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Progress in clinical and biological research最新文献

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ADP-ribosylation: role in LPS-induced phosphorylation of two cytosolic proteins (p36/38) in monocytes. adp核糖基化:在单核细胞中脂多糖诱导的两种胞质蛋白(p36/38)磷酸化中的作用。
Progress in clinical and biological research Pub Date : 1998-01-01
S Hauschildt, A J Ulmer, H D Flad, T Heyden, H Heine
{"title":"ADP-ribosylation: role in LPS-induced phosphorylation of two cytosolic proteins (p36/38) in monocytes.","authors":"S Hauschildt,&nbsp;A J Ulmer,&nbsp;H D Flad,&nbsp;T Heyden,&nbsp;H Heine","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Human monocytes respond to LPS by releasing proinflammatory cytokines such as TNF-alpha, IL-1 and IL-6. Here we show that inhibitors of ADP-ribosylation namely nicotinamide and meta-iodobenzylguanidine prevent production of TNF-alpha and IL-6 at the protein and mRNA level. The inhibitors also influence the LPS-induced phosphorylation pattern of cytosolic proteins. They consistently lead to changes of the phosphorylation state of two proteins with an apparent molecular mass of 36 kDa and 38 kDa. The changes are both time and dose dependent. The data suggest that the conditions leading to altered phosphorylation of p36/38 may correlate with conditions initiating and regulating TNF-alpha and IL-6 production.</p>","PeriodicalId":20686,"journal":{"name":"Progress in clinical and biological research","volume":"397 ","pages":"147-55"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20497205","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: 0
The pathogenic role of LBP in gram-negative sepsis and septic shock. LBP在革兰氏阴性脓毒症和感染性休克中的致病作用。
Progress in clinical and biological research Pub Date : 1998-01-01
D Heumann, S Lengacher, D Le Roy, C V Jongeneel, M P Glauser
{"title":"The pathogenic role of LBP in gram-negative sepsis and septic shock.","authors":"D Heumann,&nbsp;S Lengacher,&nbsp;D Le Roy,&nbsp;C V Jongeneel,&nbsp;M P Glauser","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":20686,"journal":{"name":"Progress in clinical and biological research","volume":"397 ","pages":"379-86"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20495701","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: 0
Natural and synthetic polypeptides that recognize the conserved lipid a binding site of lipopolysaccharides. 天然的和合成的多肽，识别保守的脂质是脂多糖的结合位点。
Progress in clinical and biological research Pub Date : 1998-01-01
M Porro, A Rustici, M Velucchi, D Agnello, P Villa, P Ghezzi
{"title":"Natural and synthetic polypeptides that recognize the conserved lipid a binding site of lipopolysaccharides.","authors":"M Porro,&nbsp;A Rustici,&nbsp;M Velucchi,&nbsp;D Agnello,&nbsp;P Villa,&nbsp;P Ghezzi","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":20686,"journal":{"name":"Progress in clinical and biological research","volume":"397 ","pages":"315-25"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20497119","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: 0
Structure-function analysis of soluble and membrane-bound CD14. 可溶性和膜结合CD14的结构-功能分析。
Progress in clinical and biological research Pub Date : 1998-01-01
T N Kirkland, S Viriyakosol
{"title":"Structure-function analysis of soluble and membrane-bound CD14.","authors":"T N Kirkland,&nbsp;S Viriyakosol","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":20686,"journal":{"name":"Progress in clinical and biological research","volume":"397 ","pages":"79-87"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20497199","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: 0
Role of nitric oxide and reactive oxygen species in endotoxin shock. 一氧化氮和活性氧在内毒素休克中的作用。
Progress in clinical and biological research Pub Date : 1998-01-01
T Yoshikawa, H Takano, M Kondo
{"title":"Role of nitric oxide and reactive oxygen species in endotoxin shock.","authors":"T Yoshikawa,&nbsp;H Takano,&nbsp;M Kondo","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":20686,"journal":{"name":"Progress in clinical and biological research","volume":"397 ","pages":"357-63"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20495699","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: 0
Cytokine regulation of inducible nitric oxide synthase in vascular smooth muscle cells. 血管平滑肌细胞诱导型一氧化氮合酶的细胞因子调控。
Progress in clinical and biological research Pub Date : 1998-01-01
J Cohen, T J Evans, J Spink
