Thematische Bibliographien / Interleukin-6

Inhaltsverzeichnis

  1. Zeitschriftenartikel
  2. Dissertationen
  3. Bücher
  4. Buchteile
  5. Konferenzberichte
  6. Berichte der Organisationen

Auswahl der wissenschaftlichen Literatur zum Thema „Interleukin-6“

Autor: Grafiati
Veröffentlicht am 4. Juni 2021
Zuletzt aktualisiert am 1. Juli 2024

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Zeitschriftenartikel zum Thema "Interleukin-6"

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&NA;. „Interleukin-3/interleukin-6“. Reactions Weekly &NA;, Nr. 550 (Mai 1995): 11. http://dx.doi.org/10.2165/00128415-199505500-00035.

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&NA;. „Interleukin-6“. Reactions Weekly &NA;, Nr. 570 (September 1995): 9. http://dx.doi.org/10.2165/00128415-199505700-00023.

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Lotz, Martin. „Interleukin-6“. Cancer Investigation 11, Nr. 6 (Januar 1993): 732–42. http://dx.doi.org/10.3109/07357909309046948.

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&NA;. „Interleukin 6“. Inpharma Weekly &NA;, Nr. 877 (März 1993): 2. http://dx.doi.org/10.2165/00128413-199308770-00001.

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&NA;. „Interleukin 6“. Reactions Weekly &NA;, Nr. 505 (Juni 1994): 8. http://dx.doi.org/10.2165/00128415-199405050-00037.

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&NA;. „Interleukin 6“. Reactions Weekly &NA;, Nr. 531 (Dezember 1994): 8. http://dx.doi.org/10.2165/00128415-199405310-00027.

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Song, Mingchen, und John A. Kellum. „Interleukin-6“. Critical Care Medicine 33, Suppl (Dezember 2005): S463—S465. http://dx.doi.org/10.1097/01.ccm.0000186784.62662.a1.

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CASTELL, JOSé V., TILO ANDUS, DIETER KUNZ und PETER C. HEINRICH. „Interleukin-6“. Annals of the New York Academy of Sciences 557, Nr. 1 (28.06.2008): 87–101. http://dx.doi.org/10.1111/j.1749-6632.1989.tb24001.x.

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LEE, FRANK, CHOY-PIK CHIU, JANUSZ WIDEMAN, PHILLIP HODGKIN, SUSAN HUDAK, LOUISE TROUTT, THERESA NG et al. „Interleukin-6“. Annals of the New York Academy of Sciences 557, Nr. 1 (28.06.2008): 215–29. http://dx.doi.org/10.1111/j.1749-6632.1989.tb24015.x.

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CLARK, STEVEN C. „Interleukin-6“. Annals of the New York Academy of Sciences 557, Nr. 1 (28.06.2008): 438–43. http://dx.doi.org/10.1111/j.1749-6632.1989.tb24036.x.

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Dissertationen zum Thema "Interleukin-6"

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Schebesta, Kathrin [Verfasser]. „Das Endothel sezerniert Interleukin-6 (IL-6) und stimuliert die adrenale Interleukin-6 und Aldosteronsynthese über einen Interleukin-6 unabhängigen Mechanismus / Kathrin Schebesta“. Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2015. http://d-nb.info/1079652612/34.

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OBAFEMI, TOLULOPE FESAYO. „THE EFFECTS OF INTERLEUKIN 6 AND INTERLEUKIN 10 ON FRAILTY IN C57BL/6 MICE“. Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/613394.

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Studies have shown that pro-inflammatory IL-6 and anti-inflammatory IL-10 interleukins may correlate to frailty and aging. This frailty can be defined in the context of clinical symptoms which include sarcopenia and osteoporosis, decreased activity level; or in the context of increased susceptibility to adverse health outcomes from a deficient immune system. In this experiment we tested a cohort of conditionally regulated IL-6 and IL-10 mice with controls (IL-6tg+.rtTA(r/r) (n=8), IL-10(-/-). IL-10tg+ rtTA(r/r) (n=10) and rtTA(r/r) (n=5)) under frailty assessments and immunological cell analysis. We were unable to successfully induce expression in the conditionally regulated mice. Subsequently, there was no difference in the frailty scores, weight, or temperature fluctuation between all three genotypes. As a preliminary study, there arose essential learning points of improvement that can be applied to future experiments concerning frailty in transgenic mice.
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Terry, Catherine. „Genetic control of Interleukin-6 gene“. Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342452.

