Objective To evaluate the values of procalcitonin (PCT)level in serum for predicting Gram-negative bacteremia (GNB).Methods Among 499 candidates for study entry,314 were GN bacteraemia,and 185 were Gram-positive bacterae-mia (GPB).The serum PCT level were measured in 499 candidates.Results PCT levels were found to be markedly higher in patients with GNB (median=5.16,0.02~450.10 ng/ml)than in those with GPB (median=0.38,0.02~44.70ng/ml) (P =0.000).The percentage of GNB were increased along with PCT level.The proportion of GNB was 100% when PCT ≥45.0 ng/ml.For prediction of GNB a PCT level of 6.00 ng/ml had a sensitivity of 49.4% and specificity of 85.2% and posi-tive predictive value of 85.6% and negative predictive value of 50.0%,respectively.The area under the receiver operating characteristic curve for discriminating GNB and GPB was 0.714,confidence interval of 95% was 0.672 ~ 0.753,SE =0.0229,P <0.0001.Conclusion PCT is an early and reliable indicator for predicting GNB.

Objective To investigate the correlation between atypical respiratory pathogens infection and serum vitamin D(VitD) level in children.Methods Serum IgM antibody levels of 11 atypical respiratory pathogens were detected in 414 serum samples of child respiratory infection by using the respiratory tract 11-items detection reagent kits (indirect immunofluorescence assay),including respiratory syncytial virus(RSV),adenovirus(ADV),influenza A virus(FluA),influenza B virus(FluB),parainfluenzavirus(PFlu),Mycoplasma pneumonia(MP),Chlalmydia pneumoniae(CP),Coxsackie virus type B(CoxB),Coxsackie virus type A(CoxA) and legionella pneumophilia(LP).At the same time the electrochemiluminescence assay was used to measure serum VitD level.Results Among 414 samples,pathogen IgM was detected out in 214 samples (51.69%),the top three places of detection rates were FluB,FluA and Mp,their positive rates were 32.13%,23.19% and 13.77% respectively;in cases of positive IgM antibody,17.63% of children developed single infection,34.06% of children developed 2 kinds of pathogen or more mixed infection;there was no statistical difference in the VitD levels between the IgM antibody positive group (median 23.60 ng/mL,3.37-71.50 ng/mL) and the IgM antibody negtive group(median 23.95 ng/mL,3.00-81.70 ng/mL).The IgM antibody positive rate,single infection positive rate and mixed infection positive rate had no statistical difference between the VitD reduce group and the VitD normal group(P>0.05).The positive rate of FluB,FluA and MP IgM antibody had no statistical difference between the VitD reduce group and the VitD normal group(P>0.05).Atypical respiratory pathogens had no correlation with VitD(r=0.005,P=0.912).Conclusion Atypical respiratory pathogens infection may had no correlation with the VitD level reduce.

In view of gemcitabine resistance has limited clinical activity of gemcitabine as a cellulotoxic drug in pancreatic cancer patients, this study is designed to investigate the effect of emodin on the sensitivity of pancreatic cancer to gemcitabine as well as its mechanism. After gemcitabine-resistant pancreatic cancer cell line (SW1990/GZ) was established by escalating doses of gemcitabine serially in pancreatic cancer cell line (SW1990). The cellular proliferation was detected by cell counting kit-8 (CCK-8) assay. Flow cytometry (FCM) was used to determine apoptosis of pancreatic cancer cells. The activity of NF-kappaB in pancreatic cancer cells was measured by electrophoretic mobility shift assay (EMSA). Western blotting was used to detect the protein expression of Bcl-2 and Survivin in SW1990/GZ cells. Metastatic model simulating human pancreatic cancer was established by orthotopic implantation of histologically intact human tumor tissue into pancreatic wall of nude mice. Also, immunohistochemistry was used to detect the positive expression of Ki-67, NF-kappaB, Bcl-2 and Survivin in the tumors. The results show that pretreatment of cells with emodin followed by gemcitabine induced a higher percentage of growth inhibition and apoptosis of pancreatic cancer cells than that of gemcitabine alone. In addition to in vitro results, emodin in combination with gemcitabine is much more effective as an antitumor agent compared to either agent alone in the orthotopic tumor model. Further study showed that the emodin with or without gemcitabine significantly down-regulates NF-kappaB and its regulated molecules such as Bcl-2 and Survivin proteins both in vitro and in vivo. It is concluded that inactivation of NF-kappaB signaling pathway by emodin resulting in the chemosensitization of pancreatic cancer to gemcitabine, which is likely to be an important and novel strategy for the treatment of pancreatic cancer.