Готові списки джерел за темами / Necrotic cell clearance

Добірка наукової літератури з теми "Necrotic cell clearance"

Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 29 січня 2023

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Статті в журналах з теми "Necrotic cell clearance"

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Poon, I. K. H., M. D. Hulett, and C. R. Parish. "Molecular mechanisms of late apoptotic/necrotic cell clearance." Cell Death & Differentiation 17, no. 3 (December 18, 2009): 381–97. http://dx.doi.org/10.1038/cdd.2009.195.

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2

Poon, Ivan K. H., Mark D. Hulett та Christopher R. Parish. "Histidine-rich glycoprotein is a novel plasma pattern recognition molecule that recruits IgG to facilitate necrotic cell clearance via FcγRI on phagocytes". Blood 115, № 12 (25 березня 2010): 2473–82. http://dx.doi.org/10.1182/blood-2009-07-234013.

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Abstract Under normal physiologic conditions, necrotic cells resulting from tissue injury are rapidly removed from the circulation and tissues by phagocytes, thus preventing the exposure of intracellular antigenic and immunostimulatory molecules that can aid the development of autoimmune disease. Histidine-rich glycoprotein (HRG), a relatively abundant plasma glycoprotein, has a multidomain structure that can interact with many ligands including components of the fibrinolytic and immune systems. Recently, it has been reported that HRG can bind strongly to cytoplasmic ligand(s) exposed in necrotic cells to enhance clearance by phagocytes. Here we describe the molecular mechanisms underpinning this process. A complex consisting of both HRG and immunoglobulin G (IgG) was found as necessary to aid necrotic cell uptake by monocytes, predominantly via an FcγRI-dependent mechanism. The findings in this study also show that HRG can potentially interact with anionic phospholipids exposed in necrotic cells. Furthermore, the enhanced phagocytosis of necrotic cells induced by HRG-IgG complexes triggers phagocytes to release proinflammatory cytokines such as interleukin-8 and tumor necrosis factor. Thus, HRG has the unique property of complexing with IgG and facilitating a proinflammatory innate immune response to promote the clearance of necrotic cells.
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3

Atkin-Smith, Georgia K. "Phagocytic clearance of apoptotic, necrotic, necroptotic and pyroptotic cells." Biochemical Society Transactions 49, no. 2 (April 12, 2021): 793–804. http://dx.doi.org/10.1042/bst20200696.

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Although millions of cells in the human body will undergo programmed cell death each day, dying cells are rarely detected under homeostatic settings in vivo. The swift removal of dying cells is due to the rapid recruitment of phagocytes to the site of cell death which then recognise and engulf the dying cell. Apoptotic cell clearance — the engulfment of apoptotic cells by phagocytes — is a well-defined process governed by a series of molecular factors including ‘find-me’, ‘eat-me’, ‘don't eat-me’ and ‘good-bye’ signals. However, in recent years with the rapid expansion of the cell death field, the removal of other necrotic-like cell types has drawn much attention. Depending on the type of death, dying cells employ different mechanisms to facilitate engulfment and elicit varying functional impacts on the phagocyte, from wound healing responses to inflammatory cytokine secretion. Nevertheless, despite the mechanism of death, the clearance of dying cells is a fundamental process required to prevent the uncontrolled release of pro-inflammatory mediators and inflammatory disease. This mini-review summarises the current understandings of: (i) apoptotic, necrotic, necroptotic and pyroptotic cell clearance; (ii) the functional consequences of dying cell engulfment and; (iii) the outstanding questions in the field.
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4

Brouckaert, Greet, Michael Kalai, Dmitri V. Krysko, Xavier Saelens, Dominique Vercammen, `Matladi Ndlovu, Guy Haegeman, Katharina D'Herde, and Peter Vandenabeele. "Phagocytosis of Necrotic Cells by Macrophages Is Phosphatidylserine Dependent and Does Not Induce Inflammatory Cytokine Production." Molecular Biology of the Cell 15, no. 3 (March 2004): 1089–100. http://dx.doi.org/10.1091/mbc.e03-09-0668.

