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  1. Article ; Online: Structural Congeners of Izenamides Responsible for Cathepsin D Inhibition: Insights from Synthesis-Derived Elucidation.

    Kim, Hyun Su / Kong, Hyejin / Kim, Taewoo / Lim, Changjin / Lee, Seungbeom / Kim, Seok-Ho / Suh, Young-Ger

    Marine drugs

    2023  Volume 21, Issue 5

    Abstract: This study aimed to elucidate the structural congeners of natural izenamides A, B, and C ( ...

    Abstract This study aimed to elucidate the structural congeners of natural izenamides A, B, and C (
    MeSH term(s) Humans ; Cathepsin D ; Protease Inhibitors/pharmacology ; Protease Inhibitors/chemistry
    Chemical Substances Cathepsin D (EC 3.4.23.5) ; Protease Inhibitors
    Language English
    Publishing date 2023-04-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2175190-0
    ISSN 1660-3397 ; 1660-3397
    ISSN (online) 1660-3397
    ISSN 1660-3397
    DOI 10.3390/md21050281
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  2. Article ; Online: Low Low-Density Lipoprotein Levels Are Associated With, But Do Not Causally Contribute to, Increased Mortality in Sepsis.

    Walley, Keith R / Boyd, John H / Kong, HyeJin Julia / Russell, James A

    Critical care medicine

    2019  Volume 47, Issue 3, Page(s) 463–466

    Abstract: Objectives: Low low-density lipoprotein levels are associated with increased mortality in sepsis. Whether low low-density lipoprotein levels contribute causally to adverse sepsis outcome is unknown.: Design: Retrospective analysis of two sepsis ... ...

    Abstract Objectives: Low low-density lipoprotein levels are associated with increased mortality in sepsis. Whether low low-density lipoprotein levels contribute causally to adverse sepsis outcome is unknown.
    Design: Retrospective analysis of two sepsis patient cohorts using a Mendelian Randomization strategy.
    Setting: Sepsis patients enrolled into clinical research cohorts at tertiary care teaching hospitals.
    Patients: The first cohort included 200 sepsis patients enrolled in an observational study in a hospital Emergency Department. The second cohort included genotyped patients enrolled in the Vasopressin and Septic Shock Trial.
    Interventions: Retrospective analysis of these patient datasets. In 632 patients enrolled in Vasopressin and Septic Shock Trial, Proprotein Convertase Subtilisin/Kexin type 9, and 3-Hydroxy-3-Methylglutaryl-CoA Reductase single nucleotide polymorphisms known to be associated with low-density lipoprotein levels were genotyped, and a genetic score related to low-density lipoprotein levels was calculated.
    Measurements and main results: In the first cohort, we replicated the finding that low low-density lipoprotein levels are associated with increased 28-day mortality. In genotyped patients in the Vasopressin and Septic Shock Trial trial, we found that the 3-Hydroxy-3-Methylglutaryl-CoA Reductase genetic score, known to be directly related to low low-density lipoprotein levels, was not associated with increased mortality. Surprisingly the Proprotein Convertase Subtilisin/Kexin type 9 genetic score, known to be directly related to low low-density lipoprotein levels, was associated with decreased (not increased) mortality.
    Conclusions: Both 3-Hydroxy-3-Methylglutaryl-CoA Reductase and Proprotein Convertase Subtilisin/Kexin type 9 genetic scores should have been associated with increased mortality if low low-density lipoprotein levels contributed causally to sepsis mortality. But this was not the case, and the opposite was observed for the Proprotein Convertase Subtilisin/Kexin type 9 genetic score. This suggests that low-density lipoprotein levels, per se, do not contribute causally to adverse sepsis outcomes. The Proprotein Convertase Subtilisin/Kexin type 9 genetic score finding raises the possibility that increased low-density lipoprotein clearance (the effect of these Proprotein Convertase Subtilisin/Kexin type 9 genotypes) may contribute to improved sepsis outcomes.
    MeSH term(s) Female ; Humans ; Hydroxymethylglutaryl CoA Reductases/genetics ; Lipoproteins, LDL/blood ; Lipoproteins, LDL/genetics ; Male ; Middle Aged ; Polymorphism, Single Nucleotide/genetics ; Proprotein Convertase 9/genetics ; Retrospective Studies ; Risk Factors ; Sepsis/blood ; Sepsis/genetics ; Sepsis/mortality
    Chemical Substances Lipoproteins, LDL ; Hydroxymethylglutaryl CoA Reductases (EC 1.1.1.-) ; PCSK9 protein, human (EC 3.4.21.-) ; Proprotein Convertase 9 (EC 3.4.21.-)
    Language English
    Publishing date 2019-01-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 197890-1
    ISSN 1530-0293 ; 0090-3493
    ISSN (online) 1530-0293
    ISSN 0090-3493
    DOI 10.1097/CCM.0000000000003551
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  3. Article ; Online: Modulation of vascular endothelial inflammatory response by proprotein convertase subtilisin-kexin type 9.

