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  • SAGE Publications  (4)
  • 1
    Online Resource
    Online Resource
    Endogenous Hydrogen Sulfide Regulates Pulmonary Artery Collagen Remodeling in Rats with High Pulmonary Blood Flow
    SAGE Publications ; 2009
    In:  Experimental Biology and Medicine Vol. 234, No. 5 ( 2009-05), p. 504-512
    Details
    In: Experimental Biology and Medicine, SAGE Publications, Vol. 234, No. 5 ( 2009-05), p. 504-512
    Abstract: The mechanisms responsible for the structural remodeling of pulmonary vasculature induced by increased pulmonary blood flow are not fully understood. This study explores the effect of endogenous hydrogen sulfide (H 2 S), a novel gasotransmitter, on collagen remodeling of the pulmonary artery in rats with high pulmonary blood flow. Thirty-two Sprague-Dawley rats were randomly divided into sham, shunt, sham+PPG (D,L-propargylglycine, an inhibitor of cystathionine-γ-lyase), and shunt+PPG groups. After 4 weeks of shunting, the relative medial thickness (RMT) of pulmonary arteries and H 2 S concentration in lung tissues were investigated. Collagen I and collagen III were evaluated by hydroxyproline assay, sirius-red staining, and immunohistochemistry. Pulmonary artery matrix metalloproteinase-13 (MMP-13), tissue inhibitor of metalloproteinase-1 (TIMP-1), and connective tissue growth factor (CTGF) were evaluated by immunohistochemistry. After 4 weeks of aortocaval shunting, resulting in an elevation of lung tissue H 2 S to 116.4%, rats exhibited collagen remodeling and increased CTGF expression in the pulmonary arteries. Compared with those of the shunt group, lung tissue H 2 S production was lowered by 23.4%, RMT of the pulmonary artery further increased by 39.5%, pulmonary artery collagen accumulation became obvious, and pulmonary artery CTGF expression elevated ( P 〈 0.01) in the shunted rats treated with PPG. However, pulmonary artery MMP-13 and TIMP-1 expressions decreased significantly in rats of shunt+PPG group ( P 〈 0.01). This study suggests that endogenous H 2 S exerts an important regulatory effect on pulmonary collagen remodeling induced by high pulmonary blood flow.
    Type of Medium: Online Resource
    ISSN: 1535-3702 , 1535-3699
    URL: Article
    DOI: 10.3181/0807-RM-230
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2009
    detail.hit.zdb_id: 2020856-X
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Autism Symptoms in Fragile X Syndrome
    SAGE Publications ; 2017
    In:  Journal of Child Neurology Vol. 32, No. 10 ( 2017-09), p. 903-909
    Details
    In: Journal of Child Neurology, SAGE Publications, Vol. 32, No. 10 ( 2017-09), p. 903-909
    Abstract: Fragile X syndrome (FXS) is recognized as the most common genetic cause of intellectual disability and autism spectrum disorder (ASD). Although symptoms of ASD are frequently observed in patients with FXS, researchers have not yet clearly determined whether the symptoms in patients with FXS differ from the symptoms in patients without ASD or nonsyndromic ASD. Behavioral similarities and differences between FXS and ASD are important to improve our understanding of the causes and correlations of ASD with FXS. Based on the evidence presented in this review, individuals with FXS and comorbid ASD have more severe behavioral problems than individuals with FXS alone. However, patients with FXS and comorbid ASD exhibit less severe impairments in the social and communication symptoms than patients with nonsyndromic ASD. Individuals with FXS also present with anxiety and seizures in addition to comorbid ASD symptoms, and differences in these conditions are noted in patients with FXS and ASD. This review also discusses the role of fragile X mental retardation 1 protein (FMRP) in FXS and ASD phenotypes.
