International congress series最新文献

{"title":"Non-protein (free and protein-bound) tryptophan content in cereal and legume seed flours","authors":"S. Comai ,&nbsp;A. Bertazzo ,&nbsp;L. Bailoni ,&nbsp;M. Zancato ,&nbsp;C.V.L. Costa ,&nbsp;G. Allegri","doi":"10.1016/j.ics.2007.07.007","DOIUrl":"10.1016/j.ics.2007.07.007","url":null,"abstract":"<div><p><span>Cereals and legumes are the major source of protein in the human diet. There is little information on the presence of non-protein tryptophan, one of the essential </span>amino acids<span><span> less represented in the vegetable proteins. Our results show that tryptophan is present not only in the free-form but also is linked either to water soluble proteins<span> or to proteins extracted at pH 8.9 both in cereal and legume flours. As regards the cereals, wheat and spelt contain the highest content of protein tryptophan and maize the lowest. Spelt, followed by barley and pearl millet flours, contains the highest amounts of free tryptophan and the rice the lowest. In addition, spelt flour shows the highest levels of tryptophan linked to both water soluble and buffered protein fractions, whereas rice contains the lowest amounts of protein-bound tryptophan. Among the legume flours, soybeans show the highest value in protein tryptophan and peas the lowest. Chick peas contain the highest concentrations of both free and protein-bound tryptophan water soluble fraction. This last fraction appears absent in </span></span>broad bean, lentil and soybean flours. In addition, beans are shown to contain the highest levels of tryptophan linked to proteins extracted at pH 8.9, and peanuts the lowest values both as free and protein-bound forms.</span></p><p>Considering that tryptophan is one of the limiting amino acids of the biological value of vegetable proteins, the determination of non-protein tryptophan in food is very useful in calculating the score.</p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 227-232"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"96902369","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":"Enhancement of 3-hydroxyanthranilic acid-induced T cell apoptosis through cinnabarinic acid generation","authors":"Rie Hiramatsu ,&nbsp;Toshiaki Hara ,&nbsp;Hidetoshi Akimoto ,&nbsp;Osamu Takikawa ,&nbsp;Tsutomu Kawabe ,&nbsp;Fumihiko Nagase","doi":"10.1016/j.ics.2007.07.023","DOIUrl":"10.1016/j.ics.2007.07.023","url":null,"abstract":"<div><p><span><span>Induction of apoptosis by 100 μM of 3-hydroxyanthranilic acid (3HAA) was enhanced by </span>SOD as well as MnCl</span>₂<span><span> and further promoted in the presence of catalase. Corresponding to apoptosis induction, the generation of cinnabarinic acid (CA) through the </span>oxidation of 3HAA was enhanced by SOD or MnCl</span>₂<span><span> in the presence of catalase. Synthesized CA possessed more than 10 times higher apoptosis-inducing activity than 3HAA. CA generated from 3HAA possesses strong apoptosis-inducing activity in thymocytes through </span>reactive oxygen species<span> (ROS) generation, loss of mitochondrial membrane potential<span> and caspase activation.</span></span></span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 209-212"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"111864186","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":"Peroxisome proliferators-activated receptor α controls tryptophan-NAD metabolism in rodents","authors":"M. Shin ,&nbsp;C. Umezawa ,&nbsp;K. Sano ,&nbsp;F.J. Gonzalez","doi":"10.1016/j.ics.2007.07.004","DOIUrl":"10.1016/j.ics.2007.07.004","url":null,"abstract":"<div><p><span><span>The effect of peroxisome-proliferators (PPs) on tryptophan (Trp)-NAD metabolism in rodents was investigated. Administration of PPs increased NAD levels in primary cultured rat hepatocytes. The time course for the NAD increase was similar to the expression of the </span>nuclear receptor<span> PPARα and its target genes. To determine the relationship between PPARα and the increase in NAD levels after PP administration, PPARα-null (−/−) and wild type (+/+) mice were examined. ACOX was up-regulated in +/+ mice by the potent PPARα ligand Wy-14,643 (Wy), but not in −/− mice. The α-Amino-β-carboxymuconate-ε-semialdehyde </span></span>decarboxylase gene (ACMSD) was down-regulated by Wy in +/+ mice and up-regulated in −/− mice compared with +/+ mice. Depending on the ligand, PPARα activation down-regulated expression of ACMSD directly or indirectly. The increase in hepatic NAD levels by Wy was observed in +/+ mice, but not in −/− mice. The contribution of altered ACMSD expression to NAD levels was determined. PPARα agonists affected Trp-NAD metabolism in rodents through PPARα-related gene expression resulting in altered hepatic NAD levels that promote fatty acid β-oxidation. Trp-NAD metabolism may also be influenced by PPARα activation by endogenous ligands.