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Journal articles on the topic 'CUA a CBA'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Dao, Thi D. "The Application of CBA to Pharmaceuticals: Going from CBA to CEA to CUA." Drug Information Journal 22, no. 3 (1988): 317–21. http://dx.doi.org/10.1177/009286158802200305.

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2

Svensson, Mikael, and Lars Hultkrantz. "A Comparison of Cost-Benefit and Cost-Effectiveness Analysis in Practice: Divergent Policy Practices in Sweden." Nordic Journal of Health Economics 5, no. 2 (2017): 41–53. http://dx.doi.org/10.5617/njhe.1592.

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This paper compares the implementation of the two economic evaluation methods Cost-Effectiveness/Utility (CEA/CUA) and Cost-Benefit Analysis (CBA) as tools for allocation of national public funds in the health and transport sector in Sweden, respectively. We compare the recommended values for important economic parameters such as the social discount rate, the marginal cost of public funds, and the explicit and implicit valuation of health, and document a number of substantial and unexplained differences in implementation. Such differences are problematic considering that the increasing use of

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3

Ward, C. A., D. McCullough, and W. D. Fraser. "Relation between complement activation and susceptibility to decompression sickness." Journal of Applied Physiology 62, no. 3 (1987): 1160–66. http://dx.doi.org/10.1152/jappl.1987.62.3.1160.

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The consequences of complement activation and the symptoms of decompression sickness are similar. Consequently, the relation between the sensitivity of individuals to complement activation by air bubbles and their susceptibility to decompression sickness has been examined. Plasma samples from 34 individuals were incubated with air bubbles, and the concentration of the fluid phase metabolites of complement activation C3a, C4a, and C5a were measured with radioimmunoassays. It was found that both the anaphylatoxins C3a and C5a were produced by the presence of air bubbles but that the anaphylatoxi

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4

Sohal, Davendra, Feng Lin, Suman Kundu, Keith McCrae, and Alok A. Khorana. "Complement levels as predictors of survival in pancreatic adenocarcinoma." Journal of Clinical Oncology 36, no. 4_suppl (2018): 315. http://dx.doi.org/10.1200/jco.2018.36.4_suppl.315.

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315 Background: Novel biomarkers to predict outcomes in pancreatic adenocarcinoma (PDA) are urgently needed. Complement activation, an important mediator of inflammatory processes, has been reported in some solid tumors but its role in PDA is unknown. We evaluated the prognostic role of complement in a prospective cohort of PDA patients. Methods: Blood samples were collected from consenting PDA patients at study entry (prior toany new regimen) in a prospective biorepository protocol at Cleveland Clinic from 2013-2016. Samples were processed for C3a, C4a, and C5a levels using ELISA on serum sam

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5

Greer, J. "Comparative Structural Anatomy of the Complement Anaphylatoxin Proteins C3a, C4a and C5a." Enzyme 36, no. 1-2 (1986): 150–63. http://dx.doi.org/10.1159/000469285.

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6

Kwon, So Hyun, Jung Eun Park, Yeong Hee Cho, and Jung Sup Lee. "Effect of Vibrio-Derived Extracellular Protease vEP-45 on the Blood Complement System." Biology 10, no. 8 (2021): 798. http://dx.doi.org/10.3390/biology10080798.

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Vibrio vulnificus is a pathogenic bacterium that can causes wound infections and fetal septicemia. We have reported that V. vulnificus ATCC29307 produces an extracellular zinc-metalloprotease (named vEP-45). Our previous results showed that vEP-45 can convert prothrombin to active thrombin and also activate the plasma kallikrein/kinin system. In this study, the effect of vEP-45 on the activation of the complement system was examined. We found that vEP-45 could proteolytically convert the key complement precursor molecules, including C3, C4, and C5, to their corresponding active forms (e.g., C3

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7

Marc, Mateja M., Peter Korosec, Mitja Kosnik, et al. "Complement Factors C3a, C4a, and C5a in Chronic Obstructive Pulmonary Disease and Asthma." American Journal of Respiratory Cell and Molecular Biology 31, no. 2 (2004): 216–19. http://dx.doi.org/10.1165/rcmb.2003-0394oc.

