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Journal articles on the topic 'APC model'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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1

Booth, JL, ES Duggan, VI Patel, et al. "ID: 106: ALVEOLAR ESCAPE BY BACILLUS ANTHRACIS SPORES DOES NOT REQUIRE A CARRIER CELL AND IS NOT ALTERED BY LETHAL TOXIN." Journal of Investigative Medicine 64, no. 4 (2016): 960.2–961. http://dx.doi.org/10.1136/jim-2016-000120.101.

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RationaleThe lung is the entry site for Bacillus anthracis in inhalation anthrax, the most deadly form of the disease. B. anthracis spores must escape from the alveolus, pass to the regional lymph nodes, germinate and enter the circulatory system as vegetative bacteria to cause systemic disease. Of the resident lung cells, three have been reported to take up B. anthracis spores: the antigen presenting cells (APC) alveolar macrophages and dendritic cells, and alveolar epithelial cells (AEC). Also, B. anthracis produces the exotoxins lethal factor and protective antigen (PA) which combine to for

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Kulkarni, Kiran, Ziguo Zhang, Leifu Chang, Jing Yang, Paula C. A. da Fonseca, and David Barford. "Building a pseudo-atomic model of the anaphase-promoting complex." Acta Crystallographica Section D Biological Crystallography 69, no. 11 (2013): 2236–43. http://dx.doi.org/10.1107/s0907444913018593.

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The anaphase-promoting complex (APC/C) is a large E3 ubiquitin ligase that regulates progression through specific stages of the cell cycle by coordinating the ubiquitin-dependent degradation of cell-cycle regulatory proteins. Depending on the species, the active form of the APC/C consists of 14–15 different proteins that assemble into a 20-subunit complex with a mass of approximately 1.3 MDa. A hybrid approach of single-particle electron microscopy and protein crystallography of individual APC/C subunits has been applied to generate pseudo-atomic models of various functional states of the comp

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Zeng, Biqing, Feng Zeng, Heng Yang, Wu Zhou, and Ruyang Xu. "Multi-task learning model for aspect term extraction and aspect polarity classification based on dual-labels." Journal of Intelligent & Fuzzy Systems 39, no. 3 (2020): 2763–74. http://dx.doi.org/10.3233/jifs-191047.

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Aspect-based sentiment analysis (ABSA) is a hot and significant task of natural language processing, which is composed of two subtasks, the aspect term extraction (ATE) and aspect polarity classification (APC). Previous researches generally studied two subtasks independently and designed neural network models for ATE and APC respectively. However, it integrates various manual features into the model, which will consume plenty of computing resources and labor. Moreover, the quality of the ATE results will affect the performance of APC. This paper proposes a multi-task learning model based on du

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Swietlicki, Elzbieta A., Shashi Bala, Jianyun Lu, et al. "Epimorphin deletion inhibits polyposis in the Apcmin/+ mouse model of colon carcinogenesis via decreased myofibroblast HGF secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 305, no. 8 (2013): G564—G572. http://dx.doi.org/10.1152/ajpgi.00486.2012.

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Interactions between the epithelium and surrounding mesenchyme/stroma play an important role in normal gut morphogenesis, the epithelial response to injury, and epithelial carcinogenesis. The tumor microenvironment, composed of stromal cells including myofibroblasts and immune cells, regulates tumor growth and the cancer stem cell niche. Deletion of epimorphin (Epim), a syntaxin family member expressed in myofibroblasts and macrophages, results in partial protection from colitis and from inflammation-induced colon cancer in mice. We sought to determine whether epimorphin deletion protects from

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Luo, Liying, and James S. Hodges. "Constraints in Random Effects Age-Period-Cohort Models." Sociological Methodology 50, no. 1 (2020): 276–317. http://dx.doi.org/10.1177/0081175020903348.

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Random effects (RE) models have been widely used to study the contextual effects of structures such as neighborhoods or schools. The RE approach has recently been applied to age-period-cohort (APC) models that are unidentified because the predictors are exactly linearly dependent. However, research has not fully explained how the RE specification identifies these otherwise unidentified APC models. We address this challenge by first making explicit that RE-APC models have greater—not less—rank deficiency than the traditional fixed-effects model, followed by two empirical examples. We then provi

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Arnljots, Björn, David Bergqvist, and Björn Dahlbäck. "Inhibition of Microarterial Thrombosis by Activated Protein C in a Rabbit Model." Thrombosis and Haemostasis 72, no. 03 (1994): 415–20. http://dx.doi.org/10.1055/s-0038-1648881.

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SummaryProtein C is the key component in a natural anticoagulant pathway. After its activation by the thrombin-thrombomodulin complex, it degrades the activated forms of coagulation cofactors VIII and V, which leads to downregulation of the coagulation process. Due to its specific anticoagulant activity, activated protein C (APC) is potentially interesting as an antithrombotic agent. The effect of bovine activated protein C on thrombus formation and haemostasis was investigated in a rabbit model of microarterial thrombosis. Segments of both central ear arteries were prepared and blood-flow int

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Zhang, Yongke, and Emma Lees. "Identification of an Overlapping Binding Domain on Cdc20 for Mad2 and Anaphase-Promoting Complex: Model for Spindle Checkpoint Regulation." Molecular and Cellular Biology 21, no. 15 (2001): 5190–99. http://dx.doi.org/10.1128/mcb.21.15.5190-5199.2001.

