Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine · 2005
[Primary exploration on immune associated genome of patients with Pi-Qi deficiency syndrome].
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Luo Yun-Jian, Xiu Zong-Chang, Huang Sui-Ping
Аннотация
OBJECTIVE: To investigate the abnormal change of immune function in patients with Pi-Qi deficiency Syndrome, and to explore the genomic mechanism of its genesis by cDNA chip techniques.
METHODS: The cross probe was made by extracting and microamplifying the total RNA and mRNA of peripheral white blood cells (WBC) in healthy subjects and patients with chronic gastritis and ulcerative colitis, which were labeled by Cy3 and Cy5 respectively. Then equal quantity of the two labeled probes were mixed and hybridized with cDNA chip, fluorescent signal of the chips were scanned with scanner. Data obtained were analyzed for comparing the difference of the expressive levels of immune associated genome in peripheral WBC in healthy subjects with those in patients.
RESULTS: Expressions of CD9, CD164, PF4 and RARB gene in WBC of patients, both gastritis and colitis, were down-regulated while those of IGKC, DEFA1 and GNLY were up-regulated.
CONCLUSION: The genesis of Pi-Qi deficiency syndrome has its immune associated genomic basis, and the immune functions are disordered in patients with that syndrome.
METHODS: The cross probe was made by extracting and microamplifying the total RNA and mRNA of peripheral white blood cells (WBC) in healthy subjects and patients with chronic gastritis and ulcerative colitis, which were labeled by Cy3 and Cy5 respectively. Then equal quantity of the two labeled probes were mixed and hybridized with cDNA chip, fluorescent signal of the chips were scanned with scanner. Data obtained were analyzed for comparing the difference of the expressive levels of immune associated genome in peripheral WBC in healthy subjects with those in patients.
RESULTS: Expressions of CD9, CD164, PF4 and RARB gene in WBC of patients, both gastritis and colitis, were down-regulated while those of IGKC, DEFA1 and GNLY were up-regulated.
CONCLUSION: The genesis of Pi-Qi deficiency syndrome has its immune associated genomic basis, and the immune functions are disordered in patients with that syndrome.