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8

Daffern, P. J., P. H. Pfeifer, J. A. Ember, and T. E. Hugli. "C3a is a chemotaxin for human eosinophils but not for neutrophils. I. C3a stimulation of neutrophils is secondary to eosinophil activation." Journal of Experimental Medicine 181, no. 6 (1995): 2119–27. http://dx.doi.org/10.1084/jem.181.6.2119.

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Inflammatory action of the potent chemotaxin C5a has been well characterized on a variety of human cell types, including neutrophils, monocytes, basophils, and eosinophils. The cellular effects of C3a are less well defined. Contradictory reports have been published for C3a activation of neutrophils. Recent reports that C3a activates both basophils and eosinophils prompted us to reinvestigate the effects of C3a stimulation on eosinophils. We hypothesized that C3a activation of eosinophils, cells that are present in most neutrophil preparations, might lead to neutrophil activation. Using neutrop

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9

Elsner, J., M. Oppermann, W. Czech, and A. Kapp. "C3a activates the respiratory burst in human polymorphonuclear neutrophilic leukocytes via pertussis toxin-sensitive G-proteins." Blood 83, no. 11 (1994): 3324–31. http://dx.doi.org/10.1182/blood.v83.11.3324.3324.

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Abstract In contrast to C5a, which represents a well-established potent activator of the respiratory burst in polymorphonuclear neutrophilic granulocytes (PMN), the functional role of C3a in the activation of PMN is, so far, poorly understood. Herein, the potential role of human C3a in the activation of the respiratory burst in human PMN was investigated. The release of reactive oxygen species (ROS) of PMN from healthy donors was measured by lucigenin-dependent chemiluminescence. C3a dose-dependently induced the production of ROS in human PMN in the range between 10 ng/mL and 1,000 ng/mL, wher

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10

Elsner, J., M. Oppermann, W. Czech, and A. Kapp. "C3a activates the respiratory burst in human polymorphonuclear neutrophilic leukocytes via pertussis toxin-sensitive G-proteins." Blood 83, no. 11 (1994): 3324–31. http://dx.doi.org/10.1182/blood.v83.11.3324.bloodjournal83113324.

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In contrast to C5a, which represents a well-established potent activator of the respiratory burst in polymorphonuclear neutrophilic granulocytes (PMN), the functional role of C3a in the activation of PMN is, so far, poorly understood. Herein, the potential role of human C3a in the activation of the respiratory burst in human PMN was investigated. The release of reactive oxygen species (ROS) of PMN from healthy donors was measured by lucigenin-dependent chemiluminescence. C3a dose-dependently induced the production of ROS in human PMN in the range between 10 ng/mL and 1,000 ng/mL, whereas C3a-d

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11

Kim, Song-Yi, Hyangsook Lee, Younbyoung Chae, Hi-Joon Park, and Hyejung Lee. "A Systematic Review of Cost-Effectiveness Analyses Alongside Randomised Controlled Trials of Acupuncture." Acupuncture in Medicine 30, no. 4 (2012): 273–85. http://dx.doi.org/10.1136/acupmed-2012-010178.

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Objective To summarise the evidence on the cost-effectiveness of acupuncture. Methods We identified full economic evaluations such as cost-effectiveness analysis (CEA), cost-utility analysis (CUA) and cost-benefit analysis (CBA) alongside randomised controlled trials (RCTs) that assessed the consequences and costs of acupuncture for any medical condition. Eleven electronic databases were searched up to March 2011 without language restrictions. Eligible RCTs were assessed using the Cochrane criteria for risk of bias and a modified version of the checklist for economic evaluation. The general ch

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12

Klos, Andreas, Elisabeth Wende, Kathryn J. Wareham, and Peter N. Monk. "International Union of Basic and Clinical Pharmacology. LXXXVII. Complement Peptide C5a, C4a, and C3a Receptors." Pharmacological Reviews 65, no. 1 (2013): 500–543. http://dx.doi.org/10.1124/pr.111.005223.

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13

Morales, Rommel, Lingjun Zhang, Yuping Wu, et al. "C3a, C4a, and C5a Complement Anaphylatoxins Are Paradoxically Decreased in Acute and Chronic Heart Failure." Journal of Cardiac Failure 26, no. 10 (2020): S19—S20. http://dx.doi.org/10.1016/j.cardfail.2020.09.063.

