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Nature 471(7337):177–182\nBriggman KL, Bock DD (2012) Volume electron microscopy for neuronal circuit reconstruction. Curr Opin Neurobiol 22(1):154–161\nBriggman KL, Helmstaedter M et al (2011) Wiring specificity in the direction-selectivity circuit of the retina. Nature 471(7337):183–188\nDenk W, Horstmann H (2004) Serial block-face scanning electron microscopy to reconstruct three-dimensional tissue nanostructure. PLoS Biol 2(11):e329\nHayworth KJ, Kasthuri N et al (2006) Automating the collection of ultrathin serial sections for large volume TEM reconstructions. Microsc Microanal 12(Suppl 2):86–87\nHelmstaedter M, Briggman KL et al (2008) 3D structural imaging of the brain with photons and electrons. Curr Opin Neurobiol 18(6):633–641\nHelmstaedter M, Briggman KL et al (2011) High-accuracy neurite reconstruction for high-throughput neuroanatomy. Nat Neurosci 14(8):1081–1088\nHelmstaedter M, Mitra PP (2012) Computational methods and challenges for large-scale circuit mapping. Curr Opin Neurobiol 22(1):162–169\nKnott G, Marchman H et al (2008) Serial section scanning electron microscopy of adult brain tissue using focused ion beam milling. J Neurosci 28(12):2959–2964\nWhite JG, Southgate E et al (1986) The structure of the nervous system of the nematode Caenorhabditis elegans. Philos Trans R Soc Lond B Biol Sci 314:1–340",{"EN":68},"The nervous system is characterized by extremely complex cell-to-cell interactions which primarily occur via chemical synapses. Mapping the structure of these intercellular networks is one of the major challenges in neuroscience. The new field of connectomics which has developed in recent years aims at the dense reconstruction of increasingly comprehensive nerve cell networks. Automated volume electron microscopy techniques are employed for image acquisition. A major obstacle, however, is data reconstruction, for which unusual solutions (e.g., mass reconstruction by crowd sourcing and online computer games) are currently being pursued.",{"EN":70},"Connectomics: novel methods for the dense reconstruction of neuronal circuits",{"VOID":72},"10.1007\u002Fs13295-013-0039-z","PUBLICATION","VERIFIED","Auto Verify","https:\u002F\u002Fwww.degruyter.com\u002Fdocument\u002Fdoi\u002F10.1007\u002Fs13295-013-0039-z\u002Fhtml",[78],{"id":79,"sortIndex":20,"researcher":19,"roles":80,"affiliations":82,"properties":94},"d87972c8-beb5-4e5e-afeb-0f9a9f788b88",[81],"AUTHOR",[83],{"id":19,"sortIndex":20,"affiliation":84,"properties":19},{"id":85,"createTime":86,"updateTime":87,"relativeEntities":88,"slug":89,"properties":90,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},"358fe8ae-10e9-4772-a5ea-2ff2ca0495bd","2023-12-02T21:14:29.446+00:00","2024-10-17T07:33:50.137+00:00",[],"Max-Planck-Institute-of-Neurobiology-Martinsried-Germany",{"title":91},{"VI":92},"Max Planck Institute of Neurobiology, Martinsried, Germany","AFFILIATION",{"title":95},{"VI":96},"M. Helmstaedter","ARTICLE",{"url":76,"publisher":99,"properties":113},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":100,"slug":10,"properties":101,"entityType":17,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20,"subjectFields":105,"manageAffiliations":106,"indexDatabases":107,"url":19,"thumbnailPath":19,"statistic":108,"gsStatistic":19,"type":53,"analyzePriority":19},[],{"issn":102,"title":103,"url":104},{"VOID":13},{"EN":10},{"VOID":16},[],[],[],{"impactFactor":20,"impactFactorByYear":109,"i10Index":30,"i10IndexLast5Year":20,"totalPublication":31,"totalPublicationByYear":110,"totalCitation":37,"totalCitationByYear":111,"totalCitationPerPublication":45,"totalCitationPerPublicationByYear":112,"hindexLast5Year":52,"hindex":52},{"2012":26,"2013":27,"2015":28,"2016":29},{"2010":33,"2011":33,"2012":33,"2013":34,"2014":35,"2015":36,"2016":34},{"2010":39,"2011":40,"2012":41,"2013":42,"2014":43,"2015":44,"2016":40},{"2010":47,"2011":48,"2012":27,"2013":30,"2014":49,"2015":50,"2016":51},{"volume":114,"pages":116},{"VOID":115},"4",{"VOID":117},"18-21","2013-03-10",2013,false,{"id":122,"createTime":123,"updateTime":124,"relativeEntities":125,"slug":126,"properties":127,"entityType":73,"verifyStatus":74,"verifyTime":124,"verifyNote":75,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20,"primaryUrl":136,"fullTextUrl":19,"authors":137,"publicationType":97,"publisherRelationship":155,"citationCount":19,"citationInfo":19,"publishDate":175,"publishYear":176,"citationAnalyzeStatus":18,"lastCitationAnalyze":19,"indexDatabases":19,"openAccess":19,"references":19,"isForceReanalyzing":120},"b2f6aa0a-829a-4f7e-a508-e8ecdb42af9f","2024-02-08T07:31:21.068+00:00","2025-01-30T22:38:45.749+00:00",[],"Hereditary-hearing-loss-in-humans-the-importance-of-genetic-approaches-for-clinical-medicine-and-basic-science",{"references":128,"abstract":130,"title":132,"doi":134},{"VOID":129},"Morton CC, Nance WE (2006) Newborn hearing screening-a silent revolution. N Engl J Med 354:2151–2164\nDavis AC (1989) The prevalence of hearing impairment and reported hearing disability among adults in Great Britain. Int J Epidemiol 18:911–917\nNoben-Trauth K, Zheng QY, Johnson KR (2003) Association of cadherin 23 with polygenic inheritance and genetic modification of sensorineural hearing loss. Nat Genet 35:21–23\nToriello HV, Smith SD (eds) (2013) Hereditary hearing loss and its syndromes (Oxford monographs on medical genetics), 3rd edn. Oxford University Press, Oxford\nWang Q, Xue Y, Zhang Y et al (2013) Genetic basis of Y-linked hearing impairment. Am J Hum Genet 92:301–306\nAltshuler D, Daly MJ, Lander ES (2008) Genetic mapping in human disease. Science 322:881–888\nBoycott KM, Vanstone MR, Bulman DE, MacKenzie AE (2013) Rare-disease genetics in the era of next-generation sequencing: discovery to translation. Nat Rev Genet 14:681–691\nLeibovici M, Safieddine S, Petit C (2008) Mouse models for human hereditary deafness. Curr Top Dev Biol 84:385–429\nVrijens K, Van Laer L, Van Camp G (2008) Human hereditary hearing impairment: mouse models can help to solve the puzzle. Hum Genet 124:325–348\nBrown SD, Hardisty-Hughes RE, Mburu P (2008) Quiet as a mouse: dissecting the molecular and genetic basis of hearing. Nat Rev Genet 9:277–290\nWhitfield TT (2002) Zebrafish as a model for hearing and