Radhika Kajekar, and Allen C. Myers. "Endogenous neurokinins facilitate synaptic transmission in guinea pig airway parasympathetic ganglia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 2 (August 1, 2002): R320—R330. http://dx.doi.org/10.1152/ajpregu.00001.2002.

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Neurokinin-containing nerve fibers were localized to guinea pig airway parasympathetic ganglia in control tissues but not in tissues pretreated with capsaicin. The purpose of the present study was to determine whether neurokinins, released during axonal reflexes or after antidromic afferent nerve stimulation, modulate ganglionic synaptic neurotransmission. The neurokinin type 3 (NK3) receptor antagonists SB-223412 and SR-142801 inhibited vagally mediated cholinergic contractions of bronchi in vitro at stimulation voltages threshold for preganglionic nerve activation but had no effect on vagally mediated contractions evoked at optimal voltage or field stimulation-induced contractions. Intracellular recordings from the ganglia neurons revealed that capsaicin-sensitive nerve stimulation potentiated subsequent preganglionic nerve-evoked fast excitatory postsynaptic potentials. This effect was mimicked by the NK3 receptor agonist senktide analog and blocked by SB-223412. In situ, senktide analog markedly increased baseline tracheal cholinergic tone, an effect that was reversed by atropine and prevented by vagotomy or SB-223412. Comparable effects of intravenous senktide analog on pulmonary insufflation pressure were observed. These data highlight the important integrative role played by parasympathetic ganglia and indicate that activation of NK3 receptors in airway ganglia by endogenous neurokinins facilitates synaptic neurotransmission.
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Dissertations / Theses on the topic "Neurokinin"

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Ore, Mikhail. "Neurokinin-1 receptor: neurokinin-1 receptor, purification and refolding." Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/96874.

