The aim of this masters thesis is hydraulic design of inducer for given pump geometry and operating parameters. The first part of this thesis deals with cavitation problematic in hydrodynamic pumps. Next section describes two-dimensional design of the inducer and according to that, the 3D CAD model of inducer is made. The later part deals with thorough CFD analysis and determination of the main hydraulic parameters of inducer itself and also with whole pump completed with this inducer. The last section is devoted to inducer design improvement.

Virginia's Smart Road, to be completed by early 2000, is a test bed for numerous research activities including snow and ice control, remote sensor testing, snow removal management, safety and human factors, and vehicle dynamics. An all-weather testing system will feature 75 automated snowmaking towers. In order to provide timely and repeatable weather scenarios, equipment operators will need to understand fully the limitations and capabilities of the snowmaking system. The research presented herein addresses the hydraulic and hydrologic variables and design methodology to implement efficient snowmaking at a transportation research facility. Design variables include nozzle configuration, water pressure and flowrate, compressed air pressure and flowrate, tower orientation, snow inducer concentration, water and compressed air temperature, and ambient weather conditions. Testing and data collection was performed at the Snow Economics, Inc. research and development site at Seven Springs Mountain Resort in Champion, PA. The results of this work will be used to guide the operators of the Smart Road on the most efficient use of the snowmaking equipment. / Master of Science

<p>Pancreatic ductal adenocarcinoma (PDAC) is a lethal cancer in part due to inherent resistance to chemotherapy, including the first-line drug gemcitabine. Gemcitabine is a nucleoside pyrimidine analog that has long been the backbone of chemotherapy for PDAC, both as a single agent, and more recently, in combination with nab-paclitaxel. Since gemcitabine is hydrophilic, it must be transported through the hydrophobic cell membrane by transmembrane nucleoside transporters. Human equilibrative nucleoside transporter-1 (hENT1) and human concentrative nucleoside transporter-3 (hCNT3) both have important roles in the cellular uptake of the nucleoside analog gemcitabine. While low expression of hENT1 and hCNT3 has been linked to gemcitabine resistance clinically, mechanisms regulating their expression in the PDAC tumor microenvironment are largely unknown. We identified that the matricellular protein Cysteine-Rich Angiogenic Inducer 61 (CYR61) negatively regulates expression of hENT1 and hCNT3. CRISPR/Cas9-mediated knockout of CYR61 significantly increased expression of hENT1 and hCNT3 and cellular uptake of gemcitabine. CRSIPR-mediated knockout of CYR61 sensitized PDAC cells to gemcitabine-induced apoptosis. Conversely, adenovirus-mediated overexpression of CYR61 decreased hENT1 expression and reduced gemcitabine-induced apoptosis. We demonstrate that CYR61 is expressed primarily by stromal pancreatic stellate cells (PSCs) within the PDAC tumor microenvironment, with Transforming Growth Factor- β (TGF-β) inducing the expression of CYR61 in PSCs through canonical TGF-β-ALK5-Smad signaling. Activation of TGF-β signaling or expression of CYR61 in PSCs promotes resistance to gemcitabine in an in vitro co-culture assay with PDAC cells. Our results identify CYR61 as a TGF-β induced stromal-derived factor that regulates gemcitabine sensitivity in PDAC and suggest that targeting CYR61 may improve chemotherapy response in PDAC patients.</p> / Dissertation

The melon crop (Cucumis melo L.) is the most exported fruit of Brazil and consist in an important agribusiness to the producers on Northeastern Region of Brazil, having as the main producers the Rio Grande do Norte and Ceará states. Among the limiting factors of this crop, root-knot nematode (Meloidogyne spp.) stand out a major treat, that causes on severed attacked plants malnourishment, poor development of the above-ground portion and shorter root system due to the galls, which is the most characteristic symptom of this disease. With the lack of management tools to the root-knot nematode, alternative measures are needed to avoid losses. In this context, the main objective of the present work was to evaluate the influence of resistance inducers and biological control agents on the control of M. incognita on melon