FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3213985589> ?p ?o ?g. }

• W3213985589 endingPage "20" @default.
• W3213985589 startingPage "14" @default.
• W3213985589 abstract "Introduction. In modern obstetrics, there are a significant number of diagnostic methods to detect fetal distress, including intrapartum. At the same time, the mechanisms of fetal adaptation to various stressors remain poorly understood. The aim of our study was to provide a clinical assessment of brain and glial neurotrophic factors (NTF) in umbilical cord blood when the fetus is exposed to stressors. Materials and methods . The study included 96 cases, which were divided into five groups depending on the data of retrospective analysis of the history of childbirth, the condition of the newborn. After delivery samples were taken, the level of BDNF (brain-derived neurotrophic factor), GDNF (glial cell-derived neurotrophic factor). Results. The mean NTF level of BDNF in group 1 was 970.3 (60.9) ng/mL, in group 2 was 1499.8 (72.12) ng/mL, in group 3 was 1243.5 (67.49) ng/mL, in group 4 was 1245.5(80.8) ng/mL, in group 5 was 573.5(43.9) ng/mL (p<0.001). Mean GDNF NTF level in group 1 was 35 pg/mL, in group 2 was 41.3 pg/mL, in group 3 was 311.00 pg/mL, in group 4 was 80.00 pg/mL, and in group 5 was 35.6 pg/mL, (p><0.001). The incidence of fetal functional impairment in labor was not established in group 1, group 2 was 18.8%, group 3 was 29.2%, group 4 was 35.3%, and group 5 was 77.8% (p=0.001). The incidence of impaired fetal functional status in labor was not established in groups 1 and 2, in group 3, 4.2%, in group 4, 17.6%, and in group 5, 77.8% (p><0.001). Discussion. Clinical study data indicate the existence of a close relationship between the level of neurotrophic factors and the realization of fetal compensatory-adaptive capabilities in the presence of fetal hypoxia development factors in labor. Conclusion. The participation of BDNF and GDNF molecules in the regulation of fetal homeostasis under intrapartum exposure to stressors has been established. High levels of BDNF and GDNF provide fetal protection as part of an endogenous system of compensatory mechanisms in the regulation of fetal homeostasis.><0.001). Mean GDNF NTF level in group 1 was 35 pg/mL, in group 2 was 41.3 pg/mL, in group 3 was 311.00 pg/mL, in group 4 was 80.00 pg/mL, and in group 5 was 35.6 pg/mL, (p<0.001). The incidence of fetal functional impairment in labor was not established in group 1, group 2 was 18.8%, group 3 was 29.2%, group 4 was 35.3%, and group 5 was 77.8% (p=0.001). The incidence of impaired fetal functional status in labor was not established in groups 1 and 2, in group 3, 4.2%, in group 4, 17.6%, and in group 5, 77.8% (p><0.001). Discussion. Clinical study data indicate the existence of a close relationship between the level of neurotrophic factors and the realization of fetal compensatory-adaptive capabilities in the presence of fetal hypoxia development factors in labor. Conclusion. The participation of BDNF and GDNF molecules in the regulation of fetal homeostasis under intrapartum exposure to stressors has been established. High levels of BDNF and GDNF provide fetal protection as part of an endogenous system of compensatory mechanisms in the regulation of fetal homeostasis.><0.001). The incidence of fetal functional impairment in labor was not established in group 1, group 2 was 18.8%, group 3 was 29.2%, group 4 was 35.3%, and group 5 was 77.8% (p=0.001). The incidence of impaired fetal functional status in labor was not established in groups 1 and 2, in group 3, 4.2%, in group 4, 17.6%, and in group 5, 77.8% (p<0.001). Discussion. Clinical study data indicate the existence of a close relationship between the level of neurotrophic factors and the realization of fetal compensatory-adaptive capabilities in the presence of fetal hypoxia development factors in labor. Conclusion. The participation of BDNF and GDNF molecules in the regulation of fetal homeostasis under intrapartum exposure to stressors has been established. High levels of BDNF and GDNF provide fetal protection as part of an endogenous system of compensatory mechanisms in the regulation of fetal homeostasis.><0.001). Discussion. Clinical study data indicate the existence of a close relationship between the level of neurotrophic factors and the realization of fetal compensatory-adaptive capabilities in the presence of fetal hypoxia development factors in labor. Conclusion . The participation of BDNF and GDNF molecules in the regulation of fetal homeostasis under intrapartum exposure to stressors has been established. High levels of BDNF and GDNF provide fetal protection as part of an endogenous system of compensatory mechanisms in the regulation of fetal homeostasis." @default.
• W3213985589 created "2021-11-22" @default.
• W3213985589 creator A5020432273 @default.
