@article{oh_see_long_galvin_2006, title={Estimates of genetic correlations between production and semen traits in boar}, volume={19}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-28844438790&partnerID=MN8TOARS}, DOI={10.5713/ajas.2006.160}, abstractNote={Currently, boars selected for commercial use as AI sires are evaluated on grow-finish performance and carcass characteristics. If AI sires were also evaluated and selected on semen production, it may be possible to reduce the number of boars required to service sows, thereby improving the productivity and profitability of the boar stud. The objective of this study was to estimate genetic correlations between production and semen traits in the boar: average daily gain (ADG), backfat thickness (BF) and muscle depth (MD) as production traits, and total sperm cells (TSC), total concentration (TC), volume collected (SV), number of extended doses (ND), and acceptance rate of ejaculates (AR) as semen traits. Semen collection records and performance data for 843 boars and two generations of pedigree data were provided by Smithfield Premium Genetics. Backfat thickness and MD were measured by real-time ultrasound. Genetic parameters were estimated from five four-trait and one five-trait animal models using MTDFREML. Average heritability estimates were 0.39 for ADG, 0.32 for BF, 0.15 for MD, and repeatability estimates were 0.38 for SV, 0.37 for TSC, 0.09 for TC, 0.39 for ND, and 0.16 for AR. Semen traits showed a strong negative genetic correlation with MD and positive genetic correlation with BF. Genetic correlations between semen traits and ADG were low. Therefore, current AI boar selection practices may be having a detrimental effect on semen production. (Asian-Aust. J. Anim. Sci. 2006. Vol 19, No. 2 : 160-164)}, number={2}, journal={Asian-Australasian Journal of Animal Sciences}, author={Oh, S.H. and See, M.T. and Long, T.E. and Galvin, J.M.}, year={2006}, pages={160–164} }
 @article{oh_lee_see_2006, title={Estimation of genetic parameters for reproductive traits between first and later parities in pig}, volume={19}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-28844484138&partnerID=MN8TOARS}, DOI={10.5713/ajas.2006.7}, abstractNote={The objective of this study was to estimate genetic parameters between first and later parities as different traits in reproductive traits of pigs using multiple trait animal model procedures. Data related to reproductive traits from a total of 2,371 individuals maintained at a farm were taken from the pedigree file. Sires and dams were consisted of Duroc, Landrace, and Yorkshire breeds, respectively. The first and later parity records were considered as different traits. Traits included in analyses were total pigs born (TB1), number of pigs born alive (NBA1), number of pigs weaned (NW1), and litter weaning weight (LWT1) in the first parity, and total pigs born (TB2), number of pigs born alive (NBA2), number of pigs weaned (NW2), litter weaning weight (LWT2) and interval between farrowing events (FTF) in later parities. Heritability estimates of TB1, NBA1, NW1 and LWT1 in the first parity were 0.27, 0.25, 0.16 and 0.20, respectively. For TB2, NBA2, NW2, LWT2 and FTF in later parities, heritabilities were estimated as 0.15, 0.15, 0.08, 0.11 and 0.07, respectively. Genetic correlations between sow reproductive traits in the first parity and in the second and later parity were estimated to be 0.89, 0.77, 0.58 and 0.66, respectively, between TB1 and TB2, NBA1 and NBA2, NW1 and NW2, and LWT1 and LWT2. While phenotypic correlations between TB1 and TB2, NBA1 and NBA2, NW1 and NW2, and LWT1 and LWT2 were estimated as 0.18, 0.15, 0.06 and 0.10, respectively. Genetic correlations between reproductive traits of first and later parities were not high indicating that reproductive traits for sows should be analyzed while considering the parities as different traits. (Asian-Aust. J. Anim. Sci. 2006. Vol 19, No. 1 : 7-12)}, number={1}, journal={Asian-Australasian Journal of Animal Sciences}, author={Oh, S.H. and Lee, D.H. and See, M.T.}, year={2006}, pages={7–12} }
 @misc{smart_oh_2003, title={Method of treating alopecia}, volume={6,555,532}, number={2003 Apr. 29}, publisher={Washington, DC: U.S. Patent and Trademark Office}, author={Smart, R. C. and Oh, H.-S.}, year={2003} }