    Leung, Alex K K / Xue, Yuan Chao / de Guzman, Antyrah / Grzelkovski, Guilherme / Kong, HyeJin Julia / Genga, Kelly R / Russell, James A / Boyd, John H / Francis, Gordon A / Walley, Keith R

    Atherosclerosis

    2022  Volume 362, Page(s) 29–37

    Abstract: Background and aims: Endotoxins carried within LDL are cleared from the circulation via hepatic LDL receptor (LDLR)-mediated endocytosis. Proprotein convertase subtilisin-kexin type 9 (PCSK9) reduces this clearance by down-regulating LDLR density on ... ...

    Abstract Background and aims: Endotoxins carried within LDL are cleared from the circulation via hepatic LDL receptor (LDLR)-mediated endocytosis. Proprotein convertase subtilisin-kexin type 9 (PCSK9) reduces this clearance by down-regulating LDLR density on hepatocytes. In addition to hepatocytes, vascular endothelial cells also express receptor targets of PCSK9, including LDLR. Therefore, we hypothesized that PCSK9 may regulate vascular endothelial cell uptake of lipopolysaccharide (LPS) and alter the vascular endothelial cell inflammatory response.
    Methods and results: We found that LPS is internalized by human umbilical vein vascular endothelial cells (HUVECs) and LPS uptake dose-dependently increased with increasing LDL concentration. Intracellular LPS co-localized with LDL. PCSK9 and, separately, blocking antibodies against LDLR, dose-dependently decreased the vascular endothelial cell uptake of LPS and, furthermore, inhibition of endocytosis using Dynasore blocked LPS uptake. In contrast, blocking antibodies against TLR4 did not alter LPS uptake. PCSK9 decreased the LPS-induced proinflammatory response (IL-6 and IL-8 gene expression and protein secretion, and VCAM-1/ICAM-1 expression) in vascular endothelial cells. In addition, a decrease in PCSK9 and increase in LDLR, mediated by triciribine or siPCSK9, increased LPS uptake and the LPS-induced proinflammatory response. Similar results were also found in aortic vascular tissue from Pcsk9
    Conclusions: Our data suggest that, similar to PCSK9 treatment in hepatocytes, PCSK9 reduces vascular endothelial cell uptake of LPS via LDLR-mediated endocytosis. Consequently, PCSK9 decreases the LPS-induced proinflammatory response in vascular endothelial cells. These results raise the possibility that PCSK9 inhibition may have additional effects on vascular endothelial inflammation via this alternative pathway, beyond the known effects of PCSK9 inhibition on LDL lowering and hepatic endotoxin clearance.
    MeSH term(s) Humans ; Mice ; Animals ; Proprotein Convertase 9/genetics ; Proprotein Convertase 9/metabolism ; Lipopolysaccharides/pharmacology ; Endothelial Cells/metabolism ; Antibodies, Blocking ; Receptors, LDL/genetics ; Receptors, LDL/metabolism ; Endotoxins ; Subtilisins
    Chemical Substances PCSK9 protein, human (EC 3.4.21.-) ; Proprotein Convertase 9 (EC 3.4.21.-) ; Lipopolysaccharides ; Antibodies, Blocking ; Receptors, LDL ; Endotoxins ; Subtilisins (EC 3.4.21.-)
    Language English
    Publishing date 2022-09-24
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 80061-2
    ISSN 1879-1484 ; 0021-9150
    ISSN (online) 1879-1484
    ISSN 0021-9150
    DOI 10.1016/j.atherosclerosis.2022.09.008
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  4. Article ; Online: 2-Aminophenylpyrimidines as Novel Inhibitors of Aminoacyl-tRNA Synthetase Interacting Multifunctional Protein 2 (AIMP2)-DX2 for Lung Cancer Treatment.

