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Little is known about the degradability of mycotoxin deoxynivalenol (DON) by the spent mushroom substrate (SMS)-derived manganese peroxidase (MnP) and lignin peroxidase (LiP) and its potential. The present study investigated the growth inhibition of Fusarium graminearum KR1 and the degradation of DON by MnP and LiP extracted from SMS. The results from the 7-day treatment period showed that mycelium inhibition of F. graminearum KR1 by MnP and LiP were 23.7% and 74.7%, respectively. Deoxynivalenol production in the mycelium of F. graminearum KR1 was undetectable after treatment with 50 U/mL of MnP or LiP for 7 days. N-acetyl-D-glucosamine (GlcNAc) content and chitinase activity both increased in the hyphae of F. graminearum KR1 after treatment with MnP and LiP for 1, 3, and 6 h, respectively. At 12 h, only the LiP-treated group had higher chitinase activity and GlcNAc content than those of the control group (p < 0.05). However, more than 60% of DON degradabilities (0.5 mg/kg, 1 h) were observed under various pH values (2.5, 4.5, and 6.5) in both MnP (50 U/g) and LiP (50 U/g) groups, while DON degradability at 1 mg/kg was 85.5% after 50 U/g of LiP treatment for 7 h in simulated pig gastrointestinal tracts. Similarly, DON degradability at 5 mg/kg was 67.1% after LiP treatment for 4.5 h in simulated poultry gastrointestinal tracts. The present study demonstrated that SMS-extracted peroxidases, particularly LiP, could effectively degrade DON and inhibit the mycelium growth of F. graminearum KR1. 相似文献
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Wanna Thongnoppakhun Surasak Jiemsup Suganya Yongkiettrakul Chompunut Kanjanakorn Chanin Limwongse Prapon Wilairat Anusorn Vanasant Nanyawan Rungroj Pa-thai Yenchitsomanus 《The Journal of molecular diagnostics : JMD》2009,11(4):334-346
A number of common mutations in the hemoglobin β (HBB) gene cause β-thalassemia, a monogenic disease with high prevalence in certain ethnic groups. As there are 30 HBB variants that cover more than 99.5% of HBB mutant alleles in the Thai population, an efficient and cost-effective screening method is required. Three panels of multiplex primer extensions, followed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry were developed. The first panel simultaneously detected 21 of the most common HBB mutations, while the second panel screened nine additional mutations, plus seven of the first panel for confirmation; the third panel was used to confirm three HBB mutations, yielding a 9-Da mass difference that could not be clearly distinguished by the previous two panels. The protocol was both standardized using 40 samples of known genotypes and subsequently validated in 162 blind samples with 27 different genotypes (including a normal control), comprising heterozygous, compound heterozygous, and homozygous β-thalassemia. Results were in complete agreement with those from the genotyping results, conducted using three different methods overall. The method developed here permitted the detection of mutations missed using a single genotyping procedure. The procedure should serve as the method of choice for HBB genotyping due to its accuracy, sensitivity, and cost-effectiveness, and can be applied to studies of other gene variants that are potential disease biomarkers.To date, 739 point mutations in the hemoglobin, β (HBB) gene causing β-thalassemia (MIM# 141900) have been reported in HbVar: A Database of Human Hemoglobin Variants and Thalassemias (http://globin.cse.psu.edu/globin/hbvar/menu.html, accessed March 2009), but each ethnic group has a limited number of common mutations and a considerable number of rarer mutations.1 The c.79G>A (also known as CD26G>A or Hb E) is the most frequent HBB variant in Southeast Asia including Thailand.2 “Thai” generally refers to speakers of Thai (Tai) languages. The ethnic groups of Thailand comprise Thais (constituting 85% of the population) and Hill Peoples living primarily in the north, as well as other groups including the Chinese and minorities in the south.3 In the Thai population, approximately 40 HBB mutations have been identified,4 of which 30 variants account for more than 99.5% of all mutant HBB alleles Common HBB mutations (13)
HBB mutations causing abnormal Hb (10)
Rare HBB mutations (7)
Common name HGVS nomenclature Common name HGVS nomenclature Common name HGVS nomenclature CD26G>A (Hb E) c.79G>A* CD147+AC (Hb Tak) c.441_442insAC*†‡ CD43G>T c.130G>T* CD41/42-TTCT c.124_127delTTCT*† CD126T>G (Hb Dhonburi) c.380T>G* CD123/125 (−8 bp) c.370_377delACC CCACC† CD17A>T c.52A>T*†‡ CD136G>A (Hb Hope) c.410G>A* −87C>A c.−137C>A† −28A>G c.−78A>G* CD6G>A (Hb C) c.19G>A*† CD15-T c.46delT† IVS2#654C>T c.316−197C>T* CD56G>A (Hb J-Bangkok) c.170G>A* CD8/9+G c.27_28insG† IVS1#5G>C c.92 + 5G>C* CD83G>A (Hb Pyrgos) c.251G>A* CD27/28+C c.84_85insC† CD19A>G (Hb Malay) c.59A>G* CD6A>C (Hb G Makassar) c.20A>C*† CD41-C c.126delC*† CD71/72 + A c.216_217insA* CD6A>T (Hb S) c.20A>T*†‡ IVS1#1G>T c.92 + 1G>T† CD121G>C (Hb D Punjab) c.364G>C* −31A>G c.−81A>G† CD1T>C (Hb Raleigh) c.5T>C† −30T>C c.−80T>C* CD35C>A c.108C>A† CD0T>G c.2T>G*