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Occurrence of 13(S)-Hydroxyoctadecadienoic Acid in Biological Samples 13(S)-羟基十八二烯酸在生物样品中的存在
Prostaglandins Pub Date : 1997-12-01 DOI: 10.1016/S0090-6980(97)00185-8
S.A Spindler , K.S Clark , M.L Blackburn , A.W Bull , R.G Reddy
{"title":"Occurrence of 13(S)-Hydroxyoctadecadienoic Acid in Biological Samples","authors":"S.A Spindler ,&nbsp;K.S Clark ,&nbsp;M.L Blackburn ,&nbsp;A.W Bull ,&nbsp;R.G Reddy","doi":"10.1016/S0090-6980(97)00185-8","DOIUrl":"10.1016/S0090-6980(97)00185-8","url":null,"abstract":"<div><p>The oxygenated metabolite of linoleic acid, 13(<em>S</em>)-hydroxyoctadecadienoic acid has recently been shown to play a role in cellular regulation. To detect this molecule in biological systems, we recently developed a specific polyclonal antibody. Using this antibody, we report the presence of 13(<em>S</em>)-hydroxyoctadecadienoic acid in human urine, cell culture media, and untreated goat serum for the first time by a specific, sensitive, and rapid enzyme immunoassay. Furthermore, the enzyme linked immunosorbent assay data are verified by gas chromatography/mass spectrometry analysis of the same samples.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(97)00185-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20456761","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: 2
Urinary Thromboxane B2 in Cardiac Transplant Patients as a Screening Method of Rejection 心脏移植患者尿血栓素B2作为排斥反应的筛查方法
Prostaglandins Pub Date : 1997-12-01 DOI: 10.1016/S0090-6980(97)00186-X
Y Zhao , N.M Katz , E.A Lefrak , M.L Foegh
{"title":"Urinary Thromboxane B2 in Cardiac Transplant Patients as a Screening Method of Rejection","authors":"Y Zhao ,&nbsp;N.M Katz ,&nbsp;E.A Lefrak ,&nbsp;M.L Foegh","doi":"10.1016/S0090-6980(97)00186-X","DOIUrl":"10.1016/S0090-6980(97)00186-X","url":null,"abstract":"<div><p>Noninvasive methods for regular monitoring of cardiac transplant patients for acute rejection are preferable to the only currently accepted method involving frequent endomyocardial biopsies. Thromboxane A<sub>2</sub> (TXA<sub>2</sub>) is synthesized in large amounts by monocytes/macrophages during organ graft rejection. It enhances T-lymphocyte clonal expansion and cytotoxic function as well as upregulating the major histocompatibility class II expression on antigen presenting cells. Experimentally increased urinary excretion of TXA<sub>2</sub> metabolites is associated with cardiac transplant rejection. We therefore compared urinary immunoreactive thromboxane B<sub>2</sub> (i-TXB<sub>2</sub>) levels to the rejection score of the endomyocardial biopsies. In addition we graded the degree of activated lymphocytes in peripheral blood. Urinary i-TXB<sub>2</sub> was significantly higher in patients exhibiting medium to severe rejection than in patients without rejection (1236 ± 372 vs. 526 ± 57 pg/mL). The urine i-TXB<sub>2</sub> (704 ± 48 pg/mL) of all patients who participated in this study, whose endomyocardial biopsy indicated rejection, was also significantly higher than in the non-rejecting group. Increased levels of urine i-TXB<sub>2</sub> were associated with increased biopsy scores. Circulating activated lymphocytes was also significantly increased in patients with moderate/severe rejection compared to patients with no rejection (66 ± 11 vs. 39 ± 4 per mm (3)) (p &lt; 0.01). Further, this study shows that urine i-TXB<sub>2</sub> is associated with increased endomyocardial biopsy scores (acute rejection scores) and blood lymphocyte activation. Thus we conclude that urine i-TXB<sub>2</sub> may be of potential value as a diagnostic screening test for helping identify cardiac transplant patients undergoing acute rejection.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(97)00186-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20457432","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: 12
Index 指数
Prostaglandins Pub Date : 1997-12-01 DOI: 10.1016/S0090-6980(98)00008-2
{"title":"Index","authors":"","doi":"10.1016/S0090-6980(98)00008-2","DOIUrl":"https://doi.org/10.1016/S0090-6980(98)00008-2","url":null,"abstract":"","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(98)00008-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137329750","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
