A Case of Successful Colonoscopic Treatment of Acute Appendiceal Bleeding by Endoclips

Lower gastrointestinal bleeding is a common disease among elderly patients. The common sources of lower gastrointestinal bleeding include vascular disease, Crohn's disease, neoplasm, inflammatory bowel disease, hemorrhoid, and ischemic colitis. However, bleeding from the appendix has been reported very rarely in patients with lower gastrointestinal tract bleeding. In general, after a colonoscopic diagnosis of appendiceal bleeding, a laparoscopic or surgical appendectomy would be recommended. We report a case of successful colonoscopic treatment of appendiceal bleeding without complications by endoclips. This report suggests that colonoscopic clipping is a safe and effective means to treat bleeding from appendiceal lesions. Further study is needed to evaluate procedure-related complications and to confirm the procedure's safety and efficacy

Massive Lower Gastrointestinal Bleeding from the Appendix

Massive rectal bleeding from the appendix, considered a rare case of lower gastrointestinal bleeding, is not easily recognized by various diagnostic modalities. A multidisciplinary approach for both a diagnosis and a differential diagnosis is important because the identification of the bleeding site is crucial to proceed to a proper intervention and there are various causes of appendiceal bleeding. Because early colonoscopy plays an important role in the diagnosis and management of lower gastrointestinal hemorrhage, we report a case of a life threatening massive rectal bleeding from the appendix diagnosed by colonoscopy. We also present a review of the literature

Pathobiological implications of mucin (MUC) expression in the outcome of small bowel cancer.

Mucins have been associated with survival in various cancer patients, but there have been no studies of mucins in small bowel carcinoma (SBC). In this study, we investigated the relationships between mucin expression and clinicopathologic factors in 60 SBC cases, in which expression profiles of MUC1, MUC2, MUC3, MUC4, MUC5AC, MUC6 and MUC16 in cancer and normal tissues were examined by immunohistochemistry. MUC1, MUC5AC and MUC16 expression was increased in SBC lesions compared to the normal epithelium, and expression of these mucins was related to clinicopathologic factors, as follows: MUC1 [tumor location (p = 0.019), depth (p = 0.017) and curability (p = 0.007)], MUC5AC [tumor location (p = 0.063) and lymph node metastasis (p = 0.059)], and MUC16 [venous invasion (p = 0.016) and curability (p = 0.016)]. Analysis of 58 cases with survival data revealed five factors associated with a poor prognosis: poorly-differentiated or neuroendocrine histological type (

Haem oxygenase delays programmed cell death in wheat aleurone layers by modulation of hydrogen peroxide metabolism

Haem oxygenase-1 (HO-1) confers protection against a variety of oxidant-induced cell and tissue injury in animals and plants. In this report, it is confirmed that programmed cell death (PCD) in wheat aleurone layers is stimulated by GA and prevented by ABA. Meanwhile, HO activity and HO-1 protein expression exhibited lower levels in GA-treated layers, whereas the hydrogen peroxide (H2O2) content was apparently increased. The pharmacology approach illustrated that scavenging or accumulating H2O2 either delayed or accelerated GA-induced PCD. Furthermore, pretreatment with the HO-1 specific inhibitor, zinc protoporphyrin IX (ZnPPIX), before exposure to GA, not only decreased HO activity but also accelerated GA-induced PCD significantly. The application of the HO-1 inducer, haematin, and the enzymatic reaction product of HO, carbon monoxide (CO) aqueous solution, both of which brought about a noticeable induction of HO expression, substantially prevented GA-induced PCD. These effects were reversed when ZnPPIX was added, suggesting that HO in vivo played a role in delaying PCD. Meanwhile, catalase (CAT) and ascorbate peroxidase (APX) activities or transcripts were enhanced by haematin, CO, or bilirubin (BR), the catalytic by-product of HO. This enhancement resulted in a decrease in H2O2 production and a delay in PCD. In addition, the antioxidants butylated hydroxytoluene (BHT), dithiothreitol (DTT), and ascorbic acid (AsA) were able not only to delay PCD but also to mimic the effects of haematin and CO on HO up-regulation. Overall, the above results suggested that up-regulation of HO expression delays PCD through the down-regulation of H2O2 production