@article{SchaefferKuehnSchmittetal.2013,
  author    = {Schaeffer, Evelin L. and K{\"u}hn, Franziska and Schmitt, Angelika and Gattaz, Wagner F. and Gruber, Oliver and Schneider-Axmann, Thomas and Falkai, Peter and Schmitt, Andrea},
  title     = {Increased cell proliferation in the rat anterior cingulate cortex following neonatal hypoxia: relevance to schizophrenia},
  series = {Journal of Neural Transmission},
  volume    = {120},
  journal   = {Journal of Neural Transmission},
  number    = {1},
  doi       = {10.1007/s00702-012-0859-y},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-125890},
  pages     = {187-195},
  year      = {2013},
  abstract  = {As a consequence of obstetric complications, neonatal hypoxia has been discussed as an environmental factor in the pathophysiology of schizophrenia. However, the biological consequences of hypoxia are unclear. The neurodevelopmental hypothesis of schizophrenia suggests that the onset of abnormal brain development and neuropathology occurs perinatally, whereas symptoms of the disease appear in early adulthood. In our animal model of chronic neonatal hypoxia, we have detected behavioral alterations resembling those known from schizophrenia. Disturbances in cell proliferation possibly contribute to the pathophysiology of this disease. In the present study, we used postnatal rats to investigate cell proliferation in several brain areas following neonatal hypoxia. Rats were repeatedly exposed to hypoxia (89 \% N2, 11 \% O2) from postnatal day (PD) 4-8. We then evaluated cell proliferation on PD 13 and 39, respectively. These investigations were performed in the anterior cingulate cortex (ACC), caudate-putamen (CPU), dentate gyrus, and subventricular zone. Rats exposed to hypoxia exhibited increased cell proliferation in the ACC at PD 13, normalizing at PD 39. In other brain regions, no alterations have been detected. Additionally, hypoxia-treated rats showed decreased CPU volume at PD 13. The results of the present study on the one hand support the assumption of chronic hypoxia influencing transient cell proliferation in the ACC, and on the other hand reveal normalization during ageing.},
  language  = {en}
}
@article{StoeberFranzekBeckmann1993,
  author    = {St{\"o}ber, Gerald and Franzek, E. and Beckmann, H.},
  title     = {Obstetric complications in distinct Schizophrenie subgroups},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-82223},
  year      = {1993},
  abstract  = {In 55 chronic DSM I11 -R schi zophre nics the occurrence of obstetr ic complica ti ons (OCs) was investigated us ing the famili al/sporael ic strategy and Leonhard's unsystemati c/systematic distin ction. The overa ll frequency and severity of OCs elid not differ be tween patie nts anel controls. A sub-sample of patients, whose genetic ri sk was supposed to be high in both class ification systems (d iagnos is 01' unsystematic anel fa mili al sc hizophre ni a), had s igni ficantly fewer OCs than controls on the Lewis anel Murray scale (P < 0.05). With reference to previous reports of inc reased morta lity rates in the offspring of schizop hre nics, high genetic risk and addition al perinatal stressors may in crease perin atal mortality. In contrast, pat ie nts whose genetic ri sk was sllpposed to be low in both systems (di agnos is of systematic and sporadic sc hizophrenia) showed a trend to an increased freqllency of OCs in the Fuchs scale. In the context of the recently reported highl y signi ficantly increased rate of matern al infections dllring midgestation in these pati e nts, it was supposed th at perin atal complications may be of so me ae tio logical importance in sc hizophrenics with low genetic ri sk.},
  subject      = {Psychiatrie},
  language  = {en}
}
@article{StoeberFranzekBeckmann1992,
  author    = {St{\"o}ber, Gerald and Franzek, E. and Beckmann, H.},
  title     = {The role of maternal infectious diseases during pregnancy in the etiology of schizophrenia in offspring},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-82216},
  year      = {1992},
  abstract  = {In 55 chronic schizophrenics, the occurrence of infectious diseases during their mothers' pregnancies was investigated. Different psychiatrie diagnostic systems were compared. Infections were reported by the mothers of familial and sporadic DSM I1I-R schizophrenics in equal proportion. However, applying Leonhard's classification, the frequency of infections was found to be significantly increased in 'systematic' schizophrenia (mainly exogenously induced in the view of Leonhard) compared to 'unsystematic' schizophrenia (mainly genetically determined according to Leonhard's findings). Most of the infections occurred during the second trimester (nine out of 13). Thus, in the 'systematic' forms of schizophrenia (low genetic loading), maternal infections in this crucial period of neurodevelopment would appear to be important causative factors in the cytoarchitectural deviance detected in the central nervous system of schizophrenics.},
  subject      = {Psychiatrie},
  language  = {en}
}
@article{LeschStoeberBallingetal.1994,
  author    = {Lesch, K. P. and St{\"o}ber, Gerald and Balling, U. and Franzek, Ernst and Li, S. H. and Ross, C. A. and Newman, M. and Beckmann, H. and Riederer, P.},
  title     = {Triplet repeats in clinical subtypes of schizophrenia: variation at the DRPLA (B37 CAG repeat) locus is not associated with periodic catatonia},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63369},
  year      = {1994},
  abstract  = {Clinical evidence for a dominant mode of inheritance and anticipation in periodic catatonia, a distinct subtype of schizophrenia, indicates that genes with triplet repeat expansions or other unstable repetitive elements affecting gene expression may be involved in the etiology of this disorder. Because patients affected with dentatorubral-pallidoluysian atrophy (DRPLA) may present with "schizophrenic" symptoms, we have investigated the DRPLA (B 37 CAG repeat) locus on chromosome 12 in 41 patients with periodic catatonia. The B 37 CAG repeat locus was highly polymorphic but all alleles in both the patient and control group had repeat sizes within the normal range. We conclude that variation at the DRPLA locus is unlikely to be associated with periodic catatonia. The evidence for dominant inheritance and anticipation as well as the high prevalence of human brain genes containing trinucleotide repeats justifies further screening for triplet repeat expansions in periodic catatonia.},
  subject      = {Schizophrenie},
  language  = {en}
}