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ABSTRACT Activation of the anaphase-promoting complex (APC) is required for anaphase initiation and for exit from mitosis in mammalian cells. Cdc20, which specifically recognizes APC substrates involved in the metaphase-to-anaphase transition, plays a pivotal role in APC activation through direct interaction with the APC. The activation of the APC by Cdc20 is prevented by the interaction of Cdc20 with Mad2 when the spindle checkpoint is activated. Using deletion mutagenesis and peptide mapping, we have identified the sequences in Cdc20 that target it to Mad2 and the APC, respectively. These se

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Hoogendoorn, H., ME Nesheim, and AR Giles. "A qualitative and quantitative analysis of the activation and inactivation of protein C in vivo in a primate model." Blood 75, no. 11 (1990): 2164–71. http://dx.doi.org/10.1182/blood.v75.11.2164.2164.

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Abstract A model of Protein C (PC) activation in vivo was used to investigate the complexing of activated PC (APC) with its plasma inhibitors, PC inhibitor (PCI) and alpha 1-antitrypsin (alpha 1AT). Chimpanzees were infused with a bolus of activated factor X (F.Xa) together with vesicles of phosphatidylcholine and phosphatidylserine (PCPS). Pre- and post-infusion plasma samples were analyzed using enzyme linked immunosorbent based assays (ELISA) for PC and APC complexes, and immunoblotting of PC from nondenaturing polyacrylamide gel electrophoresis. Within 2 minutes of infusion, a 60% decrease

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Hoogendoorn, H., ME Nesheim, and AR Giles. "A qualitative and quantitative analysis of the activation and inactivation of protein C in vivo in a primate model." Blood 75, no. 11 (1990): 2164–71. http://dx.doi.org/10.1182/blood.v75.11.2164.bloodjournal75112164.

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A model of Protein C (PC) activation in vivo was used to investigate the complexing of activated PC (APC) with its plasma inhibitors, PC inhibitor (PCI) and alpha 1-antitrypsin (alpha 1AT). Chimpanzees were infused with a bolus of activated factor X (F.Xa) together with vesicles of phosphatidylcholine and phosphatidylserine (PCPS). Pre- and post-infusion plasma samples were analyzed using enzyme linked immunosorbent based assays (ELISA) for PC and APC complexes, and immunoblotting of PC from nondenaturing polyacrylamide gel electrophoresis. Within 2 minutes of infusion, a 60% decrease in nonac

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Fosse, Ethan, and Christopher Winship. "Analyzing Age-Period-Cohort Data: A Review and Critique." Annual Review of Sociology 45, no. 1 (2019): 467–92. http://dx.doi.org/10.1146/annurev-soc-073018-022616.

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Age-period-cohort (APC) analysis has a long, controversial history in sociology and related fields. Despite the existence of hundreds, if not thousands, of articles and dozens of books, there is little agreement on how to adequately analyze APC data. This article begins with a brief overview of APC analysis, discussing how one can interpret APC effects in a causal way. Next, we review methods that obtain point identification of APC effects, such as the equality constraints model, Moore-Penrose estimators, and multilevel models. We then outline techniques that entail point identification using

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Von Drygalski, Annette, Andrew J. Gale, Laurent Burnier, Thomas J. Cramer, John H. Griffin, and Laurent O. Mosnier. "An Engineered Factor Fva Prevents Bleeding Induced By Anticoagulant Wild Type Activated Protein C." Blood 122, no. 21 (2013): 203. http://dx.doi.org/10.1182/blood.v122.21.203.203.

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Abstract Increased risk of bleeding is observed in patients receiving therapy with a variety of anticoagulant drugs, and there is an unmet need for prohemostatic agents that reduce bleeding risk. In some clinical trials, wild type (wt) APC therapy was associated with an increased risk of serious bleeding. In most animal models of inflammatory injury and disease where APC was beneficial, APC’s cytoprotective effects were responsible for the protective effects of APC therapy whereas its anticoagulant effects were neither required nor contributing. Thus, wt APC’s anticoagulant activities and asso

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Kerschen, Edward J., Brian C. Cooley, Francis J. Castellino, John H. Griffin, and Hartmut Weiler. "Protective Effect of Activated Protein C in Murine Endotoxemia: Mechanism of Action." Blood 106, no. 11 (2005): 26. http://dx.doi.org/10.1182/blood.v106.11.26.26.

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Abstract Recombinant activated protein C (APC) reduces mortality of patients with severe inflammatory disease associated with multi-organ failure. APC exerts anticoagulant, anti-inflammatory, and cytoprotective effects. The contribution of these distinct APC activities to the overall therapeutic efficacy in septic patients is unknown. The aim of the study is to delineate the mechanism underlying the protective effect of APC in mouse endotoxemia. We first establish an experimental mouse model to demonstrate that recombinant murine APC reduces 6 day mortality of mice subjected to LPS-induced end

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Gruber, A., JH Griffin, LA Harker, and SR Hanson. "Inhibition of platelet-dependent thrombus formation by human activated protein C in a primate model." Blood 73, no. 3 (1989): 639–42. http://dx.doi.org/10.1182/blood.v73.3.639.639.

