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Objective. To explore the effect and underlying mechanism of Zengye decoction (ZYD), a traditional formula from China, on the severe acute pancreatitis (SAP) rat model with acute kidney injury (AKI). Methods. The SAP-AKI model was induced by 3.5% sodium taurocholate. Rats were treated with normal saline or ZYD twice and sacrificed at 36 h after modeling. Amylase, lipase, creatinine, blood urea nitrogen, kidney injury molecule 1(KIM-1), and multiple organs' pathological examinations were used to assess the protective effect of ZYD. Gut microbiome detected by 16S rRNA sequencing analysis and serum amino acid metabolome analyzed by liquid chromatography-mass spectrometry explained the underlying mechanism. The Spearman correlation analysis presented the relationship between microflora and metabolites. Results. ZYD significantly decreased KIM-1(P < 0.05) and the pathological score of the pancreas (P < 0.05), colon (P < 0.05), and kidney (P < 0.05). Meanwhile, ZYD shifted the overall gut microbial structure (β-diversity, ANOSIM R = 0.14, P = 0.025) and altered the microbial compositions. Notably, ZYD reduced the potentially pathogenic bacteria—Bacteroidetes, Clostridiales vadin BB60 group, and uncultured_Clostridiales_bacterium, but promoted the short-chain fatty acid (SCFA) producers—Erysipelotrichaceae, Bifidobacterium, Lactobacillus, and Moryella (all P < 0.05). Moreover, principal component analysis (PCA), partial least squares-discriminant analysis (PLS-DA), and hierarchical clustering analysis (HCA) presented a remarkable change in amino acid metabolome after SAP-AKI induction and an apparent regulation by ZYD treatment (R2Y 0.878, P = 0.01 ; Q2 0.531, P = 0.01). Spearman's correlation analysis suggested that gut bacteria likely influenced serum metabolites levels (absolute r > 0.4 and FDR P < 0.02). Conclusions. ZYD attenuated SAP-AKI by modulating the gut microbiome and serum amino acid metabolome, which may be a promising adjuvant treatment. [ABSTRACT FROM AUTHOR]

Remote data auditing service is important for mobile clients to guarantee the intactness of their outsourced data stored at cloud side. To relieve mobile client from the nonnegligible burden incurred by performing the frequent data auditing, more and more literatures propose that the execution of such data auditing should be migrated from mobile client to third-party auditor (TPA). However, existing public auditing schemes always assume that TPA is reliable, which is the potential risk for outsourced data security. Although Outsourced Proofs of Retrievability (OPOR) have been proposed to further protect against the malicious TPA and collusion among any two entities, the original OPOR scheme applies only to the static data, which is the limitation that should be solved for enabling data dynamics. In this paper, we design a novel authenticated data structure called bv23Tree, which enables client to batch-verify the indices and values of any number of appointed leaves all at once for efficiency. By utilizing bv23Tree and a hierarchical storage structure, we present the first solution for Dynamic OPOR (DOPOR), which extends the OPOR model to support dynamic updates of the outsourced data. Extensive security and performance analyses show the reliability and effectiveness of our proposed scheme. [ABSTRACT FROM AUTHOR]

A hepatitis B virus (HBV) transgenic mice model was used to establish the fatty liver superimposed model by feeding the methionine choline-deficient (MCD) diet for 8 weeks, with or without the gavage of 2 mg/kg zeaxanthin dipalmitate (ZD) three times per week. Both wild-type and HBV transgenic mice, with MCD diet, gained typical non-obese non-alcoholic steatohepatitis (NASH) and HBV symptoms. Coadministration with ZD exhibited evident therapeutic effects through alleviating those pathological events. Moreover, long-term vehicle-ZD treatment was found to be safe. Thus, ZD is a promising and safe hepato-protective agent against hepatic injury induced by superimposed HBV and NASH in non-obese mice. [ABSTRACT FROM AUTHOR]

