Academic literature on the topic 'Fumigatus'

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Journal articles on the topic "Fumigatus"

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Wang, Li, Koji Yokoyama, Makoto Miyaji, and Kazuko Nishimura. "Mitochondrial Cytochrome b Gene Analysis of Aspergillus fumigatus and Related Species." Journal of Clinical Microbiology 38, no. 4 (2000): 1352–58. http://dx.doi.org/10.1128/jcm.38.4.1352-1358.2000.

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Nucleotide sequences of 426 bp from the mitochondrial (mt) cytochrome b genes of six anamorph species and two species of Neosartorya teleomophs of Aspergillussection Fumigati were determined. These sequences were used to build nucleotide- and amino acid-based trees for phylogenetic analysis. Thirteen strains of A. fumigatus including 10 clinical isolates of A. fumigatus, 1 type culture ofA. fumigatus var. fumigatus, 1 type culture ofA. fumigatus var. ellipticus, and 1 strain ofA. fumigatus var. albus, had the same nucleotide sequences. One strain of A. fumisynnematus, two strains labeled A. neoellipticus, two strains of A. viridinutans, and one strain of A. duricaulis had distinct nucleotide and amino acid sequences. Two strains of A. brevipes were divided into two types. One produced a 1,500-bp fragment that included an intron. The nucleotide sequences of its two exons were similar to those of the A. fumigatus, and the derived amino acid sequence was the same as that for A. fumigatus. The other produced a 426-bp fragment and had the same nucleotide and amino acid sequences as A. unilateralis. Neosartorya fischeri var. fischeri and N. stramenia had nucleotide sequences that differed from that ofA. fumigatus. These species possessed their own characteristic nucleotide sequences that differed from each other. In comparisons of homologous sequences from four other pathogenic species of Aspergillus, regions specific to sectionFumigati were found. The mt cytochrome b gene analysis was valuable for the identification, classification, and phylogenetic analysis of isolates of section Fumigati.
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Knox, Benjamin P., Qing Deng, Mary Rood, Jens C. Eickhoff, Nancy P. Keller, and Anna Huttenlocher. "Distinct Innate Immune Phagocyte Responses to Aspergillus fumigatus Conidia and Hyphae in Zebrafish Larvae." Eukaryotic Cell 13, no. 10 (2014): 1266–77. http://dx.doi.org/10.1128/ec.00080-14.

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ABSTRACTAspergillus fumigatusis the most common filamentous fungal pathogen of immunocompromised hosts, resulting in invasive aspergillosis (IA) and high mortality rates. Innate immunity is known to be the predominant host defense againstA. fumigatus; however, innate phagocyte responses toA. fumigatusin an intact host and their contributions to host survival remain unclear. Here, we describe a larval zebrafishA. fumigatusinfection model amenable to real-time imaging of host-fungal interactions in live animals. Following infection withA. fumigatus, innate phagocyte populations exhibit clear preferences for different fungal morphologies: macrophages rapidly phagocytose conidia and form aggregates around hyphae, while the neutrophil response is dependent upon the presence of hyphae. Depletion of macrophages rendered host larvae susceptible to invasive disease. Moreover, a zebrafish model of human leukocyte adhesion deficiency with impaired neutrophil function also resulted in invasive disease and impaired host survival. In contrast, macrophage-deficient but not neutrophil-deficient larvae exhibited attenuated disease following challenge with a less virulent (ΔlaeA) strain ofA. fumigatus, which has defects in secondary metabolite production. Taking these results together, we have established a new vertebrate model for studying innate immune responses toA. fumigatusthat reveals distinct roles for neutrophils and macrophages in mediating host defense against IA.
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Hissen, Anna H. T., Adrian N. C. Wan, Mark L. Warwas, Linda J. Pinto, and Margo M. Moore. "The Aspergillus fumigatus Siderophore Biosynthetic Gene sidA, Encoding l-Ornithine N5-Oxygenase, Is Required for Virulence." Infection and Immunity 73, no. 9 (2005): 5493–503. http://dx.doi.org/10.1128/iai.73.9.5493-5503.2005.

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ABSTRACTAspergillus fumigatusis the leading cause of invasive mold infection and is a serious problem in immunocompromised populations worldwide. We have previously shown that survival ofA. fumigatusin serum may be related to secretion of siderophores. In this study, we identified and characterized thesidAgene ofA. fumigatus, which encodesl-ornithineN5-oxygenase, the first committed step in hydroxamate siderophore biosynthesis.A. fumigatus sidAcodes for a protein of 501 amino acids with significant homology to other fungall-ornithineN5-oxygenases. A stable ΔsidAstrain was created by deletion ofA. fumigatus sidA. This strain was unable to synthesize the siderophoresN′,N",N‴-triacetylfusarinine C (TAF) and ferricrocin. Growth of the ΔsidAstrain was the same as that of the wild type in rich media; however, the ΔsidAstrain was unable to grow in low-iron defined media or media containing 10% human serum unless supplemented with TAF or ferricrocin. No significant differences in ferric reduction activities were observed between the parental strain and the ΔsidAstrain, indicating that blocking siderophore secretion did not result in upregulation of this pathway. Unlike the parental strain, the ΔsidAstrain was unable to remove iron from human transferrin. A rescued strain (ΔsidA + sidA) was constructed; it produced siderophores and had the same growth as the wild type on iron-limited media. Unlike the wild-type and rescued strains, the ΔsidAstrain was avirulent in a mouse model of invasive aspergillosis, indicating thatsidAis necessary forA. fumigatusvirulence.
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Li, Xianping, Meihua Gao, Xuelin Han, et al. "Disruption of the Phospholipase D Gene Attenuates the Virulence of Aspergillus fumigatus." Infection and Immunity 80, no. 1 (2011): 429–40. http://dx.doi.org/10.1128/iai.05830-11.

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ABSTRACTAspergillus fumigatusis the most prevalent airborne fungal pathogen that induces serious infections in immunocompromised patients. Phospholipases are key enzymes in pathogenic fungi that cleave host phospholipids, resulting in membrane destabilization and host cell penetration. However, knowledge of the impact of phospholipases onA. fumigatusvirulence is rather limited. In this study, disruption of thepldgene encoding phospholipase D (PLD), an important member of the phospholipase protein family inA. fumigatus, was confirmed to significantly decrease both intracellular and extracellular PLD activity ofA. fumigatus. Thepldgene disruption did not alter conidial morphological characteristics, germination, growth, and biofilm formation but significantly suppressed the internalization ofA. fumigatusinto A549 epithelial cells without affecting conidial adhesion to epithelial cells. Importantly, the suppressed internalization was fully rescued in the presence of 100 μM phosphatidic acid, the PLD product. Indeed, complementation ofpldrestored the PLD activity and internalization capacity ofA. fumigatus. Phagocytosis ofA. fumigatusconidia by J774 macrophages was not affected by the absence of thepldgene. Pretreatment of conidia with 1-butanol and a specific PLD inhibitor decreased the internalization ofA. fumigatusinto A549 epithelial cells but had no effect on phagocytosis by J774 macrophages. Finally, loss of thepldgene attenuated the virulence ofA. fumigatusin mice immunosuppressed with hydrocortisone acetate but not with cyclophosphamide. These data suggest that PLD ofA. fumigatusregulates its internalization into lung epithelial cells and may represent an important virulence factor forA. fumigatusinfection.
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Dhabaan, Ghulam, Julianne Kus, Deepali Kumar, Atul Humar, Shahid Husain, and Tony Mazzulli. "Molecular identification of Aspergillus fumigatus complex from lung transplant recipients using multilocus sequencing analysis (MLSA)." Official Journal of the Association of Medical Microbiology and Infectious Disease Canada 7, no. 1 (2022): 54–63. http://dx.doi.org/10.3138/jammi-2021-0004.

