International congress series最新文献

{"title":"Indole, the aromatic element of tryptophan, as a pi-donor and amphiphilic headgroup","authors":"George W. Gokel","doi":"10.1016/j.ics.2007.07.038","DOIUrl":"10.1016/j.ics.2007.07.038","url":null,"abstract":"<div><p><span>Indole<span>, the aromatic sidechain element of tryptophan, may play many biological roles. It may serve as an anchor or organizing element, a </span></span>hydrogen bond<span> donor, or a Lewis basic donor in the cation–pi sense to alkali metal or ammonium cations. Organic chemistry has been used to develop model systems that probe these interactions and give experimental data concerning their importance.</span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 1-14"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.038","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"98873187","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}

{"title":"Up-regulation of indoleamine 2,3-dioxygenase by lipopolysaccharide is regulated through activation of p38 mitogen-activated protein kinase and nuclear factor-κB","authors":"Suwako Fujigaki,&nbsp;Kanako Takahashi,&nbsp;Hidetsugu Fujigaki,&nbsp;Masao Takemura,&nbsp;Mitsuru Seishima,&nbsp;Kuniaki Saito","doi":"10.1016/j.ics.2007.07.032","DOIUrl":"10.1016/j.ics.2007.07.032","url":null,"abstract":"<div><p><span>Indoleamine 2,3-dioxygenase (IDO) is up-regulated by interferon-γ (IFN-γ)-dependent and/or -independent mechanisms. IFN-γ-dependent mechanism is regulated through signal transducer and activator of transcription 1α (STAT1α) and interferon regulatory factor 1<span> (IRF-1). On the other hand, IFN-γ-independent mechanism of IDO induction has not been identified. In this study, we explored whether IDO induction by LPS requires the STAT1α and IRF-1 signaling pathways. IDO was induced by LPS or IFN-γ in THP-1 cells and a synergistic IDO induction occurred in THP-1 cultured with a combination of tumor necrosis factor-α, interleukin-6 and interleukin-1β. An </span></span>electrophoretic mobility shift assay<span> using STAT1α and IRF-1 consensus oligonucleotide<span> probes showed no STAT1α or IRF-1 binding activities in LPS-stimulated THP-1 cells. Further, the LPS-induced IDO activity was inhibited by both p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) inhibitors. These results suggest that IDO induction by LPS is not regulated through the STAT1α or IRF-1 binding activities that are induced by IFN-γ, and may be related to the activity of the p38 MAPK pathway and/or NF-κB.</span></span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 200-204"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.032","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"96961930","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}

{"title":"Diversity of the intracellular mechanisms underlying the anti-tumor properties of indirubins","authors":"Laurent Meijer,&nbsp;Jessica Shearer,&nbsp;Karima Bettayeb,&nbsp;Yoan Ferandin","doi":"10.1016/j.ics.2007.07.041","DOIUrl":"10.1016/j.ics.2007.07.041","url":null,"abstract":"<div><p><span>Indirubin is a bis-indole isomer of indigo which can be obtained from indigo-producing plants, several species of marine </span>mollusks<span>, several recombinant bacteria and mammalian urine. Indirubin is the active ingredient of a traditional Chinese medicine<span><span> recipe, Danggui Longhui Wan, reported as a treatment for </span>chronic myelocytic leukemia<span><span><span>. Following the discovery of indirubin's interaction with cyclin-dependent kinases, numerous derivatives have been chemically synthesized aiming at the optimization of indirubins' selectivity, solubility and efficacy against tumor growth. Recent studies show that the mechanism of action of indirubins is complex. Additional targets include glycogen synthase kinase-3, c-Src and activation of the Stat3 transcription factor, </span>aryl hydrocarbon receptor<span>, glycogen phosphorylase, and other targets. Interaction with these multiple targets may contribute to the anti-proliferative and </span></span>cell death inducing effects of indirubins, and avoid the appearance of indirubin-resistant cells.</span></span></span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 60-74"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.041","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"107226669","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}

