The present study was undertaken to correlate the immunohistochemical expression of Bcl-2 oncoprotein in buffalo’s adrenal gland in the young and old ages. Paraffin-embedded sections from the adrenal glands representing the young and old ages were immunostained for Bcl-2 oncoprotein. A higher percentage of Bcl-2 immunoreactivity was detected in the adrenal cortical cells of the buffaloes at young ages. The immunoreactivity was moderate in the adrenal cortical cells of the old ages. The degree of intensity was prominent in the zona reticularis than that of the other zones, while negative immunoreactivity in the cells of the adrenal medulla. In conclusion,the immunohistochemical expression of Bcl-2 oncoprotein in the young buffalo’s adrenal gland (antiapoptotic gene) was prominent than the old ages. So the incidence of apoptosis was prominent in the adrenal gland cortical cells of the old age than that the adrenal gland cortical cells of the young ages.

Parathion is an insecticide has been demonstrated to be a highly toxic compound for animals and humans. It has been used widely in agriculture and domestic. Many cases of acute poisoning have been reported over the past few decades when exposed to parathion. The present work was designed to evaluate the protective role of lycopene against renal histopathological and biochemical changes due to exposed to insecticide parathion. The animals were divided into four groups with six in each: Group I: served as control animals received saline, Group II: receive lycopene (10 mg/kg b.w) orally. Group III: received once daily methyle parathion at a dose of 0.28 mg/kg b.w. (1/50 LD50 oral dose). Group IV: receive once daily methyle parathion at a dose of 0.28 mg/kg b.w. plus lycopene (10 mg/kg b.w.). Histological examinations revealed that parathion caused glomerular atrophy, dilated renal tubules,haemorrhage, oedema and necrosis. Immunohistochemical localization of Bax for apoptosis was performed.Methyle parathion treated animals showed positive reaction to Bax in glomerulii and renal tubules as compared with controls. Methyle parathion treated animals showed also and increased in lipid peroxidation and decreased antioxidant enzyme, glutathione. Coa-dmnistration with lycopene decrease pathological changes, apoptosis, lipid peroxidation and increase antioxidant enzyme

A hypercholesterolemia diet has been associated with the hepatic and cardiac abnormalities and the pathological changes. The present work was designed to investigate the histological and immunohistochemical changes in the liver and heart of rabbits when fed high fat diet and the possible protective role of an antioxidant “taurine”. Twenty-four male white New Zealand rabbits were divided into four groups, 6 rabbits each. Group 1, served as a control, rabbits fed with a normal diet. Group 2,(taurine group), rabbits were given orally taurine (10 mg Kg-1 b.w/day) for 8 weeks. Group 3(hypercholesterolemic group), rabbits fed (2% cholesterol-enriched diet for 8 weeks. Group 4, rabbits fed 2% cholesterol-enriched diet plus taurine (10 mg Kg-1 b.w/day) orally for the same period.Histopathological examinations revealed that high cholesterol diet caused hepatic and myocardial tissue changes compared with rabbits fed with a normal diet. Including fatty degeneration,inflammations and necrosis of Hepatocytes and vacuolar degeneration, disorganization of myofibrils and necrosis of myocardial cells. Immunohistochemistry for caspase-3 for apoptosis were performed.Caspase-3 positive cells in the liver tissue and Caspase-3 positive area in myocardial tissue increased in high cholesterol diet group.Taurine markedly attenuate hypercholesterolemia-induced cardiac and hepatic histopathological changes in the cholesterol plus taurine group compared to the cholesterol group. Thus, the results suggest that taurine could play a beneficial role against hypercholesterolemia induced complications in the liver and heart of the rabbits

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Probabilistic seismic hazard analysis in terms of peak ground acceleration (PGA) and spectral acceleration (SA) values was assessed for the Egyptian territory. Eighty-eight potential seismic sources (for shallow- and intermediate-depth seismicity) in and around Egypt were identified and characterized based on an updated and unified earthquake catalogue spanning the time period from 2200 B.C. until 2013. Earthquake recurrence rates were computed, from both instrumental and historical data, for the defined seismic sources. Six well-known ground motion attenuation models were selected to predict the ground motion for the different tectonic environments in and around Egypt. Finally, a logic tree approach was followed, after a sensitivity analysis, to consider the epistemic uncertainty in different inputs (b-value, maximum expected magnitude and ground motion attenuation model). In the present study, we show the seismic hazard deaggregation results, in terms of distance and magnitude, for the most important cities in Egypt to help understanding the relative contributions of the different seismic sources. Seismic hazard deaggregation for PGA, 0.2, 1.0 and 2.0 s SA, for 10% probability of exceedance in 50 years (return period of 475 years), was computed in detail. The deaggregation graphs were drawn considering bins of 0.5 for magnitude and 25 km for distance. The mean and modal values of magnitude and distance, to identify the distribution of control earthquakes that contribute to exceedance of the considered SA level were also computed. In general, the results at most of the cities, indicate that the distance to the seismic sources which mostly contributes to the seismic hazard is mainly controlled by the nearby seismic sources (especially for PGA). However, the more distant events contribute more to the hazard for larger spectral periods (for 1.0 and 2.0 s SA). For instance, the control earthquake for Cairo has a moment magnitude (MW) values in the range 5.0-5.5 and a focal distance between 0 and 25 km for PGA, 0.2,and 1.0 s SA, whereas for 2.0 s the distance remains the same but the magnitude become 6.0-6.5. However, for Port Said (located along the Mediterranean Sea coast), values of 7.0-7.5 MW and 375-400 km for the control earthquake has been obtained for all spectral periods. A significant result of this type of work is that seismic hazard deaggregation provides useful data on the distance and magnitude of the contributing seismic sources to the hazard in a certain place, which can be applied to generate scenario earthquakes and select acceleration records for seismic design.

