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Articles by Wenjie Xu
Total Records ( 2 ) for Wenjie Xu
  Wei Liu , Wenjie Xu , Dong Wang , Zongtian Liu and Xujie Zhang
  As the unit of human knowledge, event is used to describe all kinds of knowledge in the world. Action which is one of the main factors in event describes the changing processes of world states in a specific period of time. As we know, there are different states in different time and the main reason of states changes is caused by action. Therefore, it is necessary to embrace temporal information into the representation about action to describe these changes. In this study, we first proposed a temporal description logic T-ALC, in which the temporal information as a constraint of instances was added to ABox. It provided a kind of decidable approach to deal with the states changes of objects in action. Then, we defined the syntax and semantics of action based on T-ALC. Especially, the semantics of action can be transformed into the changing processes of interpretations and the calculation of new interpretations and ABox were also given. Finally, several inference services of action in different time were studied.
  Chunyan Xu , Wenjie Xu , Amy E. Palmer and John C. Reed
  BI-1 (Bax inhibitor-1) is an evolutionarily conserved multitransmembrane protein that resides in the endoplasmic reticulum (ER) and that has documented cytoprotective functions in both animals and plants. Recent studies indicate that BI-1 shares in common with Bcl-2/Bax family proteins the ability to regulate the amounts of Ca2+ that can be released from the ER by agents, such as the ER-Ca2+-ATPase (SERCA) inhibitor thapsigargin (TG). Using an ER-targeted, Ca2+ indicator (cameleon), with characteristics optimized for measuring ER Ca2+ ([Ca2+]er), we studied the effects of BI-1 on [Ca2+]er in resting and TG-treated cells. Similar to cells overexpressing antiapoptotic Bcl-2 or Bcl-XL, overexpression of BI-1 resulted in lower resting [Ca2+]er, with concomitantly less Ca2+ released into the cytosol upon stimulation by TG and with a higher rate of Ca2+ leakage from the ER. Co-expression of SERCA restored levels of [Ca2+]er to normal, showing opposing actions of the ER-Ca2+ATPase and BI-1 on ER Ca2+ homeostasis. Conversely, cells with deficient BI-1 have increased [Ca2+]er, and release more Ca2+ into the cytosol when challenged with TG. In BI-1-deficient cells, Bcl-XL fails to reduce [Ca2+]er, indicating that BI-1 functions downstream of Bcl-XL. In bax-/-bak-/- double knock-out cells, both BI-1 and Bcl-XL retained their ability to reduce [Ca2+]er, suggesting that BI-1 and Bcl-XL operate downstream of or parallel to Bax/Bak. The findings reveal a hierarchy of functional interactions of BI-1 with Bcl-2/Bax family proteins in regulating ER Ca2+ homeostasis.
 
 
 
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