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14

Bautsch, W., T. Kretzschmar, T. Stühmer, et al. "A recombinant hybrid anaphylatoxin with dual C3a/C5a activity." Biochemical Journal 288, no. 1 (1992): 261–66. http://dx.doi.org/10.1042/bj2880261.

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By site-directed mutagenesis of a human complement factor C5a cDNA clone, we have designed a hybrid anaphylatoxin in which three amino acid residues in the C-terminal sequence of human C5a were exchanged to create the native C-terminal human C3a (hC3a) sequence Leu-Gly-Leu-Ala-Arg. This hybrid anaphylatoxin rC5a-(1-69)-LGLAR exhibited true C3a and C5a activity when tested in the guinea pig ileum contraction assay. Quantitative measurements of ATP release from guinea pig platelets revealed about 1% intrinsic C3a activity for this hybrid, while the C5a activity was essentially unchanged. Competi

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15

Antovic, Aleksandra, Fariborz Mobarrez, Milena Manojlovic, et al. "Microparticles Expressing Myeloperoxidase and Complement C3a and C5a as Markers of Renal Involvement in Antineutrophil Cytoplasmic Antibody–associated Vasculitis." Journal of Rheumatology 47, no. 5 (2019): 714–21. http://dx.doi.org/10.3899/jrheum.181347.

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Objective.To investigate expression of terminal complement components C3a and C5a on circulating myeloperoxidase (MPO)-positive microparticles (MPO+MP) in relation to disease activity and renal involvement in patients with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV).Methods.Forty-six clinically well-characterized patients with AAV and 23 age- and sex-matched healthy controls were included. The concentration of MPO+MP expressing C3a and C5a was analyzed from citrate plasma by flow cytometry. Serum levels of C3a and C5a were determined using commercial ELISA. The asses

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16

Banadakoppa, Manu, Alex C. Vidaeff, Uma Yallampalli, Susan M. Ramin, Michael A. Belfort, and Chandra Yallampalli. "Complement Split Products in Amniotic Fluid in Pregnancies Subsequently Developing Early-Onset Preeclampsia." Disease Markers 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/263109.

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Objective. To determine the second-trimester amniotic fluid concentrations of complement split products in pregnancies subsequently affected by early-onset preeclampsia.Study Design. Cohort of 731 women with singleton pregnancies undergoing second-trimester genetic amniocentesis followed up to delivery and analyzed as a nested case-control study. Cases of preeclampsia developing before 34 weeks’ gestation (n=15) were compared with 47 uncomplicated term controls. Amniotic fluid collected at amniocentesis was tested for complement split products Bb, C4a, C3a, and C5a.Results. Women who developed

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17

Emeis, Michael, Josef Sonntag, Carsten Willam, Evelyn Strauss, Matthias M. Walka, and Michael Obladen. "Acidosis activates complement systemin vitro." Mediators of Inflammation 7, no. 6 (1998): 417–20. http://dx.doi.org/10.1080/09629359890802.

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We investigated thein vitroeffect of different form s of acidosis (pH 7.0) on the formation of anaphylatoxins C3a and C5a. Metabolic acidosis due to addition of hydrochloric acid (10 μ mol/ml blood) or lactic acid (5.5 μ mol/ml) to heparin blood(N=12)caused significant activation of C3a and C5a compared to control (bothp=0.002). Respiratory acidosis activated C3a(p=0.007)and C5a(p=0.003)compared to normocapnic controls. Making blood samples with lactic acidosis hypocapnic resulted in a median pH of 7.37. In this respiratory compensated metabolic acidosis, C3a and C5a were not increased. These

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18

Schatz-Jakobsen, Janus Asbjørn, Laure Yatime, Casper Larsen, Steen Vang Petersen, Andreas Klos, and Gregers Rom Andersen. "Structural and functional characterization of human and murine C5a anaphylatoxins." Acta Crystallographica Section D Biological Crystallography 70, no. 6 (2014): 1704–17. http://dx.doi.org/10.1107/s139900471400844x.

