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Articles by T Becker
Total Records ( 3 ) for T Becker
  J Schumacher , G Laje , R. A Jamra , T Becker , T. W Muhleisen , C Vasilescu , M Mattheisen , S Herms , P Hoffmann , A. M Hillmer , A Georgi , C Herold , T. G Schulze , P Propping , M Rietschel , F. J McMahon , M. M Nothen and S. Cichon
 

Association studies, as well as the initial translocation family study, identified the gene Disrupted-In-Schizophrenia-1 (DISC1) as a risk factor for schizophrenia. DISC1 encodes a multifunctional scaffold protein involved in neurodevelopmental processes implicated in the etiology of schizophrenia. The present study explores the contribution of the DISC locus to schizophrenia using three different approaches: (i) systematic association mapping aimed at detecting DISC risk variants in a schizophrenia sample from a central European population (556 SNPs, n = 1621 individuals). In this homogenous sample, a circumscribed DISC1 interval in intron 9 was significantly associated with schizophrenia in females (P = 4 x 10–5) and contributed most strongly to early-onset cases (P = 9 x 10–5). The odds ratios (ORs) were in the range of 1.46–1.88. (ii) The same sample was used to test for the locus-specific SNP–SNP interaction most recently associated with schizophrenia. Our results confirm the SNP interplay effect between rs1538979 and rs821633 that significantly conferred disease risk in male patients with schizophrenia (P = 0.016, OR 1.57). (iii) In order to detect additional schizophrenia variants, a meta-analysis was performed using nine schizophrenia samples from different European populations (50 SNPs, n = 10 064 individuals maximum, n = 3694 minimum). We found evidence for a common schizophrenia risk interval within DISC1 intron 4–6 (P = 0.002, OR 1.27). The findings point to a complex association between schizophrenia and DISC, including the presence of different risk loci and SNP interplay effects. Furthermore, our phenotype–genotype results—including the consideration of sex-specific effects—highlight the value of homogenous samples in mapping risk genes for schizophrenia in general, and at the DISC locus in particular.

  C Knaup , M Koesters , D Schoefer , T Becker and B. Puschner
 

Background

Feedback of treatment outcome during the course of therapy (outcome management) is increasingly considered to be beneficial for improving the quality of mental healthcare.

Aims

To review the impact of feedback of outcome to practitioners and/or patients in specialist mental health services.

Method

A systematic search and meta-analysis of controlled trials using outcome management in mental health services published in English or German language.

Results

Twelve studies met inclusion criteria. Feeding back outcome showed a small, but significant (d = 0.10; 95% CI 0.01–0.19) positive short-term effect on the mental health of individuals that did not prevail in the long run. Subgroup analysis revealed no significant differences regarding feedback modalities. Outcome management did not contribute to a reduction of treatment duration.

Conclusions

Evidence on the effects of outcome management in mental healthcare is promising. More targeted research is needed in order to identify the effective ingredients of outcome feedback and to assess its cost-effectiveness.

  Y Kamenisch , M Fousteri , J Knoch , A. K von Thaler , B Fehrenbacher , H Kato , T Becker , M. E.T Dolle , R Kuiper , M Majora , M Schaller , G. T.J van der Horst , H van Steeg , M Rocken , D Rapaport , J Krutmann , L. H Mullenders and M. Berneburg
 

Defects in the DNA repair mechanism nucleotide excision repair (NER) may lead to tumors in xeroderma pigmentosum (XP) or to premature aging with loss of subcutaneous fat in Cockayne syndrome (CS). Mutations of mitochondrial (mt)DNA play a role in aging, but a link between the NER-associated CS proteins and base excision repair (BER)-associated proteins in mitochondrial aging remains enigmatic. We show functional increase of CSA and CSB inside mt and complex formation with mtDNA, mt human 8-oxoguanine glycosylase (mtOGG)-1, and mt single-stranded DNA binding protein (mtSSBP)-1 upon oxidative stress. MtDNA mutations are highly increased in cells from CS patients and in subcutaneous fat of aged Csbm/m and Csa–/– mice. Thus, the NER-proteins CSA and CSB localize to mt and directly interact with BER-associated human mitochondrial 8-oxoguanine glycosylase-1 to protect from aging- and stress-induced mtDNA mutations and apoptosis-mediated loss of subcutaneous fat, a hallmark of aging found in animal models, human progeroid syndromes like CS and in normal human aging.

 
 
 
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