Difference between revisions of "Template:2019 New References"

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==Introduction==
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[[User:Z8600021|Mark Hill]] ([[User talk:Z8600021|talk]]) 12:23, 16 June 2019 (AEST) Added this new page to capture updated references added throughout the site in the "Some Recent Findings". Note not all new references may be added to this list.
  
[[User:Z8600021|Mark Hill]] ([[User talk:Z8600021|talk]]) 12:23, 16 June 2019 (AEST) Added this new page to capture updated references added throughout the site.
 
  
 
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{{preterm birth}}
=={{preterm birth}}==
 
 
* '''Risk of spontaneous preterm birth and fetal growth associates with fetal SLIT2'''{{#pmid:31194736|PMID31194736}} "Spontaneous preterm birth (SPTB) is the leading cause of neonatal death and morbidity worldwide. Both maternal and fetal genetic factors likely contribute to SPTB. We performed a genome-wide association study (GWAS) on a population of Finnish origin that included 247 infants with SPTB (gestational age [GA] < 36 weeks) and 419 term controls (GA 38-41 weeks). The strongest signal came within the gene encoding slit guidance ligand 2 (SLIT2; rs116461311, minor allele frequency 0.05, p = 1.6×10-6). ... Our results show that the fetal SLIT2 variant and both SLIT2 and ROBO1 expression in placenta and trophoblast cells may be correlated with susceptibility to SPTB. SLIT2-ROBO1 signaling was linked with regulation of genes involved in inflammation, PSG genes, decidualization and fetal growth. We propose that this receptor-ligand couple is a component of the signaling network that promotes SPTB."
 
* '''Risk of spontaneous preterm birth and fetal growth associates with fetal SLIT2'''{{#pmid:31194736|PMID31194736}} "Spontaneous preterm birth (SPTB) is the leading cause of neonatal death and morbidity worldwide. Both maternal and fetal genetic factors likely contribute to SPTB. We performed a genome-wide association study (GWAS) on a population of Finnish origin that included 247 infants with SPTB (gestational age [GA] < 36 weeks) and 419 term controls (GA 38-41 weeks). The strongest signal came within the gene encoding slit guidance ligand 2 (SLIT2; rs116461311, minor allele frequency 0.05, p = 1.6×10-6). ... Our results show that the fetal SLIT2 variant and both SLIT2 and ROBO1 expression in placenta and trophoblast cells may be correlated with susceptibility to SPTB. SLIT2-ROBO1 signaling was linked with regulation of genes involved in inflammation, PSG genes, decidualization and fetal growth. We propose that this receptor-ligand couple is a component of the signaling network that promotes SPTB."
  
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[[Category:2019]]
 

Revision as of 12:26, 16 June 2019

2019 New References 

Mark Hill (talk) 12:23, 16 June 2019 (AEST) Added this new page to capture updated references added throughout the site in the "Some Recent Findings". Note not all new references may be added to this list.


preterm birth

  • Risk of spontaneous preterm birth and fetal growth associates with fetal SLIT2[1] "Spontaneous preterm birth (SPTB) is the leading cause of neonatal death and morbidity worldwide. Both maternal and fetal genetic factors likely contribute to SPTB. We performed a genome-wide association study (GWAS) on a population of Finnish origin that included 247 infants with SPTB (gestational age [GA] < 36 weeks) and 419 term controls (GA 38-41 weeks). The strongest signal came within the gene encoding slit guidance ligand 2 (SLIT2; rs116461311, minor allele frequency 0.05, p = 1.6×10-6). ... Our results show that the fetal SLIT2 variant and both SLIT2 and ROBO1 expression in placenta and trophoblast cells may be correlated with susceptibility to SPTB. SLIT2-ROBO1 signaling was linked with regulation of genes involved in inflammation, PSG genes, decidualization and fetal growth. We propose that this receptor-ligand couple is a component of the signaling network that promotes SPTB."


References

  1. Tiensuu H, Haapalainen AM, Karjalainen MK, Pasanen A, Huusko JM, Marttila R, Ojaniemi M, Muglia LJ, Hallman M & Rämet M. (2019). Risk of spontaneous preterm birth and fetal growth associates with fetal SLIT2. PLoS Genet. , 15, e1008107. PMID: 31194736 DOI.

[[Category:Reference]