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Abstract The in vivo antithrombotic properties of human plasma activated protein C (APC), a natural anticoagulant enzyme, were investigated in a baboon model of thrombus formation on prosthetic vascular grafts. Infusion of 0.25 to 1.1 mg/kg/h purified, human, APC inhibited blood clotting, as measured by the activated partial thromboplastin time (APTT), and reduced vascular graft platelet deposition by 40% to 70%, as determined by the real-time scintillation camera imaging of 111In-labeled platelet deposition. APC infusion also preserved graft patency. Hemostatic plug formation remained normal,

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Gruber, A., JH Griffin, LA Harker, and SR Hanson. "Inhibition of platelet-dependent thrombus formation by human activated protein C in a primate model." Blood 73, no. 3 (1989): 639–42. http://dx.doi.org/10.1182/blood.v73.3.639.bloodjournal733639.

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The in vivo antithrombotic properties of human plasma activated protein C (APC), a natural anticoagulant enzyme, were investigated in a baboon model of thrombus formation on prosthetic vascular grafts. Infusion of 0.25 to 1.1 mg/kg/h purified, human, APC inhibited blood clotting, as measured by the activated partial thromboplastin time (APTT), and reduced vascular graft platelet deposition by 40% to 70%, as determined by the real-time scintillation camera imaging of 111In-labeled platelet deposition. APC infusion also preserved graft patency. Hemostatic plug formation remained normal, as measu

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Linden, M. D., M. Schneider, and W. N. Erber. "Factor VLEIDEN and cardiopulmonary bypass: investigation of haemostatic parameters and the effect of aprotinin using an ex vivo model." Perfusion 16, no. 6 (2001): 476–84. http://dx.doi.org/10.1177/026765910101600607.

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It has been suggested that aprotinin results in significantly increased risk for perioperative thrombotic complications in patients with Factor VLEIDEN (F5L) due to its ability to competitively inhibit activated protein C (APC) function in vitro. No clinical studies have been performed to assess the effect of aprotinin on APC function of F5L in vivo. We developed an ex vivo model to mimic the effects of cardiopulmonary bypass with the exclusion of the patient in order to assess APC function. Blood from normal ( n = 2) and F5L heterozygous donors ( n = 2) was treated with aprotinin or placebo (

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Mosnier, Laurent O., Jose A. Fernandez, Antonella Zampolli, Xia V. Yang, Zaverio M. Ruggeri, and John H. Griffin. "In Vivo Anti-Thrombotic Potency of Engineered Activated Protein C Variants." Blood 110, no. 11 (2007): 2704. http://dx.doi.org/10.1182/blood.v110.11.2704.2704.

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Abstract Activated protein C (APC) has both anticoagulant activity via inactivation of factors Va and VIIIa and cytoprotective activities on cells that include anti-apoptotic and anti-inflammatory activities, alterations of gene expression profiles and protection of endothelial barrier function. The relative importance of APC’s anticoagulant activity vs. APC’s direct cytoprotective effects on cells for reduction of mortality in severe sepsis patients and protective effects in animal injury models is not entirely clear. In this current study, genetically engineered APC variants with different a

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Souris, Jeffrey S., Hannah J. Zhang, Urszula Dougherty, et al. "A novel mouse model of sporadic colon cancer induced by combination of conditional Apc genes and chemical carcinogen in the absence of Cre recombinase." Carcinogenesis 40, no. 11 (2019): 1376–86. http://dx.doi.org/10.1093/carcin/bgz050.

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AbstractAlthough valuable insights into colon cancer biology have been garnered from human colon cancer cell lines and primary colonic tissues, and animal studies using human colon cancer xenografts, immunocompetent mouse models of spontaneous or chemically induced colon cancer better phenocopy human disease. As most sporadic human colon tumors present adenomatous polyposis coli (APC) gene mutations, considerable effort has gone into developing mice that express mutant Apc alleles that mimic human colon cancer pathogenesis. A serious limitation of many of these Apc-mutant murine models, howeve

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Kerschen, Edward J., Brian C. Cooley, Francis J. Castellino, et al. "Mechanisms for Mortality Reduction by Activated Protein C in Severe Sepsis." Blood 108, no. 11 (2006): 1. http://dx.doi.org/10.1182/blood.v108.11.1.1.

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Abstract Recombinant wild type (wt) activated protein C (APC) reduces patient mortality in severe sepsis and multi-organ failure. APC can exert both anticoagulant activity and direct cytoprotective effects on cells (anti-inflammatory, anti-apoptotic, endothelial barrier stabilization, etc.). The contribution of distinct APC activities to the overall therapeutic efficacy in septic patients is unknown. Lethal mouse endotoxemia (i.p. LPS administration) and bacterial sepsis (i.p. Staphylococcus aureus) models were used to clarify mechanisms for APC’s beneficial mortality reduction effects and to

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Uneno, Yu, Tadayuki Kou, Masashi Kanai, et al. "Prognostic model for survival in patients with advanced pancreatic cancer receiving palliative chemotherapy." Journal of Clinical Oncology 33, no. 3_suppl (2015): 248. http://dx.doi.org/10.1200/jco.2015.33.3_suppl.248.