    Lee, Seungbeom / Kim, Dae Gyu / Kim, Kyeojin / Kim, Taewoo / Lim, Semi / Kong, Hyejin / Kim, Sunghoon / Suh, Young-Ger

    Journal of medicinal chemistry

    2020  Volume 63, Issue 8, Page(s) 3908–3914

    Abstract: Aminoacyl-tRNA synthetase interacting multifunctional proteins (AIMPs) have recently been considered novel therapeutic targets in several cancers. In this publication we report the development of novel 2-aminophenylpyrimidines as new AIMP2-DX2 inhibitors. ...

    Abstract Aminoacyl-tRNA synthetase interacting multifunctional proteins (AIMPs) have recently been considered novel therapeutic targets in several cancers. In this publication we report the development of novel 2-aminophenylpyrimidines as new AIMP2-DX2 inhibitors. In particular, aminophenylpyrimidine
    MeSH term(s) A549 Cells ; Amino Acyl-tRNA Synthetases/antagonists & inhibitors ; Amino Acyl-tRNA Synthetases/metabolism ; Animals ; Cell Line, Tumor ; Female ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Mice ; Mice, Inbred BALB C ; Nuclear Proteins/antagonists & inhibitors ; Nuclear Proteins/metabolism ; Pyrimidines/chemistry ; Pyrimidines/pharmacology ; Pyrimidines/therapeutic use ; Treatment Outcome ; Xenograft Model Antitumor Assays/methods
    Chemical Substances AIMP2 protein, human ; Nuclear Proteins ; Pyrimidines ; Amino Acyl-tRNA Synthetases (EC 6.1.1.-)
    Language English
    Publishing date 2020-04-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218133-2
    ISSN 1520-4804 ; 0022-2623
    ISSN (online) 1520-4804
    ISSN 0022-2623
    DOI 10.1021/acs.jmedchem.9b01765
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  5. Article ; Online: Oligonucleotide-based Preconditioning of DCD Cardiac Donors and Its Impact on Cardiac Viability.

    Kearns, Mark J / Miller, Sally D / Kong, Hyejin J / Sirounis, Demetrios / Cheung, Anson / Bashir, Jamil / Seidman, Michael A / Boyd, John H

    Transplantation

    2019  Volume 103, Issue 12, Page(s) 2479–2485

    Abstract: Background: While clinical donation after circulatory death (DCD) cardiac transplantation is being implemented with increasing frequency to address the supply/demand mismatch of donor grafts, no research to date has examined a strategy of donor ... ...

    Abstract Background: While clinical donation after circulatory death (DCD) cardiac transplantation is being implemented with increasing frequency to address the supply/demand mismatch of donor grafts, no research to date has examined a strategy of donor preconditioning to optimize the viability of DCD hearts for transplantation. In our rat model of the DCD protocol, we investigate the impact of pretreating donors with phosphorothioate-linked cytosine and guanine rich oligodeoxynucleotides (CpG ODN) and their effects on cardiac function, injury, and a novel left ventricular (LV) mRNA biomarker panel.
    Methods: DCD rats were subjected to a withdrawal protocol, followed by 20 minutes of warm acirculatory standoff, representing a group of severely injured hearts as previously demonstrated. Beating heart controls and DCD rats were pretreated with vehicle or stimulatory CpG ODN (beating heart control and DCD stimulated with CpG ODN, BST and DST). Hearts were harvested for ex situ heart perfusion (ESHP), where LV function, histochemical injury, and differences in gene expression were characterized between groups.
    Results: Donor pretreatment with CpG ODN doubled the number of functional DCD hearts at ESHP. Pretreatment was associated with improved systolic and diastolic LV function, a reduction in histological injury, and markedly reduced elaboration of cardiac troponin-I in coronary effluent during ESHP. Pretreatment was also associated with a reduction in mRNA biomarkers associated with myocardial injury.
    Conclusions: A single dose of CpG ODN was associated with reduced biomarkers of cardiac injury and a 100% increase in cardiac viability in this rodent model of marginal DCD cardiac donation.
    MeSH term(s) Animals ; Disease Models, Animal ; Graft Rejection/physiopathology ; Graft Rejection/prevention & control ; Heart Transplantation/methods ; Myocardial Contraction/physiology ; Oligodeoxyribonucleotides/pharmacology ; Organ Preservation/methods ; Perfusion/methods ; Rats ; Rats, Sprague-Dawley ; Tissue Donors ; Ventricular Function, Left/physiology
    Chemical Substances CpG ODN 2395 ; Oligodeoxyribonucleotides
    Language English
    Publishing date 2019-07-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 208424-7
    ISSN 1534-6080 ; 0041-1337
    ISSN (online) 1534-6080
    ISSN 0041-1337
    DOI 10.1097/TP.0000000000002849
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    Zs.MO 509: Show issues