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Höschen-Lihs, Jutta. „Interleukin-6- und Interleukin-2-Rezeptor als Aktivitätsmarker bei infektiöser Endokarditis“. [S.l.] : [s.n.], 2005. http://archiv.ub.uni-marburg.de/diss/z2005/0327/.

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Siegmund, Annette. „Interleukin-11 - analog zu Interleukin-6 - ein direkter Modulator der Nebennierenrinde“. Diss., lmu, 2008. http://nbn-resolving.de/urn:nbn:de:bvb:19-83542.

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Desallais, Lucille. „Immunisation active à base de peptides, dérivés de l’IL-6 et de l’IL-1β, dans les maladies inflammatoires chroniques“. Thesis, Paris, CNAM, 2013. http://www.theses.fr/2013CNAM0867.

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Les anticorps monoclonaux anti-cytokine ont constitué une révolution dans le traitement des maladies inflammatoires chroniques, mais leur utilisation présente des inconvénients (non réponse, résistance, effets secondaires, coûts élevés).Notre équipe développe une stratégie alternative originale, l’immunisation active à base de peptides de cytokines. Elle a pour but de faire synthétiser, par l’organisme même du patient, des anticorps neutralisant les effets pathogènes dus à l’excès de cytokines.Durant ma thèse, j’ai montré que l’immunisation active contre un peptide dérivé de l’IL-6 murine est protectrice dans un modèle murin de sclérodermie systémique. L’immunisation de singes avec l’équivalent humain entraîne une réduction significative des réactions inflammatoires locales suite à l’induction d’une réaction d’HSR. De plus, l’immunisation active contre deux peptides dérivés de l’IL-1β et de l’IL-23 conduit à la réduction de la sévérité de l’EAE.Ces résultats confortent l’intérêt de cibler les cytokines par l’approche d’immunisation active à base de peptides, qui pourra permettre de diversifier l’offre thérapeutique actuellement disponible
Monoclonal antibodies have been a revolution for the treatment of chronic inflammatory diseases, but their use shows major drawbacks (non-response, resistance, side effects and prohibitive costs).Our team develops an original alternative strategy: anti-cytokine peptide-based active immunization.The aim of the approach is to make the patient’s own organism produce antibodies capable of neutralizing the pathogenic effects of cytokine overproduction.During my PhD, I have demonstrated that active immunization against an IL-6 murine peptide confers clinical protection in a murine model of systemic sclerosis. Monkeys immunized against the human peptide also showed a significant decrease of local inflammatory reactions following a delayed-type hypersensitivity reaction. Moreover, active immunization against an IL-1β and an IL-23 murinepeptide led to a reduction of the severity of the EAE in mice.These results comfort the interest of anti-cytokine peptide-based active immunization, which should eventually widen the choice of therapeutics available for the patients
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Walter, Claudia. „Bestimmung der Zytokine Interleukin-1ra, Interleukin-6, Interleukin-10 und Interleukin-12 im Vaginalsekret bei Frauen mit Bakterieller Vaginose“. Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-28461.

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Slawik, Helen Christina. „Kontinuierliche Überexpression von Interleukin-6 im Zentralnervensystem lokale Applikation des Designerzytokins Hyper-Interleukin-6 im adulten Organismus der Ratte und Auswirkungen von exzitatorischen Neurotoxinen im Interleukin-6-transgenen Mausmodell /“. [S.l.] : [s.n.], 2003. http://www.freidok.uni-freiburg.de/volltexte/842.

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Gopinathan, Ganga. „The effects of interleukin-6 on angiogenesis“. Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8186.

