TY  - JOUR
A1  - Ribitsch, Iris
A1  - Peham, Christian
A1  - Ade, Nicole
A1  - Duerr, Julia
A1  - Handschuh, Stephan
A1  - Schramel, Johannes Peter
A1  - Vogl, Claus
A1  - Walles, Heike
A1  - Egerbacher, Monika
A1  - Jenner, Florian
T1  - Structure-Function relationships of equine menisci
JF  - PLoS ONE
N2  - Meniscal pathologies are among the most common injuries of the femorotibial joint in both human and equine patients. Pathological forces and ensuing injuries of the cranial horn of the equine medial meniscus are considered analogous to those observed in the human posterior medial horn. Biomechanical properties of human menisci are site-and depth-specific. However, the influence of equine meniscus topography and composition on its biomechanical properties is yet unknown. A better understanding of equine meniscus composition and biomechanics could advance not only veterinary therapies for meniscus degeneration or injuries, but also further substantiate the horse as suitable translational animal model for (human) meniscus tissue engineering. Therefore, the aim of this study was to investigate the composition and structure of the equine knee meniscus in a site-and age-specific manner and their relationship with potential site-specific biomechanical properties. The meniscus architecture was investigated histologically. Biomechanical testing included evaluation of the shore hardness (SH), stiffness and energy loss of the menisci. The SH was found to be subjected to both age and site-specific changes, with an overall higher SH of the tibial meniscus surface and increase in SH with age. Stiffness and energy loss showed neither site nor age related significant differences. The macroscopic and histologic similarities between equine and human menisci described in this study, support continued research in this field.
KW  - Human Medial Meniscus
KW  - Articular-Cartilage
KW  - Biomechanical Properties
KW  - Compressive Properties
KW  - Human Knee
KW  - Collagen
KW  - Injuries
KW  - Models
KW  - Repair
KW  - Osteoarthritis
Y1  - 2018
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-225214
VL  - 13
IS  - 3
ER  - 
TY  - JOUR
A1  - Weis, Eva
A1  - Schoen, Holger
A1  - Victor, Anja
A1  - Spix, Claudia
A1  - Ludwig, Marco
A1  - Schneider-Raetzke, Brigitte
A1  - Kohlschmidt, Nicolai
A1  - Bartsch, Oliver
A1  - Gerhold-Ay, Aslihan
A1  - Boehm, Nils
A1  - Grus, Franz
A1  - Haaf, Thomas
A1  - Galetzka, Danuta
T1  - Reduced mRNA and Protein Expression of the Genomic Caretaker RAD9A in Primary Fibroblasts of Individuals with Childhood and Independent Second Cancer
JF  - PLoS ONE
N2  - Background: 

The etiology of secondary cancer in childhood cancer survivors is largely unclear. Exposure of normal somatic cells to radiation and/or chemotherapy can damage DNA and if not all DNA lesions are properly fixed, the mis-repair may lead to pathological consequences. It is plausible to assume that genetic differences, i.e. in the pathways responsible for cell cycle control and DNA repair, play a critical role in the development of secondary cancer. 

Methodology/Findings: 

To identify factors that may influence the susceptibility for second cancer formation, we recruited 20 individuals who survived a childhood malignancy and then developed a second cancer as well as 20 carefully matched control individuals with childhood malignancy but without a second cancer. By antibody microarrays, we screened primary fibroblasts of matched patients for differences in the amount of representative DNA repair-associated proteins. We found constitutively decreased levels of RAD9A and several other DNA repair proteins in two-cancer patients, compared to one-cancer patients. The RAD9A protein level increased in response to DNA damage, however to a lesser extent in the two-cancer patients. Quantification of mRNA expression by real-time RT PCR revealed lower RAD9A mRNA levels in both untreated and 1 Gy gamma-irradiated cells of two-cancer patients. 

Conclusions/Significance: 

Collectively, our results support the idea that modulation of RAD9A and other cell cycle arrest and DNA repair proteins contribute to the risk of developing a second malignancy in childhood cancer patients.
KW  - DNA methylation
KW  - Malignant neoplasms
KW  - Genes
KW  - Instability
KW  - Stability
KW  - Susceptibility
KW  - Checkpoints
KW  - Repair
KW  - Damage
Y1  - 2011
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-141838
VL  - 6
IS  - 10
ER  -