Objective To assess the value of serum amyloid A(SAA)in patients with acute exacerbation of chronic pulmonary diseases. Methods Seventy AECOPD patients were randomly chosen. The AECOPD patients were divided into bacterial infection induced group and non-bacterial infection induced group by sputum bacteria culture. Thirty five SCOPD patients were chosen as control group. General data was collected. Lung function ,chest X ray,blood routine,CRP,SAA,IL6 and PCT were deteced and compared in the 3 groups. The diagnostic value of SAA to distinguish bacterial infection induced AECOPD was estimated. Results SAA of both AECOPD sub-groups were significantly higher than that of healthy controls. SAA in infection group is higher that that in exacerba-tion group. In terms of ROC curve,AUC was 0.8682 for SAA to distinguish merging bacterial infection,and the cut-off value was 72.10 mg/L with sensitivity of 94.29% and specificity of 65.71%. Conclusion SAA increases in AECOPD patients,and more obviously in AECOPD patients with bacterial infection. SAA may be used as a reliable biomarker not only to distinguish AECOPD patients from SCOPD patients ,but also distinguish merging bacterial infection during AECOPD.

Objective To evaluate interventional therapy for Budd-Chiari syndrome. Methods IVC venography was first carried out, the obliteration or stenosis in the IVC was opened or dilated with the hard tip of guid wire or puncture needle and balloon, then a stent was implanted. Results The procedure was successful in 271 out of 312 cases including IVC intervention in 260 cases, and hepatic vein intervention in 11 cases. IVC stent was used in 195 cases and hepatic vein stent in 1 case. There was no pulmonary embolism happened, acute renal failure occurred in 6 cases, hepatic coma in 1 case and acute heart failure in 21 cases. One patient died in this group and 2 were complicated with acute IVC thrombosis. Follow up of 6 to 104 mos was made in 203 cases with recurrence found in 21 cases. Conclusion Interventional therapy is indicated for most types of BCS with safe and effective results.

Although the tumor suppressor P53 is known to regulate a broad network of signaling pathways, it is still unclear how certain drugs influence these P53 signaling networks. Here, we used a comprehensive single-cell multiomics view of the effects of ginsenosides on cancer cells. Transcriptome and proteome profiling revealed that the antitumor activity of ginsenosides is closely associated with P53 protein. A miRNA-proteome interaction network revealed that P53 controlled the transcription of at least 38 proteins, and proteome-metabolome profiling analysis revealed that P53 regulated proteins involved in nucleotide metabolism, amino acid metabolism and "Warburg effect". The results of integrative multiomics analysis revealed P53 protein as a potential key target that influences the anti-tumor activity of ginsenosides. Furthermore, by applying affinity mass spectrometry (MS) screening and surface plasmon resonance fragment library screening, we confirmed that 20()-protopanaxatriol directly targeted adjacent regions of the P53 DNA-binding pocket and promoted the stability of P53-DNA interactions, which further induced a series of omics changes.