 @misc{smart_oh_2001, title={Method of treating alopecia}, volume={6,204,258}, number={2001 Mar. 20}, publisher={Washington, DC: U.S. Patent and Trademark Office}, author={Smart, R. C. and Oh, H.-S.}, year={2001} }
 @article{zhu_oh_shim_sterneck_johnson_smart_1999, title={C/EBP beta modulates the early events of keratinocyte differentiation involving growth arrest and keratin 1 and keratin 10 expression}, volume={19}, DOI={10.1128/mcb.19.10.7181}, abstractNote={ABSTRACT The epidermis is a stratified squamous epithelium composed primarily of keratinocytes that become postmitotic and undergo sequential changes in gene expression during terminal differentiation. The expression of the transcription factor CCAAT/enhancer binding protein β (C/EBPβ) within mouse epidermis and primary keratinocytes has recently been described; however, the function of C/EBPβ within the epidermal keratinocyte is unknown. We report here that transient transfection of mouse primary keratinocytes with a C/EBP-responsive promoter-reporter construct resulted in a sevenfold increase in luciferase activity when keratinocytes were switched to culture conditions that induce growth arrest and differentiation. Forced expression of C/EBPβ in BALB/MK2 keratinocytes inhibited growth, induced morphological changes consistent with a more differentiated phenotype, and upregulated two early markers of differentiation, keratin 1 (K1) and keratin 10 (K10) but had a minimal effect on the expression of late-stage markers, loricrin and involucrin. Analysis of the epidermis of C/EBPβ-deficient mice revealed a mild epidermal hyperplasia and decreased expression of K1 and K10 but not of involucrin and loricrin. C/EBPβ-deficient primary keratinocytes were partially resistant to calcium-induced growth arrest. Analysis of terminally differentiated spontaneously detached keratinocytes or those induced to differentiate by suspension culture revealed that C/EBPβ-deficient keratinocytes displayed striking decreases in K1 and K10, while expression of later-stage markers was only minimally altered. Our results demonstrate that C/EBPβ plays an important role in the early events of stratified squamous differentiation in keratinocytes involving growth arrest and K1 and K10 expression.}, number={10}, journal={Molecular and Cellular Biology}, author={Zhu, S. Y. and Oh, H. S. and Shim, M. and Sterneck, E. and Johnson, P. F. and Smart, Robert}, year={1999}, pages={7181–7190} }
 @article{smart_oh_chanda_robinette_1999, title={Effects of 17-beta-estradiol and ICI 182 780 on hair growth in various strains of mice}, volume={4}, ISSN={["1529-1774"]}, DOI={10.1038/sj.jidsp.5640231}, abstractNote={17-beta-Estradiol (10 nmol per 200 microl acetone) applied topically twice weekly to the clipped dorsal surface of C57BL/6 or C3H female mouse skin prevented hair growth, as previously described in the CD-1 mouse strain. Twice weekly topical application of the estrogen receptor antagonist, ICI 182 780 (10nmol per 200microl acetone), induced the telogenanagen transition and produced early pigmentation appearance in skin and hair growth in C57BL/6 and C3H female mice. Whereas twice weekly topical application of 10nmol 17-beta-estradiol blocked hair growth, the intraperitoneal administration of this dose twice weekly did not block hair growth, suggesting a direct cutaneous effect of 17-beta-estradiol. We also evaluated the effect of 17-alpha-estradiol, 17-beta-estradiol, and ICI 182 780 on hair growth in male mice. As observed in female mice, 17-beta-estradiol was a potent inhibitor of hair growth and ICI 182 780 stimulated hair growth; however, unlike the results previously observed in female mice, 17-alpha-estradiol was a potent inhibitor of hair growth in male mice. These results demonstrate that (i) the route of administration of 17-beta-estradiol is critical for its ability to block hair growth; (ii) C57BL/6 and C3H mice, two commonly employed mouse strains for hair growth studies, responded to 17-beta-estradiol and ICI 182 780 in a manner similar to that described in CD-1 mice; and (iii) the hair follicles of male and female mice respond similarly to 17-beta-estradiol and ICI 182 780, but display striking sex differences in the response to 17-alpha-estradiol on hair growth.}, number={3}, journal={JOURNAL OF INVESTIGATIVE DERMATOLOGY SYMPOSIUM PROCEEDINGS}, author={Smart, RC and Oh, HS and Chanda, S and Robinette, CL}, year={1999}, month={Dec}, pages={285–289} }
