2010年3月，西安交通大學(xué)醫(yī)學(xué)院博士生段琛，在導(dǎo)師郭雄教授的指導(dǎo)下，與芬蘭Kuopio大學(xué)Mikko Lammi教授合作，在世界*雜志 Arthritis & Rheumatism發(fā)表了封面文章。近日又被機構(gòu)“Faculty of 1000 Medicine”特別認可為“F1000論文”。

該研究在以往研究的基礎(chǔ)上，從基因水平闡述了大骨節(jié)病和骨性關(guān)節(jié)炎的表達差異，篩選出大骨節(jié)病特征性基因，為其診斷和治療提供了理論依據(jù)和新思路，并為進一步研究骨性關(guān)節(jié)炎的發(fā)病機制提供了參考，具有實際的科學(xué)價值。

郭雄教授帶領(lǐng)的“大骨節(jié)病病因發(fā)病機制與防治研究科研創(chuàng)新團隊”受到多項國家自然科學(xué)基金、衛(wèi)生部和陜西省科研資金支持，近年在zui有影響力期刊Osteoarthritis and cartilage、The Journal of rheumatology等發(fā)表博士研究生論文。擴大了我校在該領(lǐng)域的影響；并積極將研究成果應(yīng)用到臨床防治中。

Arthritis & Rheumatism雜志在風濕病和關(guān)節(jié)炎領(lǐng)域5年平均影響因子為7.423，位居*。該文章研究成果被美國專家Amanda E Nelson和 Joanne Jordan點評，并推薦為“F1000論文”。“F1000（Faculty of 1000 Medicine）”又名“千名醫(yī)學(xué)家”，是由美國哈佛大學(xué)和英國劍橋大學(xué)等*2500 名*醫(yī)學(xué)教授組成的機構(gòu)。該機構(gòu)專家根據(jù)論文對當前世界生物醫(yī)學(xué)和臨床實踐的貢獻程度和科學(xué)價值，每年對SCI文章總數(shù)不足千分之二的精品醫(yī)學(xué)論文進行推薦和點評，并賦予“F1000論文”稱號向醫(yī)學(xué)界推薦，涵蓋了醫(yī)學(xué)各個學(xué)科，是一項很高的學(xué)術(shù)榮譽。

推薦原文出處：

Arthritis & Rheumatism DOI：10.1002/art.27282

Comparative analysis of gene expression profiles between primary knee osteoarthritis and an osteoarthritis endemic to Northwestern China, Kashin-Beck disease
Chen Duan 1, Xiong Guo 1 *, Xiao-Dong Zhang 2, Han-Jie Yu 3, Hua Yan 4, Ying Gao 4, Wei-Juan Ma 1, Zong-Qiang Gao 4, Peng Xu 5, Mikko Lammi 6

1Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi, China
2First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, China
3Northwest University, Xi'an, Shaanxi, China
4Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, China
5Xi'an Red Cross Hospital, Xi'an, Shaanxi, China
6University of Kuopio, Kuopio, Finland

Objective
To investigate the differences in gene expression profiles of adult articular cartilage from patients with Kashin-Beck disease （KBD） versus those with primary knee osteoarthritis （OA）.

Methods
The messenger RNA expression profiles of articular cartilage from patients with KBD, diagnosed according to the clinical criteria for KBD in China, were compared with those of cartilage from patients with OA, diagnosed according to the Western Ontario and McMaster Universities OA Index. Total RNA was isolated separay from 4 pairs of the KBD and OA cartilage samples, and the expression profiles were evaluated by Agilent 4×44k Whole Human Genome density oligonucleotide microarray analysis. The microarray data for selected transcripts were confirmed by quantitative real-time reverse transcription-polymerase chain reaction （RT-PCR） amplification.

Results
For 1.2 × 104 transcripts, corresponding to 58.4% of the expressed transcripts, 2-fold changes in differential expression were revealed. Expression levels higher in KBD than in OA samples were observed in a mean ± SD 6,439 ± 1,041 （14.6 ± 2.4%） of the transcripts, and expression levels were lower in KBD than in OA samples in 6,147 ± 1,222 （14.2 ± 2.8%） of the transcripts. After application of the selection criteria, 1.85% of the differentially expressed genes （P < 0.001 between groups） were detected. These included 233 genes, of which 195 （0.4%） were expressed at higher levels and 38 （0.08%） were expressed at lower levels in KBD than in OA cartilage. Comparisons of the quantitative RT-PCR data supported the validity of our microarray data.

Conclusion
Differences between KBD and OA cartilage exhibited a similar pattern among all 4 of the pairs examined, indicating the presence of disease mechanisms, mainly chondrocyte matrix metabolism, cartilage degeneration, and apoptosis induction pathways, which contribute to cartilage destruction in KBD.