deafness. J Neurobiol 53:157–171\nRead AP, Newton VE (1997) Waardenburg syndrome. J Med Genet 34:656–665\nLewis MA, Quint E, Glazier AM et al (2009) An ENU-induced mutation of miR-96 associated with progressive hearing loss in mice. Nat Genet 41:614–668\nMencía A, Modamio-Høybjør S, Redshaw N et al (2009) Mutations in the seed region of human miR-96 are responsible for nonsyndromic progressive hearing loss. Nat Genet 41:609–613\nPrezant TR, Agapian JV, Bohlman MC et al (1993) Mitochondrial ribosomal RNA mutation associated with both antibiotic- induced and non-syndromic deafness. Nat Genet 4:289–294\nEstivill X, Govea N, Barcelo E et al (1998) Familial progressive sensorineural deafness is mainly due to the mtDNA A1555G mutation and is enhanced by treatment of aminoglycosides. Am J Hum Genet 62:27–35\nJacobs HT, Hutchin TP, Kappi T et al (2005) Mitochondrial DNA mutations in patients with postlingual, nonsyndromic hearing impairment. Eur J Hum Genet 13:26–33\nAmeln S von, Wang G, Boulouiz R et al (2012) A mutation in PNPT1, encoding mitochondrial-RNA-import protein PNPase, causes hereditary hearing loss. Am J Hum Genet 91:919–927\nCheng J, Zhu Y, He S et al (2011) Functional mutation of SMAC\u002FDIABLO, encoding a mitochondrial proapoptotic protein, causes human progressive hearing loss DFNA64. Am J Hum Genet 89:56–66\nAhmed ZM, Yousaf R, Lee BC et al (2011) Functional null mutations of MSRB3 encoding methionine sulfoxide reductase are associated with human deafness DFNB74. Am J Hum Genet 88:19–29\nRichardson GP, Monvel JB de, Petit C (2011) How the genetics of deafness illuminates auditory physiology. Annu Rev Physiol 73:311–334\nDror AA, Avraham KB (2010) Hearing impairment: a panoply of genes and functions. Neuron 68:293–308\nPetit C, Richardson GP (2009) Linking genes underlying deafness to hair-bundle development and function. Nat Neurosci 12:703–710\nSafieddine S, El-Amraoui A, Petit C (2012) The auditory hair cell ribbon synapse: from assembly to function. Annu Rev Neurosci 35:509–528\nMoser T, Predoehl F, Starr A (2013) Review of hair cell synapse defects in sensorineural hearing impairment. Otol Neurotol 34:995–1004\nDel Castillo FJ, Del Castillo I (2012) Genetics of isolated auditory neuropathies. Front Biosci 17:1251–1265\nZdebik AA, Wangemann P, Jentsch TJ (2009) Potassium ion movement in the inner ear: insights from genetic disease and mouse models. Physiology 24:307–316\nAlford RL, Arnos KS, Fox M et al (2014) American College of Medical Genetics and Genomics guideline for the clinical evaluation and etiologic diagnosis of hearing loss. Genet Med 16:347–355",{"EN":131},"Hereditary hearing loss is one of the most common monogenic diseases in humans and, depending on the severity of symptoms and age of onset, dysfunction of one of the main sensory systems can cause significant problems for the affected individual and his\u002Fher social environment. The diagnostic workup of hearing impairment is complicated by a pronounced phenotypic variability and extensive genetic heterogeneity. Nevertheless, many forms of monogenic hearing impairment have been elucidated in recent years by genetic approaches. In addition to improved counselling and medical management of patients and families, these research findings have contributed significantly to the identification of functionally relevant molecules of the inner ear and have thus helped us to better understand the molecular physiology of hearing and the pathophysiology of hearing impairment.",{"EN":133},"Hereditary hearing loss in humans: the importance of genetic approaches for clinical medicine and basic science",{"VOID":135},"10.1007\u002Fs13295-014-0061-9","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs13295-014-0061-9",[138],{"id":139,"sortIndex":20,"researcher":19,"roles":140,"affiliations":141,"properties":152},"37fc2ab4-20c8-4846-98e8-c95937435dff",[81],[142],{"id":19,"sortIndex":20,"affiliation":143,"properties":19},{"id":144,"createTime":145,"updateTime":146,"relativeEntities":147,"slug":148,"properties":149,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},"00ed148d-b0c6-4d45-8bd6-b09b91e8b244","2023-12-10T07:42:40.417+00:00","2025-06-11T14:24:34.843+00:00",[],"Institute-of-Human-Genetics-University-Medical-Center-Hamburg-Eppendorf-Hamburg-Germany",{"title":150},{"VI":151},"Institute of Human Genetics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany",{"title":153},{"VI":154},"C. Kubisch",{"url":136,"publisher":156,"properties":170},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":157,"slug":10,"properties":158,"entityType":17,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20,"subjectFields":162,"manageAffiliations":163,"indexDatabases":164,"url":19,"thumbnailPath":19,"statistic":165,"gsStatistic":19,"type":53,"analyzePriority":19},[],{"issn":159,"title":160,"url":161},{"VOID":13},{"EN":10},{"VOID":16},[],[],[],{"impactFactor":20,"impactFactorByYear":166,"i10Index":30,"i10IndexLast5Year":20,"totalPublication":31,"totalPublicationByYear":167,"totalCitation":37,"totalCitationByYear":168,"totalCitationPerPublication":45,"totalCitationPerPublicationByYear":169,"hindexLast5Year":52,"hindex":52},{"2012":26,"2013":27,"2015":28,"2016":29},{"2010":33,"2011":33,"2012":33,"2013":34,"2014":35,"2015":36,"2016":34},{"2010":39,"2011":40,"2012":41,"2013":42,"2014":43,"2015":44,"2016":40},{"2010":47,"2011":48,"2012":27,"2013":30,"2014":49,"2015":50,"2016":51},{"volume":171,"pages":173},{"VOID":172},"5",{"VOID":174},"67-71","2014-09-26",2014,{"id":178,"createTime":179,"updateTime":179,"relativeEntities":180,"slug":19,"properties":181,"entityType":73,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20,"primaryUrl":190,"fullTextUrl":19,"authors":191,"publicationType":97,"publisherRelationship":222,"citationCount":19,"citationInfo":19,"publishDate":175,"publishYear":176,"citationAnalyzeStatus":18,"lastCitationAnalyze":19,"indexDatabases":19,"openAccess":19,"references":19,"isForceReanalyzing":120},"36b73e5f-f878-45a5-b8b7-da957201bc4d","2023-12-29T22:15:13.099+00:00",[],{"references":182,"abstract":184,"title":186,"doi":188},{"VOID":183},"Ashida G, Carr CE (2011) Sound localization: Jeffress and beyond. Curr Opin Neurobiol 21:745–751\nBender KJ, Trussell LO (2012) The physiology of the axon initial