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Articles by Y. Qian
Total Records ( 2 ) for Y. Qian
  S. Wilhelm , S. Alshammary and Y. Qian
  This study was conducted under a dual Line Source Irrigation System (LSIS). Both LSIS covering 380 m2 (24 by 16 m) were laid out in a West-East direction and separated by a 15 m wide turf buffer zone. The LSIS in the east side received municipal potable water [Electrical Conductivity (EC) = 0.12 dS m-1]. The west LSIS received saline well water (EC = 3.0 dS m-1). Each LSIS was then equally divided into 12 plots in which Kentucky bluegrass and tall fescue were seeded in strips along the irrigation gradients. Data were collected on turf establishment, soil salinity, soil pH and drought responses. Saline well water irrigation increased soil salinity, sodium adsorption ratio and pH. Salty well water irrigation dramatically reduced and delayed the germination of Kentucky bluegrass, whereas tall fescue germination and establishment were unaffected when compared with potable water irrigation. Grasses subjected to well water irrigation exhibited greater iron chlorosis. Under moderate drought conditions tall fescue survived drought conditions better and required less irrigation to maintain acceptable quality. However, under severe drought conditions when soil moisture was depleted in deep soil profile, tall fescue did not show advantages in drought resistance over Kentucky bluegrass.
  S Zhu , W Pan , P Shi , H Gao , F Zhao , X Song , Y Liu , L Zhao , X Li , Y Shi and Y. Qian
 

Interleukin 17 (IL-17) plays critical roles in the pathogenesis of various autoimmune diseases, including experimental autoimmune encephalomyelitis (EAE). How the signals triggered by this powerful inflammatory cytokine are controlled to avoid abnormal inflammatory responses is not well understood. In this study, we report that TRAF3 is a receptor proximal negative regulator of IL-17 receptor (IL-17R) signaling. TRAF3 greatly suppressed IL-17–induced NF-B and mitogen-activated protein kinase activation and subsequent production of inflammatory cytokines and chemokines. Mechanistically, the binding of TRAF3 to IL-17R interfered with the formation of the receptor signaling activation complex IL-17R–Act1–TRAF6, resulting in suppression of downstream signaling. TRAF3 markedly inhibited IL-17–induced expression of inflammatory cytokine and chemokine genes in vivo and consequently delayed the onset and greatly reduced the incidence and severity of EAE. Thus, TRAF3 is a negative regulator of IL-17R proximal signaling.

 
 
 
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