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R Zaman 《Tubercle》1991,72(1):51-55
Resistance to six anti-mycobacterial agents rifampicin, isoniazid, streptomycin, ethambutol, p-amino salicylic acid and cycloserine was studied. Variations in the resistance pattern among Saudi, non-Saudi and a stable National Guard King Khalid Hospital (NGKKH) population were investigated. A high percentage of relapse cases, 21%, was recorded. Among the NGKKH population this figure was much lower, 9.9%. Resistance to rifampicin alone was high at 7.2% followed by streptomycin 3.3%, isoniazid 1.8%, p-amino salicylic 1.2% and cycloserine 0.8%. Resistance to rifampicin alone was higher among 'new' cases whilst combined resistance to two or more drugs was seen more often in 'old' patients. Resistance was seen more frequently among non-Saudis, both 'old' and 'new'. An unusual finding was the prevalence of rifampicin resistance among non-pulmonary isolates. 相似文献
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Zaman Vandana Shields Donald C. Shams Ramsha Drasites Kelsey P. Matzelle Denise Haque Azizul Banik Narendra L. 《Metabolic brain disease》2021,36(5):815-827
Metabolic Brain Disease - Parkinson’s disease (PD) is a neurodegenerative disorder etiologically linked to the loss of substantia nigra (SN) dopaminergic neurons in the mid-brain. The... 相似文献
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High resolution SNP array profiling identifies variability in retinoblastoma genome stability 下载免费PDF全文
Berber M. Mol Maarten P. G. Massink Annemarie H. van der Hout Charlotte J. Dommering Johannes M. A. Zaman Machteld I. Bosscha Wijnanda A. Kors Hanne E. Meijers‐Heijboer Gertjan J. L. Kaspers Hein te Riele Annette C. Moll Jacqueline Cloos Josephine C. Dorsman 《Genes, chromosomes & cancer》2014,53(1):1-14
Both hereditary and nonhereditary retinoblastoma (Rb) are commonly initiated by loss of both copies of the retinoblastoma tumor suppressor gene (RB1), while additional genomic changes are required for tumor initiation and progression. Our aim was to determine whether there is genomic heterogeneity between different clinical Rb subtypes. Therefore, 21 Rb tumors from 11 hereditary patients and 10 nonhereditary Rb patients were analyzed using high‐resolution single nucleotide polymorphism (SNP) arrays and gene losses and gains were validated with Multiplex Ligation‐dependent Probe Amplification. In these tumors only a few focal aberrations were detected. The most frequent was a focal gain on chromosome 2p24.3, the minimal region of gain encompassing the oncogene MYCN. The genes BAZ1A, OTX2, FUT8, and AKT1 were detected in four focal regions on chromosome 14 in one nonhereditary Rb. There was a large difference in number of copy number aberrations between tumors. A subset of nonhereditary Rbs turned out to be the most genomic unstable, while especially very young patients with hereditary Rb display stable genomes. Established Rb copy number aberrations, including gain of chromosome arm 1q and loss of chromosome arm 16q, turned out to be preferentially associated with the nonhereditary Rbs with later age of diagnosis. In contrast, copy number neutral loss of heterozygosity was detected mainly on chromosome 13, where RB1 resides, irrespective of hereditary status or age. Focal amplifications and deletions and copy number neutral loss of heterozygosity besides chromosome 13 appear to be rare events in retinoblastoma. © 2013 Wiley Periodicals, Inc. 相似文献