• W3213985589 creator A5032022887 @default.
• W3213985589 creator A5054335697 @default.
• W3213985589 creator A5056853749 @default.
• W3213985589 date "2021-11-11" @default.
• W3213985589 modified "2023-10-16" @default.
• W3213985589 title "Value of BDNF and GDNF extracellular regulatory molecules in fetal umbilical cord blood. Clinical study" @default.
• W3213985589 cites W1543554996 @default.
• W3213985589 cites W1853568386 @default.
• W3213985589 cites W2002512748 @default.
• W3213985589 cites W2074362144 @default.
• W3213985589 cites W2089865358 @default.
• W3213985589 cites W2592810444 @default.
• W3213985589 cites W2598601537 @default.
• W3213985589 cites W2771760183 @default.
• W3213985589 cites W2779397213 @default.
• W3213985589 cites W2801508060 @default.
• W3213985589 cites W2889082270 @default.
• W3213985589 cites W2908506786 @default.
• W3213985589 cites W2919774896 @default.
• W3213985589 cites W3009110953 @default.
• W3213985589 doi "https://doi.org/10.52420/2071-5943-2021-20-3-14-20" @default.
• W3213985589 hasPublicationYear "2021" @default.
• W3213985589 type Work @default.
• W3213985589 sameAs 3213985589 @default.
• W3213985589 citedByCount "0" @default.
• W3213985589 crossrefType "journal-article" @default.
• W3213985589 hasAuthorship W3213985589A5020432273 @default.
• W3213985589 hasAuthorship W3213985589A5032022887 @default.
• W3213985589 hasAuthorship W3213985589A5054335697 @default.
• W3213985589 hasAuthorship W3213985589A5056853749 @default.
• W3213985589 hasBestOaLocation W32139855891 @default.
• W3213985589 hasConcept C105702510 @default.
• W3213985589 hasConcept C126322002 @default.
• W3213985589 hasConcept C134018914 @default.
• W3213985589 hasConcept C160539049 @default.
• W3213985589 hasConcept C170493617 @default.
• W3213985589 hasConcept C172680121 @default.
• W3213985589 hasConcept C185856081 @default.
• W3213985589 hasConcept C2776955114 @default.
• W3213985589 hasConcept C2779234561 @default.
• W3213985589 hasConcept C2780109559 @default.
• W3213985589 hasConcept C2780914630 @default.
• W3213985589 hasConcept C42219234 @default.
• W3213985589 hasConcept C54355233 @default.
• W3213985589 hasConcept C71924100 @default.
• W3213985589 hasConcept C86803240 @default.
• W3213985589 hasConceptScore W3213985589C105702510 @default.
• W3213985589 hasConceptScore W3213985589C126322002 @default.
• W3213985589 hasConceptScore W3213985589C134018914 @default.
• W3213985589 hasConceptScore W3213985589C160539049 @default.
• W3213985589 hasConceptScore W3213985589C170493617 @default.
• W3213985589 hasConceptScore W3213985589C172680121 @default.
• W3213985589 hasConceptScore W3213985589C185856081 @default.
• W3213985589 hasConceptScore W3213985589C2776955114 @default.
• W3213985589 hasConceptScore W3213985589C2779234561 @default.
• W3213985589 hasConceptScore W3213985589C2780109559 @default.
• W3213985589 hasConceptScore W3213985589C2780914630 @default.
• W3213985589 hasConceptScore W3213985589C42219234 @default.
• W3213985589 hasConceptScore W3213985589C54355233 @default.
• W3213985589 hasConceptScore W3213985589C71924100 @default.
• W3213985589 hasConceptScore W3213985589C86803240 @default.
• W3213985589 hasIssue "3" @default.
• W3213985589 hasLocation W32139855891 @default.
• W3213985589 hasOpenAccess W3213985589 @default.
• W3213985589 hasPrimaryLocation W32139855891 @default.
• W3213985589 hasRelatedWork W1901528025 @default.
• W3213985589 hasRelatedWork W1988051257 @default.
• W3213985589 hasRelatedWork W1993795923 @default.
• W3213985589 hasRelatedWork W2045448786 @default.
• W3213985589 hasRelatedWork W2095329316 @default.
• W3213985589 hasRelatedWork W2141521254 @default.
• W3213985589 hasRelatedWork W2355333259 @default.
• W3213985589 hasRelatedWork W2412105336 @default.
• W3213985589 hasRelatedWork W2431664838 @default.
• W3213985589 hasRelatedWork W3213985589 @default.
• W3213985589 hasVolume "20" @default.
• W3213985589 isParatext "false" @default.
• W3213985589 isRetracted "false" @default.
• W3213985589 magId "3213985589" @default.
• W3213985589 workType "article" @default.