segment. Annu Rev Neurosci 35:249–265\nBerger C, Meyer EMM, Ammer JJ, Felmy F (2014) Large somatic synapses on neurons in the ventral lateral lemniscus work in pairs. J Neurosci 34:3237–3246\nFettiplace R, Hackney CM (2006) The sensory and motor roles of auditory hair cells. Nat Rev Neurosci 7:19–29\nGoldberg JM, Brown PB (1969) Response of binaural neurons of dog superior olivary complex to dichotic tonal stimuli: some physiological mechanisms of sound localization. J Neurophysiol 32:613–636\nGolding NL, Oertel D (2012) Synaptic integration in dendrites: exceptional need for speed. J Physiol 590:5563–5569\nGrothe B, Pecka M, McAlpine D (2010) Mechanisms of sound localization in mammals. Physiol Rev 90:983–1012\nHeld H (1893) Die centrale Gehörleitung. Arch Anat Physiol A3+4:201–248\nKuenzel T, Borst JGG, Heijden M van der (2011) Factors controlling the input-output relationship of spherical bushy cells in the gerbil cochlear nucleus. J Neurosci 31:4260–4273\nLorteije JAM, Rusu SI, Kushmerick C, Borst JGG (2009) Reliability and precision of the mouse calyx of Held synapse. J Neurosci 29:13770–13784\nMcGinley MJ, Liberman MC, Bal R, Oertel D (2012) Generating synchrony from the asynchronous: compensation for cochlear traveling wave delays by the dendrites of individual brainstem neurons. J Neurosci 32:9301–9311\nMyoga MH, Lehnert S, Leibold C et al (2014) Glycinergic inhibition tunes coincidence detection in the auditory brainstem. Nat Commun 5:3790\nOertel D, Bal R, Gardner SM et al (2000) Detection of synchrony in the activity of auditory nerve fibers by octopus cells of the mammalian cochlear nucleus. Proc Natl Acad Sci U S A 97:11773–11779\nOleskevich S, Youssoufian M, Walmsley B (2004) Presynaptic plasticity at two giant auditory synapses in normal and deaf mice. J Physiol 560:709–719\nRose JE, Brugge JF, Anderson DJ, Hind JE (1967) Phase-locked response to low-frequency tones in single auditory nerve fibers of the squirrel monkey. J Neurophysiol 30:769–793\nSätzler K, Söhl LF, Bollmann JH et al (2002) Three-dimensional reconstruction of a calyx of Held and its postsynaptic principal neuron in the medial nucleus of the trapezoid body. J Neurosci 22:10567–10579\nVonderschen K, Wagner H (2014) Detecting interaural time differences and remodeling their representation. Trends Neurosci 37:289–300",{"EN":185},"Giant synapses occur in four nuclei of the auditory brainstem. They are characterized by numerous active zones concentrated on the soma of the postsynaptic neuron and by rapid postsynaptic currents. At these sites, in the ventral cochlear nucleus, the medial and lateral nucleus of the trapezoid body and the ventral nucleus of the lateral lemniscus, faithful preservation of the temporal relation of action potentials to the sound—intercellular precision—is of the utmost importance for neuronal function. The precision of action potential transfer is supported by the largely unimodal integration and homogeneity of the single postsynaptic compartment. Due to the much more rapid time constant of the synaptic currents compared with the membrane time constant, membrane capacitance dominates postsynaptic integration, enhancing precision of action potential generation. Taken together, the properties of these giant synapses reduce the temporal jitter of the transmission of information in these auditory circuits.",{"EN":187},"Giant synapses in the central auditory system",{"VOID":189},"10.1007\u002Fs13295-014-0060-x","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs13295-014-0060-x",[192,207],{"id":193,"sortIndex":20,"researcher":19,"roles":194,"affiliations":195,"properties":204},"d1b6811d-6acc-43e8-85c5-581eafe29266",[81],[196],{"id":19,"sortIndex":20,"affiliation":197,"properties":19},{"id":198,"createTime":199,"updateTime":199,"relativeEntities":200,"slug":19,"properties":201,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},"be58bd10-3ec0-437e-a497-ab558ee65d90","2023-12-29T22:15:13.120+00:00",[],{"title":202},{"VI":203},"Abteilung Neurobiologie, Biologie Department II, Ludwig-Maximilians Universität München, Planegg-Martinsried, Germany",{"title":205},{"VI":206},"F. Felmy",{"id":208,"sortIndex":41,"researcher":19,"roles":209,"affiliations":210,"properties":219},"01b5d153-a0f3-4525-8740-b6bfcd5251bb",[81],[211],{"id":19,"sortIndex":20,"affiliation":212,"properties":19},{"id":213,"createTime":214,"updateTime":214,"relativeEntities":215,"slug":19,"properties":216,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},"cff0b08d-b444-4fda-b0b8-1c46d60e46eb","2023-12-29T22:15:13.210+00:00",[],{"title":217},{"VI":218},"Institut für Biologie 2, Lehrstuhl für Zoologie\u002FTierphysiologie, RWTH Aachen, Aachen, Germany",{"title":220},{"VI":221},"T. Künzel",{"url":190,"publisher":223,"properties":237},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":224,"slug":10,"properties":225,"entityType":17,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20,"subjectFields":229,"manageAffiliations":230,"indexDatabases":231,"url":19,"thumbnailPath":19,"statistic":232,"gsStatistic":19,"type":53,"analyzePriority":19},[],{"issn":226,"title":227,"url":228},{"VOID":13},{"EN":10},{"VOID":16},[],[],[],{"impactFactor":20,"impactFactorByYear":233,"i10Index":30,"i10IndexLast5Year":20,"totalPublication":31,"totalPublicationByYear":234,"totalCitation":37,"totalCitationByYear":235,"totalCitationPerPublication":45,"totalCitationPerPublicationByYear":236,"hindexLast5Year":52,"hindex":52},{"2012":26,"2013":27,"2015":28,"2016":29},{"2010":33,"2011":33,"2012":33,"2013":34,"2014":35,"2015":36,"2016":34},{"2010":39,"2011":40,"2012":41,"2013":42,"2014":43,"2015":44,"2016":40},{"2010":47,"2011":48,"2012":27,"2013":30,"2014":49,"2015":50,"2016":51},{"volume":238,"pages":239},{"VOID":172},{"VOID":240},"53-59",{"id":242,"createTime":243,"updateTime":244,"relativeEntities":245,"slug":246,"properties":247,"entityType":73,"verifyStatus":74,"verifyTime":244,"verifyNote":75,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20,"primaryUrl":256,"fullTextUrl":19,"authors":257,"publicationType":97,"publisherRelationship":286,"citationCount":19,"citationInfo":19,"publishDate":305,"publishYear":176,"citationAnalyzeStatus":18,"lastCitationAnalyze":19,"indexDatabases":19,"openAccess":19,"references":19,"isForceReanalyzing":120},"8d28ac7c-a11b-4c21-902b-63da006e6d7c","2023-11-25T08:02:52.850+00:00","2024-12-26T21:55:14.312+00:00",[],"ADAM10-%CE%B1-secretase-in-Alzheimer-s-disease-and-regulator-of-neurobiology",{"references":248,"abstract":250,"title":252,"doi":254},{"VOID":249},"Altmeppen