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- Molecular characterization of a sodium channel gene and identification of a Phe1538 to Ile mutation in citrus red mite, Panonychus citri. [JOURNAL ARTICLE]
- Pest Manag Sci 2014 Apr 21.
The citrus red mite, Panonychus citri (McGregor), is regarded as one of the most serious citrus pests in many countries and has developed severe resistance to pyrethroids for the intensive use of these acaricides.The para sodium channel gene of P. citri (named as PcNav ) was cloned in this study, which contained an entire coding region of 6,729 bp. A total of three alternative splicing sites and twelve potential RNA editing sites were identified in PcNav . Thus, exons alt 1 and alt 3-v3 were found to be unique to PcNav . Comparison of a field fenpropathrin-resistant (WZ) and susceptible (LS) strains identified the point mutation F1538I in IIIS6 of the sodium channel, which is known to confer strong resistance to pyrethroids in mites. Moreover, we also found that the PcNav mRNA was present during all the life stages, and the transcript seems to be more abundant in larvae than in other developmental stages.These results suggest that the F1538I mutation plays an important role in fenpropathrin resistance in citrus red mites. This is the first study of sodium channel in P. citri and provides abundant information for further research on mechanism of pyrethroid resistance.
- Asymmetric dimethylarginine levels in children with β-thalassemia and their correlations to tricuspid regurgitant jet velocity. [JOURNAL ARTICLE]
- Pediatr Blood Cancer 2014 Apr 21.
Pulmonary hypertension (PHT) may be the leading cause of death in β-thalassemia patients; however, its pathophysiologic mechanisms are still unclear. Recent studies indicate that asymmetric dimethylarginine (ADMA) plays a role in the initiation and progression of a variety of diseases, especially the cardiovascular system. The aim of this study is to assess the levels of ADMA in children with β-thalassemia and their correlations with tricuspid regurgitant jet velocity.This study was carried out on 30 children with β-thalassemia major and 30 healthy children served as a control group. Both groups underwent the following investigations: Blood sampling for CBC, LDH, serum ferritin, reticulocytic count, serum bilirubin, AST, ALT, in addition to plasma levels of ADMA. Doppler echocardiography was done for thalassemic group. Patients with tricuspid regurgitant jet velocity (TRV ≥ 2.5 m/sec) were considered risky for PHT.Plasma ADMA levels were significantly higher in patients with β-thalassemia than control group with a mean value 0.91 ± 0.14 and 0.62 ± 0.10 µmol/L respectively (P = 0.001). There was a significant positive correlation between plasma ADMA levels and tricuspid regurgitant jet velocity. The prevalence of elevated tricuspid regurgitant jet velocity (TRV ≥ 2.5 m/sec) in patients with thalassemia was 33.3%, with a significant increase of elevated TVR (≥2.5 m/sec) in patients with thalassemia with splenectomy than in patients without splenectomy.High plasma ADMA levels may be implicated in the pathogenesis of PHT in children with β-thalassemia. Pediatr Blood Cancer © 2014 Wiley Periodicals, Inc.
- [Sanhuangyinchi decoction pretreatment ameliorates acute hepatic failure in rats by suppressing antioxidant stress and caspase-3 expression]. [English Abstract, Journal Article]
- Nan Fang Yi Ke Da Xue Xue Bao 2014 Apr 20; 34(4):482-6.
To observe the effects of Sanhuangyinchi decoction (SHYCD) pretreatment on acute hepatic failure (AHF) induced by D-galactosamine and lipopolysaccharide (LPS) in rats and explore the possible mechanisms involving antioxidant stress and cell apoptosis-related protein expression.Forty-eight SD rats were randomized equally into control group, AHF model group, high-, medium- and low-dose SHYCD groups, and Bicyclol group. Five days after administration of the corresponding drugs, the rats were challenged with peritoneal D-galactosamine (700 mg/kg) plus LPS (10 ug/kg) injections to induce AHF acute hepatic failure except for those in the control group. At 48 h after the injections, blood samples were collected from the rats to detect the levels of ALT, AST, TBIL, PT, INR and FIB, and pathological changes and superoxide dismutase (SOD) and malondialdehyde (MDA) contents in the liver were examined; immunohistochemistry and western blotting were used to detect caspase-3 protein expression in the liver.The levels of ALT, AST, TBIL, TP and INR in the 3 SHYCD groups and Bicyclol group significantly decreased (P<0.05) while FIB significantly increased in comparison with those in the model group. SHYCD obviously ameliorated the pathological changes, enhanced SOD activity (P<0.05), and decreased MDA levels (P<0.05) and caspase-3 expression (P<0.05) in the liver tissue. SHYCD at the medium dose produced similar effects to Bicyclol (P>0.05) and showed better effects at the high dose than Bicyclol (P<0.05).SHYCD pretreatment can dose-dependently ameliorate AHF in rats possibly by suppressing antioxidant stress and caspase-3 expression to decrease hepatic cell apoptosis.
