Abstract Introduction: Extended-spectrum β-lactamases (ESBLs), AmpC type, carbapenem resistant Enterobacteriaceae (CRE), are important mechanisms of resistance among Enterobacteriaceae. The aim of this study was to investigate the prevalence of ESBL, AmpC and CRE among Enterobacteriaceae isolates recovered from pediatric patients in Tripoli, Libya. Methods: This cross-sectional study was carried out in Tripoli Children Hospital (TCH), a total of 915 Gram negative bacteria isolates were evaluated for susceptibility to a panel of antimicrobials and were analyzed phenotypically for the ESBL, AmpC type and CRE using chromagen media, E-test and combination disc test. Results: The predominant organisms were Escherichia coli (56.8%) and Klebsiella spp. (21.4%). The overall prevalence of ESBL producing Enterobacteriaceae was 24.5% (224/915). Out of 224, Enterobacteriaceae proved ESBL producer, Klebsiella spp. (54%) and E. coli (34.4%) were the leading ESBL producers. ESBL-producers were more often resistant to major classes of antibiotics compared with non-ESBL producers, significantly high resistance rates (P < 0.001) were observed for ceftriaxone, cefepime, and ceftazidime (87.5 - 95.9%) among ESBL producers compared to non-ESBL producers (7.2 - 13.5%). MDR was documented for 50/224 (22.3%) of ESBL producers and was significantly higher (P < 0.0001) among ESBLs compared with non-ESBL producer isolates. Phenotypic detection of AmpC revealed 60/915 (6.6%) isolates as potential AmpC β-lactamase producers, E. coli exhibited a lower level of AmpC (8.3%) compared with Klebsiella spp. (56.6%). The overall prevalence of CRE was 9% (83/915). Carbapenemase-producing organisms in this study were as follows: Klebsiella spp. (44.6%); Acinetobacter spp. (24%); Pseudomonas spp. (9.6%). Conclusion: This study revealed that the prevalence of ESBL, AmpC, CRE and MDR Enterobacteriaceae isolates in Children hospital was within acceptable frequency. arabic 11 English 91
Abdulaziz Zorgani, Abdulla Bashein, (1-2017)

Environmental toxicants such as chemicals, heavy metals, and pesticides have been shown to promote transgenerational inheritance of abnormal phenotypes and/or diseases to multiple subsequent generations following parental and/ or ancestral exposures. This study was designed to examine the potential transgenerational action of the environmental toxicant trichloroethane (TCE) on transmission of liver abnormality, and to elucidate the molecular etiology of hepatocyte cell damage. A total of thirty two healthy immature female albino mice were randomly divided into three equal groups as follows: a sham group, which did not receive any treatment; a vehicle group, which received corn oil alone, and TCE treated group (3 weeks, 100 μg/kg i.p., every 4th day). The F0 and F1 generation control and TCE populations were sacrificed at the age of four months, and various abnormalities histpathologically investigated. Cell death and oxidative stress indices were also measured. The present study provides experimental evidence for the inheritance of environmentally induced liver abnormalities in mice. The results of this study show that exposure to the TCE promoted adult onset liver abnormalities in F0 female mice as well as unexposed F1 generation offspring. It is the first study to report a transgenerational liver abnormalities in the F1 generation mice through maternal line prior to gestation. This finding was based on careful evaluation of liver histopathological abnormalities, apoptosis of hepatocytes, and measurements of oxidative stress biomarkers (lipid peroxidation, protein carbonylation, and nitric oxide) in control and TCE populations. There was an increase in liver histopathological abnormalities, cell death, and oxidative lipid damage in F0 and F1 hepatic tissues of TCE treated group. In conclusion, this study showed that the biological and health impacts of environmental toxicant TCE do not end in maternal adults, but are passed on to offspring generations. Hence, linking observed liver abnormality in the offspring to environmental exposure of their parental line. This study also illustrated that oxidative stress and apoptosis appear to be a molecular component of the hepatocyte cell injury.
Mohamed A. Al-Griw , Soad A. Treesh, Rabia O. Alghazeer, Sassia O. Regeai (7-2017)

Introduction: Chronic granulomatous disease (CGD) is a rare inherited primary immune deficiency disease with prevalence of 1 in 250,000 worldwide. It is caused by mutations in the genes that encode the NADPH oxidase enzyme components responsible for the production of super oxide and other free radicals. These mutations lead to the absence or decrease of the microbicidal activity of the phagocytic cells. arabic 10 English 72
Muna Hamed Othman Elramli, Ahmed Zaid(1-2015)