Abdominal Compartment Syndrome

Abdominal compartment syndrome (ACS) is a progressively increasing intraabdominal pressure of more than 20 mm Hg with new-onset thoracoabdominal organ dysfunction. Primary abdominal compartment syndrome means increased pressure due to injury or disease in the abdominopelvic region. Secondary abdominal compartment syndrome means disease originating from outside the abdomen, such as significant burns or sepsis. As the pressure inside the abdomen increases, organ failure occurs, and the kidneys and lungs are the most frequently affected. Managements of ACS are multidisciplinary. Conservative treatment with adequate volume supple and with aggressive hemodynamic support is the first step. Decompressive laparotomy with open abdomen is indicated when ACS is refractory to conservative treatment and complicated with multiple organ failure. ACS can result in a high mortality rate, and successful treatment requires cooperation between physicians, intensivists, and surgeons

University vs. Research Institute? The Dual Pillars of German Science Production, 1950–2010

The world’s third largest producer of scientific research, Germany, is the origin of the research university and the independent, extra-university research institute. Its dual-pillar research policy differentiates these organizational forms functionally: universities specialize in advanced research-based teaching; institutes specialize intensely on research. Over the past decades this policy affected each sector differently: while universities suffered a lingering “legitimation crisis,” institutes enjoyed deepening “favored sponsorship”—financial and reputational advantages. Universities led the nation’s reestablishment of scientific prominence among the highly competitive European and global science systems after WWII. But sectoral analysis of contributions to science, technology, engineering, mathematics, and medical and health journal publications (1950–2010) finds that Germany’s small to medium-sized independent research institutes have made significant, growing contributions, particularly in publishing in higher impact journals proportionally more than their size. Simultaneously—despite dual-pillar policy implications—the university sector continues to be absolutely and relatively successful; not eclipsed by the institutes. Universities have consistently produced two-thirds of the nation’s publications in the highest quality journals since at least 1980 and have increased publications at a logarithmic rate; higher than the international mean. Indeed, they led Germany into the global mega-science style of production. Contrary to assumed benefits of functional differentiation, our results indicate that relative to their size, each sector has produced approximately similar publication records. While institutes have succeeded, the larger university sector, despite much less funding growth, has remained fundamental to German science production. Considering these findings, we discuss the future utility of the dual-pillar policy

Examining the Influence of Texas’ Strategic Plan for Increasing University Research: Loose Coupling and Research Production at Regional Public Universities

States have adopted a variety of policies to encourage universities to expand research production, with the hope of supporting economic growth and competitiveness. This paper considers whether a state-level initiative succeeded in influencing university-based research outputs among regional public universities. We test whether the Texas Research Incentive Program increased research production at a set of state universities as measured by total research spending, federally-funded research spending, the number of scholarly publications, and the share of publications published in high impact factor journals. Using a novel dataset and difference-in-differences analytic strategy, we found that TRIP adoption was associated with a 19%-25% increase in research expenditures at emerging research universities in Texas relative to a matched set of comparable universities. However, TRIP did not influence federally-funded research expenditures or journal publication outputs. We also show that federally-funded research expenditures influence publication outputs — both in amount and quality — and that number of full-time faculty influences both federal research expenditures and publication outputs. We discuss contributions to the literature on regional public universities, loose coupling, and research production, as well as implications for policy

Costunolide causes mitotic arrest and enhances radiosensitivity in human hepatocellular carcinoma cells

<p>Abstract</p> <p>Purpose</p> <p>This work aimed to investigate the effect of costunolide, a sesquiterpene lactone isolated from <it>Michelia compressa</it>, on cell cycle distribution and radiosensitivity of human hepatocellular carcinoma (HCC) cells.</p> <p>Methods</p> <p>The assessment used in this study included: cell viability assay, cell cycle analysis by DNA histogram, expression of phosphorylated histone H3 (Ser 10) by flow cytometer, mitotic index by Liu's stain and morphological observation, mitotic spindle alignment by immunofluorescence of alpha-tubulin, expression of cell cycle-related proteins by Western blotting, and radiation survival by clonogenic assay.</p> <p>Results</p> <p>Our results show that costunolide reduced the viability of HA22T/VGH cells. It caused a rapid G2/M arrest at 4 hours shown by DNA histogram. The increase in phosphorylated histone H3 (Ser 10)-positive cells and mitotic index indicates costunolide-treated cells are arrested at mitosis, not G2, phase. Immunofluorescence of alpha-tubulin for spindle formation further demonstrated these cells are halted at metaphase. Costunolide up-regulated the expression of phosphorylated Chk2 (Thr 68), phosphorylated Cdc25c (Ser 216), phosphorylated Cdk1 (Tyr 15) and cyclin B1 in HA22T/VGH cells. At optimal condition causing mitotic arrest, costunolide sensitized HA22T/VGH HCC cells to ionizing radiation with sensitizer enhancement ratio up to 1.9.</p> <p>Conclusions</p> <p>Costunolide could reduce the viability and arrest cell cycling at mitosis in hepatoma cells. Logical exploration of this mitosis-arresting activity for cancer therapeutics shows costunolide enhanced the killing effect of radiotherapy against human HCC cells.</p