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El receptor Neuroquinin-1 (NK1R) és un GPCR que es troba en el sistema nerviós central i perifèric dels vertebrats i és responsable dels processos fisiològics com la transmissió de dolor, secreció endocrina i exocrina, vasodilatació, modulació de la proliferació cel·lular i molts altres. Els antagonistes del NK1R poden ser potencials analgèsics i antidepressius i també poden ser utilitzats per al tractament del trastorn bipolar, l'alcoholisme, càncer, malalties del sistema immune i algunes infeccions. Les tècniques espectroscòpiques i les estructurals d'alta resolució com NMR i la cristal·lografia requereixen quantitats de l'ordre de mil·ligrams del receptor actiu purificat. Una de les estratègies que permet produir els GPCRs recombinants per estudis estructurals és el sistema d'expressió en E.coli. No obstant, molts GPCRs degut al seu efecte tòxic per a la cèl·lula bacteriana s'expressen en forma dels cossos d'inclusió i han de ser sotmesos al procés de renaturalització. La renaturalització dels GPCRs és una tasca complexa que implica complexos ajustaments dels tampons. La primera part d'aquest treball s'ha centrat en la renaturalització de las formes truncades hNK1R-366 i hNK1R-311 del receptor expressades en cossos d'inclusió d'E.coli. Per a l'obtenció del receptor ben plegat hem establert un original protocol de la renaturalització en columna. Hem utilitzat diferents tècniques espectroscòpiques per a estudiar el receptor renaturalitzat. Els resultats de CD han demostrat que el hNK1R-366 i el hNK1R-311 renaturalitzats en DDM presenten un percentatge d'hèlix-α similar al de la rodopsina extreta de retines bovines i solubilitzada en DDM. En els estudis de fluorescència intrínseca de triptòfans a baixes concentracions del GuHCl hem pogut observar el desplaçament cap el blau en l'espectre d'emissió, típic de triptòfans que es troben en un entorn hidrofòbic. A més a més, els espectres d'emissió del hNK1R-366 expressat en cèl·lules COS-1 i solubilitzat en DDM presenten el màxim d'emissió a 335 nm, molt similar al del receptor renaturalitzat a partir dels cossos d'inclusió, indicant la seva correcte renaturalització. El hNK1R-366, renaturalitzat en tampó fisiològic presenta agregació en 24 hores. No obstant, la presència de 0.05% DDM és capaç d'estabilitzar el receptor. Els assajos de radioligand binding de saturació del hNK1R-366 renaturalitzat indiquen que el receptor actiu constitueix l’1% de la proteïna total de la mostra. No obstant, la unió de la SP al receptor en el rang de nanomols és significatiu i és un resultat important, donat que, per primera vegada s’ha obtingut NK1 funcional a partir de E.coli. Per altre costat, no hem pogut obtenir una corba de saturació del hNK1R-311, degut possiblement al plegament defectuós del receptor per falta dels darrers 96 residus. La segona part d'aquest estudi està centrada en l'expressió, purificació i caracterització estructural del C-terminal del receptor hNK1. El domini C-terminal és important per l'acoblament de la proteïna G i la β-arrestina, i també és essencial per a la dessensibilització, internalització i reciclatge del receptor. No obstant, el paper d'aquest domini ha estat infravalorat pels investigadors durant molt temps i existeix poca informació sobre la seva estructura. Els estudis espectroscòpics de UV i de fluorescència posen de manifest anomalies en l'absorbància a 292 nm i en l'emissió intrínseca de les tirosines a 345 nm, atribuïdes a formes ionitzades de l’aminoàcid, degut a la seva proximitat a grups carboxil de residus glutàmics o aspàrtics. A partir de la predicció de l'estructura secundària i terciària i dels resultats dels estudis espectroscòpics hem proposat un model tridimensional pel C-terminal del hNK1 que conté: 25% d’hèlix-α, 27% d’estructura desordenada i 48% de fulles-β i girs-β. En conjunt, els resultat obtinguts, indiquen que el C-terminal del hNK1R no és un domini desordenat, sinó que té una estructura secundària i terciària clarament definides que poden relacionar amb les seves funcions.
Neurokinin-1 receptor (NK1R) is a GPCR found in the central and peripheral nervous system of vertebrates, responsible for such physiological processes as pain transmission, exocrine and endocrine secretion, vasodilatation, modulation of cell proliferation and many others. NK1R antagonists could be potential analgesics and anti-depressants and may also be used for treatment of bipolar disorder, alcoholism, cancer, immune system diseases and selected infections. Spectroscopic studies and high resolution structural techniques, as NMR and crystallography, require milligram amounts of active purified receptor. One of the strategies to produce recombinant GPCRs for structural studies is an E.coli expression system. However, many GPCRs due to their toxic effect for bacterial host cell are expressed in form of inclusion bodies and require refolding. The refolding of GPCRs is a complicated task that requires screening and adjustment of buffer conditions. The first part of this work was centered on the refolding of hNK1R-366 and hNK1R-311 truncated forms expressed in E.coli inclusion bodies. To obtain properly folded receptor, we established an original on-column refolding protocol. Different spectroscopic techniques were applied to study the refolded receptor. The results obtained from CD measurements showed that hNK1R-366 refolded in DDM presents similar α-helical content as rhodopsin extracted from bovine retinas and solubilized in non-denaturing DDM micelles. In the intrinsic tryptophan fluorescence studies, at low concentrations of GuHCl we observed a blue-shift in the emission spectrum peak, typical for tryptophan in hydrophobic environment. Furthermore, the emission spectra of hNK1R-366 expressed in COS-1 cells and solubilized in DDM micelles show very similar emission maximum around 335 nm to that of the receptor refolded from the inclusion bodies, which may be indicative of proper protein refolding. The refolded in physiological buffer hNK1R-366 was prone to aggregate in about 24 hours, however, the presence of 0.05% DDM was found to stabilize the receptor. Saturation radioligand-binding assays for the refolded hNK1R-366 showed that the amount of the active receptor is about 1% of the total protein the sample. However, the binding of SP to the refolded hNK1R-366 in nanomolar range is significant and can be considered as a promising result, since until now the intents to produce any detectable amounts of functional NK1 receptor in E. coli were unsuccessful. On the other hand, we were unable to get any saturation binding curve for hNK1R-311 truncated form of the receptor, which could be explained by incorrect folding caused by the lack of 96 residues of the C-terminus of the receptor. The second part of the present study is centered on hNK1R C-terminus expression, purification and characterization to elucidate its structural properties. The C-terminus domain seems to be essential for the coupling to corresponding G protein and β-arrestin, and is essential for receptor desensitization, internalization and recycling. However, the role of this domain was underestimated by researchers for a long time and as a result very little information is known about its structure. UV and fluorescence spectroscopic studies revealed abnormal tyrosine red-shifted absorbance band at 292 nm and intrinsic tyrosine emission at 345 nm which could be attributed to ionized form of tyrosine and possibly arises from the proximity of one or more tyrosines to carboxyl groups of glutamic o aspartic residues. Based on secondary and tertiary structure prediction as well as on the results of spectroscopic studies we propose a 3D-model for hNK1R C-terminus. Th following assignment of the secondary structure was made: 25% α-helix, 27% unordered structure, 48% β-sheets and β-turns. The obtained ressults give evidence that hNK1R C-terminus is not an unordered region but has clearly defined secondary and tertiary structures which certainly are tightly related to its multiple functions.
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Carelse, Tofa Kashefa. "Molecular genetic analysis of the neurokinin B (TAC3) and neurokinin B receptor (TAC3) genes as candidates for pre-eclampsia." Thesis, Stellenbosch : Stellenbosch University, 2004. http://hdl.handle.net/10019.1/50029.

