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Articles by G. Das
Total Records ( 2 ) for G. Das
  Gautam Patra , M. Ayub Ali , Kh. Victoria Chanu , L. Jonathan , L.K. Joy , M. Prava , R. Ravindran , G. Das and L. Inaotombi Devi
  The present investigation was undertaken to evaluate histo-pathological, haemotological and biochemical changes in broiler chicken naturally infected with Eimeria tenella. A Polymerase Chain Reaction (PCR) based assay was also done for the detection, identification and differentiation of pathogenic species of Eimeria in poultry. Post mortem examination revealed petechial haemorrhages, oedema, necrosis and sloughing of caecal epithelium. Histopathological evidence showed leakage of blood, oedema and necrosis. Haemotological studies revealed that coccidial infection caused significant decrease in the value of haemoglobin and Packed Cell Volume (PCV). The value of Mean Corpuscular Volume (MCV) and Mean Corpuscular Haemoglobin Concentration (MCHC) revealed that caecal coccidiosis resulted in macrocytic hypochromic anaemia. Biochemical serum analysis of coccidial infected chicken showed a significant increase in level of glucose, Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) while there was a significant decrease in the level of alkaline phosphatase (SAP) and cholesterol. In PCR using specific primers for E. tenella only the ITS 1 regions of ribosomal DNA (rDNA) could be amplified.
  J Das , G Ren , L Zhang , A. I Roberts , X Zhao , A. L.M Bothwell , L Van Kaer , Y Shi and G. Das
 

Interleukin (IL)-17–producing T helper (Th17) cells play a critical role in the pathophysiology of several autoimmune disorders. The differentiation of Th17 cells requires the simultaneous presence of an unusual combination of cytokines: IL-6, a proinflammatory cytokine, and transforming growth factor (TGF) β, an antiinflammatory cytokine. However, the molecular mechanisms by which TGF-β exerts its effects on Th17 cell differentiation remain elusive. We report that TGF-β does not directly promote Th17 cell differentiation but instead acts indirectly by blocking expression of the transcription factors signal transducer and activator of transcription (STAT) 4 and GATA-3, thus preventing Th1 and Th2 cell differentiation. In contrast, TGF-β had no effect on the expression of retinoic acid receptor–related orphan nuclear receptor t, a Th17-specific transcription factor. Interestingly, in Stat-6–/–T-bet–/– mice, which are unable to generate Th1 and Th2 cells, IL-6 alone was sufficient to induce robust differentiation of Th17 cells, whereas TGF-β had no effect, suggesting that TGF-β is dispensable for Th17 cell development. Consequently, BALB/c Stat-6–/–T-bet–/– mice, but not wild-type BALB/c mice, were highly susceptible to the development of experimental autoimmune encephalomyelitis, which could be blocked by anti–IL-17 antibodies but not by anti–TGF-β antibodies. Collectively, these data provide evidence that TGF-β is not directly required for the molecular orchestration of Th17 cell differentiation.

 
 
 
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