The aim of this study was to provide an overview of the risk factors for acute myocardial infarction in patients attending Tripoli Medical Centre, Libya. Records were reviewed for 622 patients with a mean age of 58.3 (SD 12.9) years. Diabetes mellitus (48.2%), hypertension (35.7%) and smoking (50.6%) were among the risk factors reported. There were 110 patients (17.7%) who died during hospitalization, mainly suffering cardiogenic shock (48.0%). The rate of use of thrombolytic therapy was low in patients who were female (40.4% versus 58.4% for males), older age (31.6% for those > 85 years versus 63.3% for patients < 55 years), diabetics (45.3% versus 62.0% for non-diabetic patients) and hypertensives (47.3% versus 57.8% for non-hypertensive patients). Prevention strategies should be implemented in order to improve the long-term prognosis and decrease overall morbidity and mortality from coronary artery disease in Libyan patients. arabic 20 English 112
Hawa Juma El-Shareif(4-2012)

Preterm infants have a high risk of neonatal white matter injury (WMI). WMI leads to reduced myelination, inflammation, and clinical neurodevelopmental deficits for which there are no effective treatments. Ionotropic glutamate receptor (iGluR) induced excitotoxicity contributes to oligodendrocyte (OL) lineage cell loss and demyelination in brain models of neonatal and adult WMI. Here, we hypothesized that simulated ischemia (oxygen‑glucose deprivation) damages white matter via activation of iGluR signaling, and that iGluR inhibition shortly after WMI could mitigate OL loss, enhance myelination, and suppress inflammation in an ex vivo cerebellar slice model of developing WMI. Inhibition of iGluR signaling by a combined block of AMPA and NMDA receptors, shortly after simulated ischemia, restored myelination, reduced apoptotic OLs, and enhanced OL precursor cell proliferation and maturation as well as upregulated expression of transcription factors regulating OL development and remyelination. Our findings demonstrate that iGluR inhibition post‑injury alleviates OL lineage cell loss and inflammation and promotes myelination upon developing WMI. The findings may help to develop therapeutic interventions for the WMI treatment.
Mohamed A. Al-Griw, Michael G. Salter, Ian C. Wood(1-2021)

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)