HC, Prox J, Puig B et al (2011) Lack of a-disintegrin-and-metalloproteinase ADAM10 leads to intracellular accumulation and loss of shedding of the cellular prion protein in vivo. Mol Neurodegener 6:36\nJorissen E, Prox J, Bernreuther C et al (2010) The disintegrin\u002Fmetalloproteinase ADAM10 is essential for the establishment of the brain cortex. J Neurosci 30:4833–4844\nKuhn PH, Wang H, Dislich B et al (2010) ADAM10 is the physiologically relevant, constitutive alpha-secretase of the amyloid precursor protein in primary neurons. EMBO J 29:3020–3032\nPostina R, Schroeder A, Dewachter I et al (2004) A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model. J Clin Invest 113:1456–1464\nProx J, Bernreuther C, Altmeppen H et al (2013) Postnatal disruption of the disintegrin\u002Fmetalloproteinase ADAM10 in brain causes epileptic seizures, learning deficits, altered spine morphology, and defective synaptic functions. J Neurosci 33:12915–12928\nProx, J, Rittger, A, Saftig (2012) Physiological functions of the amyloid precursor protein secretases ADAM10, BACE1, and presenilin.Exp. Brain Res 217:331–341\nProx J, Willenbrock M, Weber S et al (2012) Tetraspanin15 regulates cellular trafficking and activity of the ectodomain sheddase ADAM10. Cell Mol Life Sci 69:2919–2932\nReiss K, Saftig P (2009) The “a disintegrin and metalloprotease” (ADAM) family of sheddases: physiological and cellular functions. Semin Cell Dev Biol 20:126–137\nSuh J, Choi SH, Romano DM et al (2013) ADAM10 missense mutations potentiate β-amyloid accumulation by impairing prodomain chaperone function. Neuron 80:385–401\nSuzuki K, Hayashi Y, Nakahara S et al (2012) Activity-dependent proteolytic cleavage of neuroligin-1. Neuron 76:410–422\nWeber S, Saftig P (2013) Ectodomain shedding and ADAMs in development. Development 139:3693–3709",{"EN":251},"Proteolytic and amyloidogenic processing of amyloid precursor protein (APP) by β- and γ-secretases are pathological hallmarks of Alzheimer’s disease (AD). These proteolytic activities lead to release of the amyloid-β peptides believed to cause neurological pathology and be linked to pathological progression in AD. Due to its capability to cleave APP within the toxic peptide sequence, the metalloproteinase ADAM10 (“a disintegrin and metalloprotease”) is a known antagonist of the disease-causing pathway. ADAM10 also plays a major role in the ectodomain shedding of a number of important cell surface proteins. In addition, ADAM10 is involved in the proteolytic activation cascade of the Notch receptor, which is of crucial function in developmental processes. The study of ADAM10-deficient mice also revealed that ADAM10 regulates synaptic function and synaptogenesis. Pharmacological activation of ADAM10 is postulated to represent a valuable strategy for prevention of AD. However, due to the multiple roles of ADAM10 in the brain, it will be challenging to find a suitable therapeutic window.",{"EN":253},"ADAM10: α-secretase in Alzheimer’s disease and regulator of neurobiology",{"VOID":255},"10.1007\u002Fs13295-014-0055-7","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs13295-014-0055-7",[258,274],{"id":259,"sortIndex":41,"researcher":19,"roles":260,"affiliations":261,"properties":271},"bbbd3b35-a568-41bf-a84d-dd8f1b966bdd",[81],[262],{"id":19,"sortIndex":20,"affiliation":263,"properties":19},{"id":264,"createTime":265,"updateTime":265,"relativeEntities":266,"slug":267,"properties":268,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},"9dc275cf-a1ce-4c42-b960-a1812bc848df","2023-11-25T08:02:52.860+00:00",[],"Biochemisches-Institut-Christian-Albrechts-Universit%C3%A4t-Kiel-Kiel-Germany",{"title":269},{"VI":270},"Biochemisches Institut, Christian-Albrechts Universität Kiel, Kiel, Germany",{"title":272},{"VI":273},"J. Prox",{"id":275,"sortIndex":20,"researcher":19,"roles":276,"affiliations":277,"properties":283},"e99c2531-fc1d-4545-81d0-f1b3ff371cb7",[81],[278],{"id":19,"sortIndex":20,"affiliation":279,"properties":19},{"id":264,"createTime":265,"updateTime":265,"relativeEntities":280,"slug":267,"properties":281,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},[],{"title":282},{"VI":270},{"title":284},{"VI":285},"P. Saftig",{"url":256,"publisher":287,"properties":301},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":288,"slug":10,"properties":289,"entityType":17,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20,"subjectFields":293,"manageAffiliations":294,"indexDatabases":295,"url":19,"thumbnailPath":19,"statistic":296,"gsStatistic":19,"type":53,"analyzePriority":19},[],{"issn":290,"title":291,"url":292},{"VOID":13},{"EN":10},{"VOID":16},[],[],[],{"impactFactor":20,"impactFactorByYear":297,"i10Index":30,"i10IndexLast5Year":20,"totalPublication":31,"totalPublicationByYear":298,"totalCitation":37,"totalCitationByYear":299,"totalCitationPerPublication":45,"totalCitationPerPublicationByYear":300,"hindexLast5Year":52,"hindex":52},{"2012":26,"2013":27,"2015":28,"2016":29},{"2010":33,"2011":33,"2012":33,"2013":34,"2014":35,"2015":36,"2016":34},{"2010":39,"2011":40,"2012":41,"2013":42,"2014":43,"2015":44,"2016":40},{"2010":47,"2011":48,"2012":27,"2013":30,"2014":49,"2015":50,"2016":51},{"volume":302,"pages":303},{"VOID":172},{"VOID":304},"37-42","2014-06-14",{"id":307,"createTime":308,"updateTime":309,"relativeEntities":310,"slug":311,"properties":312,"entityType":73,"verifyStatus":74,"verifyTime":309,"verifyNote":75,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20,"primaryUrl":321,"fullTextUrl":19,"authors":322,"publicationType":97,"publisherRelationship":387,"citationCount":19,"citationInfo":19,"publishDate":406,"publishYear":407,"citationAnalyzeStatus":18,"lastCitationAnalyze":19,"indexDatabases":19,"openAccess":19,"references":19,"isForceReanalyzing":120},"466e3370-e356-4a47-90a1-7446d8dd1bd6","2024-01-04T19:56:40.412+00:00","2024-12-27T21:35:37.841+00:00",[],"Neuronal-pathways-of-embarrassment",{"references":313,"abstract":315,"title":317,"doi":319},{"VOID":314},"Frith