227 research outputs found
Opzet overlaatroutine en eerste ijking van het calamiteitenmodel CALAM
Voor de drinkwaterleidingbedrijven is in 1987, door de vakgroep Gezondheidstechniek en Waterbeheersing van de TU model CALAM ontwikkeld. CALAM moet het mogelijk maken oa in geval van calamiteuze lozingen snel en accuraat de stofverspreiding in het Noordelijk Deltabekken en de invloed van mogelijke beheersmaatregelen hierop te voorspellen. In de eerste versie van het programma bestond niet de mogelijkheid de waterbeweging en de stofverspreiding over een overlaat te berekenen. In dit rapport wordt een opzet gemaakt voor een overlaatroutine en voorts een eerste ijking van de stofverspreiding. Om de gevoeligheid van CALAM voor de grootte van de dispersiecoëfficiënten af te schatten is er een gevoeligheidsanalyse uitgevoerd. Hierbij is een geringe gevoeligheid gebleken voor de longitudinale coëfficiënt (Ix) en een grote gevoeligheid voor de transversale coëfficiënt. In geval van een zeer grote transversale coëfficiënt (Ky = 0.9) wordt de stofverspreiding afgebroken hetgeen niet overeen komt met de realiteit. Dit lijkt te worden veroorzaakt door een combinatie met takken met een kleine berging (geen kribvakken). Nadere beschouwing van berekening de berging is daarom noodzakelijk ! Tot slot is er vergelijkend onderzoek gedaan naar twee mogelijke dispersieforauleringen. Hieruit bleek dat de tweedimensionale formulering (Dx=Kx*a*ua) in de meeste gevallen het beste voldoet, maar dat vooral ter plaatse van het Haringvliet de eendimensionale dispersieformulering ( Dx=0.011*(u2.B2)/(a.ua) ) resultaten oplevert die meer in overeenstemming zijn met die van ZWENDL en DELVAQ.LWater Management and Hydraulic EngineeringCivil Engineering and Geoscience
Interne lozing in stofverspreidingsmodel t.b.v. programma CALAM
Op de Technische Universiteit te Delft is in 1986/1987 door de afstudeerders J.F.X. Urbanus en J.H.G. Vreeburg een computerprogramma ontwikkeld dat de waterbeweging en de stofverspreiding in een waterbeheerseenheid beschrijft. Dit programma "CALAM" is geschreven als calamiteitenmodel voor het Noordelijk Deltabekken waar zich belangrijke innamepunten van oppervlaktewater bevinden. Het programma "CALAM" dat geschreven is in "FORTRAN" is als uitgangspunt gebruikt voor het computerprogramma t.b.v. het afstudeerproject "De waterhuishouding van de Wieringermeer en de sanering van de afvalwaterlozingen" van A.R.M. van Nispen. Om dit programma te kunnen gebruiken voor de beschrijving van de waterbeweging en de stofverspreiding in de Wieringermeer, waren enkele verbeteringen en aanvullingen op het programma noodzakelijk. De belangrijkste aanvulling is de mogelijkheid om een lozing van stof in een interne knoop van het systeem op te geven en door te rekenen. Deze aanvulling was noodzakelijk om de verspreide afvalwaterlozingen en de effluentlozing van een rioolwater zuiveringsinstallatie op het watersysteem van de Wieringermeer polder door te rekenen. De wijze waarop deze nieuwe optie in het invoer- en rekenprogramma is aangebracht is het onderwerp van dit deelontwerp.Hydraulic EngineeringCivil Engineering and Geoscience
Guest Editorial: Public Health Approaches to Safeguarding Children
Child maltreatment is increasingly being understood within a public health framework (Barlow and Calam, 2011; Gilbert et al., 2008; Putnam-Hornstein et al., 2011; Segal and Dalziel, 2011; Shanahan et al., 2011; World Health Organization, 1998). Globally and nationally, the high numbers of children and young people affected by child abuse and neglect are increasing as knowledge and understanding about the phenomena grow, and the escalating cost measured in fiscal, social and health terms is recognised
Suppression of Helicobacter pylori reduces gastrin releasing peptide stimulated gastrin release in duodenal ulcer patients.
