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1.
International Eye Science ; (12): 454-458, 2015.
Article in Chinese | WPRIM | ID: wpr-637188

ABSTRACT

· Vascular endothelial growth factor is indispensable inducing factor in retinalangiogenesis. After the retinal neovascularization of proliferative diabetic retinopathy ( PDR ) patients, it can cause fibrovascular membrane formation, epiretinal membrane fibrosis increased, resulting in traction retinal detachment with further aggravate the condition. The recent research suggests that cytokines promote fibroblast proliferation, movement, adhesion, and secretion of extracellular matrix functions in the diabetic state of the environment changes to profibrogenic state, resulting in the accumulation and fibrosis of extracellular matrix. This paper reviewed the status quo of the correlation between vascular endothelial growth factor and fibrosis-related cytokine.

2.
International Eye Science ; (12): 2217-2219, 2014.
Article in Chinese | WPRIM | ID: wpr-637058

ABSTRACT

AlM: To measure the retinal electrical activities in patients with diabetic retinopathy ( DR ) by applying multifocal electroretinogram ( mf-ERG) and evaluate the degree of visual damage at different stages of DR METHODS:Thirty cases ( 30 eyes ) aged 50 ~70 years old, excluding other diseases, were as normal group, and 99 cases ( 99 eyes ) diagnosed with type 2 diabetes were as experiment group. The cases received mf-ERG examination in the standard state, respectively. The results were statistically analyzed RESULTS: For DR patients with early and background stage, the reaction density of mf - ERG P1 wave decreased as the disease worsened, significantly reduced in non - proliferating stage and decreased more significantly in the background of the stage Ⅲ. This showed that in the macula, electrical activity had weakened before the retina without visual or morphological changes, and with the development of the disease, the electrical activity decreased more obviously. CONCLUSlON:mf-ERG can evaluate the severity of DR, especially suit in the early and background period of DR.

3.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 392-7, 2013.
Article in English | WPRIM | ID: wpr-636466

ABSTRACT

The type I interferon and IFNAR play an important role in hepatitis B virus (HBV) infection and anti-HBV therapy. However, its mechanism of action is still poorly understood. To gain more insights into the role of type I interferon and type I interferon receptor (IFNAR) in HBV infection, we established an HBV persistent replication IFNAR knockout (IFNAR(-/-)) mouse model and preliminarily applied this model. At first, the progeny of IFNAR(-/-) mouse was reproduced. Then hydrodynamic injection with pAAV/HBV1.2 plasmid was conducted to establish the persistent HBV replication IFNAR(-/-) mouse model. At last, we applied this model to evaluate the effect of nucleoside analogues entecavir (ETV) on HBV replication. It was found that there was no difference in the serum HBsAg and HBeAg levels and HBcAg expression in the liver tissue between the ETV treated groups and normal saline (NS) treated group, but the serum HBV DNA levels were significantly suppressed 10, 25, 40 and 55 days after the ETV treatment [P=0.035, P=0.00, P=0.149 and P=0.084, IFNAR knockout (KO) control group vs. C57BL/6 ETV groups, respectively; P=0.081, P=0.001, P=0.243 and P=0.147, IFNAR KO control group vs. IFNAR KO ETV groups, respectively]. Interestingly, there was no difference in serum HBV DNA levels between the ETV treated IFNAR(-/-) and C57BL/6 mice. This result suggests that HBV suppression during ETV treatments doesn't depend on type I interferon and IFNAR. Collectively, persistent HBV replication IFNAR(-/-) mouse model that we established is a useful and convenient tool to detect the function of the type I interferon and IFNAR in HBV infection and anti-HBV treatments.

4.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 392-397, 2013.
Article in English | WPRIM | ID: wpr-343085

ABSTRACT

The type I interferon and IFNAR play an important role in hepatitis B virus (HBV) infection and anti-HBV therapy. However, its mechanism of action is still poorly understood. To gain more insights into the role of type I interferon and type I interferon receptor (IFNAR) in HBV infection, we established an HBV persistent replication IFNAR knockout (IFNAR(-/-)) mouse model and preliminarily applied this model. At first, the progeny of IFNAR(-/-) mouse was reproduced. Then hydrodynamic injection with pAAV/HBV1.2 plasmid was conducted to establish the persistent HBV replication IFNAR(-/-) mouse model. At last, we applied this model to evaluate the effect of nucleoside analogues entecavir (ETV) on HBV replication. It was found that there was no difference in the serum HBsAg and HBeAg levels and HBcAg expression in the liver tissue between the ETV treated groups and normal saline (NS) treated group, but the serum HBV DNA levels were significantly suppressed 10, 25, 40 and 55 days after the ETV treatment [P=0.035, P=0.00, P=0.149 and P=0.084, IFNAR knockout (KO) control group vs. C57BL/6 ETV groups, respectively; P=0.081, P=0.001, P=0.243 and P=0.147, IFNAR KO control group vs. IFNAR KO ETV groups, respectively]. Interestingly, there was no difference in serum HBV DNA levels between the ETV treated IFNAR(-/-) and C57BL/6 mice. This result suggests that HBV suppression during ETV treatments doesn't depend on type I interferon and IFNAR. Collectively, persistent HBV replication IFNAR(-/-) mouse model that we established is a useful and convenient tool to detect the function of the type I interferon and IFNAR in HBV infection and anti-HBV treatments.