 @misc{smart_oh_1999, title={Methods of treating alopecia}, volume={5,965,551}, number={1999 Oct. 12}, publisher={Washington, DC: U.S. Patent and Trademark Office}, author={Smart, R. C. and Oh, H.-S.}, year={1999} }
 @article{oh_smart_1998, title={Expression of CCAAT/enhancer binding proteins (C/EBP) is associated with squamous differentiation in epidermis and isolated primary keratinocytes and is altered in neoplasms}, volume={110}, ISSN={["0022-202X"]}, DOI={10.1046/j.1523-1747.1998.00199.x}, abstractNote={The epidermis is a stratified squamous epithelium composed primarily of keratinocytes that undergo sequential changes in gene expression during differentiation. CCAAT/enhancer binding proteins (C/EBP) are members of the bZIP family of DNA binding proteins/transcription factors. Northern analysis demonstrated that C/EBPalpha, C/EBPbeta, and C/EBPdelta mRNA are expressed in mouse epidermis and their mRNA levels were generally greater than those observed in other tissues known to express high levels of C/EBP. Western analysis of isolated epidermal cell nuclei demonstrated the presence of a 42 and 30 kDa C/EBPalpha protein and 35 kDa C/EBPbeta protein. Immunohistochemical localization of C/EBPalpha and C/EBPbeta in intact interfollicular epidermis revealed that C/EBPbeta expression is exclusive to the nuclei of a three-cell cluster of suprabasal keratinocytes that is morphologically consistent with the central column of the epidermal proliferative unit, and that C/EBPalpha is expressed in the nuclei and cytoplasm of suprabasal keratinocytes and weakly expressed in a perinuclear manner in some basal keratinocytes. In squamous cell carcinomas the expression of C/EBPalpha and C/EBPbeta was greatly diminished as both the intensity of nuclear staining and the number of cells expressing C/EBPalpha and C/EBPbeta were reduced. In isolated primary mouse keratinocytes, calcium-induced differentiation was accompanied by specific temporal changes in the expression of C/EBPalpha, C/EBPbeta, and C/EBPdelta mRNA and C/EBPalpha and C/EBPbeta protein. These results implicate a role for the C/EBP family in the regulation of genes involved in or specifically expressed during the process of squamous differentiation in epidermis.}, number={6}, journal={JOURNAL OF INVESTIGATIVE DERMATOLOGY}, author={Oh, HS and Smart, RC}, year={1998}, month={Jun}, pages={939–945} }
 @misc{smart_oh_1998, title={On the effect of estrogen receptor agonists and antagonists on the mouse hair follicle cycle}, volume={111}, ISSN={["1523-1747"]}, DOI={10.1046/j.1523-1747.1998.00257.x}, abstractNote={The experiments we reported in our letter were described as executed, and the mouse strains investigated were chosen for the reasons stated. The experiments were planned and conducted completely independent of one another but, unfortunately, the same mistake was made in both cases – the concentrations used were not as reported in the original report. Although we take responsibility for this oversight, we also recognize that the dosage listing is not entirely conventional to the field. Before starting the repeat experiments we consulted several independent researchers outside our respective laboratories; in all cases the understood dosage was interpreted exactly as we had. When we repeated the work using the twice weekly protocol and the concentrations used originally by Oh and Smart (Proc Natl Acad Sci 93:12525), β-estradiol did indeed inhibit the normal progression of spontaneous anagen in pigmented mice (C57B16). From additional and subsequent studies that we have since executed, we have learned several important features about the role of estrogen receptor-mediated signaling in murine hair growth control that we did not formerly appreciate. We would hope to share these data in a future report. We are indebted to Drs. Oh and Smart for calling our attention to this interesting phenomenon and regret the confusion our mistake might have caused. Note from the Editor: Due to an editorial office error, Drs. Smart and Oh were not given a chance to reply to the original letter about their paper by Drs. Stenn, Paus, and Filippi (J Invest Dermatol, 110:95 1998). We apologize to all the authors for this mistake.}, number={1}, journal={JOURNAL OF INVESTIGATIVE DERMATOLOGY}, author={Smart, RC and Oh, HS}, year={1998}, month={Jul}, pages={175–175} }