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Elevated levels of the inflammatory cytokine interleukin-6, IL-6, have been linked with poor prognosis in ovarian cancer patients by influencing tumour growth, invasion, angiogenesis and chemo-resistance. A clinical trial conducted in parallel with pre-clinical studies showed an anti-IL-6 antibody to have some activity in ovarian cancer patients and in xenograft models, via reduction in pro-inflammatory and angiogenic factors such as TNF-α, IL-8 and VEGF. Anti-IL-6 treatment also showed significant reductions in vascular area with decreased expression of an angiogenic factor Jagged1. The aim of my study was to investigate the effects of IL-6 on normal and tumour angiogenesis. I found that recombinant IL-6 stimulates angiogenesis in mouse and rat aortic ring assays and that it can also stimulate growth and migration of endothelial cells in vitro. IL-6 has similar potency as VEGF in inducing vessel sprouting. IL-6 itself does not induce VEGF in the endothelial cells I tested. Investigation of the effects of IL-6 on vessel maturation revealed a significant reduction in pericyte coverage of vessels treated with IL-6 compared with VEGF. Collectively, these data led to my hypothesis that ‘IL-6 drives aberrant angiogenesis, independent of VEGF signalling’. Investigating the mechanism by which IL-6 drives angiogenesis and leads to defective pericyte formation, I showed a link between IL-6 and the Notch ligands, Jagged1 and DLL4. My data suggested that IL-6 could stimulate Jagged1 in endothelial cells, whereas VEGF induces DLL4, the Notch ligand known to be involved in inducing stalk phenotype. Exploring previous findings to get a better understanding of the interaction of Notch ligands and pericyte recruitment also suggested a role of Angiopoeitin-2 in relation to IL-6 signalling. These observations were extended in IGROV-1 ovarian cancer xenografts treated with an anti-IL-6 antibody and by analysis of gene expression datasets from ovarian cancer biopsies. My results suggest therapeutic potential of combining inhibitors of IL-6 and VEGF in ovarian cancer.
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Sonnenberg, Sabine. „Tissue specific genetic regulation of Interleukin 6“. Thesis, University of Southampton, 2009. https://eprints.soton.ac.uk/72590/.

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Interleukin 6 (IL6) is associated with arterial disease development, progression and surgical outcome. Raised levels of IL6 may play a causal role in disease development or may be the effect of pathology. An IL6 single nucleotide polymorphism (SNP) G- 174C has been identified and reported to associate with IL6 expression. However, conflicting results have emerged and both the relationship between IL6 and vascular disease and the precise effect of SNP G-174C in vivo in humans remains obscure. The aim of this study was to establish the effect of SNP G-174C in humans, in vivo in different tissues. Varicose vein surgery patients donated adipose tissue, skeletal muscle, vein and blood samples. Patients were genotyped for SNP G-174C. A new pre-mRNA assay was developed, using gel electrophoresis, restriction digest and fluorescence quantification, to measure the ratio of heterozygous allelic pre-mRNA transcription. IL6 mRNA expression in different tissues was also measured using relative real time PCR (RT-PCR) to assess effect of tissue type on expression profiles. mRNA expression within tissues was compared between G-174C genotypes, to further quantifying the association of SNP G-174C with transcript levels. The pre-mRNA assay showed higher expression for the C-allele, though not statistically significant. The pre-mRNA assay needed to detect low levels of intron retaining allelic pre-mRNA isoforms. Replicates and controls for residual genomic DNA were used to monitor assay precision. Adipose tissue gave the greatest precision in the pre-mRNA assay. In the RT PCR assay adipose tissue expressed significantly more IL6 mRNA than all other tissues examined. In vein and leukocytes subjects with the CC genotype expressed significantly higher levels of IL6 mRNA than subjects with GC or GG genotypes. There was a trend towards higher expression for the CC genotype in all tissue types. A significant though weak correlation between IL6 mRNA expression and age was demonstrated for vein and leukocytes. Adipose tissue may be an important source of IL6 compared to other tissues. This may be relevant for obesity associated diseases. Subjects with G-174C genotype CC showed a trend towards higher IL6 RNA expression. Further studies are necessary to clarify the effect of genotype on IL6 expression.
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Bücher zum Thema "Interleukin-6"

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Tamas, Bartfai, und Ottoson David 1918-, Hrsg. Neuro-immunology of fever. Oxford [England]: Pergamon Press, 1992.

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Gregory, Bock, Marsh Joan und Widdows Kate, Hrsg. Polyfunctional cytokines: IL-6 and LIF. Chichester, Eng: Wiley, 1992.

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Young, Rosemary Irene. Cytokines and cancer: A focus on Interleukin-6. Manchester: University of Manchester, 1994.

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B, Sehgal Pravinkumar, Grieninger Gerd, Tosato Giovanna, New York Academy of Sciences. und National Foundation for Cancer Research., Hrsg. Regulation of the acute phase and immune responses: Interleukin-6. New York, N.Y: New York Academy of Sciences, 1989.

