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Corral, Pablo, E-mail: drpablocorral@gmail.com2014
AbstractAbstract
No abstract available
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Source
Available from http://dx.doi.org/10.5935/abc.20130248; Available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987394; PMCID: PMC3987394; PMID: 24652095; OAI: oai:pubmedcentral.nih.gov:3987394; This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.; Country of input: International Atomic Energy Agency (IAEA)
Record Type
Journal Article
Journal
Arquivos Brasileiros de Cardiologia; ISSN 0066-782X;
; v. 102(1); p. 5-8

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External URLExternal URL
Leyva-Illades, Dinorah; DeMorrow, Sharon, E-mail: demorrow@medicine.tamhsc.edu2013
AbstractAbstract
[en] G protein-coupled receptors (GPCRs) modulate a vast array of cellular processes. The current review gives an overview of the general characteristics of GPCRs and their role in physiological conditions. In addition, it describes the current knowledge of the physiological and pathophysiological functions of GPR55, an orphan GPCR, and how it can be exploited as a therapeutic target to combat various cancers
Primary Subject
Source
Available from http://dx.doi.org/10.2147/CMAR.S35175; Available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3706254; PMCID: PMC3706254; PMID: 23869178; PUBLISHER-ID: cmar-5-147; OAI: oai:pubmedcentral.nih.gov:3706254; Copyright (c) 2013 Leyva-Illades and DeMorrow, publisher and licensee Dove Medical Press Ltd; This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.; Country of input: International Atomic Energy Agency (IAEA)
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Journal Article
Journal
Cancer Management and Research; ISSN 1179-1322;
; v. 5; p. 147-155

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External URLExternal URL
Toyozawa, Seiko; Yamamoto, Yuki; Ishida, Yuko; Kondo, Toshikazu; Nakamura, Yasushi; Furukawa, Fukumi, E-mail: seikotoy@wakayama-med.ac.jp2010
AbstractAbstract
[en] Functional chemokine receptors are expressed in many malignant tumors. These receptors promote tumor growth and metastasis in response to endogenous chemokines. We analyzed the expression of CXCR4, CCR6 and CCR7 in fibrohistiocytic tumors, including dermatofibrosarcoma protuberance (DFSP), malignant fibrous histiocytoma (MFH), dermatofibroma (DF) using immunohistochemistry. We also investigated the relationship between CXCR4 and CD34, the latter of which is an immunohistochemical marker for DFSP. We observed a higher expression of CXCR4 in DFSP and MFH as compared with DF. Interestingly, a significantly higher expression of CXCR4 was detected in relapsed DFSP than in non-relapsed DFSP, but no significant differences were detected between non-relapsed DFSP and DFSP with CD34 immunostaining. Moreover, MFH had strong immunoreactivity for CXCR4, CCR6 and CCR7. These findings suggest that the assessment of CXCR4 immunoreactivity in fibrohistiocytic tumors is a useful tool for predicting tumor aggressiveness
Primary Subject
Source
Available from http://dx.doi.org/10.1267/ahc.10003; Available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2875858; PMCID: PMC2875858; PMID: 20514291; PUBLISHER-ID: AHC10003; OAI: oai:pubmedcentral.nih.gov:2875858; Copyright (c) 2010 The Japan Society of Histochemistry and Cytochemistry; This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.; Country of input: International Atomic Energy Agency (IAEA)
Record Type
Journal Article
Journal
Acta Histochemica et Cytochemica; ISSN 0044-5991;
; v. 43(2); p. 45-50

