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

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

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

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.

laboratorian should understand and evaluate them correctly.

It is considered that cancer-related malnutrition is caused by the imbalance of the nutritional consumption of patients,the tumor itself and the nutrient available internal.Patients with abdominal neoplasm have a great risk of getting malnutrition,which is resulting from the changes of their biochemical status,clinical symptoms and the impacts by surgery.In 1980s,people began to realize that it is important to assess the nutritional status of patients and now so do the most of doctors.Until now,there is some acceptable assessment questionnaire,by using which,we find that a large proportion of patients with abdominal cancer have malnutrition,and when it comes to different kind of abdominal cancer,the rate is not same.

Objective To study the inhibitory effect of Rompun anesthesia and operation on immune function of dogs.Methods We randomly divided 14 healthy dogs into Group A and Group B with 7 in each.Rompun anesthesia induced by intramuscular injection of 3.0 mg/kg Rompun was carried out in Group A while Rompun anesthesia and operation were applied in Group B.The venous blood samples were collected before and after anesthesia at 2,8,24,72,120 and 168 h for centrifugation to obtain sera.ELISA kit was used to evaluate the contents of serum IL-1β,IL-2,IL-4,IL-8 and TNF-α.Results Compared with those before anesthesia,the concentrations of IL-2,IL-1βand TNF-αin Group A significantly decreased at 2,8,24 and 72 h (P<0.05)and resumed the pre-anesthesia level from 120 to 168 h;however,the concentrations of IL-4 and IL-8 did not change significantly during 2 to 168 h (P>0 .05 ).Compared with those before anesthesia,the concentrations of IL-2 and IL-1βin Group B significantly decreased from 2 to 168h (P<0.05),while the concentrations of TNF-αand IL-8 significantly increased (P<0 .05 ).IL-2 and IL-1βcontents in Group B from 2 to 168 h were significantly decreased compared with those in Group A (P<0.05 ),whereas IL-8 and TNF-αincreased significantly (P<0.05 ). Conclusion Both Rompun anesthesia and operation stress can inhibit dogs'immune function,and the latter has a stronger inhibitory effect than the former.

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.