Palpation of preoperatively inserted indwelling angiocatheter facilitates intraoperative localization of obscure gastrointestinal bleeding of small intestinal origin

SummaryBackgroundPalpation of the indwelling angiographic catheter inserted before operation to localize obscure gastrointestinal bleeding of small intestinal origin during laparotomy has rarely been reported in the literature.PurposeThe purpose of the study is to investigate the role of palpable indwelling angiocatheter inserted before operation in localizing obscure gastrointestinal bleeding of small intestinal origin during laparotomy.MethodsBetween January 2003 and December 2010, seven patients who had a clinical impression of obscure gastrointestinal bleeding of small intestinal origin and angiographic extravasation from the mesenteric artery had an angiocatheter inserted into the distal mesenteric branch. During laparotomy the catheter was palpated to guide subsequent resection of the intestine. The clinical outcomes of these patients were retrospectively reviewed.ResultsDuring laparotomy the retained catheter failed to be palpated in one patient. Six patients underwent segmental resection of intestine under guidance of the palpated catheter. All six patients had positive identification of small bowel bleeding. The yield rate of intraoperative localization was 86% (6 out of 7). Two of the six patients ceased bleeding after operation, but died of underlying disease progression. Four of the six patients had an uneventful postoperative clinical course without recurrent bleeding after a median follow-up period of 25 months.ConclusionPalpation of the indwelling angiographic catheter selectively left before operation is effective for precisely locating obscure gastrointestinal bleeding of small intestinal origin during laparotomy

Src-homology 2 domain-containing tyrosine phosphatase 2 promotes oral cancer invasion and metastasis

BACKGROUND: Tumor invasion and metastasis represent a major unsolved problem in cancer pathogenesis. Recent studies have indicated the involvement of Src-homology 2 domain-containing tyrosine phosphatase 2 (SHP2) in multiple malignancies; however, the role of SHP2 in oral cancer progression has yet to be elucidated. We propose that SHP2 is involved in the progression of oral cancer toward metastasis. METHODS: SHP2 expression was evaluated in paired oral cancer tissues by using immunohistochemical staining and real-time reverse transcription polymerase chain reaction. Isogenic highly invasive oral cancer cell lines from their respective low invasive parental lines were established using a Boyden chamber assay, and changes in the hallmarks of the epithelial-mesenchymal transition (EMT) were assessed to evaluate SHP2 function. SHP2 activity in oral cancer cells was reduced using si-RNA knockdown or enforced expression of a catalytically deficient mutant to analyze migratory and invasive ability in vitro and metastasis toward the lung in mice in vivo. RESULTS: We observed the significant upregulation of SHP2 in oral cancer tissues and cell lines. Following SHP2 knockdown, the oral cancer cells markedly attenuated migratory and invasion ability. We observed similar results in phosphatase-dead SHP2 C459S mutant expressing cells. Enhanced invasiveness was associated with significant upregulation of E-cadherin, vimentin, Snail/Twist1, and matrix metalloproteinase-2 in the highly invasive clones. In addition, we determined that SHP2 activity is required for the downregulation of phosphorylated ERK1/2, which modulates the downstream effectors, Snail and Twist1 at a transcript level. In lung tissue sections of mice, we observed that HSC3 tumors with SHP2 deletion exhibited significantly reduced metastatic capacity, compared with tumors administered control si-RNA. CONCLUSIONS: Our data suggest that SHP2 promotes the invasion and metastasis of oral cancer cells. These results provide a rationale for further investigating the effects of small-molecule SHP2 inhibitors on the progression of oral cancer, and indicate a previously unrecognized SHP2-ERK1/2-Snail/Twist1 pathway that is likely to play a crucial role in oral cancer invasion and metastasis

Giant lipoma arising from deep lobe of the parotid gland

BACKGROUND: Lipomas are common benign soft tissue neoplasms but they are found very rarely in the deep lobe of parotid gland. Surgical intervention in these tumors is challenging because of the proximity of the facial nerve, and thus knowledge of the anatomy and meticulous surgical technique are essential. CASE PRESENTATION: A 71-year-old female presented with a large asymptomatic mass, which had occupied the left facial area for over the past fifteen years, and she requested surgical excision for a cosmetically better facial appearance. The computed tomography (CT) scan showed a well-defined giant lipoma arising from the left deep parotid gland. The lipoma was successfully enucleated after full exposure and mobilization of the overlying facial nerve branches. The surgical specimen measured 9 × 6 cm in size, and histopathology revealed fibrolipoma. The patient experienced an uneventful recovery, with a satisfying facial contour and intact facial nerve function. CONCLUSION: Giant lipomas involving the deep parotid lobe are extremely rare. The high-resolution CT scan provides an accurate and cost-effective preoperative investigative method. Surgical management of deep lobe lipoma should be performed by experienced surgeons due to the need for meticulous dissection of the facial nerve branches. Superficial parotidectomy before deep lobe lipoma removal may be unnecessary in selected cases because preservation of the superficial lobe may contribute to a better aesthetic and functional result

