Background Many eye diseases such as central retinal artery occlusion,glaucoma and ischemic optic neuropathy,etc.lead to retinal ischemia-reperfusion injury (RIRI) and furthmore visual functional damage.It is neeessary to study the treatment of RIRI.Objective This study was to observe and discuss the influence of aminoguanidine on the retina morphological changes and its mechanism after RIRI.Methods Eighty clean healthy male Japanese white rabbits were randomly divided into normal injury group,RIRI group and aminoguanidine (AG)treated group.The model of RIRI was established by infusing saline solution into the anterior chamber to elevate intraocular pressure (IOP) in both RIRI group and AG group.AG was intraperitoneally injected in the models of the AG group,and normal saline solution was used at the same method in tbe normal group and the RIRI group.The fundus photography and fundus fluorescein angiography(FFA) were pertormed on the rabbits at the moment of retina ischemia and 6,24 and 72 hours after reperfusion.The parts of rabbits were sacrificed 1,6,24 and 72 hours after reperfusion,followed by the enucleation of the eyeballs.Retinal section was prepared for TUNEL examination to evaluate the apoptosis of retinal cells.Nitric oxide (NO) concentration in retina was detected with nitrate reductase,and the activity of inducible nitric oxide synthase (iNOS) was measured by colorimetric detection.The use of the animals followed the Regulations for the Administration of Affairs Concerning Experimental Animals by State Science and Technology Commission.Results The fundus photography and FFA showed that the retinal edema was more mild,and the percentage of vascular occlusion was lower in the AG treatment group than that in RIRI group and the amount and area of fluorescein leakage were also smaller than the treatment group.The numbers of TUNEL positive cells in the AG treatment group were less than those in the RIRI model group at 1,6,24 and 72 hours after experiment (F分组 =2762.37,P =0.00 ; F时间 =894.24,P =0.00).Numbers of TUNEL positive cells between adjacent time points were significantly different in both RIRI model group and AG treatment group (RIRI group:q =24.475,36.591,-20.37,P＜0.05;AG group:q =20.94,16.79,-6.92,P＜0.05),with the peak value at 24 hours after experiment.NO contents were significantly higher in the RIRI model group compared to AG group at various time points(q =3.84,4.01,8.91,3.75,P＜0.05),and those between adjacent time points showed significant differences (RIRI group:q=4.77,13.403,-10.29,P＜0.05;AG group:q=4.55,9.05,-5.08,P＜0.05).iNOS activity was significantly elevated in the RIRI model group compared with AG group(q=-3.74,-4.94,-6.53,-3.98,P＜0.05),and obvious differences also were seen between the adjacent time points in both two groups(RIRI group:q =8.43,6.71,-6.39,P＜0.05 ;AG group:q =4.16,5.08,-3.93,P＜0.05).Conclusions Aminoguanidine can protect the retinal function and morpbology from oxidative stress damage after RIRI by reducing the NO level and inhibiting the iNOS activity in retina.

Humans ; Siblings ; Forensic Medicine ; Forensic Genetics

Objective To explore the epidemics of influenza viruses in Guangzhou area from 1998 to 2003. Methods The specimens for viral isolation were taken with swabs from children's throats and the material was inoculated into the MDCK cells and were incubated at 33 ℃ The supernatant of MDCK cells culture was tested with hemagglutination test. Results Influenza viruses were isolated from 264 of 3444 children; total positive rate of influenza virus isolation was 7.6%. The positive rate of influenza viruses was 16.8% in 1998; the prevailing strain of influenza viruses was H3N2. The influenza viruses isolation rate was 7.4% in 1999;the positive rate was 8.4% ; HIN1 occurred in 2000, the positive rate was 3.8%. H3N2 did not occur in 2001; the positive rate was 7.3% ; influenza B viruses was the prevailing strain in 2002; the positive rate was 1.7% in 2003. Influenza B viruses was Yamagata like strain from 1998 to 2001, Victoria like strain from 2002 to 2003. H9N2 avian influenza virus was isolated from a child. Conclusions Influenza was prevalent in Guangzhou in 1998, but not prevalent from 1999 to 2003. Most of influenza B viruses were Yamagata strain. There were cases avian influenza caused by H9N2 in 1999.