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Apoptotic cells are cleared by phagocytosis during development, homeostasis, and pathology. However, it is still unclear how necrotic cells are removed. We compared the phagocytic uptake by macrophages of variants of L929sA murine fibrosarcoma cells induced to die by tumor necrosis factor-induced necrosis or by Fas-mediated apoptosis. We show that apoptotic and necrotic cells are recognized and phagocytosed by macrophages, whereas living cells are not. In both cases, phagocytosis occurred through a phosphatidylserine-dependent mechanism, suggesting that externalization of phosphatidylserine is a general trigger for clearance by macrophages. However, uptake of apoptotic cells was more efficient both quantitatively and kinetically than phagocytosis of necrotic cells. Electron microscopy showed clear morphological differences in the mechanisms used by macrophages to engulf necrotic and apoptotic cells. Apoptotic cells were taken up as condensed membrane-bound particles of various sizes rather than as whole cells, whereas necrotic cells were internalized only as small cellular particles after loss of membrane integrity. Uptake of neither apoptotic nor necrotic L929 cells by macrophages modulated the expression of proinflammatory cytokines by the phagocytes.
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Cao, Longxing, Haishuang Chang, Xiangyi Shi, Chao Peng, and Yongning He. "Keratin mediates the recognition of apoptotic and necrotic cells through dendritic cell receptor DEC205/CD205." Proceedings of the National Academy of Sciences 113, no. 47 (November 7, 2016): 13438–43. http://dx.doi.org/10.1073/pnas.1609331113.

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Clearance of dead cells is critical for maintaining homeostasis and prevents autoimmunity and inflammation. When cells undergo apoptosis and necrosis, specific markers are exposed and recognized by the receptors on phagocytes. DEC205 (CD205) is an endocytotic receptor on dendritic cells with antigen presentation function and has been widely used in immune therapies for vaccine generation. It has been shown that human DEC205 recognizes apoptotic and necrotic cells in a pH-dependent fashion. However, the natural ligand(s) of DEC205 remains unknown. Here we find that keratins are the cellular ligands of human DEC205. DEC205 binds to keratins specifically at acidic, but not basic, pH through its N-terminal domains. Keratins form intermediate filaments and are important for maintaining the strength of cells and tissues. Our results suggest that keratins also function as cell markers of apoptotic and necrotic cells and mediate a pH-dependent pathway for the immune recognition of dead cells.
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6

Mattos, Matheus, Sofie Vandendriessche, Sara Schuermans, Romy Mittenzwei, Ari Waisman, and Pedro Elias Marques. "Natural antibodies are required for necrotic cell debris clearance and liver repair during necrotic liver injury." Journal of Hepatology 77 (July 2022): S396—S397. http://dx.doi.org/10.1016/s0168-8278(22)01141-2.

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7

Hirt, U. A., and M. Leist. "Rapid, noninflammatory and PS-dependent phagocytic clearance of necrotic cells." Cell Death & Differentiation 10, no. 10 (September 19, 2003): 1156–64. http://dx.doi.org/10.1038/sj.cdd.4401286.

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8

Krysko, Dmitri V., Katharina D’Herde, and Peter Vandenabeele. "Clearance of apoptotic and necrotic cells and its immunological consequences." Apoptosis 11, no. 10 (August 24, 2006): 1709–26. http://dx.doi.org/10.1007/s10495-006-9527-8.

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9

Zhang, Ting, and Siddharth Balachandran. "Bayonets over bombs: RIPK3 and MLKL restrict Listeria without triggering necroptosis." Journal of Cell Biology 218, no. 6 (May 16, 2019): 1773–75. http://dx.doi.org/10.1083/jcb.201905047.

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RIPK3 induces necroptosis by phosphorylating MLKL, which then induces plasma membrane rupture and necrotic cell death. In this issue, Sai et al. (2019. J. Cell Biol. https://doi.org/10.1083/jcb.201810014) show that RIPK3-MLKL signaling in epithelial cells promotes Listeria clearance by directly suppressing cytosolic bacterial replication, without activating cell death.
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10

Hyde, Dallas M., Lisa A. Miller, Ruth J. McDonald, Mary Y. Stovall, Viviana Wong, Kent E. Pinkerton, Craig D. Wegner, Robert Rothlein, and Charles G. Plopper. "Neutrophils enhance clearance of necrotic epithelial cells in ozone-induced lung injury in rhesus monkeys." American Journal of Physiology-Lung Cellular and Molecular Physiology 277, no. 6 (December 1, 1999): L1190—L1198. http://dx.doi.org/10.1152/ajplung.1999.277.6.l1190.

