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[PMID]: 29426600
[Au] Autor:Ohlemiller KK; Kaur T; Warchol ME; Withnell RH
[Ad] Address:Washington University School of Medicine, Department of Otolaryngology, Central Institute for the Deaf at Washington University School of Medicine, Fay and Carl Simons Center for Hearing and Deafness, Saint Louis MO, USA. Electronic address: kohlemiller@wustl.edu.
[Ti] Title:The endocochlear potential as an indicator of reticular lamina integrity after noise exposure in mice.
[So] Source:Hear Res;361:138-151, 2018 Apr.
[Is] ISSN:1878-5891
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The endocochlear potential (EP) provides part of the electrochemical drive for sound-driven currents through cochlear hair cells. Intense noise exposure (110 dB SPL, 2 h) differentially affects the EP in three inbred mouse strains (C57BL/6 [B6], CBA/J [CBA], BALB/cJ [BALB]) (Ohlemiller and Gagnon, 2007, Hearing Research 224:34-50; Ohlemiller et al., 2011, JARO 12:45-58). At least for mice older than 3 mos, B6 mice are unaffected, CBA mice show temporary EP reduction, and BALB mice may show temporary or permanent EP reduction. EP reduction was well correlated with histological metrics for injury to stria vascularis and spiral ligament, and little evidence was found for holes or tears in the reticular lamina that might 'short out' the EP. Thus we suggested that the genes and processes that underlie the strain EP differences primarily impact cochlear lateral wall, not the organ of Corti. Our previous work did not test the range of noise exposure conditions over which strain differences apply. It therefore remained possible that the relation between exposure severity and acute EP reduction simply has a higher exposure threshold in B6 mice compared to CBA and BALB. We also did not test for age dependence. It is well established that young adult animals are especially vulnerable to noise-induced permanent threshold shifts (NIPTS). It is unknown, however, whether heightened vulnerability of the lateral wall contributes to this condition. The present study extends our previous work to multiple noise exposure levels and durations, and explicitly compares young adult (6-7 wks) and older mice (>4 mos). We find that the exposure level-versus-acute EP relation is dramatically strain-dependent, such that B6 mice widely diverge from both CBA and BALB. For all three strains, however, acute EP reduction is greater in young mice. Above 110 dB SPL, all mice exhibited rapid and severe EP reduction that is likely related to tearing of the reticular lamina. By contrast, EP-versus-noise duration examined at 104 dB suggested that different processes contribute to EP reduction in young and older mice. The average EP falls to a constant level after ∼7.5 min in older mice, but progressively decreases with further exposure in young mice. Confocal microscopy of organ of Corti surface preparations stained for phalloidin and zonula occludens-1 (ZO-1) indicated this corresponds to rapid loss of outer hair cells (OHCs) and formation of both holes and tears in the reticular lamina of young mice. In addition, when animals exposed at 119 dB were allowed to recover for 1 mo, only young B6 mice showed collapse of the EP to ≤5 mV. Confocal analysis suggested novel persistent loss of tight junctions in the lateral organ of Corti. This may allow paracellular leakage that permanently reduces the EP. From our other findings, we propose that noise-related lateral wall pathology in young CBA and BALB mice promotes hair cell loss and opening of the reticular lamina. The heightened vulnerability of young adult animals to noise exposure may in part reflect special sensitivity of the organ of Corti to acute lateral wall dysfunction at younger ages. This feature appears genetically modifiable.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

