[1] Allander E. Kashin-Beck disease: an analysis of research and public health activities based on a bibliography 1849-1992. Scand J Rheumatol, 1994; 99, 1-36. doi:  10.3109/03009749409117126?scroll=top
[2] Suetens C, Moreno-Reyes R, Chasseur C. Epidemiological support for a multifactorial aetiology of Kashin-Beck Disease in Tibet. Int Orthop, 2001; 25, 180-87. doi:  10.1007/s002640100247
[3] Shi XW, Guo X, Lv AL, et al. Heritability estimates and linkage analysis of 23 short tandem repeat loci on chromosomes 2, 11, and 12 in an endemic osteochondropathy in China. Scand J Rheumatol, 2010; 39, 259-65. doi:  10.3109/03009740903270599
[4] Yang JB. A research report on the etiology of KBD. Chin J Endemiol, 1995; 14, 201-5. (In Chinese)
[5] Yu W, Wang Y, Jiang Y, et al. Kashin-Beck disease in children: radiographic findings in the wrist. Skeletal Radiol, 2002; 31, 222-5. doi:  10.1007/s00256-002-0475-2
[6] W Wang, S Wei, M Luo, et al. Oxidative stress and status of antioxidant enzymes in children with Kashin-Beck disease. Osteoarthritis and Cartil, 2013; 21, 1781-9 doi:  10.1016/j.joca.2013.08.002
[7] Chen J, Luo M, Wang W, et al. Altered proteolytic activity and expression of MMPs and aggrecanases and their inhibitors in Kashin-Beck disease. J Orthop Res, 2015; 33, 47-55. doi:  10.1002/jor.22708
[8] Thomas CM, Fuller CJ, Whittles CE, et al. Chondrocyte death by apoptosis is associated with cartilage matrix degradation. Osteoarthr Cartil, 2007; 15, 27-34. doi:  10.1016/j.joca.2006.06.012
[9] Hashimoto S, Ochs RL, Komiya S, et al. Linkage of chondrocyte apoptosis and cartilage degradation in human osteoarthritis. Arthritis Rheum, 1998; 41, 1632-8. doi:  10.1002/(ISSN)1529-0131
[10] Del Carlo M, Loeser R. Cell death in osteoarthritis. Curr Rheumato Rep, 2008; 10, 37-42. doi:  10.1007/s11926-008-0007-8
[11] Li SY, Cao JL, Shi ZL, et al. Promotion of the articular cartilage proteoglycan degradation by T-2 toxin and selenium protective effect. J Zhejiang Univ Sci B, 2008; 9, 22-33. doi:  10.1631/jzus.B071322
[12] Han J, Yu FF, Chang ZP, et al. Changing Grains for the Prevention and Treatment of Kashin-Beck Disease in Children: a Meta-analysis. Biomed Environ Sci, 2015; 28, 308-11. http://www.cnki.com.cn/Article/CJFDTOTAL-SWYX201504009.htm
[13] Yu FF, Han J, Wang X, et al. Salt-Rich Selenium for Prevention and Control Children with Kashin-Beck Disease: a Meta-analysis of Community-Based Trial. Biol Trace Elem Res, 2016; 170, 25-32. doi:  10.1007/s12011-015-0437-x
[14] Moreno-Reyes R, Suetens C, Mathieu F, et al. Kashin–Beck osteoarthropathy in rural Tibet in relation to selenium and iodine status. N Engl J Med, 1998; 339, 1112-20. doi:  10.1056/NEJM199810153391604
[15] Lei R, Jiang N, Zhang Q, et al. Prevalence of Selenium, T-2 Toxin, and Deoxynivalenol in Kashin-Beck Disease Areas in Qinghai Province, Northwest China. Biol Trace Elem Res, 2016; 171, 34-40. doi:  10.1007/s12011-015-0495-0