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External URLExternal URL
AbstractAbstract
[en] Dipyrone (Dp), 4-aminoantipyrine (AA), and antipyrine (At) delay liquid gastric emptying (GE) in rats. We evaluated adrenergic participation in this phenomenon in a study in male Wistar rats (250-300 g) pretreated subcutaneously with guanethidine (GUA), 100 mg·kg"−"1·day"−"1, or vehicle (V) for 2 days before experimental treatments. Other groups of animals were pretreated intravenously (iv) 15 min before treatment with V, prazosin (PRA; 1 mg/kg), yohimbine (YOH; 3 mg/kg), or propranolol (PRO; 4 mg/kg), or with intracerebroventricular (icv) administration of 25 µg PRO or V. The groups were treated iv with saline or with 240 µmol/kg Dp, AA, or At. GE was determined 10 min later by measuring the percentage of gastric retention (%GR) of saline labeled with phenol red 10 min after gavage. %GR (mean±SE, n=8) indicated that GUA abolished the effect of Dp (GUA vs V=31.7±1.6 vs 47.1±2.3%) and of At (33.2±2.3 vs 54.7±3.6%) on GE and significantly reduced the effect of AA (48.1±3.2 vs 67.2±3.1%). PRA and YOH did not modify the effect of the drugs. %GR (mean±SE, n=8) indicated that iv, but not icv, PRO abolished the effect of Dp (PRO vs V=29.1±1.7 vs 46.9±2.7%) and At (30.5±1.7 vs 49±3.2%) and significantly reduced the effect of AA (48.4±2.6 vs 59.5±3.1%). These data suggest activation of peripheral β-adrenoceptors in the delayed GE induced by phenylpyrazolone derivatives
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Available from http://dx.doi.org/10.1590/1414-431X20132975; Available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3854428; PMCID: PMC3854428; PMID: 24068187; OAI: oai:pubmedcentral.nih.gov:3854428; This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.; Country of input: International Atomic Energy Agency (IAEA)
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Journal Article
Journal
Brazilian Journal of Medical and Biological Research; ISSN 0100-879X;
; v. 46(9); p. 735-738

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External URLExternal URL
AbstractAbstract
No abstract available
Original Title
Recepteurs d'insuline: methode radioimmunologique
Primary Subject
Source
Published in abstract form only.
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Journal Article
Journal
Nouvelle Presse Medicale; ISSN 0301-1518;
; v. 8(27); p. 2235

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Liu, Yongjian; Woodard, Pamela K., E-mail: woodardp@mir.wustl.edu2019
AbstractAbstract
No abstract available
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Source
Copyright (c) 2019 American Society of Nuclear Cardiology; Country of input: International Atomic Energy Agency (IAEA)
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Journal Article
Journal
Journal of Nuclear Cardiology (Online); ISSN 1532-6551;
; v. 26(4); p. 1179-1181

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Lin, Chujiao; Zhang, Qian; Yu, Shuaitong; Lin, Yuxiu; Li, Shuchen; Liu, Huan; Chen, Zhi, E-mail: liu.huan@whu.edu.cn, E-mail: zhichen@whu.edu.cn2018
AbstractAbstract
[en] Highlights: • miR-3065-5p is significantly up-regulated during odontoblastic differentiation. • miR-3065-5p directly targets Bmpr2 and indirectly targets Adamts2. • Bmpr2 exerts different roles in the different stages of odontoblastic differentiation. Illumination of the molecular mechanisms regulating odontoblastic differentiation of dental papilla cells is of great significance for proper dentinogenesis and dental pulp regeneration. In this study, we discovered that microRNA (miR)-3065-5p is up-regulated during odontoblastic differentiation. Overexpression of miR-3065-5p promoted odontoblastic differentiation in vitro. Dual luciferase report assay verified that miR-3065-5p could bind to the 3′UTR of bone morphogenetic protein receptor type II (BMPR2), which dramatically increased in the beginning of odontoblastic differentiation but decreased in the terminal differentiation stage. Inhibition of Bmpr2 in the early stage retarded odontoblastic differentiation while knockdown of Bmpr2 in the terminal stage enhanced odontoblastic differentiation, resembling the effect of miR-3065-5p. Taken together, our present study suggests that miR-3065-5p positively regulates odontoblastic differentiation by directly binding to Bmpr2 in the terminal differentiation stage.
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S0006291X17322039; Available from http://dx.doi.org/10.1016/j.bbrc.2017.11.026; Copyright (c) 2017 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
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Journal Article
Journal
Biochemical and Biophysical Research Communications; ISSN 0006-291X;
; CODEN BBRCA9; v. 495(1); p. 493-498