plants, as the influence of these agents on melon plant development and their effects on different M. incognita stages. For these purposes, greenhouse experiments were performed. The first one aimed to verify the host status of melon hybrids to M. incognita and additional three were carried out to verify the influence of resistance inducers and biological control organisms on melon development and on the control of M. incognita on this crop (trials #1, #2 and #3). Also, an additional greenhouse trials were carried out to verify different doses of P. chlamydosporia (Rizotec&#174; ) on the control of M. incognita in melon plants and to verify the potential of culture filtrates (Cf) obtained from biological control organisms on the control of M. incognita and on the melon plant development. In these greenhouse experiments, the reproductive variables final population (Pf), reproduction factor (R value) and nematodes per gram of root (Nem/g) were obtained at the end of the experiments. Additionally, it was evaluated the fresh and dry weight of the aerial portion, the plant height, root weight, fruit weight, stem diameter (measured on stem basis, middle and apex) and chlorophyll content. Additionally, in vitro assays were performed to verify the effect of Cfs on melon seeds and to verify the effect of the Cfs and the partially purified thaxtomin A (PPT) on M. incognita egg hatching. Moreover, three additional assays were carried out to verify the effect of resistance inducers acibenzolar-S-methyl (ASM) and PPT in the penetration and post-penetration of M. incognita second stages juveniles in melon roots. As results, all tested genotypes were susceptible to M. incognita. The Pf values ranged from 2,381.06 to 7,806 nematodes, the R value ranged from 5.95 to 19.5. Also, nem/g values ranged from 271 to 1,791. In trial #1, melon plants treated with resistance inducers presented lower height; despite no statistically differences were found for fresh and dry weight. Also, plants treated with ASM (inoculated and non-inoculated), Paecilomyces lilacinus, (non-inoculated) and Pochonia chlamydosporia (inoculated) produced heavy fruits. On trial #2, all inoculated plants differed statistically on root weight and presented heavier roots than non-inoculated plants, which was due the large amount of galls caused by M. incognita. In addition, treated plants with the biological control agents presented fewer symptoms than control plants. Treated melon plants exhibited higher chlorophyll content on young leaves, when compared with both controls. Moreover, on both treatments the M. incognita population was reduced, except by P. chlamydosporia on the experiment 1. When tested separately, all P. chlamydosporia doses reduced the Pf, however the most efficient were the dose 4 (1g/plant) and dose 5 (2g/plant). Regarding Cf, promising results were obtained. Both Cf from P. lilacinus and Bacillus amyloliquefaciens reduced the M. incognita population, in greenhouse experiment. Additionally, P. lilacinus Cf increased the fruit weight, and B. amyloliquefaciens Cf increased the root weight, despite being inoculated or not. Furthermore, the tested Cfs presented suppressive effect on M. incognita egg hatching, but further evidence is necessary due to lack of statistical differences with the potato-dextrose broth medium (PD). Additionally, the filtrates improved the germination of melon seeds, despite the suppressed effect of PD broth medium on them. Also,i> P. chlamydosporia treatment induced hairy roots, which were not observed on the other treatments. Regarding the penetration assays, juveniles were not observed at 3 days after inoculation (DAI). No effect of ASM in penetration and post-penetration of M. incognita J2 was 13 observed on both experiments. Concerning PPT, penetration was not observed at 3 DAI, but it was observed on the other assessed periods. Furthermore, our data points out that the TPP may speed the nematode cycle on melon roots. In conclusion, the obtained data point out the potential of the resistance inducers, biological control organisms and their culture filtrates on the control of M. incognita on melon plants. / Atualmente, o melão (Cucumis melo L.) consiste na fruta mais exportada do Brasil, consistindo em importante agronegócio para os produtores da região Nordeste do país, tendo como maiores produtores os estados do Ceará e Rio Grande do Norte. Dentre os fatores limitantes para essa cultura, o nematoide das galhas (Meloidogyne spp.) se destaca entre as principais doenças