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  6. Article ; Online: Is Heparin-Binding Protein Inhibition a Mechanism of Albumin's Efficacy in Human Septic Shock?

    Fisher, Jane / Linder, Adam / Bentzer, Peter / Boyd, John / Kong, Hyejin Julia / Lee, Terry / Walley, Keith R / Russell, James A

    Critical care medicine

    2018  Volume 46, Issue 5, Page(s) e364–e374

    Abstract: Objectives: Our objectives were to determine first whether albumin prevents heparin-binding protein-induced increased endothelial cell permeability and renal cell inflammation and second, whether a plasma heparin-binding protein-to-albumin ratio ... ...

    Abstract Objectives: Our objectives were to determine first whether albumin prevents heparin-binding protein-induced increased endothelial cell permeability and renal cell inflammation and second, whether a plasma heparin-binding protein-to-albumin ratio predicts risk of acute kidney injury, fluid balance, and plasma cytokine levels in septic shock.
    Design: In vitro human endothelial and renal cell model and observation cohort of septic shock.
    Settings: Research laboratory and multicenter clinical trial (Vasopressin and Septic Shock Trial).
    Patients: Adult septic shock (norepinephrine dose > 5 μg/min for > 6 hr).
    Interventions: In vitro: heparin-binding protein (or thrombin) was added with or without albumin to 1) human endothelial cell monolayers to assess permeability and 2) to human renal tubular epithelial cells to assess inflammation.
    Measurements and main results: Transendothelial electrical resistance-a marker of permeability-of human endothelial cells was measured using a voltohmmeter. We measured plasma heparin-binding protein-to-albumin ratio and a panel of cytokines in septic shock patients (n = 330) to define an heparin-binding protein-to-albumin ratio that predicts risk of acute kidney injury. Albumin inhibited heparin-binding protein (and thrombin-induced) increased endothelial cell permeability at a threshold concentration of 20-30 g/L but increased renal tubular cell interleukin-6 release. Patients who developed or had worsened acute kidney injury had significantly higher heparin-binding protein-to-albumin ratio (1.6 vs 0.89; p < 0.001) and heparin-binding protein (38.2 vs 20.8 ng/mL; p < 0.001) than patients without acute kidney injury. The highest heparin-binding protein-to-albumin ratio (> 3.05), heparin-binding protein quartiles (> 69.8), and heparin-binding protein > 30 ng/mL were significantly associated with development or worsening of acute kidney injury (p < 0.001) in unadjusted and adjusted analyses and were robust to sensitivity analyses for death as a competing outcome. Heparin-binding protein and heparin-binding protein-to-albumin ratio were directly associated with positive fluid balance (p < 0.001) and with key inflammatory cytokines. Increasing quartiles of heparin-binding protein-to-albumin ratio and heparin-binding protein (but not albumin) were highly significantly associated with days alive and free of acute kidney injury and renal replacement therapy (p < 0.001), vasopressors (p < 0.001), ventilation (p < 0.001), and with 28-day mortality.
    Conclusions: Albumin inhibits heparin-binding protein-induced increased human endothelial cell permeability and heparin-binding protein greater than 30 ng/mL and heparin-binding protein-to-albumin ratio greater than 3.01-but not serum albumin-identified patients at increased risk for acute kidney injury in septic shock.
    MeSH term(s) Acute Kidney Injury/prevention & control ; Antimicrobial Cationic Peptides/antagonists & inhibitors ; Antimicrobial Cationic Peptides/blood ; Blood Proteins/antagonists & inhibitors ; Carrier Proteins/antagonists & inhibitors ; Carrier Proteins/blood ; Cell Line ; Cell Membrane Permeability/drug effects ; Cytokines/blood ; Endothelium, Vascular/cytology ; Endothelium, Vascular/drug effects ; Female ; Humans ; Kidney Tubules, Proximal/cytology ; Kidney Tubules, Proximal/drug effects ; Male ; Middle Aged ; Serum Albumin/analysis ; Serum Albumin/therapeutic use ; Shock, Septic/blood ; Shock, Septic/therapy ; Treatment Outcome
    Chemical Substances AZU1 protein, human ; Antimicrobial Cationic Peptides ; Blood Proteins ; Carrier Proteins ; Cytokines ; Serum Albumin
    Language English
    Publishing date 2018-02-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 197890-1
    ISSN 1530-0293 ; 0090-3493
    ISSN (online) 1530-0293
    ISSN 0090-3493
    DOI 10.1097/CCM.0000000000002996
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  7. Article: Erratum to: Heparin-binding protein is important for vascular leak in sepsis.

