Oesophagus

Puji syukur kami panjatkan kehadirat Tuhan Yang Maha Esa karena dengan rahmat, karunia, serta taufik dan hidayah-Nya kami dapat menyelesaikan makalah ini. Dan juga kami berteri makasih kepada Bapak Rasyid S.Si, MT selaku dosen mata kuliah Teknik Radiografi 3 yang telah memberikan tugas ini kepada kami.

SUMMARY Non-dysplastic Barrett's oesophagus (NDBE) occurs as a consequence of an inflam-matory response triggered through prolonged gastro-oesophageal reflux and it may precede the development of oesophageal adenocarcinoma. NF-kB activation as a result of inflammatory response has been shown in NDBE, but the possible mechanism involved in the process is unknown. The aim of this study was to assess, using immunohistochemistry, Survivin and Bcl3 expression as potential biomarkers for NF-kB activation along the oesophageal metaplasia–dysplasia–adenocarcinoma sequence. Survivin is an NF-kB-inducible anti-apoptotic protein, and Bcl3 is a negative regulator of NF-kB. There was progressive upregulation of Survivin expression along the oesophageal metaplasia–dysplasia–adenocarcinoma sequence. Bcl3 expression was upregulated in non-dysplastic Barrett's oesophagus, low-grade, high-grade dysplasia and oesophageal adenocarcinoma when compared to squamous group. The study shows the differential expression of Bcl3 between the squamous and Barrett's stage, suggesting that Bcl3 could be a surrogate marker for early event involving constitutive NF-kB activation. In addition, the study suggests that NF-jB activation may infer resistance to apoptosis through the expression of anti-apoptotic genes such as Survivin, which showed progressive increase in expression throughout the oeso-phageal metaplasia–dysplasia–adenocarcinoma sequence. This ability to avoid apop-tosis may underlie the persistence and malignant predisposition of Barrett's metaplasia.

Background Information. Carcinoma of the oesophagus is the sixth leading cause of cancer death in the western world and is associated with a 5-year survival of less than 15%. Recent evidence suggests that stromal–epithelial interactions are fundamental in carcinogenesis. The advent of co-culture techniques permits the investigation of cross-talk between the stroma and epithelium in a physiological setting. We have characterized a histologically representative oesophageal organotypic model and have used it to compare the most commonly used squamous oesophageal cell line, HET-1A, with primary oesophageal squamous cells for use in studies of the oesophageal epithelium in vitro. Results. When grown in an organotypic culture with normal fibroblasts, the oesophageal carcinoma cell lines OE21 (squamous) and OE19 (adenocarcinoma) morphologically resembled the tumour of origin with evidence of stromal invasion and mucus production, respectively. However, HET-1A cells, which were derived from normal squamous oesophageal cells, appeared dysplastic and failed to display evidence of squamous differentiation. By comparison with primary oesophageal epithelial cells, the HET-1A cells were highly proliferative and did not express the epithelial markers E-cadherin or CK5/6 (casein kinase 5/6), or the stratified epithelial marker Np63, but did express the mesenchymal markers vimentin and N-cadherin. Conclusion. Studies of epithelial carcinogenesis will benefit from culture systems which allow manipulation of the stromal and epithelial layers independently. We have developed an organotypic culture using primary oesophageal squamous cells and fibroblasts in which a stratified epithelium with a proliferative basal layer that stains strongly for Np63 develops. This model will be suitable for the study of the molecular events in the development of Barrett's oesophagus. The most commonly used normal oesophageal squamous cell line, HET-1A, does not have the characteristics of normal oesophageal squamous cells and should not be used in models of the normal oesophageal epithelium. Until more representative cell lines are available, future studies in oesophageal cancer will be reliant on the availability and manipulation of primary tissue. 1 These authors contributed equally to this work. 2 To whom correspondence should be addressed (email tju@soton.ac.uk).

Aim: The aim of the study was to set up a porcine ex vivo model of acid-induced damage and to evaluate its performance by means of multichannel intraluminal impedance and pH (MII-pH) live recording, histology, and Evans blue (EB) permeability assay. Materials and Methods: Thirteen esophagi, collected at a slaughterhouse, were ablated of their sphincters, pinned upright on a support, and placed in a thermostatic hood at 37°C with two infusion tubes and an MII-pH probe inserted in the top end. Three esophagi (histology controls) were only left in the hood for 3.5 h before sampling, while the remaining organs underwent the experimental protocol including saline infusion and recovery recording, and acid solution infusion and recovery recording. Results: MII-pH analysis highlighted a significantly stronger decrease during acid infusion when compared to saline, but a better post-infusion recovery for saline solution. At the end of the protocol, MII was still statistically lower than basel...