Objective To evaluate the limit of detection of eight enzyme-linked immunosorbent assay (ELISA) according to hospital grade assessment and ISO15189:2012.Methods According to the new health industry standard WS/T 514-2017:"Establishment and verification of detection capability for clinical laboratory measurement procedures",the limit of detection (LoD) was established,in the sameset of detection system,using two reagent lot,each lot for 5 consecutive days 4 consecutive days to assess the value of the concentration of five specimens were detected repeatedly,calculated the corresponding hit rate,then transform into probability units,and the corresponding concentration value production regression model,the hit rate of 95 ％ corresponds to the probability unit 1.645 substituted into the equation,the resulting concentration value was LoD estimates.The detection limit values were tested for 3 consecutive days of detection of two LoD concentrations near the declared concentration of the sample (diluted by the standard material) was detected 4 times repeatedly to calculate the positive result was greater than or equal to the percentage of LoD statement,greater than or equal to the critical value of 87％,then verified success.Results HBsAg:0.100 IU/ml,HBsAb:9.642 mIU/ml,HBeAg:0.666 NCU/ml,HBeAb:3.700 NCU/ml,HBcAb:0.786 IU /ml,HCV:0.506 NCU/ml,TP:2.236 mIU/ml and HIV:0.135 NCU/ml.The detection limit estimates were passed.Conclusion The verification limit of the verification project in the testing method and detection system of the laboratory meet the requirements Objective.

OBJECTIVETo study the effect of celecoxib on chronic hypoxia and hypercapnic pulmonary hypertension.

METHODSSD rats were randomly divided into normal control group (A), hypoxic hypercapnic group (B), hypoxic hypercapnia+ celecoxib group (C). The content of TXB2 and 6-keto-PGF1alpha in plasma and lung were detected by the technique of radioimmunology.

RESULTS(1) Mean pulmonary arteria pressure(mPAP) was significantly higher in rats of B group than those of A group. mPAP was significantly higher in rats of C group than those of B group. Differences of mPAP were not significant in three groups. (2) The content of TXB2 in plasma and lung and the ratio of TXB2/6-keto-PGF1alpha were significantly higher in rats of B group than those of A group. The ratio of TXB2/6-keto-PGF1alpha was significantly higher and the content of 6-keto-PGF1alpha in plasma and lung was significantly lower in rats of C group than those of B group. (3) Light microscopy showed that WA/TA (vessel wall area/total area) and PAMT (the thickness of medial smooth cell layer) were significantly higher in rats of B group than those of A group. WA/TA and PAMT were significantly higher in rats of C group than those of B group. (4) Electron microscopy showed the thickening of vessel wall and the proliferation of collagen fiber in B group and augmentation of smooth muscle cell and abundance of myofilament in pulmonary arterioles in C group.

CONCLUSIONCelecoxib can aggravate hypoxic hypercapnia pulmonary hypertension and pulmonary vessel remodeling by increasing the ratio of TXA2/PGI2.

Animals ; Celecoxib ; Chronic Disease ; Cyclooxygenase 2 Inhibitors ; adverse effects ; pharmacology ; Epoprostenol ; blood ; Hypercapnia ; complications ; Hypertension, Pulmonary ; etiology ; physiopathology ; Hypoxia ; complications ; Male ; Pyrazoles ; adverse effects ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Sulfonamides ; adverse effects ; pharmacology ; Thromboxane A2 ; blood

The cardiovascular circulation feedback control treatment instrument (CFCTI) is an automatic feedback control treatment system, which has the function of monitoring, alarming, trouble self-diagnosis and testing on the line in the closed loop. The instrument is designed based on the successful clinical experiences and the data are inputted into the computer in real-time through a pressure sensor and A/D card. User interface window is set up for the doctor's choosing different medicine. The orders are outputted to control the dose of medicine through the transfusion system. The response to medicine is updated continually. CFCTI can avoid the man-made errors and the long interval of sampling. Its reliability and accuracy in rescuing the critical patients are much higher than the traditional methods.
Automation ; instrumentation ; Cardiovascular System ; Feedback ; Medication Systems

