To determine the effect of different doses of Salmonella enteritidis on immunocompetent cells, the thymus, bursa of Fabricius, and peripheral blood were examined. One-day-old chickens were orally infected with 2 × 102CFU/ml (low dose) and 2 × 108 CFU/ml(high dose) of S. enteritidis PT4. Subsets of T lymphocytes (CD3, CD4, and CD8), and BU1b cells using an indirect immunofluorescent method and flow cytometry were analysed on days 7, 10, 14, 21, and 27 postinoculation (dpi). The actual number of lymphocytes in the peripheral blood showed a significant increase in the low dose group (P < 0.05) on day 21 pi, and in the high dose group on day 27 pi (P< 0.001) compared to controls. The increase of CD3+, CD4+, and CD8+ T cells was observed in both infected groups compared to the controls from day 14 pi, significant on day 21 pi (P < 0.05) in the high dose group. The subpopulation of CD8+ was higher also on day 27 pi (P < 0.01) compared with the values of the control group. The subpopulation of BU1b+ B cells in both infected groups showed higher values, but without significant differences from controls. The thymus T lymphocytes showed a significant decline in CD3+ T cells on day 7 pi, whereas CD4+ T cells were significantly (P < 0.05) increased on day 7 pi in both infected groups. The bursal lymphocytes showed a decrease in BU1b+ B cells in both infected groups compared with the control group, significant in the high dose group on day 21 pi (P < 0.05). These results indicate that S. enteritidis infection induced the changes in immunocompetent cells, included cellular and humoral immune response. Salmonella infection accelerated the maturation and differentiation of thymus T cells in the first phase of infection, what was secondarily reflected by increased number of studied T lymphocyte subpopulations in the peripheral blood from day 14 to 27 after infection. Similarly, it appears that the activation of B cells in bursa of Fabricius caused the decrease number of bursal B lymphocytes and increased number of these cells in the peripheral blood from day 14 to 27 pi in both infected groups.
A. A. Asheg(3-2003)

The 11p15 region is organised into two independent imprinted domains controlled by imprinting control regions, which carry opposite germline imprints. Dysregulation of 11p15 genomic imprinting results in two human fetal growth disorders (Silver-Russell syndrome (SRS, MIM 180860) and Beckwith-Wiedemann syndrome (BWS, MIM 130650)) with opposite growth phenotypes. The mouse orthologous region on distal chromosome 7 (dist7) is well conserved in its organisation and its regulation. Targeted mutagenesis in mice has provided highly valuable clues in terms of the mechanisms involved in the regulation of genomic imprinting of the 11p15/dist7 imprinted region. On the other hand, the recent identification of unexpected genetic defects in BWS and SRS patients also brought new insights into the mechanisms of 11p15 imprinting regulation. However, some mouse models and human genetic defects show contradictions in term of growth phenotypes and parental transmission. In this review, we extensively analyse those various mouse and human models and more particularly models with mutations affecting the two imprinting centres, in order to improve our understanding of regulation of 11p15/dist7 genomic imprinting. arabic 21 English 117
Mansur Ennuri Moftah Shmela, C. F. Gicquel(1-2013)

Vibrio vulnificus, a zoonotic bacterial pathogen was isolated for the first time from kidneys of black scorpionfish Scorpaena porcus collected from the south Mediterranean basin (western coast of Tripoli, Libya) during the early summer of 2013. Fish exhibited typical signs of Vibriosis with furuncle like lesions, skin hemorrhages, fin rot and congested spleen. The abdominal cavity, liver, intestinal wall, and gonads were suffering from mild larval nematode infection. Interestingly, a huge portion of the kidney tissue was replaced with the anisakids nematode Anisakis pegreffi. This is considered the first report ofV. vulnificus / A. pegreffi in the Mediterranean black scorpionfish. The identities of the retrieved V. vulnificus isolates were confirmed using morpho-chemical and molecular tools. The research lead us to conclude that the deteriorated nature of the sewage polluted seawater at the western coast of Tripoli could have played a detrimental role in facilitating the invasion with the two diverse etiological agents (V. vulnificus and A.pegreffi) . We also hypothesize that V. vulnificus was lodged within nematode worms or at one of its life stages before invading fish intestine with consequent spread into other internal organs during its visceral larval migration stage.
Abdulwahab Kammon(5-2015)