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BACKGROUND: Aspergillus infection causes significant morbidity and mortality among lung transplant recipients (LTRs). It is primarily caused by Aspergillus fumigatus. Other closely related species belonging to the section Fumigati have also been found. These cryptic species are often misidentified as A. fumigatus. Thus, we used multilocus sequencing analysis (MLSA) of the calmodulin, β-tubulin, and hydrophobin gene sequences to identify these species and to determine the frequency with which they occur among LTRs. METHODS: A total of 81 A. fumigatus isolates were initially isolated from bronchoalveolar lavage fluid or sputum specimens collected from lung transplant patients. These isolates were then sub-cultured and genotyped using MLSA. Of these isolates, 53, 17, and 11 were isolated from double LTRs, single LTRs, and pre-LTRs, respectively. RESULTS: All isolates (100%) carried DNA sequences identical to those of A. fumigatus reference strains and thus clustered in the same clade with A. fumigatus. Analysis of the MLSA data revealed that A. fumigatus species were the only species recovered in this population of LTRs. The MLSA results were consistent with those routinely obtained by conventional mycological procedures in the microbiology laboratory. CONCLUSIONS: A. fumigatus appears to be the primary causative agent of colonization or invasive aspergillosis among LTRs. No cryptic species were identified.
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Sabino, Raquel, Paulo Gonçalves, Aryse Martins Melo, et al. "Trends on Aspergillus Epidemiology—Perspectives from a National Reference Laboratory Surveillance Program." Journal of Fungi 7, no. 1 (2021): 28. http://dx.doi.org/10.3390/jof7010028.

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Identification of Aspergillus to species level is important since sibling species may display variable susceptibilities to multiple antifungal drugs and also because correct identification contributes to improve the knowledge of epidemiological studies. Two retrospective laboratory studies were conducted on Aspergillus surveillance at the Portuguese National Mycology Reference Laboratory. The first, covering the period 2017–2018, aimed to study the molecular epidemiology of 256 Aspergillus isolates obtained from patients with respiratory, subcutaneous, or systemic infections and from environmental samples. The second, using our entire collection of clinical and environmental A. fumigatus isolates (N = 337), collected between 2012 and 2019, aimed to determine the frequency of azole-resistant A. fumigatus isolates. Aspergillus fumigatus sensu stricto was the most frequent species in both clinical and environmental samples. Overall, and considering all Aspergillus sections identified, a high frequency of cryptic species was detected, based on beta-tubulin or calmodulin sequencing (37% in clinical and 51% in environmental isolates). Regarding all Fumigati isolates recovered from 2012–2019, the frequency of cryptic species was 5.3% (18/337), with the identification of A. felis (complex), A. lentulus, A. udagawae, A. hiratsukae, and A. oerlinghauensis. To determine the frequency of azole resistance of A. fumigatus, isolates were screened for azole resistance using azole-agars, and 53 possible resistant isolates were tested by the CLSI microdilution reference method. Nine A. fumigatus sensu stricto and six Fumigati cryptic isolates showed high minimal inhibitory concentrations to itraconazole, voriconazole, and/or posaconazole. Real-time PCR to detect cyp51A mutations and sequencing of cyp51A gene and its promoter were performed. The overall frequency of resistance to azoles in A. fumigatus sensu stricto was 3.0%. With this retrospective analysis, we were able to detect one azole-resistant G54R mutant A. fumigatus environmental isolate, collected in 2015. The TR34/L98H mutation, linked to environmental transmission route of azole resistance, was the most frequently detected mutation (N = 4; 1.4%). Our findings underline the demand for correct identification and susceptibility testing of Aspergillus isolates.
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WONGSUK, Thanwa, and Passanesh SUKPHOPETCH. "Effect of Quarum Sensing Molecules on Aspergillus fumigatus." Walailak Journal of Science and Technology (WJST) 17, no. 4 (2019): 348–58. http://dx.doi.org/10.48048/wjst.2020.6172.

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Aspergillus fumigatus is an opportunistic fungal pathogen to which immunocompromised patients are especially susceptible. A. fumigatus can form biofilms both in vitro and in vivo. Quorum sensing molecules (QSMs) have activity against some fungi. This study aimed to determine the activity of the QSMs farnesol, tyrosol, phenylethanol and tryptophol against the growth A. fumigatus on solid media, and against its ability to form biofilms. The activity of each QSM against planktonic A. fumigatus growth was assessed using the CLSI M38-A2 broth microdilution assay, while QSM inhibition of A. fumigatus’s biofilm formation was measured in crystal violet, and 2, 3-bis (2-methoxy-4-nitro-5-sulfo-phenyl)-2H-tetrazolium-5-caboxanilide (XTT) assays. The QSMs reduced the colony diameter of the studied strains in a QSM-dependent pattern. Tryptophol showed the best effect and tyrosol showed the poorest effect. The minimum inhibitory concentrations (MICs) for farnesol, tyrosol, phenylethanol and tryptophol tested against A. fumigatus were > 32, > 32, 16 and 8 mM, respectively. The effective concentration each QSM required to inhibit A. fumigatus biofilm formation were higher than the planktonic MICs. In this study, the performance of QSMs against A. fumigatus ranked from best to worst as follows: tryptophol, phenylethanol, farnesol and tyrosol. Because of phenylethanol and tryptophol showed the strongest effect to the growth and biofilm formation of A. fumigatus. Therefore, the cytotoxic activities of phenylethanol and tryptophol in A549 cells (lung alveolar epithelial cells) were determined. However, phenylethanol and tryptophol induced A549 cell damage (at MIC level), as demonstrated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) and lactate dehydrogenase (LDH) assays.
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Szewczyk, Edyta, and Sven Krappmann. "Conserved Regulators of Mating Are Essential for Aspergillus fumigatus Cleistothecium Formation." Eukaryotic Cell 9, no. 5 (2010): 774–83. http://dx.doi.org/10.1128/ec.00375-09.