Index 指数
Prostaglandins Pub Date : 1997-12-01 DOI: 10.1016/S0090-6980(98)00007-0
{"title":"Index","authors":"","doi":"10.1016/S0090-6980(98)00007-0","DOIUrl":"https://doi.org/10.1016/S0090-6980(98)00007-0","url":null,"abstract":"","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(98)00007-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137329749","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 Isoprostanes: A Perspective 异前列腺素:一个视角
Prostaglandins Pub Date : 1997-12-01 DOI: 10.1016/S0090-6980(97)00183-4
J. Rokach , S.P. Khanapure , S.-W. Hwang , M. Adiyaman , J.A. Lawson , G.A. FitzGerald
{"title":"The Isoprostanes: A Perspective","authors":"J. Rokach ,&nbsp;S.P. Khanapure ,&nbsp;S.-W. Hwang ,&nbsp;M. Adiyaman ,&nbsp;J.A. Lawson ,&nbsp;G.A. FitzGerald","doi":"10.1016/S0090-6980(97)00183-4","DOIUrl":"10.1016/S0090-6980(97)00183-4","url":null,"abstract":"<div><p>The isoprostanes are a new class of natural products produced in vivo by a non-enzymatic free-radical-induced peroxidation of polyunsaturated fatty acid. In the case of arachidonic acid, for example, four classes of isoprostanes can be produced. Because of the specific structural features distinguishing them from other free-radical-generated products, e.g., HETEs, etc., the isoprostanes can provide an exclusive and selective index for the oxidant component of several inflammatory and degenerative diseases. The possible mechanisms of formation of the individual isoprostanes is discussed in detail. Class III products, such as 8-iso-PGF<sub><em>2α</em></sub> and 8-iso-PGE<sub><em>2</em></sub> have been shown to be vasoconstrictors and modulate platelet function. Several synthetic representatives from the four classes of arachidonic-acid-derived isoprostanes have already been prepared by total synthesis. These synthetic standards have been used for the identification and quantitation of these isoprostanes in biological fluids using gas chromatography/mass spectrometry methodology.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(97)00183-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20456759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 114
Tomoxiprole Selectively Inhibits Cyclooxygenase-2 托莫昔普洛勒选择性抑制环氧合酶-2
Prostaglandins Pub Date : 1997-12-01 DOI: 10.1016/S0090-6980(97)00187-1
R.E West Jr , S.M Williams , H.S She , N.I Carruthers , R.W Egan , M Motasim Billah
{"title":"Tomoxiprole Selectively Inhibits Cyclooxygenase-2","authors":"R.E West Jr ,&nbsp;S.M Williams ,&nbsp;H.S She ,&nbsp;N.I Carruthers ,&nbsp;R.W Egan ,&nbsp;M Motasim Billah","doi":"10.1016/S0090-6980(97)00187-1","DOIUrl":"10.1016/S0090-6980(97)00187-1","url":null,"abstract":"<div><p>Tomoxiprole is a nonsteroidal anti-inflammatory compound that was reported to have low ulcerogenic potential, a quality that would be expected of a cyclooxygenase-2-selective inhibitor, and, in fact, we find it is selective for this isozyme. In stably transfected COS cells, the compound inhibits recombinant human cyclooxygenase-2 (IC<sub>50</sub> = 7 nM) more potently than recombinant cyclooxygenase-1 (IC<sub>50</sub> = 240 nM), and similar results are obtained with partially pure ovine enzyme preparations. The compound is thus a very potent as well as selective inhibitor of cyclooxygenase-2. As is true of some other cyclooxygenase-2-selective inhibitors, tomoxiprole inhibition of cyclooxygenase-2 but not cyclooxygenase-1 is time-dependent.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(97)00187-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20457433","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: 2
Nomenclature of Isoprostanes: A Proposal 异前列腺素的命名:一个建议
Prostaglandins Pub Date : 1997-12-01 DOI: 10.1016/S0090-6980(97)00184-6
J Rokach , S.P Khanapure , S.-W Hwang , M Adiyaman , J.A Lawson , G.A FitzGerald