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Thesis (MSc)--Stellenbosch University, 2004.
ENGLISH ABSTRACT: Hypertensive conditions of pregnancy, such as pre-eclampsia, are the principal direct cause of maternal morbidity and mortality and affect up to 10% of first pregnancies worldwide. The placenta is vital in the pathogenesis of pre-eclampsia since the condition only occurs in the presence of placental tissue and the only cure is delivery of the placenta and the fetus. It has been hypothesised that the placenta may be the source of a circulating factor(s), which transports freely in the maternal system, resulting in the multi-systemic and immunological responses that are characteristic of pre-eclampsia. Among the potential "circulating" candidates currently being investigated worldwide, is the tachykinin member, neurokinin B (NKB). The aim of this project was to use a novel approach and investigate the role of Neurokinin B in pre-eclampsia on a genetic level. This would be achieved by bioinformatie characterisation of the neurokinin B (TAC3) and neurokinin B receptor (TACR3) genes. Samples from thirty pre-eclampsia patients (of whom 10 also had abruptio placentae) and twenty control individuals were used for mutation detection analysis involving Multiphor gel electrophoresis and automated sequencing. Three sequence variants were identified in the TAC3 gene and include: (i) 5' UTR variant (-25 c-t); (ii) intronic variant IVS3-53 (t-g) and (iii) 3' UTR variant exon 7 (479, t-c). Only the -25 c-t variant had been reported before (SNP database). A further two variants were identified in the TACR3 gene: (i) exon 3 variant (nt 857, a-t) and (ii) 3' UTR variant, amplicon 5b (nt 1471, t-c), of which the latter had previously been reported in the SNP database. In the analysis of allele and genotype frequencies, only variant homozygosity for TAC3 -25 c-t could be associated with increased risk of pre-eclampsia (RR 3.33, p=0.03). Follow-up work will include extended genotyping in further stratified and larger patient cohorts and transfection studies to assess splicing potential and functional consequences of the mutant alleles. These data represent the first documented mutation screen of the TAC3 and TACR3 genes and report novel variants in patients with pre-eclampsia. This study contributes to the knowledge of neurokinin B as a circulatory molecule and confirms the heterogeneity of pre-eclampsia.
AFRIKAANSE OPSOMMING: Die belangrikste direkte oorsaak van moedersterftes is hipertensiewe toestande in swangerskap, insluitende pre-eklampsie. Hierdie toestande kompliseer wêreldwyd 10% van alle swangerskappe. Die plasenta is kardinaal in die ontwikkeling van die siekte aangesien dit slegs voorkom terwyl die plasenta in-situ is en die simptome opklaar na verlossing van die plasenta. 'n Moontlike hipotese is dat die plasenta 'n sirkulerende agens afskei wat in die moederlike sisteem beland en die uiteenlopende multi-sistemiese simptome en tekens van die siekte veroorsaak, asook aktivering van die immuunsisteem. Een van die moontlike kandidate wat tans wêreldwyd ondersoek word as moontlike sirkulerende agens, is Neurokinien B (NKB), 'n lid van die Tachikinien familie. Die unieke benadering van hierdie projek was om die rol van Neurokinien B in pre-eklampsie te ondersoek op 'n genetiese grondslag. Dit is bereik deur bio-informatiewe karakterisering van die neurokinien B (TAC3) en neurokinien B reseptor (TACR3) en deur mutasie sifting op DNA monsters van 30 pasiënte met pre-eklampsie (waarvan 10 ook abruptio placentae gehad het) en twintig kontrole individue met behulp van Multiphor gel elektroforese en ge-outomatiseerde volgorde bepaling. Drie volgorde variasies is geïdentifiseer in die TAC3 geen en sluit in: (i) 5' UTR variant (-25 c-t); (ii) introniese variant IVS3-53 (t-g) en (iii) 3' UTR variant in ekson 7 (479, t-e). Slegs die -25 c-t variasie is voorheen raporteer (SNP databasis). Nog twee variante is ook gevind in die TACR3 geen: (i) ekson 3 variant (nt 857, a-t) en (ii) 3' UTR variant, amplikon 5b (nt 1471, t-e); hierdie laaste een is al in die SNP databasis raporteer. In 'n analise van genotipe en allele frekwensies is slegs homosigositeit vir variant TAC3 -25 c-t geassosieër met 'n verhoogde risiko vir preeklampsie (RR 3.33, p=0.03). Verdere werk sal nou fokus op die genotipering van groter en gestratifiseerde pasiënt kohorte en transfeksie studies om splitsing potensiaal en funksionele gevolge van mutante allele te ondersoek. Hierdie data is die eerste gedokumenteerde mutasie sifting van die TAC3 en TACR3 gene en verslag word gelewer van unieke variasies in pasiënte met pre-eklampsie.
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Sandoval-Guzman, Tatiana. "Neurokinin B and the hypothalamic regulation of reproduction." Diss., The University of Arizona, 2003. http://hdl.handle.net/10150/280447.