Purpose: We aim to examine whether honey ameliorates hepatic injury in non-alcoholic steatohepatitis (NASH) animal and cell line steatosis models. Methods: NASH was induced in female Sprague-Dawley rat by 8-week feeding with a high-fat diet. During the experiment, 5 g/kg honey was intragastrically fed daily. Rat normal hepatocyte BRL-3A cell was treated with sodium palmitate (SP) to induce steatosis in the absence or presence of honey pre-treatment or specific siRNA/overexpress plasmid of thioredoxin-interacting protein (TXNIP) or antagonist/agonist of Nod-like receptor protein 3 (NLRP3). Results: Honey significantly improved the high-fat-diet-induced hepatic injury, steatosis, fibrosis, oxidative stress, and inflammation in rats. Honey also inhibited the overexpression of TXNIP and the activation of NLRP3 inflammasome. These effects were replicated in BRL-3A cell line which showed that the down-regulation of TXNIP or inhibition of NLRP3 contributed to the suppression of NLRP3 inflammasome activation, inflammation, and re-balanced lipid metabolism. In contrast, overexpression of TXNIP or agonism of NLRP3 exacerbated the cellular damage induced by SP. Conclusion: Suppression of the TXNIP-NLRP3 inflammasome pathway may partly contribute to the amelioration of hepatic injury during the progression of NASH by honey. Targeting hepatic TXNIP-NLRP3 inflammasome pathway is a potential therapeutic way for the prevention and treatment of NASH. [ABSTRACT FROM AUTHOR]

Objective: To investigate the correlations among persistent viral infection, heart function and Chinese medicine (CM) difined-syndromes in patients with dilated cardiomyopathy (DCM). Methods: Fifty patients with DCM in the First Affiliated Hospital of Zhejiang Chinese Medical University from October 2009 to December 2011 were selected as the research subjects, and 30 healthy people were simultaneously selected as the normal control group to detect persistent viral infections after admission. The CM syndrome type and grade of heart function were then evaluated. The expression level of Coxsackie adenovirus receptor (CAR) was detected using the flow cytometry (FCM) technique, coxsackie virus RNA (CVB-RNA) using reverse transcription polymerase chain reaction (RTPCR), and the plasma brain natriuretic peptide (BNP) level with a Triage meter plus diagnosis instrument. Finally, the parameters such as left ventricular end diastolic diameter (LVEDd) and left ventricular ejection fraction (LVEF) were measured by ultrasonic cardiogram. Person correlation analysis was used for measured data, Spearman correlation analysis for rating data, and the Chi-square test for numerical data. Results: CVB-RNA was positive in 22 patients (44%) with DCM, while only 6 cases (20%) were CVB-RNA-positive in the normal control group, with a significant difference between the two groups ( P<0.01). The expression level of CAR was significantly elevated in the DCM group compared with the normal control group ( P<0.01). In CVB-RNA-positive patients (22 cases), the expression level of CAR was significantly higher than in CVB-RNA-negative patients (28 cases; P<0.01). In the DCM patients, there was a positive correlation between the CAR expression and the BNP level ( r=0.34, P<0.05), while no significant difference was found between the CAR expression and the LVEF and LVEDd ( r=−0.32, 0.30, P>0.05). There was no clear correlation between virus infection and the CM syndrome types in DCM patients ( r=−0.22, P>0.05). According to the sequence of syndrome types: phlegm → qi deficiency → blood stasis → hydroretention with asthenic yang (from low to high), a positive correlation was existed between the BNP levels and CM syndrome types ( r=0.139, P<0.05). Conclusion: The expression of CAR on the surface of white cells could be used to detect persistent viral infection. The expression level of CAR and heart function in DCM patients were highly correlated. The expression level of BNP may serve as an objective index for differentiating CM syndromes for patients with DCM. [ABSTRACT FROM AUTHOR]

In this study, The fingerprints of Cuscutae Semen and its processed products such as qing chao pin (QCP), jiu zhi pin (JZP), and yan zhi pin (YZP) were performed using high performance liquid chromatography. Ten chromatographic peaks were selected as characteristic peaks, the relative peak areas (RPA) of which were calculated for quantitative expression of the HPLC fingerprints. The RPA of 10 chromatographic peaks were subjected to principal component analysis (PCA) in order to classify raw Cuscutae Semen and its processed products. Principal component analysis (PCA) of the analytical data showed that raw Cuscutae Semen and its processed products could be clustered reasonably into four different groups corresponding to different processed procedure. The chemical markers of different samples given by the loadings plot of PCA were identified tentatively by electrospray ionization iontrap mass spectrometry and partially verified by the available reference standards. The results from this study indicate that the proposed method is reliable, and it has been successfully applied to the identification of raw Cuscutae Semen and its processed products used in Traditional Chinese Medicine (TCM). [ABSTRACT FROM AUTHOR]

