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Situ Expression (situ + expression)
Selected AbstractsIdentification of novel markers expressed during fin regeneration by microarray analysis in medaka fishDEVELOPMENTAL DYNAMICS, Issue 9 2007Masanobu Nishidate Abstract Urodeles and fish have a remarkable ability to regenerate lost body parts, whereas many higher vertebrates, including mammals, retain only a limited capacity. It is known that the formation of specialized cell populations such as the wound epidermis or blastema is crucial for regeneration; however, the molecular basis for their formation has not been elucidated. Recently, approaches using differential display and microarray have been done in zebrafish for searching molecules involved in regeneration. Here, we used the medaka fish, a distantly diverged fish species, for microarray screening of transcripts up-regulated during regeneration. By setting criteria for selecting transcripts that are reliably and reproducibly up-regulated during regeneration, we identified 140 transcripts. Of them, localized in situ expression of 12 transcripts of 22 tested was detected either in differentiating cartilage, basal wound epidermis, or blastema. Our results provide useful molecular markers for dissecting the regeneration process at a fine cellular resolution. Developmental Dynamics 236:2685,2693, 2007. © 2007 Wiley-Liss, Inc. [source] Changes in retinoblastoma gene expression during cervical cancer progressionINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 6 2002Mauricio Salcedo Summary. The role of tumour suppressor genes in the development of human cancers has been studied extensively. In viral carcinogenesis, the inactivation of suppressor proteins such as retinoblastoma (pRb) and p53, and cellular oncogenes overexpression, such as c-myc, has been the subject of a number of investigations. In uterine-cervix carcinomas, where high-risk human papillomavirus (HPV) plays an important role, pRb and p53 are inactivated by E7 and E6 viral oncoproteins, respectively. However, little is known about the in situ expression of some of these proteins in pre-malignant and malignant cervical tissues. On the other hand, it has also been demonstrated that c-myc is involved in cervical carcinogenesis, and that pRb participates in the control of c-myc gene expression. By using immunostaining techniques, we investigated pRb immunodetection pattern in normal tissues, squamous intraepithelial lesions (SILs) and invasive carcinomas from the uterine cervix. Our data show low pRb detection in both normal cervical tissue and invasive lesions, but a higher expression in SILs. C-Myc protein was observed in most of the cellular nuclei of the invasive lesions, while in SILs was low. These findings indicate a heterogeneous pRb immunostaining during the different stages of cervical carcinogenesis, and suggest that this staining pattern could be a common feature implicated in the pathogenesis of uterine-cervix carcinoma. [source] Expression of IFN-, before and after treatment of oral lichen planus with 0.1% fluocinolone acetonide in orabaseJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 9 2009Pornpan Youngnak-Piboonratanakit Background:, Oral lichen planus (OLP) is a common chronic inflammatory mucosal disease in which T-cell-mediated immune responses are implicated in the pathogenesis. The purpose of this study was to investigate the effect of 0.1% fluocinolone acetonide in orabase (FAO) on the in situ expression of IFN-, in patients with OLP. Methods:, Twenty OLP patients were enrolled in this study. Biopsy specimens and serum samples were obtained before and 1-month after the treatment with 0.1% FAO. In situ expression and serum levels of IFN-, were determined using immunohistochemistry and ELISA, respectively. Results:, The number of IFN-,-positive mononuclear cells in OLP lesions before the treatment was significantly higher as compared with that after the treatment. Similarly, the mean number of total mononuclear cells was clearly decreased after the treatment. However, the serum levels of IFN-, were not detectable. Conclusions:, Our results suggest that IFN-, expression in OLP tissue may involve in the immunopathogenesis and the treatment with 0.1% FAO had an immunomodulating effect on the decrease of IFN-,. [source] Prognostic analysis in chronic hepatitis B patients: a retrospective study of 216 cases about Scheuer scores, in situ expression of viral antigens and tissue hepatitis B virus DNA levelsLIVER INTERNATIONAL, Issue 1 2006Rong Zhu Abstract: Background: Most of the previous studies of patients with chronic hepatitis B virus (HBV) infection concentrated on serum samples. Liver biopsy specimens for HBV have not been systematically analyzed. This study was performed to analyze some histopathological indicators (Scheuer scores, the expression of HBV antigens in situ, HBV DNA quantification) in the biopsy samples and showed the relationship among them and the prognosis of chronic hepatitis. Methods: A total of 216 consecutive chronic HBV-infected patients were followed up by clinical and laboratory data and classified into two groups at first: carcinogenesis