| 1. |
- Li, Ping, et al.
(författare)
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Phosphane and phosphite unsymmetrically disubstituted diiron complexes related to the Fe-only hydrogenase active site
- 2007
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Ingår i: European Journal of Inorganic Chemistry. - : Wiley. - 1434-1948 .- 1099-1948 .- 1099-0682. ; :23, s. 3718-3727
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Tidskriftsartikel (refereegranskat)abstract
- A series of unsymmetrically disubstituted diiron complexes [(mu-pdt){Fe(CO)(2)L-1]{Fe(CO)(2)L-2}] [pdt = 1,3-propanedithiolato; L-1 = PMe3, L-2 = PMe2Ph, 4; PPh3, 5; PCy3, 6; P(OEt)(3), 7; L-1= PMe2Ph, L-2 = PPh3, 8; P(OEt)(3), 9; L-1 = P(OEt)(3), L-2 = PPh3, 10; PCy3, 11] and [(mu-edt){Fe(CO)(2)PMe3)}{Fe(CO)(2)PPh3}] (edt = 1, 2-ethane dithiolato, 12) were prepared by means of step-wise CO displacements of [(mu-pdt)Fe-2(CO)(6)] and [(mu-edt)-Fe-2(CO)(6)] by different tertiary phosphane and phosphite ligands. The interconversion of the irondithiacyclohexane ring and the rotation of the [Fe(CO)(2)PR3] subunit were studied using by variable-temperature P-31{H-1} NMR spectroscopy of 4, 6 and 12 in solution. The molecular structures of 4-6, 8-10 and 12 show that complexes 4-6, 8, 9 and 12 possess an apical/basal coordination mode and complex 10 has an apical/apical conformation. The X-ray analyses indicate that the PMe2Ph ligand in the apical position of the starting complex [(mu-pdt){Fe(CO)(3)}{FeCO2(PMe2Ph)}] rotates to the basal position on conversion to the products 8 and 9. Cyclic voltammograms of 4-11 were studied both under argon and CO. The influences of the phosphane and phosphite ligands on the redox properties of the unsymmetrically disubstituted diiron complexes are discussed. ((C) Wiley-VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
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| 2. |
- Wang, Xiaoyang, 1965, et al.
(författare)
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Lipopolysaccharide Sensitizes Neonatal Hypoxic-Ischemic Brain Injury in a MyD88-Dependent Manner
- 2009
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Ingår i: Journal of Immunology. - : The American Association of Immunologists. - 0022-1767 .- 1550-6606. ; 183:11, s. 7471-7477
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Tidskriftsartikel (refereegranskat)abstract
- Neurological deficits in children, including cerebral palsy, are associated with prior infection during the perinatal period. Experimentally, we have shown that pre-exposure to the Gram-negative component LPS potentiates hypoxic-ischemic (HI) brain injury in newborn animals. LPS effects are mediated by binding to TLR4, which requires recruitment of the MyD88 adaptor protein or Toll/IL-1R domain-containing adapter inducing IFN-beta for signal transduction. In this study, we investigated the role of MyD88 in neonatal brain injury. MyD88 knockout (MyD88 KO) and wild-type mice were subjected to left carotid artery ligation and 10% O(2) for 50 min on postnatal day 9. LPS or saline were administered i.p. at 14 h before HI. At 5 days after HI in wild-type mice, LPS in combination with HI caused a significant increase in gray and white matter tissue loss compared with the saline-HI group. By contrast, in the MyD88 KO mice there was no potentiation of brain injury with LPS-HI. MyD88 KO mice exhibited reduced NFkappaB activation and proinflammatory cytokine-chemokine expression in response to LPS. The number of microglia and caspase-3 activation was increased in the brain of MyD88 KO mice after LPS exposure. Collectively, these findings indicate that MyD88 plays an essential role in LPS-sensitized HI neonatal brain injury, which involves both inflammatory and caspase-dependent pathways.
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| 3. |
- Wang, Xiaoyang, 1965, et al.
(författare)
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White matter damage after chronic subclinical inflammation in newborn mice.
- 2009
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Ingår i: Journal of child neurology. - : SAGE Publications. - 1708-8283 .- 0883-0738. ; 24:9, s. 1171-8
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Tidskriftsartikel (refereegranskat)abstract
- Preterm infants exposed to inflammation are at increased risk of white matter injury and/or cerebral palsy. To investigate the effect of chronic inflammation on the developing white matter, we administered low-dose lipopolysaccharide once a day from postnatal days 3 to 11, examined white matter changes at postnatal day 12, and monitored serum levels of insulin-like growth factor 1 and insulin-like factor binding protein-3. A single injection of lipopolysaccharide decreased the serum insulin-like growth factor 1 level but not the insulin-like factor binding protein-3 level. At postnatal day 12, quantification of immunohistochemical staining for axonal, myelin, and oligodendrocyte markers revealed impaired myelination in subcortical white matter. In addition, brain gray matter volume decreased and spleen and liver weight increased at postnatal day 12. These data suggest chronic subclinical inflammation hampers development of white and gray matter in early life, which may be associated with insulin-like growth factor 1 deficiency.
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| 4. |
- Zhu, Changlian, 1964, et al.
(författare)
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Irradiation to the immature brain attenuates neurogenesis and exacerbates subsequent hypoxic-ischemic brain injury in the adult.
- 2009
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Ingår i: Journal of neurochemistry. - : Wiley. - 1471-4159 .- 0022-3042. ; 111:6, s. 1447-1456
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Tidskriftsartikel (refereegranskat)abstract
- Abstract Cranial radiotherapy is common in pediatric oncology. Our purpose was to investigate if irradiation (IR) to the immature brain would increase the susceptibility to hypoxic- ischemic injury in adulthood. The left hemisphere of postnatal day 10 (P10) mice was irradiated with 8 Gy and subjected to hypoxia-ischemia (HI) on P60. Brain injury, neurogenesis and inflammation were evaluated 30 days after HI. IR alone caused significant hemispheric tissue loss, or lack of growth (2.8 +/- 0.42 mm(3), p<0.001). Tissue loss after HI (18.2 +/- 5.8 mm(3), p<0.05) was synergistically increased if preceded by IR (32.0 +/- 3.5 mm(3), p<0.05). Infarct volume (5.1 +/- 1.6 mm(3)) nearly doubled if HI was preceded by IR (9.8 +/- 1.2 mm(3), p<0.05). Pathological scoring revealed that IR aggravated hippocampal, cortical and striatal, but not thalamic, injury. Hippocampal neurogenesis decreased >50% after IR but was unchanged by HI alone. The number of newly formed microglia was three times higher after IR+HI than after HI alone. In summary, IR to the immature brain produced long-lasting changes, including decreased hippocampal neurogenesis, subsequently rendering the adult brain more susceptible to HI, resulting in larger infarcts, increased hemispheric tissue loss and more inflammation than in non-irradiated brains.
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