    Bentzer, Peter / Fisher, Jane / Kong, HyeJin Julia / Mörgelin, Mattias / Boyd, John H / Walley, Keith R / Russell, James A / Linder, Adam

    Intensive care medicine experimental

    2017  Volume 5, Issue 1, Page(s) 6

    Language English
    Publishing date 2017-01-20
    Publishing country Germany
    Document type Published Erratum
    ZDB-ID 2740385-3
    ISSN 2197-425X
    ISSN 2197-425X
    DOI 10.1186/s40635-017-0119-4
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  8. Article ; Online: Very Low Density Lipoprotein Receptor Sequesters Lipopolysaccharide Into Adipose Tissue During Sepsis.

    Shimada, Tadanaga / Topchiy, Elena / Leung, Alex K K / Kong, HyeJin J / Genga, Kelly R / Boyd, John H / Russell, James A / Oda, Shigeto / Nakada, Taka-Aki / Hirasawa, Hiroyuki / Walley, Keith R

    Critical care medicine

    2019  Volume 48, Issue 1, Page(s) 41–48

    Abstract: Objectives: Obese patients have lower sepsis mortality termed the "obesity paradox." We hypothesized that lipopolysaccharide, known to be carried within lipoproteins such as very low density lipoprotein, could be sequestered in adipose tissue during ... ...

    Abstract Objectives: Obese patients have lower sepsis mortality termed the "obesity paradox." We hypothesized that lipopolysaccharide, known to be carried within lipoproteins such as very low density lipoprotein, could be sequestered in adipose tissue during sepsis; potentially contributing a survival benefit.
    Design: Retrospective analysis.
    Setting: University research laboratory.
    Subjects and patients: Vldlr knockout mice to decrease very low density lipoprotein receptors, Pcsk9 knockout mice to increase very low density lipoprotein receptor, and Ldlr knockout mice to decrease low density lipoprotein receptors. Differentiated 3T3-L1 adipocytes. Caucasian septic shock patients.
    Interventions: We measured lipopolysaccharide uptake into adipose tissue 6 hours after injection of fluorescent lipopolysaccharide into mice. Lipopolysaccharide uptake and very low density lipoprotein receptor protein expression were measured in adipocytes. To determine relevance to humans, we genotyped the VLDLR rs7852409 G/C single-nucleotide polymorphism in 519 patients and examined the association of 28-day survival with genotype.
    Measurements and main results: Lipopolysaccharide injected into mice was found in adipose tissue within 6 hours and was dependent on very low density lipoprotein receptor but not low density lipoprotein receptors. In an adipocyte cell line decreased very low density lipoprotein receptor expression resulted in decreased lipopolysaccharide uptake. In septic shock patients, the minor C allele of VLDLR rs7852409 was associated with increased survival (p = 0.010). Previously published data indicate that the C allele is a gain-of-function variant of VLDLR which may increase sequestration of very low density lipoprotein (and lipopolysaccharide within very low density lipoprotein) into adipose tissue. When body mass index less than 25 this survival effect was accentuated and when body mass index greater than or equal to 25 this effect was diminished suggesting that the effect of variation in very low density lipoprotein receptor function is overwhelmed when copious adipose tissue is present.
    Conclusions: Lipopolysaccharide may be sequestered in adipose tissue via the very low density lipoprotein receptor and this sequestration may contribute to improved sepsis survival.
    MeSH term(s) Adipocytes/metabolism ; Adipose Tissue/metabolism ; Adult ; Aged ; Animals ; Cells, Cultured ; Female ; Humans ; Lipopolysaccharides/metabolism ; Male ; Mice ; Middle Aged ; Receptors, LDL/metabolism ; Retrospective Studies ; Sepsis/metabolism
    Chemical Substances Lipopolysaccharides ; Receptors, LDL ; VLDL receptor
    Language English
    Publishing date 2019-10-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 197890-1
    ISSN 1530-0293 ; 0090-3493
    ISSN (online) 1530-0293
    ISSN 0090-3493
    DOI 10.1097/CCM.0000000000004064
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  9. Article ; Online: Inhibition of Cholesteryl Ester Transfer Protein Preserves High-Density Lipoprotein Cholesterol and Improves Survival in Sepsis.