[16] Sun LY, Li Q, Meng FG, et al.. T-2 toxin contamination in grains and selenium concentration in drinking water and grains in Kaschin-Beck disease endemic areas of Qinghai Province. Biol Trace Elem Res, 2012; 150, 371-5. doi:  10.1007/s12011-012-9469-7
[17] Guan F, Li S, Wang Z, et al. Histopathology of chondronecrosis development in knee articular cartilage in a rat model of Kashin-Beck disease using T-2 toxin and selenium deficiency conditions. Rheumatol Int, 2013; 33, 157-66. doi:  10.1007/s00296-011-2335-7
[18] Chen J, Chu Y, Cao J, et al. T-2 toxin induces apoptosis, and selenium partly blocks, T-2 toxin induced apoptosis in chondrocytes through modulation of the Bax/Bcl-2 ratio. Food Chem Toxicol, 2006; 44, 567-73 doi:  10.1016/j.fct.2005.09.004
[19] Mistry D, Oue Y, Chambers MG, et al. Chondrocyte death during murine osteoarthritis. Osteoarthr Cartil, 2004; 12, 131-41. doi:  10.1016/j.joca.2003.10.006
[20] Wang SJ, Guo X, Zuo H, et al. Chondrocyte Apoptosis and Expression of Bcl-2, Bax, Fas, and iNOS in Articular Cartilage in Patients with Kashin-Beck Disease. J Rheumatol, 2006; 33, 615-9. https://www.researchgate.net/publication/7265772_Chondrocyte_apoptosis_and_expression_of_Bcl-2_Bax_Fas_and_NOS_in_articular_cartilage_in_patients_with_Kashin-Beck_disease
[21] Liu J, Wang L, Guo X, et al. The Role of Mitochondria in T-2 Toxin-Induced Human Chondrocytes Apoptosis. PLoS One, 2014; 9, e108394. doi:  10.1371/journal.pone.0108394
[22] D'Lima D, Hermida J, Hashimoto S, et al. Caspase inhibitors reduce severity of cartilage lesions in experimental osteoarthritis. Arthritis Rheum, 2006; 54, 1814-21. doi:  10.1002/(ISSN)1529-0131
[23] Hashimoto S, Takahashi K, Amiel D, et al. Chondrocyte apoptosis and nitric oxide production during experimentally induced osteoarthritis. Arthritis Rheum, 1998; 41, 1266-74. doi:  10.1002/(ISSN)1529-0131
[24] Wei L, Sun XJ, Wang Z, et al. CD95-induced osteoarthritic chondrocyte apoptosis and necrosis: dependency on p38 mitogen-activated protein kinase. Arthritis Res Ther, 2006; 8, R37. doi:  10.1186/ar1891
[25] Matsuo M, Nishida K, Yoshida A, et al. Expression of caspase-3 and -9 relevant to cartilage destruction and chondrocyte apoptosis in human osteoarthritic cartilage. Acta Med Okayama, 2001; 55, 333-40. https://www.researchgate.net/publication/283492658_Chondrocyte_Apoptosis_in_the_Pathogenesis_of_Osteoarthritis
[26] Lo MY, Kim HT. Chondrocyte apoptosis induced by collagen degradation: Inhibition by caspase inhibitors and IGF-1. J Orthop Res, 2004; 22, 140-4 doi:  10.1016/S0736-0266(03)00117-7
[27] Yang JB, Wang ZW, Liu JX. Diagnostic criteria of Kashin-Beck disease. Chin J Endemiol, 1994; 13, 24-32. (In Chinese)
[28] Philip GR, Forrest HN, George C JR. AIN-93 Purified Diets for Laboratory Rodents: Final Report of the American Institute of Nutrition Ad Hoc Writing Committee on the Reformulation of the AIN-76A Rodent Diet. J Nutr, 1993; 123, 1939-51.