The present study was to explore the effects of insulin on proliferation of skeletal myoblast cells in rats. Separated and cultured primary skeletal myoblast cells from rats were treated by insulin. By means of the incorporation of (3)H-TdR, BrdU assay and MTT assay, the proliferation of skeletal myoblast cells was detected. Western blot was used to check the phosphorylation of Akt and ERK of myoblast cells. The results showed that insulin significantly promoted the incorporation of (3)H-TdR into cultured skeletal myoblast cells in a dose-dependent manner. MTT assay and BrdU assay also showed insulin promoted the proliferation of skeletal myoblast cells. The promotion of skeletal myoblast cells proliferation by insulin was inhibited by PI3K inhibitor wortmannin or MEK inhibitor U0126, and the same phenomenon was shown in L6 and C2C12 cells. Also, insulin increased the phosphorylation of Akt and ERK in myoblast cells. These results suggest that insulin may promote proliferation of skeletal myoblast cells through PI3K/Akt and MEK/ERK pathways.
Androstadienes ; pharmacology ; Animals ; Butadienes ; pharmacology ; Cell Proliferation ; Cells, Cultured ; Enzyme Inhibitors ; pharmacology ; Insulin ; pharmacology ; MAP Kinase Signaling System ; Myoblasts, Skeletal ; cytology ; drug effects ; Nitriles ; pharmacology ; Phosphatidylinositol 3-Kinases ; metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; metabolism ; Rats

OBJECTIVETo investigate the clinical features of thyroid disease occurring in response to antiviral therapy in patients with chronic hepatitis C (CHC).

METHODSEighty-two patients diagnosed with CHC were recruited for study from our hospital between 2009 and 2010. All patients were given a 48-week course of antiviral combination therapy with pegylated-interferon (Peg-IFN; 180 mug qw ih) and ribavirin (RBV; 15 mg/kg bw). Patient sera was collected prior to treatment (baseline), at treatment weeks 24 and 48, and post-treatment week 24, and used to detect changes in levels of thyroid function markers, thyroid-specific and other autoantibodies, complement factors, and immunoglobulins (Igs). Differential expression of biomarkers was assessed between patients who developed thyroid disorder and those who did not.

RESULTSAt treatment week 48, 13.4% (11/82) of cases developed hypothyroidism, 3.7% (3/82) developed hyperthyroidism, 20.7% (17/82) tested positive for thyroglobulin antibody, and 22.0% (18/82) tested positive for thyroid peroxidase antibody. The patients who did not develop thyroid disease had significantly higher post-treatment levels (vs. baseline) of IgG (14.84 +/- 2.61 vs. 12.95 +/- 3.32 g/L, F = 10.458, P = 0.002) and C4 (0.26 +/- 0.09 vs. 0.22 +/- 0.08 g/L, F = 6.835, P = 0.011) and significantly lower IgM (0.86 +/- 0.48 vs. 1.00 +/- 0.42 g/L, F = 9.106, P = 0.003). The patients who developed thyroid disease showed no significant differences in the baseline and post-treatment levels of IgG, C4, or IgM. When the two groups of patients who did or did not develop thyroid disease were compared, there was no difference in the amount of patients who achieved sustained virological response.

CONCLUSIONAntiviral-induced thyroid disease in patients with refractory hepatitis C manifests as clinically-detectable abnormalities in serum levels of thyroid autoantibody and markers of hypothyroidism. Levels of other autoantibodies and Igs do not correlate with the development of thyroid disease in these patients, and thyroid disease does not appear to affect the efficacy of Peg-IFN + RBV antiviral therapy.