and non-carcinogenesis. The non-carcinogenesis also included two groups: cirrhosis and non-cirrhosis. The non-cirrhosis was still divided into fluctuation and normalization at last. Histological activity index was described by Scheuer scores. Two-step immunohistochemical staining showed the expression of viral antigens in situ. Tissue HBV DNA levels were determined by fluorescence quantitative real-time PCR. Results: Regression analysis revealed significant positive correlations between the expression of hepatitis B e antigen (HBeAg) and grading, as well as between hepatitis Bx (HBx) protein and grading or staging of Scheuer scores. Positive correlations between grading or staging and prognosis were statistically significant. The expressions of HBeAg and HBx protein were higher in patients with cirrhosis than those without cirrhosis. Scheuer score was the most important indicator of prognosis. Conclusions: HBeAg and HBx protein can be used as indicators of hepatitis activity and their positive expressions increase the risk for cirrhosis remarkably. In addition to be a marker of liver damage, Scheuer score is the most reliable indicator of the prognosis. [source] atz gene expressions during atrazine degradation in the soil drilosphereMOLECULAR ECOLOGY, Issue 4 2010C. MONARD Abstract One of the various ecosystemic services sustained by soil is pollutant degradation mediated by adapted soil bacteria. The pathways of atrazine biodegradation have been elucidated but in situ expression of the genes involved in atrazine degradation has yet to be demonstrated in soil. Expression of the atzA and atzD genes involved in atrazine dechlorination and s -triazine ring cleavage, respectively, was investigated during in situ degradation of atrazine in the soil drilosphere and bulked samples from two agricultural soils that differed in their ability to mineralize atrazine. Interestingly, expression of the atzA gene, although present in both soils, was not detected. Atrazine mineralization was greatest in Epoisses soil, where a larger pool of atzD mRNA was consistently measured 7 days after atrazine treatment, compared with Vezin soil (146 vs. 49 mRNA per 10616S rRNA, respectively). Expression of the atzD gene varied along the degradation time course and was profoundly modified in soil bioturbated by earthworms. The atzD mRNA pool was the highest in the soil drilosphere (casts and burrow-linings) and it was significantly different in burrow-linings compared with bulk soil (e.g. 363 vs. 146 mRNA per 10616S rRNA, 7 days after atrazine treatment in Epoisses soil). Thus, consistent differences in atrazine mineralization were demonstrated between the soil drilosphere and bulk soil. However, the impact of bioturbation on atrazine mineralization depended on soil type. Mineralization was enhanced in casts, compared with bulk soil, from Epoisses soil but in burrow-linings from Vezin soil. This study is the first to report the effects of soil bioturbation by earthworms on s -triazine ring cleavage and its spatial variability in soil. [source] Vascular endothelial growth factor, FLT-1, and FLK-1 analysis in a pancreatic cancer tissue microarray,CANCER, Issue 8 2006Gina G. Chung M.D. Abstract BACKGROUND Measures of vascular endothelial growth factor (VEGF) expression in pancreatic cancer typically have been qualitative or semiquantitative. The objective of this study was to use a series of algorithms called AQUA that quantitatively assesses protein expression on tissue microarrays (TMAs) to compare in situ expression of VEGF and its primary receptors, VEGF receptor 1 (FLT-1) and VEGF receptor 1 (FLK-1), on a pancreatic cancer TMA. METHODS TMAs were constructed by arraying 1.5-mm cores from 76 samples of pancreatic adenocarcinoma (1996-2002) that were obtained from the archives of the Yale Department of Pathology. The staining for AQUA was similar to standard immunohistochemistry and involved antigen retrieval and the application of primary antibodies, but with epifluorescence detection. Slides were counterstained with 4,,6-diamidino-2-phenylindole for nuclear visualization and cytokeratin for membrane visualization. The primary antibodies used were VEGF, FLT-1, FLK-1, and cytokeratin. RESULTS Disease stage was highly prognostic for outcome, as expected. Total amounts of VEGF and its receptors were assessed within the tumor mask and were divided into quartiles. Kaplan,Meier survival curves showed that VEGF and FLK-1 were not associated clearly with outcome. However, the expression of FLT-1 was correlated significantly, and the patients who had tumors with the lowest expression FLT-1 levels had the worst survival (P = .0038). In multivariate analysis, FLT-1 expression was an independent prognostic factor for overall survival (P = .0044). CONCLUSIONS VEGF and its 2 principal receptors were expressed to varying degrees in tumors of the pancreas. A significant association was found between low expression of FLT-1 and both poor prognosis and advanced stage, suggesting that tumor expression of this VEGF receptor is a marker of less aggressive disease. Cancer 2006. © 2006 American Cancer Society. 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