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AbstractAbstract
[en] Growth arrest specific 1 (GAS1) is a signaling mediator for the development of the central nervous system that works as a co-receptor for sonic hedgehog (SHH) to induce the amplification of neural progenitors during the patterning of the mammalian neural tube and establishing granular cells in the cerebellum. Recently, we confirmed that Gas1 is also expressed by neural progenitors of the developing cortex and the dentate gyrus of the hippocampus. The presence of GAS1 in progenitor stages indicates that one of its principal roles is the maintenance of these cells during neurogenic events. However, the signals responsible for the expression of Gas1 in progenitor cells are unknown, an aspect that is relevant to understand its functions during neurogenesis. Here, we focused on elucidating the mechanisms of the transcriptional regulation of Gas1 and using comparative genomics methods found two highly conserved E-boxes in the Gas1 promoter which mediate its up-regulation by NeuroD1. Additionally, we found that GAS1 and NeuroD1 co-localize in the neocortex, the dentate gyrus of the hippocampus and the external granular layer of the cerebellum, suggesting a previously unsuspected regulatory relationship. Our data indicate that Gas1 is a direct target of NeuroD1 during the induction of the neurogenic program.
Primary Subject
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S0014482718300466; Available from http://dx.doi.org/10.1016/j.yexcr.2018.01.034; Copyright (c) 2018 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
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Journal Article
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He, Qianqian; Shen, Zhongxia; Ren, Lie; Wang, Xing; Qian, Mincai; Zhu, Jianying; Shen, Xinhua, E-mail: heqianqian205@163.com, E-mail: snowszx@sina.com, E-mail: renliemeidu@126.com, E-mail: 1439612777@qq.com, E-mail: 1311956613@qq.com, E-mail: 54037360@qq.com, E-mail: prozac1216@sina.com2018
AbstractAbstract
[en] In previous studies, neuropeptide S (NPS) and its cognate receptor (NPSR) have been involved in the pathogenesis of anxiety disorders in previous studies. Here, we aimed to investigate the association of NPSR1 polymorphism with generalized anxiety disorder (GAD) and its treatment response in Chinese Han population. Three hundred and thirty seven patients and one hundred and seventy seven healthy controls were involved in our study for 8 weeks. Further, Hamilton Anxiety Scale (HAMA) was used to assess anxiety symptom at baseline and the 1st, 2nd, 4th, 8th week. And all participants were genotyped for NPSR1 (rs324981) variants by polymerase chain reaction. Using Repeated-measures analysis, it showed significant reduction on HAMA scores in patients treated with escitalopram (F = 1.03, P = 0.362) and venlafaxine (F = 0.27, P = 0.763) respectively through 8 weeks treatment. Additionally, patients with AA and TT homozygous genotypes treated with venlafaxine XR had a higher reduction of HAMA scores compared to AT heterozygotic carriers (F = 4.18, P = 0.004), while no significant differences were found in patients treated with escitalopram (F = 1.05, P = 0.383). Thus, our study provides preliminary evidence that NPSR1 AA and TT homozygous genotypes have better treatment responses to venlafaxine XR in Chinese GAD patients, but not to escitalopram. Further studies are needed to verify the observation.
Primary Subject
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S0006291X18318394; Available from http://dx.doi.org/10.1016/j.bbrc.2018.08.145; Copyright (c) 2018 Published by Elsevier Inc.; Country of input: International Atomic Energy Agency (IAEA)
Record Type
Journal Article
Journal
Biochemical and Biophysical Research Communications; ISSN 0006-291X;
; CODEN BBRCA9; v. 504(1); p. 137-142

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Krenning, Eric; Kwekkeboom, Dik; Jong, Marion de, E-mail: r.valkema@erasmusmc.nl
International Atomic Energy Agency, Industrial Applications and Chemistry Section, Vienna (Austria)2010
International Atomic Energy Agency, Industrial Applications and Chemistry Section, Vienna (Austria)2010
AbstractAbstract
No abstract available
Primary Subject
Source
Mar 2010; 68 p; Technical meeting on therapeutic radiopharmaceuticals; Vienna (Austria); 16-20 Nov 2009; Published as PowerPoint presentation only; Working material
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Report
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