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Articles by Younes Anzabi
Total Records ( 2 ) for Younes Anzabi
  Yousef Doustar , Daryoush Mohajeri , Younes Anzabi and Mehrdad Nazeri
  Influenza virus produces cell death in animals and human. Since cell death can be caused by either necrosis or apoptosis. We investigated the types of cell death that occur in chickens infected with avian influenza virus, A/chicken/Iran/772/2000(H9N2). In experimental study 60 SPF chickens at 3 weeks old were divided to two groups. The first group was infected with 107.5 EID50 titer of the virus intranasaly and the second group was treated with saline normal. Following 72 hrs, renal tissues were collected and fixed in 10% formalin solution. The prepared microscopic sections with the thickness of 5-6 micron were stained using TUNEL method. In comparison to the control group, there were significant mean difference of apoptotic cells in renal tubular cells of the infected group (p<0.005). We demonstrated that A/chicken/Iran/772/2000 (H9N2) is able to induce apoptosis in renal tubular cells.
  Yousef Doustar , Younes Anzabi , Amirreza Ebadi and Behbood Jafari
  Influenza is a viral disease which has been known in 1901AD in 1955, a kind of influenza virus was known as a factor caused disease that later on called avian plague because of high rate mortality. In the present study, the sub-type H9N2 of avian influenza virus (obtained from Razi Serum Producing and Research Center) which was cloned two times in embryonic eggs was inoculated to the SPF (Valo, Lohman, Germany) at their 3rd week by nasal drops: At first, SPF chickens were divided to 2 groups of 10 subjects; a group as a treatment group and another one as a control group. Then treatment group was infected by H9N2 sub-type of influenza virus with dosage of 107.5 EID50. The control group obtained normal saline serum nasally equal to the inoculated viral solution volume. In histopathological studies of lung and pleura of treated chicks with H9N2 sub-type influenza virus, propagated pneumonia which accompanies hyperemia and severs hemorrhage was observed in to allele and pleurisy sacs. In microscopic view, there is sever hyperemia and hemorrhage in allelic sacs, edama infiltration of fibrin and inflammatory cells, especially heterophylus in pulmonary' tissue inter-space. In the present study, the apoptosis of primary bronchial cells was observable in some cases which demonstrate significant changes compared with control group. Probably, the expression of apoptosis induction channel which has been discussed in Brydon's studies is a suitable justification for these changes. So, it must be noted that there are various channels in occurrence of cell death following infection by influenza virus and knowing these channels needs extensive studies.
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