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Complement is an ancient part of the innate immune system that plays a pivotal role in protection against invading pathogens and helps to clear apoptotic and necrotic cells. Upon complement activation, a cascade of proteolytic events generates the complement effectors, including the anaphylatoxins C3a and C5a. Signalling through their cognate G-protein coupled receptors, C3aR and C5aR, leads to a wide range of biological events promoting inflammation at the site of complement activation. The function of anaphylatoxins is regulated by circulating carboxypeptidases that remove their C-terminal a

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19

Pham, Duc-Truc, Huy Tien Ngo, Stephen F. Lincoln, Bruce L. May та Christopher J. Easton. "Synthesis of C6A-to-C6A and C3A-to-C3A diamide linked γ-cyclodextrin dimers". Tetrahedron 66, № 15 (2010): 2895–98. http://dx.doi.org/10.1016/j.tet.2010.02.005.

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20

TAKEMATSU, H., K. OHKOHCHI, and H. TAGAMI. "Demonstration of anaphylatoxins C3a, C4a and C5a in the scales of psoriasis and inflammatory pustular dermatoses." British Journal of Dermatology 114, no. 1 (1986): 1–6. http://dx.doi.org/10.1111/j.1365-2133.1986.tb02773.x.

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21

Kasuya, Hidetoshi, and Takashi Shimizu. "Activated complement components C3a and C4a in cerebrospinal fluid and plasma following subarachnoid hemorrhage." Journal of Neurosurgery 71, no. 5 (1989): 741–46. http://dx.doi.org/10.3171/jns.1989.71.5.0741.

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✓ The cerebrospinal fluid (CSF) and plasma levels of the complement components C3a and C4a in 40 patients suffering from subarachnoid hemorrhage (SAH) were quantitated by radioimmunoassay. Serial measurements of the lumbar CSF levels revealed that the C3a and C4a levels were significantly elevated in the initial stage of SAH, but decreased rapidly. Within 48 hours after SAH, the mean C3a and C4a levels in the cisternal, lumbar, and ventricular CSF were significantly higher in patients with delayed ischemic neurological deficits (DIND) than in those without DIND. The serially measured plasma le

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22

Rua-Figueroa, I., O. Arencibia-Mireles, M. Elvira, et al. "Factors involved in the progress of preclinical atherosclerosis associated with systemic lupus erythematosus: a 2-year longitudinal study." Annals of the Rheumatic Diseases 69, no. 6 (2009): 1136–39. http://dx.doi.org/10.1136/ard.2008.104349.

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ObjectivesTo assess the changes in carotid intima-media thickness (IMT) and the associated risks factors in patients with low severity systemic lupus erythematosus (SLE).MethodsCommon carotid IMT measurements were obtained by ultrasound from 101 patients with SLE at an interval of 2 years. Cardiovascular risk factors, disease activity, accumulated damage, severity (Katz index) and biochemical parameters (including high sensitivity C-reactive protein, interleukin 6, C3a, C4a, C5a and homocysteine) were also assessed. Multiple linear regression was used to assess the effect of these variables on

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23

Strey, C. W., B. Siegmund, R. Marquez-Pinilla, E. Oppermann, and W. O. Bechstein. "C3a, C4a and C5a plasma levels change after liver resection in correlation with a systemic chemokine response." Molecular Immunology 44, no. 1-3 (2007): 245. http://dx.doi.org/10.1016/j.molimm.2006.07.232.

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24

KATO, Y. "Purification and functional assessment of C3a, C4a and C5a of the common carp (Cyprinus carpio) complement*1." Developmental & Comparative Immunology 28, no. 9 (2004): 901–10. http://dx.doi.org/10.1016/j.dci.2004.01.006.

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25

Deb-Chatterji, Milani, Christian W. Keller, Simon Koch, et al. "Profiling Complement System Components in Primary CNS Vasculitis." Cells 10, no. 5 (2021): 1139. http://dx.doi.org/10.3390/cells10051139.

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Complement activation has been implicated in the pathogenesis of many vasculitic syndromes such as anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides. Using an array-based multiplex system, we simultaneously quantified serum and CSF levels of activated and regulatory complement system proteins in patients with primary CNS vasculitis (PACNS; n = 20) compared to patients with non-inflammatory conditions (n = 16). Compared to non-inflammatory controls, levels of C3a, C5a, and SC5b-9, indicative for general activation of the complement system, of C4a, specific for the activation o

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Pham, Duc-Truc, Huy Tien Ngo, Stephen F. Lincoln, Bruce L. May та Christopher J. Easton. "ChemInform Abstract: Synthesis of C6A-to-C6A and C3A-to-C3A Diamide Linked γ-Cyclodextrin Dimers." ChemInform 41, № 29 (2010): no. http://dx.doi.org/10.1002/chin.201029205.

