@article{sperry_kathariou_edwards_wolf_2009, title={Multiple-Locus Variable-Number Tandem-Repeat Analysis as a Tool for Subtyping Listeria monocytogenes Strains (vol 46, pg 1435, 2008)}, volume={47}, ISSN={["0095-1137"]}, DOI={10.1128/jcm.00730-09}, number={6}, journal={JOURNAL OF CLINICAL MICROBIOLOGY}, author={Sperry, Katharine E. Volpe and Kathariou, Sophia and Edwards, Justin S. and Wolf, Leslie A.}, year={2009}, month={Jun}, pages={1984–1984} }
 @article{gebreyes_thakur_dorr_tadesse_post_wolf_2009, title={Occurrence of spvA Virulence Gene and Clinical Significance for Multidrug-Resistant Salmonella Strains}, volume={47}, ISSN={["0095-1137"]}, DOI={10.1128/JCM.01660-08}, abstractNote={
            Nontyphoidal
            Salmonella
            strains are important reservoirs of antimicrobial resistance. An important issue that has not been investigated is whether the multiresistant
            Salmonella
            strains are more virulent than their susceptible counterparts.
            Salmonella
            isolates collected from clinical human (
            n
            = 888) and porcine (
            n
            = 2,120) cases at the same time period and geographic location were investigated. Antimicrobial susceptibility, PCR analysis for the
            spvA
            virulence gene, and pulsed-field gel electrophoresis (PFGE) genotyping were done. Carriage of
            spvA
            was associated with multidrug-resistant (MDR) type ACSSuT strains (odds ratio, 7.1;
            P
            < 0.05), a type often implicated in bacteremic human cases. PFGE revealed that clinical isolates from pigs were more clonally related to those of human origin than the nonclinical porcine isolates. The findings suggest that MDR strains that also carry specific virulence factors are more likely to be of clinical significance.
          }, number={3}, journal={JOURNAL OF CLINICAL MICROBIOLOGY}, author={Gebreyes, Wondwossen A. and Thakur, Siddhartha and Dorr, Paul and Tadesse, Daniel A. and Post, Karen and Wolf, Leslie}, year={2009}, month={Mar}, pages={777–780} }
 @article{sperry_kathariou_edwards_wolf_2008, title={Multiple-locus variable-number tandem-repeat analysis as a tool for subtyping Listeria monocytogenes strains}, volume={46}, ISSN={["1098-660X"]}, DOI={10.1128/JCM.02207-07}, abstractNote={ABSTRACT}, number={4}, journal={JOURNAL OF CLINICAL MICROBIOLOGY}, author={Sperry, Katharine E. Volpe and Kathariou, Sophia and Edwards, Justin S. and Wolf, Leslie A.}, year={2008}, month={Apr}, pages={1435–1450} }
 @article{wolf_laster_1999, title={Characterization of arachidonic acid-induced apoptosis}, volume={30}, DOI={10.1007/bf02738119}, abstractNote={Tumor necrosis factor (TNF) can induce apoptosis in a number of different cell types. This response often depends on the activity of cytosolic phospholipase A2 (cPLA2), which catalyzes the release of arachidonic acid from the sn-2 position of membrane phospholipids. In this study, we investigate the ability of arachidonic acid itself to cause cell death. We show that in assays with 10% fetal bovine serum (FBS) arachidonic acid will not kill, nor does act synergistically with TNF. In contrast, by lowering the concentration of FBS to 2%, it is possible to use arachidonic acid to induce cell death. Arachidonic acid-induced cell death was judged to be apoptotic based on morphology and the cleavage of poly(ADP)ribose polymerase. Arachidonic acid was able to kill all cell lines tested including two human melanoma-derived cell lines, and susceptibility to arachidonic acid was not influenced by adenovirus gene products that control susceptibility to TNF. Finally, we show that arachidonic acid is unique among 20 carbon fatty acids for its ability to induce apoptosis and that several other unsaturated, but not saturated fatty acids can also induce apoptosis.}, number={3}, journal={Cell Biochemistry and Biophysics}, author={Wolf, L. A. and Laster, S. M.}, year={1999}, pages={353–368} }
 @article{coulombe_yang_wolf_gill_1999, title={Tolerance to antigen-presenting cell-depleted islet allografts is CD4 T cell dependent}, volume={162}, number={5}, journal={Journal of Immunology}, author={Coulombe, M. and Yang, H. and Wolf, L. A. and Gill, R. G.}, year={1999}, pages={2503–2510} }