Subjects: Medicine, Pharmacy >> Preclinical Medicine submitted time 2017-12-07 Cooperative journals: 《南方医科大学学报》
Abstract： Objective To observe epithelial-mesenchymal phenotypes and oxidative stress related protein expressions of the liver cells in a rat model of liver fibrosis induced by bile duct ligation and recanalization. Methods Twenty-four male Wistar rats were randomized into 4 groups, including a sham-operated group, two bile duct ligation groups with ligation for 2 and 4 weeks, and a bile duct ligation group with a 2-week ligation followed by a 2-week recanalization. HE staining and Masson staining were used to assess liver fibrosis in the rats, and immunohistochemistry and Western blotting were employed to detect expressions of the epithelial and mesenchymal marker proteins and oxidative stress-related proteins. Results Compared with the sham-operated group, the rats with bile duct ligation showed obvious liver fibrosis, which worsened as the ligation time extended, accompanied by significantly increased expression of α-SMA, collagen I, NOX4 and vimetin and reduced E-cadherin expression. Compared with the rats with bile duct ligation for 4 weeks, the rats in bile duct ligation-recanalization group showed obviously lessened liver fibrosis, significantly lowered expressions of NOX4 and mesenchymal cell maker proteins, and enhanced expressions of epithelial cell marker proteins. Conclusion Bile duct ligation up-regulates mesenchymal phenotype-related proteins and NOX4 protein expression and down-regulates the expression of epithelial phenotype-related proteins, and these changes can be reversed by subsequent bile duct recanalization.
Subjects: Medicine, Pharmacy >> Preclinical Medicine submitted time 2017-12-07 Cooperative journals: 《南方医科大学学报》
Abstract： Objective To investigate the value of the junction fragments between the breakpoints of introns in identifying deletional Duchenne muscular dystrophy (DMD) carriers. Methods A DMD family (including the index patient III2 and the suspected carrier II3) and a sporadic DMD case (including the patient II1 and his mother I2) were studied. The patient III2 of the DMD family was identified as having exons 31-43 deletion of the DMD gene, and the sporadic patient II1 had exons 45-54 deletion. A PCR-based genome-walking method was used to locate the breakpoints in the corresponding introns. The junction fragments of the patients and their female relatives waiting for a diagnosis were amplified by PCR with primers adjacent to the deletion junctions. Results PCR amplification yielded identical positive results for the female suspected carrier II3 of and the index patient of the DMD family, and the former was thus diagnosed as a carrier of DMD. PCR amplification of the sporadic patient’s mother I2 showed a negative result, but the patient II1 had a positive result, so that the patient's mother was excluded as being a carrier of DMD. Conclusion Routine PCR technique for detecting the junction fragments allows identification of carriers among female relatives of patients with deletional DMD.
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