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27

Bajic, Goran, Laure Yatime, Andreas Klos, and Gregers Rom Andersen. "Human C3a and C3a desArg anaphylatoxins have conserved structures, in contrast to C5a and C5a desArg." Protein Science 22, no. 2 (2012): 204–12. http://dx.doi.org/10.1002/pro.2200.

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28

Youn, So Won. "Transition-Metal-Catalyzed Annulative Coupling Cascade for the Synthesis of 3-Methyleneisoindolin-1-ones." Synthesis 52, no. 06 (2020): 807–18. http://dx.doi.org/10.1055/s-0039-1690046.

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This short review describes the recent progress made on transition-metal-catalyzed annulative couplings for the synthesis of 3-methyleneisoindolin-1-ones, which are useful intermediates for the synthesis of numerous alkaloids and can be often found in a wide range of natural products and pharmaceuticals. In particular, new one-pot multiple C–C/C–N bond-forming processes for the construction of the 5-methylenepyrrol-2-one nucleus of such compounds are summarized.1 Introduction2 Intramolecular Cyclization Reactions: C3–N or C3–C3a and C–C Bond Formation3 Intermolecular Annulative Coupling Reacti

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29

Pfeifer, Philippe H., Marleen S. Kawahara, and Tony E. Hugli. "Possible Mechanism for in Vitro Complement Activation in Blood and Plasma Samples: Futhan/EDTA Controls in Vitro Complement Activation." Clinical Chemistry 45, no. 8 (1999): 1190–99. http://dx.doi.org/10.1093/clinchem/45.8.1190.

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Abstract Background: Ongoing in vitro complement (C) activation in citrate or EDTA plasma has prevented an accurate analysis of C-activation products generated in vivo. The aim of this study was to characterize handling and storage conditions required to prevent in vitro C activation in blood and plasma samples collected with Futhan/EDTA. Methods: BiotrakTM RIAs were used to quantitatively measure C3a and C4a in blood and/or plasma samples from healthy individuals (controls) and from liver transplant patients. Blood samples were routinely drawn into either EDTA (1 g/L) tubes or into tubes cont

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Prendecki, Maria, Candice Clarke, Nicholas Medjeral-Thomas, et al. "Temporal changes in complement activation in haemodialysis patients with COVID-19 as a predictor of disease progression." Clinical Kidney Journal 13, no. 5 (2020): 889–96. http://dx.doi.org/10.1093/ckj/sfaa192.

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Abstract Background Complement activation may play a pathogenic role in patients with severe coronavirus disease 2019 (COVID-19) by contributing to tissue inflammation and microvascular thrombosis. Methods Serial samples were collected from patients receiving maintenance haemodialysis (HD). Thirty-nine patients had confirmed COVID-19 and 10 patients had no evidence of COVID-19. Plasma C5a and C3a levels were measured using enzyme-linked immunosorbent assay. Results We identified elevated levels of plasma C3a and C5a in HD patients with severe COVID-19 compared with controls. Serial sampling id

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Schraufstaetter, Ingrid U., Richard DiScipio, and Sophia K. Khaldoyanidi. "Complement C3a Enhances the Repair Potential of Human Mesenchymal Stem Cells." Blood 118, no. 21 (2011): 1324. http://dx.doi.org/10.1182/blood.v118.21.1324.1324.

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Abstract Abstract 1324 Mesenchymal stem cells (MSCs) contribute to the regulatory network in the bone marrow by generating the cellular compartment of the hematopoietic microenvironment including osteoblasts and stromal fibroblasts, and by producing a variety of trophic and growth factors. Because of these properties, MSCs are starting to find clinical application in a variety of pathological conditions including hematological disorders. However, the full regenerative potential of MSCs has not been realized due to poor tissue homing and limited cell survival following transplantation. One fact

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Strey, Christoph W., Maciej Markiewski, Dimitrios Mastellos, et al. "The Proinflammatory Mediators C3a and C5a Are Essential for Liver Regeneration." Journal of Experimental Medicine 198, no. 6 (2003): 913–23. http://dx.doi.org/10.1084/jem.20030374.