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ABSTRACT Sexual reproduction of the human pathogen Aspergillus fumigatus (teleomorph: Neosartorya fumigata) was assumed to be absent or cryptic until recently, when fertile crosses among geographically restricted environmental isolates were described. Here, we provide evidence for mating, fruiting body development, and ascosporogenesis accompanied by genetic recombination between unrelated, clinical isolates of A. fumigatus, and this evidence demonstrates the generality and reproducibility of this long-time-undisclosed phase in the life cycle of this heterothallic fungus. Successful mating requires the presence of both mating-type idiomorphs MAT1-1 and MAT1-2, as does expression of genes encoding factors presumably involved in this process. Moreover, analysis of an A. fumigatus mutant deleted for the nsdD gene suggests a role of this conserved regulator of cleistothecium development in hyphal fusion and hence heterokaryon formation.
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Werner, Jessica L., Melissa A. Gessner, Lauren M. Lilly, et al. "Neutrophils Produce Interleukin 17A (IL-17A) in a Dectin-1- and IL-23-Dependent Manner during Invasive Fungal Infection." Infection and Immunity 79, no. 10 (2011): 3966–77. http://dx.doi.org/10.1128/iai.05493-11.

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ABSTRACTWe have previously reported that compromised interleukin 17A (IL-17A) production in the lungs increased susceptibility to infection with the invasive fungal pathogenAspergillus fumigatus. Here we have shown that culturing lung cells fromA. fumigatus-challenged miceex vivodemonstrated Dectin-1-dependent IL-17A production. In this system, neutralization of IL-23 but not IL-6, IL-1β, or IL-18 resulted in attenuated IL-17A production.Il23mRNA expression was found to be lower in lung cells fromA. fumigatus-challenged Dectin-1-deficient mice, whereas bone marrow-derived dendritic cells from Dectin-1-deficient mice failed to produce IL-23 in response toA. fumigatusin vitro. Addition of recombinant IL-23 augmented IL-17A production by wild-type (WT) and Dectin-1-deficient lung cells, although the addition of IL-6 or IL-1β did not augment the effect of IL-23. Intracellular cytokine staining of lung cells revealed lower levels of CD11b+IL-17A+and Ly-6G+IL-17A+cells inA. fumigatus-challenged Dectin-1-deficient mice. Ly-6G+neutrophils purified from the lungs ofA. fumigatus-challenged Dectin-1-deficient mice displayed lowerIl17amRNA expression but surprisingly had intactRorcandRoramRNA expression. We further demonstrated that Ly-6G+neutrophils required the presence of myeloid cells for IL-17A production. Finally, uponin vitrostimulation withA. fumigatus, thioglycolate-elicited peritoneal neutrophils were positive for intracellular IL-17A expression and produced IL-17A in a Dectin-1- and IL-23-dependent manner. In summary, Dectin-1-dependent IL-17A production in the lungs during invasive fungal infection is mediated in part by CD11b+Ly-6G+neutrophils in an IL-23-dependent manner.
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Castro-Fuentes, Carlos Alberto, María Guadalupe Frías-De-León, María del Carmen González-Villaseñor, et al. "Evaluation of Primers OPF-01, P54, and 1253 to Identify A. fumigatus, A. flavus, and A. niger from Polymorphic Patterns Obtained by RAPD-PCR." Pathogens 13, no. 7 (2024): 574. http://dx.doi.org/10.3390/pathogens13070574.

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We evaluated the specificity of the primers OPF-01, P54, and 1253 to identify A. fumigatus, A. flavus, and A. niger, respectively, with the RAPD-PCR method. Eighty-two isolates belonging to the sections Fumigati, Flavi, and Nigri were used. The isolates were identified by phenotypic (macro- and micromorphology) and genotypic (partial sequences of the BenA gene) methods. The RAPD-PCR method was used to obtain polymorphic patterns with the primers OPF-01, P54, and 1253. The specificity of the polymorphic patterns of the isolates of each species was evaluated through the UPGMA clustering method and logistic regression model. All isolates of the genus Aspergillus were identified at the section level by macro- and micromorphology showing the typical morphology of the sections Fumigati, Flavi, and Nigri, and the species were identified by the construction of the phylogeny of the partial sequence of the BenA gene. The patterns’ polymorphic strains obtained with the primers OPF-01, P54, and 1253 for the isolates of A. fumigatus, A. flavus, and A niger, respectively, showed the same polymorphic pattern as the reference strains for each species. To verify the specificity of the primers, they were tested with other species from the sections Fumigati, Flavi and Nigri. The results support that the primers OPF-01, P54, and 1253 generate polymorphic patterns by RAPD-PCR species specific to A. fumigatus, A. flavus, and A. niger, respectively.
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Dissertations / Theses on the topic "Fumigatus"

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Weaver, Sean. "Heterokaryon incompatibility in Aspergillus fumigatus." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/heterokaryon-incompatibility-in-aspergillus-fumigatus(c0db26be-8326-4a93-8bcb-2648069e256c).html.

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Invasive aspergillosis (IA) is associated with high mortality rates and can be difficult and expensive to treat with current drugs. The drugs used to treat IA are also associated with undesirable, and often severe, side-effects of the patient. The main causative agent of this disease is the opportunistic pathogen Aspergillus fumigatus. This study identifies genes which play a role in a fungal-specific type of programmed cell death (PCD) in A. fumigatus, known as heterokaryon incompatibility. The development of drugs specifically targeting the products of these genes could lead to fewer side-effects than those arising from currently available anti-fungal drugs. The drug amphotericin B is currently used to treat IA and has been shown to induce an apoptotic-like phenotype in A. fumigatus; however, the sterols targeted are present in both fungal and mammalian cell membranes. HI is a fungal-specific self/non-self recognition system that results in rapid compartmentalisation and cell death of hyphal fusion sites if the two fusing fungi are not genetically compatible. The HI system could be exploited as a novel drug target against invasive fungal pathogens through targeting a component of the molecular pathway to induce cell death. In contrast to current drugs, novel drugs could target HI components to induce PCD without affecting non-desirable targets that cause side-effects. The non-self recognition systems used by Neurospora crassa, Aspergillus Nidulans and Podospora anserina are the well characterised, and they each differ significantly in their modes of action. BLAST searches found 30 homologues of HI genes from other the systems of characterised species in A. fumigatus, with 8 containing the fungal-specific het domain. The first assay to determine whether disruption of het genes could affect HI was to observe the barrage phenotype between incompatible A. fumigatus individuals. However, there was no barrage visible as the leading edge of colonies stopped growing when in close proximity to another colony. Instead, nitrate non-utilising (Nit) A. fumigatus mutant strains were generated using chlorate and pair-wise crosses of 46 environmentally and clinically isolates on nitrate-containing media resulted in the formation of 16 viable heterokaryons. All of the heterokaryons fell into exclusive compatibility groups where no intergroup crossing was possible. Homologous recombination was used to disrupt five of the identified het domain genes with gene replacement cassettes, generated through fusion-PCR, in an akuB(KU80Delta) A. fumigatus strain. The mutant strains displayed both detrimental growth on standard agar growth media and reduced ability to recognise non-self strains. Full and partial heterokaryons were formed during intergroup pair-wise compatibility crosses using the mutants and strains that the akuB(KU80Delta) parent strain was previously incompatible with. This was followed with a non-bias approach of gene disruption using the Fusarium oxysporum impala160 transposable element in a Nit A. fumigatus mutant. Inducing transposon mutagenesis through exposure to low temperature generated a mutant library of spores in which the transposon had disrupted different open reading frames at different locations across the A. fumigatus genome. The mutant spore library was also screened for the ability to form viable intergroup heterokaryons with strains belonging to different compatibility groups. PCR recovery and DNA sequencing was able to identify the locus of impala160 in three isolates able to form viable heterokaryons. The sequences revealed the transposable element had disrupted the same gene, AFUA_2G05070, in each of the three isolates. This gene encodes an uncharacterised conserved hypothetical protein which may be a critical component for non-self recognition in A. fumigatus HI, and a potential target for novel anti-fungal drugs to induce PCD.
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MOUTAOUAKIL, MOHAMMED. "Caracterisation des exoantigenes d'aspergillus fumigatus." Paris 7, 1992. http://www.theses.fr/1992PA077137.