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Michel, Revel, Hrsg. IL-6: Physiopathology and clinical potentials. New York: Raven Press, 1992.

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Schwarze, Melinda Margarete K. Mechanisms of prevention of apoptosis in an interleukin-6-dependent myeloma cell line. Ottawa: National Library of Canada, 1995.

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Moldoveanu, Andrei Ion. Effects of prolonged endurance exercise on the gene expression and plasma levels of interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha. Ottawa: National Library of Canada, 1999.

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Cournoyer, Micheline. Circulating endotoxin, interleukin-6 and tumor necrosis factor alpha in a porcine model of intraabdominal sepsis. Ottawa: National Library of Canada, 1995.

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1946-, Kluger Matthew J., Oppenheim Joost J. 1934- und Powanda M. C, Hrsg. The Physiologic, metabolic, and immunologic actions of interleukin-1: Proceedings of a symposium held in Ann Arbor, Michigan, June 4-6, 1985. New York: Liss, 1985.

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Some aspects of induced protein synthesis in liver cells: Regulatory effects of interleukin-6, insulin, glicated proteins and polyglucans. Kraków: Wydawn. Uniwersytetu Jasgiellońskiego, 1997.

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Buchteile zum Thema "Interleukin-6"

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Hirano, T., und T. Kishimoto. „Interleukin-6“. In Peptide Growth Factors and Their Receptors I, 633–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-49295-2_14.

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Van Snick, J., und R. P. Nordan. „Interleukin 6“. In Growth Factors, Differentiation Factors, and Cytokines, 163–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74856-1_12.

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Chen, Taosheng. „Interleukin-6“. In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_3099-3.

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Tanaka, Toshio, Masashi Narazaki und Tadamitsu Kishimoto. „Interleukin-6“. In Encyclopedia of Medical Immunology, 579–87. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_38.

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Gressner, A. M., und O. A. Gressner. „Interleukin-6“. In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1597-1.

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Gressner, A. M., und O. A. Gressner. „Interleukin-6“. In Springer Reference Medizin, 1265–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1597.

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Kishimoto, Tadamitsu, und Toshio Tanaka. „Interleukin 6“. In Compendium of Inflammatory Diseases, 686–92. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_179.

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Hirano, T., und T. Kishimoto. „Interleukin-6“. In Peptide Growth Factors and Their Receptors I, 633–65. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4612-3210-0_14.

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Chen, Taosheng. „Interleukin-6“. In Encyclopedia of Cancer, 2317–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_3099.

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Chen, Taosheng. „Interleukin-6“. In Encyclopedia of Cancer, 1895–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3099.

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Konferenzberichte zum Thema "Interleukin-6"

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Jenkins, Brendan J., Louise McLeod, Alistair Miller, Jessica Jones, Steven Bozinovski, Ross Vlahos, Phillip Bardin, Gary P. Anderson und Saleela Ruwanpura. „Interleukin-6 Promotes Emphysema By Apoptosis“. 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.a5800.

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Gopinathan, Ganga, Carla Milagre, Oliver M. T. Pearce, Louise Reynolds, Kairbaan Hodivala-Dilke, Andrew Leinster, Haihong Zhong et al. „Abstract 4162: Interleukin–6 stimulates defective angiogenesis“. In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4162.

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Pereira da Silva, F., F. Luís, F. Jesus, É. Almeida, S. Braga, J. Ribeiro, R. Natal, J. Costa, M. Tavares und L. Ferreira. „Interleukin-6 in SARS-CoV2 risk stratification“. In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.2216.

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Perea, Beatrice, Miriana D’Alessandro, Laura Bergantini, Sara Gangi, Benedetta Zilio, Paolo Cameli und Elena Bargagli. „Interleukin-6 and krebs von den lungen-6 in lymphangioleiomyomatosis patients“. In ERS International Congress 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/13993003.congress-2023.pa3949.

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Wiegertjes, R., A. van Caam, H. van Beuningen, P. van der Kraan, F. van de Loo und E. Blaney Davidson. „P078 Transforming growth factor-beta dampens pro-inflammatory interleukin-6 signaling in chondrocytes by decreasing the interleukin-6 receptor“. In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.67.

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Tadjibayeva, K., und T. R. Romanovskaya. „REGULATORY ROLE OF INTERLEUKINS-4, 5 AND 6 IN THE DEVELOPMENT OF GLOMERULONEPHRITIS OF VARIOUS ETIOLOGIES“. In SAKHAROV READINGS 2022: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2022. http://dx.doi.org/10.46646/sakh-2022-2-24-27.