    Type of Medium: Online Resource
    ISSN: 0883-0738 , 1708-8283
    URL: Article
    DOI: 10.1177/0883073817712875
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2017
    detail.hit.zdb_id: 2068710-2
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  • 3
    Online Resource
    Online Resource
    Sulfur dioxide derivatives improve the vasorelaxation in the spontaneously hypertensive rat by enhancing the vasorelaxant response to nitric oxide
    SAGE Publications ; 2012
    In:  Experimental Biology and Medicine Vol. 237, No. 7 ( 2012-07), p. 867-872
    Details
    In: Experimental Biology and Medicine, SAGE Publications, Vol. 237, No. 7 ( 2012-07), p. 867-872
    Abstract: The present study was designed to explore the role of sulfur dioxide (SO 2 ) in the regulation of vasorelaxation in the spontaneously hypertensive rat (SHR). Twenty-two Wistar rats and 15 SHRs were divided randomly into the following groups: Wistar-Kyoto (WKY) control ( n = 8), WKY+Na 2 SO 3 /NaHSO 3 ( n = 8), WKY+l-aspartic acid- β-hydroxamate (HDX) ( n = 6), SHR control ( n = 8) and SHR+Na 2 SO 3 /NaHSO 3 ( n = 7). Their blood pressure in vivo was measured by tail plethysmography. The vasorelaxant response of the thoracic aorta to acetylcholine (Ach) and sodium nitroprusside (SNP) in all rats was tested, respectively, in the experiment. At the same time, the SO 2 content of the WKY aorta after incubation with HDX and the vasorelaxant response to Ach after incubation with HDX were quantified. Nitric oxide (NO) production in the aorta of all rats was determined. We also measured the vasorelaxant responses of WKY aorta to different concentrations of SO 2 after incubation with the NO inhibitor, N G -nitro-l-arginine methyl ester (l-NAME). The blood pressure decreased significantly in SHRs treated with SO 2 derivatives ( P 〈 0.05). Reduction of endogenous SO 2 in WKY vessels resulted in a decrease in the vasorelaxation induced by Ach. Vasorelaxation in response to both Ach and SNP increased in SHRs treated with SO 2 derivatives compared with SHR controls, but decreased in WKY given HDX compared with WKY controls ( P 〈 0.05). The NO level in arterial tissues increased in SHRs treated with SO 2 derivatives ( P 〈 0.05). However, the vasorelaxant response to SO 2 derivatives in the presence of l-NAME decreased markedly compared with WKY controls. The results suggest that SO 2 reduced blood pressure and increased vasorelaxation in SHR arteries via enhancing the vasorelaxant response to NO in isolated aortic rings and increasing the NO level of aortic tissues.
    Type of Medium: Online Resource
    ISSN: 1535-3702 , 1535-3699
    URL: Article
    DOI: 10.1258/ebm.2012.011304
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2012
    detail.hit.zdb_id: 2020856-X
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Regulatory Effects of Hydrogen Sulfide on IL-6, IL-8 and IL-10 Levels in the Plasma and Pulmonary Tissue of Rats with Acute Lung Injury
    SAGE Publications ; 2008
    In:  Experimental Biology and Medicine Vol. 233, No. 9 ( 2008-09), p. 1081-1087
    Details
    In: Experimental Biology and Medicine, SAGE Publications, Vol. 233, No. 9 ( 2008-09), p. 1081-1087
    Abstract: We examined the possible role of hydrogen sulfide (H 2 S) in the pathogenesis of oleic acid (OA)-induced acute lung injury (ALI) and its regulatory effects on the inflammatory response. Compared to control rats, the OA-treated rats had decreased partial pressure of oxygen in the arterial blood (PaO 2 ) levels, an increased pulmonary wet/dry weight (W/D) ratio, increased index of quantitative assessment (IQA) score and increased frequency of polymorphonuclear (PMN) cells in the lung 2, 4 or 6 h after OA injection (0.1 ml/kg, intravenous injection). In addition, significantly increased IL-6, IL-8 and IL-10 levels together with decreased H 2 S levels were observed in the plasma and lung tissue of OA-treated rats compared to controls. Administration of the H 2 S donor sodium hydrosulfide (NaHS, 56 μmol/L, intraperitoneal injection) into OA-treated rats increased the PaO 2 level, reduced the lung W/D ratio and infiltration of PMN cells, and alleviated the degree of ALI (measured by the IQA score). In addition, NaHS decreased IL-6 and IL-8 levels but increased IL-10 levels in the plasma and lung tissues, suggesting that H 2 S may regulate the inflammatory response during ALI via regulation of IL-6, IL-8 and IL-10. Thus, the down-regulation of endogenous H 2 S production might be involved in the pathogenesis of OA-induced ALI in rats.
    Type of Medium: Online Resource
    ISSN: 1535-3702 , 1535-3699
    URL: Article
    DOI: 10.3181/0712-RM-354
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2008
    detail.hit.zdb_id: 2020856-X
    SSG: 12
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