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A. Fumigatus est un pathogene opportuniste qui est responsable de plusieurs types de mycoces: asthme allergique, aspergillose broncho-pulmonaire allergique, aspergillome et aspergillose invasive. Le diagnostic de l'aspergillose est base sur la detection soit d'anticorps circulants specifiques (igg ou/et ige en fonction de la maladie) soit d'antigenes circulants dans le cas de l'aspergillose invasive. A ce jour, moins d'une dizaine d'antigenes ont ete purifies. L'identification et la purification des antigenes est donc une des etapes essentielles a franchir en vue d'ameliorer les tests de detection deja existant ou de mettre au point de nouveaux tests originaux. Les antigenes secretes par a. Fumigatus sont identiques d'une souche a l'autre mais varient en fonction des conditions de culture. Ces antigenes ont des poids moleculaires apparents compris entre 10 et 205 kda. Quatre antigenes secretes par a. Fumigatus in vitro ont ete caracterises. L'antigene de 35 kda est reconnu de facon specifique par 55% des serums de patients. Sa purification reste difficile car cet antigene est present en tres faibles quantites dans le filtrat de culture. L'antigene de 18 kda a ete purifie a homogeneite. Cet antigene fait partie de la famille des ribotoxines capables de bloquer la synthese proteique. Cette proteine a ete detectee dans les urines de patients atteints d'aspergillose invasive et pourrait donc servir pour le developpement d'une nouvelle methode diagnostique. L'antigene de 33 kda est une serine protease purifiee a partir du filtrat de culture lorsque a. Fumigatus est cultive dans un milieu a base de collagene ou d'hydrolysats de proteines si le ph est maintenu entre 7 et 8. A cause de leur activite enzymatique et de leur presence in vivo, la proteine de 33 kda et la ribotoxine de 18 kda pourrait jouer un role dans la pathogenicite de ce champignon. L'antigene de 94 kda a ete purifie a partir du filtrat de culture d'a. Fumigatus produit dans un milieu contenant exclusivement de l'extrait de levure. Les souris ayant survecu a une infection aspergillaire ont des anticorps diriges de facon quasi exclusive contre cet antigene de 94 kda, ce qui suggere un role protecteur de ces anticorps contre l'infection par a. Fumigatus. Enfin la comparaison des antigenes produits par a. Fumigatus in vitro et in vivo dans les poumons de souris infectees a permis l'identification d'un grand nombre d'antigenes dont deux seulement avec des poids moleculaires de 20 et 38 kda semblent specifiquement produits in vivo
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Robertson, Maura Diane. "Host defences against Aspergillus fumigatus." Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/26892.

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The potential of the filamentous fungus Aspergillus fumigatus to act as an opportunistic pathogen may be related to its ability to resist the host defence network. Whilst phagocytic cells are clearly important in host defences against invading microorganisms their precise role in the killing of A. fumigatus remains undefined. The purpose of this study was to examine the basic interactions between phagocytic cells, from humans and rodents, with spores of A. fumigatus. In particular the mechanisms whereby phagocytic cells bind and kill spores of A. fumigatus, when compared with the relatively non-pathogenic fungus Penicillium ochrochloron were investigated. In order to investigate why people with asthma may develop some hypersensitivity reactions to A. fumigatus, in particular, rather than to the many other fungi in the atmosphere, the possibility that there may be a defect in the handling of the fungus by such patients has been tested. A comparison of the fungal handling by phagocytes from asthmatic patients, both sensitised and unsensitised to A. fumigatus with phagocytes from non-asthmatic subjects has been made. The principal findings from this study are that spores of A. fumigatus bind to the surface of the phagocytic cell yet are relatively resistant to phagocytosis. The spores also fail to trigger the phagocytic cells into releasing the potentially microbicidal reactive oxygen intermediates. These results may be related to a further finding which is that spores of A. fumigatus release a low molecular weight substance (diffusate) which interferes with various aspects of phagocytic cell activation. Spore diffusates were shown to inhibit the phagocytosis of radiolabelled antibody-coated sheep red blood cells and to suppress the spontaneous release of reactive oxygen intermediates by Corynebacterium parvum stimulated mouse peritoneal exudate cells. In addition spores diffusates inhibited the ability of phagocytic cells to spread on glass and reduce the number of phagocytic cells migrating towards a known chemoattractant. Studies on spore killing showed that spores of A. fumigatus opsonised in autologous serum were more resistant to killing by phagocytic cells from humans and rodents than similarly opsonised spores of P. ochrochloron. However, the ability of the phagocytic cells to kill spores of A. fumigatus was substantially increased when the spores were opsonised in sera which had been heat-treated for 30 minutes at 56?C. No increased killing was found with P. ochrochloron. People with asthma sensitised to A. fumigatus showed significant differences in their handling of A. fumigatus in vitro when compared with the control group. Monocytes from these sensitised patients killed significantly fewer spores of A. fumigatus (opsonised in auto? logous sera) whilst their polymorphonuclear leucocytes killed significantly more. No such differences were found for P. ochrochloron. The work reported in this Thesis has given us a clearer understanding of why Aspergillus fumigatus is an important cause of disease in man, and how the defence mechanisms that it has evolved in its natural environment the soil, enable it to act as a saprophyte or parasite in the lungs of humans and animals. The results also suggest a mechanism whereby heat-labile serum components may be an advantage to the survival of the fungus, thus perhaps explaining why it may be a particular problem in the airways of asthmatic patients.
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Melloul, Elise. "Aspergillose aviaire : développement d’un modèle d’aspergillose chez la dinde (Meleagris gallopavo) et évaluation de l’efficacité de l’énilconazole." Thesis, Paris Est, 2015. http://www.theses.fr/2015PEST1183/document.