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248 Background: The prognosis of patients with advanced pancreatic cancer (APC) is extremely poor. Several clinical and laboratory factors have been known to be associated with prognosis of APC patients. However, there are few clinically available prognostic models predicting survival in APC patients receiving palliative chemotherapy. Methods: To construct a prognostic model to predict survival in APC patients receiving palliative chemotherapy, we analyzed the clinical data from 306 consecutive patients with pathologically confirmed APC who received palliative chemotherapy. We selected six ind

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Lazic, Divna, Abhay P. Sagare, Angeliki M. Nikolakopoulou, John H. Griffin, Robert Vassar, and Berislav V. Zlokovic. "3K3A-activated protein C blocks amyloidogenic BACE1 pathway and improves functional outcome in mice." Journal of Experimental Medicine 216, no. 2 (2019): 279–93. http://dx.doi.org/10.1084/jem.20181035.

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3K3A-activated protein C (APC), a cell-signaling analogue of endogenous blood serine protease APC, exerts vasculoprotective, neuroprotective, and anti-inflammatory activities in rodent models of stroke, brain injury, and neurodegenerative disorders. 3K3A-APC is currently in development as a neuroprotectant in patients with ischemic stroke. Here, we report that 3K3A-APC inhibits BACE1 amyloidogenic pathway in a mouse model of Alzheimer’s disease (AD). We show that a 4-mo daily treatment of 3-mo-old 5XFAD mice with murine recombinant 3K3A-APC (100 µg/kg/d i.p.) prevents development of parenchyma

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Livnat, Tami, Yael Nisgav, Ivan Budnik, et al. "Activated Protein C Induces Stabilization of the Outer Retinal Barrier and Inhibits Laser Induced Choroidal Neovascularization in a Murine Model." Blood 132, Supplement 1 (2018): 73. http://dx.doi.org/10.1182/blood-2018-99-111375.

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Abstract Introduction: Age-related macular degeneration (AMD) is considered one of the main causes of severe vision loss in older adults. Wet AMD is characterized by choroidal neovascular membrane developed under or into the sensory retina, breaking the outer blood-retina barrier (oBRB) and causing leakage and bleeding. Protein C (PC) is a plasma serine protease zymogen whose active form, activated protein C (APC), exerts diverse homeostatic cell signaling pathways apart from its anticoagulant activity. APC activities are mediated mainly through endothelial PC receptor (EPCR) and protease acti

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Wang, Chongkai, Ching Ouyang, Jaideep Singh Sandhu, Michael Kahn, and Marwan Fakih. "Wild-type APC and prognosis in metastatic colorectal cancer." Journal of Clinical Oncology 38, no. 4_suppl (2020): 223. http://dx.doi.org/10.1200/jco.2020.38.4_suppl.223.

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223 Background: Somatic mutations at adenomatous polyposis coli ( APC) gene, found in ~75% of colorectal cancers (CRC), are under-represented in microsatellite instable (MSI-H) tumors. While several studies have suggested worse outcomes for CRC patients (pts) with wild-type APC ( APC-WT), the prognostic implication of this genomic alteration in metastatic CRC (mCRC) is not well defined. Methods: APC prognostic value was evaluated in 331 stage IV microsatellite stable (MSS) CRC pts treated in our institution. Next-generation genomic analysis (FoundationOne) was used to characterize the molecula

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Teixeira da Silva, Jaime A. "Three new suggested guidelines for increased transparency regarding open access article processing charges (APCs)." Epistēmēs Metron Logos, no. 4 (July 21, 2020): 4. http://dx.doi.org/10.12681/eml.24208.

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The article processing charge (APC) lies at the heart of the gold open access (GOA) business model. Small and larger society-based, as well as commercial publishers, rely – to different extents – on the APC and the GOA model to thrive. There is wide debate regarding what amount of APC is considered to be exploitative, and the issue of low APCs is often erroneously associated with “predatory” OA publishing. Independent of this debate, there is still, surprisingly, considerable opacity related to the APC used to cover the cost of GOA. In a bid to increase transparency, a simple 3-point plan at i

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Tucker, Erik I., Melani Helm, Owen JT McCarty, Sawan Hurst, David Gailani, and Andras Gruber. "Factor XI Inhibitor Antibody Treatment Improves Survival In a Murine Polymicrobial Sepsis Model." Blood 116, no. 21 (2010): 820. http://dx.doi.org/10.1182/blood.v116.21.820.820.

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Abstract Abstract 820 Sepsis results in a systemic inflammatory state that is frequently accompanied by intravascular coagulation and fibrinolysis, resulting in a coagulopathy with thrombotic and hemorrhagic components (disseminated intravascular coagulation– DIC). We have shown that the plasma coagulation protease factor XI (FXI) contributes substantially to experimental thrombus formation in baboons and mice, but does not appear to be essential for hemostasis. These results are supported by studies in human populations that show FXI deficiency confers a decreased risk of thrombotic ischemic

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Kwak, Kyeongmin, Sung-il Cho, and Domyung Paek. "Future Incidence of Malignant Mesothelioma in South Korea: Updated Projection to 2038." International Journal of Environmental Research and Public Health 18, no. 12 (2021): 6614. http://dx.doi.org/10.3390/ijerph18126614.