- [Effect of emodin on expression of farnesoid X receptor in rats with acute cholestatic hepatitis]. [English Abstract, Journal Article]
- Zhongguo Dang Dai Er Ke Za Zhi 2014 Apr; 16(4):424-9.
To investigate the expression of farnesoid X receptor (FXR) and the effect of emodin on FXR expression in a rat model of acute cholestatic hepatitis.Ninety adult Sprague-Dawley rats were randomly divided into normal control, model, and emodin groups (n=30 each). The model and emodin groups were given alpha-naphthylisothiocyanate (ANIT) 50 mg/kg by gavage to establish an animal model of cholestatic hepatitis, while the normal control group was given an equal volume of sesame oil. The emodin group was given emodin by gavage every day from 4 days before the model was prepared until the time of sacrifice, while the model and normal control groups were given an equal volume of sodium carboxymethyl cellulose solution. At 24, 48 and 72 hours after the model was prepared, serum level of total bilirubin (TB), direct bilirubin (DB), alanine aminotransferase (ALT), and total bile acids (TBA) were measured by Aeroset automatic biochemical analyzer, and the mRNA expression of FXR in the liver tissue was measured by real-time PCR.At all time points FXR mRNA expression in the model group decreased, but serum levels of TB, DB, ALT and TBA increased significantly compared with the normal control group (P<0.05). The emodin group had significantly higher mRNA expression of FXR and significantly lower serum levels of TB, DB, ALT, and TBA compared with the model group (P<0.05).Emodin can significantly reduce serum levels of TB, DB, ALT, and TBA in rats with ANIT-induced cholestatic hepatitis, probably by promoting FXR expression.
- The Pan-Caspase Inhibitor Emricasan (IDN-6556) Decreases Liver Injury and Fibrosis in a Murine Model of Non-Alcoholic Steatohepatitis. [JOURNAL ARTICLE]
- Liver Int 2014 Apr 22.
Hepatocyte apoptosis, the hallmark of Non-alcoholic steatohepatitis (NASH) contributes to liver injury and fibrosis. Although, both the intrinsic and extrinsic apoptotic pathways are involved in the pathogenesis of NASH, the final common step of apoptosis is executed by a family of cysteine-proteases termed caspases. Thus, our aim was to ascertain if administration of Emricasan, a pan-caspase inhibitor, ameliorates liver injury and fibrosis in a murine model of NASH. Methods: C57/BL6J-mice were fed regular chow or high fat diet (HFD) for 20 weeks. All mice were treated with vehicle or Emricasan.Mice fed a HFD diet demonstrate a 5-fold increase in hepatocyte apoptosis by the TUNEL assay and a 1.5-fold and 1.3-fold increase in caspase-3 and-8 activities respectively; this increase in apoptosis was substantially attenuated in mice fed a HFD treated with Emricasan (HFD-Em). Likewise, liver injury and inflammation were reduced in mice fed HFD-Em as compare to HFD by measuring serum AST and ALT levels, NAS histologic score and IL 1-β, TNF-α, MCP-1 and CXCL2 qPCR. These differences could not be attributed to differences in hepatic steatosis as liver triglycerides content were similar in both HFD groups. Hepatic fibrosis was reduced by Emricasan in HFD animals by decreasing αSMA (a marker for HSC activation), fibrosis score, Sirius red staining, hydroxyproline liver content and profibrogenic cytokines by qPCR. In Conclusion, these data demonstrate that in a murine model of NASH, liver injury and fibrosis are suppressed by inhibiting hepatocytes apoptosis and suggests that Emricasan may be an attractive anti-fibrotic therapy in NASH This article is protected by copyright. All rights reserved.
- Comparative time efficiency of aligner therapy and conventional edgewise braces. [Journal Article]
- Angle Orthod 2014 May; 84(3):391-6.