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Aspergillus fumigatus est un agent pathogène respiratoire majeur chez les oiseaux d’ornement comme de production. L’aspergillose qui peut être responsable de mortalités importantes et de chutes de performances est difficile à traiter. Nous avons développé un modèle d’aspergillose aiguë chez le dindonneau en inoculant différents lots d’oiseaux âgés de moins d’une semaine via une aérosolisation intratrachéale de doses croissantes de conidies (105 à 108/animal) en utilisant un MicroSprayer®. Le développement de la masse fongique a été évalué par qPCR, dosage du galactomannane (GM), culture fongique et évaluation histopathologique dans le but de comparer les résultats obtenus en fonction du nombre de conidies inoculées. Une mortalité significative a été observée dans les 4 jours suivant l’inoculation uniquement pour l’inoculum le plus concentré. Les résultats des différents marqueurs du développement du champignon (culture, qPCR et GM), sont très bien corrélés avec la dose de l’inoculum administrée. Les moyennes d’équivalents conidies/g de poumon obtenues par qPCR étaient 1,3 log10 plus importantes que les numérations obtenues par culture sur gélose. Ce nouveau modèle incluant une combinaison inédite de biomarqueurs chez la dinde a été utilisé pour évaluer l’efficacité de l’énilconazole, seule molécule utilisée en élevage avicole pour lutter contre l’aspergillose<br>Aspergillus fumigatus remains a major respiratory pathogen in both ornamental and poultry. Aspergillosis can be responsible for high mortality rates and induces significant economic losses, particularly in turkey production, and it is still difficult to treat. We developed a new model of acute aspergillosis in young turkeys by inoculating few-days-old turkeys via intratracheal aerosolization with increasing concentrations (105 up to 108) of conidia using a MicroSprayer® device. The fungal burden was assessed and compared by real-time PCR, galactomannan (GM) dosage, fungal colony (CFU) counting and by histopathology. Early death occurred in the first 96 h post-inoculation only at the highest inoculum dose. We observed a correlation between inoculum size and results obtained by real-time PCR, GM dosage and CFU counting. The mean fungal burden detected by qPCR was 1.3 log10 units higher than the mean values obtained by CFU measurement. Furthermore, this new model, with its unique combination of markers, has been used to evaluate the efficacy of enilconazole
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Bernard-Cardona, Muriel. "Protéines et paroi chez Aspergillus fumigatus." Phd thesis, INAPG (AgroParisTech), 2003. http://tel.archives-ouvertes.fr/tel-00005702.

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La paroi du champignon filamenteux A. fumigalus conditionne la croissance et est responsable du maintien de l'intégrité cellulaire lors de l'infection. Les protéines de la paroi de ce champignon filamenteux n'avaient pas été étudiées jusqu'à présent alors qu'elles semblent jouer un rôle essentiel dans la structuration de la paroi de la levure modèle S. cereviciae. Une approche essentiellement biochimique a permis de caractériser les protéines associées à la paroi de A..fumigatus. La majorité des protéines pariétales chez A. fumigatus sont des protéines solubles. Une seule protéine est relarguée à partir de la paroi par un traitement f3- (1 .3) glucanase : c'est une phosphatase acide qui possède une ancre GPl et dont l'expression est réprimée en présence de phosphate inorganique. Par ailleurs, une étude des protéines GPl chez A. fumigatus par génomique comparative a montré que les protéines GPI décrites comme associées de façon covalente à la paroi chez la levure n'ont pas d'homologue chez A. fumigatus. Ainsi. l'organisation des protéines au sein de la paroi de A..fumigatus est différente de celle de la levure : les protéines pariétales ne semblent pas avoir un rôle essentiel dans l'élaboration de la paroi. Ensuite, une nouvelle famille de glycoprotéines portant un N-glycane lié à un galactofuranose en position terminale a été décrite. Cette famille comprend une phospholipase C, une phosphatase alcaline et une phytase. Enfin, une analyse morphologique de deux mutants chitine synthase et gluconosyltransférase a permis d'associer la réduction de la croissance à un hyper-branchement du mycélium et à une diminution de la taille de la cellule apicale sans que l'organisation globale des polysaccharides pariétaux et le taux de croissance spécifique soient affectés.
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Brown, Jeremy Stuart. "Signature tagged-mutagenesis of aspergillus fumigatus." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322287.

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Kong, Yun-cheung, and 江潤祥. "Multilocus sequence typing of aspergillus fumigatus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B4593972X.

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Marsh, Rachael. "Cytochrome P450 studies in Aspergillus fumigatus." Thesis, University of Sheffield, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364267.

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Rosa, Carla Maria de Gouveia. "Detecção de Aspergillus fumigatus em Hemoculturas." Master's thesis, Faculdade de Farmácia da Universidade do Porto, 2007. http://hdl.handle.net/10216/9491.

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SPENTCHIAN, MARC. "Interaction aspergillus fumigatus - laminine : etude preliminaire." Nantes, 1990. http://www.theses.fr/1990NANT016M.

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Books on the topic "Fumigatus"

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Latgé, Jean-Paul, and William J. Steinbach, eds. Aspergillus fumigatus and Aspergillosis. ASM Press, 2008. http://dx.doi.org/10.1128/9781555815523.

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1948-, Latgé Jean-Paul, and Steinbach William J, eds. Aspergillus fumigatus and aspergillosis. ASM Press, 2009.

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A, Brakhage Axel, Jahn Bernhard, and Schmidt Axel 1962-, eds. Aspergillus fumigatus: Biology, clinical aspects, and molecular approaches to pathogenicity. Karger, 1999.

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Holland, Tracey Michelle. The utilisation of a waste lignocellulosic by Aspergillus fumigatus IMI 255091. University of Birmingham, 1989.

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Hanahoe, Belinda. Detection of IgG and IgE antibodies to Aspergillus fumigatus in cystic fibrosis patients. The Author], 1993.

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Mambula, Salamatu Sangaljala. The application of B-cell epitope mapping on Aspergillus fumigatus alkaline protease in the search for diagnostic and therapeutic targets. University of Manchester, 1996.

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Seiber, James N., James E. Woodrow, Marylynn V. Yates, James A. Knuteson, N. Lee Wolfe, and S. R. Yates, eds. Fumigants. American Chemical Society, 1996. http://dx.doi.org/10.1021/bk-1997-0652.

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Taylor, R. W. D. Using phosphine as an effective commodity fumigant. Natural Resources Institute, 1996.

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Barse, Joseph R. Economic effects of banning soil fumigants. U.S. Dept. of Agriculture, Economic Research Service, 1988.

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Montana. Environmental Management Division. Technical Services Bureau. Controlling burrowing rodents with burrow fumigants. Montana Dept. of Agriculture, Environmental Management Division, Technical Services Bureau, 1985.

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Book chapters on the topic "Fumigatus"

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D’Enfert, C. "Aspergillus fumigatus." In Fungal Pathology. Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-015-9546-9_1.

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Rhodes, Judith C., and David S. Askew. "Aspergillus fumigatus." In Cellular and Molecular Biology of Filamentous Fungi. ASM Press, 2014. http://dx.doi.org/10.1128/9781555816636.ch43.

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Lydyard, Peter M., Michael F. Cole, John Holton, et al. "Aspergillus fumigatus." In Case Studies in Infectious Disease, 2nd ed. CRC Press, 2023. http://dx.doi.org/10.1201/9781003155447-1.

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d�Enfert, C., G. Weidner, P. C. Mol, and A. A. Brakhage. "Transformation Systems of Aspergillus fumigatus." In Aspergillus fumigatus. KARGER, 1999. http://dx.doi.org/10.1159/000060292.

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Bouchara, J. P., M. Sanchez, K. Esnault, and G. Tronchin. "Interactions between Aspergillus fumigatus and Host Matrix Proteins." In Aspergillus fumigatus. KARGER, 1999. http://dx.doi.org/10.1159/000060293.

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Monod, M., K. Jaton-Ogay, and U. Reichard. "Aspergillus fumigatus-Secreted Proteases As Antigenic Molecules and Virulence Factors." In Aspergillus fumigatus. KARGER, 1999. http://dx.doi.org/10.1159/000060294.

