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lllggghhh4 发表于 2010-7-28 09:28

求助PUBMED文献4篇

【题名】:Vascular endothelial growth factor and transforming growth factor-beta1 are highly expressed in the cerebrospinal fluid of premature infants with posthemorrhagic hydrocephalus
【作者】:Heep A, Stoffel-Wagner B, Bartmann P, Benseler S, Schaller C, Groneck P, Obladen M, Felderhoff-Mueser U.
【杂志名全称】:Pediatric research
【年, 卷(期), 起止页码】:2004 Nov;56(5):768-74. Epub 2004 Aug 19.
【DOI】:
【全文链接】:[url]http://www.ncbi.nlm.nih.gov/pubmed/15319463[/url]
【摘要信息】:The expression of specific growth factors such as vascular endothelial growth factor (VEGF) and transforming growth factor-beta1 (TGF-beta1) is of importance during brain development and in the pathogenesis of neurodegenerative disorders. VEGF and TGF-beta1 was studied in the cerebrospinal fluid (CSF) of neonates with posthemorrhagic hydrocephalus (PHHC) and nonhemorrhagic hydrocephalus. For determining the interference of inflammatory cytokine interaction with the expression of VEGF and TGF-beta1, IL-6 and IL-10 CSF concentrations were measured. Eighteen neonates who had PHHC and underwent serial reservoir puncture and nine neonates who had congenital nonhemorrhagic hydrocephalus (CHC) and underwent first shunt surgery were included in the study. CSF samples of 11 neonates with lumbar puncture for the exclusion of meningitis served as control subjects. VEGF, TGF-beta1, IL-6, and IL-10 concentrations in the CSF were measured by ELISA technique. VEGF concentrations in the CSF of patients with PHHC were significantly higher (median: 377 pg/mL; range: 101-1301 pg/mL) when compared with patients with CHC (median: 66 pg/mL; range: 3-1991; p < 0.001) and control subjects (median: 2 pg/mL; range: 0-12 pg/mL; p < 0.0001). TGF-beta1 CSF concentrations did not differ from control infants in all groups. Median IL-6 and IL-10 concentrations in the CSF were found to be low in all patient groups. Increased release of VEGF in the CSF of neonates with PHHC and nonhemorrhagic hydrocephalus may serve as an indicator of brain injury from progressive ventricular dilation. TGF-beta1 CSF concentrations are not elevated in the phase of acute fibroproliferative reactions in patients with PHHC
【求助者email】:[email]lllggghhh4@126.com[/email]

【题名】:A reassessment of vascular endothelial growth factor in central nervous system pathology.
【作者】:Merrill MJ, Oldfield EH.
【杂志名全称】:Journal of neurosurgery
【年, 卷(期), 起止页码】:2005 Nov;103(5):853-68
【DOI】:
【全文链接】:[url]http://www.ncbi.nlm.nih.gov/pubmed/16304990[/url]
【摘要信息】:Overexpression of vascular endothelial growth factor (VEGF) is associated with several central nervous system (CNS) diseases and abnormalities, and is often postulated as a causative factor and promising therapeutic target in these settings. The authors' goal was to reassess the contribution of VEGF to the biology and pathology of the CNS. The authors review the literature relating to the following aspects of VEGF: 1) the biology of VEGF in normal brain; 2) the involvement of VEGF in CNS disorders other than tumors (traumatic and ischemic injuries arteriovenous malformations, inflammation); and 3) the role of VEGF in brain tumor biology (gliomas and the associated vasogenic edema, and hemangioblastomas). The authors conclude the following: first, that VEGF overexpression contributes to the phenotype associated with many CNS disorders, but VEGF is a reactive rather than a causative factor in many cases; and second, that use of VEGF as a therapeutic agent or target is complicated by the effects of VEGF not only on the cerebral vasculature, but also on astrocytes, neurons, and inflammatory cells. In many cases, therapeutic interventions targeting the VEGF/VEGF receptor axis are likely to be ineffective or even detrimental. Clinical manipulation of VEGF levels in the CNS must be approached with caution
【求助者email】:[email]lllggghhh4@126.com[/email]

【题名】:Vascular endothelial growth factor increases neurogenesis after traumatic brain injury.
【作者】:Thau-Zuchman O, Shohami E, Alexandrovich AG, Leker RR.
【杂志名全称】:Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
【年, 卷(期), 起止页码】:2010 May;30(5):1008-16. Epub 2010 Jan 13
【DOI】:
【全文链接】:[url]http://www.ncbi.nlm.nih.gov/pubmed/20068579[/url]
【摘要信息】:[url]http://www.ncbi.nlm.nih.gov/pubmed/20068579[/url]
【求助者email】:[email]lllggghhh4@126.com[/email]

【题名】:Breakdown of the blood-brain barrier after fluid percussive brain injury in the rat. Part 1: Distribution and time course of protein extravasation
【作者】:Tanno H, Nockels RP, Pitts LH, Noble LJ.
【杂志名全称】:Journal of neurotrauma
【年, 卷(期), 起止页码】:1992 Spring;9(1):21-32.
【DOI】:
【全文链接】:[url]http://www.ncbi.nlm.nih.gov/pubmed/1619673[/url]
【摘要信息】:Experimental brain injury is associated with marked vasogenic edema, as evidenced by an increase in brain water content. This prominent and widespread response raises questions about the vulnerability of microvasculature in the brain to injury. In the present report we further characterize the vascular response by evaluating the integrity of the blood-brain barrier to circulating proteins. Vascular permeability to endogenous immunoglobulins (IgG) and to the protein horseradish peroxidase (HRP) was examined after a lateral, fluid percussive brain injury in the rat. In study 1 IgG was immunolocalized in brain sections 1-24 hr after injury. In studies 2 and 3 HRP was given intravenously either before impact (study 2) or 10 min before sacrifice (study 3). Permeability to this protein was assessed at 1-6 hr (study 2) or at 1-72 hr (study 3) after injury. In studies 1 and 2 the extravascular accumulation of proteins was evaluated. Pronounced abnormal permeability to IgG and HRP occurred within the first hour after injury and was widespread throughout both hemispheres. The intensity of immunostaining for IgG increased with time up to 24 hr after injury. In contrast, maximal extravascular accumulation of HRP occurred within the first hour after injury. In study 3 the time course for re-establishment of the blood-brain barrier to HRP was determined. Maximal permeability occurred at 1 hr after injury. At 24 hr abnormal permeability was restricted to the impact site and this area remained permeable up to 72 hr after injury. In summary this study demonstrates that breakdown of the blood-brain barrier to plasma proteins is a prominent feature of experimental brain injury. This abnormal permeability is characterized by its transient expression and widespread distribution. The time course for re-establishment of the blood-brain barrier to circulating proteins is most delayed at the impact site.

【求助者email】:[email]lllggghhh4@126.com[/email]

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