000 | 03191cam a2200349 a 4500 | ||
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003 | EG-GiCUC | ||
005 | 20250223031708.0 | ||
008 | 170327s2016 ua h f m 000 0 eng d | ||
040 |
_aEG-GiCUC _beng _cEG-GiCUC |
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041 | 0 | _aeng | |
049 | _aDeposite | ||
097 | _aM.Sc | ||
099 | _aCai01.08.08.M.Sc.2016.Ma.E | ||
100 | 0 | _aMarwa Gamal Ahmed Ahmed Elhennawy | |
245 | 1 | 4 |
_aThe effect of Ü1-antitrypsin deficiency and bacterial loads on the efficacy of chronic obstructive pulmonary disease pharmacotherapy in Egyptian patients / _cMarwa Gamal Ahmed Elhennawy ; Supervised Yosri Akl , Nirmeen A. Sabry , Ahmed Sherif Attia |
246 | 1 | 5 | _aانتيتريبسين و الاحمال الجرثومية على فعالية المعالجة الدوائية لمرض الانسداد الرئوى المزمن فى المرضى المصريين {u٢١٦٠}Ü تأثير نقص |
260 |
_aCairo : _bMarwa Gamal Ahmed Ahmed Elhennawy , _c2016 |
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300 |
_a118 P. : _bfacsimiles ; _c25cm |
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502 | _aThesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmaceutics | ||
520 | _aChronic obstructive pulmonary disease (COPD) is associated with slowly progressive airflow obstruction. Chronic obstructive pulmonary disease (COPD) is caused by the combination of smoking, genetic susceptibility and exacerbated by infection. The genetic cause of COPD is {uF061}1-antitrypsin (AAT) deficiency where the gene encoding this protein shows genetic polymorphisms increasing the complexity of COPD predisposing factors. In addition, the development of pulmonary infections with different bacterial species is associated with exacerbation of COPD. How the different genotypes when combined with different types and loads of bacterial infections could affect the outcome of COPD and its responsiveness to therapy remain unclear. This is especially true regarding Egyptian patients where COPD is widespread and at the same time genotyping of these patients is almost absent. Screen for the AAT deficiency alleles phenotypically and genotypically and hence assess the contribution of two of the most common deficiencies (Pi*S and Pi*Z) and two of the rare deficiencies alleles that were predicted to be prevalent in Egypt (Pi*Mmalton and Pi*Q0Cairo) in the development of COPD in Egypt. Compare this study results to the results collected in North African countries to study the mutation pattern in North Africa. Determine the effects of AATD on the efficacy of COPD conventional pharmacotherapy. Fifty-nine subjects (29 controls and 30 COPD patients) were tested for genetic AATD and respiratory function. The bacterial loads were determined to the patients{u2019} group who were then given a long acting beta-agonist and corticosteroid inhaler for 6 months | ||
530 | _aIssued also as CD | ||
653 | 4 | _aAAT deficiency | |
653 | 4 | _aBacteria | |
653 | 4 | _aChronic obstructive pulmonary disease | |
700 | 0 |
_aAhmed Sherif Attia , _eSupervisor |
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700 | 0 |
_aNirmeen Ahmed Sabry , _eSupervisor |
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700 | 0 |
_aYosri Akl , _eSupervisor |
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856 | _uhttp://172.23.153.220/th.pdf | ||
905 |
_aNazla _eRevisor |
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905 |
_aSamia _eCataloger |
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942 |
_2ddc _cTH |
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999 |
_c60437 _d60437 |