Helicobacter pylori increases gastrin release in duodenal ulcer patients. This may be through disruption or changes in the mucus layer affecting the access of luminal stimulants to gastrin releasing cells. The effect of suppressing H pylori on gastrin release stimulated by a non-luminal stimulus, gastrin releasing peptide (GRP), was examined. Eleven patients with active duodenal ulcer disease and colonised with H pylori received an intravenous infusion of GRP (2.9 pmol/kg/minute for 30 minutes) and the plasma gastrin response was measured. Basal and peak pentagastrin stimulated acid output were also determined. Patients were treated with tripotassium dicitratobismuthate (De-Nol) and metronidazole to suppress H pylori and the tests were repeated. Suppression of H pylori decreased plasma gastrin concentrations during GRP infusion, but acid output was not affected. Chromatographic analysis of the forms of gastrin in plasma showed a significant fall in gastrin 17, the predominant form found in the gastric antrum. Gastrin 34 did not fall significantly. This study shows that suppression of H pylori decreases the hypergastrinaemia caused by the nonluminal stimulant, GRP, mainly via decreasing gastrin 17
Voyages en zigzag ou excursions d'un pensionnat en vacances dans les cantons suisses et sur le revers italien des alpes
par R. Topffer; illustrés d'après des dessins de l'auteur et ornés de 15 grands dessins par M. Calam
Canadian Education: A History
In 1959, W. J. Gage published The Development of Education in Canada by C. E. Phillips. Prior to this event, the average Canadian student of educational history seemed destined for W. S. Gilbert\u27s little list in that he so often studied "all centuries but this, and every country but his own." After the appearance of Phillips\u27 book, however, student historical attention sometimes took a more introspective turn, thanks to scholars like F. Henry Johnson and Louis-Philippe Audet whose subsequent provincial and national interpretations built productively on the Phillips theme of Canadian unity in diversity.
Gastric antral vascular ectasia in a patient with GIST after treatment with imatinib: Case report and literature review
Imatinib mesylate is a receptor kinase inhibitor approved by the Food and Drug Administration for the treatment of malignant metastatic and-or unresectable gastrointestinal stromal tumors and chronic myelogenous leukemia. Although imatinib is generally well tolerated, certain adverse drug reactions are common. These include gastrointestinal side-effects such as diarrhea, nausea and vomiting, as well as hematological side-effects and other miscellaneous side-effects such as fatigue, edema, dermatitis and dyspnea. We present a previously unreported adverse effect of imatinib, gastric antral vascular ectasia, in a 74-year-old woman with gastrointestinal stromal tumor in remission treated with adjuvant imatinib. Endoscopy performed prior to starting imatinib showed normal gastric mucosa, but 8 months after starting imatinib showed diffuse gastric inflammation. Repeat endoscopy 1 month after discontinuing imatinib showed significant improvement in gastric inflammation. © The Author 2012. Published by Oxford University Press. All rights reserved.Bowmick BK, 1993, J ROY SOC MED, V86, P52; CALAM J, 1980, DIGEST DIS SCI, V25, P236, DOI 10.1007-BF01308145; Debiec-Rychter M, 2004, J PATHOL, V202, P430, DOI 10.1002-path.1546; DeMatteo RP, 2009, LANCET, V373, P1097, DOI 10.1016-S0140-6736(09)60500-6; Demetri GD, 2002, NEW ENGL J MED, V347, P472, DOI 10.1056-NEJMoa020461; Dulai GS, 2004, ENDOSCOPY, V36, P68; Dunne KA, 2006, EUR J GASTROEN HEPAT, V18, P455, DOI 10.1097-00042737-200604000-00024; GOSTOUT CJ, 1992, J CLIN GASTROENTEROL, V15, P256, DOI 10.1097-00004836-199210000-00019; Hecker A, 2010, WORLD J SURG ONCOL, V8, DOI 10.1186-1477-7819-8-47; Heinrich MC, 2003, SCIENCE, V299, P708, DOI 10.1126-science.1079666; JABBARI M, 1984, GASTROENTEROLOGY, V87, P1165; Kwan V, 2006, AM J GASTROENTEROL, V101, P58, DOI 10.1111-j.1572-0241.2006.00370.x; Lorenzi