مقاله انگلیسی رایگان در مورد نقش جهش های ژن pncA W68R و W68G در مقاومت پری زینامید – وایلی 2017

 

مشخصات مقاله
انتشار مقاله سال 2017
تعداد صفحات مقاله انگلیسی 36 صفحه
هزینه دانلود مقاله انگلیسی رایگان میباشد.
منتشر شده در نشریه وایلی
نوع مقاله ISI
عنوان انگلیسی مقاله Role of pncA gene mutations W68R and W68G in Pyrazinamide resistance
ترجمه عنوان مقاله نقش جهش های ژن pncA W68R و W68G در مقاومت پری زینامید
فرمت مقاله انگلیسی  PDF
رشته های مرتبط زیست شناسی
گرایش های مرتبط علوم سلولی و مولکولی
مجله مجله بیوشیمی سلولی – Journal of Cellular Biochemistry
دانشگاه School of Biotechnology – Jawaharlal Nehru University – New Delhi
کلمات کلیدی میکروسکوپیک توبرکلوزیس، اتصال، شبیه سازی دینامیک مولکولی، پریزینامیداز، مقاومت PZA
کلمات کلیدی انگلیسی Mycobacterium tuberculosis, docking, molecular dynamics simulation, pyrazinamidase, PZA resistance
کد محصول E5969
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Introduction

Among humans, Tuberculosis (TB) which, spreads by aerosols is one of the leading cause of infection related deaths. Tuberculosis (TB) manifests upon infection by its bacterial causative agent, Mycobacterium tuberculosis (Mtb) [Organization, 2015]. As on 2015, 10.4 million individuals were infected with TB which led to the death of 1.5 million individuals around the world. One of the major reasons for this alarming rise in spread of TB is due to the emergence of drug resistant strains [Stehr et al., 2015]. In 2015, > 4.7 million new cases of Multi drugresistant tuberculosis (MDR-TB) were detected which, resulted in about 250000 deaths [Organization, 2016]. Moreover, 9.7% people with MDR-TB were reported to have Extensively drug-resistant tuberculosis (XDR-TB) [Organization, 2015]. This burgeoning phenomenon of antibiotic resistance is believed to be the result of several point mutations in specific key resistance genes [Chan et al., 2007]. Thereby there is an urgent need to combat this disease. The World Health Organization recommended protocol of treatment for new TB patients is DOTS (directly observed treatment, short-course), which is a six months course involving four first-line drugs; isoniazid, rifampin, pyrazinamide and ethambutol [Organization, 2015]. However, this therapy is marred by the poor efficacy of first line anti-tubercular drugs and high toxic side effects of second line drugs [Dooley et al., 2012]. It is due to the fact that Mtb is impervious to numerous anti-toxins produced by other bacteria due to the presence of highly hydrophobic cell envelope acting as a permeability barrier [Cole et al., 1998]. Pyrazinamide (PZA), a derivative of nicotinamide, has the unique ability to kill persistent bacilli which resides in the low pH environment of the host macrophages, hence reducing the period of chemotherapy [Gu et al., 2015; Mitchison, 1985]. Nicotinamide was reported to have activity against Mycobacterium in animal models by Chorine in 1945 [Ryan, 1993]. PZA was identified as an active analog of nicotinamide by direct testing on a mouse model of TB infection [Malone et al., 1952; McKenzie et al., 1948; Solotorovsky et al., 1952]. Its role as an anti-tuberculosis drug was discovered in 1952 [Yeager et al., 1952]. In 1996, it was confirmed that pncA gene was strongly associated with intrinsic PZA resistance in Mtb [Scorpio and Zhang, 1996] and in 1997 it was found that mutations in pncA gene constituted the significant reason behind PZA resistance [Scorpio and Zhang, 1996].