do meloeiro. Plantas sob alta infestação apresentam deficiência nutricional, baixo desenvolvimento da porção aérea e deformação do sistema radicular devido as galhas, que consiste no sintoma mais característico dessa doença. Com a falta de ferramentas de manejo, medidas alternativas são necessárias para evitar maiores perdas. Nesse contexto, o presente trabalho teve por objetivo avaliar a influência de agentes de controle biológico e indutores de resistência no controle de M. incognita em plantas de melão, bem como a influência desses agentes no desenvolvimento do meloeiro em casa de vegetação, além de seus efeitos em diferentes estádios de M. incognita. Dessa forma, experimentos de casa-de-vegetação foram conduzidos, sendo um para verificar a reação de hospedeiro de híbridos de melão à M. incognita, três para verificar a influência de indutores de resistência e agentes de controle biológico no desenvolvimento do meloeiro e no controle de M. incognita (Experimento 1, 2 e 3). Adicionalmente, um experimento foi conduzido para verificar a dose-resposta de Pochonia chlamydosporia (Rizotec&#174;) para controle de M. incognita e dois para verificar o uso potencial de filtrados obtidos a partir de organismos de controle biológico no desenvolvimento do meloeiro e no controle de M. incognita. Nesses experimentos, o fator de reprodução (valor R), população final (Pf) e nematoides por grama de raiz (Nem/g) foram obtidos ao final dos ensaios. Adicionalmente, foram avaliados a massa fresca e seca da parte aérea, altura das plantas, massa das raízes, massa dos frutos por planta, diâmetro do caule (base, meio e ápice) e conteúdo de clorofila. Ademais, realizou-se um experimento para se verificar o efeito de filtrados nas sementes de melão e três para verificar o efeito dos filtrados e da taxtomina parcialmente purificada (TPP) na eclosão dos ovos de M. incognita. Adicionalmente, três experimentos foram realizados para verificar o efeito de indutores de resistência na penetração e desenvolvimento de juvenis J2 de M. incognita nas raízes de meloeiro. Como resultados, todos os genótipos testados foram suscetíveis a M. incognita. A Pf variou de 2.381 à 7.806 nematoides, o valor R variou de 5,7 à 19,5 e o Nem/g foi de 271 à 1.791. No experimento 1, meloeiros tratados com indutores de resistência apresentaram menor altura, embora, nenhuma diferença estatística foi encontrada nas massas frescas e secas das plantas. Adicionalmente, plantas tratadas com acibenzolar-S-metil (ASM) (inoculadas e não inoculadas), P. lilacinus (-N) e P. chlamydosporia (+N) apresentaram frutos mais pesados. Com relação ao experimento 2, todos os tratamentos inoculados apresentaram maior peso das raízes, quando comparada aos tratamentos não inoculados, causado pela deformação da porção radicular. Adicionalmente, plantas tratadas com agentes de controle biológico apresentaram raízes com menos sintomas, quando comparados ao controle. Ademais, plantas tratadas apresentaram maior quantidade de clorofila em folhas jovens, quando comparadas aos controles. Todos os tratamentos, com exceção a P. chlamydosporia no experimento 1, reduziram a população final de M. incognita. Quando testado separadamente, todas as doses de P. chlamydosporia reduziram a Pf de M. incognita, embora as mais eficientes tenham sido a dose 4 (1g/planta) e dose 5 (2g/planta). Com relação aos filtrados, resultados promissores foram obtidos. Os filtrados obtidos a partir de B. amyloliquefaciens e P. lilacinus reduziram as populações finais de M. incognita, embora apenas B. amyloliquefaciens tenha diferido estatisticamente. Adicionalmente, aumento na massa das raízes e na massa dos frutos foram observados para plantas tratadas com filtrados de B. amyloliquefaciens e P. lilacinus, respectivamente. Ademais, todos os filtrados aceleraram a germinação das sementes quando comparado ao meio batata- dextrose, que suprimiu a germinação. Sementes tratadas com o filtrado obtido a partir de P. chlamydosporia apresentaram radículas pilosas, o que não foi observado nos outros tratamentos. Com relação aos experimentos de penetração, juvenis J2 de M. incognita foram observados no interior das raízes em todos os ensaios. Nenhum efeito do ASM foi observado em ambos os experimentos. Com relação a TPP, os dados apontam que o tratamento acelerou o ciclo do nematoide no interior das raízes. Conclui-se, que os dados obtidos apontam para o potencial dos indutores de resistência e agentes de controle biológico e seus filtrados no controle de M. incognita em meloeiro.