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Complement has been implicated in liver repair after toxic injury. Here, we demonstrate that complement components are essential for liver regeneration, and mediate their effect by interacting with key signaling networks that promote hepatocyte proliferation. C3- or C5-deficient mice exhibited high mortality, parenchymal damage, and impaired liver regeneration after partial hepatectomy. Mice with dual C3 and C5 deficiency had a more exacerbated phenotype that was reversed by combined C3a and C5a reconstitution. Interception of C5a receptor signaling resulted in suppression of IL-6/TNFα inducti

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33

Foley, J. H., and E. M. Conway. "Basic weapons to degrade C3a and C5a." Journal of Thrombosis and Haemostasis 16, no. 5 (2018): 987–90. http://dx.doi.org/10.1111/jth.13999.

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Gutzmer, Ralf, Brigitta Köther, Jörg Zwirner, et al. "Human Plasmacytoid Dendritic Cells Express Receptors for Anaphylatoxins C3a and C5a and Are Chemoattracted to C3a and C5a." Journal of Investigative Dermatology 126, no. 11 (2006): 2422–29. http://dx.doi.org/10.1038/sj.jid.5700416.

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35

NAGATA, S., and M. GLOVSKY. "Activation of human serum complement with allergensI. Generation of C3a, C4a, and C5a and induction of human neutrophil aggregation." Journal of Allergy and Clinical Immunology 80, no. 1 (1987): 24–32. http://dx.doi.org/10.1016/s0091-6749(87)80186-0.

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Perret, J. J., E. Raspe, G. Vassart, and M. Parmentier. "Cloning and functional expression of the canine anaphylatoxin C5a receptor. Evidence for high interspecies variability." Biochemical Journal 288, no. 3 (1992): 911–17. http://dx.doi.org/10.1042/bj2880911.

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A cDNA clone, DTJP03, encoding an orphan receptor, was isolated from a canine thyroid library, and found to exhibit 68.6% amino-acid identity with the recently described human C5a receptor. This relatively low similarity first suggested that DTJP03 encoded either a C5a receptor subtype, or the presumably related C3a receptor. Binding studies performed on membranes from COS-7 cells expressing the recombinant receptor demonstrated that DTJP03 encoded a high-affinity C5a receptor, with a Kd of 1.2 nM. C3a was unable to compete for C5a binding. Intracellular free calcium concentrations were measur

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Jalili, Ali, Neeta Shirvaikar, Chris Korol, and Anna Janowska-Wieczorek. "The Role of C5a in the Mobilization of Hematopoietic Stem/Progenitor Cells." Blood 112, no. 11 (2008): 3472. http://dx.doi.org/10.1182/blood.v112.11.3472.3472.

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Abstract The complement system, a vital component of the immune system, has been shown to play a role in hematopoietic stem/progenitor cell (HSPC) trafficking. C3a is known to be important in the retention of HSPC in the bone marrow (BM) as C3a-deficient mice are good mobilizers, and C5a is important in the mobilization of HSPC because C5a-deficient mice are poor mobilizers (Stem Cells2007; 25: 3093). Further, granulocyte-colony stimulating factor (G-CSF) activates the complement system via the classical pathway, down-regulates stromal-derived factor (SDF)-1 in BM stromal cells and decreases e

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Freyria, A. M., Ph Leitienne, C. N. Veysseyre, J. P. Bringuier, and J. Traeger. "Complement C3 and C5 Degradation Products during Hemodialysis Treatment: Study of an Index of Membrane Bioincompatibility." International Journal of Artificial Organs 11, no. 2 (1988): 111–18. http://dx.doi.org/10.1177/039139888801100211.