AR, 2001, ANN RHEUM DIS, V60, P796, DOI 10.1136-ard.60.8.796; McCormick PA, 1998, GUT, V42, P750; Miettinen M, 2006, AM J SURG PATHOL, V30, P477, DOI 10.1097-00000478-200604000-00008; Miettinen M, 2005, AM J SURG PATHOL, V29, P52, DOI 10.1097-01.pas.0000146010.92933.de; Nilsson B, 2005, CANCER, V103, P821, DOI 10.1002-cncr.20862; PARK RHR, 1990, POSTGRAD MED J, V66, P720; RIDER JA, 1953, GASTROENTEROLOGY, V24, P118; Samelis GF, 2007, EJSO-EUR J SURG ONC, V33, P942, DOI 10.1016-j.ejso.2006.11.025; Sebastian S, 2003, ALIMENT PHARM THERAP, V18, P157, DOI 10.1046-j.0269-2813.2003.01617.x; Selinger CP, 2008, DIGESTION, V77, P131, DOI 10.1159-000124339; Spahr L, 1999, GUT, V44, P739; Takahashi T, 2006, INT J HEMATOL, V83, P467, DOI 10.1532-IJH97.06052; Tran T, 2005, AM J GASTROENTEROL, V100, P162, DOI 10.1111-j.1572-0241.2005.40709.x; Ward EM, 2004, J CLIN GASTROENTEROL, V38, P898, DOI 10.1097-00004836-200411000-0001322
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Candidatus Liberibacter americanus induces significant reprogramming of the transcriptome of the susceptible citrus genotype
In Brazil, Huanglongbing (HLB) is caused by Candidatus Liberibacter americanus (CaLam) and Ca. L. asiaticus (CaLas). Both species are vectored by the Asian citrus psyllid and are restricted to the phloem of infected citrus, where they promote a severe imbalance in the translocation of nutrients and other important substances along the plant. Several studies of the transcriptional response of citrus to HLB have been reported, but only for infection caused by CaLas. This study evaluated the transcriptional reprogramming of a susceptible genotype (Pera sweet orange) challenged with CaLam, using a customized 385K microarray chip. The analyses showed that a large number of genes and biological processes were significantly altered upon CaLam infection. Among the changes we highlight induction of zinc transporters, modulation of enzymes related to sugar metabolism, decreased photosynthesis, induction of several defense-related genes and modulation of enzymes regulating ROS production. Several biological processes reported as differentially modulated upon infection with CaLas responded similarly to CaLam. The large number of receptor-like proteins, PR genes, NBS-LRR and transcription factors (such as WRKY and MYB) found showed that even a susceptible citrus genotype is able to actively respond to infection by CaLam, as reported for CaLas. Twenty candidate genes were selected for validation in symptomatic and asymptomatic PCR-positive leaves of Hamlin sweet orange infected with CaLas or CaLam. Finally, using in
silico approaches, we compared our results with all published studies using CaLas to hypothesize a global feature of the defense/susceptibility mechanisms of citrus in response to the bacteria. These results have been explored in selection of target genes for genetic engineering to control HLB. Also, further transcriptome (RNAseq) experiments using tolerant and susceptible citrus genotypes infected with CaLam or CaLas using different time points are in progress to investigate the dynamics of expression of these genes during early stages of infection
Candidatus Liberibacter americanus induces significant reprogramming of the transcriptome of the susceptible citrus genotype
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Background: Citrus huanglongbing (HLB) disease is caused by endogenous, phloem-restricted, Gram negative, uncultured bacteria named Candidatus Liberibacter africanus (CaLaf), Ca. L. asiaticus (CaLas), and Ca. L. americanus (CaLam), depending on the continent where the bacteria were first detected. The Asian citrus psyllid vector, Diaphorina citri, transmits CaLas and CaLam and both Liberibacter species are present in Brazil. Several studies of the transcriptional response of citrus plants manifesting HLB symptoms have been reported, but only for CaLas infection. This study evaluated the transcriptional reprogramming of a susceptible genotype of sweet orange challenged with