Probabilistic seismic hazard analysis in terms of peak ground acceleration (PGA) and spectral acceleration (SA) values was assessed for the Egyptian territory. Eighty-eight potential seismic sources (for shallow- and intermediate-depth seismicity) in and around Egypt were identified and characterized based on an updated and unified earthquake catalogue spanning the time period from 2200 B.C. until 2013. Earthquake recurrence rates were computed, from both instrumental and historical data, for the defined seismic sources. Six well-known ground motion attenuation models were selected to predict the ground motion for the different tectonic environments in and around Egypt. Finally, a logic tree approach was followed, after a sensitivity analysis, to consider the epistemic uncertainty in different inputs (b-value, maximum expected magnitude and ground motion attenuation model). In the present study, we show the seismic hazard deaggregation results, in terms of distance and magnitude, for the most important cities in Egypt to help understanding the relative contributions of the different seismic sources. Seismic hazard deaggregation for PGA, 0.2, 1.0 and 2.0 s SA, for 10% probability of exceedance in 50 years (return period of 475 years), was computed in detail. The deaggregation graphs were drawn considering bins of 0.5 for magnitude and 25 km for distance. The mean and modal values of magnitude and distance, to identify the distribution of control earthquakes that contribute to exceedance of the considered SA level were also computed. In general, the results at most of the cities, indicate that the distance to the seismic sources which mostly contributes to the seismic hazard is mainly controlled by the nearby seismic sources (especially for PGA). However, the more distant events contribute more to the hazard for larger spectral periods (for 1.0 and 2.0 s SA). For instance, the control earthquake for Cairo has a moment magnitude (MW) values in the range 5.0-5.5 and a focal distance between 0 and 25 km for PGA, 0.2,and 1.0 s SA, whereas for 2.0 s the distance remains the same but the magnitude become 6.0-6.5. However, for Port Said (located along the Mediterranean Sea coast), values of 7.0-7.5 MW and 375-400 km for the control earthquake has been obtained for all spectral periods. A significant result of this type of work is that seismic hazard deaggregation provides useful data on the distance and magnitude of the contributing seismic sources to the hazard in a certain place, which can be applied to generate scenario earthquakes and select acceleration records for seismic design.

Type 1 diabetes mellitus (T1D) is associated with increased type 1 interferon (IFN) levels and subsequent severe defects in lymphocyte function, which increase susceptibility to infections. The blockade of type 1 IFN receptor 1 (IFNAR1) in non-obese diabetic mice has been shown to delay T1D onset and decrease T1D incidence by enhancing spleen CD4+ T cells and restoring B cell function. However, the effect of type 1 IFN blockade during T1D on splenic CD8+ T cells has not previously been studied. Therefore, we investigated, for the first time, the effect of IFNAR1 blockade on the survival and architecture of spleen-homing CD8+ T cells in a streptozotocin-induced T1D mouse model. Three groups of mice were examined: a non-diabetic control group; a diabetic group; and a diabetic group treated with an anti-IFNAR1blocking antibody. We observed that T1D induction was accompanied by a marked destruction of β cells followed by a marked reduction in insulin levels and increased IFN-α and IFN-β levels in the diabetic group. The diabetic mice also exhibited many abnormal changes including an elevation in blood and spleen free radical (reactive oxygen species and nitric oxide) and pro-inflammatory cytokine (IL-6 and TNF-α) levels, a significant decrease in IL-7 levels, and subsequently, a significant decrease in the numbers of spleen-homing CD8+ T cells. This decrease in spleen-homing CD8+ T cells resulted from a marked reduction in the CCL21-mediated entry of CD8+ T cells into the spleen and from increased apoptosis due to a marked reduction in IL-7-mediated STAT5 and AKT phosphorylation. Interestingly, type 1 IFN signaling blockade in diabetic mice significantly restored the numbers of splenic CD8+ T cells by restoring free radical, pro-inflammatory cytokine and IL-7 levels. These effects subsequently rescued splenic CD8+ T cells from apoptosis through a mechanism that was dependent upon CCL21- and IL-7-mediated signaling. Our data suggest that type 1 IFN is an essential mediator of pathogenesis in T1D and that this role results from the negative effect of IFN signaling on the survival of splenic CD8+ T cells.