@article{HaeussingerHeinzelHahnetal.2011,
  author    = {Haeussinger, Florian B. and Heinzel, Sebastian and Hahn, Tim and Schecklmann, Martin and Ehlis, Ann-Christine and Fallgatter, Andreas J.},
  title     = {Simulation of Near-Infrared Light Absorption Considering Individual Head and Prefrontal Cortex Anatomy: Implications for Optical Neuroimaging},
  series = {PLoS ONE},
  volume    = {6},
  journal   = {PLoS ONE},
  number    = {10},
  doi       = {10.1371/journal.pone.0026377},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-142311},
  pages     = {e26377},
  year      = {2011},
  abstract  = {Functional near-infrared spectroscopy (fNIRS) is an established optical neuroimaging method for measuring functional hemodynamic responses to infer neural activation. However, the impact of individual anatomy on the sensitivity of fNIRS measuring hemodynamics within cortical gray matter is still unknown. By means of Monte Carlo simulations and structural MRI of 23 healthy subjects (mean age: (25.0 +/- 2.8) years), we characterized the individual distribution of tissue-specific NIR-light absorption underneath 24 prefrontal fNIRS channels. We, thereby, investigated the impact of scalp-cortex distance (SCD), frontal sinus volume as well as sulcal morphology on gray matter volumes (V(gray)) traversed by NIR-light, i.e. anatomy-dependent fNIRS sensitivity. The NIR-light absorption between optodes was distributed describing a rotational ellipsoid with a mean penetration depth of (23.6 +/- 0.7) mm considering the deepest 5\% of light. Of the detected photon packages scalp and bone absorbed (96.4 +/- 9: 7)\% and V(gray) absorbed (3.1 +/- 1.8)\% of the energy. The mean V(gray) volume (1.1 +/- 0.4)cm(3) was negatively correlated (r = - .76) with the SCD and frontal sinus volume (r = - .57) and was reduced by 41.5\% in subjects with relatively large compared to small frontal sinus. Head circumference was significantly positively correlated with the mean SCD (r = .46) and the traversed frontal sinus volume (r = .43). Sulcal morphology had no significant impact on V(gray). Our findings suggest to consider individual SCD and frontal sinus volume as anatomical factors impacting fNIRS sensitivity. Head circumference may represent a practical measure to partly control for these sources of error variance.},
  language  = {en}
}
@article{CeteciXuCetecietal.2011,
  author    = {Ceteci, Fatih and Xu, Jiajia and Ceteci, Semra and Zanucco, Emanuele and Thakur, Chitra and Rapp, Ulf R.},
  title     = {Conditional Expression of Oncogenic C-RAF in Mouse Pulmonary Epithelial Cells Reveals Differential Tumorigenesis and Induction of Autophagy Leading to Tumor Regression},
  series = {Neoplasia},
  volume    = {13},
  journal   = {Neoplasia},
  number    = {11},
  doi       = {10.1593/neo.11652},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134347},
  pages     = {1005-1018},
  year      = {2011},
  abstract  = {Here we describe a novel conditional mouse lung tumor model for investigation of the pathogenesis of human lung cancer. On the basis of the frequent involvement of the Ras-RAF-MEK-ERK signaling pathway in human non-small cell lung carcinoma (NSCLC), we have explored the target cell availability, reversibility, and cell type specificity of transformation by oncogenic C-RAF. Targeting expression to alveolar type II cells or to Clara cells, the two likely precursors of human NSCLC, revealed differential tumorigenicity between these cells. Whereas expression of oncogenic C-RAF in alveolar type II cells readily induced multifocal macroscopic lung tumors independent of the developmental state, few tumors with type II pneumocytes features and incomplete penetrance were found when targeted to Clara cells. Induced tumors did not progress and were strictly dependent on the initiating oncogene. Deinduction of mice resulted in tumor regression due to autophagy rather than apoptosis. Induction of autophagic cell death in regressing lung tumors suggests the use of autophagy enhancers as a treatment choice for patients with NSCLC.},
  language  = {en}
}
@article{AllignolSchumacherWanneretal.2011,
  author    = {Allignol, Arthur and Schumacher, Martin and Wanner, Christoph and Drechsler, Christiane and Beyersmann, Jan},
  title     = {Understanding competing risks: a simulation point of view},
  series = {BMC Medical Research Methodology},
  volume    = {11},
  journal   = {BMC Medical Research Methodology},
  number    = {86},
  doi       = {10.1186/1471-2288-11-86},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-142811},
  pages     = {1-13},
  year      = {2011},
  abstract  = {Background: Competing risks methodology allows for an event-specific analysis of the single components of composite time-to-event endpoints. A key feature of competing risks is that there are as many hazards as there are competing risks. This is not always well accounted for in the applied literature. Methods: We advocate a simulation point of view for understanding competing risks. The hazards are envisaged as momentary event forces. They jointly determine the event time. Their relative magnitude determines the event type. 'Empirical simulations' using data from a recent study on cardiovascular events in diabetes patients illustrate subsequent interpretation. The method avoids concerns on identifiability and plausibility known from the latent failure time approach. Results: The 'empirical simulations' served as a proof of concept. Additionally manipulating baseline hazards and treatment effects illustrated both scenarios that require greater care for interpretation and how the simulation point of view aids the interpretation. The simulation algorithm applied to real data also provides for a general tool for study planning. Conclusions: There are as many hazards as there are competing risks. All of them should be analysed. This includes estimation of baseline hazards. Study planning must equally account for these aspects.},
  language  = {en}
}