U, Frith CD (2003) Development and neurophysiology of mentalizing. Philos Trans R Soc Lond B Biol Sci 358:459–473\nGilovich T, Medvec VH, Savitsky K (2000) The spotlight effect in social judgment: an egocentric bias in estimates of the salience of one’s own actions and appearance. J Pers Soc Psychol 78:211–222\nKeltner D, Buswell BN (1997) Embarrassment: its distinct form and appeasement functions. Psychol Bull 122:250–270\nKeysers C, Gazzola V (2006) Towards a unifying neural theory of social cognition. Prog Brain Res 156:379–401\nKrach S, Cohrs JC, Echeverría LNC de, Kircher T, Sommer J, Jansen A, Paulus FM (2011) Your flaws are my pain: Linking empathy to vicarious embarrassment. PLoS ONE 6:e18675\nLamm C, Decety J, Singer T (2011) Meta-analytic evidence for common and distinct neural networks associated with directly experienced pain and empathy for pain. Neuroimage 54:2492–2502\nMüller-Pinzler L, Krach S, Krämer U, Paulus FM (2016) The social neuroscience of interpersonal emotions. In: Wöhr M, Krach S (eds) Social Behavior from Rodents to Humans: Neural Foundations and Clinical Implications Curr Topic. Springer, Berlin\nMüller-Pinzler L, Rademacher L, Paulus FM, Krach S (2016) When your friends make you cringe: social closeness modulates vicarious embarrassment-related neural activity. Soc Cogn Affect Neurosci. 11(3):466-75. DOI: 10.1093\u002Fscan\u002Fnsv130\nPaulus FM, Müller-Pinzler L, Jansen A, Gazzola V, Krach S (2015) Mentalizing and the role of the posterior superior temporal sulcus in sharing others’ embarrassment. Cereb Cortex 25:2065–2075\nTangney JP, Stuewig J, Mashek DJ (2007) Moral emotions and moral behavior. Annu Rev Psychol 58:345–372\nVignemont F de, Singer T (2006) The empathic brain: how, when and why? Trends Cogn Sci 10:435–441\nWager TD, Atlas LY, a LM, Roy M, Woo C‑W, Kross E (2013) An fMRI-based neurologic signature of physical pain. N Engl J Med 368:1388–1397",{"EN":316},"Embarrassment is a genuine human emotion that we experience while being publicly exposed in unfavorable situations. The embarrassment we feel informs us how we perform according to prevalent norms and moral values and helps to regulate the impression we make on others. One cornerstone of embarrassment is the capacity to take another’s perspective and reflect on the thoughts, feelings, and intentions of others. On the neural systems level, these processes of perspective taking are linked to neural activation in the medial prefrontal cortex and precuneus. In addition, the mishap and the expected negative evaluation induce affective arousal and activity in the anterior insula and anterior cingulate cortex. Both networks contribute to the experience of embarrassment and it is their orchestrated activity in the (para-)limbic system that accounts for this complex emotional phenomenon. From a conceptual point of view embarrassment thus presupposes the presence of others. This witnessing audience however also reacts to the mishaps of others and embarrassment may also be experienced vicariously. Here, processes of perspective taking also play an important role, while bystanders embody threats to another’s social integrity. Such interpersonal emotional phenomena gain particular relevance in the context of psychiatric disorders. Specifically, autism spectrum disorders and social anxiety disorders have core symptoms in the social domain that manifest in social interactions causing disturbances in social behavior and reduced well-being of affected individuals.",{"EN":318},"Neuronal pathways of embarrassment",{"VOID":320},"10.1007\u002Fs13295-016-0024-4","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs13295-016-0024-4",[323,338,351,363,375],{"id":324,"sortIndex":41,"researcher":19,"roles":325,"affiliations":326,"properties":335},"1d2a96a8-b930-47bc-b94c-a25a2b423f5b",[81],[327],{"id":19,"sortIndex":20,"affiliation":328,"properties":19},{"id":329,"createTime":330,"updateTime":330,"relativeEntities":331,"slug":19,"properties":332,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},"f4d08fb3-9865-4ccf-988b-143329b31b8a","2024-01-04T19:56:40.438+00:00",[],{"title":333},{"VI":334},"Klinik für Psychiatrie und Psychotherapie,  Social Neuroscience Lab at the Center of Brain, Behavior and Metabolism (CBBM), Universität zu Lübeck, Lübeck, Germany",{"title":336},{"VI":337},"Laura Müller-Pinzler",{"id":339,"sortIndex":340,"researcher":19,"roles":341,"affiliations":342,"properties":348},"469dc639-ca1a-4101-9594-dfaca2cf1627",4,[81],[343],{"id":19,"sortIndex":20,"affiliation":344,"properties":19},{"id":329,"createTime":330,"updateTime":330,"relativeEntities":345,"slug":19,"properties":346,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},[],{"title":347},{"VI":334},{"title":349},{"VI":350},"Frieder Michel 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Krach",{"id":376,"sortIndex":40,"researcher":19,"roles":377,"affiliations":378,"properties":384},"8054ed12-6370-4143-9795-6055d0a4c46b",[81],[379],{"id":19,"sortIndex":20,"affiliation":380,"properties":19},{"id":329,"createTime":330,"updateTime":330,"relativeEntities":381,"slug":19,"properties":382,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},[],{"title":383},{"VI":334},{"title":385},{"VI":386},"Lena Rademacher",{"url":321,"publisher":388,"properties":402},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":389,"slug":10,"properties":390,"entityType":17,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20,"subjectFields":394,"manageAffiliations":395,"indexDatabases":396,"url":19,"thumbnailPath":19,"statistic":397,"gsStatistic":19,"type":53,"analyzePriority":19},[],{"issn":391,"title":392,"url":393},{"VOID":13},{"EN":10},{"VOID":16},[],[],[],{"impactFactor":20,"impactFactorByYear":398,"i10Index":30,"i10IndexLast5Year":20,"totalPublication":31,"totalPublicationByYear":399,"totalCitation":37,"totalCitationByYear":400,"totalCitationPerPublication":45,"totalCitationPerPublicationByYear":401,"hindexLast5Year":52,"hindex":52},{"2012":26,"2013":27,"2015":28,"2016":29},{"2010":33,"2011":33,"2012":33,"2013":34,"2014":35,"2015":36,"2016":34},{"2010":39,"2011":40,"2012":41,"2013":42,"2014":43,"2015":44,"2016":40},{"2010":47,"2011":48,"2012":27,"2013":30,"2014":49,"2015":50,"2016":51},{"volume":403,"pages":405},{"VOID":404},"7",{"VOID":304},"2016-05-18",2016,{"id":409,"createTime":410,"updateTime":411,"relativeEntities":412,"slug":413,"properties":414,"entityType":73,"verifyStatus":74,"verifyTime":427,"verifyNote":75,"syncStatus":18,"languages":19,"translateLanguages":428,"viewCount":20,"primaryUrl":430,"fullTextUrl":19,"authors":431,"publicationType":97,"publisherRelationship":500,"citationCount":19,"citationInfo":19,"publishDate":519,"publishYear":119,"citationAnalyzeStatus":18,"lastCitationAnalyze":19,"indexDatabases":19,"openAccess":19,"references":19,"isForceReanalyzing":120},"c8c1857a-1b2b-4626-92e3-2a1f92fc4ee0","2024-02-08T00:03:19.955+00:00","2025-01-06T20:59:03.416+00:00",[],"The-brain-s-role-in-human-obesity",{"references":415,"abstract":417,"title":420,"doi":423,"keywords":425},{"VOID":416},"Hare