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The relationship between the concentration of interleukin-4, 5, and 6 with the content of eosinophils and the level of C-reactive protein in patients with chronic glomerulonephritis was established. An increase in eosinophils was found in patients with chronic glomerulonephritis with a predominance of interleukin-4 compared with patients with a predominance of interleukin-5 and 6, which may be an important diagnostic marker of glomerulonephritis.
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Kura, Yurie, Marco A. De Velasco, Yasuyuki Kobayashi, Naomi Ando, Emiko Fukushima, Yutaka Yamamoto, Yuji Hatanaka et al. „Abstract 1226: Interleukin-6 (IL-6) as a therapeutic target in prostate cancer.“ In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1226.

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Hippenstiel, S., J. Lorenz, J. Zahlten, B. Opitz, J. Eitel, A. Flieger, S. Scharf, N. Suttorp und BT Schmeck. „Legionella Pneumophila Induced IkappaBzeta-Dependent Expression of Interleukin-6.“ In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3248.

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Tam, A., X. Shi Wen, B. Ahmed-Abdi, C. Denton, D. Abraham und V. Ong. „AB0166 Interleukin-6-polarised macrophages promote dermal myofibroblast differentiation“. In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4868.

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Räsänen, Kati A., Laura Hautala, Ulf-Håkan Stenman und Hannu Koistinen. „Abstract 439: Interleukin-6 induces SPINK1 in colorectal cancer“. In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-439.

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Berichte der Organisationen zum Thema "Interleukin-6"

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Keller, Evan T. Interleukin-6 and Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, Juli 2001. http://dx.doi.org/10.21236/ada398242.

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Keller, Evan T. Interleukin-6 and Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, Juli 2002. http://dx.doi.org/10.21236/ada407280.

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Keller, Evan T. Interleukin-6 and Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, Juli 2003. http://dx.doi.org/10.21236/ada418080.

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Rokita, Hanna, Ruta Neta und Jean D. Sipe. Increased Fibrinogen Synthesis in Mice During the Acute Phase Response: Co-Operative Interaction of Interleukin 1, Interleukin 6, and Interleukin 1 Receptor Antagonist. Fort Belvoir, VA: Defense Technical Information Center, September 1993. http://dx.doi.org/10.21236/ada280464.

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Knudsen, Beatrice S. Hepatocyte Growth Factor and Interleukin-6 in Prostate Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, März 2005. http://dx.doi.org/10.21236/ada435856.

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Knudsen, Beatrice S. Hepatocyte Growth Factor and Interleukin-6 in Prostate Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, März 2004. http://dx.doi.org/10.21236/ada428439.

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Knudesen, Beatrice S. Hepatocyte Growth Factor and Interleukin-6 in Prostate Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, März 2003. http://dx.doi.org/10.21236/ada416620.

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Knudsen, Beatrice S. Hepatocyte Growth Factor and Interleukin-6 in Prostate Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, Juni 2006. http://dx.doi.org/10.21236/ada467982.

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Huang, Xinyi, Manman Zhang, Jiaojiao Wang und Fuyong Hu. Association between interleukin-6 levels and stroke：a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, Mai 2024. http://dx.doi.org/10.37766/inplasy2024.5.0089.

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Jafrin, Sarah, Md Abdul Aziz und Mohammad Safiqul Islam. Elevated levels of pleiotropic interleukin-6 (IL-6) and interleukin-10 (IL-10) are critically involved with the severity and mortality of COVID-19: An updated longitudinal meta-analysis and systematic review on 147 studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0046.

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Annotation:
Review question / Objective: How were serum IL-6 and IL-10 linked with the severity and mortality of COVID-19 patients? To evaluate the role of IL-6 and IL-10 in the development of the severity or morality of COVID-19 patients. The outcomes (mean difference) were calculated between the severe vs. non-severe COVID-19 patients and non-survival vs. survival patients to evaluate the risk of severity or mortality. Condition being studied: Severity and mortality among the COVID-19 patients. Information sources: The international scientific authorized databases such as Google Scholar, PubMed, Embase, CNKI, Cochrane Library, and Web of science were used as primary sources to identify and collect the eligible literature. Additional secondary databases were also comprehensively searched to extract more related studies.
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