    Trinder, Mark / Wang, Yanan / Madsen, Christian M / Ponomarev, Tatjana / Bohunek, Lubos / Daisely, Brendan A / Julia Kong, HyeJin / Blauw, Lisanne L / Nordestgaard, Børge G / Tybjærg-Hansen, Anne / Wurfel, Mark M / Russell, James A / Walley, Keith R / Rensen, Patrick C N / Boyd, John H / Brunham, Liam R

    Circulation

    2020  Volume 143, Issue 9, Page(s) 921–934

    Abstract: Background: The high-density lipoprotein hypothesis of atherosclerosis has been challenged by clinical trials of cholesteryl ester transfer protein (CETP) inhibitors, which failed to show significant reductions in cardiovascular events. Plasma levels of ...

    Abstract Background: The high-density lipoprotein hypothesis of atherosclerosis has been challenged by clinical trials of cholesteryl ester transfer protein (CETP) inhibitors, which failed to show significant reductions in cardiovascular events. Plasma levels of high-density lipoprotein cholesterol (HDL-C) decline drastically during sepsis, and this phenomenon is explained, in part, by the activity of CETP, a major determinant of plasma HDL-C levels. We tested the hypothesis that genetic or pharmacological inhibition of CETP would preserve high-density lipoprotein levels and decrease mortality in clinical cohorts and animal models of sepsis.
    Methods: We examined the effect of a gain-of-function variant in
    Results: A fixed-effect meta-analysis of all 7 cohorts found that the
    Conclusions: Clinical genetics and humanized mouse models suggest that inhibiting CETP may preserve high-density lipoprotein levels and improve outcomes for individuals with sepsis.
    MeSH term(s) Animals ; Anticholesteremic Agents/therapeutic use ; Apolipoprotein A-I/blood ; Apolipoprotein E3/genetics ; Cholesterol Ester Transfer Proteins/antagonists & inhibitors ; Cholesterol Ester Transfer Proteins/genetics ; Cholesterol Ester Transfer Proteins/metabolism ; Cholesterol, HDL/blood ; Cytokines/metabolism ; Disease Models, Animal ; Female ; Gain of Function Mutation ; Humans ; Mice ; Mice, Transgenic ; Oxazolidinones/therapeutic use ; Placebo Effect ; Polymorphism, Single Nucleotide ; Risk Factors ; Sepsis/drug therapy ; Sepsis/mortality ; Sepsis/pathology ; Survival Rate
    Chemical Substances Anticholesteremic Agents ; Apolipoprotein A-I ; Apolipoprotein E3 ; CETP protein, human ; Cholesterol Ester Transfer Proteins ; Cholesterol, HDL ; Cytokines ; Oxazolidinones ; anacetrapib (P7T269PR6S)
    Language English
    Publishing date 2020-11-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.120.048568
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Correction: Lipopolysaccharide Is Cleared from the Circulation by Hepatocytes via the Low Density Lipoprotein Receptor.

    Topchiy, Elena / Cirstea, Mihai / Kong, HyeJin Julia / Boyd, John H / Wang, Yingjin / Russell, James A / Walley, Keith R

    PloS one

    2016  Volume 11, Issue 7, Page(s) e0160326

    Abstract: This corrects the article DOI: 10.1371/journal.pone.0155030.]. ...

    Abstract [This corrects the article DOI: 10.1371/journal.pone.0155030.].
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Published Erratum
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0160326
    Database MEDical Literature Analysis and Retrieval System OnLINE

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