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In 10 hemodialyses (HD) with cuprophan (CU) and 10 with polyacrylonitrile (PAN), signs of complement activation were investigated by following arterial and venous levels of C3a, C3d and C5a, in order to propose a marker of bioincompatibility. Despite large individual variabilities, significant increases of these molecules were detected at t 20 min, particularly with CU device in the artery and more marked in the vein except for C3d with PAN. During the later stage of HD, while C3a and C5a levels gradually declined, but remained significantly higher than t 0 in all the patients treated with CU,

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Westcott, Stephen A., Nicholas J. Taylor та Todd B. Marder. "Reactions of (η5-C9H7)Rh(η2-C2H4)2 with quinones: molecular structure of [(η5-C9H7)Rh(2,3,5,6-C6O2(CH3)4)]". Canadian Journal of Chemistry 77, № 2 (1999): 199–204. http://dx.doi.org/10.1139/v98-228.

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Reactions of (η5-C9H7)Rh(η2-C2H4)2 (1) with quinones were investigated. Substitution of the labile ethylene ligands was observed upon addition of either duroquinone (2,3,5,6-tetramethyl-1,4-benzoquinone) or 1,4-benzoquinone to complex 1. The molecular structure of neutral (η5-C9H7)Rh(2,3,5,6-C6O2(CH3)4) (3), determined by X-ray diffraction, shows that the duroquinone ligand lies in a plane nearly parallel to the indenyl group. The carbonyl moieties of duroquinone lie in a plane incorporating Rh, C2, and the midpoint between C3a and C7a of the indenyl ring. The slip parameter (Δ= d(average Rh-C

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Fareed, Jawed, Debra A. Hoppensteadt, Fred Leya, Omer Iqbal, Helmut Wolf, and Roger Bick. "Useful laboratory tests for studying thrombogenesis in acute cardiac syndromes." Clinical Chemistry 44, no. 8 (1998): 1845–53. http://dx.doi.org/10.1093/clinchem/44.8.1845.

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Abstract We review laboratory tests that evaluate thrombogenesis during acute coronary syndromes. These tests have been found to be valuable research tools in more clearly understanding the pathophysiology of acute coronary syndromes. In particular, we describe tissue factor, tissue factor pathway inhibitor, prothrombin fragment 1.2, thrombin-antithrombin complex, fibrinopeptide A, tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), t-PA-PAI complex, Bβ 15–42-related peptides, fibrinogen degradation products, fibrin degradation products, D-dimer, platelet factor 4,

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Jayakody Arachchillage, Deepa, Ian J. Mackie, Maria Efthymiou, et al. "Rivaroxaban Limits Complement Activation Compared to Warfarin in Antiphospholipid Syndrome Patients with Venous Thromboembolism." Blood 126, no. 23 (2015): 2328. http://dx.doi.org/10.1182/blood.v126.23.2328.2328.

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Abstract Background Complement activation may play a role in the pathogenesis of thrombosis and other pathological processes in the antiphospholipid syndrome (APS). Since coagulation proteases, such as factor Xa, can cleave complement proteins, we investigated complement activation in thrombotic APS patients receiving rivaroxaban, a direct factor Xa inhibitor. Aims To assess markers of complement activation (C3a, C5a, terminal complement complex (SC5b-9) and Bb fragment) in patients with thrombotic APS treated with rivaroxaban or warfarin in a prospective randomised controlled trial. Methods 1

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Schleuning, M., M. Schmid-Haslbeck, H. Utz, et al. "Complement activation during storage of blood under normal blood bank conditions. Effects of proteinase inhibitors and leukocyte depletion." Blood 79, no. 11 (1992): 3071–75. http://dx.doi.org/10.1182/blood.v79.11.3071.3071.

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Abstract During storage of CPD-A1 preserved whole blood factors of the complement cascade become activated, as evidenced by a rapid increase in the concentrations of C3a-desArg and C4a-desArg. After 10 to 14 days of whole blood storage, the elevations of C3a and C4a levels were highly significant. This increase was paralleled by an increase in the concentration of the lysosomal proteinase elastase from polymorphonuclear (PMN) granulocytes. By contrast, the concentration of the C3 activator complex C4b2b remained unchanged even after 3 weeks of storage. The supplementation of the anticoagulant

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Schleuning, M., M. Schmid-Haslbeck, H. Utz, et al. "Complement activation during storage of blood under normal blood bank conditions. Effects of proteinase inhibitors and leukocyte depletion." Blood 79, no. 11 (1992): 3071–75. http://dx.doi.org/10.1182/blood.v79.11.3071.bloodjournal79113071.

