31 research outputs found

    Long-Term Outcomes of Patients with Acute Cholecystitis after Successful Percutaneous Cholecystostomy Treatment and the Risk Factors for Recurrence: A Decade Experience at a Single Center

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    <div><p>Background</p><p>Percutaneous cholecystostomy tube (PCT) has been effectively used for the treatment of acute cholecystitis (AC) for patients unsuitable for early cholecystectomy. This retrospective study investigated the recurrence rate after successful PCT treatment and factors associated with recurrence.</p><p>Methods</p><p>We reviewed patients treated with PCT for AC from October 2004 through December 2013. Patients with successful PCT treatment were those who were free from persistent PCT drainage. We used multivariable logistic regression analysis sequentially to identify factors associated with each outcome.</p><p>Results</p><p>The study included 184 patients (mean age: 70.1 years). The average duration for parenteral antibiotics was 14.4 days and 20.0 days for PCT drainage. The one-year recurrence rate was 9.2% (17/184) with most recurrences occurring within two months (6.5%, 12/184) of the procedure. Complicated cholecystitis (odds ratio [OR]: 4.67; 95% confidence interval [CI]: 1.44–15.70; <i>P</i> = 0.01) and PCT drainage duration >32 days (OR: 4.92; 95% CI: 1.03–23.53; <i>P</i> = 0.05) positively correlated with one-year recurrence; parenteral antibiotics duration >10 days (OR: 0.21; 95% CI: 0.05–0.68; <i>P</i> = 0.01) was inversely associated with one-year recurrence.</p><p>Conclusions</p><p>The recurrence rate was low for patients after successful PCT treatment. Predictors for recurrence included the severity of initial AC and subsequently provided treatments.</p></div

    Molecular Imaging of Ischemia and Reperfusion in Vivo with Mitochondrial Autofluorescence

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    Ischemia and reperfusion (IR) injury constitutes a pivotal mechanism of tissue damage in pathological conditions such as stroke, myocardial infarction, vascular surgery, and organ transplant. Imaging or monitoring of the change of an organ at a molecular level in real time during IR is essential to improve our understanding of the underlying pathophysiology and to guide therapeutic strategies. Herein, we report molecular imaging of a rat model of hepatic IR with the autofluorescence of mitochondrial flavins. We demonstrate a revelation of the histological characteristics of a liver in vivo with no exogenous stain and show that intravital autofluorescent images exhibited a distinctive spatiotemporal variation during IR. The autofluorescence decayed rapidly from the baseline immediately after 20-min ischemia (approximately 30% decrease in 5 min) but recovered gradually during reperfusion (to approximately 99% of the baseline 9 min after the onset of reperfusion). The autofluorescent images acquired during reperfusion correlated strongly with the reperfused blood flow. We show further that the autofluorescence was produced predominantly from mitochondria, and the distinctive autofluorescent variation during IR was mechanically linked to the altered balance between the flavins in the oxidized and reduced forms residing in the mitochondrial electron-transport chain. Our approach opens an unprecedented route to interrogate the deoxygenation and reoxygenation of mitochondria, the machinery central to the pathophysiology of IR injury, with great molecular specificity and spatiotemporal resolution and can be prospectively translated into a medical device capable of molecular imaging. We envisage that the realization thereof should shed new light on clinical diagnostics and therapeutic interventions targeting IR injuries of not only the liver but also other vital organs including the brain and heart

    C1GALT1 regulates cell adhesion, migration, and invasion.

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    <p>(<i>a</i>) Overexpression and knockdown of C1GALT1 in HCC cell lines. Overexpression of C1GALT1 with <i>C1GALT1</i>/pcDNA3.1 plasmid compared with pcDNA3.1 empty plasmid (mock) transfection in HCC36 and Sk-Hep1 cells. Knockdown of C1GALT1 with two <i>C1GALT1</i> siRNAs compared with control (Ctr) siRNA in HA22T cells and HepG2 cells. GAPDH was used as a loading control. (<i>b</i>) C1GALT1 regulated transwell cell migration and (<i>c</i>) Matrigel invasion. Overexpression of C1GALT1 significantly enhanced migration and invasion in HCC36 and HA22T cells (left), and knockdown of C1GALT1 suppressed migration and invasion in HA22T and HepG2 cells (right). All results are represented as means ± SD from three independent experiments. * <i>P</i><0.05; **<i>P</i><0.01. (<i>d</i>) C1GALT1 regulated cell adhesion. C1GALT1 overexpressed (left) or knockdown (right) cells were allowed to attach on collagen IV-, fibronectin-, and laminin-coated plates. Adherent cells were counted. BSA was used as a non-ECM protein control. Results are represented as the means ± SD from three independent experiments. * <i>P</i><0.05; **<i>P</i><0.01.</p
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