Generally accepted standards for the therapy of advanced gastric carcinomas do not exist. In cases where the therapeutic strategy is surgical exploration, no preoperative staging is necessary. In cases with differentiated treatment strategies, the accuracy of EUS is not sufficient for the selection of patients for endoscopic resection. Its accuracy for submucosal cancer invasion and for the detection of lymph node metastases needs to be further enhanced. If only multimodal therapy is considered, EUS staging seems to be absolutely mandatory. Patients classified preoperatively as T1 to T3 can be operated on primarily with sufficient security. In patients where radical resection of the tumor seems doubtful, we recommend that a diagnostic laparoscopy be performed to confirm the diagnosis.

Purpose Transcriptomic profiling has enabled the neater genomic characterization of several cancers, among them colorectal cancer (CRC), through the derivation of genes with enhanced causal role and informative gene sets. However, the identification of small-sized gene signatures, which can serve as potential biomarkers in CRC, remains challenging, mainly due to the great genetic heterogeneity of the disease. Methods We developed and exploited an analytical framework for the integrative analysis of CRC datasets, encompassing transcriptomic data and positron emission tomography (PET) measurements. Profiling data comprised two microarray datasets, pertaining biopsy specimen from 30 untreated patients with primary CRC, coupled by their F-18-Fluorodeoxyglucose (FDG) PET values, using tracer kinetic analysis measurements. The computational framework incorporates algorithms for semantic processing, multivariate analysis, data mining and dimensionality reduction. Results Transcriptomic and PET data feature sets, were evaluated for their discrimination performance between primary colorectal adenocarcinomas and adjacent normal mucosa. A composite signature was derived, pertaining 12 features: 7 genes and 5 PET variables. This compact signature manifests superior performance in classification accuracy, through the integration of gene expression and PET data. Conclusions This work represents an effort for the integrative, multilayered, signature-oriented analysis of CRC, in the context of radio-genomics, inferring a composite signature with promising results for patient stratification.

The rat is an established model for studying intestinal adaptations following abdominal surgery. In the study of functional and morphological adaptations of the small intestine, it is helpful to estimate the mucosal surface area. In order to simplify measurements and calculation we developed a new mathematical model for calculation of the mucosal surface area on histological sections. In contrast to other methods, it requires only cross-sections of small intestine and includes the measurement of only three histological parameters: length and width of villus and width of crypt. The new approach was compared with the most commonly used procedures, the Harris and the Fisher-Parsons methods, under experimental conditions. An animal study including single-pass perfusion, fixation, staining and subsequent histomorphometry of jejunum and ileum using these different methods was performed. The new method showed the least work and presented no significant differences compared with the precise Harris method. In conclusion, the method described is an adequate tool to estimate the mucosal surface area with less work and with comparable results to established methods. The less-complex method may be a valuable tool in experimental research of small intestine adaptations in rats.

Both methods provide a good operative outcome with low complication rates. We do recommend the loop ileostomy in all patients in which dehydration is not to be expected since wound infection rate is lower and hospital stay is shorter during stoma reversal.

18 F-FDG kinetics are primarily dependent on the expression of genes associated with glucose transporters and hexokinases but may be modulated by other genes. The dependency of 18 F-FDG kinetics on angiogenesis-related gene expression was evaluated in this study. Methods: Patients with primary colorectal tumors (n 5 25) were examined with PET and 18 F-FDG within 2 days before surgery. Tissue specimens were obtained from the tumor and the normal colon during surgery, and gene expression was assessed using gene arrays. Results: Overall, 23 angiogenesis-related genes were identified with a tumor-to-normal ratio exceeding 1.50. Analysis revealed a significant correlation between k1 and vascular endothelial growth factor (VEGF-A, r 5 0.51) and between fractal dimension and angiopoietin-2 (r 5 0.48). k3 was negatively correlated with VEGF-B (r 5 20.46), and a positive correlation was noted for angiopoietin-like 4 gene (r 5 0.42). A multiple linear regression analysis was used for the PET parameters to predict the gene expression, and a correlation coefficient of r 5 0.75 was obtained for VEGF-A and of r 5 0.76 for the angiopoietin-2 expression. Thus, on the basis of these multiple correlation coefficients, angiogenesis-related gene expression contributes to about 50% of the variance of the 18 F-FDG kinetic data. The global 18 F-FDG uptake, as measured by the standardized uptake value and influx, was not significantly correlated with angiogenesisassociated genes. Conclusion: 18 F-FDG kinetics are modulated by angiogenesis-related genes. The transport rate for 18 F-FDG (k1) is higher in tumors with a higher expression of VEGF-A and angiopoietin-2. The regression functions for the PET parameters provide the possibility to predict the gene expression of VEGF-A and angiopoietin-2.