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To test the hypothesis that neutrophil influx is important for the removal of necrotic airway epithelial cells, rhesus monkeys were treated with a function-blocking monoclonal antibody (MAb) against CD18 followed by exposure to ozone or filtered air. CD18 MAb-treated, ozone-exposed monkeys showed a significant inhibition of neutrophil emigration and an accumulation of necrotic airway epithelial cells. In a subsequent experiment, monkeys were given CD18 MAb or an isotype control immunoglobulin before ozone or filtered-air exposure. Complement 5a was instilled into lobes of the right lung at the end of the exposure. Lavage neutrophils were significantly elevated in the right lobes compared with those in the contralateral left lobes; consequently, there were significantly fewer necrotic cells in the airways of the right lung, whereas large aggregations of necrotic cells were observed in the contralateral airways of the left lung. These data indicate that neutrophil influx in ozone-induced injury in primates is CD18 dependent and that neutrophils contribute to the repair of airway epithelium by removal of injured epithelial cells.
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Більше джерел

Дисертації з теми "Necrotic cell clearance"

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McPhillips, Kathleen Ann. "The role of oxidants in the clearance of apoptotic cells /." Connect to full text via ProQuest. IP filtered, 2006.

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Анотація:
Thesis (Ph.D. in Cancer Biology) -- University of Colorado at Denver and Health Sciences Center, 2006.
Typescript. Includes bibliographical references (leaves 112-124). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
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2

Sarter, Kerstin. "The role of galectins in clearance and immunogenicity of apoptotic and secondary necrotic cells = Die Rolle der Galektine in der Clearance und Immunogenität apoptotischer und sekundär nekrotischer Zellen." kostenfrei, 2010. http://d-nb.info/1002479827/34.

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Poon, Ivan Ka Ho. "The role of histidine-rich glycoprotein in necrotic cell clearance and regulation of degradative enzymes." Phd thesis, 2009. http://hdl.handle.net/1885/7156.

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Анотація:
Histidine-rich glycoprotein (HRG) is an abundant multi-functional protein that is present in the plasma of many vertebrates. HRG has a multi-domain structure that allows the molecule to interact with many ligands including heparin, heparan sulfate (HS), Fcy receptors (FcyR), plasminogen, fibrinogen, IgG, Clq, haem and Zn2+. The ability of HRG to interact with various ligands simultaneously has suggested that HRG can act as an adaptor molecule and regulate numerous biological processes such as immune complex/necrotic cell/pathogen clearance, cell adhesion, angiogenesis, coagulation and fibrinolysis. Although HRG is thought to play an important role in both immunity and vascular biology, the molecular mechanisms underpinning its action remain largely undefined. Thus, the aim of this thesis was to characterize the molecular components that are involved in HRG-mediated uptake of necrotic cells and to further examine the role of HRG in regulating degradative enzymes, such as plasminogen/plasmin and heparanase...In summary, the studies presented in this thesis have delineated the molecular mechanisms underlying necrotic cell removal mediated by plasma-derived HRG and may have important implications for the development of autoimmune disease caused by defective clearance of dying/dead cells. In addition, the ability of HRG to regulate degradative enzymes, such as plasmin and heparanase, further supports the view that HRG may play an important role in angiogenesis, leukocyte migration and cancer metastasis.
The Australian Government, John Curtin School of Medical Research, Australian National University, National Health and Medical Research Council, Australasian Society for Immunology, Australian Society for Medical Research, Federation of Immunological Societies of Asia-Oceania and Riken Research Center for Allergy and Immunology.
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Sarter, Kerstin [Verfasser]. "The role of galectins in clearance and immunogenicity of apoptotic and secondary necrotic cells = Die Rolle der Galektine in der Clearance und Immunogenität apoptotischer und sekundär nekrotischer Zellen / vorgelegt von Kerstin Sarter." 2010. http://d-nb.info/1002479827/34.

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Частини книг з теми "Necrotic cell clearance"

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Gachanja, Naomi N., David A. Dorward, Adriano G. Rossi, and Christopher D. Lucas. "Assays of Eosinophil Apoptosis and Phagocytic Uptake." In Methods in Molecular Biology, 113–32. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1095-4_10.

