Patients with a failed ileoanal pouch may be offered redo pouch surgery with a high likelihood of success in terms of function and QOL.

Preoperative exposure to biologics is associated with an increased risk of pelvic sepsis after total proctocolectomy with IPAA. This risk is mitigated by the performance of an initial subtotal colectomy.

Concentrations of organic carbon (OC) and elemental carbon (EC) in atmospheric particles were measured in Tianjin during January, April, July and October in 2008. The 24-h PM 2.5 (particles with aerodynamic diameters less than 2.5 micrometer [μm]) and PM 10 (particles with aerodynamic diameters less than 10 micrometer [μm]) samples were simultaneously collected every day during sampling periods. These samples were analyzed for OC/EC by thermal/optical reflectance (TOR) following the Interagency Monitoring of Protected Visual Environments (IMPROVE) protocol. The annual average concentration was 109.8 ± 48.5 μg/m 3 in PM 2.5 , and 196.2 ± 86.1 μg/m 3 in PM 10 , respectively. The average ratio of PM 2.5 /PM 10 was 57.9%, indicating the PM 2.5 had been one of the main contaminations affecting urban atmospheric environmental quality in Tianjin. The concentrations of OC and EC in PM 2.5 and PM 10 were all relatively higher in winter and fall and lower in summer and spring. This seasonal variation could be attributed to the cooperative effects of changes in emission rates and seasonal meteorological conditions. The annual average concentration of the estimated secondary organic carbon (SOC) was 14.9 μg/m 3 and occupied 61.7% of the total OC in PM 2.5 , while those in PM 10 were 23.4 μg/m 3 and 61.2%, respectively, indicating SOC had been an important contributor to organic aerosol in Tianjin. The distribution of eight carbon fractions (OC1, OC2, OC3, OC4, EC1, EC2, EC3 and OP) was also reported and found that the biomass burning, coal-combustion and motor-vehicle exhaust were all contributed to the carbonaceous particles in Tianjin.

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The fate of temporary faecal diversion in patients with perianal Crohn's disease is adversely affected by aggressive disease characteristics. No particular treatment, including biological therapy, was associated with an improved outcome.

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Purpose: Our aim was to determine the effects of cyclin D1 inhibition on tumor-associated neovascularization and endothelial cell growth. Experimental Design: We have generated adenovirus system for antisense to cyclin D1 (AS CyD1) and evaluated in vitro and in vivo effects. Small interfering RNA against cyclin D1 was also used to analyze cyclin D1 inhibition-associated vascular endothelial growth factor (VEGF) regulation. Results: The xenografts treated with adenoviral AS CyD1 showed less vessel density and displayed smaller tumor size in colon cancer cell lines HCT116 and DLD1. In vitro studies indicated that AS CyD1 decreased VEGF protein expression in DLD1 but not in HCT116. Cyclin D1 small interfering RNA caused a decrease in VEGF expression at protein and RNA levels in DLD1. A modest decrease was noted in the VEGF promoter activity, with inactivation of the STAT3 transcription factor through dephosphorylation. On the hand, the cyclin D1inhibition plus STAT3 inhibitor markedly decreased VEGF expression in HCT116, although VEGF did not change by the STAT3 inhibitor alone. In cultures of human umbilical vein endothelial cells (HUVEC), VEGF augmented cyclin D1expression and cell growth. AS CyD1significantly inhibited HUVEC growth even in the presence of VEGF. AS CyD1 also significantly suppressed in vitro tube formation in VEGF-treated HUVEC and in vivo macroaneurysm formation inVEGF-treated Matrigel plug. Conclusions: Our results suggest that cyclin D1 may play a role in the maintenance of VEGF expression and that AS CyD1could be potentially useful for targeting both cancer cells and their microenvironment of tumor vessels.Cyclin D1, a putative G 1 cyclin, preferentially associates with CDK4 and positively regulates the cell cycle transition from G 1 to S phase (1). Cyclin D1 is considered an oncogene because forced expression in rodent fibroblasts induces tumorigenicity in nude mice and cyclin D1 transgenic mice develop tumors of breast, esophagus, stomach, and tongue (2 -4). In human carcinomas, increased expression of cyclin D1 is one of the most frequent abnormalities because it is detected in f60% of breast cancers, 40% of colorectal cancers, 40% of squamous carcinomas of the head and neck, and 20% of prostate cancers (5 -8). Furthermore, overexpression of cyclin D1 is associated with poor prognosis of patients with carcinomas of colorectum, esophagus, stomach, pancreas, and liver (9 -13). Therefore, cyclin D1 is a crucial target for various types of human malignancies.To suppress the malignant potential of carcinomas, the strategy of antisense to cyclin D1 (AS CyD1) was first assessed in human esophageal squamous cell carcinoma and colon cancer cells (14,15). These studies clearly showed that AS CyD1 reversed the transformed phenotype of tumor cells, inhibited cell growth of tumor cells, and resulted in loss of tumorigenicity. Subsequently, AS CyD1 was found to enhance chemosensitivity of 5-fluorouracil, mitoxantrone, and cisplatinum in pancreatic cancer cells and head and neck cancer cells and...

Preoperative clinical deterioration is associated with an adverse outcome after laparoscopic TAC for UC.