{"title":"Nomenclature of Isoprostanes: A Proposal","authors":"J Rokach ,&nbsp;S.P Khanapure ,&nbsp;S.-W Hwang ,&nbsp;M Adiyaman ,&nbsp;J.A Lawson ,&nbsp;G.A FitzGerald","doi":"10.1016/S0090-6980(97)00184-6","DOIUrl":"10.1016/S0090-6980(97)00184-6","url":null,"abstract":"<div><p>We have proposed a nomenclature system for the isoprostanes, a new class of natural products formed in vivo by the free-radical peroxidation of polyunsaturated fatty acids. Our proposed nomenclature is based on the assignment of four isoprostanes, <strong>1</strong>, <strong>9</strong>, <strong>17,</strong> and <strong>25</strong>, as representatives of the four classes of isoprostanes derived from arachidonic acid (AA). We have attempted as much as possible to retain elements from the familiar prostaglandin nomenclature. In this proposal, we have used the abbreviation iP for isoprostane. We have classified isoprostane classes or types based on ω-carbon as being the starting reference. Roman numerals I-VI refer the six types of isoprostanes derived from eicosapentaenoic acid (EPA) and III-VI refer to the four types derived from AA. This nomenclature can be applied to isoprostanes derived from other PUFAs also.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(97)00184-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20456760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 144
Gastrin-Releasing Peptide-Induced Expression of Prostaglandin Synthase-2 in Swiss 3T3 Cells 胃泌素释放肽诱导的前列腺素合成酶-2在瑞士3T3细胞中的表达
Prostaglandins Pub Date : 1997-11-01 DOI: 10.1016/S0090-6980(97)00162-7
J.Randolph Hecht, Javier Duque, Srinivasa T Reddy , Harvey R Herschman , John H Walsh, Lee W Slice
{"title":"Gastrin-Releasing Peptide-Induced Expression of Prostaglandin Synthase-2 in Swiss 3T3 Cells","authors":"J.Randolph Hecht,&nbsp;Javier Duque,&nbsp;Srinivasa T Reddy ,&nbsp;Harvey R Herschman ,&nbsp;John H Walsh,&nbsp;Lee W Slice","doi":"10.1016/S0090-6980(97)00162-7","DOIUrl":"10.1016/S0090-6980(97)00162-7","url":null,"abstract":"<div><p>Prostaglandins, produced in response to mitogens and cytokines, are potent modulators of gastrointestinal physiology and pathophysiology. We investigated modulation of Prostaglandin synthase 2 (PGS-2) expression by the gastrin-releasing peptide (GRP) receptor in Swiss 3T3 cells. PGS-2 mRNA expression in Swiss 3T3 cells was determined by Northern blot analysis. PGS-2 protein expression in Swiss 3T3 cells was measured by Western blot analysis. GRP caused a transient induction of PGS-2 mRNA in Swiss 3T3 cells that resulted in GRP-dependent expression of PGS-2 protein. Transcriptional activation of PGS-2 by GRP was independent of de novo protein synthesis and was not affected by pertussis toxin. Comparison of signaling pathways used by PMA or EGF to those used by GRP showed that PGS-2 induction by GRP increased under conditions that inhibit PKC activity. Dexamethasone, which blocks PMA and EGF induction of PGS-2, also inhibited GRP-induced accumulation of PGS-2 mRNA. These results show that PGS-2 expression in Swiss 3T3 cells is not only controlled by PKC and receptor tyrosine kinase pathways but also by G-protein coupled receptor signaling pathways.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(97)00162-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20415406","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: 7
Angiopeptin, a Somatostatin Analogue, Inhibits Rat Coronary Artery and Aorta Smooth Muscle Cell Proliferation Induced by the Thromboxane A2 Mimetic U46619 一种生长抑素类似物Angiopeptin抑制血栓素A2模拟物U46619诱导的大鼠冠状动脉和主动脉平滑肌细胞增殖
Prostaglandins Pub Date : 1997-11-01 DOI: 10.1016/S0090-6980(97)00160-3
Yejun Zhao, Marie L Foegh
{"title":"Angiopeptin, a Somatostatin Analogue, Inhibits Rat Coronary Artery and Aorta Smooth Muscle Cell Proliferation Induced by the Thromboxane A2 Mimetic U46619","authors":"Yejun Zhao,&nbsp;Marie L Foegh","doi":"10.1016/S0090-6980(97)00160-3","DOIUrl":"10.1016/S0090-6980(97)00160-3","url":null,"abstract":"<div><p>Thromboxane A<sub>2</sub> (TXA<sub>2</sub>) is a potent mitogenic agent. Its synthesis is increased in transplant patients during rejection episodes, which is the suspected etiology of accelerated transplant arteriosclerosis. Angiopeptin, a stable analogue of somatostatin, inhibits arterial myointimal thickening in a number of vascular balloon injury models of angioplasty and in vivo models of transplant arteriosclerosis. In