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Horiuchi, H., and M. Takagi. "Chitin Synthase Genes of Aspergillus Species." In Aspergillus fumigatus. KARGER, 1999. http://dx.doi.org/10.1159/000060295.

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Brakhage, A. A., K. Langfelder, G. Wanner, A. Schmidt, and B. Jahn. "Pigment Biosynthesis and Virulence." In Aspergillus fumigatus. KARGER, 1999. http://dx.doi.org/10.1159/000060296.

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Samson, R. A. "The Genus Aspergillus with Special Regard to the Aspergillus fumigatus Group." In Aspergillus fumigatus. KARGER, 1999. http://dx.doi.org/10.1159/000060298.

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Schmidt, A., and D. I. Schmidt. "J.B. Georg W. Fresenius and the Description of the Species Aspergillus fumigatus." In Aspergillus fumigatus. KARGER, 1999. http://dx.doi.org/10.1159/000060300.

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Conference papers on the topic "Fumigatus"

1

Bhadoria, Dharam P., Mitesh Kumar, Kanika Bhadoria, et al. "Novel Allergenic Proteins Of Aspergillus Fumigatus." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4303.

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Everaerts, Stephanie, Erna Van Hoeyveld, Kristina Vermeersch, et al. "Aspergillus fumigatus sensitization in COPD and smokers." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3610.

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Tiew, Pei Yee, Micheal Mac Aogain, Tavleen Kaur Jaggi, et al. "Environmental Aspergillus fumigatus associates with COPD exacerbations." In ERS International Congress 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/13993003.congress-2023.pa2188.

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Ajayan, Teena, P. Sony, Janu R. Panicker, and S. Shailesh. "Clustering DNA Sequences of Aspergillus Fumigatus Using Incremental Multiple Medoids." In 2015 Fifth International Conference on Advances in Computing & Communications (ICACC). IEEE, 2015. http://dx.doi.org/10.1109/icacc.2015.19.

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Huang, Valentina, Leah Daly, Kirstie Lucas, and Kazuhiro Ito. "Accelerated evolution of azole resistant Aspergillus fumigatus by diesel particles." In ERS International Congress 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/13993003.congress-2023.pa2182.

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REGINATTO, C., F. P. NORONHA, C. ROSSI, et al. "EFEITO DO INÓCULO NA OBTENÇÃO DE PECTINASES POR Aspergillus fumigatus." In XX Congresso Brasileiro de Engenharia Química. Editora Edgard Blücher, 2015. http://dx.doi.org/10.5151/chemeng-cobeq2014-0693-24401-178109.

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Engel, Tobias, Ellen Erren, Koen Vanden Driessche, et al. "Transmission-frequency of Aspergillus fumigatus in cystic fibrosis patients through coughing." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa1328.

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Bals, Robert, and Christoph Beisswenger. "Aspergillus Fumigatus Conidia Induce IFN-Beta Signaling In Respiratory Epithelial Cells." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2091.

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Matsuse, Hiroto, Susumu Fukahori, Tomoko Tsuchida, Tetsuya Kawano, Chizu Fukushima, and Shigeru Kohno. "Clearance Of Aspergillus Fumigatus Is Impaired In The Allergic Airway Inflammation." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5639.

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GUIMARÃES, J. R., E. C. O. ARAÚJO, J. C. F. QUEIROZ, and G. D. COELHO. "Produção de biossurfactante por Aspergillus fumigatus utilizando o sisal como substrato." In XXII Congresso Brasileiro de Engenharia Química. Editora Blucher, 2018. http://dx.doi.org/10.5151/cobeq2018-pt.0896.

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Reports on the topic "Fumigatus"

1

สุขวัฒนาสินิทธิ์, มงคล, та อนวัช อาชวาคม. การผลิตอาหารเสริมสุขภาพเพื่อป้องกันโรคข้อกระดูกเสื่อมจากเปลือกอาหารทะเล : รายงานการวิจัย. จุฬาลงกรณ์มหาวิทยาลัย, 2007. https://doi.org/10.58837/chula.res.2007.47.

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การย่อยไคตินจากแกนหมึกด้วยเอนไซม์จากรา Aspergillus fumigatus และโคลนแบคทีเรีย Serratia sp. สามารถผลิตเอ็น-แอซีทิล-ดี-กลูโคซามีน (GlcNAc) และเอ็น,เอ็น-ไดแอซทิลไคโตไบโอส [(GIcNAc)2] อย่างเฉพาะเจาะจงได้ เอนไซม์จากรา Aspergillus fumigatus (4 U/1 g of chitin) สามารถย่อยไคติน (3% w/v) ที่ pH เป็น 3 อุณหภูมิ 40 ํC ได้ผลิตภัณฑ์เป็น GIcNAc ด้วยเปอร์เซ็นต์ผลผลิต 72% ภายในเวลา 2 วัน การย่อยไคติน (3% w/v) ด้วยเอนไซม์จากโคลนแบคทีเรีย Serratia sp. (1 U/1 g of chitin) ที่ pH เท่ากับ 6 อุณหภูมิ 37 ํC ทำการบ่มเป็นเวลา 6 วันให้ผลิตภัณฑ์เป็น (GIcNAc)2 และ GIcNAc ด้วยเปอร์เซ็นต์ผลิตภัณฑ์ 43% และ 2.6% ตามลำดับ การทำให้ GlcNac และ (GlcNAc)2 บริสุทธิ์สามารถทำได้โดยการตกตะกอนด้วยเอทานอล ตามด้วยการกำจัดสีด้วยผงถ่านกัมมันต์หรือใช้คอลัมน์ที่มีผงถ่านกัมมันต์ให้ GIcNAc บริสุทธิ์ด้วยเปอร์เซ็นต์ผลผลิต 64% และ (GlcNac)2 บริสุทธิ์ด้วยเปอร์เซ็นต์ผลผลิต 40% การย่อยไคตินด้วยกรดไฮโดรคลอริกเข้มข้น โดยการใช้และไม่ใช้คลื่นอัลตราโซนิคเพื่อให้ได้เกลือกลูโคซามีน ไฮโดรคลอไรด์ (GIcNHCI) ซึ่งสภาวะที่ใช้ในการเตรียมเกลือ GIcNHCI คืออัตราส่วนไคตินต่อกรดไฮโดรคลอริกเข้มข้น 1:1 (w/w) ขณะนี้การทดลองของการย่อยไคตินด้วยกรดไฮโดรคลอริกเข้มข้นอยู่ในระหว่างการเก็บข้อมูล
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สุขวัฒนาสินิทธิ์, มงคล, та อนวัช อาชวาคม. การผลิตอาหารเสริมสุขภาพเพื่อป้องกันโรคข้อกระดูกเสื่อมจากเปลือกอาหารทะเล : รายงานการวิจัย. จุฬาลงกรณ์มหาวิทยาลัย, 2008. https://doi.org/10.58837/chula.res.2008.42.