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The morphology and gene expression of neurokinin B (NKB) neurons is altered in the human infundibular (arcuate) nucleus in association with the ovarian failure of menopause. Also, gonadotropin releasing-hormone (GnRH) mRNA is elevated and proopiomelanocortin (POMC) mRNA decreased. To determine if loss of ovarian steroids could produce comparable changes in gene expression in primates, we measured the effects of ovariectomy on NKB and GnRH in young cynomolgus monkeys. We also measured POMC gene expression, serum leptin and body weight to examine the consequences of ovariectomy on energy balance. Neurokinin B neurons in the infundibular nucleus of ovariectomized monkeys were larger, more numerous and displayed increased levels of NKB mRNA than the intact controls. Ovariectomy increased the number of neurons expressing GnRH gene transcripts. In contrast, the energy balance parameters were unchanged by ovariectomy. This study provides strong support for the hypothesis that ovarian failure contributes to the morphological changes and increased NKB and GnRH gene expression observed in postmenopausal women. We hypothesized that hypothalamic NKB neurons participate in the hypothalamic circuitry regulating LH. We determined if intracerebral infusion of a NK 3 receptor agonist alters serum LH in the ovariectomized estrogen-treated rat. A significant inhibition of serum LH was observed after senktide injection, accompanied by changes in Fos expression in medial preoptic area, arcuate, paraventricular and supraoptic nuclei. This study provides evidence that stimulation of the NK3 receptor may inhibit LH secretion via activation of hypothalamic neurons. To further investigate the role of NKB in gonadotropin regulation, we infused an antisense oligodeoxynucleotide targeted to the NKB gene in gonadectomized rats. In support of our hypothesis, the downregulation of NKB decreased serum LH by 25%. To analize the participation of the NKB receptor, NK3, we targeted an antisense to the receptor. Rats injected with the NK3 antisense exhibited no change in serum LH. Furthermore, injection of SB-222200, a NK3 antagonist, did not modify serum LH. These data suggest that NKB may regulate gonadotropin secretion through more than one receptor. Taken together, these studies provide some of the first detailed information on the relationship between NKB neurons, and the reproductive axis.
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Dacks, Penny Ann Frances. "THE NEURONAL CIRCUITRY OF ESTROGENIC EFFECTS ON THERMOREGULATION." Diss., The University of Arizona, 2010. http://hdl.handle.net/10150/195591.