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[PMID]: 29352609
[Au] Autor:Setz C; Benischke AS; Pinho Ferreira Bento AC; Brand Y; Levano S; Paech F; Leitmeyer K; Bodmer D
[Ad] Address:Department of Biomedicine, University of Basel, Hebelstrasse 20, 4031, Basel, Switzerland; Clinic for Otolaryngology, Head and Neck Surgery, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland.
[Ti] Title:Induction of mitophagy in the HEI-OC1 auditory cell line and activation of the Atg12/LC3 pathway in the organ of Corti.
[So] Source:Hear Res;361:52-65, 2018 Apr.
[Is] ISSN:1878-5891
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Autophagy is a highly evolutionary conserved quality control defense mechanism within cells, which has also been implicated in cell death processes. In the mammalian inner ear, autophagy has been shown to play a role during early morphogenesis as well as in adult cochlear hair cells exposed to ototoxic insults. Mitophagy, a selective autophagic cell process targeting mitochondria, hasn't been studied in the inner ear so far. On this work, we searched for molecular indicators of mitophagy within House Ear Institute-Organ of Corti-1 (HEI-OC1) cells as well as in the organ of Corti (OC). We first tested for the expression of Pink1/Park2 mRNA in 5-day-old C57BL/6 mice's cochleae using RT-PCR. We focused on the induction of mitophagy in HEI-OC1 cells as well as in the OC and investigated a possible mitophagic potential of the aminoglycoside agent gentamicin. The induction of mitophagy in HEI-OC1 cells was detected by objectivizing the translocation of fluorescence-tagged LC3 to mitochondria using confocal microscopy after a 6-h incubation with a well-described mitochondrial uncoupler and mitophagy-inducing agent: carbonyl cyanide m-chlorophenyl hydrazone (CCCP). Incubation with gentamicin generated no mitochondrial translocation of LC3. Protein levels of COXIV, Atg5/12 and LC3 were evaluated by an immunoblot analysis after a 24-h CCCP treatment as well as gentamicin. We demonstrated mitophagy after CCCP exposure in HEI-OC1 cells by showing a downregulation of COXIV. A downregulation of COXIV could also be visualized in the OC after CCCP. A significant oxygen consumption rate (OCR) changed in cells treated with CCCP as well as significant morphological changes of mitochondria by electron microscopy (EM) strengthen this assumption. Gentamicin exposure generated no impact on OCR or mitochondrial morphological changes by EM. Finally, we demonstrated changes in the expression of Atg12 and LC3 proteins in both the OC and HEI-OC1 cells after CCCP exposure but not after gentamicin. Our data indicate that gentamicin had no impact in the activation of mitophagy-neither in the HEI-OC1 cell line nor in the OC. Therefore, we speculate that mitophagic-independent mechanisms may underly aminoglycoside ototoxicity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  3 / 5293 MEDLINE  
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[PMID]: 28450830
[Au] Autor:Elliott KL; Kersigo J; Pan N; Jahan I; Fritzsch B
[Ad] Address:Department of Biology, University of IowaIowa City, IA, USA.
[Ti] Title:Spiral Ganglion Neuron Projection Development to the Hindbrain in Mice Lacking Peripheral and/or Central Target Differentiation.
[So] Source:Front Neural Circuits;11:25, 2017.
[Is] ISSN:1662-5110
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:We investigate the importance of the degree of peripheral or central target differentiation for mouse auditory afferent navigation to the organ of Corti and auditory nuclei in three different mouse models: first, a mouse in which the differentiation of hair cells, but not central auditory nuclei neurons is compromised ( ); second, a mouse in which hair cell defects are combined with a delayed defect in central auditory nuclei neurons ( ), and third, a mouse in which both hair cells and central auditory nuclei are absent ( ). Our results show that neither differentiated peripheral nor the central target cells of inner ear afferents are needed (hair cells, cochlear nucleus neurons) for segregation of vestibular and cochlear afferents within the hindbrain and some degree of base to apex segregation of cochlear afferents. These data suggest that inner ear spiral ganglion neuron processes may predominantly rely on temporally and spatially distinct molecular cues in the region of the targets rather than interaction with differentiated target cells for a crude topological organization. These developmental data imply that auditory neuron navigation properties may have evolved before auditory nuclei.
[Mh] MeSH terms primary: Basic Helix-Loop-Helix Transcription Factors/deficiency
Cell Differentiation/genetics
Hair Cells, Auditory/physiology
Nervous System Malformations/pathology
PAX2 Transcription Factor/deficiency
Rhombencephalon/pathology
Spiral Ganglion
[Mh] MeSH terms secundary: Animals
Animals, Newborn
Auditory Pathways/embryology
Basic Helix-Loop-Helix Transcription Factors/genetics
Cochlear Nucleus/cytology
Cochlear Nucleus/embryology
Cochlear Nucleus/growth & development
Embryo, Mammalian
Mice
Mice, Knockout
Nervous System Malformations/genetics
PAX2 Transcription Factor/genetics
Spiral Ganglion/embryology
Spiral Ganglion/growth & development
Spiral Ganglion/pathology
beta-Galactosidase/genetics
beta-Galactosidase/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Atoh1 protein, mouse); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (PAX2 Transcription Factor); 0 (Pax2 protein, mouse); EC 3.2.1.23 (beta-Galactosidase)
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[Js] Journal subset:IM
[Da] Date of entry for processing:170429
[St] Status:MEDLINE
[do] DOI:10.3389/fncir.2017.00025

