ObjectiveTo investigate the mechanism of Huangqin Tang （HQT） in regulating metabolic reprogramming during the inflammation-cancer transformation in colitis-associated colorectal cancer （CAC）. MethodsCAC mouse model was established using the carcinogen azoxymethane （AOM） combined with the inflammatory agent dextran sulfate sodium （DSS）. HQT treatment was adopted. Serum metabolomics analysis was performed at three stages （inflammation， proliferation， and tumor formation） using liquid chromatography-tandem mass spectrometry （LC-MS/MS） untargeted metabolomics coupled with multivariate statistical analysis to explore the mechanism of HQT intervention in metabolism in CAC. ResultsThe results revealed that HQT significantly reversed the disturbance of key metabolites in CAC mice. A total of 52， 67， and 45 differential metabolites were identified in the model group， compared to the normal group， during inflammation， proliferation， and tumor stages， respectively. Lactate， linoleic acid， oleic acid， elaidic acid， and betaine were characteristic metabolites persistently enriched throughout colitis-cancer transformation. Pathway enrichment analysis of differential metabolites showed that linoleic acid metabolism and arachidonic acid metabolism were the most significantly disturbed in CAC pathogenesis. The proliferation stage featured expanded amino acid metabolic networks， while the tumor stage uniquely exhibited two new pathways of nicotinate and nicotinamide metabolism and phosphoinositide metabolism. HQT exerted stage-specific regulatory effects： targeting arachidonic acid metabolism in the inflammation stage， correcting the dysregulation of choline-carnitine metabolism in the proliferation stage， and rescuing nicotinamide and tryptophan metabolic collapse in the tumor stage. ConclusionHQT exerts regulatory effects on metabolic disorders at various stages of the colitis-cancer transformation process， thereby effectively slowing the progression from colitis to cancer. The study also reveals the dynamic metabolic characteristics of colorectal "inflammation-cancer transformation，"providing new insights for research on the targeted mechanisms of traditional Chinese medicine in anti-tumor therapy based on metabolic reprogramming.

Objective: To analyze the correlation between the Spondyloarthritis Research Consortium of Canada (SPARCC) magnetic resonance imaging (MRI) sacroiliac joint inflammation score (SPARCC score)/structural score (SSS) and the disease activity as well as the functional indexs. The correlation between the MRI score and inflammatory indicators [erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)] in patients with active axial spondyloarthritis (axSpA) before and after treatment was explored. In addition, the contribution of the two MRI scoring method in evaluating conditions was also explored. Methods: According to the inclusion criteria, 24 patients with active axial SpA were recruited and received the recombinant hauman tumor necrosis factor (TNF)-α receptor Ⅱ: IgG Fc fusion protein(rhTNFR:Fc), sulfasalazine and thalidomide for 12 weeks. Subjects were scored at week 0 and 12 by SPARCC/SSS scores. Bath ankylosing spondylitis disease activity index (BASDAI), Assessment of Spondyloarthritis Intemational Society (ASAS)-endorsed disease activity score(ASDAS)-CRP, bath ankylosing spondylitis functional index (BASFI). Bath ankylosing spondylitis metrology index(BASMI), ESR and CRP. The correlation between the SPARCC/SSS scores and that of clinical indicators were analyzed. Paired sample t test, Wilcoxon signedrank test, Spearman correlation analysis and Pearson correlation analysis were used for statistical analysis, and receiver operating characteristic curve (ROC) was used to evaluate the effectiveness of SPARCC score decline as a response to treatment. Results: ① Compared with baseline, after 12 weeks treatment, SPARCC scores [(15±4) and(33±10)], BASDAI [(3.2±0.9) and (5.2±1.1)], BASFI [(2.3±0.6) and (4.6±1.0)], BASMI [(2.3±0.7) and (4.1±1.1)], ASDAS-CRP scores [(2.0±0.8) and (3.7±0.9)], ESR [(16±12) mm/1 h and (49±26) mm/1 h], CRP [(7.2±2.8) mg/L and (30.4±19.3) mg/L] were significantly decreased (t values were 7.822, 6.950, 10.707, 7.204, 6.281,-4.015 and-4.257, respectively), and the differences were statistically significant (P=0.000). There was no significant difference in SSS scores between baseline [(20±6) and (19±7)] and after 12 weeks treatment (t=-0.761, P=0.455). ② Before treatment, SPARCC score showed positive linear correlation with BASDAI (r=0.630, P=0.001), ASDAS-CRP (r=0.646, P=0.001), CRP (r=0.574, P=0.003) and ESR (r=0.559, P=0.004), and the correlation of the above indexes disappeared after treatment (P>0.05). The association between SPARCC structral scores and the above indicators was not significant before and after treatment. ③ Areas under curve(AUC) of ROC for assessing treatment response by reduced SPARCC scores was 0.809. The cut-off value for response to treatment was 20.5, with the sensitivity of 68.8% and specificity of 75.0%. Conclusion The SPARCC MRI SIJ inflamm-ation score has certain value in evaluating disease activity and efficacy, while the SPARCC SSS is not.

