2007 Fiscal Year Final Research Report Summary
ELUCIDATION OFMOLECULAR MECHANISMS OF FETAL AND PLACENTAL UNIT FUNCTIONS AND THERAPEUTIC INTERVENTIONS OF PERINATAL PATHOGENETIC CONDITIONS
Project/Area Number |
17390299
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Pediatrics
|
Research Institution | University of Fukui |
Principal Investigator |
MAYUMI Mitsufumi University of Fukui, Faculty of Medical Sciences, Professor (70135581)
|
Co-Investigator(Kenkyū-buntansha) |
TSUKAHARA Hirokazu University of Fukui, Hospital, Lecturer (90207340)
|
Project Period (FY) |
2005 – 2007
|
Keywords | Fetus / Placenta / Perinatal period / Neonate / Biological responses / Oxidative stress / Breast milk / Bronchopulmonary dvsplasia |
Research Abstract |
The results of the present research project are described in the following (1) Human breast milk contains high amounts of thioredoxin and other antioxidants and VEGF and other cell growth factors. We concluded that human breast milk might contribute to the successful neonatal adaptation and postnatal development and growth (2) Nitric oxide (NO) and other antioxidants reduce the inflammatory injuries caused by TNF-a in human microvascular endothelial cells. We concluded that these factors might provide novel therapeutic strategies for inflammatory endothelial injuries and dysfunctions. (3) Preterm infants, especially those showing respiratory distress and requiring oxygen supplementation, excrete high amounts of oxidative stress biomarkers. We concluded that these infants might sustain enhanced systemic oxidative stress in the neonatal period. (4) Asymmetric dimethylarginine (ADMA) levels are higher and NO levels are lower in younger children than in older subjects. We concluded that ADMA m
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ight contribute to blood pressure maintenance and peripheral perfusion in younger children. (5) Patients with Wilson disease, congenital portal-venous shunt or certain urea cycle enzyme defects (e.g., ASS defect) showed systemic enhancement of oxidative stress and endothelial injuries. We concluded that antioxidative strategies might help improve the sick conditions in these patients. (6) We identified the second case of congenital heme oxygenase type 1 defect in a three-year-old Turkish boy presenting persistent hemolysis, systemic inflammation and multiorgan injuries but not hyperbilirubinemia. We showed that the genetic defect was localized at the homologue missense mutation (Gly 139 Val) in this case. (7) We summarized recent research works and future views of oxidative-reductive chemistry and biology and emphasized the importance of determination of oxidative-reductive biomarkers in clinical medicine. (8) We also summarized recent progress and views of NO chemistry and biology in the field of clinical nephrology. Less
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Research Products
(8 results)