Digital Repository for Department of Histology

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)

Evidence based medicine, clinical reasoning, self-directed critical thinking and problem solving approach are mandatory in order to acquire better retained and usable knowledge in a clinical context through student-centered teaching, and team interpersonal skills promotion. Adoption of new and high standards methods of teaching such as 3D models [24,25], along with updated responsive teaching materials are mandatory and represent pre-requirements for accredited medical schools
Aisha Nasef, Mohamed A Al-Griw, Adel El Taguri(5-2020)

Exposure to chemicals has been shown to adversely affect CNS health in rodents and humans. The objective was to evaluate, in-vivo, the effects of trichloroethane (TCE), a ubiquitous environmental contaminant, on the integrity of neural cells. A group of albino mice was injected intraperitoneally twice weekly for three weeks with TCE (100 and 400 µg/kg). Animals were followed up for signs of toxicity and death. Alterations in neural tissues have also been investigated by histopathology The results showed a large number of degenerative neural cells (pyknosis of nuclei, DNA fragmentation, chromatin condensation) in the 100 and 400 µg/kg TCE-treated groups comparing to controls. Although there were no significant effect on the neural cell counts, the pattern of increased degenerative cells in TCE-treated groups was higher compared to controls. The results also showed that TCE led to a significant increase in the percent of degenerative neurons. There was also a significant reduction in the percent of neurons. These results correlated with the increase in the percent of glia. This study indicates that TCE exposure had detrimental impact on neural cells, and that neurons are more vulnerable to TCE than glia in this in-vivo mouse model.
Mohamed A. Al-Griw, Naser M. Salama, Soad A. Treesh, Lubna N. Algadi, Abdul hakim Elnfati(7-2015)

The present in vivo murine study was aimed to investigate the long-term effect of repeated administration of low-dose of the environmental toxicant trichloroethane (TCE) over three weeks on the spleen and peripheral blood cells, and the possible role of oxidative stress in TCE-induced toxicity. The results showed neither adverse clinical signs nor mortality on the TCE-treated mice. However, significant changes were noticed in the spleen of those animals. Grossly, the spleen of TCE-treated group was congested and enlarged (splenomegaly). Histpathologically, the splenic tissues of TCE-treated mice showed signs of toxicity as highly activated germinal centers of the white pulp with minimal apoptotic reaction as well as a prominent megakarocytosis and infiltration of the red pulp by comparatively increased number of eosinophiIs and mature lymphocytes were detected. In addition, lymphocyte numbers were decreased in peripheral blood as well as basophils. In contrast, there was an increase in monocyte numbers in the peripheral circulation. In addition, lipid peroxidation/ malondialdehyde formation, a biomarker of oxidative stress, was significantly induced by TCE treatment in the sera and spleen of mice, suggesting an overall increase in oxidative stress. These results provide further support to a role of oxidative stress in TCE-induced cell death, which could result in an impaired spleen function. This study concludes that attenuation of TCE-induced splenic damage in mice provides an approach for preventive and/or therapeutic strategies
Massaud S. Maamar, Mohamed A. Al-Griw, Rabia O. Al-Ghazeer, Seham A. Al-Azreg, Naser M. Salama, Emad M. Bennour(3-2016)

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)

Mutations in the TAL1 (T-cell acute leukemia 1) gene were recently described in patients with T-cell acute lymphoblastic leukaemia (T-ALL) and in those with lymphoblastic T-cell non-Hodgkin’s lymphoma (T-NHL). The purpose of this pilot study was to assess the prevalence of mutations in TAL1 gene in T-ALL and TNHL. DNA samples from 15 unrelated healthy controls, 20 T-ALL patients, and 10 T-NHL patients were analyzed using DNA-PCR and direct DNA sequencing to identify sequence genetic variations in TAL1 gene (exons 2 and 3). TAL1 exon 2 mutations were identified in 7.7% adult and 12.5% adolescent T-ALL patients analyzed. TAL1 exon 2 mutations were detected in 16.7% of the adult TNHL patients analyzed. Sequencing of TAL1 exon 3 showed no sequence variation for the T-ALL and T-NHL cancer patients analyzed. No sex difference where observed in the incidences of TAL1 exons 2 mutations between T-ALL and T-NHL patients with and without TAL1 mutations. TAL1 exon 2 missense and frame-shift mutations were present in 44.4% (4/9) and 55.6% (5/9) of T-ALL patients, respectively. However, the frame-shift and missense mutations in the T-NHL patients accounted for, where respectively, 60% (3/5) and 40% (4/5) of all TAL1 exon 2 mutations. Comparing the clinical features showed that there are no differences in PLT and WBC counts as well as the average age between T-ALL and T-NHL patients with and without TAL1 mutations. Overall, these findings indicate that TAL1 mutations are too rare to be of clinical relevance, and do not seem to be significantly associated with the increased T-ALL and T-NHL susceptibility, implying different pathways with respect to TAL1 genetic polymorphisms as a risk factor for T-ALL and T-NHL at least in this population of Libyans.
Amal E. Elarifi, Othman A. El-Ansari, Mohamed A. Al-Griw(12-2016)

