Background: To diagnose between intestinal tuberculosis (ITB) and Crohn's disease (CD) is a difficult problem, because disease presentation and endoscopic findings mimic inflammatory conditions such as CD and malignancies.So we evaluated the usefulness of the QuantiFERON-TB Gold In-Tube test (QFN-GIT) for differential diagnosis between ITB and other inflammatory bowel diseases.Methods: 75 patients with abnormal endoscopic findings and gastrointestinal trouble were enrolled between October 2007 and December 2011.The QFN-GIT, comprises three tubes: a test tube containing antigens from ESAT-6, CFP-10 and part of the sequence of TB7.7; a positive control tube (containing phytohaemagglutinin); and a negative control tube.The three tubes are inoculated with the patient's blood, incubating for 16 24 hours, and the IFN-gamma concentration measured by an ELISA.We evaluated the usefulness of QFN-GIT blood test comparing the results to the final diagnosis.Results: 23, 9 and 42 patients were revealed to be positive, intermediate, and negative in the QFN-GIT.Among the 23 patients with positive results, 13 patients (56.5%) were finally diagnosed as ITB, 5 patients were diagnosed as infective enteritis, 2 patients were diagnosed as Behcet's disease (BD), 1 patients were diagnosed as TB lymphadenitis, and 2 patients were unspecific colitis.Of the 9 patients indeteminated group, 3 patients (33.3%) were diagnosed as CD, 2 patients (22.2%) were diagnosed as ITB, and 4 patients were diagnosed as unspecific colitis.42 patients with negative group, 11 patients (26.2%) were diagnosed as CD, 9 patients (21.4%) were diagnosed as ITB, 3 patients diagnosed as ulcerative colitis, 2 patients diagnosed as BD and others were diagnosed as infective or unspecific colitis.The sensitivity and specificity of QFN-GIT for ITB were 54.2% and 64.2%, respectively.Positive and negative predictive values of QFN-GIT for ITB were 56.5% and 79.1%, respectively.Conclusions: For differential diagnosis between CD and ITB, the diagnostic value of In Vitro Interferon-gamma Assay doesn't have effective evidence in this study.
Ethnopharmacological relevance: Hedera helix L. (HH) leaves and Coptidis rhizoma (CR) have traditionally been used to treat respiratory conditions. AG NPP709, which is formulated using extracts of both these herbs, has been developed as an expectorant and antitussive.Aim of the studyThe objective was to evaluate the subchronic toxicity and toxicokinetic characteristics of AG NPP709 in laboratory rats.Materials and methodsAG NPP709 was orally administered to rats at doses of up to 2.0 g/kg/day for a duration of 13 weeks. Throughout the treatment period, various health parameters were measured and at the end of the treatment, a necropsy was conducted and additional parameters were analyzed. Toxicokinetic analyses were also performed on hederacoside C and berberine, the active components of HH leaves and CR, respectively, in the plasma of rats treated with AG NPP709.ResultsSome health issues were observed in AG NPP709-treated rats, including a reduced feed intake, altered differential white blood cell (WBC) count, and increased plasma Alb/Glo ratio in females, in addition to reduced kidney weight in males. However, these changes appeared to be incidental and fell within the typical range for healthy animals of this species. Additionally, toxicokinetic analysis of hederacoside C and berberine showed no accumulation in the plasma of rats during the repeated treatments with AG NPP709.ConclusionsOur study demonstrates that AG NPP709 does not have any harmful effects on rats under experimental conditions. Based upon these findings, the no observed adverse effect level of AG NPP709 can be estimated to be 2.0 g/kg/day in rats.
To clarify the role of stem cells in hepatocarcinogenesis, the expression of epithelial cell adhesion molecule (EpCAM) and proliferating cell nuclear antigen (PCNA) was investigated in mouse hepatic tumors and embryonic cell lineages. Ten ICR mice were treated with diethylnitrosamine (DEN) at 14 days of age and sacrificed at 36 weeks subsequent to DEN treatment to obtain the hepatic tumors. Mouse embryonic stem cells, hepatic progenitor cells and hepatocyte-like cells, representing 0, 22 and 40 days of differentiation, respectively, were treated in vitro with DEN at four doses (0, 1, 5 and 15 mM; G1, G2, G3 and G4, respectively) for 24 h and RNA was isolated. A total of 71 hepatic tumors were obtained from the DEN-treated mice. EpCAM expression was increased mainly in hepatic tumor cells, although it was also detected in the surrounding visually normal cells. Double staining showed that EpCAM and PCNA were co-expressed in numerous tumor cells. In vitro, EpCAM expression was significantly different for G4 at day 0 (P<0.01) and for G2, G3 and G4 at day 40 (P<0.01) compared with the control (G1) at the corresponding time-point. PCNA expression was significantly different for G3 and G4 at day 0 (P<0.01), for G2, G3 and G4 at day 22 (P<0.01) and for G2 at day 40 (P<0.01) compared with G1 at the corresponding time-point. In summary, the expression of EpCAM and PCNA was increased in DEN-induced tumors and the expression of EpCAM and PCNA was altered by DEN treatment in cultured cells. This suggests that EpCAM expression may be modulated in the progeny of adult liver stem cells during their differentiation toward hepatocytes and may be increased during DEN-induced hepatocarcinogenesis.
Cytochrome P450 1A2 (CYP1A2) is constitutively expressed in the mouse liver, but the constitutive expression progressively declines to an undetectable level in isolated hepatocytes. In this study, CYP1A2 was induced in hepatocytes exposed to the histone deacetylase inhibitors trichostatin A (TSA) and sodium butyrate (SB), but only well after constitutive CYP1A2 expression was silenced. However, cotreatment with the arylhydrocarbon receptor (AhR) ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and either TSA or SB reduced the induction of CYP1A2 with the same time course as TSA or SB increased its induction. These results suggest that histone modification is involved in CYP1A2 regulation in hepatocytes through pathways that are independent of AhR.
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