Cyclin‐dependent kinase‐like 2 (CDKL2), a new member of the cyclin‐dependent kinase family, may be involved in gastric cancer (GC) progression. Thus, we conducted this study to explore the clinical effect of CDKL2 in GC. Immunohistochemistry was used to measure CDKL2 levels in gastric tissues. The association of a high CDKL2 level with clinical and pathological characteristics, and the correlation between the CDKL2 level and disease‐free and overall survival were analyzed. Transfection was employed to overexpress CDKL2 in GC cells and to investigate the effect of CDKL2 overexpression on cell proliferation and invasion. Loss of CDKL2 was positively correlated with several clinical and pathological characteristics, and patients with a low CDKL2 level had significantly poorer disease‐free and overall survival than those with a high level (P = .005 and .001, respectively). Univariate analysis using the Cox proportional hazards model indicated that a low CDKL2 level was a prognosticator for inferior disease‐free survival (P = .007). Based on immmunoblotting data, AGS and HGC‐27 GC cells were chosen for CDKL2 overexpression. Cellular studies revealed that CDKL2 overexpression impaired cell proliferation and invasion. Loss of CDKL2 may serve as a biomarker for predicting GC patient outcomes and a potential therapeutic target for GC treatment.

Although gastric cancer (GC) is one of the most common cancers, knowledge of its development and carcinogenesis is limited. To date, expression of ubiquitin‐specific protease 3 (USP3) in all types of cancer, including GC, is still unknown. The present study explored the involvement of USP3 in the carcinogenesis and prognosis of GC. We measured USP3 expression in normal and GC tissues and cell lines. Correlations between USP3 protein level and clinicopathological parameters, as well as the significance of USP3 protein level for disease‐free survival were assessed. Small hairpin RNA technology and transfection were used to investigate the effect of USP3 manipulation on cell proliferation and spreading. Moreover, xenograft proliferation and metastasis were used to explore the influence of USP3 on tumor growth and metastasis in animals. An increase in USP3 expression was observed in GC cells and tissues. The overexpression of USP3 was significantly correlated with several clinicopathological parameters and poor disease‐free survival. Multivariate Cox regression analysis showed that the overexpression of USP3 was an independent prognostic biomarker. Silencing of USP3 suppressed GC cell proliferation and spreading in vitro as well as xenograft proliferation and metastasis in vivo; however, opposite results were obtained when USP3 was overexpressed. Further studies showed that USP3 influenced cell proliferation and spreading by regulating the cell cycle control‐ and epithelial‐mesenchymal transition‐related molecules. This study suggests that USP3 overexpression can be a useful biomarker for predicting the outcomes of GC patients and that USP3 targeting represents a potential modality for treating GC.

cAMP signaling controls a variety of cellular functions. In addition to the well-known signal transducer cAMP-dependent protein kinase, a more recently discovered transducer is the exchange protein directly activated by cAMP (EPAC). EPAC responses are mediated by small G proteins, which regulate biologic functions such as cell adhesion, migration and proliferation. Recently, the clinical importance of EPAC1 has received increased attention. This study investigated the correlations between the expression of EPAC1 and various clinicopathologic parameters as well as the survival of the patients with gastric cancer (GC). The patient cohort in this study consisted of 141 cases of GC that presented from 1999 through 2011; documented clinicopathologic parameters and clinical outcomes were available for all cases. Immunoblotting, immunohistochemistry and quantitative real-time PCR were used to examine EPAC1 expression in gastric cells and tissues. siRNA technology was used to study the effect of EPAC1 knockdown on cell proliferation and invasion. An increase in EPAC1 expression was found in GC cells and tissues. The overexpression of EPAC1 was associated with the depth of invasion (P=0.0021), stage (P=0.0429), and vascular invasion (P=0.0049) and was correlated with poor disease-free survival (P=0.0029) and overall survival (P=0.0024). A univariate Cox regression analysis showed that the overexpression of EPAC1 was a prognostic marker for GC (P=0.038). Furthermore, cell studies indicated that the knockdown of EPAC1 in GC cells suppressed cell proliferation and invasion. The overexpression of EPAC1 can be used as a marker to predict the outcome of patients with GC, and EPAC1 represents a potential therapeutic modality for treating GC.

Background: As one of the most common malignancies in the world, little is known about the molecular mechanism underlying gastric cancer (GC) and its progression. In this study, we aimed to investigate the clinical impact of the mitochondrial GTPase mitofusin 2 (MFN2) in GC.Methods: Immunohistochemistry was used to examine the expression levels of MFN2 in gastric tissues obtained from 141 patients with GC. The correlations between MFN2 protein level and clinicopathologic parameters, as well as the significance of MFN2 protein level for overall and disease-free survival were assessed. siRNA technology was used to study the effect of MFN2 knockdown on cell proliferation and invasion.Results: The overexpression of MFN2 was positively associated with depth of invasion (P = 0.0430), stage (P = 0.0325) and vascular invasion (P = 0.0077). Patients with high expression levels of MFN2 had a significantly lower overall survival rate and disease-free survival rate compared with those with low expression levels (P = 0.003 and 0.001, respectively). Multivariate Cox regression analysis showed that the overexpression of MFN2 was an independent prognostic marker for inferior overall survival and disease-free survival (P = 0.015 and 0.025, respectively). In addition, studies conducted in GC cells indicated that knockdown of MFN2 suppressed cell proliferation and invasion.Conclusions: Overexpression of MFN2 can be used as a marker to predict the outcome of patients with GC. Furthermore, targeting MFN2 might provide a new therapeutic modality for the treatment of GC.