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During storage of CPD-A1 preserved whole blood factors of the complement cascade become activated, as evidenced by a rapid increase in the concentrations of C3a-desArg and C4a-desArg. After 10 to 14 days of whole blood storage, the elevations of C3a and C4a levels were highly significant. This increase was paralleled by an increase in the concentration of the lysosomal proteinase elastase from polymorphonuclear (PMN) granulocytes. By contrast, the concentration of the C3 activator complex C4b2b remained unchanged even after 3 weeks of storage. The supplementation of the anticoagulant CPD-A1 wi

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Hartmann, Karin, Beate M. Henz, Sabine Krüger-Krasagakes, et al. "C3a and C5a Stimulate Chemotaxis of Human Mast Cells." Blood 89, no. 8 (1997): 2863–70. http://dx.doi.org/10.1182/blood.v89.8.2863.

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Abstract The factors that control migration of mast cells to sites of inflammation and tissue repair remain largely undefined. Whereas several recent studies have described chemotactic factors that induce migration of murine mast cells, only stem cell factor (SCF ) is known to induce migration of human mast cells. We report here that the anaphylatoxins C3a and C5a are chemotactic factors for the human mast cell line HMC-1, human cord blood-derived mast cells (CBMC) and cutaneous mast cells in vitro. The presence of an extracellular matrix protein, laminin, was required for chemotaxis in respon

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Chiummiento, Lucia, Rosarita D’Orsi, Maria Funicello, and Paolo Lupattelli. "Last Decade of Unconventional Methodologies for the Synthesis of Substituted Benzofurans." Molecules 25, no. 10 (2020): 2327. http://dx.doi.org/10.3390/molecules25102327.

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This review describes the progress of the last decade on the synthesis of substituted benzofurans, which are useful scaffolds for the synthesis of numerous natural products and pharmaceuticals. In particular, new intramolecular and intermolecular C–C and/or C–O bond-forming processes, with transition-metal catalysis or metal-free are summarized. (1) Introduction. (2) Ring generation via intramolecular cyclization. (2.1) C7a–O bond formation: (route a). (2.2) O–C2 bond formation: (route b). (2.3) C2–C3 bond formation: (route c). (2.4) C3–C3a bond formation: (route d). (3) Ring generation via in

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Issekutz, Andrew C., Dennis M. Roland, and Richard A. Patrick. "The effect of FUT-175 (nafamstat mesilate) on C3a, C4a and C5a generation in vitro and inflammatory reactions in vivo." International Journal of Immunopharmacology 12, no. 1 (1990): 1–9. http://dx.doi.org/10.1016/0192-0561(90)90062-r.

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Francis, Karen, B. Mary Lewis, Peter N. Monk, and Jack Ham. "Complement C5a receptors in the pituitary gland: expression and function." Journal of Endocrinology 199, no. 3 (2008): 417–24. http://dx.doi.org/10.1677/joe-08-0110.

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Communication between the immune and endocrine system is important for the control of inflammation that is primarily mediated through the hypothalamic–pituitary–adrenal axis. The innate immune system rapidly responds to pathogens by releasing complement proteins that include the anaphylatoxins C3a and C5a. We previously reported the existence of C3a receptors in the anterior pituitary gland and now describe the presence of C5a receptors in the gland. C5a and its less active derivative (C5adR) can bind to its own receptor and to another receptor called C5L2. Using RT-PCR and immunocytochemistry

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Peng, Qi, Ke Li, Lesley A. Smyth, et al. "C3a and C5a Promote Renal Ischemia-Reperfusion Injury." Journal of the American Society of Nephrology 23, no. 9 (2012): 1474–85. http://dx.doi.org/10.1681/asn.2011111072.

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OHKOHCHI, K., H. TAKEMATSU, and H. TAGAMI. "Increased anaphylatoxins (C3a and C4a) in psoriatic sera." British Journal of Dermatology 113, no. 2 (1985): 189–96. http://dx.doi.org/10.1111/j.1365-2133.1985.tb02064.x.

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Mastroroberto, Pasquale, Massimo Chello, and Antonietta R. Marchese. "Plasma C3a and C5a concentrations during cardiopulmonary bypass." Annals of Thoracic Surgery 57, no. 3 (1994): 781–82. http://dx.doi.org/10.1016/0003-4975(94)90599-1.

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