@article{thompson_zhu_hall_house_ranjan_burr_he_owens_smart_2011, title={C/EBP alpha Expression Is Downregulated in Human Nonmelanoma Skin Cancers and Inactivation of C/EBP alpha Confers Susceptibility to UVB-Induced Skin Squamous Cell Carcinomas}, volume={131}, ISSN={["0022-202X"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-79956039252&partnerID=MN8TOARS}, DOI={10.1038/jid.2011.31}, abstractNote={Human epidermis is routinely subjected to DNA damage induced by UVB solar radiation. Cell culture studies have revealed an unexpected role for C/EBPα (CCAAT/enhancer-binding protein-α) in the DNA damage response network, where C/EBPα is induced following UVB DNA damage, regulates the G<sub>1</sub> checkpoint, and diminished or ablated expression of C/EBPα results in G<sub>1</sub> checkpoint failure. In the current study we observed that C/EBPα is induced in normal human epidermal keratinocytes and in the epidermis of human subjects exposed to UVB radiation. The analysis of human skin precancerous and cancerous lesions (47 cases) for C/EBPα expression was conducted. Actinic keratoses, a precancerous benign skin growth and precursor to squamous cell carcinoma (SCC), expressed levels of C/EBPα similar to normal epidermis. Strikingly, all invasive SCCs no longer expressed detectable levels of C/EBPα. To determine the significance of C/EBPα in UVB-induced skin cancer, SKH-1 mice lacking epidermal C/EBPα (CKOα) were exposed to UVB. CKOα mice were highly susceptible to UVB-induced SCCs and exhibited accelerated tumor progression. CKOα mice displayed keratinocyte cell cycle checkpoint failure <i>in vivo</i> in response to UVB that was characterized by abnormal entry of keratinocytes into S phase. Our results demonstrate that C/EBPα is silenced in human SCC and loss of C/EBPα confers susceptibility to UVB-induced skin SCCs involving defective cell cycle arrest in response to UVB.}, number={6}, journal={JOURNAL OF INVESTIGATIVE DERMATOLOGY}, author={Thompson, Elizabeth A. and Zhu, Songyun and Hall, Jonathan R. and House, John S. and Ranjan, Rakesh and Burr, Jeanne A. and He, Yu-Ying and Owens, David M. and Smart, Robert C.}, year={2011}, month={Jun}, pages={1339–1346} }
 @article{olby_blot_thibaud_phillips_dp o'brien_burr_berg_brown_breen_2004, title={Cerebellar cortical degeneration in adult American Staffordshire Terriers}, volume={18}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2004)18<201:CCDIAA>2.0.CO;2}, abstractNote={Journal of Veterinary Internal MedicineVolume 18, Issue 2 p. 201-208 Open Access Cerebellar Cortical Degeneration in Adult American Staffordshire Terriers Natasha Olby, Corresponding Author Natasha Olby Department of Clinical Sciences, North Carolina State University, Raleigh, NC College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, NC 27606;e-mail: [email protected].Search for more papers by this authorStephane Blot, Stephane Blot Ecole Nationale Ve-terinaire d'Alfort, Paris, FranceSearch for more papers by this authorJean-Laurent Thibaud, Jean-Laurent Thibaud Ecole Nationale Ve-terinaire d'Alfort, Paris, FranceSearch for more papers by this authorJeff Phillips, Jeff Phillips Department of Clinical Sciences, North Carolina State University, Raleigh, NCSearch for more papers by this authorDennis P. O'Brien, Dennis P. O'Brien Department of Clinical Sciences, University of Missouri, Columbia, MOSearch for more papers by this authorJeanne Burr, Jeanne Burr Department of Clinical Sciences, North Carolina State University, Raleigh, NCSearch for more papers by this authorJason Berg, Jason Berg VCA County Animal Clinic, Yonkers, NYSearch for more papers by this authorTalmage Brown, Talmage Brown Department of Population Health and Pathobiology, North Carolina State University, Raleigh, NCSearch for more papers by this authorMatthew Breen, Matthew Breen Department of Molecular Biomedical Sciences, North Carolina State University, Raleigh, NC.Search for more papers by this author Natasha Olby, Corresponding Author Natasha Olby Department of Clinical Sciences, North Carolina State University, Raleigh, NC College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, NC 27606;e-mail: [email protected].Search for more papers by this authorStephane Blot, Stephane Blot Ecole Nationale Ve-terinaire d'Alfort, Paris, FranceSearch for more papers by this authorJean-Laurent Thibaud, Jean-Laurent Thibaud Ecole Nationale Ve-terinaire d'Alfort, Paris, FranceSearch for more papers by this authorJeff Phillips, Jeff Phillips Department of Clinical Sciences, North Carolina State University, Raleigh, NCSearch for more papers by this authorDennis P. O'Brien, Dennis P. O'Brien Department of Clinical Sciences, University of Missouri, Columbia, MOSearch for more papers by this authorJeanne Burr, Jeanne Burr Department of Clinical Sciences, North Carolina State University, Raleigh, NCSearch for more papers by this authorJason Berg, Jason Berg VCA County Animal Clinic, Yonkers, NYSearch for more papers by this authorTalmage Brown, Talmage Brown Department of Population Health and Pathobiology, North Carolina State University, Raleigh, NCSearch for more papers by this authorMatthew Breen, Matthew Breen Department of Molecular Biomedical Sciences, North Carolina State University, Raleigh, NC.Search for more papers by this author First published: 28 June 2008 https://doi.org/10.1111/j.1939-1676.2004.tb00161.xCitations: 47AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract Adult-onset cerebellar cortical degeneration recently has been reported in American Staffordshire Terriers. We describe the clinical and histopathologic features of this disease and examine its mode of inheritance in 63 affected dogs. The age at which neurologic deficits 1st were recognized varied from 18 months to 9 years, with the majority of dogs presented to veterinarians between 4 and 6 years of age. Time from onset of clinical signs to euthanasia varied from 6 months to 6.5 years, with the majority of affected dogs surviving from 2 to 4 years. Initial neurologic findings included stumbling, truncal sway, and ataxia exacerbated by lifting the head up and negotiating stairs. Signs progressed to obvious ataxia characterized by dysmetria, nystagmus, coarse intention tremor, variable loss of menace reaction, marked truncal sway, and falling with transient opisthotonus. With continued progression, dogs became unable to walk without falling repeatedly. Cerebellar atrophy was visible on magnetic resonance images and on gross pathology. Histopathologic findings included marked loss of Purkinje neurons with thinning of the molecular and granular layers and increased cellularity of the cerebellar nuclei. The closest common ancestor of the dogs was born in the 1950s and inheritance was most consistent with an autosomal recessive mode of transmission with a prevalence estimated at 1 in 400 dogs. This inherited disease is comparable to the group of diseases known as spinocerebellar ataxias in humans. Many spinocerebellar ataxias in humans are caused by nucleotide repeats, and this genetic aberration merits investigation as a potential cause of the disease in American Staffordshire Terriers. References 1 de Lahunta A. Abiotrophy in domestic animals: A review. 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Arch Neurol 2002; 59: 623–629. 27 Vuillaume I., Devos D., Schraen-Maschke S., et al. A new locus for spinocerebellar ataxia (SCA21) maps to chromosome 7p21.3-p15.1. Ann Neurol 2002; 52: 666–670. 28 Jardim LB, Silveira I., Pereira ML, et al. A survey of spinocerebellar ataxia in South Brazil–6new caseswith Machado-Joseph disease, SCA7, SCA8, or unidentified disease-causing mutations. J Neurol 2001; 248: 870–876. 29 Zhuchenko O., Bailey J., Bonnen P., et al. Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the a1A-voltage dependent calcium channel. Nat Genet 1997; 15: 62–69. 30 Sinke RJ, Ippel EF, Diepstraten CM, et al. Clinical and molecular correlations in spinocerebellar ataxia type 6. Arch Neurol 2001; 58: 1839–1844. 31 Pujana MA, Corral J., Gratacos M., et al. Spinocerebellar ataxias in Spanish patients: Genetic analysis of familial and sporadic cases. Hum Genet 1999; 104: 516–522. 32 Gabsi S., Gouider-Khouja N., Belal S., et al. Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. Eur J Neurol 2001; 8: 477–481. 33 Van Swieten JC, Brusse E., de Graaf BM, et al. A mutation in the fibroblast growth factor 14 gene is associated with autosomal dominant cerebellar ataxia. Am J Hum Genet 2003; 77: 191–199. Citing Literature Volume18, Issue2March 2004Pages 201-208 ReferencesRelatedInformation}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Olby, N and Blot, S and Thibaud, JL and Phillips, J and DP O'Brien and Burr, J and Berg, J and Brown, T and Breen, M}, year={2004}, pages={201–208} }
 @article{olby_harris_burr_munana_sharp_keene_2004, title={Recovery of pelvic limb function in dogs following acute intervertebral disc herniations}, volume={21}, ISSN={["1557-9042"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-0942290535&partnerID=MN8TOARS}, DOI={10.1089/089771504772695940}, abstractNote={Chondrodystrophoid breeds of dog are prone to explosive herniation of mineralized disc material into the thoracolumbar spinal canal. The resulting acute spinal cord injury may represent an excellent spontaneous model of acute traumatic spinal cord injury. The aims of this study were to quantify the recovery of dogs following acute disc herniations, to evaluate external factors that influence recovery, and to identify a group of dogs suitable for use in clinical trials on neuroprotective drugs. The gait of 88 dogs with thoracolumbar disc herniations was scored at the time of injury and 2, 4, and 12 weeks after surgical decompression. Dogs were placed into four groups dependent on the severity of presenting signs; dogs in group 1 had the most severe injury severity. Group 1 dogs showed a variable but incomplete recovery by 12 weeks. Dogs in groups 2 and 3 recovered uniformly but more completely, while dogs in group 4 made a rapid and excellent recovery and were deemed unsuitable for clinical trials. Combining dogs in groups 1, 2 and 3 produced a population of dogs with incomplete recovery by 12 weeks. Power analysis revealed that 87 such dogs would be needed per treatment group to detect a 20% change in function with a power of 95%. The number needed reduced drastically to 19 by eliminating dogs in group 1, but this produced less room for functional improvement. External factors did not appear to influence outcome. We conclude that dogs with spontaneous disc herniations provide a useful model of acute spinal cord injury for clinical trials.}, number={1}, journal={JOURNAL OF NEUROTRAUMA}, author={Olby, N and Harris, T and Burr, J and Munana, K and Sharp, N and Keene, B}, year={2004}, month={Jan}, pages={49–59} }