  4 / 5293 MEDLINE  
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[PMID]: 29513056
[Au] Autor:Tillinger JA; Gupta C; Ila K; Ahmed J; Mittal J; Van De Water TR; Eshraghi AA
[Ad] Address:a Department of Otolaryngology, Hearing Research Laboratory , Miller School of Medicine University of Miami , Miami , FL , USA.
[Ti] Title:l-N-acetylcysteine protects outer hair cells against TNFα initiated ototoxicity in vitro.
[So] Source:Acta Otolaryngol;:1-9, 2018 Mar 07.
[Is] ISSN:1651-2251
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: The present study is aimed at determining the efficacy and exploring the mechanisms by which l-N-acetylcysteine (l-NAC) provides protection against tumor necrosis factor-alpha (TNFα)-induced oxidative stress damage and hair cell loss in 3-day-old rat organ of Corti (OC) explants. Previous work has demonstrated a high level of oxidative stress in TNFα-challenged OC explants. TNFα can potentially play a significant role in hair cell loss following an insult to the inner ear. l-NAC has shown to provide effective protection against noise-induced hearing loss in laboratory animals but mechanisms of this otoprotective effect are not well-defined. DESIGN: Rat OC explants were exposed to either: (1) saline control (N = 12); (2) TNFα (2 µg/ml, N = 12); (3) TNFα+l-NAC (5 mM, N = 12); (4) TNFα+l-NAC (10 mM, N = 12); or (5) l-NAC (10 mM, N = 12). Outer hair cell (OHC) density, levels of reactive oxygen species (ROS), lipid peroxidation of cell membranes, gluthathione activity, and mitochondrial viability were assayed. RESULTS: l-NAC (5 and 10 mM) provided protection for OHCs from ototoxic level of TNFα in OC explants. Groups treated with TNFα+l-NAC (5 mM) showed a highly significant reduction of both ROS (p < 0.01) and 4-hydroxy-2-nonenal immunostaining (p < 0.001) compared to TNFα-challenged explants. Total glutathione levels were low in TNFα-challenged explants compared to control and TNFα+l-NAC (5 mM) treated explants (p < 0.001). CONCLUSIONS: l-NAC is a promising treatment for protecting auditory HCs from TNFα-induced oxidative stress and subsequent loss via programmed cell death.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.1080/00016489.2018.1440086

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[PMID]: 29436578
[Au] Autor:Zhong C; Jiang Z; Guo Q; Zhang X
[Ad] Address:Department of Otolaryngology, Southwest Hospital, The Third Military Medical University, Chongqing 400038, P.R. China.
[Ti] Title:Protective effect of adenovirus-mediated erythropoietin expression on the spiral ganglion neurons in the rat inner ear.
[So] Source:Int J Mol Med;41(5):2669-2677, 2018 May.
[Is] ISSN:1791-244X
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:The aim of the present study was to evaluate the expression of erythropoietin (Epo) and the Epo receptor (Epo­R) in the spiral ganglion neurons (SGNs) of the rat inner ear, and to assess the effect of Epo adenovirus vector (Ad­Epo) on the spontaneous apoptosis of SGNs. A total of 60 ears from 30 healthy neonatal (2­3 days postnatal) Sprague­Dawley rats were used to examine the expression of Epo in the SGNs. The rats were divided into three groups: The negative control group, the vector control group [infected with a green fluorescent protein expression vector (Ad­GFP)] and the Ad­Epo group (infected with Ad­Epo). The expression of Epo and Epo­R was detected by immunohistochemistry and dual immunofluorescence staining using polyclonal antibodies directed against Epo and Epo­R, followed by confocal laser­scanning microscopy. An adenovirus vector was constructed and used to transfect the cultured SGNs. Following adenovirus infection, apoptosis of the SGNs was evaluated and Epo protein expression was assessed. Epo and Epo­R were widely expressed in the plasma membrane and the cytoplasm of the SGNs, as well as in the organ of Corti and the stria vascularis within the inner ear. Epo protein expression was upregulated in the Ad­Epo group compared with that in the other two groups (P<0.05). Apoptotic cells were seldom observed at day 4 of SGN culture in the negative control group. At day 7, marked apoptotic cells were detected in the negative control group and the vector control group. The apoptosis level in the Ad­Epo group was significantly decreased compared with that in the negative control group or the vector control group at day 7 (P<0.05). In conclusion, Epo and Epo­R are expressed in the SGNs of the inner ear of the rat, and Ad­Epo can decrease the spontaneous apoptosis of SGNs, which may provide a basis for the prevention or alleviation of sensorineural hearing loss.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Process
[do] DOI:10.3892/ijmm.2018.3455