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Malignant mesothelioma (MM) is a cancer that is largely caused by exposure to asbestos. Although asbestos is no longer used in South Korea, the incidence of MM continues to increase due to its long latent period. We aimed to update the previous prediction of MM incidence until 2038. We predicted the incidence of MM over the next 20 years (2019–2038) in South Korea using Møller’s age–period–cohort (APC) model and a Poisson regression model based on asbestos consumption. The APC model predicted that the crude incidence rate would increase sharply in men and slowly in women. Despite the sex discr

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Vleminckx, Kris, Ellen Wong, Kathy Guger, Bonnee Rubinfeld, Paul Polakis, and Barry M. Gumbiner. "Adenomatous Polyposis Coli Tumor Suppressor Protein Has Signaling Activity in Xenopus laevis Embryos Resulting in the Induction of an Ectopic Dorsoanterior Axis." Journal of Cell Biology 136, no. 2 (1997): 411–20. http://dx.doi.org/10.1083/jcb.136.2.411.

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Mutations in the adenomatous polyposis coli (APC) tumor suppressor gene are linked to both familial and sporadic human colon cancer. So far, a clear biological function for the APC gene product has not been determined. We assayed the activity of APC in the early Xenopus embryo, which has been established as a good model for the analysis of the signaling activity of the APC-associated protein β-catenin. When expressed in the future ventral side of a four-cell embryo, full-length APC induced a secondary dorsoanterior axis and the induction of the homeobox gene Siamois. This is similar to the phe

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Lane, Steven W., Stephen M. Sykes, Fatima Al-Shahrour, et al. "The Apcmin mouse has altered hematopoietic stem cell function and provides a model for MPD/MDS." Blood 115, no. 17 (2010): 3489–97. http://dx.doi.org/10.1182/blood-2009-11-251728.

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Abstract Apc, a negative regulator of the canonical Wnt signaling pathway, is a bona-fide tumor suppressor whose loss of function results in intestinal polyposis. APC is located in a commonly deleted region on human chromosome 5q, associated with myelodysplastic syndrome (MDS), suggesting that haploinsufficiency of APC contributes to the MDS phenotype. Analysis of the hematopoietic system of mice with the Apcmin allele that results in a premature stop codon and loss of function showed no abnormality in steady state hematopoiesis. Bone marrow derived from Apcmin mice showed enhanced repopulatio

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Livnat, Tami, Yehonatan Weinberger, José A. Fernández, et al. "Activated Protein C (APC) and 3K3A-APC-Induced Regression of Choroidal Neovascularization (CNV) Is Accompanied by Vascular Endothelial Growth Factor (VEGF) Reduction." Biomolecules 11, no. 3 (2021): 358. http://dx.doi.org/10.3390/biom11030358.

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The activated protein C (APC) ability to inhibit choroidal neovascularization (CNV) growth and leakage was recently shown in a murine model. A modified APC, 3K3A-APC, was designed to reduce anticoagulant activity while maintaining full cytoprotective properties, thus diminishing bleeding risk. We aimed to study the ability of 3K3A-APC to induce regression of CNV and evaluate vascular endothelial growth factor (VEGF) role in APC’s activities in the retina. CNV was induced by laser photocoagulation on C57BL/6J mice. APC and 3K3A-APC were injected intravitreally after verification of CNV presence

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Kowalska, M. Anna, Shawn A. Mahmud, Michele P. Lambert, Mortimer Poncz, and Arne Slungaard. "Endogenous platelet factor 4 stimulates activated protein C generation in vivo and improves survival after thrombin or lipopolysaccharide challenge." Blood 110, no. 6 (2007): 1903–5. http://dx.doi.org/10.1182/blood-2007-03-081901.

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AbstractPharmacologic infusion of activated protein C (APC) improves survival in severe sepsis, and platelet factor 4 (PF4) accelerates APC generation in a primate thrombin-infusion model. We now tested whether endogenous platelet PF4 content affects APC generation. Mice completely deficient in PF4 (mPF4−/−) had impaired APC generation and survival after thrombin infusion, similar to the impairment seen in heterozygote protein C–deficient (PC+/−) mice. Transgenic mice overexpressing human PF4 (hPF4+) had increased plasma APC generation. Overexpression of platelet PF4 compensated for the defect

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van ’t Veer, Cornelis, Joris Roelofs, Bruce Gerlitz, et al. "Recombinant activated protein C attenuates coagulopathy and inflammation when administered early in murine pneumococcal pneumonia." Thrombosis and Haemostasis 106, no. 12 (2011): 1189–96. http://dx.doi.org/10.1160/th11-06-0438.

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SummaryRecombinant human activated protein C (APC), which has both anticoagulant and anti-inflammatory properties, improves survival of patients with severe sepsis. This beneficial effect is especially apparent in patients with pneumococcal pneumonia. Earlier treatment with APC in sepsis has been associated with a better therapeutic response as compared to later treatment. In a mouse model it was recently confirmed that recombinant murine (rm-)APC decreases coagulation activation and improves survival in pneumococcal pneumonia; however, APC did not impact on the inflammatory response. The aim

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Nold-Petry, Claudia, Doris Fischer, Bernd Richter, et al. "Activated protein C downregulates p38 mitogen-activated protein kinase and improves clinical parameters in an in-vivo model of septic shock." Thrombosis and Haemostasis 98, no. 11 (2007): 1118–26. http://dx.doi.org/10.1160/th07-01-0052.

