The presence of IGHG1 in pancreatic cancer cells might constitute an important element responsible for tumor cell proliferation and immune evasion mechanisms.

Approximately 30% of the patients with ulcerative colitis (UC) would ultimately require colectomy for medically refractory UC or UC‐associated neoplasia. Restorative proctocolectomy with ileal pouch‐anal anastomosis has become the surgical treatment of choice for these patients. However, this procedure does not completely abolish the risk for neoplasia of the pouch. The main risk factor for pouch neoplasia is a preoperative diagnosis of UC‐associated dysplasia or cancer. Although the natural history and prognosis of pouch dysplasia are not clear, mortality associated with pouch cancer, once diagnosed, appears to be high. Conversely, not all pouch neoplasia follows the chronic inflammation‐dysplasia‐cancer sequence, which makes pouch endoscopy with biopsy, the current gold standard for surveillance, challenging. In addition, the findings that pouch neoplasia is not common and that pouch endoscopy still misses dysplasia lead to controversy on the need and time interval of routine endoscopic surveillance. However, based on reports in the literature and their own experience, the authors recommend surveillance endoscopy to be performed in patients at risk, such as those with a precolectomy diagnosis of UC‐associated neoplasia. This review appraises issues in the prevalence and incidence, risk factors, technical aspects of pouch construction, clinical and pathological features, natural history, surveillance examination, diagnosis, and management of pouch neoplasia. Cancer 2011. © 2011 American Cancer Society.

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The aim of this study was to explore the preventive effect and possible mechanisms of transcutaneous electrical acustimulation (TEA) on stroke-induced constipation. A total of 86 ischemic stroke patients were randomly allocated to 2-wk TEA or sham-TEA group. Bowel dairy and Bristol Stool Form Scale were recorded daily. Constipation and dyspeptic symptom assessment was performed at the end of the 14-day treatment. Electrocardiogram was recorded for the assessment of autonomic function. The correlation between autonomic function at admission and stroke severity was assessed. The univariate and multivariate regression analyses were performed to investigate the risk factors for stroke-induced constipation. The cumulative incidence of stroke-induced constipation was 68.2% at the acute stage. Sympathetic nerve activity at admission was positively correlated with stroke severity ( R = 0.47, P < 0.001). Sympathetic nerve activity and stroke severity were independent risk factors for stroke-induced constipation. TEA decreased cumulative incidence of stroke-induced constipation (42.9 vs. 68.2%, P = 0.029). TEA significantly increased frequency of bowel movements (4.5 vs. 5.5, P = 0.001) and spontaneous bowel movements (3.0 vs. 4.5, P = 0.003) per week. TEA decreased straining defecations (0.2 vs. 0, P < 0.001) and laxative use (1 vs. 0, P < 0.001). TEA improved stool consistency and patients' quality of life ( P < 0.05, resp.). TEA increased vagal activity ( P < 0.001 vs. baseline) and decreased sympathetic activity ( P < 0.001 vs. baseline). Ischemic stroke patients are predisposed to autonomic function imbalance. TEA was effective in the prevention of stroke-induced constipation, and the effect was possibly mediated via the autonomic function. NEW & NOTEWORTHY This study illustrated that the brain-gut dysfunction, primarily autonomic function imbalance, was correlated with the stroke-induced constipation. This was the first study to report that transcutaneous electrical acustimulation had a preventive effect on stroke-induced constipation, suggesting a potential novel therapy for bowel problem management. The effect was possibly mediated via the autonomic function.

