FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4229020912> ?p ?o ?g. }

• W4229020912 endingPage "26" @default.
• W4229020912 startingPage "18" @default.
• W4229020912 abstract "The purpose of the study was to identify specific links between genotypic and phenotypic changes in the body that can lead to inflammatory skin diseases and dysbiosis. Materials and methods. Medline / PubMed, Embase, Web of Science databases were searched and research studies related to inflammatory skin diseases: immunity, genetics, epigenetics, epidermal barrier, skin microbiome, etc. were analyzed. The results of microbiome studies based on cultivation methods were excluded from the study. Results and discussion. Inflammatory skin diseases often lead to physical or psychological disorders, but the cause of these diseases is still unclear. Pathogenesis of inflammatory skin diseases includes heredity, environmental impact, immunity changes, epidermal barrier dysfunction, mental disorders, infections, and more. A better understanding of the role of microbiome, genetic abnormalities and phenotypic changes may help to predict the occurrence of seborrheic dermatitis in humans. The human microbiome is directly involved in the formation of host immunity. In particular, skin residents maintain the stability of the skin barrier, regulate inflammation and the immune response. Mutualistic symbioses provide homeostasis of the human-host relationship and the microbiome. However, under the influence of the external environment, genetic and physiological changes, the balance of the microbial community and man is disturbed, which can negatively regulate the condition of the host and cause disease. Most symbiotic skin microbiota coexists peacefully with the host and become pathogenic only under certain conditions. The transition from symbiosis to pathogenicity is a complex process, because the skin is well resistant to aggressive factors. Potential attackers must induce gene expression to enable adhesion, invasion, and avoidance of the immune response. The skin microbiome induces inflammation and skin healing. Also it may change its qualitative and quantitative composition to adapt to existing inflammatory conditions. Conclusion. Microorganisms grown under conditions of homeostasis perfectly interact with the human-host in a healthy symbiotic relationship. Under conditions of impaired immune system response, abnormal gene expression or dysfunction of the skin barrier microbiome residents use a variety of defense mechanisms to survive, that plays an important role in the pathogenesis of inflammatory skin diseases. Understanding the species composition of the microbiome, its dynamic changes and effects on human skin makes it possible to predict the possible occurrence of seborrheic dermatitis, control inflammation and prevent exacerbations" @default.
• W4229020912 created "2022-05-08" @default.
• W4229020912 creator A5003379039 @default.
• W4229020912 creator A5039287953 @default.
• W4229020912 date "2022-05-06" @default.
• W4229020912 modified "2023-09-27" @default.
• W4229020912 title "The Role of Genes and Skin Microbiome in the Development of Seborrheic Dermatitis" @default.
• W4229020912 cites W1623761777 @default.
• W4229020912 cites W1968661266 @default.
• W4229020912 cites W1971079822 @default.
• W4229020912 cites W1977686320 @default.
• W4229020912 cites W1980496604 @default.
• W4229020912 cites W1982704806 @default.
• W4229020912 cites W1983952381 @default.
• W4229020912 cites W1998541797 @default.
• W4229020912 cites W1999151001 @default.
• W4229020912 cites W2002178604 @default.
• W4229020912 cites W2003258181 @default.
• W4229020912 cites W2003768155 @default.
• W4229020912 cites W2042926093 @default.
• W4229020912 cites W2054259512 @default.
• W4229020912 cites W2060130170 @default.
• W4229020912 cites W2061913303 @default.
• W4229020912 cites W2072982170 @default.
• W4229020912 cites W2073396586 @default.
• W4229020912 cites W2077590888 @default.
• W4229020912 cites W2089606456 @default.
• W4229020912 cites W2101046603 @default.
• W4229020912 cites W2125732695 @default.
• W4229020912 cites W2143105792 @default.
• W4229020912 cites W2151051787 @default.
• W4229020912 cites W2293713895 @default.
• W4229020912 cites W2378861546 @default.
• W4229020912 cites W2396875337 @default.
• W4229020912 cites W2537139861 @default.
• W4229020912 cites W2542762131 @default.
• W4229020912 cites W2555202449 @default.
• W4229020912 cites W2556917229 @default.
• W4229020912 cites W2568590455 @default.
• W4229020912 cites W2574978917 @default.
• W4229020912 cites W2736056004 @default.
• W4229020912 cites W2742350697 @default.
• W4229020912 cites W2772747033 @default.
• W4229020912 cites W2773553976 @default.
• W4229020912 cites W2792597482 @default.
• W4229020912 cites W2894824333 @default.
• W4229020912 cites W2911520506 @default.
• W4229020912 cites W2919964671 @default.
• W4229020912 cites W2939998169 @default.
• W4229020912 cites W2952250112 @default.
• W4229020912 cites W2964939904 @default.
• W4229020912 cites W3013877382 @default.
• W4229020912 cites W3048255267 @default.
• W4229020912 cites W3161328221 @default.
• W4229020912 cites W4255570858 @default.
• W4229020912 doi "https://doi.org/10.26693/jmbs07.02.018" @default.
• W4229020912 hasPublicationYear "2022" @default.
• W4229020912 type Work @default.
• W4229020912 citedByCount "0" @default.
• W4229020912 crossrefType "journal-article" @default.
• W4229020912 hasAuthorship W4229020912A5003379039 @default.
• W4229020912 hasAuthorship W4229020912A5039287953 @default.
• W4229020912 hasBestOaLocation W42290209121 @default.
• W4229020912 hasConcept C104317684 @default.
• W4229020912 hasConcept C127716648 @default.
• W4229020912 hasConcept C142724271 @default.
• W4229020912 hasConcept C143098186 @default.
• W4229020912 hasConcept C143121216 @default.
• W4229020912 hasConcept C16005928 @default.
• W4229020912 hasConcept C203014093 @default.
• W4229020912 hasConcept C2777165150 @default.
• W4229020912 hasConcept C2777484424 @default.
• W4229020912 hasConcept C2779134260 @default.
• W4229020912 hasConcept C2779341262 @default.
• W4229020912 hasConcept C41091548 @default.
• W4229020912 hasConcept C54355233 @default.
• W4229020912 hasConcept C71924100 @default.
• W4229020912 hasConcept C86803240 @default.
• W4229020912 hasConcept C8891405 @default.
• W4229020912 hasConceptScore W4229020912C104317684 @default.
• W4229020912 hasConceptScore W4229020912C127716648 @default.
• W4229020912 hasConceptScore W4229020912C142724271 @default.
• W4229020912 hasConceptScore W4229020912C143098186 @default.
• W4229020912 hasConceptScore W4229020912C143121216 @default.
• W4229020912 hasConceptScore W4229020912C16005928 @default.
• W4229020912 hasConceptScore W4229020912C203014093 @default.
• W4229020912 hasConceptScore W4229020912C2777165150 @default.
• W4229020912 hasConceptScore W4229020912C2777484424 @default.
• W4229020912 hasConceptScore W4229020912C2779134260 @default.
• W4229020912 hasConceptScore W4229020912C2779341262 @default.
• W4229020912 hasConceptScore W4229020912C41091548 @default.
• W4229020912 hasConceptScore W4229020912C54355233 @default.
• W4229020912 hasConceptScore W4229020912C71924100 @default.
• W4229020912 hasConceptScore W4229020912C86803240 @default.
• W4229020912 hasConceptScore W4229020912C8891405 @default.
• W4229020912 hasIssue "2" @default.
• W4229020912 hasLocation W42290209121 @default.
• W4229020912 hasOpenAccess W4229020912 @default.

• next