Alterations in genes encoding the xenobiotic-metabolizing enzymes contribute to the variability in susceptibility to various cancers. In this study, we assessed the possible association between the CYP1A1 variants and lung cancer (LC) risk in a population of Libyan males. For this study, we selected 20 unrelated healthy controls and 32 patients with LC. DNA samples from the controls and patients were screened by DNA-PCR and direct DNA sequence analysis to search for genetic sequence variations in CYP1A1 gene (exon 7 and 3’ non-coding region). CYP1A1 mutations were identified in 11.5 % adult subjects and cases analyzed, and all were males. Overall, 11 CYP1A1 mutations were documented in this study implicating exon 7 and 3’ non-coding region. Nonsense, missense, and frame-shift mutations accounted for, respectively, 27.3 %, 63.6 % and 9.1 % of all CYP1A1 mutations. Three missense mutations namely CYP1A1*2B/m2 (rs1048943), CYP1A1*4/m4 (rs1799814), and CYP1A1*2A/m1 (rs4646903) have already been reported. The remaining mutations have not been described previously. We observed two apparently heterozygous carriers of mutation CYP1A1*2B/m2 (CYP1A1 4889A/G [642Ile/Val] genotype) in control group. We also observed two heterozygotic genotypes one containing mutation m4 (CYP1A1 4887C/A [461Thr/Asp]) and another containing mutation m1 (6235T/C) in cancer group. The mutations m2, m4, and m1 accounted for, respectively, 18.2 %, 9.1 % and 9.1 % of all CYP1A1 mutations. Comparing the clinical features showed that PLT and WBC counts were lower in CYP1A1 mutant than in CYP1A1 wild type, but they have not reached statistical significant (P > 0.05). The average age of CYP1A1 mutant was lower than in CYP1A1 wild type. Overall, these findings suggest that genetic alterations in the metabolic gene CYP1A1 are too rare to be of clinical relevance in this study, implying different pathways for the LC risk with respect to CYP1A1 polymorphisms as a risk factor for LC at least in this study.
Najah A. Fares, Othman A. El-Ansari, Mohamed A. Al-Griw(4-2017)

Exposures to a wide variety of environmental substances are negatively associated with many biological cell systems both in humans and rodents. Trichloroethane (TCE), a ubiquitous environmental toxicant, is used in large quantities as a dissolvent, metal degreaser, chemical intermediate, and component of consumer products. This increases the likelihood of human exposure to these compounds through dermal, inhalation and oral routes. The present in vivo study was aimed to investigate the possible cellular and molecular etiology of liver abnormality induced by early exposure to TCE using a murine model. The results showed a significant increase in liver weight. Histopathological examination revealed a TCE-induced hepatotoxicity which appeared as heavily congested central vein and blood sinusoids as well as leukocytic infiltration. Mitotic figures and apoptotic changes such as chromatin condensation and nuclear fragments were also identified. Cell death analysis demonstrates hepatocellular apoptosis was evident in the treated mice compared to control. TCE was also found to induce oxidative stress as indicated by an increase in the levels of lipid peroxidation, an oxidative stress marker. There was also a significant decrease in the DNA content of the hepatocytes of the treated groups compared to control. Agarose gel electrophoresis also provided further biochemical evidence of apoptosis by showing internucleosomal DNA fragmentation in the liver cells, indicating oxidative stress as the cause of DNA damage. These results suggest the need for a complete risk assessment of any new chemical prior to its arrival into the consumer market.
Mohamed M. Al-Griw, Rabia O. Alghazeer, S. A. Al-Azreg, Emad M. Bennour(9-2016)