Publications by authors named "Yun-Chang Yuan"

Background: Long non-coding RNA H19 (lncRNA H19) has been widely reported in esophageal cancer (EC), and previous study had found that lncRNAH19 was up-regulated in EC and promoted cell proliferation and metastasis. However, the mechanism still needs further studied.

Methods: Levels of lncRNA H19 were analyzed by qRT-PCR in matched samples from 30 patients.

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Background/purpose: Chronic rejection limits the long-term success of cardiac transplantation and the underlying cause of the disease is unknown. Connective tissue growth factor (CTGF) is considered as a mitogenic and chemotactic factor for fibroblasts, and is associated with cell proliferation and collagen synthesis. We evaluated the expression of CTGF in a rat model of heart allograft chronic rejection.

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Objective: To detect the expression of connective tissue growth factor (CTGF) in acute heart allograft rejection in rats and to investigate the relationship between CTGF expression and cardiac allograft fibrosis.

Methods: Sixteen Wister rats served as donors and another 16 Sprague-Dawely (SD) rats served as recipients. Intra-abdominal heterotopic heart transplantation was performed.

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Objective: To evaluate the therapeutic effect of remaining integrated mediastinal pleura upon the aortic arch and performing the anastomosis at the left cervix in radical operation for esophageal carcinoma.

Methods: Ninety-eight patients with esophageal carcinoma were treated with the operation mentioned above. Among them, 56 patients had cancer in the middle, 12 in the upper-middle, 24 in the lower-middle segments, and 6 had double-primary tumors, with carcinoma length of (5.

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Objective: To investigate the role of connective tissue growth factor (CTGF) in pulmonary allograft fibrosis in rats.

Methods: The lungs of 20 Wistar rats were transplanted into 20 Sprague-Dawley(SD) rats. Ten allograft lungs were harvested 1 week postoperatively (acute rejection group,AR); the other 10 allografts were harvested 6 weeks postoperatively (chronic rejection group,CR); and ten normal Wistar rats served as a control group(normal lung, NL).

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Background & Objective: The genesis of lung cancer was associated with mutation or abnormal expression of PTEN, p16, p21, and p53. Tissue microarray provides a high throughout tool for genes expression. But little is reported about expression of PTEN, p16, p21, and p53 in lung cancers with tissue microarray.

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