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Approximately 75% of menopausal women in the United States experience hot flushes but the etiology of this thermoregulatory disorder is unknown. The dominant theory is that estrogen withdrawal sensitizes thermoregulatory areas of the brain, leading to the inappropriate activation of heat loss effectors in response to mild stimuli. This dissertation examines the circuitry of estrogen effects on thermoregulation. First, a rodent model was characterized. In ovariectomized rats, estradiol treatment decreased tail skin vasodilatation, a primary heat loss mechanism, and raised the ambient temperature threshold for tail skin vasodilatation. These results indicate that estradiol does not alter the maximal ability of blood vessels to constrict and dilate, but rather shifts the threshold for thermoregulatory activation in rats. Using this animal model, we examined how estradiol treatment and ambient temperature affect neuronal activity in brain areas involved with thermoregulation and reproduction. Out of 14 examined regions, only 3 areas were significantly affected by both estradiol and temperature and only the median preoptic nucleus (MnPO) exhibited increased activity at warmer ambient temperature. Interestingly, the effects of estradiol and ambient temperature on MnPO activity closely resembled their effects on tail skin vasodilatation. These results identify the MnPO as a plausible site for the integration of estrogen with skin vasodilatation. In the third study, we examined whether thermoregulation can be modified by neurokinin 3 (NK3) receptors, the dominant receptor for neurokinin B (NKB). Core temperature in ovariectomized rats was decreased by microinfusion of a selective NK3 receptor agonist into the MnPO and adjacent septal areas. This transient hypothermia was accompanied by a lack of homeostatic tail skin vasoconstriction but was not caused by tail skin vasodilatation or a global impairment in thermoregulation. These results demonstrate that thermoregulation in rats is modified by NK3 receptors in brain areas that receive projections from NKB neurons. In humans, menopause is associated with hot flushes and the hypertrophy and increased NKB gene expression in arcuate (infundibular) neurons. We propose a novel theory that estrogen withdrawal causes hot flushes by enhancing NKB release from arcuate (infundibular) neurons onto NK3 receptors.
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Murnin, Mark Anthony. "Structure-activity studies on some analogues of neurokinin A." Thesis, University of Ulster, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260519.

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Wang, Linhong. "Differential processing of circulating substance P and neurokinin A /." The Ohio State University, 1995. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487862972134708.

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Shanab, Ahmed Ayesh Abu. "Synthesis and biological testing of some analogues of neurokinin A." Thesis, Queen's University Belfast, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335458.

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Misu, Ryosuke. "Development of Neuropeptide Receptor Ligands for the Control of Reproductive Systems." 京都大学 (Kyoto University), 2015. http://hdl.handle.net/2433/199501.

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Wong, Chui Mae. "Substance P and neurokinin A as markers of pain in neonates." Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/25329.

