Mechanism of benign biliary stricture: a morphological and immunohistochemical study.

AIM: To explore the mechanism of benign biliary stricture. METHODS: A model of trauma of bile duct was established in 28 dogs. The anastomosed tissues were resected and examined by light and electron microscopes on day 3, in wk 1, 3 and mo 3, 6 after operation. CD68, TGF-beta1 and alpha-SMA were examined by immunohistochemical staining, respectively. RESULTS: The mucosal epithelium of the bile duct was slowly recovered, chronic inflammation lasted for a long time, fibroblasts proliferated actively, extracellular matrix was over-deposited. Myofibroblasts functioned actively and lasted through the whole process. The expression of macrophages in lamina propria under mucosa, TGF-beta1 in granulation tissue, fibroblasts and endothelial cells of blood vessels, alpha-SMA in myofibroblasts were rather strong from the 1st wk to the 6th mo after operation. CONCLUSION: The type of healing occurring in bile duct belongs to overhealing. Myofibroblasts are the main cause for scar contracture and stricture of bile duct. High expressions of CD68, TGF-beta1 and alpha-SMA are closely related to the active proliferation of fibroblasts, extracellular matrix over-deposition and scar contracture of bile duct.

Relationship between inducible nitric oxide synthase expression and angiogenesis in primary gallbladder carcinoma tissue.

AIM: To explore the relationship between angiogenesis and biological behaviors of primary gallbladder carcinoma (PGBC), the relationship between the expression of inducible nitric oxide synthase (iNOS) and biological behaviors of PGBC and its relationship with the expression of iNOS and angiogenesis of PGBC. METHODS: The expression of iNOS and micro-vessel density (MVD) were assessed by immunohistochemical method and image analysis system in 40 specimens of PGBC and in 8 specimens of normal gallbladder. The immunostaining results and related clinicopathologic materials were analyzed by statistical methods. RESULTS: MVD in PGBC was significantly higher than that in normal gallbladder tissue (46+/-14 vs 14+/-6, P<0.05), and was not related with age, gender, tumor size and histological type. MVD of poorly and undifferentiated tumor tissues was higher than that of moderately-differentiated and well-differentiated tumor tissues (52+/-9 vs 43+/-9 vs 33+/-6, P<0.01). MVD of Nevin IV and V stages was higher than that of Nevin I, II and III stages (52+/-8 vs 37+/-13, P<0.01). MVD of cases with lymphatic or liver metastasis was significantly higher than that without liver metastasis (55+/-6 vs 42+/-10, P<0.05)or lymphatic metastasis (53+/-8 vs 38+/-8, P<0.01). The positive level index (PLI) of iNOS in PGBC was 0.435+/-0.134, and was not related with age, gender, tumor size, histological type, differentiation and clinical stage of PGBC. The PLI of iNOS in cases with lymphatic metastasis was higher than that without lymphatic metastasis (0.573+/-0.078 vs 0.367+/-0.064, P<0.01). The PLI of iNOS in cases with liver metastasis was higher than that without liver metastasis (0.533+/-0.067 vs 0.424+/-0.084, P<0.05). There was a significant correlation between PLI of iNOS and MVD in PGBC (P<0.05). CONCLUSION: Angiogenesis of PGBC is significantly related to the biological behaviors of PGBC. The expression of iNOS is related to the biological behaviors of PGBC. The detection of MVD and the expression of iNOS in PGBC can be used as parameters to determine the degree of malignancy and prognosis.

[GC-box is not a key cis-acting element in human insulin gene promoter].

OBJECTIVE: To identify whether GC-box (-348 to -338) in human insulin gene promoter is a key cis-acting element. METHODS: Human insulin gene promoter was sub-cloned into secreted alkaline phosphatase (SEAP) reporter plasmid. The deletion and mutation of GC-box in insulin gene promoter was performed. The activity of human insulin gene promoter was determined by evaluating the activity of SEAP in the supernatant of cell culture after the reporter plasmids were transfected in beta cell line betaTC3. RESULT: Deletion and mutation of GC box in human insulin gene promoter did not result in significant changes of the activity of the promoter in betaTC3. CONCLUSION: The GC-box is not a key cis-acting element in human insulin gene promoter.