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1.  A call for transparent reporting to optimize the predictive value of preclinical research 
Nature  2012;490(7419):187-191.
The US National Institute of Neurological Disorders and Stroke convened major stakeholders in June 2012 to discuss how to improve the methodological reporting of animal studies in grant applications and publications. The main workshop recommendation is that at a minimum studies should report on sample-size estimation, whether and how animals were randomized, whether investigators were blind to the treatment, and the handling of data. We recognize that achieving a meaningful improvement in the quality of reporting will require a concerted effort by investigators, reviewers, funding agencies and journal editors. Requiring better reporting of animal studies will raise awareness of the importance of rigorous study design to accelerate scientific progress.
doi:10.1038/nature11556
PMCID: PMC3511845  PMID: 23060188
2.  Willingness to Donate Human Samples for Establishing a Dermatology Research Biobank: Results of a Survey 
Biopreservation and Biobanking  2011;9(3):265-271.
There is a rising need for biomaterial in dermatological research with regard to both quality and quantity. Research biobanks as organized collections of biological material with associated personal and clinical data are of increasing importance. Besides technological/methodological and legal aspects, the willingness to donate samples by patients and healthy volunteers is a key success factor. To analyze the theoretical willingness to donate blood and skin samples, we developed and distributed a questionnaire. Six hundred nineteen questionnaires were returned and analyzed. The willingness to donate samples of blood (82.5%) and skin (58.7%) is high among the population analyzed and seems to be largely independent of any expense allowance. People working in the healthcare system, dermatological patients, and higher qualified individuals seem to be in particular willing to donate material. An adequate patient insurance as well as an extensive education about risks and benefits is requested. In summary, there is a high willingness to donate biological samples for dermatological research. This theoretical awareness fits well with our own experiences in establishing such a biobank.
doi:10.1089/bio.2011.0009
PMCID: PMC3178419  PMID: 21977242
3.  Test systems for the determination of glucocorticoid receptor ligand induced skin atrophy 
Dermato-endocrinology  2011;3(3):175-179.
Topical glucocorticoids are highly anti-inflammatory effective but limited by their side effect potential, with skin atrophy being the most prominent one. Thus, determining the atrophogenic potential of novel compounds targeting the glucocorticoid receptor is important. Significant progress in the understanding of glucocorticoid receptor mediated molecular action has been made providing the basis for novel glucocorticoid receptor ligands with a potentially superior effect/side effect profile. Such compounds, however, need to be tested. The present gold standard for the reliable prediction of glucocorticoid induced skin atrophy are still in vivo models, however, in vitro models may replace them to some extent in the future. Indeed, advances in technologies to determine the atrophogenic potential of compounds in vitro has been made recently and promising novel test models like the human full thickness skin models are emerging. Their full predictive value, however, needs to be further evaluated. Currently, a screening approach starting with a combination of several in vitro test systems followed by subsequent testing of the most promising compounds in rodent models is recommended prior entering clinical studies with selected development compounds.
doi:10.4161/derm.3.3.15065
PMCID: PMC3219167  PMID: 22110776
glucocorticoid; glucocorticoid receptor ligands; skin atrophy; skin model; in vitro assay; in vivo assay
4.  RNA interference-mediated gene silencing in murine T cells: in vitro and in vivo validation of proinflammatory target genes 
Background
T cells play a central role in many inflammatory diseases, hence the identification and validation of T cell-specific target genes will increase the understanding of T cell function in pathologic inflammatory situations. RNA interference (RNAi), with its ability to induce specific gene silencing in mammalian cells, represents a powerful technology to investigate and validate the function of pharmaceutical target genes in vitro and in vivo. The aim of the present study was to systematically explore RNAi-mediated gene-silencing of known T cell-specific model signaling molecules in primary murine T cells in vitro and in vivo.
Results
We demonstrate that siRNA delivery and subsequent silencing of T cell specific genes is substantially increased, if murine T cells were activated prior siRNA transfection. Silencing of ZAP70, p56Lck as well as PLC-γ1 protein expression resulted in impaired function of T cells in vitro. Furthermore, delayed type hypersensitivity (DTH) was ameliorated in vivo after adoptive transfer of ZAP70-silenced T cells.
Coclusion
The combination of RNAi-mediated gene silencing and adoptive transfer of gene-silenced T cells, thus, may allow the identification and analysis of T cell-specific targets for therapeutic intervention. Additionally, this model system may represent an alternative to conventional time consuming and cost intensive gene targeting approaches.
doi:10.1186/1478-811X-6-3
PMCID: PMC2517589  PMID: 18684324
5.  Selectin and selectin ligand binding: a bittersweet attraction 
Journal of Clinical Investigation  2003;112(7):980-983.
Inhibition of leukocyte migration into target organs has long been an attractive, though challenging, basis for anti-inflammatory strategies. However, to date, the manipulation of leukocyte rolling along blood vessels has not yielded successful new therapies. An important study may now open new avenues in this exciting field of anti-inflammatory therapies by introducing a putative inhibitor of poly-N-acetyllactosamine biosynthesis that affects selectin ligand activity and shows efficacy in a rodent skin inflammation model.
doi:10.1172/JCI200319962
PMCID: PMC198533  PMID: 14523033

Results 1-5 (5)