Cont-IONM is feasible and safe to use during transoral endoscopic thyroidectomies and may assist in the early detection of adverse EMG changes, thereby preventing paralysis of the RLNs.

Liver abscess secondary to fish bone migration from the duodenuma ns_5665 206..214 A 59-year-old woman was admitted with persistent fever for 2 weeks in spite of medication treatment and progressive persistent epigastric dullness after fever onset 10 days later. Abdominal computed tomography revealed a linear high-density lesion between the liver abscess and the duodenal bulb. Percutaneous abscess drainage and antibiotics treatment were performed. The panendoscopy demonstrated a healed duodenal ulcer without any foreign body. Therefore, she underwent the lateral segmentectomy, fistulectomy and duodenorrhaphy. Operative findings revealed one 4-cm fish bone within the duodenohepatic fistula, which was located at the duodenal bulb attached to the liver (Fig. 1). She was discharged on post-operative day 12 and felt well during outpatient department follow-up.Liver abscess combined with hepato-enteric fistula is a rare clinical manifestation. There are two mechanisms of relation between liver abscess and hepato-enteric fistula. One is liver abscess rupture into alimentary tract. 1 The other is perforated bowel wall leading to liver abscess formation. 2 Intestinal perforation by foreign body ingestion is one of the bowel perforation factors and the incidence is approximately 1%. 2 In the past, liver abscess secondary to foreign body penetrating from the alimentary tract was a surgical indication. Recently, some reports suggest non-operative treatment by abscess drainage, antibiotics administration and endoscopic removal of foreign body. 2,3 We combined operative and non-operative therapy for this complicated case. According to the patient's history, the process by which this fish bone penetrated through the duodenal wall may be slow ongoing and migration is more likely. When it 'migrated' out of the duodenal serosa and then the fistular orifice was covered by new growing mucosa, this duodenohepatic fistula and the fish bone became invisible. This is the possible mechanism of the liver abscess secondary to fish bone migration from the duodenum.The case series were presented at the

BackgroundOutbreaks of several serious infectious diseases have occurred in recent years. In response, to mitigate public health risks, countries worldwide have dedicated efforts to establish an information system for effective disease monitoring, risk assessment, and early warning management for international disease outbreaks. A cloud computing framework can effectively provide the required hardware resources and information access and exchange to conveniently connect information related to infectious diseases and develop a cross-system surveillance and control system for infectious diseases.ObjectiveThe objective of our study was to develop a Hospital Automated Laboratory Reporting (HALR) system based on such a framework and evaluate its effectiveness.MethodsWe collected data for 6 months and analyzed the cases reported within this period by the HALR and the Web-based Notifiable Disease Reporting (WebNDR) systems. Furthermore, system evaluation indicators were gathered, including those evaluating sensitivity and specificity.ResultsThe HALR system reported 15 pathogens and 5174 cases, and the WebNDR system reported 34 cases. In a comparison of the two systems, sensitivity was 100% and specificity varied according to the reported pathogens. In particular, the specificity for Streptococcus pneumoniae, Mycobacterium tuberculosis complex, and hepatitis C virus were 99.8%, 96.6%, and 97.4%, respectively. However, the specificity for influenza virus and hepatitis B virus were only 79.9% and 47.1%, respectively. After the reported data were integrated with patients’ diagnostic results in their electronic medical records (EMRs), the specificity for influenza virus and hepatitis B virus increased to 89.2% and 99.1%, respectively.ConclusionsThe HALR system can provide early reporting of specified pathogens according to test results, allowing for early detection of outbreaks and providing trends in infectious disease data. The results of this study show that the sensitivity and specificity of early disease detection can be increased by integrating the reported data in the HALR system with the cases’ clinical information (eg, diagnostic results) in EMRs, thereby enhancing the control and prevention of infectious diseases.

Colorectal cancer is one of the most prevalent and lethal malignancies, affecting approximately 900,000 individuals each year worldwide. Patients with colorectal cancer are found with elevated serum interleukin-6 (IL-6), which is associated with advanced tumor grades and is related to their poor survival outcomes. Although IL-6 is recognized as a potent inducer of colorectal cancer progression, the detail mechanisms underlying IL-6-induced colorectal cancer epithelial–mesenchymal transition (EMT), one of the major process of tumor metastasis, remain unclear. In the present study, we investigated the regulatory role of IL-6 signaling in colorectal cancer EMT using HCT116 human colorectal cancer cells. We noted that the expression of epithelial marker E-cadherin was reduced in HCT116 cells exposed to IL-6, along with the increase in a set of mesenchymal cell markers including vimentin and α-smooth muscle actin (α-SMA), as well as EMT transcription regulators—twist, snail and slug. The changes of EMT phenotype were related to the activation of Src, FAK, ERK1/2, p38 mitogen-activated protein kinase (p38MAPK), as well as transcription factors STAT3, κB and C/EBPβ. IL-6 treatment has promoted the recruitment of STAT3, κB and C/EBPβ toward the Twist promoter region. Furthermore, the Src-FAK signaling blockade resulted in the decline of IL-6 induced activation of ERK1/2, p38MAPK, κB, C/EBPβ and STAT3, as well as the decreasing mesenchymal state of HCT116 cells. These results suggested that IL-6 activates the Src-FAK-ERK/p38MAPK signaling cascade to cause the EMT of colorectal cancer cells. Pharmacological approaches targeting Src-FAK signaling may provide potential therapeutic strategies for rescuing colorectal cancer progression.