Objective To investigate the mechanism of miRNA-129-5p in epithelial-mesenchymal transition (EMT)of biliary atresia.Methods Constructed bile duct epithelial EMT cell model (the experimental group) induced by TGF-β1,detected the expressions of EMT related markers and miRNA-129-5p.While miRNA-129-5p precursor was transfected,the expressions of EMT related markers and extracellular matrix were contrasted between the original and the renovated biliary epithelial cells.Results In the experimental group,extrahepatic bile duct showedEMT,the expression of miRNA-129-5p was decreased (P＜0.05),overexpression of miRNA-129-5p could inhibit the progression of EMT (P＜0.05).Conclusion miRNA-129-5p may relate to EMT by regulating the expression of TGF-β1.

BACKGROUND:At present, there is no effective treatment strategy for cavernous transformation of portal vein and basic research about its etiology is rarely reported.
OBJECTIVE:To establish the models of cavernous transformation of portal vein, detect the expression of matrix metal oproteinase-2,-9 (MMP-2, MMP-9) and tissue inhibitors 1, 2 of metal oproteinase (TIMP-1, TIMP-2) in rat portal vein and peripheral tissue, and discuss the roles in the process of peripheral angiogenesis.
METHODS:Eighty Sprague-Dawley rats were randomly divided into three groups. The rat models of cavernous transformation of portal vein were established with partial coarctation in portal vein by using 21 G blunt pinhead. Control group was normal rats without operation (samples were harvested after portal vein radiography). Model group and sham operation group were divided into three groups respectively according to different time points, namely 2, 4 and 6 weeks after operation. Rats of each group were randomly chosen at week 2, 4 and 6 after operation to observe the formation of col ateral circulation of portal vein and its peripheral tissues by performing portal vein radiography. CD31 was detected by immunohistochemistry. The expression of MMP-2, MMP-9, TIMP-1, TIMP-2 mRNA and protein in portal vein and peripheral tissue were determined by RT-PCR and immunohistochemistry respectively.
RESULTS AND CONCLUSION:Peripheral angiogenesis of model group was increased obviously by portal vein radiography and immunohistochemistry. RT-PCR and immunohistochemistry results demonstrated that, compared with the control group and sham operation group, the expression of MMP-2 mRNA and protein in model group were significantly increased at weeks 2, 4, and 6 (P<0.01, P<0.05), while expression of MMP-9 mRNA and protein at week 2 in model group were significantly higher than that in the control group and sham operation group. Expression of TIMP-1 and TIMP-2 in model group showed no significant difference compared with control group and sham operation group at weeks 2, 4, and 6 (P>0.05). Ratio of MMP-2/TIMP-2 of model group was significantly higher than that of control group and sham operation group (P<0.05) at week 2. the rat models of cavernous transformation of portal vein have low mortality, high success rate and are stable. Upregulation of the expression of MMP-2, MMP-9 and the disbanlance of the ratio of MMP-2/TIMP-2 might contribute to the peripheral angiogenesis in rats with cavernous transformation of portal vein.

Objective To investigate the incidence and CT imaging features of abdominal splenosis with a previous splenectomy.Methods 94 consecutive patients with a history of splenectomy underwent abdominal contrast CT examination between April 2010 and December 2012 and were recruited for this study.These patients were devided into two groups according to the reason for which splenectomy was performed.Descriptive statistics were calculated for clinical incidence of abdominal splenosis,and subsequently CT imaging features and diagnosis of abdominal splenosis were discussed.Results In this series,29 cases (30.85％) with abdominal splenosis were found in 94 patients.Abdominal splenosis was found in all of 20 cases with more than one year history of posttraumatic splenectomy,and in 17.31％ (9 of 52) of cases with more than one year history of non-traumatic splenectomy (P ＜ 0.05).There were 60 nodules found on CT examinations in these 29 cases.All nodules were 50 mm or smaller.All nodules appeared of homogeneous soft-tissue density on plain CT scan.The nodules showed significant enhancement during arterial phase on postcontrast CT scan,with continuous significant homogeneous enhancement during portal venous phase.Conclusions Abdominal splenosis following posttraumatic splenectomy are more common than previously suggested.Knowledge of typical CT imaging appearances and the history of splenectomy may prevent mistaking as tumors.