Presence of pink-color sign within 1 min after iodine staining has high diagnostic accordance rate for esophageal high-grade intraepithelial neoplasia/invasive cancer.

BACKGROUND/AIM: The dramatic color change after iodine staining (from white-yellow to pink after 2-3 min), designated as the "pink-color sign" (PCS), is indicative of esophageal high-grade intraepithelial neoplasia (HGIN) or an invasive lesion. However, no study has yet examined the association between the time of PCS appearance and histopathology. We investigated the association between the time of PCS appearance and esophageal histopathology in 456 lesions of 438 patients who were examined for suspected esophageal cancer. MATERIALS AND METHODS:: The records of 495 consecutive patients who had suspected esophageal cancer based on gastroscopy and who underwent Lugol's chromoendoscopy from January 2015 to March 2018 were retrospectively reviewed. The time of PCS appearance was recorded in all patients, and tissue specimens were examined. RESULTS: We examined 456 lesions in 438 patients. Use of PCS positivity at 2 min for the diagnosis of HGIN/invasive cancer had a sensitivity of 84.1%, a specificity of 72.7%, and an accuracy of 80.4%. We classified the PCS-positive patients in whom the time of PCS appearance was recorded (168 lesions) into 4 groups: 0-30, 31-60, 61-90, and 91-120 s. Based on a 60-s time for appearance of the PCS, the area under the receiver operating characteristic curve was 0.897, indicating good validity. At the optimal cutoff value of 60 s, the sensitivity was 90.2% and the specificity was 82.3%. The appearance of the PCS within 60 s had a diagnostic accordance rate of 88.6%, significantly higher than appearance of the PCS within 2 min (79.7%, P < 0.05). CONCLUSION: Appearance of the PCS within 1 min after iodine staining has a higher diagnostic accordance rate for esophageal HGIN/invasive cancer than appearance of the PCS at 2 min.

[The protective effects of bifidobacterial adhesin on ischemic reperfusion injury of intestine in rats].

OBJECTIVE: To investigate the protection effect of bifidobacterial adhesin for intestine ischemia/reperfusion (I/R) injury on gut barrier function in rat. METHODS: Seventy-two male SD rats were randomly divided into sham operation group (n = 24), I/R model group (n = 24) and pretreatment group of bifidobacterial adhesin (pretreatment group, n = 24). Six rats were anatomized at 6 h, 1 d, 4 d and 7d after inducing I/R model in each group, respectively. The pathological changes of the terminal ilea and the blood levels of TNFα, IL-6, IL-10, diamine oxidase (DAO), and the activity and content of D-lactic acid were observed. RESULTS: The blood levels of TNFα, IL-6, DAO and D-lactic acid in I/R model group were significantly higher than sham operation group at all time points (P < 0.05), while the blood level of IL-10 was no significantly change. The activity of IL-6 and DAO in pretreatment group was significantly lower than I/R model group at all time points (P < 0.05), the blood level of TNFα in pretreatment group was significantly lower than I/R model group at 1 d, the blood level of D-lactic was significantly lower than I/R model group at 4 d and 7 d (P < 0.05). Intestinal pathological damages were obviously milder in pretreatment group than I/R model group at all time points (Chiu's pathological scores: 6 h, 3.22 ± 0.22 vs 3.57 ± 0.20; 1 d, 3.77 ± 0.13 vs 3.90 ± 0.12; 4 d, 2.93 ± 0.23 vs 3.07 ± 0.21; 7 d, 2.10 ± 0.30 vs 2.22 ± 0.17, all P < 0.05). CONCLUSION: The pretreatment of bifidobacterial adhesin could protect the intestinal mucosa from I/R injury, and alleviate intestinal ischemic reperfusion injury.

[Effects of catalase on the mitochondria and apoptosis of SW480 cells].

OBJECTIVE: To investigate the effects of catalase on the mitochondria and apoptotic behavior of SW480 cells treated by lipopolysaccharide (LPS), and the changes in intracellular expression of nuclear factor kappaB (NF-kappaB). METHODS: LPS-stimulated SW480 cells were treated with catalase and the changes in their mitochondria and apoptotic behavior were observed by transmission electron microscopy. The expression of NF-kappaB was detected by immunohistochemical method. RESULTS: Mitochondria damages and apoptosis were slightly diminished in the LPS-stimulated cells with catalase pretreatment, and the NF-kappaB expression was also decreased. CONCLUSION: Catalase protect the mitochondria of SW480 cells from damages by LPS and inhibit the cell apoptosis, possibly due to the activation of NF-kappaB.

Competitive inhibition of adherence of enterotoxigenic Escherichia coli, enteropathogenic Escherichia coli and Clostridium difficile to intestinal epithelial cell line Lovo by purified adhesin of Bifidobacterium adolescentis 1027.

AIM: To observe competitive inhibition of adherence of enterotoxigenic Escherichia coli (ETEC), enteropathogenic Escherichia coli (EPEC) and Clostridium difficile (C. difficile) to intestinal epithelial cell line Lovo by purified adhesin of Bifidobacterium adolescentis 1027 (B. ado 1027). METHODS: The binding of bacteria to intestinal epithelial cell line Lovo was counted by adhesion assay. The inhibition of adherence of ETEC, EPEC and C. difficile to intestinal epithelial cell line Lovo by purified adhesin of B. ado 1027 was evaluated quantitatively by flow cytometry. RESULTS: The purified adhesin at the concentration of 10 microg/mL, 20 microg/mL and 30 microg/mL except at 1 microg/mL and 5 microg/mL could inhibit significantly the adhesion of ETEC, EPEC and C. difficile to intestinal epithelial cell line Lovo. Moreover, we observed that a reduction in bacterial adhesion was occurred with increase in the concentration of adhesin, and MFI (Mean fluorescent intensity) was decreased with increase in the concentration of adhesin. CONCLUSION: The purified adhesin of B. ado 1027 can inhibit the adhesion of ETEC, EPEC and C. difficile to intestinal epithelial cell line Lovo in a dose-dependent manner.