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SummaryDespite the success of the anti-coagulant protease protein C (PC) in treating septic shock in humans, the signaling pathways used are still unclear. To explore the effects of treatment with PC zymogen and its activated form aPC in a setting of sepsis, we employed a piglet model of endotoxic shock. In the aPC group, we observed a 65%-90% reduction in plasmaTNF-alpha levels and a concomitant clinical improvement. Unexpectedly, administration of aPC also resulted in stabilization of the plasma pH above 7.2. Moreover, phosphorylated p38 mitogen-activated protein kinase (p38MAPK) was virtual

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Borges, Anne Karin da Mota, Adalberto Miranda-Filho, Sérgio Koifman, and Rosalina Jorge Koifman. "Thyroid Cancer Incidences From Selected South America Population-Based Cancer Registries: An Age-Period-Cohort Study." Journal of Global Oncology, no. 4 (December 2018): 1–11. http://dx.doi.org/10.1200/jgo.17.00024.

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Purpose The incidence of thyroid cancer (TC) has increased substantially worldwide. However, there is a lack of knowledge about age-period-cohort (APC) effects on incidence rates in South American countries. This study describes the TC incidence trends and analyzes APC effects in Cali, Colombia; Costa Rica; Goiânia, Brazil; and Quito, Ecuador. Materials and Methods Data were obtained from the Cancer Incidence in Five Continents series, and the crude and age-standardized incidence rates were calculated. Trends were assessed using the estimated annual percentage change, and APC models were estim

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Tanner, Scott M., Joseph G. Daft, Stephanie A. Hill, Colin A. Martin, and Robin G. Lorenz. "Altered T-Cell Balance in Lymphoid Organs of a Mouse Model of Colorectal Cancer." Journal of Histochemistry & Cytochemistry 64, no. 12 (2016): 753–67. http://dx.doi.org/10.1369/0022155416672418.

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The adenomatous polyposis coli ( APC) gene is a known tumor suppressor gene, and mice with mutations in Apc (ApcMin/+) spontaneously form multiple intestinal neoplasms. In this model of human colorectal cancer (CRC), it has been reported that CD4+ T-cell-derived interleukin 17 (IL-17) promotes intestinal tumor development, but it is not known if the Apc mutation actually directly alters T-cell function and subsequently tumor immunosurveillance. To investigate the ApcMin/+ mutation on T-cell function, flow cytometric, histochemical, and immunofluorescent studies on both wild-type (Apc+/+) and A

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Pellequer, Jean-Luc, Andrew Gale, Elizabeth Getzoff, and John Griffin. "Three-dimensional Model of Coagulation Factor Va Bound to Activated Protein C." Thrombosis and Haemostasis 84, no. 11 (2000): 849–57. http://dx.doi.org/10.1055/s-0037-1614127.

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SummaryA complete molecular model of blood coagulation factor Va (FVa) bound to anticoagulant activated protein C (APC) and to a phospholipid membrane was constructed. The three homologous A domains and the two homologous C domains of FVA were modeled based on the X-ray crystallographic structures of ceruloplasmin and C2 domain of factor V, respectively. The final arrangement of the five domains in the complete FVa model bound to a membrane incorporated extensive published experimental data. FVa binds the phospholipid membrane through its C2 domain while the A-domain trimer is located from 40

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Meledeo, Michael A., James E. Campbell, Armando C. Rodriguez, Melanie V. Valenciana, and Andrew P. Cap. "Activated Protein C Levels Found In Trauma Patients Are Insufficient To Inactivate Platelet Factor Va and Produce Coagulopathy In An In Vitro Model." Blood 122, no. 21 (2013): 4767. http://dx.doi.org/10.1182/blood.v122.21.4767.4767.

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Background A subset of severe trauma victims suffering from uncontrolled hemorrhage present to the emergency room with an acute coagulopathy of trauma (ACoT). This condition occurs within the first 30 min following injury, is not the result of resuscitation-associated dilutional effects, and is defined by an INR > 1.2. The mechanisms behind this coagulopathy have not been completely identified, but recent studies posit that the exuberant activation of protein C is a key contributor to ACoT. Protein C is activated through the interaction of thrombin and thrombomodulin on the endothelial surf

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Lu, Xiyuan, Hong Liu, Lianguo Wang та Saul Schaefer. "Activation of NF-κB is a critical element in the antiapoptotic effect of anesthetic preconditioning". American Journal of Physiology-Heart and Circulatory Physiology 296, № 5 (2009): H1296—H1304. http://dx.doi.org/10.1152/ajpheart.01282.2008.

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Anesthetic preconditioning (APC), defined as brief exposure to inhalational anesthetics before cardiac ischemia-reperfusion (I/R), limits injury in both animal models and in humans. APC can result in the production of reactive oxygen species (ROS), and prior work has shown that APC can modify activation of NF-κB during I/R, with consequent reduction in the expression of inflammatory mediators. However, the role of NF-κB activation before I/R is unknown. Therefore, these experiments tested the hypothesis that APC-induced ROS results in activation of NF-κB before I/R, with consequent increased e

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Madhusudhan, Thati, Hongjie Wang, Sandra Müller-Krebs, et al. "PAR-3 Activation by Activated Protein C: a Novel Podocyte Protective Signalling Pathway." Blood 116, no. 21 (2010): 329. http://dx.doi.org/10.1182/blood.v116.21.329.329.