Antiviral Agents ; therapeutic use ; Drug Therapy, Combination ; Hepatitis C, Chronic ; drug therapy ; Humans ; Interferon-alpha ; therapeutic use ; Polyethylene Glycols ; therapeutic use ; Ribavirin ; therapeutic use ; Thyroid Diseases ; chemically induced

BACKGROUND AND OBJECTIVEBC047440 is a new gene related to cancer growth and proliferation. Due to the lack of specific antibodies, how BC047440 protein influences the liver cancer growth is unclear. This study aimed to determine the relationship between BC047440 protein expression and clinicopathologic parameters of hepatocellular carcinoma (HCC), and to evaluate the prognostic value of BC047440 for HCC patients.

METHODSWe prepared the polyclonal antibodies of BC047440, and used Western blot and immunohistochemical staining to detect BC047440 expression in 68 specimens of HCC. The correlations of BC047440 expression to clinicopathologic features and prognosis of HCC patients were analyzed.

RESULTSThe polyclonal antibodies could effectively recognize endogenous BC047440 in HCC tissues. The positive rate of BC047440 protein was significantly higher in HCCs than in adjacent tissues (44.1% vs. 23.5%, P<0.05); the rate was significantly higher in patients with larger tumor (P<0.05) and portal vein invasion (P<0.01). The HCC patients with high BC047440 expression showed a significantly poorer prognosis than those with low BC047440 expression (P<0.05).

CONCLUSIONBC047440 can promote the growth and invasion of HCC.

Adaptor Proteins, Signal Transducing ; immunology ; metabolism ; Adult ; Age Factors ; Aged ; Antibodies ; analysis ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Female ; Humans ; Liver Neoplasms ; metabolism ; pathology ; Male ; Middle Aged ; Neoplasm Invasiveness ; Portal Vein ; pathology ; Prognosis ; Survival Rate ; Tumor Burden

OBJECTIVETo observe the effects of Nrf2 gene expression induced by RU486 at different doses on A549 cell damage induced by paraquat (PQ).

METHODSAfter A549 cells transfected with Ad-RUNrf2 were treated by RU486 at the doses of 10(-10), 10(-9), 10(-8) and 10(-7) mol/L for 6 h, A549 cell cultures were exposed to 10(-3) mol/L of PQ for 48 h. Then qRT-PCR and EMSA assays were used to detect the expression of Nrf2 gene, and qRT-PCR and ELISA assays were utilized to measure the effects of Nrf2 gene on the expression of the inflammatory cytokines IL-6, IL-10 and TNF-α, apoptotic factors Caspase-3, Caspase-9 and Cytochrome C. The oxidation factors (CAT and MDA protein contents) were observed by Chemical Colorimetric Analysis.

RESULTSNrf2 gene relative expression and protein contents increased with RU486 concentrations, and the above expression was the highest when the concentration of RU486 was 10(-7) mol/L, which was significantly higher than those in control and PQ exposure groups (P < 0.01 or P < 0.05). The relative gene expression and protein expression of IL-6 and TNF-α enhanced with the reduced concentrations of RU486, which were the lowest when RU486 concentration was 10(-7) mol/L, as compared with control and PQ exposure groups (P < 0.01 or P < 0.05), while the change of IL-10 content was the opposite. The relative expression of Caspase3, Caspase9 and Cytochrome C genes also increased with the reduced concentrations of RU486, which were the lowest when RU486 concentration was 10(-7) mol/L, as compared with control and PQ exposure groups (P < 0.01 or P < 0.05). The content of CAT enhanced with RU486 concentration, which was the highest when RU486 concentration was 10(-7) mol/L, as compared with control and PQ exposure groups (P < 0.05). But the change of MDA content was the contrary.

CONCLUSIONNrf2 expression induced by RU486 can promote the balance of oxidation-antioxidation system in A549 cells and inhibit the inflammation and apoptosis factors, which has a protective effect on A549 cell injury induced by PQ.

Cell Line ; Gene Expression ; drug effects ; Humans ; Interleukin-10 ; metabolism ; Interleukin-6 ; metabolism ; Mifepristone ; administration & dosage ; pharmacology ; NF-E2-Related Factor 2 ; genetics ; Paraquat ; toxicity ; Tumor Necrosis Factor-alpha ; metabolism