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[PMID]: 29495686
[Au] Autor:Marnell D; Jabeen T; Nam JH
[Ad] Address:Department of Biomedical Engineering, University of Rochester, 204 Goergen Hall, Rochester, New York 14627, USA.
[Ti] Title:Hydrostatic measurement and finite element simulation of the compliance of the organ of Corti complex.
[So] Source:J Acoust Soc Am;143(2):735, 2018 Feb.
[Is] ISSN:1520-8524
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In the mammalian cochlea, the geometrical and mechanical properties of the organ of Corti complex (OCC, consisting of the tectorial membrane, the organ of Corti, and the basilar membrane) have fundamental consequences for understanding the physics of hearing. Despite efforts to correlate the mechanical properties of the OCC with cochlear function, experimental data of OCC stiffness are limited due to difficulties in measurement. Modern measurements of the OCC stiffness use microprobes exclusively, but suffer ambiguity when defining the physiologically relevant stiffness due to the high nonlinearity in the force-displacement relationship. The nonlinearity stems from two sources. First, microprobes apply local force instead of fluid pressure across the OCC. Second, to obtain the functionally relevant stiffness, the OCC is deformed well beyond in vivo levels (>10 µm). The objective of this study was to develop an alternative technique to overcome challenges intrinsic to the microprobe method. Using a custom-designed microfluidic chamber system, hydrostatic pressures were applied to the excised gerbil cochlea. Deformations of the OCC due to hydrostatic pressures were analyzed through optical-axis image correlation. The pressure-displacement relationship was linear within nanoscale displacement ranges (<1 µm). To compare the results in this paper with existing measurements, a three-dimensional finite element model was used.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:In-Data-Review
[do] DOI:10.1121/1.5023206

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[PMID]: 29174619
[Au] Autor:Elliott SJ; Ni G
[Ad] Address:Institute of Sound and Vibration Research, University of Southampton, Southampton, SO17 1BJ, UK. Electronic address: sje@isvr.soton.ac.uk.
[Ti] Title:An elemental approach to modelling the mechanics of the cochlea.
[So] Source:Hear Res;360:14-24, 2018 Mar.
[Is] ISSN:1878-5891
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The motion along the basilar membrane in the cochlea is due to the interaction between the micromechanical behaviour of the organ of Corti and the fluid movement in the scalae. By dividing the length of the cochlea into a finite number of elements and assuming a given radial distribution of the basilar membrane motion for each element, a set of equations can be separately derived for the micromechanics and for the fluid coupling. These equations can then be combined, using matrix methods, to give the fully coupled response. This elemental approach reduces to the classical transmission line model if the micromechanics are assumed to be locally-reacting and the fluid coupling is assumed to be entirely one-dimensional, but is also valid without these assumptions. The elemental model is most easily formulated in the frequency domain, assuming quasi-linear behaviour, but a time domain formulation, using state space method, can readily incorporate local nonlinearities in the micromechanics. Examples of programs are included for the elemental model of a human cochlea that can be readily modified for other species.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1711
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:In-Data-Review