Antimicrobial Susceptibility and Multiplex PCR Screening of AmpC Genes From Isolates of Enterobacter cloacae, Citrobacter freundii, and Serratia marcescens

Background/PurposeThe emergence of multiple drug resistance in Enterobacteriaceae is of particular concern. The aim of this study was to evaluate the antimicrobial susceptibility and screen for the ampC gene in three members of the Enterobacteriaceae family (Enterobacter cloacae, Citrobacter freundii, and Serratia marcescens) found at Taichung Veterans General Hospital during the past 5 years using multiplex polymerase chain reaction (PCR).MethodsThe susceptibility of thirty isolates from each of the three Enterobacteriaceae family members to five antimicrobial agents (ceftazidime, flomoxef, imipenem, moxifloxacin, and colistin) was assessed. The susceptibility was analyzed by disk diffusion, screening and confirmatory tests for extended-spectrum β-lactamases (ESBL) and minimum inhibitory concentration tests according to the recommendations of the Clinical and Laboratory Standards Institute. The detection of ampC genes (3 families, including DHA, EBC and CIT) was performed by multiplex PCR. To detect the coexistence of ESBL genes, PCR was performed using five primer pairs: TEM, SHV, SHV-5, CTX-M-3, and CTX-M-14.ResultsOf the 90 isolates, 53 (58.9%) were positive in the screening test for ESBL. Resistance genes were detected in 12 (22.6%) of these isolates: ampC gene of DHA type in one E. cloacae isolate and EBC type in three E. cloacae isolates; ampC gene of CIT type in four C. freundii isolates; CTX-M-3-like in one C. freundii isolate and one S. marcescens isolate; TEM in three E. cloacae isolates, three C. freundii isolates and two S. marcescens isolates; SHV in one C. freundii isolate.ConclusionAntibiotic phenotypes cannot accurately distinguish the resistance mechanisms caused by ampC or ESBL, and especially in ESBL-ampC combinations. However, PCR is a useful technique for the identification of the different types of resistance genes

Clinical Outcome of Mycobacterium abscessus Infection and Antimicrobial Susceptibility Testing

Background/PurposeMycobacterium abscessus is the most resistant and rapidly growing mycobacterium and causes a wide range of clinical infectious diseases. The relationship between antimicrobial susceptibility and clinical outcome needs to be further evaluated.MethodsForty M. abscessus isolates were obtained from clinical specimens of 40 patients at the Taichung Veterans General Hospital from January 2006 to December 2008. Antimicrobial susceptibility testing was performed using the broth microdilution method according to the recommendations of the National Committee for Clinical Laboratory Standards. The clinical manifestations and outcomes were reviewed from medical records.ResultsTwenty-two patients were diagnosed with M. abscessus infection. Cough (86.3%), hemoptysis (31.8%) and fever (18.1%) were the most common symptoms. The radiographic findings included reticulonodular opacities (50.0%), consolidation (31.8%) and cavitary lesions (18.1%). The 40 isolates were susceptible to amikacin (95.0%), cefoxitin (32.5%), ciprofloxacin (10.0%), clarithromycin (92.5%), doxycycline (7.5%), imipenem (12.5%), moxifloxacin (22.5%), sulfamethoxazole (7.5%) and tigecycline (100%). The rate of treatment failure was 27.3% at the end of the 12th month after the start of treatment, although these patients were treated with a combination of clarithromycin and other antimicrobial agents.ConclusionM. abscessus is naturally susceptible to clarithromycin and amikacin, variably susceptible to cefoxitin and imipenem, and resistant to most other antimicrobial drugs. Combination therapy with clarithromycin, amikacin and other active antimicrobial agents may lead to clinical improvement; however, the rate of treatment failure is still high