</p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 222-226"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"94471676","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":"Aetiology of antisocial behaviour","authors":"Essi Viding ,&nbsp;Henrik Larsson","doi":"10.1016/j.ics.2007.07.040","DOIUrl":"10.1016/j.ics.2007.07.040","url":null,"abstract":"<div><p><span>In this paper we briefly and selectively review the current knowledge base of the nature and nurture for persistent, early-onset antisocial behaviour, with a particular focus on studies that have examined potential etiologic distinctions such as callous-unemotional subtype of antisocial behaviour. First, we discuss results from recent studies that indicate that callous-unemotional traits can be used to distinguish two different subtypes of conduct problems at a behavioural, cognitive–affective, and possibly neural level. Second, we review genetically informative studies on antisocial behaviour keeping in mind the distinction of callous-unemotional subtype. Data from these two lines of research (i.e., </span>genetic, neurocognitive studies) to date suggest that antisocial children with callous-unemotional traits are genetically more vulnerable to antisocial behaviour than their antisocial peers and that this genetic vulnerability may manifest in a distinct neurocognitive signature. In this paper we also highlight the complex interplay between nature and nurture and provide examples of how putative environmental risk factors for antisocial behaviour can be studied using behavioural genetic research designs. Finally, we give some pointers of new research strategies in the field and draw out implications of this research to practice.</p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 121-132"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.040","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"106460167","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":"Kynurenic acid actions in brain and periphery","authors":"F. Moroni,&nbsp;S. Fossati,&nbsp;A. Chiarugi,&nbsp;A. Cozzi","doi":"10.1016/j.ics.2007.07.016","DOIUrl":"10.1016/j.ics.2007.07.016","url":null,"abstract":"<div><p><span><span>Kynurenic acid (KYNA) is commonly considered a non-competitive NMDA </span>receptor antagonist<span><span>. It has been recently shown that KYNA also antagonizes the alpha 7 nicotine receptors and reduces </span>glutamate<span><span> and dopamine release in the rat striatum. Finally, it has been demonstrated that KYNA interacts with GPR35, an </span>orphan receptor negatively coupled to G</span></span></span>_i proteins.</p><p><span>We noticed that in a macrophage cell line (RAW 264.7) KYNA reduces the LPS-induced release of pro-inflammatory cytokines. In mice treated with lethal doses of </span>LPS<span>, a septic shock<span> model, KYNA administration (200 mg/kg i.p.x 3 times) significantly reduced the mortality rate. Thus KYNA has receptors both in the nervous and peripheral tissues where it may play an interesting regulatory role in cell activation and survival.</span></span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 305-313"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"101751887","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 metabolism via serotonin in human CSF of different brain sites using a new neuroendoscopic technique","authors":"P. Longatti ,&nbsp;S. Comai ,&nbsp;A. Perin ,&nbsp;A. Bertazzo ,&nbsp;V. Rizzo ,&nbsp;E. Ragazzi ,&nbsp;C.V.L. Costa ,&nbsp;G. Allegri","doi":"10.1016/j.ics.2007.07.009","DOIUrl":"10.1016/j.ics.2007.07.009","url":null,"abstract":"<div><p><span>A new neuroendoscopic technique has permitted a precise and accurate exploration of all the cerebral ventricles, making possible the study of the CSF of the </span>lateral ventricles<span><span><span><span> and, above all, the CSF adjacent to the walls of the third ventricle in humans. The concentrations of </span>tryptophan and its metabolites via serotonin were measured in the CSF of different sites of the cerebral cavity, in particular in the third ventricle. Patients affected with non-communicating </span>hydrocephalus<span><span> undergoing neuroendoscopic third ventriculostomy were enrolled in the study. As controls, subjects not suffering from any </span>neurological disease<span>, who underwent lumbar subarachnoid anaesthesia for minor surgical procedures, provided lumbar CSF, and patients affected by </span></span></span>Chiari malformation<span> provided cisternal and right ventricular CSF. Tryptophan concentration was higher in right ventricular CSF than in lumbar CSF. Serotonin (5-HT) was detectable in the CSF of the right ventricle<span> of hydrocephalic individuals. 5-Hydroxyindoleacetic acid (5-HIAA) was higher in the right ventricular CSF than in the cisternal and lumbar CSF both in controls and hydrocephalic subjects. However, the 5-HIAA level was higher in the right ventricular and cisternal CSF in hydrocephalic individuals in comparison to controls. 5-HT presented the highest concentration in the pineal recess<span>, whereas the highest amounts of 5-HIAA were found in the choroids plexus<span>, third and right ventricles and the lowest in the pineal recess, subarachnoid space<span> and intepeduncular cistern. Melatonin is more concentrated within the ventricles, in particular the third ventricle, and in the CSF pineal recess.</span></span></span></span></span></span></p><p>The use of this neuroendoscopic technique in hydrocephalic patients provides new insight into the metabolic pathway of tryptophan via serotonin in the CSF.