In den Firmicutes wird der Induktorausschluss (Katabolitrepression) durch das am Serin46 phosphorylierte HPr (PTS) vermittelt. Der genaue Mechanismus war jedoch unklar. Um diese Frage auf der Grundlage von isolierten Proteinen zu klären, wurde ein zum Escherichia coli Maltose-/Maltodextrin-ABC-Transporter homologes System aus Lactobacillus casei BL23 (MalE1-MalF1G1K12) als Modellsystem genutzt. Im Rahmen der Promotion wurde über isothermale Titrationskalorimetrie und Fluoreszenzspektroskopie gezeigt, dass das Bindeprotein MalE1 lineare und zyklische Maltodextrine, aber keine Maltose bindet. Experimentell ermittelte dreidimensionale Strukturen von MalE1 im Komplex mit diesen Zuckern belegten eine vergleichbar geschlossene Konformation und dienten zusätzlich als Grundlage, um die fehlende Maltosebindung zu erklären. Die Stimulierung der ATPaseaktivität des in Liposomen und Nanodiscs eingebauten Komplexes wurde jedoch hauptsächlich durch eine MalE1-Beladung mit linearen Maltodextrinen bewirkt. Eine bis zu 85 %ige Inhibierung der ATPaseaktivität durch P-Ser46-HPr belegte erstmals in vitro eine Interaktion von mehr als einem phosphorylierten Protein mit dem Transporter. Analog zum EIIAGlc-Inhibitor des homologen Systems aus E. coli wurden über Quervernetzungsexperimente und massenspektrometrische Analysen Interaktionen mit dem MalK1-Dimer als interagierende Komplexeinheit in der Nähe des Walker A-Motivs nachgewiesen. Über Fluoreszenzmessungen in Anwesenheit des ATP-Analogons TNP-ATP wurde eine unbeeinflusste ATP-Bindung und damit eine fehlende Blockade der γ-Phosphatbindestelle des Walker-A Motivs durch die Phosphorylgruppe von P-Ser46-HPr bestimmt. Die folgende Substitution verschiedener positiv geladener MalK1-Reste, die als potenzielle Interaktionsstellen für die Phosphorylgruppe fungieren könnten, identifizierte K63 in der Nähe des Walker A-Motivs als ersten möglichen Partner. Der genaue Mechanismus der Inhibierung bleibt jedoch unklar. / Catabolite repression is a global mechanism which controls the utilization of carbohydrates in bacteria. In Firmicutes HPr, a component of the phosphoenolpyruvate carbohydrate phosphotransferase system, prevents the uptake of less preferred sugars but only when it is phosphorylated at serine46. However the exact mechanism was unclear. To address this question the purified ATP-binding cassette transporter from Lactobacillus casei BL23 (MalE1-MalF1G1K12) was used as a model system, which is homologous to the Escherichia coli maltose/maltodextrin ABC importer. Isothermal titration calorimetry and fluorescence spectroscopy revealed that the binding protein MalE1 binds linear and cyclic maltodextrins but not maltose. Experimentally determined three-dimensional structures from MalE1 in complex with these sugars show a comparably closed conformation and served as a basis to explain the lack of maltose binding. The stimulation of the ATPase activity of the transporter incorporated in liposomes and nanodiscs however, was mainly caused by MalE1 loaded with linear maltodextrins. For the first time an inhibition of ATPase activity by P-Ser46-HPr up to 85 % and an interaction of more than one phosphorylated protein with the transporter was demonstrated. Analogous to the EIIAGlc inhibitor of the homologous system from E. coli, cross-linking experiments and mass spectrometric analyzes revealed interactions with the MalK1 dimer near the Walker A motif. Fluorescence measurements in the presence of the ATP analogue TNP-ATP, however, revealed an unaffected ATP binding and thus a lack of blockade of the γ-phosphate binding site (Walker A motif) by the phosphoryl group from P-Ser46-HPr. The following substitution of several positively charged MalK1 residues that could act as potential sites of interaction for the phosphoryl group, identified K63 near the Walker A motif as the first potential partner. The exact mechanism of inhibition, however, remains unclear.

