Lang, Christine

[["dc.bibliographiccitation.firstpage","135"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Psychiatry Research"],["dc.bibliographiccitation.lastpage","146"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Weniger, Godehard"],["dc.contributor.author","Lange, C."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Irle, Eva"],["dc.date.accessioned","2018-11-07T10:45:28Z"],["dc.date.available","2018-11-07T10:45:28Z"],["dc.date.issued","2004"],["dc.description.abstract","The goal of this study was to assess facial affect recognition abilities in subjects with various schizophrenia subtypes and subjects with major depression. A total of six disorganized, 21 paranoid and 18 residual subjects with schizophrenia (DSM-IV criteria) were compared with 21 subjects with major depression (DSM-1V criteria) and 30 matched healthy control subjects. Two experimental tasks requiring the sorting and rating of emotional facial expressions were applied. Disorganized and paranoid subjects showed strong impairments in the sorting of emotional facial expressions. Depressive subjects displayed only minor deficits, and residual subjects were unimpaired. Subjects with disorganized schizophrenia rated emotional facial expressions as more aroused, and depressive subjects rated them as less aroused, than the other study groups. Our study demonstrates strong deficits in facial affect recognition in subjects with schizophrenia and pronounced disorganized or psychotic symptoms. Deficits in facial affect recognition are specific to schizophrenia. They may be considered as a state marker of schizophrenia. (C) 2004 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.psychres.2003.12.027"],["dc.identifier.isi","000224994600004"],["dc.identifier.pmid","15488956"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47509"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0165-1781"],["dc.title","Differential impairments of facial affect recognition in schizophrenia subtypes and major depression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","International Journal of Medical Microbiology"],["dc.bibliographiccitation.volume","294"],["dc.contributor.author","Lang, C."],["dc.contributor.author","Algner, M."],["dc.contributor.author","Gross, U."],["dc.contributor.author","Luder, C. G. K."],["dc.date.accessioned","2018-11-07T10:45:58Z"],["dc.date.available","2018-11-07T10:45:58Z"],["dc.date.issued","2004"],["dc.format.extent","120"],["dc.identifier.isi","000224456000084"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47632"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Urban & Fischer Verlag"],["dc.publisher.place","Jena"],["dc.relation.conference","Annual Meeting of the DGHM"],["dc.relation.eventlocation","Munster, GERMANY"],["dc.relation.issn","1438-4221"],["dc.title","Differential effects of Toxoplasma gondii and parasite lysate on GAS-containing promoters driving IFN-gamma-responsive genes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","PII S0921-5093(02)00677-9"],["dc.bibliographiccitation.firstpage","119"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","MATERIALS SCIENCE AND ENGINEERING A-STRUCTURAL MATERIALS PROPERTIES MICROSTRUCTURE AND PROCESSING"],["dc.bibliographiccitation.lastpage","125"],["dc.bibliographiccitation.volume","353"],["dc.contributor.author","Lang, C."],["dc.contributor.author","Schmitz, G."],["dc.date.accessioned","2018-11-07T10:37:37Z"],["dc.date.available","2018-11-07T10:37:37Z"],["dc.date.issued","2003"],["dc.description.abstract","The dependence of thin-film microstructure on the curvature of the substrate is investigated by field ion microscopy (FIM) and transmission electron microscopy (TEM). For this purpose, Cu-Au multilayers were deposited on W single crystals, which are prepared both as curved (radius of curvature similar to50 nm) and as planar substrates. 3D atom probe analysis shows that the curved substrates lead to heterogeneous reaction patterns by grain boundary reaction beside planar reaction patterns. This result is explained by local variations of microstructure. Grain boundary reaction is dependent on the atomic structure of the grain boundary and can lead to the early formation of intermetallics. At temperatures too low for significant volume diffusion, interdiffusion between enriched grain boundaries and neighbored grains is observed under the formation of ordered compounds. The elastic strain, which is caused by a considerable atomic size mismatch, is found to hinder interdiffusion and to cause alloying under grain boundary motion (DIGM). The introduction of a Co diffusion barrier between Au and Cu slows down interdiffusion, resulting in higher reaction temperatures. Thus, it is possible to observe that the grain boundary reaction in the An layer disappears at elevated temperatures, at which volume diffusion of Cu in An gets possible, whereas in the Cu layer the grain boundary reaction is still observed. (C) 2002 Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0921-5093(02)00677-9"],["dc.identifier.isi","000183607100021"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45615"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Sa"],["dc.publisher.place","Lausanne"],["dc.relation.conference","47th International Field Emission Symposium (FIELD EMISSION 2001)"],["dc.relation.eventlocation","BERLIN, GERMANY"],["dc.relation.issn","0921-5093"],["dc.title","Structure-controlled interdiffusion of Cu/Co/Au thin films investigated by three-dimensional atom probe"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","833"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","International Journal for Parasitology"],["dc.bibliographiccitation.lastpage","844"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Luder, Carsten G. K."],["dc.contributor.author","Algner, Michaela"],["dc.contributor.author","Lang, Christine"],["dc.contributor.author","Bleicher, Nadja"],["dc.contributor.author","Groß, Uwe"],["dc.date.accessioned","2018-11-07T10:37:35Z"],["dc.date.available","2018-11-07T10:37:35Z"],["dc.date.issued","2003"],["dc.description.abstract","Production of nitric oxide by activated murine macrophages is thought to represent an important mechanism to restrict replication of the obligate intracellular parasite Toxoplasma gondii. In this study, we characterised the effect of T. gondii on nitric oxide production and expression of the inducible nitric oxide synthase and determined the functional significance of a parasite-induced evasion of this potential effector mechanism. Infection of primary bone marrow-derived macrophages or monocytic/macrophage RAW264.7 cells with a mouse-avirulent T. gondii strain significantly decreased nitric oxide production that had been induced by activation with either interferon-gamma or lipopolysaccharide or interferon-gamma plus lipopolysaccharide. Importantly, down-regulation of nitric oxide production by T. gondii enabled considerable parasite replication in macrophages activated with interferon-gamma alone or lipopolysaccharide, alone. Furthermore, supplementation of endogenous nitric oxide by addition of sodium nitroprusside to levels as observed in uninfected interferon-gamma- or lipopolysaccharide-activated macrophages almost completely abrogated replication of T. gondii. Although T. gondii also partially inhibited the vigorous nitric oxide production induced by interferon-gamma along with lipopolysaccharide, the magnitude of inhibition did not suffice to allow intracellular propagation of the parasite in these synergistically activated macrophages. Inhibition of interferon-gamma-, lipopolysaccharide- and interferon--y plus lipopolysaccharide-induced nitric oxide production coincided with reduced inducible nitric oxide synthase protein levels. Such down-regulation required the presence of intracellular parasites as determined by immunofluorescence microscopy. Inducible nitric oxide synthase transcripts induced by interferon--y alone or in combination with lipopolysaccharide were also dose-dependently down-regulated after infection of RAW264.7 cells with T gondii. In conclusion, this evasion strategy enables parasite replication in macrophages moderately activated by interferon-gamma or lipopolysaccharide, but does not suffice to evade the anti-parasitic activity of macrophages fully activated by interferon-gamma plus lipopolysaccharide. Nitric oxide production and its partial inhibition by the parasite may modulate the parasite-host equilibrium during toxoplasmosis. (C) 2003 Australian Society for Parasitology Inc. Published by Elsevier Science Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0020-7519(03)00092-4"],["dc.identifier.isi","000184375800007"],["dc.identifier.pmid","12865083"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45603"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","0020-7519"],["dc.title","Reduced expression of the inducible nitric oxide synthase after infection with Toxoplasma gondii facilitates parasite replication in activated murine macrophages"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1994"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Microbes and Infection"],["dc.bibliographiccitation.lastpage","2005"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Lang, Christine"],["dc.contributor.author","Algner, Michaela"],["dc.contributor.author","Beinert, Nicole"],["dc.contributor.author","Gross, Uwe"],["dc.contributor.author","Lueder, Carsten Guenter Kurt"],["dc.date.accessioned","2018-11-07T09:38:13Z"],["dc.date.available","2018-11-07T09:38:13Z"],["dc.date.issued","2006"],["dc.description.abstract","The intracellular parasite Toxoplasma gondii is able to establish persistent infections in immunocompetent hosts and this may be facilitated by different immune evasion mechanisms. In the present study, we describe that infection of marine monocyte/macrophage RAW 264.7 cells with T. gondii blocks the IFN-gamma-induced upregulation of major