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Both substance P (SP) and neurokinin A (NKA) have been postulated to be involved in persistent pain in adult studies, but never previously researched in newborn infants. Methods of sample handling and analysis were developed to accommodate neonatal microsamples.  Sample extraction was found to be essential, as were speed of sample collection and the use of polypropylene materials during sample handing. The clinical study enrolled 174 infants of different gestational ages, who had serial measurements of SP, NKA, and cortisol performed in plasma and saliva samples. Plasma SP concentrations in neonates ranged from 0.0-11.2 pmol/L (median 1.7 pmol/L) and NKA concentrations from 1.8-74.6 pmol/L (median 6.0 pmol/L). Gestation and birth weight had no significant correlation with peptide concentrations. Postnatally, there was a gradual rise in median plasma SP and NKA during the first three days which decreased again by days 7 to 14. Perinatal factors such as labour, the mode of delivery, and epidural analgesia affected NKA but not SP concentrations. With regard to either pain or assisted ventilation, plasma SP concentrations did not appear to be a useful marker of persistent pain or distress.  Conversely, plasma NKA concentrations showed significant changes with ventilation, which were further modulated by the use of analgesia. Cortisol responses in the same group of infants demonstrated significant changes with ventilation, but not with the administration of analgesia. This suggests that although cortisol is a useful indicator of overall stress, NKA might be more specific for pain. There was a weak correlation between plasma SP and NKA. Plasma SP did not correlate with plasma cortisol or other physiological measures of pain used in this study.
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McLeod, Amber L. "Synaptic organization of the neurokinin system in the sensory spinal cord." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0026/NQ50219.pdf.

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Books on the topic "Neurokinin"

1

Murrin, Mark Anthony. Structure - activity studies on some analogues of Neurokinin A. [S.l: The Author], 1993.

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Yamamoto, Koki. Structure–Activity Relationships for Development of Neurokinin-3 Receptor Antagonists. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-2965-8.

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Henry, James L., Rejean Couture, A. Claudio Cuello, Georges Pelletier, Remi Quirion, and Domenico Regoli, eds. Substance P and Neurokinins. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4612-4672-5.

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Yamamoto, Koki. Structure–Activity Relationships for Development of Neurokinin-3 Receptor Antagonists: Reducing Environmental Impact. Springer, 2020.

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Yamamoto, Koki. Structure-Activity Relationships for Development of Neurokinin-3 Receptor Antagonists: Reducing Environmental Impact. Springer Singapore Pte. Limited, 2021.

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Abt, Simon Dominik. Nachweis des Neurokinin-1-Rezeptors und des Calcitonin-Gene-Related-Peptide-Rezeptors und Untersuchung ihres Vorkommens auf parenchymalen und nicht-parenchymalen Zellen der menschlichen Leber. 2011.

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Placenza, Franca M. The role of substance P and brain neurokinin-1 receptors in relapse to drug-seeking behaviour, drug-induced locomotor activity and drug self-administration: Y Franca M. Placenza. 2006.

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Henry, J. L. Substance P and Neurokinins: Proceedings of Substance P and Neurokinins-Montreal '86 a Satellite Symposium of the Xxx International Congress of the I. Springer, 1987.

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Henry, James L. Substance P and Neurokinins: Proceedings of "Substance P and Neurokinins - Montreal '86": A Satellite Symposium of the XXX International Congress of The International Union of Physiological Sciences. Springer-Verlag Berlin and Heidelberg GmbH & Co. KG, 1987.

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L, Henry J., International Union of Physiological Sciences. Congress, and IUPS Satellite Symposium "Substance P and Neurokinins - Montreal '86" (1986 : McGill University), eds. Substance P and neurokinins: Proceedings of "substance P and neurokinins--Montreal '86" : a satellite symposium of the XXX International Congress of the International Union of Physiological Sciences. New York: Springer-Verlag, 1987.