Purpose: To investigate the protective mechanisms of an 85 % pure extract of (−) epigallocatechin gallate (EGCG) in the development of fibrosis, oxidative stress and inflammation in a recently developed dietary-induced animal model of non-alcoholic fatty liver disease (NAFLD). Methods: Female Sprague-Dawley rats were fed with either normal rat diet or high-fat diet for 8 weeks to develop NAFLD. For both treatments, rats were treated with or without EGCG (50 mg/kg, i.p. injection, 3 times per week). At the end, blood and liver tissue samples were obtained for histology, molecular, and biochemical analyses. Results: Non-alcoholic fatty liver disease (NAFLD) rats showed significant amount of fatty infiltration, necrosis, fibrosis, and inflammation. This was accompanied by a significant expressional increase in markers for fibrosis, oxidative stress, and inflammation. TGF/SMAD, PI3 K/Akt/FoxO1, and NF-κB pathways were also activated. Treatment with EGCG improved hepatic histology (decreased number of fatty score, necrosis, and inflammatory foci), reduced liver injury (from ~0.5 to ~0.3 of ALT/AST ratio), attenuated hepatic changes including fibrosis (reduction in Sirius Red and synaptophysin-positive stain) with down-regulation in the expressions of key pathological oxidative (e.g. nitrotyrosine formation) and pro-inflammatory markers (e.g. iNOS, COX-2, and TNF-α). EGCG treatment also counteracted the activity of TGF/SMAD, PI3 K/Akt/FoxO1, and NF-κB pathways. Treatment with EGCG did not affect the healthy rats. Conclusions: Epigallocatechin gallate (EGCG) reduced the severity of liver injury in an experimental model of NAFLD associated with lower concentration of pro-fibrogenic, oxidative stress, and pro-inflammatory mediators partly through modulating the activities of TGF/SMAD, PI3 K/Akt/FoxO1, and NF-κB pathways. Therefore, green tea polyphenols and EGCG are useful supplements in the prevention of NAFLD. [ABSTRACT FROM AUTHOR]

PURPOSE: To evaluate and compare the treatment efficiency of Empower interactive self-ligating brackets and traditional brackets in Class II division I extraction patients. METHODS: Forty patients with Class II division I malocclusion were randomly divided into 2 groups. Twenty patients received Empower self-ligating technique (group A) and the other 20 patients received MBT technique (group B). Four first premolars were extracted and without any other anchorage devices added in both groups. The duration of treatment, the number of visits and chair -side time were recorded. Cephalometric analysis was performed before and after treatment. The data was analyzed with SPSS 13.0 software package for paired t test. RESULTS: Treatment time and number of visits in group A were more than in group B, but there was no significant difference between the 2 groups. Chair-side time in group A reduced 151.15s on average compared with group B. Significant changes were observed in both groups after treatment. Upper and lower anterior teeth retracted and convex profile improved.U1-SN, U1-NA, L1-MP, L1-NB, UI-PTV, LI-PTV, UL-EP, LL-EP decreased. Significant differences were found in UM -PTV between the 2 groups (P <0.05). CONCLUSIONS: Compared with traditional brackets, Empower self-ligating brackets can save chair-side time, control anterior teeth torque and posterior teeth anchorage effectively, but can not reduce the treatment time or number of visits. Supported by Youth Research Project of Shanghai Municipal Health Bureau(2010Y155). [ABSTRACT FROM AUTHOR]

