ROGERS, T. E., & GALGIANI, J. N. (1986). ACTIVITY OF FLUCONAZOLE (UK-49,858) AND KETOCONAZOLE AGAINST CANDIDA-ALBICANS INVITRO AND INVIVO. ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 30(3), 418-422.
Donovan, F., Malo, J., Zangeneh, T. T., & Galgiani, J. N. (2017). Top Questions in Diagnosis and Treatment of Coccidioidomycosis. Open Forum Infectious Diseases.
DEFELICE, R., JOHNSON, D. G., & GALGIANI, J. N. (1981). GYNECOMASTIA WITH KETOCONAZOLE. ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 19(6), 1073-1074.
Taroumian, S., Knowles, S. L., Lisse, J. R., Yanes, J., Ampel, N. M., Vaz, A., Galgiani, J. N., & Hoover, S. E. (2012). Management of coccidioidomycosis in patients receiving biologic response modifiers or disease-modifying antirheumatic drugs. Arthritis care & research, 64(12), 1903-9.
Coccidioidomycosis (valley fever) is an endemic fungal infection of the American Southwest, an area with a large population of patients with rheumatic diseases. There are currently no guidelines for management of patients who develop coccidioidomycosis while under treatment with biologic response modifiers (BRMs) or disease-modifying antirheumatic drugs (DMARDs). We conducted a retrospective study of how both concurrent diseases were managed and the patient outcomes at 2 centers in Tucson, Arizona.
Stafford, P., Halperin, R., Legutki, J. B., Magee, D. M., Galgiani, J., & Johnston, S. A. (2012). Physical characterization of the "immunosignaturing effect". Molecular & cellular proteomics : MCP, 11(4), M111.011593.
Identifying new, effective biomarkers for diseases is proving to be a challenging problem. We have proposed that antibodies may offer a solution to this problem. The physical features and abundance of antibodies make them ideal biomarkers. Additionally, antibodies are often elicited early in the ontogeny of different chronic and infectious diseases. We previously reported that antibodies from patients with infectious disease and separately those with Alzheimer's disease display a characteristic and reproducible "immunosignature" on a microarray of 10,000 random sequence peptides. Here we investigate the physical and chemical parameters underlying how immunosignaturing works. We first show that a variety of monoclonal and polyclonal antibodies raised against different classes of antigens produce distinct profiles on this microarray and the relative affinities are determined. A proposal for how antibodies bind the random sequences is tested. Sera from vaccinated mice and people suffering from a fugal infection are individually assayed to determine the complexity of signals that can be distinguished. Based on these results, we propose that this simple, general and inexpensive system could be optimized to generate a new class of antibody biomarkers for a wide variety of diseases.