(3aR,4S,5aR,6R,9aS,9bR)-6-Hydroxy-5a,9-dimethyl-3-methylene-2-oxo-2,3,3a,4,5,5a,6,7,9a,9b-decahydronaphtho[1,2-b]furan-4-yl methacrylate/2-Propenoic acid, 2-methyl-, (3aR,4S,5aR,6R,9aS,9bR)-2,3,3a,4,5,5a,6,7,9a,9b-decahydro-6-hydroxy-5a,9-dimethyl-3-methylene-2-oxonaphtho[1,2-b]furan-4-yl ester
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
488.9±45.0 °C at 760 mmHg
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Personal Projective Equipment
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Azole-resistance in Aspergillus fumigatus is an emerging worldwide threat as it precludes the use of one of the 3 major classes of antifungal drugs to treat chronic and invasive aspergillosis . In addition to the well-known environmental emergence of azole-resistant A. fumigatus strains, associated with the use of fungicides in agriculture , , the development of in-host resistance, facilitated by medical antifungal use, has been described . Investigations involving linked sets of (isogenic) clinical isolates of A. fumigatus sequentially recovered from individual patients, are extremely important in order to improve our understanding of how azole resistance develops in-host. Here we present the whole genome sequences of 13 clinical isogenic A. fumigatus isolates. These isolates were cultured from a single patient suffering from invasive aspergillosis over a period of 2 years. This patient underwent a wide range of antifungal therapies and the resultant isolates acquired multiple azole resistance in-host during the course of infection. The data presented here is related to our research paper titled “In-host microevolution of Aspergillus fumigatus: a phenotypic and genotypic analysis” which describes the phenotypic characterisation of these clinical isolates . The raw sequence data was deposited in the NCBI Sequence Read Archive (https://www.ncbi.nlm.nih.gov/sra), under BioProject ID number PRJNA528395.
Raw genome sequence data for 13 isogenic Aspergillus fumigatus strains isolated over a 2 year period from a patient with chronic granulomatous disease
Eloise Ballard,a Jan Zoll,b Willem J.G. Melchers,b Alistair J.P. Brown,a Adilia Warris,a and Paul E. Verweijb,?
Mutations in the ataxia-telangiectasia mutated (ATM) and checkpoint kinase 2 (CHEK2) genes and amplification of the v-erb-b2 avian erythroblastic leukemia viral oncogene homolog 2 (ERBB2) gene have been suggested to have an important role in breast cancer aetiology. However, whether common variation in these genes has a role in the development of breast cancer or breast cancer survival in humans is still not clear.
We performed a comprehensive haplotype analysis of the ATM, CHEK2 and ERBB2 genes in a Swedish population-based study, which included 1,579 breast cancer cases and 1,516 controls. We followed the cases for 8.5 years, on average, and retrieved information on the date and cause of death during that period from the nationwide Swedish causes of death registry. We selected seven haplotype-tagging SNPs (tagSNPs) in the ATM gene, six tagSNPs in the CHEK2 gene and seven tagSNPs in the ERBB2 gene that predicted both haplotypic and single locus variations in the respective genes with R2 values ≥ 0.8. These tagSNPs were genotyped in the complete set of cases and controls. We computed expected haplotype dosages of the tagSNP haplotypes and included the dosages as explanatory variables in Cox proportional hazards or logistic regression models.
We found no association between any genetic variation in the ATM, CHEK2 or ERBB2 genes and breast cancer survival or the risk of developing tumours with certain characteristics.
Our results indicate that common variants in the ATM, CHEK2 or ERBB2 genes are not involved in modifying breast cancer survival or the risk of tumour-characteristic-defined breast cancer.
Comprehensive analysis of the ATM, CHEK2 and ERBB2 genes in relation to breast tumour characteristics and survival: a population-based case-control and follow-up study
Kristjana Einarsdottir,corresponding author1 Lena U Rosenberg,1 Keith Humphreys,1 Carine Bonnard,2 Juni Palmgren,1,3 Yuqing Li,2 Yi Li,4 Kee S Chia,5 Edison T Liu,2 Per Hall,1 Jianjun Liu,2 and Sara Wedren1
Mycoplasmas are regarded to be useful models for studying the minimum genetic complement required for independent survival of an organism. Mycoplasma bovis is a globally distributed pathogen causing pneumonia, mastitis, arthritis, otitis media and reproductive tract disease, and genome sequences of three strains, the type strain PG45 and two strains isolated in China, have been published. In this study, several Tn4001 based transposon constructs were generated and used to create a M. bovis PG45 insertional mutant library. Direct genome sequencing of 319 independent insertions detected disruptions in 129 genes in M. bovis, 48 of which had homologues in Mycoplasma mycoides subspecies mycoides SC and 99 of which had homologues in Mycoplasma agalactiae. Sixteen genes found to be essential in previous studies on other mycoplasma species were found to be dispensable. Five of these genes have previously been predicted to be part of the core set of 153 essential genes in mycoplasmas. Thus this study has extended the list of non-essential genes of mycoplasmas from that previously generated by studies in other species.
Genes Found Essential in Other Mycoplasmas Are Dispensable in Mycoplasma bovis
Shukriti Sharma, Philip F. Markham, and Glenn F. Browning *