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การย่อยไคตินจากแกนหมึกด้วยเอนไซม์จากรา Aspergillus fumigatus และโคลนแบคทีเรีย Serratia sp. สามารถผลิตเอ็น-แอซีทิล-ดี-กลูโคซามีน (GlcNAc) และเอ็น,เอ็น-ไดแอซีทิลไคโตไบโอส [(GlcNAc)2] อย่างเฉพาะเจาะจงได้ เอนไซม์จากรา Aspergillus fumigatus (4 u/1 g of chitin) สามารถย่อยไคติน (3% w/v) ที่ pH เป็น 3 อุณหภูมิ 40oC ได้ผลิตภัณฑ์เป็น GlcNAc ด้วยเปอร์เซ็นต์ผลผลิต 72% ภายในเวลา 2วัน การย่อยไคติน (3% w/v) ด้วยเอนไซม์จากโคลนแบคทีเรีย Serratia sp. (1 u/1 g of chitin) ที่ pH เท่ากับ 6 อุณหภูมิ 37oC บ่มเป็นเวลา 6 วันให้ผลผลิตเป็น (GlcNAc)2 และ GlcNAc ด้วยเปอร์เซ็นต์ผลิตภัณฑ์ 43% และ2.6% ตามลำดับ การทำให้ GlcNAc และ (GlcNAc)2 บริสุทธิ์สามารถทำได้โดยการตกตะกอนของเอทานอล ตามด้วยการกำจัดสีด้วยผงถ่านกัมมันต์หรือใช้คอลัมน์ที่มีผงถ่านกัมมันต์ให้ GlcNAc บริสุทธิ์ด้วยเปอร์เซ็นต์ผลผลิต 64% และ (GlcNAc)2 บริสุทธิ์ด้วยเปอร์เซ็นต์ผลผลิต 40% และด้วยกรรมวิธีการทำให้บริสุทธิ์ที่พัฒนาแล้วสามารถเพิ่มความบริสุทธิ์ของผลิตภัณฑ์สูงถึง 100% การย่อยไคตินด้วยกรดไฮโดรคลอริกเข้มข้น โดยการใช้และไม่ใช้คลื่นอัตราโซนิคเพื่อให้ได้เกลือกลูโคซามีน ไฮโดรคลอไรด์ (GlcNHCL) ซึ่งสภาวะที่ใช้ในการเตรียมเกลือ GlcNHCL คืออัตราส่วนไคตินต่อกรดไฮโดรคลอริกเข้มข้น 1:1 (w/v) และที่อุณหภูมิ 40oC ได้ผลการย่อยที่มีประโยชน์และสามารถนำไปใช้ในการทดลองในขั้นต่อไป ขณะนี้การทดลองของการย่อยไคตินด้วยกรดไฮโดรคลอริกเข้มข้นด้วยสภาวะต่างๆ อยู่ในระหว่างการเก็บข้อมูล
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Konkler, Matthew J., Mark A. Newbill, Stan Lebow, and Jeffrey J. Morrell. Performance of two solid fumigants in covered bridges. U.S. Department of Agriculture, Forest Service, Forest Products Laboratory, 2017. http://dx.doi.org/10.2737/fpl-rp-346.

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Barger, Jack H., Richard W. Hall, Alden M. Townsend, and Alden M. Townsend. Elm leaf beetle performance on ozone-fumigated elm. U.S. Department of Agriculture, Forest Service, North Central Research Station, 1992. http://dx.doi.org/10.2737/ne-rp-661.

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สุขวัฒนาสินิทธิ์, มงคล, та อนวัช อาชวาคม. การผลิตอาหารเสริมสุขภาพเพื่อป้องกันโรคข้อกระดูกเสื่อมจากเปลือกอาหารทะเล : รายงานการวิจัย. จุฬาลงกรณ์มหาวิทยาลัย, 2009. https://doi.org/10.58837/chula.res.2009.41.

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การย่อยไคตินจากแกนหมึกด้วยเอนไซม์จากรา Aspergillus fumigates และโคลนแบคทีเรีย Serratia sp. สามารถผลิตเอ็น-แอซีทิล-ดี-กลูโคซามีน (GIcNAc) และเอ็น,เอ็น-ไดแอซีทิลไคโตไบโอส [(GIcNAc)2] อย่างเฉพาะเจาะจงได้ เอนไซม์จากรา Aspergillus fumigates (4 U/1 g of chitin) สามารถย่อยไคติน (3% w/v) ที่ pH เป็น 3 อุณหภูมิ 40°C ได้ผลิตภัณฑ์เป็น GIcNAc ด้วยเปอร์เซ็นต์ผลผลิต 72% ภายในเวลา 2 วัน การย่อยไคติน (3% w/v) ด้วยเอนไซม์จากโคลนแบคทีเรีย Serratia sp. (1 U/1 g of chitin) ที่ pH เท่ากับ 6 อุณหภูมิ 37°C ทำการบ่มเป็นเวลา 6 วันให้ผลิตภัณฑ์เป็น (GIcNAc)2 และ GIcNAc ด้วยเปอร์เซ็นต์ผลิตภัณฑ์ 43% และ 2.6% ตามลำดับ การทำให้ GIcNAc และ (GIcNAc)2 บริสุทธิ์สามารถทำได้โดยการตกตะกอนด้วยเอทานอล ตามด้วยการกำจัดสีด้วยผงถ่านกัมมันต์หรือใช้คอลัมน์ที่มีผงถ่านกัมมันต์ให้ GIcNAc บริสุทธิ์ด้วยเปอร์เซ็นต์ผลผลิต 64% และ (GIcNA)2 บริสุทธิ์ด้วยเปอร์เซ็นต์ผลผลิต 40% และด้วยกรรมวิธีการทำให้บริสุทธิ์ที่พัฒนาแล้วสามารถเพิ่มความบริสุทธิ์ของผลิตภัณฑ์สูงถึง 100% การย่อยไคตินด้วยกรดไฮโดรคลอริกเข้มข้น โดยการใช้และไม่ใช้คลื่นอัลตราโซนิคเพื่อให้ได้เกลือกลูโคซามีน ไฮโดรคลอไรด์ (GIcNHCI) ซึ่งสภาวะที่ใช้ในการเตรียมเกลือ GIcNHCI คืออัตราส่วนไคตินต่อกรดไฮโดรคลอริกเข้มข้น 1:1 (w/w) และที่อุณหภูมิ 40°C ได้ผลการย่อยที่มีประโยชน์และสามารถนำไปใช้ในการทดลองในขั้นต่อไป การย่อยไคตินด้วยกรดไฮโดรคลอริกเข้มข้นโดยการใช้คลื่นไมโครเวฟซึ่งสภาวะที่ใช้ในการเตรียมเกลือ GIcNHCI คืออัตราส่วนไคตินต่อกรดไฮโดรคลอริกเข้มข้น 1:3 (w/w) ที่พลังงาน 850 วัตต์เป็นเวลา 12 นาทีทำให้ได้เปอร์เซ็นต์ผลิตภัณฑ์ 52% ขณะนี้การปรับปรุงเปอร์เซ็นต์ผลิตภัณฑ์ของการย่อยโดยการใช้คลื่นไมโครเวฟอยู่ในระหว่างการเก็บข้อมูล
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6

Hochman, Ayala, Thomas Nash III, and Pamela Padgett. Physiological and Biochemical Characterization of the Effects of Oxidant Air Pollutants, Ozone and Gas-phase Nitric Acid, on Plants and Lichens for their Use as Early Warning Biomonitors of these Air Pollutants. United States Department of Agriculture, 2011. http://dx.doi.org/10.32747/2011.7697115.bard.