histocompatibility complex (MHC) class II mRNAs and proteins. Heat inactivation of the parasites prior to host cell invasion, but not inhibition of the intracellular replication of T. gondii abolished the inhibition of MHC class II upregulation. Interestingly, a T. gondii lysate (TL) mimicked the inhibitory effect of viable parasites on MHC class II expression. Nuclear translocation of the signal transducer and activator of transcription in response to IFN-gamma were normal both in cells incubated with TL or infected with viable parasites. Transcript levels of the class II transactivator and consequently H2-Ab were nevertheless diminished by both viable parasites and TL. In contrast, interferon regulatory factor-1 mRNA was only decreased in response to viable T. gondii. Luciferase reporter assays confirmed differential effects of viable parasites and TL on minimal or complex IFN-gamma-responsive promoters. Furthermore, only TL, and not viable parasites, strongly induced the secretion of IL-10 by marine macrophages. Whereas TL also inhibited MHC class II expression in macrophages from IL-10-deficient mice, increased IL-10 secretion by wild type macrophages did not mediate the block in MHC class II upregulation. In conclusion, T. gondii employs different mechanisms to inhibit MHC class II expression, suggesting a complex regulation of this immune evasion strategy. (c) 2006 Elsevier SAS. All rights reserved."],["dc.identifier.doi","10.1016/j.micinf.2006.02.031"],["dc.identifier.isi","000241115100002"],["dc.identifier.pmid","16824778"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33024"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1286-4579"],["dc.title","Diverse mechanisms employed by Toxoplasma gondii to inhibit IFN-gamma-induced major histocompatibility complex class II gene expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E146"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","E147"],["dc.bibliographiccitation.volume","81"],["dc.contributor.author","Bergner, C. G."],["dc.contributor.author","Lang, C."],["dc.contributor.author","Spreer, A."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Mohr, Alexander"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2017-09-07T11:47:04Z"],["dc.date.available","2017-09-07T11:47:04Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1212/01.wnl.0000435307.33389.f7"],["dc.identifier.gro","3142253"],["dc.identifier.isi","000330770100003"],["dc.identifier.pmid","24190004"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6232"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Teaching NeuroImages: Ma2 encephalitis presenting as acute panhypopituitarism in a young man"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","330"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Psychiatrica Scandinavica"],["dc.bibliographiccitation.lastpage","331"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Irle, Eva"],["dc.contributor.author","Lange, C."],["dc.contributor.author","Sachsse, Ulrich"],["dc.contributor.author","Weniger, Godehard"],["dc.date.accessioned","2018-11-07T08:30:49Z"],["dc.date.available","2018-11-07T08:30:49Z"],["dc.date.issued","2009"],["dc.identifier.doi","10.1111/j.1600-0447.2009.01351.x"],["dc.identifier.isi","000263855500012"],["dc.identifier.pmid","19207126"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16984"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.relation.issn","0001-690X"],["dc.title","Further evidence that post-traumatic stress disorder but not dissociative disorders are related to amygdala and hippocampal size reduction in trauma-exposed individuals"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","20"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Seizure"],["dc.bibliographiccitation.lastpage","32"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Exner, C."],["dc.contributor.author","Boucsein, K."],["dc.contributor.author","Lange, C."],["dc.contributor.author","Winter, H."],["dc.contributor.author","Weniger, Godehard"],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Irle, Eva"],["dc.date.accessioned","2018-11-07T10:33:47Z"],["dc.date.available","2018-11-07T10:33:47Z"],["dc.date.issued","2002"],["dc.description.abstract","The search for a special neuropsychological profile of frontal lobe epilepsy subjects (FLE) has so far led to inconclusive results. In this paper we compared the preoperative neuropsychological performance of FLE and temporal lobe epilepsy (TLE) subjects. We further investigated whether frontal lobe lesions of epileptogenic cause produce the same type of cognitive dysfunction as do tumours of the frontal lobe. Sixteen FLE subjects were compared to 16 TLE subjects as well as to a group of 10 subjects after the removal of frontal lobe tumors (TUM) and a healthy control group, A set of neuropsychological test measures routinely used for presurgical evaluation, an emotional conceptualization task and two associative learning tasks were administered. We