CaLam, using a customized 385K microarray containing approximately 32,000 unigene transcripts. We analyzed global changes in gene expression of CaLam-infected leaves of sweet orange during the symptomatic stage of infection and compared the results with previously published microarray studies that used CaLas-infected plants. Twenty candidate genes were selected to validate the expression profiles in symptomatic and asymptomatic PCR-positive leaves infected with CaLas or CaLam. Results: The microarray analysis identified 633 differentially expressed genes during the symptomatic stage of CaLam infection. Among them, 418 (66%) were upregulated and 215 (34%) were down regulated. Five hundred and fourteen genes (81%) were orthologs of genes from Arabidopsis thaliana. Gene set enrichment analysis (GSEA) revealed that several of the transcripts encoded transporters associated with the endomembrane system, especially zinc transport. Among the most biologically relevant gene transcripts in GSEA were those related to signaling, metabolism and/or stimulus to hormones, genes responding to stress and pathogenesis, biosynthesis of secondary metabolites, oxidative stress and transcription factors belonging to different families. Real time PCR of 20 candidate genes validated the expression pattern of some genes in symptomatic and asymptomatic leaves infected with CaLam or CaLas. Conclusions: Many gene transcripts and biological processes are significantly altered upon CaLam infection. Some of them had been identified in response to CaLas infection, while others had not been previously reported. These data will be useful for selecting target genes for genetic engineering to control HLB.14Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)EMBRAPA-Monsanto AgreementFlorida Research and Development Foundation, Inc. [Machado-ma2-132]Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Florida Research and Development Foundation, Inc. [Machado-ma2-132
Helicobacter felis infection is associated with lymphoid follicular hyperplasia and mild gastritis but normal gastric secretory function in cats
The relationship of Helicobacter felis, a bacterium observed in the stomachs of cats, to gastric disease is unclear. The objective of this study was to determine if H. felis infection alters gastric histopathology, proinflammatory cytokine expression, and secretory function and evokes a humoral immune response in cats. Five specific-pathogen-free (SPF) Helicobacter-free cats were studied before and for 1 year after oral inoculation with H. felis (ATCC 49179). Four SPF H. felis-uninfected cats served as controls. The stomachs of all five H. felis-inoculated cats became colonized, as determined by urease activity, histopathology, PCR, culture, and transmission electron microscopy of serial gastric biopsies at 0, 3, 5, 8, and 12 months. Uninoculated cats remained Helicobacter free. Lymphoid follicular hyperplasia, atrophy, and fibrosis were observed primarily in the pylorus of infected cats. Mild mononuclear inflammation was detected in both infected and uninfected cats, but was more extensive in infected cats, with pangastric inflammation, eosinophilic infiltrates, and cardia gastritis observed only in infected cats. No upregulation of antral mucosal interleukin 1alpha (IL-1alpha), IL-1beta, or tumor necrosis factor alpha was detected by reverse transcription-PCR in any cat. The gastric secretory axes, assessed by fasting plasma gastrin, antral mucosal gastrin and somatostatin immunoreactivity, and pentagastrin-stimulated gastric acid secretion, were similar in both infected and uninfected cats. Gradual seroconversion (immunoglobulin G) was observed in four of five infected cats, with enzyme-linked immunosorbent assay values reaching 4x to 12x baseline 12 months postinfection. These findings indicate that H. felis infection in cats induces lymphoid follicular hyperplasia, mild gastritis, and seroconversion, but is associated with normal gastric secretory function
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