[29] Chen JH, Xue S, Li S, et al. Oxidant Damage in Kashin-Beck disease and a rat Kashin-Beck disease model by employing T-2 toxin treatment under selenium deficient conditions. J Orthop Res, 2012; 30, 1229-37. doi:  10.1002/jor.22073
[30] Zhou X, Wang ZL, Wang W, et al. Increased levels of IL-6, IL-1β and TNF-α in Kashin-Beck disease and rats induced by T-2 toxin and selenium deficiency. Rheumatol Int, 2013; 33, 412-16. doi:  10.1007/s00296-013-2862-5
[31] Zhou X, Yang H, Guan F, et al. T-2 Toxin Alters the Levels of Collagen Ⅱ and Its Regulatory Enzymes MMPs/TIMP-1 in a Low-Selenium Rat Model of Kashin-Beck Disease. Biol Trace Elem Res, 2016; 169, 237-46. doi:  10.1007/s12011-015-0408-2
[32] Ramamurthy NS, Vernillo AT, Greenwald RA, et al. Reactive oxygen species activate and tetracyclines inhibit rat osteoblast collagenase. J Bone Miner Res, 1993; 8, 1247-53. http://www.academia.edu/14004999/Reactive_oxygen_species_activate_and_tetracyclines_inhibit_rat_osteoblast_collagenase
[33] Tiku ML, Liesch JB, Robertson FM. Production of hydrogen peroxide by rabbit articular chondrocytes: enhancement by cytokines. J Immunol, 1990; 145, 690-96.
[34] Goldring MB. Osteoarthritis and cartilage: the role of cytokines. Curr Rheumatol Rep, 2000; 2, 459-65 doi:  10.1007/s11926-000-0021-y
[35] Yasuhara R, Miyamoto Y, Akaike T, et al. Interleukin-1beta induces death in chondrocyte-like ATDC5 cells through mitochondrial dysfunction and energy depletion in a reactive nitrogen and oxygen species-dependent manner. Biochem J, 2005; 15(Pt 2), 315-23 doi:  10.1007/s00441-016-2551-2
[36] Del Carlo M Jr, Loeser RF. Cell death in osteoarthritis. Curr Rheumatol Rep, 2008; 10, 37-42. doi:  10.1007/s11926-008-0007-8
[37] Del Carlo M Jr, Loeser RF. Nitric oxide-mediated chondrocyte cell death requires the generation of additional reactive oxygen species. Arthritis Rheum, 2002; 46, 394-403. doi:  10.1002/(ISSN)1529-0131
[38] Daheshia M1, Yao JQ. The interleukin 1beta pathway in the pathogenesis of osteoarthritis. J Rheumatol, 2008; 35, 2306-12. doi:  10.3899/jrheum.080346
[39] Rich T, Allen RL, Wyllie AH. Defying death after DNA damage. Nature, 2000; 407, 777-83. doi:  10.1038/35037717
[40] Vousden KH. P-53: death star. Cell, 2000; 103, 691-4. doi:  10.1016/S0092-8674(00)00171-9
[41] Evan G, Littlewood T. A matter of life and cell death. Science, 1998281, 1317-22. doi:  10.1126/science.281.5381.1317
[42] Vogelstein B, Lane D, Levine AJ. Surfing the P-53 network. Nature, 2000; 408, 307-10. J Pharmacol Exp Ther, 2005; 312, 525-36.
[43] Schneider-Stock R, Diab-Assef M, Rohrbeck A, et al. 5-Aza-cytidine is a potent inhibitor of DNA methyltransferase 3a and induces apoptosis in HCT-116 colon cancer cells via Gadd45-and p53-dependent mechanisms. J Biol Chem, 2011, 286, 14744-52. doi:  10.1074/jbc.M111.221259
[44] Landesman Y, Bringold F, Milne DD, et al. Modifications of p53 protein and accumulation of p21 and gadd45 mRNA in TGF-beta 1 growth inhibited cells. Cell Signal, 1997; 9, 291-8. doi:  10.1016/S0898-6568(97)89890-7
[45] Cory S, Adams JM. The Bcl-2 family: regulators of the cellular life-or-death switch. Nature Reviews. Nat Rev Cancer, 2002; 2, 647-56. doi:  10.1038/nrc883
[46] Chen JH, Chu YL, Wang ZL, et al. T-2 toxin-induced apoptosis involving Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 signaling pathways in human chondrocytes. Zhejiang Univ Sci B, 2008; 9, 455-63. doi:  10.1631/jzus.B0820013