TA, Camerer CF, Rangel A (2009) Self-control in decision-making involves modulation of the vmPFC valuation system. Science 324(5927):646–648\nHorstmann A, Busse F, Mathar D et al (2011) Obesity-related differences between women and men in brain structure and goal-directed behavior. Front Hum Neurosci 5. doi:10.3389\u002Ffnhum.2011.00058\nHorstmann A, Kovacs P, Kabisch S et al (2013) Common genetic variation near MC4R has a sex-specific impact on human brain structure and eating behavior. (F. J. Esteban, Ed.) PLoS One 8(9):e74362\nKenny PJ (2011) Reward mechanisms in obesity: new insights and future directions. Neuron 69(4):664–679\nKullmann S, Heni M, Veit R et al (2012) The obese brain: association of body mass index and insulin sensitivity with resting state network functional connectivity. Hum Brain Mapp 33(5):1052–1061\nMueller K, Anwander A, Möller HE et al (2011) Sex-dependent influences of obesity on cerebral white matter investigated by diffusion-tensor imaging. PLoS One 1–30\nSpeliotes EK, Willer CJ, Berndt SI et al (2010) Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index. Nat Genet 42(11):937–948\nStanek KM, Grieve SM, Brickman AM et al (2011) Obesity is associated with reduced white matter integrity in otherwise healthy adults. Obesity (Silver Spring) 19(3):500–504\nStice E, Yokum, S, Blum K, Bohon C (2010) Weight gain is associated with reduced striatal response to palatable food. J Neurosci 30(39):13105–13109\nWiller CJ, Speliotes EK, Loos RJF et al (2009) Six new loci associated with body mass index highlight a neuronal influence on body weight regulation. Nat Genet 41(1):25–34",{"VI":418,"EN":419},"Nguyên nhân phổ biến nhất gây béo phì là sự mất cân bằng năng lượng dương, tức là năng lượng tiêu thụ nhiều hơn năng lượng tiêu hao. Sự gia tăng tỷ lệ béo phì không thể được giải thích chỉ dựa trên môi trường tạo điều kiện cho béo phì, vì tồn tại sự khác biệt lớn về tình trạng cân nặng giữa các cá nhân. Do đó, nguyên nhân có khả năng cao là do sự tương tác giữa hành vi cá nhân và môi trường đã thay đổi của chúng ta. Điều này đòi hỏi việc điều tra vai trò của não trong sự phát triển và duy trì béo phì, thực sự đã trở thành một lĩnh vực đang ngày càng mở rộng trong ngành khoa học thần kinh. Bài báo này sẽ cung cấp cái nhìn tổng quan về các phát hiện trong hình ảnh não liên quan đến béo phì ở người. Hơn nữa, bài báo này sẽ làm sáng tỏ mối quan hệ giữa biến thể di truyền phổ biến, hành vi ăn uống và cấu trúc não trong bối cảnh béo phì. Cuối cùng, các câu hỏi quan trọng còn bỏ ngỏ trong lĩnh vực này sẽ được tóm tắt.","The most common cause for obesity is a positive energy balance, i.e. more energy is being consumed than is expended. The rise in obesity rates cannot be explained on the basis of our obesogenic environment alone, because large interindividual differences in weight status exist between people. Therefore, the cause is most probably to be found in an interaction between individual behaviour and our changed environment. This warrants the investigation of the brain’s role in the development and maintenance of obesity that indeed has become a growing field in the neurosciences. This article will give an overview about the findings in neuroimaging associated with human obesity. Further, this article will elucidate the relationship between common genetic variation, eating behaviour and brain structure in the context of obesity. Finally, important open questions in the field will be summarised.",{"VI":421,"EN":422},"Vai trò của não trong béo phì ở người","The brain’s role in human obesity",{"VOID":424},"10.1007\u002Fs13295-013-0048-y",{"VI":426},"béo phì, năng lượng, cấu trúc não, hành vi ăn uống, khoa học thần kinh","2024-12-31T09:09:38.398+00:00",[429],"VI","https:\u002F\u002Fwww.degruyter.com\u002Fdocument\u002Fdoi\u002F10.1007\u002Fs13295-013-0048-y\u002Fhtml",[432,459],{"id":433,"sortIndex":20,"researcher":19,"roles":434,"affiliations":435,"properties":456},"f1dd4d3d-83e3-41c6-bd05-7f65002cf646",[81],[436,444],{"id":19,"sortIndex":20,"affiliation":437,"properties":19},{"id":438,"createTime":439,"updateTime":439,"relativeEntities":440,"slug":19,"properties":441,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},"acdd9ee3-9ce7-47a7-8080-1b74bd0cdd9b","2024-02-08T00:03:19.987+00:00",[],{"title":442},{"VI":443},"IFB Adiposity Diseases, Leipzig University Medical Centre, Leipzig, Germany",{"id":445,"sortIndex":41,"affiliation":446,"properties":455},"65f95fee-51ea-4fdb-ad1f-d312c4103c1d",{"id":447,"createTime":448,"updateTime":449,"relativeEntities":450,"slug":451,"properties":452,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},"b0d39e9f-1651-4553-9c7e-8936d9221612","2024-01-14T16:20:32.748+00:00","2024-12-28T09:13:04.149+00:00",[],"Department-of-Neurology-Max-Planck-Institute-for-Human-Cognitive-and-Brain-Sciences-Leipzig-Germany",{"title":453},{"VI":454},"Department of Neurology, Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany",{},{"title":457},{"VI":458},"A. Horstmann",{"id":460,"sortIndex":41,"researcher":19,"roles":461,"affiliations":462,"properties":497},"83a01bf5-74c8-451b-8dc3-34feed6c23d5",[81],[463,475,482,492],{"id":464,"sortIndex":40,"affiliation":465,"properties":474},"29486478-0f92-4aa6-81f6-1e4e158dad41",{"id":466,"createTime":467,"updateTime":468,"relativeEntities":469,"slug":470,"properties":471,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},"d24a5898-1768-4b7f-84a5-34637fd426e8","2023-12-28T19:55:36.422+00:00","2024-09-30T04:27:07.510+00:00",[],"Clinic-for-Cognitive-Neurology-University-Hospital-Leipzig-Germany",{"title":472},{"VI":473},"Clinic