Objective:To compare the time efficiency of aligner therapy (ALT) and conventional edgewise braces (CEB) based on large samples of patients treated by the same highly experienced orthodontist, with the same treatment goals for both groups of patients. Materials and
Methods:The retrospective portion of the study evaluated 150 CEB patients who were matched, based on mandibular crowding and number of rotated teeth, to 150 ALT patients. All records were obtained at one orthodontist's office. All of the patients had mild-to-moderate Class I malocclusions (≤5 mm incisor crowding) and were treated nonextraction. Age, gender, total treatment time, total number of appointments, types of appointments, materials used, mandibular crowding, and number of rotated teeth were recorded from the patients' records. The prospective portion of the study timed the various types of appointments for both treatments with a stopwatch.
Results:Compared to ALT, CEB required significantly (P < .01) more visits (approximately 4.0), a longer treatment duration (5.5 months), more emergency visits (1.0), greater emergency chair time (7.0 minutes), and greater total chair time (93.4 minutes). However, ALT showed significantly (P < .01) greater total material costs and required significantly more total doctor time than CEB (P < .01).
Conclusions:Whether the greater time efficiency of ALT offsets the greater material costs and doctor time required depends on the experience of the orthodontist and the number of ALT case starts.
- Induction of hepatic Bach1 mRNA expression by carbon tetrachloride-induced acute liver injury in rats. [JOURNAL ARTICLE]
- Biomed Rep 2014 May; 2(3):359-363.
Hepatic oxidative stress is a major contributor to the pathogenesis of several acute liver diseases. Diagnostic markers of hepatic oxidative stress may facilitate early detection and intervention. Bach1 is an oxidative stress-responsive transcription factor that represses heme oxygenase 1 (HO-1), the rate-limiting enzyme in the catabolism of heme, a potent pro-oxidant. We previously demonstrated that carbon tetrachloride (CCl4) causes oxidative hepatic injury in rats, exacerbated by free heme, suggesting that CCl4 may affect Bach1 gene expression. In the present study, we used northern blot analysis to measure Bach1, HO-1 and δ-aminolevulinate synthase (ALAS1; a heme biosynthesis enzyme) mRNA expression levels during acute hepatic injury induced by CCl4 (at doses of 0.1, 1.0 and 2.0 ml/kg body weight). Oxidative injury was assessed by measuring serum alanine aminotransferase (ALT), hepatic malondialdehyde (MDA) and glutathione (GSH) content. Treatment with CCl4 induced a significant dose-dependent increase in Bach1 mRNA 1-3 h after administration. Bach1 mRNA peaked at 6 h after CCl4 treatment (1 ml/kg), followed by a rapid decrease and gradual return to baseline by 12 h after treatment. The timecourse of transient Bach1 mRNA induction roughly mirrored that of HO-1 mRNA, while ALAS1 mRNA was inversely downregulated. Serum ALT levels and hepatic MDA concentration were significantly increased at 24 h after CCl4 treatment, while the hepatic GSH content was significantly reduced within 3 h of treatment. Serum ALT levels were positively correlated with Bach1 mRNA levels. These findings indicate that Bach1 mRNA is transiently induced in rat liver by CCl4, possibly as a regulatory mechanism to restore HO-1 to baseline following free heme catabolism. Our findings also suggest that Bach1 mRNA expression may be a novel indicator of the extent of oxidative hepatic injury caused by free heme.
- Evaluation of the relation between hepatic fibrosis and basic laboratory parameters in patients with chronic hepatitis B fibrosis and basic laboratory parameters. [Journal Article]
- Hepat Mon 2014 Apr; 14(4):e16975.
The hepatitis B virus is an important healthcare problem. According to current clinical practice, a liver biopsy is required for the diagnosis and treatment of chronic liver disease. However, a liver biopsy is an invasive, inconvenient procedure, which requires an expert pathologist opinion. Therefore requirement of biochemical tests, which are considered to indicate hepatic fibrosis and may be repeated easily, increases gradually today.This study evaluated the correlation between hepatic fibrosis and routine laboratory values in patients with chronic hepatitis B.The files of 456 patients with CHB (chronic hepatitis B) who were referred to the infectious diseases and clinical microbiology clinic between January 2009 and March 2012 were screened retrospectively. Liver biopsy samples were examined according to Ishak scoring. Laboratory parameters and histopathology reports were recorded, and correlations between the fibrosis grade and laboratory parameters were analyzed.There were 320 male and 136 female patients, with a mean age 36.7 ± 12.1 years. According to liver biopsy results, a low fibrosis score (stage 0-2) was detected in 281 patients (61.6%), and a high fibrosis score (stage 3-5) was detected in 175 patients (38.4%). Patients with a high fibrosis score had significantly higher ALT (alanine amino transferase), AST (aspartate aminotransferase), and HBV-DNA values and a significantly lower platelet count compared with those with a low fibrosis score (P = 0.001, 0.001, 0.025, and 0.001, respectively). A positive correlation was detected between the fibrosis score and age, BMI, HAI, ALT, and AST values, and a negative correlation was detected between the fibrosis score and albumin and platelet counts. In the regression analysis performed to evaluate the factors associated with high-stage fibrosis, fibrosis was determined to be associated with thrombosis, ALT, and gender. The results of the regression analysis demonstrated that the risk of fibrosis was 4.6 fold higher in men.According to the results obtained in our study, advanced age, higher BMI, AST, ALT, and HBV-DNA levels, and low albumin and platelet levels are correlated with advanced fibrosis in patients with CHB.
