• Wisconsin Alumni Research Foundation, 1989-2016, Special Innovations Award

• 7,541,349 - 2-methylene-19-nor-(23S)-25-dehydro-1.alpha.-hydroxyvitamin D.sub.3-26,23-lactone and 2-methylene-19-nor-(23R)-25-dehydro-1.alpha.-hydroxyvitamin D.sub.3-26,23-lactone, granted Jun 2009.
• 7,541,348 - 2-methylene-19-nor-(20S)-1.alpha.-hydroxy-trishomopregnacalciferol, granted Jun 2009.
• 7,538,098 - 19-nor-vitamin D analogs with 1,2 or 3,2 heterocyclic ring, granted May 2009.
• 7,534,778 - (20S)-1.alpha.-hydroxy-2-methylene-19-nor-bishomopregnacalciferol and its uses, granted May 2009.
• 7,534,777 - Des-C,D analogs of 1.alpha.,25-dihydroxy-19-norvitamin D.sub.3, granted May 2009.

• "UV radiation supresses experimental autoimmune encephalomyelitis independent of vitamin D production"

Becklund BR, Severson KS, Vang SV, Deluca HF, Proceedings of the National Academy of Sciences of the United States of America 107(14): 6418-6423 Apr 2010.  Results suggest that UVR is likely suppressing disease independent of vitamin D production, and that vitamin D supplementation alone may not replace the ability of sunlight to reduce MS susceptibility. 

• "The calcitonin/calcitonin gene related peptide-alpha gene is not required for 1 alpha,25-dihydroxyvitamin D-3-mediated suppression of experimental autoimmune encephalomyelitis"

Becklund BR, James BJ, Gagel RF, et al., Archives of Biochemistry and Biophysics 488 (2): 105-108 Aug 2009. To determine the importance of CT in EAE we have utilized a mouse strain in which the gene encoding CT and its alternative splice product, calcitonin gene related peptide-alpha (CGRP), have been deleted. Deletion of the CT/CGRP gene had no effect on EAE progression. Furthermore, treatment with 1,25(OH)(2)D-3 suppressed EAE in CT/CGRP knock-out mice equal to that in wild type mice. Therefore, we conclude that CT is not necessary for 1,25(OH)(2)D-3-mediated suppression of EAE

• "Vitamin D and the parenteral nutrition patient"

DeLuca HF, Gastroenterology 137 (5): S79-S91 Suppl. 1 Nov 2009. Vitamin D is a prohormone produced in the skin epidermis when irradiated with sunlight or ultraviolet light B. It is also absorbed from food or supplements. Vitamin D must be converted to 25-hydroxyvitamin D-3 (circulating form) and finally to the hormone, 1a,25-dihydroxyvitamin D-3, before it can function. This hormone acts through a single nuclear receptor. The details of these conversions and molecular biology of the action of vitamin D-3 are summarized.

• "Removal of the 20-methyl group from 2-methylene-19-nor-(20S)-1 alpha,25-dihydroxyvitamin D-3 (2MD) selectively eliminates bone calcium mobilization activity"

Barycki R, Sicinski RR, Plum LA, et al., Bioorganic & Medical Chemistry 17 (22): 7658-7669 Nov 2009. The 18-nor (7), 21-nor (8) and 18,21-dinor (9) analogs of (20S)-1 alpha,25-dihydroxy-2-methylene-19-norvitamin D-3 (6, 2MD) were prepared by convergent syntheses. The known phosphine oxide 10 was coupled by the Wittig-Horner process with the corresponding C, D-fragments (13-15), obtained by a multi-step procedure from commercial vitamin D-2. The goal of our studies was to examine the influence of removal of the methyl groups located at carbons 13 and 20 on the biological potency of 2MD in the hope of finding analogs with improved therapeutic profiles.

• "Enhancement of 1,25-dihydroxyvitamin D-3-mediated suppression of experimental autoimmune encephalomyelitis by calcitonin"

Becklund BR,  Hansen DW, DeLuca HF, Proceedings of the National Academy of Sciences of the USA 106 (13): 5276-5281 Mar 2009. Because calcitonin (CT) is believed to be released by hypercalcemia and has been shown to be anti-inflammatory, we examined whether suppression of EAE by 1,25(OH)(2)D-3 could be mediated either in part or entirely by CT. Keywords: Calcium Homeostasis; Multiple Sclerosis; Allergic Encephalomyelitis; Vitamin D; Rheumatoid Arthritis.