{"title":"Cytokine regulation of inducible nitric oxide synthase in vascular smooth muscle cells.","authors":"J Cohen,&nbsp;T J Evans,&nbsp;J Spink","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>NO is an important mediator in sepsis. It has been unequivocally established that it is the major determinant in the vasodilatation and consequent hypotension in experimental animals following the administration of LPS. It is cytotoxic, particularly in combination with superoxide anions, and exerts negative inotropic and chronotropic effects on the heart. The exact role that these functions play in sepsis, however, remain unclear. Similarly, its immunomodulatory and cerebral effects, although potentially important, remain of uncertain significance in sepsis. Regulation of such a pivotal molecule is clearly extremely important: the data described here show that not only is this regulation extremely complex, but it appears to vary in different cell types. The implication of this finding for future clinical work is clear. NO production is not all bad: in some circumstances, it may be desirable to differentially regulate iNOS activity such that production is restricted in some cell types but not in others. The work described here begins to offer the possibility of identifying new molecular targets which allow this kind of differential regulation.</p>","PeriodicalId":20686,"journal":{"name":"Progress in clinical and biological research","volume":"397 ","pages":"169-77"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20497104","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: 0
Molecular mechanisms responsible for endotoxin tolerance. 内毒素耐受的分子机制。
Progress in clinical and biological research Pub Date : 1998-01-01
B Yoza, K LaRue, C McCall
{"title":"Molecular mechanisms responsible for endotoxin tolerance.","authors":"B Yoza,&nbsp;K LaRue,&nbsp;C McCall","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Bacterial lipopolysaccharide endotoxin (LPS) is a potent activator of a number of inflammatory genes, including interleukin-1 (IL-1). IL-1 and other cytokines such as tumor necrosis factor alpha (TNF alpha) are essential mediators in inducing severe sepsis syndromes (SS). Major cellular targets of LPS are blood or tissue leukocytes, such as macrophages and neutrophils. These cells can respond and adapt to LPS, the latter phenomenon is known as LPS tolerance. In animals, LPS tolerance is a highly effective mechanism of protection against the lethal syndrome of severe sepsis. Two models are used to investigate the molecular basis of LPS tolerance. The first model employs blood leukocytes isolated from patients with SS. The second model employs the promonocytic cell line, THP-1 in vitro. In the SS model, LPS tolerance of involves repression at the level of IL-1 beta mRNA. Suppression of IL-1 beta mRNA is under the control of a labile repressor protein. In contrast to suppression of IL-1 beta, mRNA is under the control of a labile repressor protein. In contrast to suppression of IL-1 beta, there is increased expression of the Type 2 IL-1 receptor mRNA and protein in leukocytes from patients with SS. The THP-1 model of LPS tolerance also involves repression of LPS induction of IL-1 beta gene expression. The repression of THP-1 cell IL-1 beta expression is at the level of transcription, and like the SS model is under the control of a labile protein. LPS tolerance in both models is stimulus-specific. We further find that transcription factors such as NF kappa B and AP-1 may participate in regulating LPS tolerance.</p>","PeriodicalId":20686,"journal":{"name":"Progress in clinical and biological research","volume":"397 ","pages":"209-15"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20497108","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: 0
The role of scavenger receptors in LPS-induced macrophage activation. 清道夫受体在lps诱导的巨噬细胞活化中的作用。
Progress in clinical and biological research Pub Date : 1998-01-01
T Kirikae, T Kodama, F Kirikae, H Suzuki, M Nakano
{"title":"The role of scavenger receptors in LPS-induced macrophage activation.","authors":"T Kirikae,&nbsp;T Kodama,&nbsp;F Kirikae,&nbsp;H Suzuki,&nbsp;M Nakano","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":20686,"journal":{"name":"Progress in clinical and biological research","volume":"397 ","pages":"97-105"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20497201","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: 0
The role of tyrosine kinases and map kinases in LPS-induced signaling. 酪氨酸激酶和map激酶在脂多糖诱导的信号传导中的作用。
Progress in clinical and biological research Pub Date : 1998-01-01
A L DeFranco, M T Crowley, A Finn, J Hambleton, S L Weinstein
{"title":"The role of tyrosine kinases and map kinases in LPS-induced signaling.","authors":"A L DeFranco,&nbsp;M T Crowley,&nbsp;A Finn,&nbsp;J Hambleton,&nbsp;S L Weinstein","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":20686,"journal":{"name":"Progress in clinical and biological research","volume":"397 ","pages":"119-36"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20497203","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: 0
Production of nontoxic lipid A by chemical modification and its antagonistic effect on LPS activity. 化学修饰制备无毒脂质A及其对LPS活性的拮抗作用。
Progress in clinical and biological research Pub Date : 1998-01-01
K Tanamoto
{"title":"Production of nontoxic lipid A by chemical modification and its antagonistic effect on LPS activity.","authors":"K Tanamoto","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":20686,"journal":{"name":"Progress in clinical and biological research","volume":"397 ","pages":"269-80"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20497115","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: 0
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