</p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 150-158"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"100257235","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":"Variety of natural products derived from tryptophan and stereoselective synthesis of tetrahydro-β-carboline derivatives of pharmacological importance","authors":"Piotr Roszkowski ,&nbsp;Stefan Czarnocki ,&nbsp;Jan K. Maurin ,&nbsp;Aleksandra Siwicka ,&nbsp;Anna Zawadzka ,&nbsp;Joanna Szawkało ,&nbsp;Andrzej Leniewski ,&nbsp;Zbigniew Czarnocki","doi":"10.1016/j.ics.2007.07.003","DOIUrl":"10.1016/j.ics.2007.07.003","url":null,"abstract":"<div><p>The use of chiral inductors belonging to different classes of compounds is elaborated. Tetrahydro-β-carboline derivatives were constructed stereoselectively by the use of (<em>R</em>)-1-arylethylamine and <span>l</span>-amino acids. Asymmetric transfer hydrogenation was proven highly effective in enantioselective synthesis of several alkaloids.</p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 46-59"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132005029","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 the brain indoleamine 2,3-dioxygenase activity in a mouse model of Alzheimer's disease by systemic endotoxin challenge","authors":"Hidetoshi Akimoto,&nbsp;Akiko Yamada,&nbsp;Osamu Takikawa","doi":"10.1016/j.ics.2007.07.026","DOIUrl":"10.1016/j.ics.2007.07.026","url":null,"abstract":"<div><p><span><span>Inflammation is suspected to be a critical component of the progression and severity of neurodegeneration<span> in Alzheimer's disease (AD). The </span></span>kynurenine<span><span><span> pathway (KP), which is the major route for tryptophan degradation, is activated in </span>central nervous system (CNS) inflammation. The activation of KP, which is caused by the up-regulation of indoleamine 2,3-dioxygenase (IDO), leads to the production of some neurotoxic metabolites (e.g., quinolinic acid). To address the hypothesis that the KP may play a role in the pathogenesis of the AD brain, we examined the IDO activity in the brain of the </span>Tg2576<span> transgenic mouse<span> model of AD. The IDO activity was detected in the brain of the mouse model of AD, but the level was not significantly different from that of the age-matched nontransgenic control mice. In contrast, when CNS inflammation was induced in this mouse model by a single intraperitoneal injection of </span></span></span></span>lipopolysaccharide<span> (LPS), a marked (3-fold) increase in the IDO activity was observed, but not in the control mice with the same treatment<span>. These results suggest that peripheral inflammation activates the CNS KP in the AD brain, leading to the production of neurotoxic metabolites and thereby inducing neuronal death.</span></span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 357-361"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134596546","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":"Rapid, simple and simultaneous measurement of kynurenine and tryptophan in plasma by column switching-HPLC method","authors":"K. Kawai ,&nbsp;H. Ishikawa ,&nbsp;K. Ohashi ,&nbsp;Y. Itoh ,&nbsp;R. Teradaira","doi":"10.1016/j.ics.2007.07.005","DOIUrl":"10.1016/j.ics.2007.07.005","url":null,"abstract":"<div><p><span>We established a highly reproducible, simple and rapid simultaneous measurement method in which blood plasma can be directly injected into high-performance liquid chromatography (HPLC) without conducting conventional extraction of kynurenine<span> (Kyn) and tryptophan (Trp) from blood plasma. In this method, Kyn and Trp were first separated from proteins present in blood plasma using a pre-column. Then, by column-switching, the separated Kyn and Trp were automatically injected into a separation column. The recoveries of Kyn and Trp determined in blood plasma by this method were 100.0</span></span> <!-->±<!--> <!-->0.9 and 100.0<!--> <!-->±<!--> <!-->1.4%, respectively.</p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 415-419"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"95577846","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":"Clinical aspects of indoleamine 2,3-dioxygenase (IDO)-initiated tryptophan metabolism: IDO is a target of drug discovery for various diseases","authors":"O. Takikawa","doi":"10.1016/j.ics.2007.07.029","DOIUrl":"10.1016/j.ics.2007.07.029","url":null,"abstract":"<div><p><span><span><span>Indoleamine 2,3-dioxygenase (IDO) catalyzes the first and rate-limiting step in the major metabolic pathway of tryptophan (Trp) in mammals. In healthy conditions, IDO is modestly expressed in many tissues but highly up-regulated locally or systemically by immune activation and inflammation. Considerable attention has been focused on IDO because of its detrimental effects in a variety of diseases. The activity of IDO plays a role in: 1) the cytokine (IFN-γ/IL-12) cascade inducing dangerous systemic Trp depletion that possibly results in a reduction of serotonin synthesis, 2) the escape of malignant tumors from </span>immune surveillance by inducing </span>immune tolerance through localized Trp depletion and production of </span>immunosuppressive<span><span><span> Trp metabolites, 3) neurodegenerative disorders such as Alzheimer`s disease via aberrant production of the </span>neurotoxin, </span>quinolinic acid<span>, and 4) age-related cataract due to “Kynurenilation,” a novel post-translational modification of lens proteins<span> with Trp-derived UV filters. Therefore IDO is an ideal pharmacological target for intervention in these diseases. The properties of currently available IDO inhibitors are also described.</span></span></span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 290-297"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.029","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"109995300","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}