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  • 1
    Keywords: brain ; FOLLOW-UP ; magnetic resonance imaging ; ABNORMALITIES ; SCALE ; SENSORIMOTOR CORTEX ; MR-IMAGES ; VOXEL-BASED MORPHOMETRY ; DYSFUNCTION ; 1ST-EPISODE SCHIZOPHRENIA ; CEREBELLAR VOLUME ; Heidelberg scale ; Schizophrenia Neurological soft signs ; SOFT SIGNS
    Abstract: Neurological soft signs (NSS) comprise a broad range of minor motor and sensory deficits which are frequently found in schizophrenia. However, the cerebral changes underlying NSS are only partly understood. We therefore investigated the cerebral correlates of NSS by using magnetic resonance imaging (MRI) in 102 patients with first episode schizophrenia. NSS were assessed after remission of acute psychotic symptoms using the Heidelberg scale (HS), which consists of five NSS subscales ("motor coordination", "complex motor tasks", "orientation", "integrative functions", and "hard signs"). Correlations between NSS scores and cerebral changes were established by optimized voxel-based morphometry. NSS total scores were significantly associated with reduced gray matter densities in the precentral and postcentral gyri, the inferior parietal lobule and the inferior occipital gyrus. Both of the NSS subscales "motor coordination" and "complex motor tasks", referred to motor strip changes but showed differential correlations with parietal, insular, cerebellar or frontal sites, respectively. The NSS subscales "orientation" and "integrative functions" were associated with left frontal, parietal, and occipital changes or bihemispheric frontal changes, respectively. The NSS subscale "hard signs" was associated with deficits in the right cerebellum and right parastriate cortex. Repeated analyses for white matter changes revealed similar results. These findings confirm the associations between NSS and cerebral changes in areas important for motor and sensory functioning. This variety of cerebral sites corresponds to the heterogeneity of NSS and are consistent with the hypothesis that NSS reflect both a rather generalized cerebral dysfunction and localized deficits specific for particular signs.
    Type of Publication: Journal article published
    PubMed ID: 21498055
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  • 2
    Keywords: CANCER ; EXPRESSION ; SURVIVAL ; CELL ; Germany ; GENE ; MARKER ; prognosis ; polymorphism ; single nucleotide polymorphism ; TRIAL ; AGE ; MUTATION ; SNP ; leukemia ; MARKERS ; MUTATIONS ; HIGH-RISK ; GLIOMAS ; GENE-MUTATIONS ; STUDY-GROUP ULM ; ONCOLOGY ; overall survival ; MYELOID-LEUKEMIA ; PROGNOSTIC-FACTOR ; ALLELES ; methods ; PREDICTS ; STEM ; GROUP-B ; outcome ; IDH1 ; CODON 132 ; single nucleotide ; NUCLEOPHOSMIN ; clinical oncology ; AML STUDY-GROUP ; YOUNGER ADULTS 16
    Abstract: Purpose We assessed the prognostic impact of IDH1 R132 mutations and a known single nucleotide polymorphism (SNP) located in the same exon of the IDH1 gene in patients with cytogenetically normal acute myeloid leukemia (CN-AML) in the context of other prognostic markers. Patients and Methods IDH1 exon four was directly sequenced in 275 CN-AML patients from two subsequent AML multicenter treatment trials and 120 healthy volunteers. Moreover, mutations in NPM1, FLT3, CEBPA, and WT1 were analyzed, and mRNA expression of IDH1 was quantified. Results IDH1 R132 mutations were found in 10.9% of CN-AML patients. IDH1 SNP rs11554137 was found in 12% of CN-AML patients and 11.7% of healthy volunteers. IDH1 R132 mutations had no impact on prognosis. In contrast, IDH1 SNP rs11554137 was an adverse prognostic factor for overall survival in univariate and multivariate analysis. Other significant factors were age, NPM1/FLT3 mutational status, WT1 SNP rs16754, and platelet count. The impact of IDH1 SNP rs11554137 was most pronounced in the NPM1/FLT3 high-risk patients (either NPM1 wild-type or FLT3-internal tandem duplication positive). Patients with IDH1 SNP rs11554137 had a higher expression of IDH1 mRNA than patients with two wild-type alleles. Conclusion IDH1 SNP rs11554137 but not IDH1 R132 mutations are associated with an inferior outcome in CN-AML
    Type of Publication: Journal article published
    PubMed ID: 20368538
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