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Effect of a rapid response system on code rates and in-hospital mortality in medical wards
Hong Yeul Lee,이진우,Sang-Min Lee,Sulhee Kim,양은진,Hyun Joo Lee,Hannah Lee,류호걸,Seung-Young Oh,Eun Jin Ha,Sang-Bae Ko,조재영 대한중환자의학회 2019 Acute and Critical Care Vol.34 No.4
Background: To determine the effects of implementing a rapid response system (RRS) on code rates and in-hospital mortality in medical wards. Methods: This retrospective study included adult patients admitted to medical wards at Seoul National University Hospital between July 12, 2016 and March 12, 2018; the sample comprised 4,224 patients admitted 10 months before RRS implementation and 4,168 patients admitted 10 months following RRS implementation. Our RRS only worked during the daytime (7 AM to 7 PM) on weekdays. We compared code rates and in-hospital mortality rates between the preintervention and postintervention groups. Results: There were 62.3 RRS activations per 1,000 admissions. The most common reasons for RRS activation were tachypnea or hypopnea (44%), hypoxia (31%), and tachycardia or brady cardia (21%). Code rates from medical wards during RRS operating times significantly decreased from 3.55 to 0.96 per 1,000 admissions (adjusted odds ratio [aOR], 0.29; 95% confidence interval [CI], 0.10 to 0.87; P=0.028) after RRS implementation. However, code rates from medical wards during RRS nonoperating times did not differ between the preintervention and postintervention groups (2.60 vs. 3.12 per 1,000 admissions; aOR, 1.23; 95% CI, 0.55 to 2.76; P=0.614). In-hospital mortality significantly decreased from 56.3 to 42.7 per 1,000 admissions after RRS implementation (aOR, 0.79; 95% CI, 0.64 to 0.97; P=0.024). Conclusions: Implementation of an RRS was associated with significant reductions in code rates during RRS operating times and in-hospital mortality in medical wards.
Lee, Jung-Eun,Kim, Chan,Yang, Hannah,Park, Intae,Oh, Nuri,Hua, Serenus,Jeong, Haneul,An, Hyun Joo,Kim, Sun Chang,Lee, Gyun Min,Koh, Gou Young,Kim, Ho Min American Association for Cancer Research 2015 Molecular Cancer Therapeutics Vol.14 No.2
<P>Antiangiogenic therapies targeting VEGFA have been commonly used in clinics to treat cancers over the past decade. However, their clinical efficacy has been limited, with drawbacks including acquisition of resistance and activation of compensatory pathways resulting from elevated circulating VEGFB and placental growth factor (PlGF). To bypass these disadvantages, we developed a novel glycosylated soluble decoy receptor fusion protein, VEGF-Grab, that can neutralize VEGFA, VEGFB, and PlGF. VEGF-Grab has the second and third immunoglobulin (Ig)-like domains of VEGF receptor 1 (VEGFR1) fused to IgG1 Fc, with three potential glycosylation sites introduced into the third Ig-like domain of VEGF-Grab by mutagenesis. Compared with VEGF-Trap, VEGF-Grab showed more potent decoy activity against VEGF and PlGF, mainly attributed to the VEGFR1 backbone. Most importantly, the negatively charged <I>O</I>-glycans attached to the third Ig-like domain of VEGFR1 counterbalanced the originally positively charged VEGFR1 backbone, minimizing nonspecific binding of VEGF-Grab to the extracellular matrix, and resulting in greatly improved pharmacokinetic profile. These advancements led to stronger and more durable antiangiogenic, antitumor, and antimetastatic efficacy in both implanted and spontaneous tumor models as compared with VEGF-Trap, while toxicity profiles were comparable with VEGF-Trap. Collectively, our results highlight VEGF-Grab as a promising therapeutic candidate for further clinical drug development. <I>Mol Cancer Ther; 14(2); 470–9. ©2014 AACR</I>.</P>
Lee, Jin Ju,Kim, Dae Geun,Kim, Dong Hyeok,Simborio, Hannah Leah,Min, Wongi,Lee, Hu Jang,Her, Moon,Jung, Suk Chan,Watarai, Masahisa,Kim, Suk American Society for Biochemistry and Molecular Bi 2013 The Journal of biological chemistry Vol.288 No.39
<P>Lipid raft-associated clathrin is essential for host-pathogen interactions during infection. <I>Brucella abortus</I> is an intracellular pathogen that circumvents host defenses, but little is known about the precise infection mechanisms that involve interaction with lipid raft-associated mediators. The aim of this study was to elucidate the clathrin-mediated phagocytic mechanisms of <I>B. abortus</I>. The clathrin dependence of <I>B. abortus</I> infection in HeLa cells was investigated using an infection assay and immunofluorescence microscopy. The redistribution of clathrin in the membrane and in phagosomes was investigated using sucrose gradient fractionation of lipid rafts and the isolation of <I>B. abortus</I>-containing vacuoles, respectively. Clathrin and dynamin were concentrated into lipid rafts during <I>B. abortus</I> infection, and the entry and intracellular survival of <I>B. abortus</I> within HeLa cells were abrogated by clathrin inhibition. Clathrin disruption decreased actin polymerization and the colocalization of <I>B. abortus</I>-containing vacuoles with clathrin and Rab5 but not lysosome-associated membrane protein 1 (LAMP-1). Thus, our data demonstrate that clathrin plays a fundamental role in the entry and intracellular survival of <I>B. abortus</I> via interaction with lipid rafts and actin rearrangement. This process facilitates the early intracellular trafficking of <I>B. abortus</I> to safe replicative vacuoles.</P>
( Hannah Leah Tadeja Simborio ),( Alisha Wehdnesday Bernardo Reyes ),( Huynh Tan Hop ),( Lauren Togonon Arayan ),( Wongi Min ),( Hu Jang Lee ),( Jin Ju Lee ),( Hong Hee Chang ),( Suk Kim ) 한국미생물 · 생명공학회 2016 Journal of microbiology and biotechnology Vol.26 No.3
Brucellosis affects a wide range of host species, including humans and many livestock animals. Chronic infections of the disease make antibiotic treatment costly, and the current vaccine used in livestock has not been approved for human use. This study investigated the possible use of the Brucella abortus outer membrane protein A (OmpA) as a candidate subunit vaccine in an infected mouse model. The ompA gene was cloned and overexpressed, and the recombinant OmpA (rOmpA) protein fused to maltose binding protein (MBP) was purified in Escherichia coli. Immunogenicity was verified through western blotting, and mice were immunized and challenged to evaluate its protective effect. Mice treated with rOmpA exhibited induced humoral and host cell-mediated responses, with a significant increase in immunoglobulin G (IgG1 and IgG2a) and cytokine levels, especially TNF-α and IL-12, compared with the control groups treated with either MBP or PBS. In conclusion, rOmpA should be highly considered as a future subunit vaccine for brucellosis, and further studies regarding rOmpA and its protective ability are suggested.