- Bile acids override steatosis in farnesoid X receptor deficient mice in a model of non-alcoholic steatohepatitis. [JOURNAL ARTICLE]
- Biochem Biophys Res Commun 2014 Apr 17.
Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases, and the pathogenesis is still not well known. The farnesoid X receptor (FXR) is a member of the nuclear hormone receptor superfamily and plays an essential role in maintaining bile acid and lipid homeostasis. In this study, we study the role of FXR in the pathogenesis of NFALD. We found that FXR deficient (FXR(-/-)) mice fed methionine- and choline-deficient (MCD) diet had higher serum ALT and AST activities and lower hepatic triglyceride levels than wild-type (WT) mice fed MCD diet. Expression of genes involved in inflammation (VCAM-1) and fibrosis (α-SMA) was increased in FXR(-/-) mice fed MCD diet (FXR(-/-)/MCD) compared to WT mice fed MCD diet (WT/MCD). Although MCD diet significantly induced hepatic fibrosis in terms of liver histology, FXR(-/-)/MCD mice showed less degree of hepatic steatosis than WT/MCD mice. Moreover, FXR deficiency synergistically potentiated the elevation effects of MCD diet on serum and hepatic bile acids levels. The super-physiological concentrations of hepatic bile acids in FXR(-/-)/MCD mice inhibited the expression of genes involved in fatty acid uptake and triglyceride accumulation, which may be an explanation for less steatosis in FXR(-/-)/MCD mice in contrast to WT/MCD mice. These results suggest that hepatic bile acids accumulation could override simple steatosis in hepatic injury during the progression of NAFLD and further emphasis the role of FXR in maintaining hepatic bile acids homeostasis in liver disorders and in hepatic protection.
- Effects of vanadium (III, IV, V)-chlorodipicolinate on glycolysis and antioxidant status in the liver of STZ-induced diabetic rats. [JOURNAL ARTICLE]
- J Inorg Biochem 2014 Mar 31.:47-56.
Vanadium compounds exert various insulin-mimetic and anti-diabetic effects both in vitro and in vivo. Vanadium(III, IV, V)-chlorodipicolinate (Vdipic-Cl) compounds, including H[V(III)(dipic-Cl)2]·5H2O (V3dipic-Cl), V(IV)O(dipic-Cl)(H2O)2 (V4dipic-Cl) and K[V(V)O2(dipic-Cl)] (V5dipic-Cl), were synthesized with the indicated oxidation states. The present study was conducted to investigate if chemical valence and anti-oxidation effects of vanadium compounds are involved in the anti-diabetic effects observed in streptozotocin (STZ)-induced diabetic rats treated with these vanadium compounds. V3dipic-Cl, V4dipic-Cl, V5dipic-Cl, inorganic vanadium salts vanadyl sulfate (VOSO4) or sodium metavanadate (NaVO3) were orally administered in drinking water (50μgV/ml) to STZ-induced diabetic rats for 28days. The results showed that Vdipic-Cl treatment significantly improved hyperglycemia and glucose intolerance, as well as increased hepatic glycogen synthesis in diabetic rats. The mRNA levels of key glycolytic enzymes in liver, phosphoenolpyruvate carboxykinase (PEPCK), glucokinase (GK), and L-pyruvate kinase (L-PK) altered in diabetic animals were significantly restored towards normal values by treatment with some of the vanadium compounds. Moreover, the diabetes elevated activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) in serum were significantly decreased after treatment with Vdipic-Cl complexes. Furthermore, treatment of diabetic rats with V4dipic-Cl and V5dipic-Cl compounds significantly reduced malondialdehyde (MDA) production and increased glutathione peroxidase (GSH-Px) and catalase (CAT) activities. These data suggest that vanadium compounds with the indicated chemical valence promote glycogen synthesis and recover suppressed glycolysis in the liver of diabetic rats due to their capacity to reduce oxidative stress by stimulating antioxidant enzymes.