Aim– This paper aims to review the existing literature relevant to the subject of ISO/IEC 17025 within Arabic countries and Libyan Research Centres Laboratories (LRCL), especially to the Critical Success Factors (CSFs) that effect the implementation of ISO/IEC 17025 standards. Therefore, a review of the literature revealed a major gap in studies in this area of quality standards for testing and calibration laboratories. Methodology– The aspects listed were based on a review of the literature. This paper summaries the key findings result within LRCL using SWOT and Template analysis to analyse the data collected from existing literature and LRCL data. Findings –The findings revealed that despite some organisations have faced challenges undertaking ISO/IEC 17025 implementations, many others have enjoyed the benefits that the systems have brought to the organisations. Outcomes of the research are important for Arabic and Libyan organisations implementing ISO/IEC 17025 systems and for consulting companies assisting with ISO/IEC 17025 implementation. The distribution of the current study results will lead to knowledge transfer and help organisations, among Arabic and developing countries including Libya, in the process of achieving standardisation. Originality, Value – The novelty of this research paper stems from the realisation of critical factors determining a successful implementation of ISO/IEC 17025 within research centers and Laboratories in Arabic countries and LRCL. The originality and value of this research paper is to fill the gap in knowledge in this area, which is explicit to the Arabic countries and Libya in particular. In addition, it contributes to the literature and professional practice by offering new insights into the CSFs for the implementation of ISO/IEC 17025 in Arabic countries and LRCL.
Anwar Salih Ali Al-mijrab, Maged Elmabruk Elgharib, Mohamed A. Al-Griw(5-2019)

Ischaemic injury during brain development correlates with long-term neurological problems resulting in part from oligodendrocytes (OL) damage and a loss of appropriate myelination. The molecular and cellular mechanisms responsible remain partially understood and there is no effective clinical treatment. Here we develop and characterise an ex-vivo slice culture ischaemia model to elucidate the cellular mechanisms to aid the search for therapeutic interventions. Cerebellar slices from 7 day-old rats were cultured for 10 days and their developmental profile in culture and their response to oxygen-glucose deprivation (OGD) was assessed. During the culture period development of white matter progressed as in-vivo, the numbers of oligodendrocyte precursor cells (OPC) decreased and the numbers of mature OLs increased and there was extensive myelination of axons as judged by colocalisation of myelin basic protein and neurofilament. Cultured slices were exposed to a short period of OGD at 7 days in-vitro and reperfused to mimic in-vivo conditions. Twenty minutes of OGD was found to result in significant injury as judged by a 58.6% reduction in cell viability 3 days post-injury. Treatment of cultures with OGD resulted in a loss of OLs and a loss of myelination of axons. In summary we have developed a paradigm for studying the damage to OLs and loss of myelination associated with ischaemic periods during development which should facilitate the search for understanding the mechanisms responsible and identifying potential therapeutic interventions.
Mohamed A M Al Griw , Mohamed A. Al-Griw, Ian C. Wood, Michael G. Salter(11-2017)

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)