{"title":"Tryptophan metabolites as potent inhibitors of aldehyde dehydrogenase activity and potential alcoholism-aversion therapeutic agents","authors":"Abdulla A.-B. Badawy ,&nbsp;Christopher J. Morgan","doi":"10.1016/j.ics.2007.07.020","DOIUrl":"10.1016/j.ics.2007.07.020","url":null,"abstract":"<div><p><span><span>Alcoholism aversion therapy involves administration of a </span>drug which inhibits the activity of the liver mitochondrial (or low </span><em>K</em>_m<span><span><span>) enzyme </span>aldehyde dehydrogenase<span><span><span> (AlDH; EC 1. 2.1.3), so that if a person consumes alcohol while on such medication, s/he will experience the unpleasant symptoms and effects of acetaldehyde. Our work on the tryptophan (Trp) and serotonin status of patients with the </span>chronic fatigue syndrome and observations of alcohol consumption </span>behaviour of such patients led us to identify 4 Trp metabolites as potent inhibitors of AlDH activity from both yeast and rat </span></span>liver mitochondria<span><span>. Three of these inhibitors are kynurenine<span><span><span> metabolites [3-hydroxykynurenine (3HK), 3-hydroxyanthranilic acid (3HAA), and kynurenic acid<span> (KA)], whereas the fourth is the Trp transamination product indol-3-ylpyruvic acid (IPA). At a range of concentrations of 2–100 μM, the 4 metabolites caused inhibition of the mammalian liver mitochondrial </span></span>enzyme activity similar to or stronger than that produced by the classical AlDH inhibitor </span>disulfiram. For example, at 2 μM, inhibition was 55, 46, 40 and 30% respectively, against 42% by disulfiram. We propose these Trp metabolites as potential alcoholism-aversion therapeutic agents. Our preferred strategy is to ensure accumulation of adequate concentrations of these AlDH-inhibitory metabolites by administration of Trp with metabolic blockade of the kynurenine pathway at the </span></span>kynureninase<span><span><span> step. Advantages of this new therapy over existing aversion drugs and of the proposed strategy are the following: (1) a much greater safety profile; (2) production at the required site of action (the liver); (3) decreased neuronal hyperexcitability (an important determinant of relapse by detoxified alcoholics) by the cytoprotective kynurenic acid and (4) by the decreased formation of the neurotoxin </span>quinolinic acid by kynureninase inhibition; (5) provision of serotonin from Trp, thus counteracting the other important determinants of relapse, namely anxiety and depression. Our proposed therapy, which enjoys intellectual property protection, represents a novel, comprehensive and unique concept in alcoholism </span>treatment, which merits clinical development.</span></span></span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 344-351"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"104094348","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}

{"title":"The role of serotonin in risky choice and the acquisition of reciprocal cooperative behaviour: 2 investigations using tryptophan depletion","authors":"Robert D. Rogers","doi":"10.1016/j.ics.2007.08.001","DOIUrl":"10.1016/j.ics.2007.08.001","url":null,"abstract":"<div><p><span>Making decisions between risky actions involves weighing the pros and cons of each, and considering the relative probabilities with which good and bad outcomes will occur. In this paper, I review 2 recent studies suggesting that serotonin modulates the cognitive and emotional processes involved in such decision-making in both non-social and social contexts. First, we have found that tryptophan depletion – leading to diminishes central serotonin activity – alters attention towards the gains associated with risky options. Second, we have found that tryptophan depletion alters the acquisition of socially cooperative </span>behaviour in an iterated Prisoner's Dilemma game. These findings highlight the significance of serotonin in altered non-social and social risky choice in psychiatric illnesses.</p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 144-149"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.08.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"93281383","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}

{"title":"Post-translational modification of indoleamine 2,3-dioxygenase: N-terminal modification and nitration","authors":"Hidetsugu Fujigaki ,&nbsp;Kanako Takahashi ,&nbsp;Suwako Fujigaki ,&nbsp;Junichi Masuda ,&nbsp;Osamu Takikawa ,&nbsp;Sanford P. Markey ,&nbsp;Mitsuru Seishima ,&nbsp;Kuniaki Saito","doi":"10.1016/j.ics.2007.07.017","DOIUrl":"10.1016/j.ics.2007.07.017","url":null,"abstract":"<div><p>Indoleamine 2,3-dioxygenase (IDO) induction can deplete <span>l</span><span><span><span><span>-Trp in target cells, and this effect is partially responsible for the antimicrobial, antiviral, and antiproliferative activities of several cytokines. Although a lot of studies have indicated the biological importance of IDO, the post-translational modification of IDO remains unknown. In this study, we analyzed IDO protein by liquid chromatography and tandem mass spectrometry (LC-MS/MS) to find post-translational modifications. LC-MS/MS analysis revealed that: (1) immunoprecipitated-IDO from a human </span>monocyte cell line has been processed to cleave the N-terminal </span>methionine<span>, and the resulting N-terminal alanine is acetylated; (2) </span></span>peroxynitrite, an NO-derived reactive species, which can modify proteins via formation of 3-nitrotyrosine, induced nitration and inactivation of recombinant IDO, specifically nitrating Tyr15, 345, and 353 residues. We successfully revealed these two types of post-translational modifications of IDO, and further findings of the post-translational modification may shed light on the mechanisms of IDO induction.</span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 41-45"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"102042505","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}

