LncRNA SNHG16 predicts poor prognosis in ESCC and promotes cell proliferation and invasion by regulating Wnt/ß-catenin signaling pathway.

OBJECTIVE: Increasing evidence indicated that small nucleolar RNA host gene 16 (SNHG16) acted as a key regulator in the proliferation and metastasis of several cancers, including esophageal squamous cell carcinoma (ESCC). In this research, we aimed to explore biological functions, clinical significance and the underlying molecular mechanisms of SNHG16 in ESCC. PATIENTS AND METHODS: qRT-PCR was performed to examine the expression of SNHG16 in ESCC cell lines and clinical ESCC tissue samples. The association of SNHG16 expression with clinicopathological factors and prognosis was statistically analyzed. Cell Counting Kit-8, flow cytometry, and transwell invasion assays were performed to determine the effect of SNHG16 in the regulation of biological behaviors of ESCC cells. Luciferase assay and Western blot were performed to determine the activation of Wnt/ß-catenin signaling pathway RESULTS: We observed that SNHG16 expression levels were significantly upregulated in ESCC tissues and cell lines compared with the corresponding normal tissues and normal esophageal cell line, respectively. In addition, increased expression of SNHG16 were strongly linked to tumor stage (p = 0.019), lymph nodes metastasis (p = 0.007) and clinical stage (p = 0.026). Kaplan-Meier assay showed that the survival time of patients with high SNHG16 expression was significantly shorter than those with low SNHG16 expression (p = 0.0017). Univariate and multivariate analyses showed that high SNHG16 expression in ESCC was an independent predictor of poor survival. Loss-of-function experiments revealed that knockdown of SNHG16 suppressed proliferation and invasion and induced apoptosis of ESCC cells. Mechanistically, Wnt/ß-catenin signaling pathways were actively modulated by SNHG16 in ESCC cells. CONCLUSIONS: Our findings reveal that SNHG16 plays an important role in ESCC proliferation/metastasis via modulating Wnt/ß-catenin signaling pathways and could represent a novel biomarker for predicting poor survival as well a promising therapeutic target.

Age adjusted Charlson Co-morbidity Index is an independent predictor of mortality over long-term follow-up in infective endocarditis.

BACKGROUND: Infective endocarditis (IE) is associated with high morbidity and mortality. The epidemiology of IE is changing, affecting more elderly patients with increased medical comorbidities. We aimed to assess the ability of the age adjusted Charlson Co-morbidity Index (ACCI) to predict early and late outcomes. METHODS: Between 1998 and 2010, adult patients with definite IE according to the modified Duke criteria were identified. The primary outcome was in-hospital and all-cause mortality. The secondary outcome was predictors of the primary outcome incorporating ACCI. RESULTS: 148 patients with IE were followed up for a mean of 3.8 ± 3 years. The mean age was 57 ± 17 years and 66% were male. In-hospital mortality and all-cause mortality were 24 and 47% respectively. Comorbid conditions included diabetes mellitus (DM) (21%); ischaemic heart disease (16%); heart failure (HF) (14%); renal failure (eGFR <60 ml/min/1.73 m(2)) (19%); and anaemia (64%). The most common causative organism was Staphylococcus aureus (53%). ACCI was >3 in 59% of patients. Cardiac surgery was performed in 45% of patients. On Cox regression analysis, ACCI >3 (HR=3.0 [1.5-6.0], p<0.002), new onset HF (HR=2.2 [1.3-3.6], p<0.003), anaemia (HR=1.8 [1.1-3.2], p=0.04) and age-per decade (HR=1.4 [1.1-1.7]. p=0.004) were independently associated with all-cause mortality. ACCI >3 was the strongest predictor of in-hospital mortality (OR=8.4 [2.8-24], p<0.001). Of the individual ACCI components, prior HF, DM with complications and metastatic disease were independent predictors of all-cause mortality. CONCLUSION: In-hospital and all-cause mortality of IE remain high. An ACCI >3 was a strong predictor of mortality, in addition to age, new HF and anaemia.

Mycobacterium genavense duodenitis following allogeneic peripheral blood stem cell transplantation.

A 56-year-old man was diagnosed with Mycobacterium genavense duodenitis 21 months after an allogeneic peripheral stem cell transplant complicated by graft-versus-host disease requiring intense immunosuppression. This duodenitis responded to prolonged therapy with clarithromycin, ciprofloxacin, and rifabutin and reduction of immunosuppression.

Design and application of compliant mechanisms for surgical tools.

This paper introduces the benefits of exploiting elasticity in the engineering design of surgical tools, in general, and of minimally invasive procedures, in particular. Compliant mechanisms are jointless mechanisms that rely on elastic deformation to transmit forces and motion. The lack of traditional joints in these single-piece flexible structures offers many benefits, including the absence of wear debris, pinch points, crevices, and lubrication. Such systems are particularly amenable to embedded sensing for haptic feedback and embedded actuation with active-material actuators. The paper provides an overview of design synthesis methods developed at the Compliant Systems Design Laboratory and focuses specifically on surgical applications. Compliant systems have potential to integrate. well within the constraints of laparoscopic procedures and telerobotic surgery. A load-path representation is used within a genetic algorithm to solve two gripper example problems. In addition, the paper illustrates the design and construction of an organ (kidney) manipulator for use in minimally invasive procedures.