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Book chapters on the topic "Neurokinin"

1

Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "Neurokinin 1." In Encyclopedia of Psychopharmacology, 854. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_4403.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "Neurokinin 2." In Encyclopedia of Psychopharmacology, 854. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_4404.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "Neurokinin 3." In Encyclopedia of Psychopharmacology, 854. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_4405.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "Neurokinin-α." In Encyclopedia of Psychopharmacology, 854. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_6030.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "Neurokinin A." In Encyclopedia of Psychopharmacology, 854–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1652.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "Neurokinin B." In Encyclopedia of Psychopharmacology, 855. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1653.

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Muñoz, Miguel, Marisa Rosso, and Rafael Coveñas. "Neurokinin-1 Receptor." In Encyclopedia of Signaling Molecules, 3437–45. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101781.

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Muñoz, Miguel, Marisa Rosso, and Rafael Coveñas. "Neurokinin-1 Receptor." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101781-1.

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Muñoz, Miguel, and Rafael Coveñas. "Neurokinin/Tachykinin Receptors." In Encyclopedia of Molecular Pharmacology, 1–11. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-21573-6_202-1.

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Muñoz, Miguel, and Rafael Coveñas. "Neurokinin/Tachykinin Receptors." In Encyclopedia of Molecular Pharmacology, 1093–103. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_202.

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Conference papers on the topic "Neurokinin"

1

Calzetta, Luigino, Paola Rogliani, Francesco Facciolo, Barbara Rinaldi, Maria Gabriella Matera, and Mario Cazzola. "N-Acetylcysteine protects human bronchi via inhibiting neurokinin A." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa1807.

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Harle, Amelie, Fiona Blackhall, Alex Molassiotis, Kim Holt, Rachel Dockry, Philip Russell, Katy Burns, et al. "Neurokinin-1 receptor antagonism for the treatment of cough in lung cancer." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa5060.

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Ewer, M., S. Grunberg, S. Ranganathan, S. Lane, and M. Russo. "Cardiac Safety Data for Casopitant, a Neurokinin-1 Receptor Antagonist, Given with Anthracycline." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-1118.

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Kokhan, Viktor, Petr Anokhin, Denis Abaimov, Irina Tarabarko, and Inna Shamakina. "NEUROKININ-1 RECEPTOR AS POTENTIAL TARGET FOR PHARMACOTHERAPY OF RELAPSE TO ALCOHOL-SEEKING." In XVIII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2022. http://dx.doi.org/10.29003/m2800.sudak.ns2022-18/183-184.

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Smith, Jaclyn, Elizabeth Ballantyne, Mary Kerr, Lorcan Mcgarvey, Alyn Morice, Mandel Sher, Michael Trower, and Stephen Pawsey. "Late Breaking Abstract - The neurokinin-1 receptor antagonist orvepitant improves chronic cough symptoms: results from a Phase 2b trial." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa600.

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Adams, Laurel M., Stefano Zamuner, Paolo Fina, Michela Peroni, Brendan M. Johnson, and Sofia Fernandes. "Abstract C133: Effect of casopitant, a novel neurokinin‐1 receptor antagonist, on the pharmacokinetics (PK) of the oral contraceptive pill (OCP)." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-c133.

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Kokhan, Viktor. "NEUROKININ-1 RECEPTOR ANTAGONIST INHIBITS PSYCHO-EMOTIONAL AND COGNITION ALTERATIONS CAUSED BY GALACTIC COSMIC RAYS' EXPOSURE OF RATS IN A GROUND-BASED MODEL." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m1108.sudak.ns2020-16/275-276.

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Derom, Eric, Yannick van Durme, Bihiyga Salhi, Christina Vander Stichele, Fré Bauters, Josseline Sele, Renaud Louis, and Guy F. Joos. "Tiotropium Bromide Protects Against Methacholine-, But Not Against Neurokinin A-Induced Bronchoconstriction In Patients With Asthma: A Randomized, Double-Blind, Placebo-Controlled, Crossover Study." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4500.

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