Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement最新文献_第9页

Antidotes: availability, use and cost in hospital and extra-hospital emergency services of Catalonia (Spain). 解毒剂:加泰罗尼亚(西班牙)医院和院外急救服务的供应、使用和费用。

Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement Pub Date : 1997-01-01 DOI: 10.1007/978-3-642-60682-3_27

S Nogué, D Soy, P Munné, J Millá

引用次数: 8

Neuropathy target esterase (NTE): molecular characterisation and cellular localisation. 神经病变靶酯酶(NTE):分子特征和细胞定位。

Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement Pub Date : 1997-01-01 DOI: 10.1007/978-3-642-60682-3_30

P Glynn

引用次数: 7

Mechanisms and models of neurotoxicity of n-hexane and related solvents. 正己烷及相关溶剂的神经毒性机制和模型。

Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement Pub Date : 1997-01-01 DOI: 10.1007/978-3-642-60682-3_32

H Tähti, M Engelke, L Vaalavirta

引用次数: 0

Mineral fiber-induced oxidative stress in phagocytes. 矿物质纤维诱导的吞噬细胞氧化应激。

Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement Pub Date : 1996-01-01 DOI: 10.1007/978-3-642-61105-6_24

K M Savolainen, M Ruotsalainen

引用次数: 1

Drug treatment in the perinatal period and the risk of functional teratogenicity. 围产期药物治疗与功能性致畸风险。

Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement Pub Date : 1996-01-01 DOI: 10.1007/978-3-642-61105-6_10

O. Benešová

引用次数: 3

Sentinel screening for human immunotoxicity. 人类免疫毒性哨点筛查。

Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement Pub Date : 1996-01-01 DOI: 10.1007/978-3-642-61105-6_4

J Descotes, B Nicolas, E Pham, T Vial

引用次数: 8

Genetic predisposition in occupational toxicology. 职业毒理学中的遗传易感性。

Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement Pub Date : 1996-01-01 DOI: 10.1007/978-3-642-61105-6_34

H M Bolt

引用次数: 1

Cytokines in human lung fibrosis. 细胞因子在人肺纤维化中的作用。

Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement Pub Date : 1996-01-01 DOI: 10.1007/978-3-642-61105-6_14

Y Martinet, O Menard, P Vaillant, J M Vignaud, N Martinet

{"title":"Cytokines in human lung fibrosis.","authors":"Y Martinet, O Menard, P Vaillant, J M Vignaud, N Martinet","doi":"10.1007/978-3-642-61105-6_14","DOIUrl":"https://doi.org/10.1007/978-3-642-61105-6_14","url":null,"abstract":"Fibrosis is a pathological process characterized by the replacement of normal tissue by mesenchymal cells and the extracellular matrix produced by these cells. The sequence of events leading to fibrosis of an organ involves the subsequent processes of injury with inflammation and disruption of the normal tissue architecture, followed by tissue repair with accumulation of mesenchymal cells in the area of derangement. The same sequence of events occurs in wound healing with normal granulation tissue and scar formation, but, while normal scar formation is very localized and transient, in contrast, in fibrosis, the repair process is exaggerated and usually widespread and can be chronic. Inflammatory cells (mainly mononuclear phagocytes), platelets, endothelial cells, and type II pneumocytes play a direct and indirect role in tissue injury and repair. The evaluation of three human fibrotic lung diseases, two diffuse [idiopathic pulmonary fibrosis (IPF), and the adult respiratory distress syndrome (ARDS)], and one focal (tumor stroma in lung cancer), has shown that several cytokines participate to the local injury and inflammatory reaction [interleukin-1 (IL-1), interleukin-8 (IL-8), monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-alpha)], while other cytokines are involved in tissue repair and fibrosis [platelet-derived growth factor (PDGF), insulin-like growth factor-1 (IGF-1), transforming growth factor-beta (TGF-beta), and basic-fibroblast growth factor (b-FGF)]. A better understanding of the cytokines and cytokine networks involved in lung fibrosis leads to the possibility of new therapeutic approaches.","PeriodicalId":8353,"journal":{"name":"Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement","volume":"18 ","pages":"127-39"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-3-642-61105-6_14","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19653137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 86

Mechanistical studies of the inhibition of intercellular communication by organochlorine compounds. 有机氯化合物抑制细胞间通讯的机理研究。

Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement Pub Date : 1996-01-01 DOI: 10.1007/978-3-642-61105-6_16

L Wärngárd, Y Bager, Y Kato, K Kenne, U G Ahlborg

{"title":"Mechanistical studies of the inhibition of intercellular communication by organochlorine compounds.","authors":"L Wärngárd, Y Bager, Y Kato, K Kenne, U G Ahlborg","doi":"10.1007/978-3-642-61105-6_16","DOIUrl":"https://doi.org/10.1007/978-3-642-61105-6_16","url":null,"abstract":"Many hydrocarbons are environmental pollutants that, due to their lipophilicity and chemical stability, accumulate in biological systems including milk and body fat. A number of investigations have demonstrated that many organochlorine compounds can act as tumour promoters in vivo and inhibit gap junctional intercellular communication between cells in culture. In the present study we have investigated the dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), different polychlorinated biphenyls, chlorinated paraffins and the pesticide endosulfan. Using techniques of scrape loading dye/transfer and Western blot analysis the function, expression and phosphorylation of different connexins in vitro and in vivo were studied. The results show a good correlation between the ability to act as a tumour promoter and to interfere with gap junctional intercellular communication. All tested compounds inhibited the intercellular communication in a liver derived cell line (IAR 20). However, the results show that the time to inhibition varies between the different agents. Endosulfan and chlorinated paraffins inhibit the communication within one hour, whereas dioxin like substances need to expose the cells for 48 hours before the communication is affected.","PeriodicalId":8353,"journal":{"name":"Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement","volume":"18 ","pages":"149-59"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19653139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Risk assessment for the harmful effects of UVB radiation on the immunological resistance to infectious diseases. UVB辐射对传染病免疫抵抗力有害影响的风险评估。

Archives of toxicology. Supplement. = Archiv fur Toxikologie. Supplement Pub Date : 1996-01-01 DOI: 10.1007/978-3-642-61105-6_3

H Van Loveren, W Goettsch, W Slob, J Garssen

引用次数: 11