{"title":"LIFE (losartan intervention for endpoint reduction in hypertension) study and its substudies","authors":"Claudio Borghi ,&nbsp;Sibel Ertek","doi":"10.1016/j.ics.2007.03.014","DOIUrl":"10.1016/j.ics.2007.03.014","url":null,"abstract":"<div><p><span>Hypertension is one of the most important causes of mortality and morbidity in modern world. Its treatment with renin–angiotensin system blockade provides beneficial effects especially in special patient groups. The LIFE (losartan intervention for endpoint reduction in hypertension) study analysed the differences between an </span>angiotensin receptor<span><span> blocker (losartan) and a beta-blocker (atenolol) antihypertensive treatments </span>in patients<span> with hypertension and left ventricular hypertrophy<span><span><span><span>. Despite similar blood pressure reductions, </span>losartan showed beneficial effects in primary endpoints, and also new-onset diabetes, stroke, </span>albuminuria, left ventricular hypertrophy regression and in </span>atrial fibrillation. Although there are some restrictions on the study, the results show the beneficial effects of angiotensin receptor blockers in hypertensive patients with high risk, with probably mechanisms other than blood pressure reduction.</span></span></span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1303 ","pages":"Pages 129-137"},"PeriodicalIF":0.0,"publicationDate":"2007-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.03.014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"113853999","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}

{"title":"Insulin signaling in hypertension","authors":"Bruno Trimarco,&nbsp;Salvatore Crispo,&nbsp;Carmine Morisco","doi":"10.1016/j.ics.2007.04.005","DOIUrl":"10.1016/j.ics.2007.04.005","url":null,"abstract":"<div><p><span><span><span><span>Insulin resistance has been described in several diseases that increase cardiovascular risk and mortality, such as diabetes mellitus, obesity, essential hypertension, </span>metabolic syndrome, and heart failure. In last years it has been clarified the role of insulin resistance in the pathogenesis of hypertension and target organ damage. Dysregulation of sympathetic nervous and renin–angiotensin systems resulting in enhanced stimulation of both adrenergic (ARs) and </span>angiotensin<span> II receptors (AT) are typical features of hypertension. Overactivity of the renin–angiotensin system observed in hypertension is likely to impair insulin signaling and contribute to insulin resistance. Actually, Ang II acting through the AT1 receptor inhibits the actions of insulin in </span></span>vascular tissue<span><span><span>, in part, by interfering with insulin signaling through PI3K and downstream Akt signaling pathways via generation of </span>reactive oxygen species (ROS) by </span>NADPH oxidase. On the contrary, stimulation of βARs is able to induce insulin resistance through the activation of different serine/threonine kinases that blunt the insulin signal by phosphorylating </span></span>IR<span><span> or IRS-1. Hypertension is also associated with an endothelial chronic inflammatory response characterized by altered cytokine production and activation of inflammatory signaling pathways, this activation results in an impairment of insulin signaling. Understanding the molecular mechanisms which can interfere with the impairment insulin signalling may be useful to improve </span>blood pressure control as well as cardiac and cerebral protection in hypertension.</span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1303 ","pages":"Pages 41-47"},"PeriodicalIF":0.0,"publicationDate":"2007-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.04.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"110128547","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}

{"title":"Oxidative stress, inflammation and atherosclerotic plaque development","authors":"Francesco Cipollone,&nbsp;Maria Luigia Fazia,&nbsp;Andrea Mezzetti","doi":"10.1016/j.ics.2007.02.064","DOIUrl":"10.1016/j.ics.2007.02.064","url":null,"abstract":"<div><p>Although the pathophysiological mechanisms underlying atherosclerosis<span> are not completely understood, it is widely recognized that both inflammation and oxidative stress<span><span><span> play important roles in all of the phases of atherosclerosis evolution. The oxidative modification hypothesis of atherosclerosis supports the concept that oxidation<span> of circulating low density lipoprotein<span> (LDL) plays a key role in the early phases of atherogenesis. However, in addition to LDL oxidation, other oxidative events are worth noting in the setting of atherosclerosis, such as the generation of </span></span></span>oxygen reactive species<span>. These compounds are crucial mediators in the signaling pathways underlying </span></span>vascular inflammation<span>, from the initial phases of fatty streak formation to atherosclerotic plaque evolution toward instability and rupture. In this manuscript, we summarize the newest evidence linking oxidative signaling to inflammation and atherosclerosis evolution.</span></span></span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1303 ","pages":"Pages 35-40"},"PeriodicalIF":0.0,"publicationDate":"2007-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.02.064","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"110386050","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}

{"title":"Coronary heart disease in diabetes","authors":"Angelo Avogaro,&nbsp;Gianpaolo Fadini,&nbsp;Saula Vigili de Kreutzenberg,&nbsp;Antonio Tiengo","doi":"10.1016/j.ics.2007.04.006","DOIUrl":"10.1016/j.ics.2007.04.006","url":null,"abstract":"<div><p>Type Diabetes Mellitus is a chronic disease, whose incidence is alarmingly growing. It is associated with severe metabolic abnormalities and increased cardiovascular morbidity and mortality. The first detectable alteration in the pathogenesis of atherosclerosis<span><span> is endothelial dysfunction which is linked to alteration in </span>microcirculation. Detection of microvascular dysfunction in diabetes would force physician to implement early aggressive therapeutic intervention.</span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1303 ","pages":"Pages 70-73"},"PeriodicalIF":0.0,"publicationDate":"2007-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.04.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"94340584","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}