[Effect of Bifidobacterial adhesin on lipopolysaccharide- and H2O2-induced proliferation and apoptosis of intestinal epithelial cells in vitro].

OBJECTIVE: To study the effect of Bifidobacterial adhesin on proliferation and apoptosis of intestinal epithelial cell induced by lypopolysaccharide (LPS) and H(2)O(2) in vitro. METHODS: With (3)H-TdR incorporation method, flow cytometry and fluorochrome staining, the proliferation and apoptosis of intestinal epithelial cells induced by LPS and H(2)O(2) in vitro were studied. RESULTS: LPS at the dose of 100 microg/L effectively stimulated the proliferation and apoptosis of cells, whereas H(2)O(2) at the dose of 200 micromol/L obviously restrained the proliferative ability while enhanced the apoptosis of the cells. Fluorochrome staining showed cell shrinkage, nuclear condensation and fragmentation under microscope. After treatment with Bifidobacterial adhesin, the cell proliferation and apoptosis decreased significantly in LPS group, and in H(2)O(2) group, cell apoptosis was significantly decreased. CONCLUSIONS: Bifidobacterial adhesin can protect intestinal epithelial cells from the damage by LPS and H(2)O(2), and maintain the balance between the proliferation and apoptosis of the cells.

Effect of eIF-4E inhibition on heparanase mRNA and its expression in colon adenocarcinoma cell.

OBJECTIVE: To verify whether inhibition of the overexpressed eukaryotic initiation factor-4E (eIF-4E) in human colon adenocarcinoma cell line LS-174T may facilitate the degradation of heparanase mRNA and alter the translation and expression levels of heparanase protein. METHODS: A 20-mer antisense s-oligodeoxynucleotide (asODN) targeted against the translation start site of eIF-4E mRNA was introduced into LS-174T cells by means of lipid-mediated DNA-transfection, followed by Western blotting analysis and reverse transcription-PCR to determine eIF-4E protein and mRNA levels, respectively. Northern methods was applied to determine heparanase mRNA expression level, with the alterations of heparanase expression assessed by Western blotting analysis. RESULTS: The 20-mer asODN against eIF-4E specifically and significantly inhibited eIF-4E protein expression, and as a result, a significant reduction in heparanase mRNA level was observed by Northern blotting in conjunction with significantly decreased heparanase protein expression. CONCLUSION: The inhibition of eIF-4E strongly reduces the stability of heparanase mRNA in colon adenocarcinoma cell line LS-174T and results in an apparent reduction in the expression of heparanase protein.

[Study of angiogenesis in human colorectal carcinoma and its modulation by p53 and K-ras gene].

OBJECTIVE: To investigate the angiogenesis in human colorectal carcinoma and its modulation by p53 and K-ras gene. METHODS: The positive rate of p53 and K-ras gene mutation, the expression of vascular endothelial growth factor (VEGF) and microvessel density in 68 cancer tissue, peritumoral tissue samples and 20 normal controls were studied by PCR-SSCP and immunohistochemical methods. RESULTS: The positive rate of p53 and K-ras gene mutation and the expression of VEGF in cancer tissue (47.1%, 32/68; 44.1%, 30/68; 55.9%, 38/68) were significantly higher than in peritumoral tissue (13.2%, 9/68; 7.4%, 5/68; 11.8%, 8/68). p53, K-ras gene mutation and the expression of VEGF were not detected in 20 normal tissue. The expression of VEGF was closely related with the angiogenesis and metastasis of colorectal carcinoma (r = 0.820, P < 0.01). VEGF expression correlated with both p53 and K-ras gene mutation (P < 0.01). CONCLUSIONS: p53 and K-ras gene upregulated the expression of VEGF. p53 and K-ras gene might play an important role in modulating tumor angiogenesis.

[Uptake and distribution of adriamycin in multidrug-resistant LoVo/Adr cells].

OBJECTIVE: To investigate adriamycin (Adr) uptake and distribution features in multidrug-resistant LoVo/Adr cells and explore the drug-resistance mechanism of the cells. METHODS: Adr uptake in LoVo/Adr cells was observed by flow cytometry and the distribution of the drug examined by fluorescence microscope. Immunohistochemical method was employed to detect the expression of P-glycoprotein (P-gp) by the cells. RESULTS: In comparison with that in LoVo/Adr cells, Adr level in LoVo cells was significantly higher, but after treatment with verapamil, the former cells showed an increased Adr level. Adr distributed mainly in the nucleus in the drug-sensitive LoVo cells, with only a small quantity in the cytoplasm, while in multidrug-resistant LoVo/Adr cells, significantly reduction of Adr quantity in the nucleus and relative increase in the cytoplasm were observed. In response to verapamil treatment, the Adr uptake in LoVo/Adr cells increased and the distribution of the drug was similar to that in sensitive cells. P-gp expression was positive in LoVo/Adr cells, while negative in LoVo cells. CONCLUSION: Abnormal Adr uptake and distribution in drug-resistant cells is related to P-gp expression which is one of the mechanisms for multidrug resistance.