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Abstract Abstract 329 Activated protein C (APC) has anti-coagulant and cytoprotective effects. Recently we have shown that APC protects against diabetic nephropathy by inhibiting endothelial and podocyte apoptosis. The cytoprotecive effects of APC in endothelial cells require endothelial protein C receptor (EPCR) and protease activated recetor-1 (PAR-1). However, the signalling mechanism through which APC exerts its cytoprotective effects in podocytes is not known. Here we have used a mouse model of LPS-mediated podocyte injury and show that APC protects against LPS induced podocyte apoptosis

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Montalvo Corral, Maricela, Lucinda Puebla Clark, Guadalupe López Robles, Itzel Reyes Duarte, Guillermo López Cervantes, and Silvia Yolanda Moya Camarena. "Conjugated linoleic acid enhances intestinal mucosal innate immunity against parasite Giardia lamblia in a murine model." Nova Scientia 10, no. 21 (2018): 228–46. http://dx.doi.org/10.21640/ns.v10i21.1578.

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Introduction: Giardia lamblia, a protozoan intestinal parasite is able to evade or suppress defense mechanisms, such as innate response. Antigen presenting cells (APC) like dendritic cells may orchestrate an immune response and support a more effective adaptive defense. Conjugated linoleic acid (CLA), a dietary lipid, has shown biological activity on APC. The aim was to evaluate the effect of CLA in intestinal innate response measuring the frequency of mucosal APC populations in Giardia lamblia murine infection.Method: The giardiasis infection model was established in C3H/HeN mice (n=32), and

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Maitra, Radhashree, Thongthai Thavornwatanayong, Madhu Kumar Venkatesh, et al. "Development and Characterization of a Genetic Mouse Model of KRAS Mutated Colorectal Cancer." International Journal of Molecular Sciences 20, no. 22 (2019): 5677. http://dx.doi.org/10.3390/ijms20225677.

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Patients with KRAS mutated colorectal cancer (CRC) represent a cohort with unmet medical needs, with limited options of FDA-approved therapies. Representing 40–45% of all CRC patients, they are considered ineligible to receive anti-EGFR monoclonal antibodies that have added a significant therapeutic benefit for KRAS wild type CRC patients. Although several mouse models of CRC have been developed during the past decade, one genetically resembling the KRAS mutated CRC is yet to be established. In this study C57 BL/6 mice with truncated adenomatous polyposis coli (APC) floxed allele was crossed w

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Okonogi, Siriporn, Pimpak Phumat, Sakornrat Khongkhunthian, Pisaisit Chaijareenont, Thomas Rades, and Anette Müllertz. "Development of Self-Nanoemulsifying Drug Delivery Systems Containing 4-Allylpyrocatechol for Treatment of Oral Infections Caused by Candida albicans." Pharmaceutics 13, no. 2 (2021): 167. http://dx.doi.org/10.3390/pharmaceutics13020167.

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Clinical use of 4-Allylpyrocatechol (APC), a potential antifungal agent from Piper betle, is limited because of its low water solubility. The current study explores the development of the self-nanoemulsifying drug delivery system (SNEDDS) containing APC (APC-SNEDDS) to enhance APC solubility. Results demonstrated that excipient type and concentration played an important role in the solubility of APC in the obtained SNEEDS. SNEDDS, comprising 20% Miglyol 812N, 30% Maisine 35-1, 40% Kolliphor RH40, and 10% absolute ethanol, provided the highest loading capacity and significantly increased water

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Lee, Margaret S., Karen A. D'Amour та Jackie Papkoff. "A yeast model system for functional analysis of β-catenin signaling". Journal of Cell Biology 158, № 6 (2002): 1067–78. http://dx.doi.org/10.1083/jcb.200204063.

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We have developed a novel Saccharomyces cerevisiae model system to dissect the molecular events of β-catenin (β-cat) signaling. Coexpression of mammalian β-cat with TCF4 or LEF1 results in nuclear accumulation of these proteins and a functional complex that activates reporter gene transcription from constructs containing leukocyte enhancer factor (LEF)/T cell factor (TCF) response elements. Reporter transcription is constitutive, requires expression of both β-cat and TCF4 or LEF1, and is not supported by mutated LEF/TCF binding elements or by TCF4 or LEF1 mutants. A cytoplasmic domain of E-cad

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Lee, Chang Moo, Hyun Tae Joo, and Je Sun Han. "Forecasting Long-term Housing Demand based on APC Model." Korean Association for Housing Policy Studies 25, no. 1 (2017): 5–34. http://dx.doi.org/10.24957/hsr.2017.25.1.05.

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Stoddart, Angela, Jianghong Wang, Chunmei Hu, et al. "Inhibition of WNT signaling in the bone marrow niche prevents the development of MDS in the Apcdel/+ MDS mouse model." Blood 129, no. 22 (2017): 2959–70. http://dx.doi.org/10.1182/blood-2016-08-736454.

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Key Points Loss of 1 copy of Ctnnb1 (encoding β-catenin) in an Apc-haploinsufficient microenvironment prevents the development of MDS. Modulation of WNT signaling in the niche using pyrvinium inhibits the development of MDS in Apc-haploinsufficient mice.

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Schuettrumpf, Joerg, Alexander Schlachterman, Jianxiang Zou, Christian Furlan Freguia, Stefano Baila, and Valder R. Arruda. "Assessing the Role of Continuous Activated Protein C (APC) Expression in Murine Thrombosis Models." Blood 106, no. 11 (2005): 1030. http://dx.doi.org/10.1182/blood.v106.11.1030.1030.