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Introduction. Ozone and related oxidants are regarded as the most important phytotoxic air pollutant in many parts of the western world. A previously unrecognized component of smog, nitric acid, may have even greater deleterious effects on plants either by itself or by augmenting ozone injury. The effects of ozone on plants are well characterized with respect to structural and physiological changes, but very little is known about the biochemical changes in plants and lichens exposed to ozone and/or HNO3. Objectives.To compare and contrast the responses of crop plants and lichens to dry deposition of HNO3 and O3., separately, and combined in order to assess our working hypothesis that lichens respond to air pollution faster than plants. Lichens are most suitable for use as biomonitors because they offer a live-organism-based system that does not require maintenance and can be attached to any site, without the need for man-made technical support systems. Original Immediate aims To expose the tobacco (Nicotiana tabacum L.) cultivar Bel-W3 that is ozone supersensitive and the ozone sensitive red kidney bean (Phaseolusvulgaris) and the lichen Ramalinamenziesii to controlled HNO3 and O3 fumigations and combined and to follow the resulting structural, physiological and biochemical changes, with special reference to reactive oxygen species related parameters. Revised. Due to technical problems and time limitations we studied the lichen Ramalinamenziesii and two cultivar of tobacco: Bel-W3 that is ozone supersensitive and a resistant cultivar, which were exposed to HNO3 and O3 alone (not combined). Methodology. Plants and lichens were exposed in fumigation experiments to HNO3 and O3, in constantly stirred tank reactors and the resulting structural, physiological and biochemical changes were analyzed. Results. Lichens. Exposure of Ramalinamenziesiito HNO3 resulted in cell membrane damage that was evident by 14 days and continues to worsen by 28 days. Chlorophyll, photosynthesis and respiration all declined significantly in HNO3 treatments, with the toxic effects increasing with dosage. In contrast, O3 fumigations of R. menziesii showed no significant negative effects with no differences in the above response variables between high, moderate and low levels of fumigations. There was a gradual decrease in catalase activity with increased levels of HNO3. The activity of glutathione reductase dropped to 20% in thalli exposed to low HNO3 but increased with its increase. Glucose 6-phosphate dehydrogenase activity increase by 20% with low levels of the pollutants but decreased with its increase. Tobacco. After 3 weeks of exposure of the sensitive tobacco cultivar to ozone there were visible symptoms of toxicity, but no danmage was evident in the tolerant cultivar. Neither cultivar showed any visible symptoms after exposure to HNO3.In tobacco fumigated with O3, there was a significant decrease in maximum photosynthetic CO2 assimilation and stomatal conductance at high levels of the pollutant, while changes in mesophyll conductance were not significant. However, under HNO3 fumigation there was a significant increase in mesophyll conductance at low and high HNO3 levels while changes in maximum photosynthetic CO2 assimilation and stomatal conductance were not significant. We could not detect any activity of the antioxidant enzymes in the fumigated tobacco leaves. This is in spite of the fact that we were able to assay the enzymes in tobacco leaves grown in Israel. Conclusions. This project generated novel data, and potentially applicable to agriculture, on the differential response of lichens and tobacco to HNO3 and O3 pollutants. However, due to experimental problems and time limitation discussed in the body of the report, our data do not justify yet application for a full, 4-year grant. We hope that in the future we shall conduct more experiments related to our objectives, which will serve as a basis for a larger scale project to explore the possibility of using lichens and/or plants for biomonitoring of ozone and nitric acid air pollution.
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7

Freeman, Stanley, and Daniel Legard. Epidemiology and Etiology of Colletotrichum Species Causing Strawberry Diseases. United States Department of Agriculture, 2001. http://dx.doi.org/10.32747/2001.7695845.bard.

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Diseases caused by Colletotrichum spp. are one of the most important limitations on international strawberry production, affecting all vegetative and fruiting parts of the plant. From 1995 to 1997, C. acutatum infections reached epidemic levels in Israeli strawberry nurseries, causing extensive loss of transplants in fruit-bearing fields and additional reductions in yield. Although C. acutatum also occurs on strawberry in Florida, recent crown rot epidemics have been primarily caused by C. gloeosporioides. Little is known about the basic epidemiology of these important diseases on strawberry. The source of initial inoculum for epidemics in Israel, Florida (other US states including California) and the rest of the world is not well understood. Subspecies relationships between Colletotrichum isolates that cause the different diseases on strawberry (i.e. attack different tissues) are also not well understood. Objectives of this proposal were to detennine the potential of infested soil, strawberry debris and other hosts as sources of primary inoculum for strawberry diseases caused by Colletotrichum spp. in Israel and Florida. In addition, traditional (ie. morphological characteristics, benomyl sensitivity, vegetative compatibility grouping) and DNA based methods were used to investigate the etiology of these diseases in order to resolve epidemiologically important subspecies variation. In Israel it was found that C. gloeosporioides and C. acutatum infecting strawberry could remain viable in sterilized soil for up to one year and in methyl-bromide fumigated soil for up to 4 months; inoculum in mummified fruit remained viable for at least 5 months under field conditions whereas that in infected crowns was not recovered. Therefore, the contribution of these inocula to disease epidemics should be considered. The host range and specificity of C. acutatum from strawberry was examined on pepper, eggplant, tomato, bean and strawberry under greenhouse conditions. The fungus was recovered from all plant species over a three-month period but caused disease symptoms only on strawberry. C. acutatum was also isolated from healthy looking, asymptomatic plants of the weed species, Vicia and Conyza, growing in infected strawberry fruiting fields. Isolates of C. acutatum originating from strawberry and anemone infected both plant species in artificial inoculations. The habitation of a large number of plant species including weeds by C. acutatum suggests that although it causes disease only on strawberry and anemone in Israel, these plants may serve as a potential inoculum source for strawberry infection and pennit survival of the pathogen between seasons. In Florida, isolates of Colletotrichum spp. from diseased strawberry fruit and crowns were evaluated to detennine their etiology and the genetic diversity of the pathogens. Only C. acutatum was recovered from fruit and C. gloeosporioides were the main species recovered from crowns. These isolates were evaluated at 40 putative genetic loci using random amplified polymorphic DNA (RAPD). Genetic analysis of RAPD markers revealed that the level of linkage disequilibrium among polymorphic loci in C. gloeosporioides suggested that they were a sexually reproducing population. Under field conditions in Florida, it was detennined that C. gloeosporioides in buried crowns survived
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8

NTP Technical Report on the Toxicity Studies of Aspergillus fumigatus Administered by Inhalation to B6C3F1/N Mice. NIEHS, 2021. http://dx.doi.org/10.22427/ntp-tox-100.

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9

Fumigator falls off roof during tenting and dies in California. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, 1998. http://dx.doi.org/10.26616/nioshsface98ca002.

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