for Cognitive Neurology, University Hospital Leipzig, Germany",{},{"id":476,"sortIndex":41,"affiliation":477,"properties":481},"d5294787-b870-458f-8795-9cfb9e0734c3",{"id":447,"createTime":448,"updateTime":449,"relativeEntities":478,"slug":451,"properties":479,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},[],{"title":480},{"VI":454},{},{"id":483,"sortIndex":30,"affiliation":484,"properties":491},"3d20cb01-5427-49fd-89ba-4aa94c82dd4a",{"id":485,"createTime":486,"updateTime":486,"relativeEntities":487,"slug":19,"properties":488,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},"b915f782-f8d5-4393-a282-e0a4bd761220","2024-02-08T00:03:20.003+00:00",[],{"title":489},{"VI":490},"Mind and Brain Institute, Berlin School of Mind and Brain, Humboldt-University and Charité, Berlin, Germany",{},{"id":19,"sortIndex":20,"affiliation":493,"properties":19},{"id":438,"createTime":439,"updateTime":439,"relativeEntities":494,"slug":19,"properties":495,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},[],{"title":496},{"VI":443},{"title":498},{"VI":499},"A. 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Likewise, genotypes asso­ciated with an increased risk for, e.g., schizophrenia are regularly found to also increase the risk for uni- and\u002For bipolar affective dis­orders. Therefore, one major research strategy of the last decade was to avoid correlation of genetic variation with complex clinical dis­orders and instead to focus on so-called intermediate or endophenotypes, i.e., neurobiological variables such as in vivo receptor expression or neuronal activation patterns, which are hypothetically more closely related to direct gene effects. We describe one such attempt and show that intermediate phenotypes such as brain activation patterns elic­ited by more or less complex cognitive tasks underlie complex regulations and influences and may thus not be the best target for neurobiological research. We suggest that in­stead of reifying brain activation as correlates of mental disorders, such disorders may best be conceptualized as results of alterations\u002Fbiases in basic learning mechanisms (e.g., Pav­lovian and operant conditioning) interacting with individual and social environments and that neuroscientific research can rely on animal models and computationalized modeling to reveal their neurobiological correlates.\u003C\u002Fjats:p>",{"EN":534},"Neurobiological research in psychiatry—classification of dimensions of learning mechanisms instead of reification of categories?",{"VOID":536},"10.1007\u002Fs13295-011-0024-3",[538],"EN","https:\u002F\u002Fwww.degruyter.com\u002Fdocument\u002Fdoi\u002F10.1007\u002Fs13295-011-0024-3\u002Fhtml",[541,562],{"id":542,"sortIndex":20,"researcher":19,"roles":543,"affiliations":544,"properties":555},"d5181bbb-1d79-4f86-9f0f-c484184303a3",[],[545],{"id":546,"sortIndex":20,"affiliation":547,"properties":19},"9d38565d-77aa-4297-a4cf-ad4f96d1c8ac",{"id":548,"createTime":549,"updateTime":549,"relativeEntities":550,"slug":551,"properties":552,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},"1d06ecc6-83aa-4450-8dd1-dbb9dfe20088","2024-04-21T20:57:09.709+00:00",[],"Department-of-Psychiatry-and-Psychotherapy-Charit%C3%A9-Universit%C3%A4tsmedizin-Berlin-Charit%C3%A9-Campus-Mitte-Charit%C3%A9platz-1-10117-Berlin-Germany",{"title":553},{"EN":554},"Department of Psychiatry and Psychotherapy, Charité – Universitätsmedizin Berlin, Charité Campus Mitte Charitéplatz 1, 10117 Berlin, Germany",{"openalex":556,"orcid":558,"title":560},{"VOID":557},"A5002906123",{"VOID":559},"https:\u002F\u002Forcid.org\u002F0000-0002-2362-417X",{"EN":561},"Andreas Heinz",{"id":563,"sortIndex":41,"researcher":19,"roles":564,"affiliations":565,"properties":572},"7bb6e7d3-7d2b-44f5-b450-229088681853",[],[566],{"id":567,"sortIndex":20,"affiliation":568,"properties":19},"801a8e37-c8e9-495d-b6d0-290db4936914",{"id":548,"createTime":549,"updateTime":549,"relativeEntities":569,"slug":551,"properties":570,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},[],{"title":571},{"EN":554},{"openalex":573,"title":575},{"VOID":574},"A5019518940",{"EN":576},"Anne Beck",{"url":19,"publisher":578,"properties":592},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":579,"slug":10,"properties":580,"entityType":17,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20,"subjectFields":584,"manageAffiliations":585,"indexDatabases":586,"url":19,"thumbnailPath":19,"statistic":587,"gsStatistic":19,"type":53,"analyzePriority":19},[],{"issn":581,"title":582,"url":583},{"VOID":13},{"EN":10},{"VOID":16},[],[],[],{"impactFactor":20,"impactFactorByYear":588,"i10Index":30,"i10IndexLast5Year":20,"totalPublication":31,"totalPublicationByYear":589,"totalCitation":37,"totalCitationByYear":590,"totalCitationPerPublication":45,"totalCitationPerPublicationByYear":591,"hindexLast5Year":52,"hindex":52},{"2012":26,"2013":27,"2015":28,"2016":29},{"2010":33,"2011":33,"2012":33,"2013":34,"2014":35,"2015":36,"2016":34},{"2010":39,"2011":40,"2012":41,"2013":42,"2014":43,"2015":44,"2016":40},{"2010":47,"2011":48,"2012":27,"2013":30,"2014":49,"2015":50,"2016":51},{"volume":593,"pages":595,"issue":597},{"VOID":594},"17",{"VOID":596},"88-94",{"VOID":115},{"total":40,"publishYear":19,"statisticByYear":599},{"2013":41,"2015":41},"2011-12-01",2011,[603,607,610,613,617,620,623,627,631,634,638,642,645,649,653,657,661,665,669,672,676,679,683,686,689,693,697,701,705,708,712,715,718,721,724,728],{"id":19,"text":604,"url":19,"identifiers":605},"Heinz, 2000, A rela - 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J Hand Surg Am 30:513–518\nBoyd JG, Gordon T (2003) Neurotrophic factors and their receptors in axonal regeneration and functional recovery after peripheral nerve injury. Mol Neurobiol 27:277–324\nBozkurt A, Deumens R, Beckmann C et al (2009) In vitro cell alignment obtained with a Schwann cell enriched microstructured nerve guide with longitudinal guidance channels. Biomaterials 30:169–179\nChew SY, Mi R, Hoke A, Leong KW (2007) Aligned protein-polymer composite fibers enhance nerve regeneration: a potential tissue-engineering platform. Adv Funct Mater 17:1288–1296\nClements IP, Kim Y-T, English