IntroductionGloboid cell leukodystrophy (GLD) is a severe disorder of the central and peripheral nervous system caused by the absence of galactocerebrosidase (GALC) activity. Cell-based therapies are highly promising strategies for GLD. In this study, G-Olig2 mouse embryonic stem cells (ESCs) were induced into oligodendrocyte progenitor cells (OPCs) and were implanted into the brains of twitcher mice, an animal model of GLD, to explore the therapeutic potential of the cells.MethodsThe G-Olig2 ESCs were induced into OPCs by using cytokines and a multi-step differentiation procedure. Oligodendrocyte markers were detected by reverse transcription-polymerase chain reaction (RT-PCR) and immunocytochemistry. The toxicity of psychosine to OPCs was determined by a cell proliferation assay kit. The GALC level of OPCs was also examined. OPCs were labeled with Dir and transplanted into the brains of twitcher mice. The transplanted cells were detected by in-Vivo Multispectral Imaging System and real-time PCR. The physiological effects of twitcher mice were assessed.ResultsOligodendrocyte markers were expressed in OPCs, and 76% ± 5.76% of the OPCs were enhanced green fluorescent protein (eGFP)-positive, eGFP was driven by the Olig2 promoter. The effect of psychosine on cell viability indicated that OPCs were more resistant to psychosine toxicity. The GALC level of OPCs was 10.0 ± 1.23 nmol/hour per mg protein, which was significantly higher than other cells. Dir-labeled OPCs were injected into the forebrain of post-natal day 10 twitcher mice. The transplanted OPCs were myelin basic protein (MBP)-positive and remained along the injection tract as observed by fluorescent microscopy. The level of the Dir fluorescent signal and eGFP mRNA significantly decreased at days 10 and 20 after injection, as indicated by in-Vivo Multispectral Imaging System and real-time PCR. Because of poor cell survival and limited migration ability, there was no significant improvement in brain GALC activity, MBP level, life span, body weight, and behavioral deficits of twitcher mice.ConclusionsESC-derived OPC transplantation was not sufficient to reverse the clinical course of GLD in twitcher mice.

BackgroundSerine/arginine protein kinase 1 (SRPK1) is a protein kinase that belongs to the serine/arginine-rich domain family of splicing factors which are essential for splice-site selection, especially the modulation for RNA metabolism, localization, and translation. High expression of SRPK1 has been found in numerous human cancers, but its mechanism in colorectal cancer (CRC) is still rarely reported.PurposeTo investigate the expression of SRPK1 in CRC tissues and cells and determine its functions and mechanism in CRC.MethodsThe expression of SRPK1 was explored in human CRC patients and cells by immunohistochemistry, real-time quantitative PCR, and Western blot; Cell Counting Kit-8, Transwell, flow cytometry, and tube formation assay were used to investigate the CRC cell viability, migration, apoptosis, and angiogenesis, respectively.ResultsSRPK1 was overexpressed in CRC tumor tissues and cells, and correlated with tumor node metastasis stage; inhibition of SRPK1 by siRNA resulted in decreased cell growth and migration, significantly increased apoptosis, and suppressed angiogenesis.ConclusionSRPK1 can be a prognostic indicator of CRC and may be a therapeutic target for CRC.

Colon adenocarcinoma (COAD), having high malignancy and poor prognosis, is the main pathological type of colon cancer. Previous studies show that Keratin 17 (KRT17) plays an important role in the development of many malignant tumors. However, its role and the molecular mechanism underlying COAD remain unclear. Using TCGA and ONCOMINE databases, as well as immunohistochemistry, we found that the expression of KRT17 was higher in COAD tissues as compared to that in the adjacent normal tissues. Cell- and animal-based experiments showed that overexpression of KRT17 promoted the invasion and metastasis of colon cancer cells while knocking down KRT17 reversed these processes both in vitro and in vivo . In addition, we also showed that KRT17 promoted the formation of new blood vessels. Mechanistically, KRT17 could regulate the WNT/β-catenin signaling pathway, and APC may be involved in this process by interacting with KRT17. In summary, these findings suggested that high expression of KRT17 could promote cell metastasis and angiogenesis of colon cancer cells by regulating the WNT/β-catenin signaling pathway. Thus, KRT17 could be a potential therapeutic target for COAD treatment.

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