This HTML5 document contains 43 embedded RDF statements represented using HTML+Microdata notation.

The embedded RDF content will be recognized by any processor of HTML5 Microdata.

Namespace Prefixes

PrefixIRI
dctermshttp://purl.org/dc/terms/
n13http://purl.org/net/nknouf/ns/bibtex#
n12http://localhost/temp/predkladatel/
n18http://linked.opendata.cz/resource/domain/vavai/projekt/
n6http://linked.opendata.cz/resource/domain/vavai/riv/tvurce/
n24http://linked.opendata.cz/resource/domain/vavai/subjekt/
n23http://linked.opendata.cz/ontology/domain/vavai/
n10http://linked.opendata.cz/resource/domain/vavai/vysledek/RIV%2F00216208%3A11120%2F12%3A43902754%21RIV13-MSM-11120___/
n20https://schema.org/
n7http://linked.opendata.cz/resource/domain/vavai/zamer/
shttp://schema.org/
skoshttp://www.w3.org/2004/02/skos/core#
rdfshttp://www.w3.org/2000/01/rdf-schema#
n4http://linked.opendata.cz/ontology/domain/vavai/riv/
n19http://bibframe.org/vocab/
n2http://linked.opendata.cz/resource/domain/vavai/vysledek/
rdfhttp://www.w3.org/1999/02/22-rdf-syntax-ns#
n16http://linked.opendata.cz/ontology/domain/vavai/riv/klicoveSlovo/
n14http://linked.opendata.cz/ontology/domain/vavai/riv/duvernostUdaju/
xsdhhttp://www.w3.org/2001/XMLSchema#
n21http://linked.opendata.cz/ontology/domain/vavai/riv/jazykVysledku/
n8http://linked.opendata.cz/ontology/domain/vavai/riv/aktivita/
n22http://linked.opendata.cz/ontology/domain/vavai/riv/druhVysledku/
n9http://linked.opendata.cz/ontology/domain/vavai/riv/obor/
n11http://reference.data.gov.uk/id/gregorian-year/

Statements

Subject Item
n2:RIV%2F00216208%3A11120%2F12%3A43902754%21RIV13-MSM-11120___
rdf:type
skos:Concept n23:Vysledek
rdfs:seeAlso
http://cdn.intechopen.com/pdfs/35958/InTech-Oxidative_stress_in_human_autoimmune_joint_diseases.pdf
dcterms:description
Living with oxygen is basically unsafe, but vital. During evolution, oxygen originally a waste product of the metabolism in primitive unicellular organisms became normal product of the metabolism in higher animal species involving humans. Even when oxidative reactions are toxic, and destructive, they are tolerated by all organisms to some extent. The fact has opened the discussion about efficiency of antioxidant mechanisms. The classical enzyme antioxidant defence alone does not explain high tolerance of the organism for oxygen. Moreover, enzyme antioxidant mechanisms are not hundred percent effective in preventing oxidation what allows oxidative damage to continue. The pathogenesis of autoimmune joint inflammatory diseases is related to activation of native immune system. At site of inflammation, activated neutrophils and macrophages consume large amounts of oxygen, whose corollary is the increase of reactive oxygen species (ROS) production. There are several mechanisms how oxidative stress is involved into the pathogenesis of autoimmune joint inflammatory diseases. Excess production of ROS in the joint area encourages process of re-oxygenation, which then promotes joint inflammation. ROS further inhibit connective tissue cell proliferation, in some cases ROS have been shown to induce cell death to these cells inducing apoptosis Living with oxygen is basically unsafe, but vital. During evolution, oxygen originally a waste product of the metabolism in primitive unicellular organisms became normal product of the metabolism in higher animal species involving humans. Even when oxidative reactions are toxic, and destructive, they are tolerated by all organisms to some extent. The fact has opened the discussion about efficiency of antioxidant mechanisms. The classical enzyme antioxidant defence alone does not explain high tolerance of the organism for oxygen. Moreover, enzyme antioxidant mechanisms are not hundred percent effective in preventing oxidation what allows oxidative damage to continue. The pathogenesis of autoimmune joint inflammatory diseases is related to activation of native immune system. At site of inflammation, activated neutrophils and macrophages consume large amounts of oxygen, whose corollary is the increase of reactive oxygen species (ROS) production. There are several mechanisms how oxidative stress is involved into the pathogenesis of autoimmune joint inflammatory diseases. Excess production of ROS in the joint area encourages process of re-oxygenation, which then promotes joint inflammation. ROS further inhibit connective tissue cell proliferation, in some cases ROS have been shown to induce cell death to these cells inducing apoptosis
dcterms:title
Chapter 19: Oxidative stress in human autoimmune joint diseases Chapter 19: Oxidative stress in human autoimmune joint diseases
skos:prefLabel
Chapter 19: Oxidative stress in human autoimmune joint diseases Chapter 19: Oxidative stress in human autoimmune joint diseases
skos:notation
RIV/00216208:11120/12:43902754!RIV13-MSM-11120___
n23:predkladatel
n24:orjk%3A11120
n4:aktivita
n8:S n8:P n8:Z
n4:aktivity
P(LC554), S, Z(MSM0021620816)
n4:dodaniDat
n11:2013
n4:domaciTvurceVysledku
n6:9044833
n4:druhVysledku
n22:C
n4:duvernostUdaju
n14:S
n4:entitaPredkladatele
n10:predkladatel
n4:idSjednocenehoVysledku
126758
n4:idVysledku
RIV/00216208:11120/12:43902754
n4:jazykVysledku
n21:eng
n4:klicovaSlova
inflammatory synovitis; arthritis; oxidative stress
n4:klicoveSlovo
n16:inflammatory%20synovitis n16:oxidative%20stress n16:arthritis
n4:kontrolniKodProRIV
[DE139B9DAAD3]
n4:mistoVydani
Rijeka
n4:nazevZdroje
Oxidative stress and diseases [on-line]
n4:obor
n9:EB
n4:pocetDomacichTvurcuVysledku
1
n4:pocetStranKnihy
610
n4:pocetTvurcuVysledku
1
n4:projekt
n18:LC554
n4:rokUplatneniVysledku
n11:2012
n4:tvurceVysledku
Škurlová, Martina
n4:zamer
n7:MSM0021620816
s:numberOfPages
19
n19:doi
10.5772/33460
n13:hasPublisher
InTech
n20:isbn
978-953-51-0552-7
n12:organizacniJednotka
11120