<p>In sera remitted for anti-nuclear antibody (ANA) analysis, the supplement of a sensitive anti-SSA/Ro ELISA to the conventional ANA screening by immunofluorescence (IF) revealed that one fourth of the individuals with IF-ANA negative, but SSA/Ro ELISA positive sera, had systemic lupus erythematosus (SLE) or cutaneous LE. Consequently, adding a sensitive anti-SSA/Ro ELISA to the ANA screening is valuable for the serological detection of ANA negative SLE/LE patients.</p><p>SLE patients often have measurable interferon-alpha (IFN-α) levels in serum, and IFN-α treatment of patients with non-autoimmune diseases can induce SLE. Thus, the type I IFN system seems to be important in SLE and was therefore investigated. Initially, a decreased IFN-α producing capacity, due to a 70-fold reduction in the number of circulating natural IFN-α producing cells (NIPC), was noted in peripheral blood mononuclear cells (PBMC) from SLE patients. SLE-sera contained an endogenous IFN-α inducing factor (SLE-IIF), consisting of IgG and DNA in the form of small immune complexes (300-1000 kD). The SLE-IIF selectively activated NIPC and was more common in sera from patients with active disease compared to individuals with inactive disease. IFN-α producing cells could be detected by immunohistochemistry in both lesional and unaffected skin from SLE patients, and IFN-α gene transcription could be verified by in situ hybridisation in some of the skin biopsies. A reduced number of NIPC, detected by expression of the blood dendritic cell antigen (BDCA)-2, was noted among SLE-PBMC. The IFN-α production triggered by SLE-IIF in SLE-PBMC was inhibited by monoclonal antibodies (mAbs) to BDCA-2 and markedly decreased by anti-BDCA-4 mAbs. </p><p>The observations in the present thesis may explain the ongoing IFN-α production in SLE patients, indicate an important role for the activated type I IFN system in the pathogenesis, and suggest that direct targeting of SLE-NIPC may constitute a new therapeutic principle in SLE.</p>

<p>Patients with systemic lupus erythematosus (SLE) have an activated type I interferon (IFN) system with an ongoing IFN-α synthesis. This may be caused by circulating immune complexes, consisting of anti-DNA antibodies (Abs) and DNA, with IFN-α inducing capacity. Produced IFN-α may be crucial in the pathogenesis, because this cytokine can break tolerance and promote autoimmunity.</p><p>In the present thesis, possible mechanisms of the IFN-α production in SLE were studied. To investigate whether IFN-α inducing material could be derived from apoptotic cells, IgG from SLE patients (SLE-IgG) were combined with apoptotic cells. This combination induced high IFN-α production in normal peripheral blood mononuclear cells (PBMC). The IFN-α induction was associated to presence of anti-RNP Abs, but not to anti-dsDNA Abs, indicating that two inducers could be active in SLE, one containing DNA and the other RNA.</p><p>Apoptotic cells and SLE-IgG exclusively activated the natural interferon producing cells (NIPC) and the IFN-α response was enhanced by type I IFN and inhibited by IL-10 and TNF-α. The IFN-α induction was dependent on FcγRII, because blocking this receptor reduced IFN-α production and NIPC were found to express FcγRIIa.</p><p>To further elucidate the role of different autoantibodies in the IFN-α induction, sera from patients with Sjögren´s syndrome (SS), containing autoantibodies to RNA binding proteins (SSA, SSB, RNP and/or Sm) were investigated. The combination of SS or SLE sera and apoptotic or necrotic cell material induced high IFN-α production in PBMC. RNA, but not DNA, was required for IFN-α induction, indicating that RNA and Abs to RNA-binding proteins form potent IFN-α inducing complexes.</p><p>The findings in this thesis can explain central mechanisms for the activation of NIPC in SLE, and perhaps also other autoimmune diseases. This activation is mediated by interferogenic immune complexes, and modulating the NIPC activation may be a novel therapeutic approach in SLE.</p>

In sera remitted for anti-nuclear antibody (ANA) analysis, the supplement of a sensitive anti-SSA/Ro ELISA to the conventional ANA screening by immunofluorescence (IF) revealed that one fourth of the individuals with IF-ANA negative, but SSA/Ro ELISA positive sera, had systemic lupus erythematosus (SLE) or cutaneous LE. Consequently, adding a sensitive anti-SSA/Ro ELISA to the ANA screening is valuable for the serological detection of ANA negative SLE/LE patients. SLE patients often have measurable interferon-alpha (IFN-α) levels in serum, and IFN-α treatment of patients with non-autoimmune diseases can induce SLE. Thus, the type I IFN system seems to be important in SLE and was therefore investigated. Initially, a decreased IFN-α producing capacity, due to a 70-fold reduction in the number of circulating natural IFN-α producing cells (NIPC), was noted in peripheral blood mononuclear cells (PBMC) from SLE patients. SLE-sera contained an endogenous IFN-α inducing factor (SLE-IIF), consisting of IgG and DNA in the form of small immune complexes (300-1000 kD). The SLE-IIF selectively activated NIPC and was more common in sera from patients with active disease compared to individuals with inactive disease. IFN-α producing cells could be detected by immunohistochemistry in both lesional and unaffected skin from SLE patients, and IFN-α gene transcription could be verified by in situ hybridisation in some of the skin biopsies. A reduced number of NIPC, detected by expression of the blood dendritic cell antigen (BDCA)-2, was noted among SLE-PBMC. The IFN-α production triggered by SLE-IIF in SLE-PBMC was inhibited by monoclonal antibodies (mAbs) to BDCA-2 and markedly decreased by anti-BDCA-4 mAbs. The observations in the present thesis may explain the ongoing IFN-α production in SLE patients, indicate an important role for the activated type I IFN system in the pathogenesis, and suggest that direct targeting of SLE-NIPC may constitute a new therapeutic principle in SLE.