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AbstractEosinophil apoptosis (programmed cell death) plays an important role in several inflammatory and allergic conditions. Apoptosis triggers various mechanisms including activation of cysteine-aspartic proteases (caspases) and is characterized by morphological and biochemical changes. These include cellular condensation, nuclear fragmentation, increased mitochondrial permeability with loss of membrane potential, and exposure of phosphatidylserine on the cell membrane. A greater understanding of apoptotic mechanisms, subsequent phagocytosis (efferocytosis), and regulation of these processes is critical to understanding disease pathogenesis and development of potential novel therapeutic agents. Release of soluble factors and alterations to surface marker expression by eosinophils undergoing apoptosis aid them in signaling their presence to the immediate environment, and their subsequent recognition by phagocytic cells such as macrophages. Uptake of apoptotic cells usually suppresses inflammation by restricting proinflammatory responses and promoting anti-inflammatory and tissue repair responses. This, in turn, promotes resolution of inflammation. Defects in the apoptotic or efferocytosis mechanisms perpetuate inflammation, resulting in chronic inflammation and enhanced disease severity. This can be due to increased eosinophil life span or cell necrosis characterized by loss of cell membrane integrity and release of toxic intracellular mediators. In this chapter, we detail some of the key assays that are used to assess eosinophil apoptosis, as well as the intracellular signaling pathways involved and phagocytic clearance of these cells.
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Li, Zao, Nan Lu, Xiangwei He, and Zheng Zhou. "Monitoring the Clearance of Apoptotic and Necrotic Cells in the Nematode Caenorhabditis elegans." In Methods in Molecular Biology, 183–202. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-383-1_14.

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3

Krysko, Dmitri V., Tom Vanden Berghe, Eef Parthoens, Katharina D'Herde, and Peter Vandenabeele. "Chapter 16 Methods for Distinguishing Apoptotic from Necrotic Cells and Measuring Their Clearance." In Programmed Cell Death,General Principles forStudying Cell Death, Part A, 307–41. Elsevier, 2008. http://dx.doi.org/10.1016/s0076-6879(08)01416-x.

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4

Tadiparth, Sujatha, and Kayvan Shokrollahi. "Frostbite." In Burns (OSH Surgery), 353–66. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199699537.003.0042.

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Frostbite is the damage sustained by tissues when exposed to temperatures below their freezing point (<0°C). Extremities such as fingers, toes, nose and ears are most commonly affected. A number of extrinsic and intrinsic factors predispose to frostbite. The severity of frostbite can be classified into four degrees. Tissue injury occurs firstly, by direct cell damage and death from the formation of intracellular ice crystals and secondly, by vascular insufficiency and tissue ischaemia which result from vasoconstriction, endothelial injury and thromboembolism. Treatment is focused on gentle rewarming in a warm circulating bath (40–41°C). Tissues should be allowed to demarcate with rewarming and then surgical debridement or amputation performed if necrotic tissue is present. Tissue plasminogen activator can lead to rapid clearance of vascular thromboses, restore arterial perfusion and improve tissue salvage. Long-term sequelae can result including, cold hypersensitivity, sensory deficits, chronic pain, heterotropic calcification, and pigmentary changes.
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5

Tiberi, Simon. "Tuberculosis and Other Mycobacterial Infections." In Tutorial Topics in Infection for the Combined Infection Training Programme. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198801740.003.0035.

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Mycobacterium tuberculosis (MTB) is a thin, aerobic, non-spore forming, slow-growing (doubling time twelve hours) non-motile rod-shaped bacteria, belonging to the family Mycobacteriaceae. Mycobacterium tuberculosis complex is made up of several species, including M. tuberculosis, M. bovis, Bacillus Calmette-Guerin (BCG), M. africanum, M. canetii, M.caprae, M. microti, and others. Transmission is via inhalation of aerosolized respiratory secretions. After inhalation, majority of bacilli are captured in the upper respiratory tract by mucus and removed through a process called clearance, although bacteria in small droplets can reach the alveoli where the bacilli are ingested by macrophages. If clearance is not effective infection may result. With the involvement of CD4 lymphocytes, interferon-γ and tumour necrosis factor-α, a granuloma is formed, and bacilli may be destroyed. In many cases, the bacilli are not destroyed and can spread into lymphatics or via blood to other sites (any organs) where it can lie dormant for years. This asymptomatic situation is called latent TB infection (LTBI). It may reactivate in 10% of people throughout their lifetime; this increases with immunosuppression and HIV infection. The course of illness is chronic and indolent. However, rapid progression to fulminant disease may result if the host is immunocompromised. Pulmonary TB is the most common and important form of TB because it is the infectious form of the disease. In areas where reactivation predominates (like the UK), there is a higher proportion of extrapulmonary TB. Tuberculosis bacilli resist destaining with acid alcohol treatment hence the term. This retention is due to complexing of the carbolfuschin Ziehl-Neelsen stain with mycolic acids present in the waxy cell wall, including lipoarabinomannan (which facilitates survival in macrophages). Microscopy will diagnose TB in 80% of smear-positive patients with a first sputum sample, a further 15% with the second, and 5% with a third. In endemic areas finding acid-fast bacilli in sputum has a 98% specificity, but this is not the case in the UK, a low-prevalence setting, where atypical mycobacteria can have a similar prevalence. In the best settings only 60% of culture-positive patients are also sputum smear-positive as liquid culture, the gold standard, and most sensitive test.
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Тези доповідей конференцій з теми "Necrotic cell clearance"

