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Additional file 2. Table S1. The information of siRNA and primer sequences used in this study. Table S2. The information of antibodies used in this study. Table S3. E xpression patterns of 100 di fferentially expressed genes in SC between the sham and CCI model groups by Microarray Profiling (mixed sample, n = 3). Table S4. Expression patterns of 100 differentially expressed genes in SC between the sham and CCI model groups by RNA-seq (n = 4).

Additional file 1. Figure S1. Clec7a knockdown alleviated LPS and ATP induced BV2 cells pyroptosis. Figure S2. C/EBP β knockdown alleviated LPS and ATP induced BV2 cells pyroptosis.

Additional file 6: Table S2. Quantification analysis of calcium in Gypsum Fibrosum and full prescription BHGZD by ICP-AES.

Additional file 2: Figure S2. The chromatograms of mixed standards and serum sample after BHGZD gavage.

Additional file 1: Figure S1. The chemical structure and corresponding mass spectrum of absorbed components in vivo.

Additional file 3: Figure S3. The chromatogram of selectivity of the analytes in rat serum.

Additional file 5: Table S1. Identification of chemical profile of BHGZD in vitro by UFLC-Q-TOF-MS/MS.

Additional file 1: Table S1. Includes detailed information of all enzyme-linked immunosorbent assay kits. Table S2. Includes 672 putative target genes of CRT predicted using ETCM database and TCMIP v2.0 platform. Table S3. Includes 3472 DKD-related genes from Human Phenotype Ontology (HPO), DisGeNet and Drugbank databases. Table S4. Includes enrichment results of clinical symptoms of 390 CRT putative targets. Table S5. Includes enrichment results of functional modules of 390 CRT putative targets. Table S6. Includes 231 candidate targets of CRT against DKD in ���Disease Gene-Drug Target��� interaction networks based on calculated network topological features. Table S7. Includes enrichment results of functional modules of 231 CRT candidate targets.

Additional file 4: Figure S4. Graphical abstract.

ObjectiveTo investigate the clinical characteristic and long-term prognosis risk factor of patients with hepatitis B virus-related acute-on-chronic liver failure(HBV-ACLF). MethodsThe clinical data of 1116 HBV-ACLF patients who were hospitalized in Southwest Hospital of Third Military Medical University from January 2010 to January 2015 were analyzed retrospectively. The risk factors for 1-year survival time and prognosis were observed, and the Cox regression model was used to determine the independent risk factors for the prognosis of these patients. The t-test or t′-test was applied for comparison of continuous data between groups, and the chi-square test was applied for comparison of categorical data between groups. ResultsA total of 562 patients died within the 1-year follow-up period, and the fatality rate was 50.4%. The comparison between the survival group and the death group showed that age, alanine aminotransferase, total bilirubin, urea nitrogen, serum creatinine, international normalized ratio, serum Na+, white blood cell (WBC), percentage of neutrophils, platelet (PLT), HBV DNA load, Model for End-Stage Liver Disease (MELD) score, ascites, spontaneous bacterial peritonitis, gastrointestinal bleeding, pulmonary infection, sepsis, electrolyte disturbance, hepatic encephalopathy, and acute kidney injury (AKI) were the risk factors for death within 1 year (all P＜0.05). The Cox regression analysis showed that age, WBC, MELD score, hepatic encephalopathy, electrolyte disturbance, AKI, and PLT were the independent risk factors for the 1-year fatality in HBV-ACLF patients (all P＜0.05). ConclusionOur findings show that HBV-ACLF has a high fatality rate and is often accompanied by serious complications. The major risk factors affecting the 1-year fatality in HBV-ACLF patients are age, WBC, MELD score, hepatic encephalopathy, electrolyte disturbance, AKI, and PLT.

OBJECTIVE: To assess the efficacy and safety of decernotinib (VX-509), an oral selective inhibitor of JAK-3, in patients with rheumatoid arthritis (RA) in whom the response to methotrexate treatment was inadequate.METHODS: In this 24-week, double-blind, randomized phase IIb study, 358 patients with active RA received either placebo (n = 71) or VX-509 at dosages of 100 mg/day (n = 71), 150 mg/day (n = 72), 200 mg/day (n = 72), or 100 mg twice daily (n = 72). Primary measures of efficacy at week 12 were the response rate according to the American College of Rheumatology 20% improvement criteria (ACR20) and change from baseline in the Disease Activity Score in 28 joints using the C-reactive protein level (DAS28-CRP).RESULTS: At week 12, the ACR20 response rates were 46.5%, 66.7%, 56.9%, and 68.1% in the groups receiving VX-509 at dosages of 100 mg/day, 150 mg/day, 200 mg/day, and 100 mg twice daily, respectively, and 18.3% in the placebo group (P < 0.001 for all comparisons). At week 12, the mean change from baseline in the DAS28-CRP was significantly greater in each VX-509 group compared with the placebo group (P < 0.001). Improvements were maintained at week 24, as shown by the ACR20, ACR50, and ACR70 response rates and mean change from baseline in the DAS28-CRP. The most common adverse event in the VX-509 group was headache (8.7%), and elevated levels of transaminases, lipoproteins, and creatinine were observed.CONCLUSION: VX-509 significantly improved the signs and symptoms of RA at weeks 12 and 24 compared with the placebo group when it was administered in combination with methotrexate. Safety signals included infection and increases in liver transaminase and lipid levels.

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Few data are available from prospective trials to define the hepatotoxicity of diclofenac, the most widely prescribed non-steroidal anti-inflammatory drug (NSAID) in the world. We determined the rate of laboratory and clinical adverse hepatic effects in a large double-blind trial of diclofenac.Patientsor = 50 years with rheumatoid arthritis or osteoarthritis were randomly assigned to diclofenac (150 mg daily) or etoricoxib (60 or 90 mg daily). Patients with hepatic disease or who reportedor = 14 alcoholic drinks weekly were excluded. Patients had visits (with liver tests) every 4 months and were contacted by phone between visits and every 6 months after discontinuation until the end of the study. Causality assessment was performed for liver-related hospitalizations, Hy's cases (serious adverse events with AST or ALT3 x upper limit of normal (ULN) and bilirubin2 xULN), and liver failure/transplant/death.A total of 17,289 patients received diclofenac for a mean of 18 months. Liver end points with diclofenac were ALT/AST3 xULN: 527(3.1%); ALT/AST10 xULN: 86(0.5%); liver-related hospitalizations: 4(0.023%); Hy's cases: 2(0.012%); liver failure/death/transplant: 0. Aminotransferase elevations occurred primarily within the first 4-6 months of therapy, whereas liver-related hospitalizations occurred between 9 days and 21 months.Diclofenac is commonly associated with aminotransferase elevations, generally in the first 4-6 months of therapy. Clinical liver events requiring hospitalization are relatively rare (23/100,000 patients), but may develop early or late in therapy. The markedly increased rate of aminotransferase elevation with diclofenac may not be paralleled by a proportional marked increase in clinical liver events, although clinical events potentially also may be decreased with regular monitoring in a clinical trial setting.