A et al (2009) Thin-film enhanced nerve guidance channels for peripheral nerve repair. Biomaterials 30:3834–3846\nDalton PD, Mey J (2009) Neural interactions with materials. Front Biosci 14:769–795\nRuiter GC de, Malessy MJ, Yaszemski MJ et al (2009) Designing ideal conduits for peripheral nerve repair. Neurosurg Focus 26:E5\nDodla MC, Bellamkonda RV (2008) Differences between the effect of anisotropic and isotropic laminin and nerve growth factor presenting scaffolds on nerve regeneration across long peripheral nerve gaps. Biomaterials 29:33–46\nGeiger B, Bershadsky A, Pankov R, Yamada KM (2001) Extracellular matrix–cytoskeleton crosstalk. Nat Rev Mol Cell Biol 2:794–805\nHadlock T, Elisseeff J, Langer R et al (1998) A tissue-engineered conduit for peripheral nerve repair. Arch Otolaryngol Head Neck Surg 124:1081–1086\nInada Y, Hosoi H, Yamashita A et al (2007) Regeneration of peripheral motor nerve gaps with a polyglycolic acid-collagen tube: technical case report. Neurosurgery 61:E1105–E1107\nKawaja MD, Boyd JG, Smithson LJ et al (2009) Technical strategies to isolate olfactory ensheathing cells for intraspinal implantation. J Neurotrauma 26:155–177\nKim YT, Haftel VK, Kumar S, Bellamkonda RV (2008) The role of aligned polymer fiber-based constructs in the bridging of long peripheral nerve gaps. Biomaterials 29:3117–3127\nKlinkhammer K, Bockelmann J, Simitzis C et al (2010) Functionalization of electrospun fibers of poly (epsilon-caprolactone) with star shaped NCO-poly (ethylene glycol)-stat-poly (propylene glycol) for neuronal cell guidance. J Mater Sci Mater Med. Doi:10.1007\u002Fs10856-010-4112-7\nKoh HS, Yong T, Chan CK, Ramakrishna S (2008) Enhancement of neurite outgrowth using nano-structured scaffolds coupled with laminin. Biomaterials 29:3574–3582\nLietz M, Dreesmann L, Hoss M et al (2006) Neuro tissue engineering of glial nerve guides and the impact of different cell types. Biomaterials 27:1425–1436\nMatsumoto K, Ohnishi K, Kiyotani T et al (2000) Peripheral nerve regeneration across an 80-mm gap bridged by a polyglycolic acid (PGA)-collagen tube filled with laminin-coated collagen fibers: a histological and electrophysiological evaluation of regenerated nerves. Brain Res 868:315–328\nMeek MF, Coert JH (2008) US Food and Drug Administration\u002FConformit Europe-approved absorbable nerve conduits for clinical repair of peripheral and cranial nerves. Ann Plast Surg 60:466–472\nMohanna PN, Young RC, Wiberg M, Terenghi G (2003) A composite poly-hydroxybutyrate-glial growth factor conduit for long nerve gap repairs. J Anat 203:553–565\nSchmidt CE, Baier Leach J (2003) Neural tissue engineering: strategies for repair and regeneration. Annu Rev Biomed Eng 5:293–347\nSchnell E, Klinkhammer K, Balzer S et al (2007) Guidance of glial cell migration and axonal growth on electrospun nanofibers of poly-å-caprolactone and a collagen\u002Fpoly-å-caprolactone blend. Biomaterials 28:3012–3025\nSulaiman OAR, Boyd JG, Gordon T (2005) Axonal regeneration in the peripheral nervous system of mammals. In: Kettenmann H, Ransom BR (eds) Neuroglia. Oxford University, Oxford New York, pp 454–466\nWang W, Itoh S, Matsuda A et al (2008) Enhanced nerve regeneration through a bilayered chitosan tube: the effect of introduction of glycine spacer into the CYIGSR sequence. J Biomed Mater Res A 85:919–928\nWang X, Hu W, Cao Y et al (2005) Dog sciatic nerve regeneration across 30 mm defect bridged by a chitosan\u002FPGA artificial nerve graft. Brain 128:1897–1910\nWangensteen KJ, Kalliainen LK (2009) Collagen tube conduits in peripheral nerve repair: a retrospective analysis. J Hand (N Y). doi:10.1007\u002Fs11552-009-9245-0\nWebb K, Budko E, Neuberger TJ et al (2001) Substrate-bound human recombinant L1 selectively promotes neuronal attachment and outgrowth in the presence of astrocytes and fibroblasts. Biomaterials 22:1017–1028\nWeber RA, Breidenbach WC, Brown RE et al (2000) A randomized prospective study of polyglycolic acid conduits for digital nerve reconstruction in humans. Plast Reconstr Surg 106:1036–1046",{"EN":927},"Axonal regeneration is possible in the peripheral nervous system. Therefore, nerve lesions can be cured by suturing the dissociated nerve stumps or by grafting an autologous nerve. Since nerve transplantations cause a sensory deficit at the donor site, it is desirable to develop artificial implants for nerve regeneration. Artificial implants have to promote and guide axonal growth, the migration of Schwann cells and must not cause inflammation. Hollow tubes as nerve bridges are already used in the clinic. However, with these it is not possible to achieve nerve regeneration over distances much longer than 30 mm. For this purpose, a number of natural and synthetic materials have already been tested. Biocompatible tubes are being developed which contain orientated fibers or gels with longitudinal channels. In addition, artificial guidance materials are endowed with specific biological functions. Most frequently, extracellular matrix proteins or synthetic peptides that activate integrin receptors are coupled to the materials. Other approaches use gradients of neurotrophins or incorporate living cells. In the long run, a major goal of research is to develop cell-free artificial implants which allow a similar degree of regeneration as is possible with autologous nerve transplants.",{"EN":929},"Artificial implants for the regeneration of peripheral nerves",{"VOID":931},"10.1007\u002Fs13295-010-0009-7","https:\u002F\u002Fwww.degruyter.com\u002Fdocument\u002Fdoi\u002F10.1007\u002Fs13295-010-0009-7\u002Fhtml",[934,949],{"id":935,"sortIndex":20,"researcher":19,"roles":936,"affiliations":937,"properties":946},"f53ba9e4-fa9f-419e-95ea-8e55d8e6d5b7",[81],[938],{"id":19,"sortIndex":20,"affiliation":939,"properties":19},{"id":940,"createTime":941,"updateTime":941,"relativeEntities":942,"slug":19,"properties":943,"entityType":93,"verifyStatus":18,"verifyTime":19,"verifyNote":19,"syncStatus":18,"languages":19,"translateLanguages":19,"viewCount":20},"e0a1ae48-f5b1-4e1a-9582-098b0e0d0c7c","2024-01-26T18:40:11.329+00:00",[],{"title":944},{"VI":945},"Institut für Biologie II, RWTH Aachen, Aachen, Deutschland",{"title":947},{"VI":948},"I. 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