Adult ; Biomarkers, Tumor ; metabolism ; Calbindin 2 ; Female ; Follow-Up Studies ; Humans ; Mesothelioma ; metabolism ; pathology ; surgery ; Mucin-1 ; metabolism ; Peritoneal Neoplasms ; metabolism ; pathology ; surgery ; S100 Calcium Binding Protein G ; metabolism

Child ; Child, Preschool ; Humans ; Hypersensitivity, Immediate ; prevention & control ; Infant ; Primary Prevention

Communicable Diseases ; Disease Outbreaks ; Humans ; Infection Control ; Science

Anti-Asthmatic Agents ; therapeutic use ; Asthma ; diagnosis ; drug therapy ; Emphysema ; Female ; Humans ; Male

Asthma ; diagnosis ; therapy ; Child ; Chronic Disease ; Cough ; diagnosis ; therapy ; Humans

Asthma ; diagnosis ; therapy ; Child ; Humans

laboratorian should understand and evaluate them correctly.

A large number of laboratory and clinical researches have indicated that the occurrence of restenosis after percutaneous transluminal angioplasty is mainly related to the following factors: the inflammatory reaction, the injury of vascular wall, the aggregation of platelet, the formation of thrombus, the hyperplasia of vascular endotheliocyte, etc. The corresponding parameters related to the above mentioned factors can be regarded as the clinical predictors of restenosis after pereutaneous transluminal angioplasty. This paper aims to make a summarization of some kinds of clinical predictors which are related to inflammation.

A large number of laboratory and clinical researches have indicated that the occurrence of restenosis after percutaneous transluminal angioplasty is mainly related to the following factors: the inflammatory reaction,the injury of vascular wall,the aggregation of platelet,the formation of thrombus,the hyperplasia of vascular endotheliocyte,etc.The corresponding parameters related to the above mentioned factors can be regarded as the clinical predictors of restenosis after percutaneous transluminal angioplasty.This paper aims to make a summarization of some kinds of clinical predictors which are related to inflammation.

MAPKKK (MEKK1 or ASK1)/MAPKK (SEK1 or MKK7)/JNK signal cascade is an important pathway which mediates apoptosis. MAPK phosphotase can deactivate JNK by dephosphorylation of JNK.The interaction between JNK and c-Jun can also be negatively regulated by NO through S-nitrosylation. SGK1 or Akt can result in deactivation of SEK1 through its phosphorylation at the Ser78 site.The c-FLIPL can block this cascade through binding with MKK7.GST Mu1-1 interferes and suppresses MEKK1-mediated apoptosis. GST Pi 1-1 and TRX have a dose-dependent inhibitory effect on ASK1 through forming protein complex. The deactivation of JNK can enhance drug resistance of tumor cells and counteract the injury from a wide variety of stimulus. Here,how these proteins induce deactivation of the pathway and mediate anti-apoptosis has been discussed.