Subject(s)
Animals , Female , Humans , Male , Mice , Chronic Disease , Disease Models, Animal , Hepatitis B , Genetics , Virology , Hepatitis B virus , Physiology , Mice, Inbred C57BL , Mice, Knockout , Receptor, Interferon alpha-beta , Genetics , Metabolism , Virus Replication , Genetics
5.
Chinese Journal of Hepatology ; (12): 794-797, 2012.
Article in Chinese | WPRIM | ID: wpr-296812

ABSTRACT

<p><b>OBJECTIVE</b>To explore the mitochondrial toxicities induced by zidovudine (AZT) and adefovir dipivoxil (ADV) antiviral drugs using a rat model system.</p><p><b>METHODS</b>Twelve healthy Sprague-Dawley rats were randomly divided into three equal groups and treated by oral gavage with zidovudine (125 mg/kg/day), adefovir (40 mg/kg/day), or saline (equal volume) for 28 days. The rats' body weights were measured once a week, and blood was collected every two weeks for blood and biochemical tests. All animals were sacrificed at the end of treatment, and liver, kidney, skeletal muscle, and cardiac muscle were collected by necropsy. Mitochondria were isolated from the respective tissue samples, and the activities of respiratory chain complexes were measured. DNA was purified from each sample and the mitochondrial DNA (mtDNA) content was monitored by quantitative real time PCR. Mitochondrial morphology was analyzed under electron microscope.</p><p><b>RESULTS</b>No significant adverse effects, including body weight loss, abnormal blood or biochemistry, were observed in rats treated with AZT or ADV. The activities of mitochondrial cytochrome c oxidase in liver and cardiac muscle were slightly decreased in rats treated with AZT (liver: 9.44+/-3.09 vs. 17.8+/-12.38, P?=?0.21; cardiac muscle: 32.74+/-5.52 vs. 24.74+/-20.59, P?=?0.28; kidney: 4.42+/-1.53 vs. 14.45+/-13.75, P?=?0.18; skeletal muscle: 33.75+/-8.74 vs. 40.04+/-2.49, P?=?0.45). The mtDNA content was significantly decreased in cardiac muscle of AZT-treated rats (cardiac muscle: 0.15+/-0.13 vs. 0.32+/-0.42, P?=?0.85). The morphology of mitochondria in liver, kidney, skeletal muscle, and cardiac muscle was significantly altered in the AZT-treated rats and included disappearance of the outer membrane, severely damaged structure, and swollen or completely absent cristae. No obvious effects were noted in the ADV- or saline-treated rats.</p><p><b>CONCLUSION</b>Significant adverse effects related to mitochondrial toxicity were observed in rats treated with AZT. The slightly decreased mtDNA content in ADV-treated rats may suggest that this antiviral drug can also cause mitochondrial toxic effects.</p>


Subject(s)
Animals , Female , Rats , Adenine , DNA, Mitochondrial , Electron Transport Complex IV , Metabolism , Kidney , Liver , Mitochondria , Metabolism , Mitochondria, Heart , Mitochondria, Liver , Mitochondria, Muscle , Muscle, Skeletal , Myocardium , Organophosphonates , Rats, Sprague-Dawley , Zidovudine
6.
International Eye Science ; (12): 951-953, 2011.
Article in Chinese | WPRIM | ID: wpr-641832

ABSTRACT

AIM: To analyze the clinical feature and treatment of endogenous endophthalmitis caused by liver abscess. METHODS: A total of 9 eyes (7 cases) with endogenous endophthalmitis caused by liver abscess in our hospital from 2005 to 2010 were analyzed retrospectively. Microorganism was cultivated with blood or vitreous in all patients.4 eyes were performed vitrectomy. 2 eyes were injected antibiotics in vitreous cavity. 3 eyes were only treated with antibiotics.RESULTS: Two cases (2 eyes) were diagnosed with endophthalmitis firstly, then found liver abscess; 4 eyes were with diabetes mellitus, and 1 eye with abnormal glucose tolerance. Cultivation of microorganism was positive in 6 eyes (67%), including Pneumonia cray-research, Candida albicans and Escherichia coli. 5 eyes had useful vision after treatment, 1 eye had light perception,3 eyes became blindness. CONCLUSION: As an ocular emergency, endogenous endophthalmitis caused by liver abscess can severely damage visual function. Timely consultation, early diagnosis, proper systemic and topical anti-infective and anti-inflammatory treatment are the most effective methods for controlling infection. Vitrectomy with intravitreal antibiotics plays an important role in preserving useful vision function in patients.

7.
Journal of Southern Medical University ; (12): 2059-2063, 2009.
Article in Chinese | WPRIM | ID: wpr-336021

ABSTRACT

<p><b>OBJECTIVE</b>To establish a loop-mediated isothermal amplification (LAMP) method for rapid diagnosis of Vibrio cholerae.</p><p><b>METHODS</b>Based on the ompW nucleic sequence of Vibrio cholerae, a pair of primers was designed for LAMP. The reaction conditions were optimized, and the specificity, sensitivity, and practicability of LAMP were tested using 47 bacterial strains and simulated contaminated sites.</p><p><b>RESULTS</b>The results of viable bacterium count showed that LAMP was capable of detecting Vibrio cholerae at a level as low as 1.6x10(2) cfu/ml. The minimal detectable concentration was 1.6+10(3) cfu/ml for simulated contaminated samples such as feces and seawater, and 1.6+10(4) cfu/ml for contaminated milk. All the 21 strains of Vibrio cholerae yielded positive results in LAMP, and the 26 strains of other bacteria all showed negative results, with a detection specificity of 100%.</p><p><b>CONCLUSION</b>The established LAMP method has high specificity and sensitivity for detecting Vibrio cholerae and is applicable in field monitoring and epidemiological study of Vibrio cholerae.</p>


Subject(s)
Humans , Bacterial Proteins , Genetics , Cholera , Diagnosis , Microbiology , Clinical Laboratory Techniques , Methods , Nucleic Acid Amplification Techniques , Methods , Sensitivity and Specificity , Vibrio cholerae , Genetics
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