this study, we investigated whether TXA<sub>2</sub>-induced smooth muscle cell proliferation is inhibited by Angiopeptin in vitro. Primary rat coronary and aorta smooth muscle cells were cultured in the presence of U46619, a TXA<sub>2</sub> mimetic. Proliferation induced by U46619, as determined by <sup>3</sup>H-thymidine incorporation, was abrogated by two specific thromboxane receptor antagonists, SQ 30741 and SQ 29548, indicating that the effect of U46619 on smooth muscle cells is a specific receptor-mediated response. We found Angiopeptin to inhibit proliferation following exposure of both coronary and aorta smooth muscle cells to varying concentrations of U46619 for 3 and 6 days. This study demonstrates that U46619 exerts a specific receptor-mediated response stimulating the rat coronary and aorta smooth muscle cell proliferation. This mitogenic effect is obtained by increasing the G<sub>1</sub> to S transition rate. Angiopeptin inhibits thromboxane-induced cell proliferation to the same extent as a thromboxane antagonist. This inhibition is obtained by maintaining the noncycling fraction in that Angiopeptin prevents a progression from G<sub>0</sub>–G<sub>1</sub> to S phase.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(97)00160-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20415869","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: 10
Time Course Study for Airway Inflammation and Responsiveness by Repeated Provocation of Aeroantigen in Guinea Pigs 反复刺激空气抗原对豚鼠气道炎症反应的时间过程研究
Prostaglandins Pub Date : 1997-11-01 DOI: 10.1016/S0090-6980(97)00158-5
Hiroshi Takeda, Akifumi Kogame, Hiroyuki Tanaka, Hiroichi Nagai
{"title":"Time Course Study for Airway Inflammation and Responsiveness by Repeated Provocation of Aeroantigen in Guinea Pigs","authors":"Hiroshi Takeda,&nbsp;Akifumi Kogame,&nbsp;Hiroyuki Tanaka,&nbsp;Hiroichi Nagai","doi":"10.1016/S0090-6980(97)00158-5","DOIUrl":"10.1016/S0090-6980(97)00158-5","url":null,"abstract":"<div><p>To investigate the mechanisms of airway hyperresponsiveness (AHR), we examined the time course for asthmatic responses (including immediate asthmatic response (IAR), late asthmatic response (LAR), and AHR), airway inflammation (including edema in the airway, accumulation of inflammatory cells in bronchoalveolar lavage fluid (BALF), and mediator release including histamine and thromboxane A<sub>2</sub> (TXA<sub>2</sub>) in BALF after the repeated provocation of aeroantigen in sensitized guinea pigs. Furthermore, we examined the effect of S-1452, a TXA<sub>2</sub> receptor antagonist, on the antigen-induced airway obstruction and AHR in guinea pigs.</p><p>We found that IAR occurred 1 min after every antigen inhalations. LAR was observed every 4 h after the inhalation of antigen without 1st or 2nd challenge. AHR was initially observed 4 h after the 5th inhalation of antigen, and then AHR was observed at every time measured even after the 6th provocation. The water content of the airway increased after the 2nd antigen inhalation. A number of leukocytes, especially eosinophils in BALF, was observed 30 min after the 2nd antigen inhalation. Desquamation of epithelia was observed 30 min after the 5th antigen inhalation. TXB<sub>2</sub> and histamine in BALF were detected after the first antigen inhalation. These results suggest that LAR is caused by repeated airway inflammation such as eosinophilia and mediator release including TXA<sub>2</sub>. AHR may appear with the damages of lung tissue such as desquamation of epithelia. Oral administration of S-1452 (1 and 10 mg/kg) significantly inhibited LAR and AHR, assessed after the 6th antigen challenge.</p><p>The present findings suggest that repeated antigen challenge causes airway inflammation and leads to the onset of LAR and AHR when became chronic. Furthermore, persistent generated TXA<sub>2</sub> plays an important role in the pathogenesis of antigen-induced late-phase obstruction and AHR.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(97)00158-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20415872","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: 16
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