The tendency towards sphincter-preserving resection for distal rectal cancers has led to the technique of straight coloanal anastomosis (CAA) and colonic J-pouch anal anastomosis (CPA) after low anterior resection. The aim of the present study was to compare complication rate, anorectal physiology and functional results after both types of reconstruction after ultra-low intersphincteric resection. A total of 31 patients who had undergone CPA were followed up prospectively using anorectal manometry and a standardised questionnaire and were compared with 63 patients who had undergone CAA and were followed up in the same way. The complication rate after CPA did not differ significantly from that after CAA. One year postoperatively, the median stool frequency and urgency were reduced after CPA (1.7+/-2.2/day; 7% vs. 2.4+/-3.6/day; 14%; P<0.05). Three months after colostomy/ileostomy closure, the maximum tolerable volume, threshold volume and compliance were decreased after CAA when compared with CPA (55+/-12, 34+/-12, and 3.9+/-0.3 ml/mmHg vs. 85+/-21, 53+/-11 and 6.2 ml/mmHg, respectively; P<0.05). Anal manometry revealed no significant differences in the anal resting and squeeze pressure. One year postoperatively, continence also did not differ significantly between CPA and CAA. Colonic J-pouch reconstruction seems to be superior to the straight coloanal anastomosis, especially during the first postoperative year. In view of the often poor prognosis of the patients, it is the reconstruction of choice after ultra-low resections of the rectum.

SUMMARY Seven patients with epidermolysis bullosa dystrophica and chronic and recurrent oesophageal lesions such as spasm, strictures, and complete occlusion were studied. Dysphagia could be cured with drugs if it was caused by bullae formation or spasm. If oesophageal strictures were present, endoscopy and bouginage with corticosteroid prophylaxis during the quiescent phase of the disease was a safe and useful procedure. We have also given corticosteroids, which reduced the oedema caused by bullae formation and oral phenytoin, which reduced epithelial detachment by inhibiting collagenase activity. Verapamil counteracted oesophageal spasm and pureed food during periods of dysphagia reduced blistering of the upper oesophagus.Epidermolysis bullosa dystrophica is a group of hereditary mechanobullous disorders affecting both the skin and gastrointestinal mucosa (table). In the recessive type, trauma is followed by a separation of skin at the dermoepidermal junction and at the lamina propria of the mucous membrane, probably because of an increase in mutant collagenase activity.1 The recessive type can be further subdivided into two forms, localised and generalised, on the electron microscopic appearance of the dermoepidermal junction in non-blistered skin. In the localised form there are recognisable anchoring fibrils below the basement membrane, but they are attenuated in appearance and sparse. In the generalised form (which is clinically more severe) the anchoring fibrils are absent.2In the recessive type the bullous lesions of the skin are usually present at birth and they quickly spread to affect the skin and mouth. Healing is slow, with chronic scarring that leads to digital fusion (syndactyly) and flexion contractures of the fingers and toes. The mucosa of the mouth, pharynx, and oesophagus is often affected. Oesophageal problems develop insidiously and are caused by bullae formation, ulceration, and oedema, which ultimately lead to stricture formation that may in turn cause complete oesophageal obstruction with regurgitation of blood stained secretions. In the dominant form of epidermolysis bullosa dystrophica the skin disease is milder, but patients may develop tight webs in the upper oesophagus. These develop several years later than in the recessive type.

There is a fundamental disorder of collagen metabolism in patients with haemorrhoidal disease. It remains unclear whether this is due to exogenous or endogenous influences.