Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.10.3.2 (laccase)
 4,656 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We propose a new process using a vapor phase bioreactor (VPB) to simultaneously (i) delignify sugar-cane bagasse, a residue of sugar production that can be recycled in paper industry, and (ii) produce laccase, an enzyme usable to bleach paper pulp. Ethanol vapor, used as laccase inducer, was blown up through a VPB packed with bagasse and inoculated with Pycnoporus cinnabarinusss3, a laccase-hyperproducing fungal strain. After 28 days, the laccase activity in the ethanol-treated bagasse was 80-fold higher (80 U g(ds)(-)(1)) and the bagasse delignification percentage was 12-fold (12%) higher than in the reference samples produced in the absence of ethanol, corresponding to a high overall pulp yield of 96.1%. In the presence of ethanol, the total soluble phenols amount was 2.5-fold (3 mg FA g(ds)(-)(1)) higher than that without ethanol. Six monomeric phenols were detected: p-coumaric (4-hydroxyphenyl-2-propenoic), ferulic (4-hydroxy-3-methoxyphenyl-2-propenoic), syringic (4-hydroxy-3,5-dimethoxybenzoic), vanillic (4-hydroxy-3-methoxybenzoic) and 4-hydroxybenzoic acids, and 2-methoxyhydroquinone. Higher concentrations of phenolic compounds were observed when ethanol vapor was added, confirming a more efficient bagasse delignification. After 28 days, the fungal-treated bagasse (with ethanol addition) was pulped and refined. For a freeness of 81 mL CSF, this processing required 50% less energy than with untreated bagasse (without inoculation and ethanol addition), which indicated a significant potential economy for the pulp and paper industry. Handsheets were made from pulp obtained after fungal-treated and untreated bagasse. Comparison of bagasse-pulp characteristics for freeness of 35 and 181 mL CSF showed an average increment by 35% for tensile index and breaking strength and length. VPB allowed a simultaneous production of laccase (90 U g(ds)(-)(1), after pressing of the bagasse) that improved the overall profitability of the process.
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PMID:New process for fungal delignification of sugar-cane bagasse and simultaneous production of laccase in a vapor phase bioreactor. 1671 6

Cryptococcal meningitis is a major cause of mortality throughout the developing world, yet little is known about the genetic markers underlying Cryptococcal virulence and patient outcome. We studied a cohort of 230 Cryptococcus neoformans (Cn) isolates from HIV-positive South African clinical trial patients with detailed clinical follow-up using multi-locus sequence typing and in vitro phenotypic virulence assays, correlating these data with clinical and fungal markers of disease in the patient. South African Cn displayed high levels of genetic diversity and locus variability compared to globally distributed types, and we identified 50 sequence types grouped within the main molecular types VNI, VNII and VNB, with 72% of isolates typed into one of seven 'high frequency' sequence types. Spatial analysis of patients' cryptococcal genotype was not shown to be clustered geographically, which might argue against recent local acquisition and in favour of reactivation of latent infection. Through comparison of MLST genotyping data with clinical parameters, we found a relationship between genetic lineage and clinical outcome, with patients infected with the VNB lineage having significantly worse survival (n=8, HR 3.35, CI 1.51-7.20, p=0.003), and this was maintained even after adjustment for known prognostic indicators and treatment regimen. Comparison of fungal genotype with in vitro phenotype (phagocytosis, laccase activity and CSF survival) performed on a subset of 89 isolates revealed evidence of lineage-associated virulence phenotype, with the VNII lineage displaying increased laccase activity (p=0.001) and ex vivo CSF survival (p=0.0001). These findings show that Cryptococcus neoformans is a phenotypically heterogeneous pathogen, and that lineage plays an important role in cryptococcal virulence during human infection. Furthermore, a detailed understanding of the genetic diversity in Southern Africa will support further investigation into how genetic diversity is structured across African environments, allowing assessment of the risks different ecotypes pose to infection.
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PMID:Genotypic Diversity Is Associated with Clinical Outcome and Phenotype in Cryptococcal Meningitis across Southern Africa. 2611 Sep 2

Cryptococcus neoformans and Cryptococcus gattii are fungal pathogens that cause diseases in humans. Cryptococcal species mainly enter the body by inhalation and in most cases are eliminated by host defense mechanisms. Some cases, however, progress to pneumonia and subsequent dissemination of the infection to the central nervous system (CNS), leading to meningoencephalitis. Cryptococcus can cross the blood-brain barrier transcellularly, paracellularly and through infected phagocytes (the Trojan horse mechanism). The reason for the tropism of Cryptococcus to the CNS could be partially explained by the abundance of inositol in the brain, which causes the hyaluronic acid in fungal cells to bind to host CD44 receptors. There are differences in the clinical characteristics of C. neoformans and C. gattii. HIV infection is the most common risk factor for cryptococcosis due to C. neoformans, whereas C. gattii infection with CNS involvement is frequently found in otherwise healthy individuals exposed to plant propagules found in tropical and subtropical regions. As the virulence traits of C. neoformans contributing to CNS disease, high macrophage uptake and laccase activity are associated with the fungal burden and the rate of clearance of the infection from the brain. Recent reports suggested that the C. gattii VGII strain suppresses host immune responses in the lung and causes more lung infections than CNS diseases. Furthermore, the anti-GM-CSF autoantibodies are a risk factor for CNS infection by the C. gattii VGI strain. To understand the mechanism by which Cryptococcus causes CNS disease, it is important to consider the specific characteristics of the species and the molecular types.
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PMID:[Mechanism of Cryptococcus Meningoencephalitis]. 2693 49