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Abstract The protein C (PC) pathway plays a major role in the interface between coagulation and inflammation. APC has both anticoagulant and anti-inflammatory properties and is the only effective treatment in patients with severe sepsis. However, assessment of APC’s therapeutic effect on other complex disease models has been compromised by its short half-life (15 min) and by difficulties in monitoring protein levels. To overcome this limitation we used adeno-associated viral (AAV) vectors encoding the PC zymogen or APC for hepatocyte specific gene expression. For direct APC secretion we introd

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van den Boom, Frans M., and Kees de Rijk. "The Schorerstichting Model AIDS Program." AIDS Patient Care 4, no. 6 (1990): 41–46. http://dx.doi.org/10.1089/apc.1990.4.41.

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46

Zhang, Ziguo, Jing Yang, Eric H. Kong, et al. "Recombinant expression, reconstitution and structure of human anaphase-promoting complex (APC/C)." Biochemical Journal 449, no. 2 (2012): 365–71. http://dx.doi.org/10.1042/bj20121374.

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Mechanistic and structural studies of large multi-subunit assemblies are greatly facilitated by their reconstitution in heterologous recombinant systems. In the present paper, we describe the generation of recombinant human APC/C (anaphase-promoting complex/cyclosome), an E3 ubiquitin ligase that regulates cell-cycle progression. Human APC/C is composed of 14 distinct proteins that assemble into a complex of at least 19 subunits with a combined molecular mass of ~1.2 MDa. We show that recombinant human APC/C is correctly assembled, as judged by its capacity to ubiquitinate the budding yeast AP

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Mizutani, Akio, Kenji Okajima, Mitsuhiro Uchiba, and Takayuki Noguchi. "Activated protein C reduces ischemia/reperfusion-induced renal injury in rats by inhibiting leukocyte activation." Blood 95, no. 12 (2000): 3781–87. http://dx.doi.org/10.1182/blood.v95.12.3781.

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Abstract We examined whether activated protein C (APC) reduces ischemia/reperfusion (I/R)–induced renal injury by inhibiting leukocyte activation. In a rat model, intravenous administration of APC markedly reduced I/R-induced renal dysfunction and histological changes, whereas intravenous administration of dansyl glutamylglycylarginyl chloromethyl ketone–treated factor Xa (DEGR-FXa; active-site–blocked factor Xa), heparin or diisopropyl fluorophosphate–treated APC (DIP-APC; inactive derivative of ARC) had no effect. Furthermore, APC significantly inhibited the I/R-induced decrease in renal tis

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Mizutani, Akio, Kenji Okajima, Mitsuhiro Uchiba, and Takayuki Noguchi. "Activated protein C reduces ischemia/reperfusion-induced renal injury in rats by inhibiting leukocyte activation." Blood 95, no. 12 (2000): 3781–87. http://dx.doi.org/10.1182/blood.v95.12.3781.012k18_3781_3787.

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We examined whether activated protein C (APC) reduces ischemia/reperfusion (I/R)–induced renal injury by inhibiting leukocyte activation. In a rat model, intravenous administration of APC markedly reduced I/R-induced renal dysfunction and histological changes, whereas intravenous administration of dansyl glutamylglycylarginyl chloromethyl ketone–treated factor Xa (DEGR-FXa; active-site–blocked factor Xa), heparin or diisopropyl fluorophosphate–treated APC (DIP-APC; inactive derivative of ARC) had no effect. Furthermore, APC significantly inhibited the I/R-induced decrease in renal tissue blood

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Griffin, John H., Berislav V. Zlokovic, and Laurent O. Mosnier. "Activated protein C, protease activated receptor 1, and neuroprotection." Blood 132, no. 2 (2018): 159–69. http://dx.doi.org/10.1182/blood-2018-02-769026.

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Abstract Protein C is a plasma serine protease zymogen whose active form, activated protein C (APC), exerts potent anticoagulant activity. In addition to its antithrombotic role as a plasma protease, pharmacologic APC is a pleiotropic protease that activates diverse homeostatic cell signaling pathways via multiple receptors on many cells. Engineering of APC by site-directed mutagenesis provided a signaling selective APC mutant with 3 Lys residues replaced by 3 Ala residues, 3K3A-APC, that lacks >90% anticoagulant activity but retains normal cell signaling activities. This 3K3A-APC mutant ex

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Joyce, David E., Haifeng Xu, Sumeet Mathur, and Francis J. Castellino. "Performance of Murine Soluble Thrombomodulin (rmsTM) in a Murine Model of Endotoxin-Induced Sepsis." Blood 108, no. 11 (2006): 3933. http://dx.doi.org/10.1182/blood.v108.11.3933.3933.

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Abstract The endothelial surface protein thrombomodulin (TM) generates activated protein C (aPC) that protects from sepsis-related DIC, vascular inflammation, and apoptosis. The purpose of this study is to evaluate a novel recombinant mouse soluble TM (Eli Lilly, Indianapolis, IN) in a murine lethal endotoxin (LPS) sepsis model to determine both kinetic and survival endpoints. A dose effective in rodent reperfusion studies was employed in this sepsis model (D. Berg, Eli Lilly). C57BL6 mice were injected concomitantly with rmsTM 5 mg/kg (s.c.) and LPS 14 ug/g (i.p.) at time zero. Plasma concent

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