Patients with systemic lupus erythematosus (SLE) have an activated type I interferon (IFN) system with an ongoing IFN-α synthesis. This may be caused by circulating immune complexes, consisting of anti-DNA antibodies (Abs) and DNA, with IFN-α inducing capacity. Produced IFN-α may be crucial in the pathogenesis, because this cytokine can break tolerance and promote autoimmunity. In the present thesis, possible mechanisms of the IFN-α production in SLE were studied. To investigate whether IFN-α inducing material could be derived from apoptotic cells, IgG from SLE patients (SLE-IgG) were combined with apoptotic cells. This combination induced high IFN-α production in normal peripheral blood mononuclear cells (PBMC). The IFN-α induction was associated to presence of anti-RNP Abs, but not to anti-dsDNA Abs, indicating that two inducers could be active in SLE, one containing DNA and the other RNA. Apoptotic cells and SLE-IgG exclusively activated the natural interferon producing cells (NIPC) and the IFN-α response was enhanced by type I IFN and inhibited by IL-10 and TNF-α. The IFN-α induction was dependent on FcγRII, because blocking this receptor reduced IFN-α production and NIPC were found to express FcγRIIa. To further elucidate the role of different autoantibodies in the IFN-α induction, sera from patients with Sjögren´s syndrome (SS), containing autoantibodies to RNA binding proteins (SSA, SSB, RNP and/or Sm) were investigated. The combination of SS or SLE sera and apoptotic or necrotic cell material induced high IFN-α production in PBMC. RNA, but not DNA, was required for IFN-α induction, indicating that RNA and Abs to RNA-binding proteins form potent IFN-α inducing complexes. The findings in this thesis can explain central mechanisms for the activation of NIPC in SLE, and perhaps also other autoimmune diseases. This activation is mediated by interferogenic immune complexes, and modulating the NIPC activation may be a novel therapeutic approach in SLE.

Made available in DSpace on 2014-07-29T14:52:10Z (GMT). No. of bitstreams: 1 abadia tese.pdf: 6055071 bytes, checksum: 41810223bb4492258f77c027a3385652 (MD5) Previous issue date: 2009-02-17 / The search of alternative products for tomato bacterial spot has been promoting by the lack of effectiveness registered by the traditional products available. The objective of this work was to evaluate a range of chemical products by in vitro tests, in experiments seedlings and field experiments. The products studied were: acibenzolar-S-methyl; benzalkonium chloride; phosphite; copper hydroxide, copper oxicloreto; metiram + pyraclostrobin and famoxadone + mancozebe. The in vitro tests were carried out at Embrapa Hortaliça, Brasília-DF, in July of 2007. The bactericide action was evaluated on Xanthomonas perforans and X. gardneri. The trial was in a complete randomized block design with four replications and plot was constituted by a Petri plate impregnated with solidified bacterial suspension. The halo of inhibition formed was evaluated. The experiments with seedlings were carried out with the hybrid Heinz 9553 at the commercial nursery VIVATI in Rio Verde, Goiás, in August to September and November to December of 2008. There were three trials in a complete randomized block design with three replications. The products were sprayed by using CO2 portable sprayer. The inoculation occurred 29 days after sowing, with an isolated of X. gardneri. Disease severity was evaluated on 15 leaflets per plot at 14 and 16 days after inoculation of the first and second experiment, respectively. Data was expressed as percentage of leaf affected by program Quant. It was also suggested a possible interaction between the regulator of growth paclobutrazol and the behavior of certain products in the reduction of the severity of the disease. Two field trials were carried out at the experimental farm of Unilever Bestfoods, in Goiânia-GO, from February to June of 2007 and April to August of 2008. The first was with the hybrid Heinz 9992 in a complete randomized block design, with 15 treatments and three replications, and inoculated with X. perforans. The second was in a split plot completely randobized block design with three replications. Variety (Hypeel 108 and U2006) was ascertained for factor A and the 10 treatments for factor B. Xanthomonas perforans and X. gardneri were inoculated in different moments. In both trials foliage severity, number of fruits with symptoms and yield were evaluated. In the second trial fruits with sun scald was also taken. In the in vitro test, the products to which X. perforans and X. gardneri were sensitive in the recommended dose were the benzalkonium chloride and famoxadone + mancozeb. Methiram + pyraclostrobin had action in the dosage recommended only for X. gardneri. Xanthomonas perforans was sensitive to this product only starting from ten times more. The products of copper base did not have action in the bacteria at the recommended dose, being sensitive only at a hundred time more. For the trials of seedlings it was noticed that metiram + pyraclostrobin, copper oxicloreto, famoxadone + mancozebe, phosphite and copper hydroxide reduced the severity under certain conditions. In the field trials, in generally, acibenzolar-S-methyl and famoxadone + mancozeb lead to the better results. / A pouca disponibilidade de produtos eficazes tem propiciado a busca por alternativas de controle da mancha bacteriana do tomateiro. Sendo assim, este trabalho teve como objetivo avaliar uma gama de produtos químicos em testes in vitro, experimentos com mudas e em experimentos de campo. Foram estudados: acibenzolar-S-metil; cloretos de benzalcônio; fosfitos; hidróxido de cobre, oxicloreto de cobre; metiram + piraclostrobina e famoxadona + mancozebe. Os testes in vitro foram conduzidos na Embrapa Hortaliças, Brasília-DF, em julho de 2007. A ação bactericida dos produtos foi avaliada sobre Xanthomonas perforans e X. gardneri. O ensaio foi em blocos casualizados com quatro repetições e a parcela foi constituída por uma placa de Petri impregnada com suspensão bacteriana solidificada. Avaliou-se o halo de inibição formado. Os experimentos de mudas foram conduzidos com o híbrido Heinz 9553 no viveiro comercial VIVATI em Rio Verde GO, de agosto a setembro e de novembro a dezembro de 2008. Foram três ensaios inteiramente casualizados com três repetições. Os tratamentos (produtos) foram pulverizados na parte aérea utilizando pulverizador costal de barra. A inoculação foi aos 29 dias após a semeadura, com um isolado de X. gardneri. Avaliou-se a severidade da doença em 15 folíolos por parcela aos 14 e 16 dias após a inoculação do primeiro e segundo experimento, respectivamente. Esta foi expressa em porcentagem de área foliar atacada processada pelo programa Quant. É sugerido uma possível interação entre o regulador de crescimento paclobutrazol e o comportamento de certos produtos na redução da severidade da doença. Dois ensaios de campo foram conduzidos na área experimental da Unilever Bestfoods, em Goiânia-GO, de fevereiro a junho de 2007 e de abril a agosto de 2008. O primeiro foi com o híbrido Heinz 9992 em delineamento experimental blocos casualizados, com 15 tratamentos e três repetições. Inoculou-se X. perforans. Já o segundo ensaio foi fatorial em parcelas subdivididas em blocos ao acaso e três repetições. O fator A foi hídrido (Hypeel 108 e U2006) e o fator B (tratamentos). Inoculou-se X. perforans e X. gardneri em momentos distintos. Em ambos ensaios foram avaliados severidade foliar, número de frutos com sintomas e produtividade. No segundo ensaio tomou-se também número de frutos com escaldadura. No teste in vitro os produtos aos quais X. perforans e X. gardneri foram sensíveis na dose recomendada foram os cloretos de benzalcônio e a famoxadona + mancozebe. Metiram + piraclostrobina tiveram ação na dosagem recomendada somente para X. gardneri. Xanthomonas perforans foi sensível ao produto somente a partir de dez vezes maior a dosagem recomendada. Os produtos à base de cobre não tiveram ação nas bactérias na dosagem recomendada, sendo sensíveis apenas na dose cem vezes maior a dosagem recomendada. Em mudas metiram + piraclostrobina, oxicloreto de cobre, famoxadona + mancozebe, fosfito e hidróxido de cobre reduziram a severidade em mudas no ensaio realizado em agosto. Em campo, notou-se que, de maneira geral acibenzolar-S-metil e famozadona + mancozebe estão entre os melhores resultados.