1

Napirei, M., H. Karsunky, R. Paddenberg, B. Zevnik, S. Wulf, T. Möröy, and HG Mannherz. "OP0075 Chromatin clearance from necrotic cells by a concerted action of dnase 1 and serine proteases resembles apoptotic dna-degradation." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.1239.

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2

Han, Ji-Young, Ye-Ji Lee, Keung-Sub Song, and Jihee L. Kang. "Tumor Necrosis Factor Alpha-Converting Enzyme Metalloproteinase Iinhibitor-0 Promotes Apoptotic Cell Clearance And Suppresses Inflammation And Apoptosis In Bleomycin-Induced Lung Injury." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5986.

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3

Shimp, Samuel K., Christopher M. Reilly, and Marissa Nichole Rylander. "Empirical Modeling the Effect of Hsp90 Inhibition on Cytokines Associated With Impaired Biotransport of Apoptotic Debris." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19572.

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Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disorder that can affect nearly every organ in the body. A link has been established between abnormal biotransport of apoptotic cell debris and pathogenesis of SLE [1]. Lupus mice are hyper-responsive to immune stimulation and overproduce inflammatory mediators including IL-6, IL-12, and nitric oxide (NO) [2]. Extracellular expression and transport of inflammatory cytokines are thought to be involved with the inhibited clearance of cellular debris [1]. Hsp90 has a prominent role in folding and conformational regulation of several client proteins, including proteins involved with production of inflammatory mediators [3]. Hsp90 readily binds ATP at the amino (N-) terminal domain. This binding event causes a conformational change in Hsp90 making it “clamp down” on its client protein [3]. Geldanamycin (Geld) is a known inhibitor of Hsp90 that out competes ATP binding at the N-terminal. This prevents chaperone capability and ultimately leads to client protein deactivation, destabilization, and degradation [3]. Hsp90 inhibitors have been shown to suppress immune stimulated release of interleukin 6 (IL-6), IL-12, tumor necrosis factor alpha (TNF-α), and nitric oxide (NO) [4].
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4

De Angelis, V., M. Zambon, L. Toffolo, C. Donada, G. L. Molaro, and R. Zuin. "ACTIVATION OF FACTOR VII IS RELATED TO BLEEDING TENDENCY IN LIVER CIRRHOSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644800.

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Coagulation abnormalities are among the number of potential risk factors toinitiate the bleeding episodes from gastrcr-esophageal varices in liver cirrhosis. The impairment of liver clearance of activated coagulation factors, the release of thromboplastin-like activity from the necrotic liver cells and the hemodynamic changes due to expanded bollaterals may all contribute to activate the coagulation cascade.However, little is known about the mechanisms leading to this activation. Activated Factor VII (FVIIa) is known totrigger both intrinsec and extrinsec coagulation pathway. Therefore, we measured FVIIa in a group of 33 cirrhotic patients in order to see if a difference between bleeders and non-bleeders patients would correlate with Factor VII activation. The patients were divided in two groups according to the presence or the absence of major bleeding from gastroesophageal varices; haemorragic episodes were confirmed by a gastroscopic examination performed during or immediately after bleeding episodes. Factor VII coagulant assay (VII:C - one stage clotting method) and Factor VII coupled amidolytic assay (VII:CHR) were performed and a factor VII activity ratio (VIIa) was calculated as VII:C/VII:CHR. The results (mean ± S.E.) are summarized in this table:No difference in Vila distribution was seen when the patients were divided on the base of liver impairment (according to Child’s criteria) .Our study shows that FVII activation is related to bleeding from esophageal varices but not to the degree of liver impairment and strongly suggests the existence of an hypercoagulable state in liver cirrhosis, probably related to major bleeding from gastroesophageal varices in cirrhotic patients.
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