قسم الكيمياء الحيوية

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حول قسم الكيمياء الحيوية

حقائق حول قسم الكيمياء الحيوية

نفتخر بما نقدمه للمجتمع والعالم

30

المنشورات العلمية

6

هيئة التدريس

0

الطلبة

0

الخريجون

من يعمل بـقسم الكيمياء الحيوية

يوجد بـقسم الكيمياء الحيوية أكثر من 6 عضو هيئة تدريس

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أ.د. عبدالله مسعود بشين بشين

عبدالله بشين هو احد اعضاء هيئة التدريس بقسم الكيمياء الحيوية بكلية الطب البشري. يعمل السيد عبدالله بشين بجامعة طرابلس كـأستاذ منذ 2007-04-15 وله العديد من المنشورات العلمية في مجال تخصصه

منشورات مختارة

بعض المنشورات التي تم نشرها في قسم الكيمياء الحيوية

Co-Occurrence of Plasmid-Mediated AmpC β-Lactamase Activity Among Klebsiella pneumoniae and Escherichia Coli

Introduction: Extended-spectrum β-lactamases (ESBLs), including the AmpC type, are important mechanisms of resistance among Klebsiella pneumoniae and Escherichia coli isolates. Objective: The aim of the study was to investigate the occurrence of AmpC-type β-lactamase producers isolated from two hospitals in Tripoli, Libya. Methods: All clinical isolates (76 K. pneumoniae and 75 E. coli) collected over two years (2013-2014) were evaluated for susceptibility to a panel of antimicrobials and were analyzed phenotypically for the ESBL and AmpC phenotype using E-test and ESBL and AmpC screen disc test. Both ESBL and AmpC-positive isolates were then screened for the presence of genes encoding plasmid-mediated AmpC β-lactamases by polymerase chain reaction (PCR). Results: Of the K. pneumoniae and E. coli tested, 75% and 16% were resistant to gentamicin, 74% and 1.3% to imipenem, 71% and 12% to cefoxitin, 80% and 12% to cefepime, 69% and 22.6% to ciprofloxacin, respectively. None of the E. coli isolates were multidrug resistant compared with K. pneumoniae (65.8%). K. pneumoniae ESBL producers were significantly higher (85.5%) compared with (17.3%) E. coli isolates (P
Abdulaziz Zorgani, Abdulla Bashein(1-2017)
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Development of hydrolysis probe real-time polymerase chain reaction and high-resolution melting analysis protocols for screening of e280k and c.1055del.g mutations in phenylalanine hydroxylase gene

Background: Phenylketonuria (PKU) is one of the most common inborn errors of amino acids metabolism. It is an autosomal recessive disease that is caused by mutations in phenylalanine hydroxylase (PAH) gene. In the North Africa and Eastern Mediterranean region, E280K missense mutation and c.1055del.G frameshift mutation in PAH gene are one of the most common pathogenic mutations seen in PKU patients. Materials and Methods: In this study, we developed molecular protocols for rapid screening of the PKU patients for these two mutations. These protocols are based on hydrolysis probe real-time polymerase chain reaction technique using allele-specific probes labeled with 6-carboxyfluorescein (FAM) for wild-type (WT) and hexachloro-6-carboxyfluorescein (HEX) for mutant genotypes and Black Hole Quencher 1 as a quencher and high-resolution melting analysis using EvaGreen saturating dye. Results: There was complete accordance between the developed protocols in differentiating genotypes and they proved to be rapid, sensitive, and efficient for the detection and differentiation between WT, mutant, and heterozygous genotypes of the E280K and c.1055del.G mutations. Conclusions: These protocols allow easy molecular screening of the mutations studied among the families of affected people, especially for premarital screening. arabic 27 English 170
Abdulla Bashein(1-2017)
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Gene inactivation of proprotein convertase subtilisin/kexin type 9 reduces atherosclerosis in mice

Background— The proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes independently of its enzymatic activity the degradation of the low-density lipoprotein (LDL) receptor. PCSK9 gain of function in humans leads to autosomal dominant hypercholesterolemia, whereas the absence of functional PCSK9 results in ≈7-fold lower levels of LDL cholesterol. This suggests that lowering PCSK9 may protect against atherosclerosis. Methods and Results— We investigated the role of PCSK9 in atherosclerosis in C57BL/6 wild-type (WT), apolipoprotein E–deficient, and LDL receptor–deficient mouse models. Circulating cholesterol levels, fast protein liquid chromatography profiles, aortic cholesteryl esters (CE), and plaque sizes were determined. Intima-media thicknesses were measured by ultrasound biomicroscopy. First, mice expressing null (knockout [KO]), normal (WT), or high (transgenic [Tg]) levels of PCSK9 … arabic 12 English 86
Maxime Denis, Ahmed Zaid(1-2012)
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