found that subjects with frontal lobe damage were significantly impaired relative to controls on a wide range of cognitive functions independent of neurological cause. FLE subjects could hardly be discriminated from TLE subjects as both groups showed a similarly reduced level of neuropsychological performance. Our results demonstrate the devastating effect that frontal lobe epilepsy can have on cognitive functioning. Routinely used neuropsychological test measures lack the specificity to distinguish between frontal and temporal lobe epilepsy. Highly specialized measures are necessary to reveal differences. (C) 2002 BEA Trading Ltd."],["dc.identifier.doi","10.1053/seiz.2001.0572"],["dc.identifier.isi","000174109800004"],["dc.identifier.pmid","11888256"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44700"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co Ltd"],["dc.relation.issn","1059-1311"],["dc.title","Neuropsychological performance in frontal lobe epilepsy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1059"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Psychological Medicine"],["dc.bibliographiccitation.lastpage","1064"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Lange, C."],["dc.contributor.author","Irle, Eva"],["dc.date.accessioned","2018-11-07T10:47:04Z"],["dc.date.available","2018-11-07T10:47:04Z"],["dc.date.issued","2004"],["dc.description.abstract","Background. Evidence is increasing that amygdala and hippocampus show significant structural abnormalities in affective disorders. Two previous studies found enlarged amygdala size in subjects with recent-onset major depression. Method. Amygdala and hippocampal volumes were assessed in 17 young women with major depressive disorder and 17 healthy matched control subjects by use of three-dimensional structural magnetic resonance imaging. The severity of depressive symptoms was assessed using the Hamilton Depression Scale and the Beck Depression Inventory. Results. Compared with control subjects, depressive subjects had significantly larger (+13%) amygdala volumes and significantly smaller (-12%) hippocampal volumes. Amygdala and hippocampal volumes were not significantly correlated with disorder-related variables. Conclusions. Our results are consistent with previous findings of structural abnormalities of amygdala and hippocampus in subjects with recent-onset major depression. It may be suggested that the size of the amygdala is enlarged in the first years of the disorder, and may decrease with prolonged disorder duration."],["dc.identifier.doi","10.1017/S0033291703001806"],["dc.identifier.isi","000224104300010"],["dc.identifier.pmid","15554576"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47886"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cambridge Univ Press"],["dc.relation.issn","0033-2917"],["dc.title","Enlarged amygdala volume and reduced hippocampal volume in young women with major depression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Epilepsia"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Weber, Yvonne G."],["dc.contributor.author","Storch, Alexander"],["dc.contributor.author","Wuttke, Thomas V."],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Kempfle, Judith"],["dc.contributor.author","Maljevic, Snezana"],["dc.contributor.author","Margari, Lucia"],["dc.contributor.author","Kamm, Christoph"],["dc.contributor.author","Schneider, S."],["dc.contributor.author","Huber, Stephan M."],["dc.contributor.author","Pekrun, Arnulf"],["dc.contributor.author","Roebling, Robert"],["dc.contributor.author","Seebohm, Guiscard"],["dc.contributor.author","Koka, Saisudha"],["dc.contributor.author","Lang, C."],["dc.contributor.author","Kraft, Eduard"],["dc.contributor.author","Blazevic, Dragica"],["dc.contributor.author","Salvo-Vargas, Alberto"],["dc.contributor.author","Fauler, Michael"],["dc.contributor.author","Mottaghy, Felix M."],["dc.contributor.author","Muenchau, Alexander"],["dc.contributor.author","Edwards, M. J."],["dc.contributor.author","Presicci, Anna"],["dc.contributor.author","Margari, Francesco"],["dc.contributor.author","Gasser, Thomas"],["dc.contributor.author","Lang, F."],["dc.contributor.author","Bhatia, Kailash P."],["dc.contributor.author","Lehmann-Horn, Frank"],["dc.contributor.author","Lerche, Holger"],["dc.date.accessioned","2018-11-07T08:29:05Z"],["dc.date.available","2018-11-07T08:29:05Z"],["dc.date.issued","2009"],["dc.format.extent","21"],["dc.identifier.isi","000265770600073"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16567"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.publisher.place","Malden"],["dc.relation.conference","6th Joint Meeting of the German, Austrian, and Swiss Sections of the International-League-Against-Epilepsy"],["dc.relation.eventlocation","Rostock, GERMANY"],["dc.relation.issn","0013-9580"],["dc.title","GLUT1 MUTATIONS IN PATIENTS WITH PAROXYSMAL EXERTION-INDUCED DYSKINESIA"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]