Well-differentiated gall bladder hepatoid carcinoma producing alpha-fetoprotein: a case report

<p>Abstract</p> <p>Introduction</p> <p>Gall bladder carcinoma is rare, and metastatic gall bladder carcinoma from hepatocellular carcinoma has been reported in only a few patients.</p> <p>Case presentation</p> <p>We present a 73-year-old man with a history of hepatitis B virus-related liver cirrhosis and hepatocellular carcinoma. He received transcatheter arterial chemoembolization, and was diagnosed to have an alpha-fetoprotein producing gall bladder tumor with intraluminal growth. Open cholecystectomy was performed. Pathologic examination of the lesion revealed a well-differentiated hepatoid carcinoma. The lesion was thought most likely to be a metastatic lesion from previous hepatocellular carcinoma. His alpha-fetoprotein level dropped to normal levels five months after the surgery.</p> <p>Conclusion</p> <p>This unusual intraluminal growing tumor proved to be a well-differentiated hepatoid carcinoma, most likely a metastatic lesion from previous hepatocellular carcinoma. This case reminds clinicians that in looking for likely hepatocellular carcinoma recurrence, when no detectable hepatic lesion can account for an elevated alpha-fetoprotein level, the gall bladder should be included in the search for the site of metastasis.</p

The dimer interface of the SARS coronavirus nucleocapsid protein adapts a porcine respiratory and reproductive syndrome virus-like structure

AbstractWe have employed NMR to investigate the structure of SARS coronavirus nucleocapsid protein dimer. We found that the secondary structure of the dimerization domain consists of five α helices and a β-hairpin. The dimer interface consists of a continuous four-stranded β-sheet superposed by two long α helices, reminiscent of that found in the nucleocapsid protein of porcine respiratory and reproductive syndrome virus. Extensive hydrogen bond formation between the two hairpins and hydrophobic interactions between the β-sheet and the α helices render the interface highly stable. Sequence alignment suggests that other coronavirus may share the same structural topology

ATF3 Sustains IL-22-Induced STAT3 Phosphorylation to Maintain Mucosal Immunity Through Inhibiting Phosphatases

In gut epithelium, IL-22 transmits signals through STAT3 phosphorylation (pSTAT3) which provides intestinal immunity. Many components in the IL-22-pSTAT3 pathway have been identified as risk factors for inflammatory bowel disease (IBD) and some of them are considered as promising therapeutic targets. However, new perspectives are still needed to understand IL-22-pSTAT3 signaling for effective clinical interventions in IBD patients. Here, we revealed activating transcription factor 3 (ATF3), recently identified to be upregulated in patients with active IBD, as a crucial player in the epithelial IL-22-pSTAT3 signaling cascade. We found ATF3 is central to intestinal homeostasis and provides protection during colitis. Loss of ATF3 led to decreased crypt numbers, more shortened colon length, impaired ileal fucosylation at the steady state, and lethal disease activity during DSS-induced colitis which can be effectively ameliorated by rectal transplantation of wild-type colonic organoids. Epithelial stem cells and Paneth cells form a niche to orchestrate epithelial regeneration and host-microbe interactions, and IL-22-pSTAT3 signaling is a key guardian for this niche. We found ATF3 is critical for niche maintenance as ATF3 deficiency caused compromised stem cell growth and regeneration, as well as Paneth cell degeneration and loss of anti-microbial peptide (AMP)-producing granules, indicative of malfunction of Paneth/stem cell network. Mechanistically, we found IL-22 upregulates ATF3, which is required to relay IL-22 signaling leading to STAT3 phosphorylation and subsequent AMP induction. Intriguingly, ATF3 itself does not act on STAT3 directly, instead ATF3 regulates pSTAT3 by negatively targeting protein tyrosine phosphatases (PTPs) including SHP2 and PTP-Meg2. Furthermore, we identified ATF3 is also involved in IL-6-mediated STAT3 activation in T cells and loss of ATF3 leads to reduced capacity of Th17 cells to produce their signature cytokine IL-22 and IL-17A. Collectively, our results suggest that via IL-22-pSTAT3 signaling in the epithelium and IL-6-pSTAT3 signaling in Th17 cells, ATF3 mediates a cross-regulation in the barrier to maintain mucosal homeostasis and immunity