Purpose: To investigate the hepato-protective properties and underlying mechanisms of SAMC in a non-alcoholic fatty liver disease (NAFLD) rat model. Methods: Female rats were fed with a diet comprising highly unsaturated fat diet (30% fish oil) for 8 weeks to develop NAFLD with or without an intraperitoneal injection of 200 mg/kg SAMC three times per week. After euthanasia, blood and liver samples of rats were collected for histological and biochemical analyses. Results: Co-treatment of SAMC attenuated NAFLD-induced liver injury, fat accumulation, collagen formation and free fatty acids (FFAs). At the molecular level, SAMC decreased the lipogenesis marker and restored the lipolysis marker. SAMC also reduced the expression levels of pro-fibrogenic factors and diminished liver oxidative stress partly through the inhibition in the activity of cytochrome P450 2E1-dependent pathway. NAFLD-induced inflammation was also partially mitigated by SAMC treatment via reduction in the pro-inflammatory mediators, chemokines and suppressor of cytokine signaling. The protective effect of SAMC is also shown partly through the restoration of altered phosphorylation status of FFAs-dependent MAP kinase pathways and diminished in the nuclear transcription factors (NF-κB and AP-1) activity during NAFLD development. Conclusions: SAMC is a novel hepato-protective agent against NAFLD caused by abnormal liver functions. Garlic or garlic derivatives could be considered as a potent food supplement in the prevention of fatty liver disease. [ABSTRACT FROM AUTHOR]

Background Thromboxane levels are increased in rats fed ethanol ( Et OH), whereas thromboxane inhibitors reduce alcoholic liver injury. The aim of this study is to determine whether thromboxane inhibitors could attenuate the already established alcoholic liver injury. Methods Rats were fed Et OH and liquid diet for 6 weeks by intragastric infusion to induce liver injury after which EtOH was continued for 2 more weeks, and the rats were treated with either a thromboxane synthase inhibitor ( TXSI) or a thromboxane receptor antagonist ( TXRA). Liver pathology, lipid peroxidation, nuclear factor-kappa- B ( NF-κ B) activity, tumor necrosis factor-α ( TNF-α), cyclooxygenase-2 ( COX-2), and transforming growth factor-beta1 ( TGF-β1) were evaluated. Results Administration of fish oil and Et OH caused fatty liver, necrosis, inflammation and fibrosis accompanied by increased in lipid peroxidation, NF-κ B activity, and expression of TNF-α, COX-2, and TGF-β1. Treatment with the thromboxane inhibitors ameliorated a certain level of the pathological and biochemical abnormalities. In particular, TXSI in addition to reducing necrosis, inflammation and fibrosis also decrease the severity of fatty liver. Conclusions Thromboxane inhibitors attenuated the alcoholic liver injury, inflammation and fibrotic changes despite continued Et OH administration. Inhibition of the production of thromboxane by thromboxane inhibitor and receptor antagonists may be a useful treatment strategy in clinical alcoholic liver disease. [ABSTRACT FROM AUTHOR]

Purpose: To study the protective effects and underlying molecular mechanisms of SAMC on carbon tetrachloride (CCl)-induced acute hepatotoxicity in the mouse model. Methods: Mice were intraperitoneally injected with CCl (50 μl/kg; single dose) to induce acute hepatotoxicity with or without a 2-h pre-treatment of SAMC intraperitoneal injection (200 mg/kg; single dose). After 8 h, the blood serum and liver samples of mice were collected and subjected to measurements of histological and molecular parameters of hepatotoxicity. Results: SAMC reduced CCl-triggered cellular necrosis and inflammation in the liver under histological analysis. Since co-treatment of SAMC and CCl enhanced the expressions of antioxidant enzymes, reduced the nitric oxide (NO)-dependent oxidative stress, and inhibited lipid peroxidation induced by CCl. SAMC played an essential antioxidative role during CCl-induced hepatotoxicity. Administration of SAMC also ameliorated hepatic inflammation induced by CCl via inhibiting the activity of NF-κB subunits p50 and p65, thus reducing the expressions of pro-inflammatory cytokines, mediators, and chemokines, as well as promoting pro-regenerative factors at both transcriptional and translational levels. Conclusions: Our results indicate that SAMC mitigates cellular damage, oxidative stress, and inflammation in CCl-induced acute hepatotoxicity mouse model through regulation of NF-κB. Garlic or garlic derivatives may therefore be a potential food supplement in the prevention of liver damage. [ABSTRACT FROM AUTHOR]