  8 / 5293 MEDLINE  
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[PMID]: 29485861
[Au] Autor:Kempfle JS; Nguyen K; Hamadani C; Koen N; Edge AS; Kashemirov BA; Jung DH; McKenna CE
[Ad] Address:Department of Otolaryngology and The Eaton-Peabody Laboratories, Massachusetts Eye and Ear Infirmary , Boston, Massachusetts 02114, United States.
[Ti] Title:Bisphosphonate-Linked TrkB Agonist: Cochlea-Targeted Delivery of a Neurotrophic Agent as a Strategy for the Treatment of Hearing Loss.
[So] Source:Bioconjug Chem;, 2018 Feb 27.
[Is] ISSN:1520-4812
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hearing loss affects more than two-thirds of the elderly population, and more than 17% of all adults in the U.S. Sensorineural hearing loss related to noise exposure or aging is associated with loss of inner ear sensory hair cells (HCs), cochlear spiral ganglion neurons (SGNs), and ribbon synapses between HCs and SGNs, stimulating intense interest in therapies to regenerate synaptic function. 7,8-Dihydroxyflavone (DHF) is a selective and potent agonist of tropomyosin receptor kinase B (TrkB) and protects the neuron from apoptosis. Despite evidence that TrkB agonists can promote survival of SGNs, local delivery of drugs such as DHF to the inner ear remains a challenge. We previously demonstrated in an animal model that a fluorescently labeled bisphosphonate, 6-FAM-Zol, administered to the round window membrane penetrated the membrane and diffused throughout the cochlea. Given their affinity for bone mineral, including cochlear bone, bisphosphonates offer an intriguing modality for targeted delivery of neurotrophic agents to the SGNs to promote survival, neurite outgrowth, and, potentially, regeneration of synapses between HCs and SGNs. The design and synthesis of a bisphosphonate conjugate of DHF (Ris-DHF) is presented, with a preliminary evaluation of its neurotrophic activity. Ris-DHF increases neurite outgrowth in vitro, maintains this ability after binding to hydroxyapatite, and regenerates synapses in kainic acid-damaged cochlear organ of Corti explants dissected in vitro with attached SGNs. The results suggest that bisphosphonate-TrkB agonist conjugates have promise as a novel approach to targeted delivery of drugs to treat sensorineural hearing loss.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:Publisher
[do] DOI:10.1021/acs.bioconjchem.8b00022

  9 / 5293 MEDLINE  
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[PMID]: 29481711
[Au] Autor:Rathinam R; Rosati R; Jamesdaniel S
[Ad] Address:Institute of Environmental Health Sciences, Wayne State University, Detroit, Michigan.
[Ti] Title:Cover Image, Volume 119, Number 4, April 2018.
[So] Source:J Cell Biochem;119(4):i, 2018 Apr.
[Is] ISSN:1097-4644
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cover: The cover image, by Rajamani Rathinam et al, is based on the Original Research Article, CRISPR/Cas9-mediated knockout of Lim-domain only four retards organ of Corti cell growth, DOI: 10.1002/jcb.26529.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180226
[Lr] Last revision date:180226
[St] Status:In-Data-Review
[do] DOI:10.1002/jcb.26785

  10 / 5293 MEDLINE  
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[PMID]: 29460824
[Au] Autor:Serinan E; Altun Z; Aktas S; Çeçen E; Olgun N
[Ad] Address:Department of Basic Oncology, Dokuz Eylül University Institute of Oncology, Izmir, Turkey.
[Ti] Title:Comparison of Cisplatin with Lipoplatin in Terms of Ototoxicity.
[So] Source:J Int Adv Otol;, 2018 Feb 20.
[Is] ISSN:1308-7649
[Cp] Country of publication:Turkey
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Cisplatin (CDDP) is an anti-neoplastic agent that has been used in treatments of both pediatric and adult cancers. It has many side effects, such as ototoxicity, nephrotoxicity, and neurotoxicity. Lipoplatin (LIPO) is a nanomolecule with 110 nm diameter and composed of lipids and CDDP. In this study, we aimed to compare the toxic effects of LIPO with CDDP in the cochlear cells with anti-tumoral doses determined in neuroblastoma cells. MATERIALS AND METHODS: House Ear Institute Organ Corti 1 (HEI-OC1), MYC-N amplified KELLY, and MYC-N non-amplified SH-SY5Y human neuroblastoma cells were used in this study. Firstly, anti-tumoral lethal dose 50 (LD50) of LIPO and CDDP were determined using the WST-1 assay in both neuroblastoma cells. Then anti-tumoral doses of CDDP and LIPO were applied on HEI-OC1 cells for evaluating the toxic effects. The apoptotic cell death was measured using flow cytometric analysis of annexin-V/7-amino-actinomycin (7-AAD) and cell cycle tests. RESULTS: LIPO or CDDP inhibited cell viability in a dose- and time-dependent manner in both neuroblastoma and HEI-OC1 cells. LD50 values were selected as 20 mM for CDDP and 750 mM for LIPO in neuroblastoma cells. After the 48-hour incubation, KELLY cells treated with 20 mM CDDP and 750 mM LIPO had a 53% viability; SH-SY5Y cells treated 20 mM CDDP and 750 mM LIPO had a 45% and 58% viability, respectively; and HEI-OC1 cells treated with 20 mM CDDP and 750 mM LIPO had a 65% and 82% viability, respectively. CONCLUSION: LIPO showed less toxic effects in the HEI-OC1 cells compared to CDDP at anti-tumoral doses.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[St] Status:Publisher
[do] DOI:10.5152/iao.2018.4097


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