Although the facility is a teaching facility we have a strong focus on basic and translational research in human disease. The facility proactively acts to support funding applications and project research outputs directly and indirectly through the services listed within these pages. In order to maintain these high standards and to ensure that the facility is constantly resourcing advanced research technologies as they become commercially available, we request that researchers using the facility help to support both the facility and the staff within by acknowledging their input. This support acts to strengthen cases for capital equipment grant awards and helps the facility to synergistically evolve it's capabilities with your own research needs.
Although the Facility is a charged service in order to recover most of its operating costs, the full costs (including capital equipment purchases) are not passed on to the end user.
The Faculty of Medicine & Health look at the quantity and quality of publications from the University research and assess the research output related to work using our core facility. This is used as a metric of facility performance (alongside the number of usage hours and cost recovery) and affects the degree of long term support that the facility receives. As a result the facility requests acknowledgment in your research outputs including posters, talks and publications to help maintain its research profile.
Using data generated within the Facility
In a publication that includes data (main figures or supplemental) generated within the FCCF, please state:
“We acknowledge the University of Leeds FoMH Flow Cytometry & Imaging Facility for assistance with the generation of Flow Cytometry & Light Microscopy data”
Significant Input from Facility Support Staff
If a member of the Facility support team have worked closely with you on a project, you should acknowledge this. It is good practice to include their name in the acknowledgement section at least.
In situations where they have made significant intellectual input, you can offer them a co-authorship. This should be discussed at the earliest opportunity.
(Under construction TBA)
1. Meade JL et al (2009) Proteolytic activation of the cytotoxic phenotype during human NK cell development. Journal of Immunology 183, 803-813.
2. Holmes TD et al (2011) A human NK cell activation/inhibition threshold allows small changes in the target cell surface phenotype to dramatically alter susceptibility to NK cells. Journal of Immunology 186:1538-45
3. Scott GB et al (2010). Identification of the BCL2/Adenovirus E1B-19K protein-interacting protein 2 (BNIP-2) as a granzyme B target during human natural killer cell-mediated killing. Biochemical Journal 431, 423-4314.
4. Churchman S et al (2012) Native CD271(+) multipotential stromal cells (MSCs) have a transcript profile indicative of multiple fates with prominent osteogenic and Wnt pathway signalling activity. Arthritis and Rheumatism in press; doi: 10.1002/art.34434.
5. Jones E et al (2010) Large-scale extraction and characterization of CD271+ multipotential stromal cells from trabecular bone in health and osteoarthritis: implications for bone regeneration strategies based on uncultured or minimally cultured multipotential stromal cells. Arthritis and Rheumatism 62:1944-54.
6. Jones E et al (2010) Mesenchymal stem cells in rheumatoid synovium: enumeration and functional assessment in relation to synovial inflammation level. Annals Rheumatic Diseases 69:450-7.
7. Hoogenkamp M et al (2009) Early chromatin unfolding by RUNX1: a molecular explanation for differential requirements during specification versus maintenance of the hematopoietic gene expression program. Blood 114:299-309
8. Barnes NA et al (2012) BLIMP-1 and STAT3 counter-regulate microRNA-21 during plasma cell differentiation. Journal of Immunology in press.
9. Doody GM et al (2007) PRDM1/BLIMP-1 Modulates IFN-γ-Dependent Control of the MHC Class I Antigen-Processing and Peptide-Loading Pathway. Journal of Immunology 179:7614-23.
10. Barnes NA et al (2009) Amino Acid Deprivation Links BLIMP-1 to the Immunomodulatory Enzyme Indoleamine 2,3-Dioxygenase. Journal of Immunology 183:5768-77.