Objective To prepare and characterize the monoclonal antibodies (McAbs) against recombinant adhesion protein 33 (AP33) of Trichomonas vaginalis. Methods The purified recombinant fusion protein AP33 was used as antigen to immunize BALB/c mice. Sp2/0 myeloma cells were fused with the splenocytes from immunized BALB/c mice. After ELISA screening and 4 times of limited dilution, 5 positive hybridoma cell lines were obtained, and the biological properties of the McAbs were identified by Western blotting. Indirect immunofluorescent antibody test (IFAT) was performed and the inhibition effect of McAbs on the cytoadherence of T.richomonas vaginalis to HeLa cell was assayed. Results Western blotting demonstrated that 5 McAbs, designated as 4A2, 4F11, 4F8, 4E7 and 4H11, specifically combined with the recombinant AP33 of T.vaginalis. The McAbs were IgG1 isotypes. Four of them (4F11, 4F8, 4E7 and 4H11) showed parasite recognition by IFAT. Parasite cytoadherence to a monolayer of HeLa cells was inhibited in vitro with a inhibition rate of 50.08%, 65.03%, 50.70% and 49.08% by the 4 McAbs under a concentration of 200, 200, 400 and 200?g/ml, respectively. Conclusions The prepared McAbs against the recombinant AP33 show a protective inhibition on cytoadherence of Trichomonas vaginalis in vitro.

BACKGROUND:Cirrhosis is a long-term consequence of chronic hepatic injury, which has no effective therapy. Mesenchymal stem cels have been shown to play a potential role in the treatment of liver fibrosis/cirrhosis. OBJECTIVE:To investigate the therapeutic effect and mechanism of human umbilical cord-derived mesenchymal stem cels on CCl4 induced liver fibrosis/cirrhosis in rats. METHODS:A CCl4-induced liver fibrotic/cirrhotic rat model was used, and human umbilical cord-derived mesenchymal stem cels were injectedvia the tail vein after modeling. Liver biochemical profile was measured by Beckman Coulter analyzer. Histopathological changes were assessed by Sirius red staining. The expressions of colagen type I, colagen type III, matrix metaloproteinases-2 and tissue inhibitor of matrix metaloproteinases-2 protein and mRNA in liver tissues were observed by immunohistochemistry, western blot and real-time PCR, respectively. RESULTS AND CONCLUSION:Liver biochemical profile indicated the transplantation of human umbilical cord-derived mesenchymal stem cels could improve the liver function of rats with liver fibrosis and cirrhosis. After cel transplantation, except 1-week cel transplantation group, the expressions of the matrix metaloproteinases-2 mRNA and protein were significantly increased, while the expressions of colagen type I, colagen type III and tissue inhibitor of matrix metaloproteinases-2 mRNA and protein significantly decreased, compared with the corresponding model groups. Human umbilical cord-derived mesenchymal stem cels play a role in the treatment of liver fibrosis and cirrhosis through upregulating the expression of matrix metaloproteinases-2 and lowering the expression of inhibitor of matrix metaloproteinases-2. With the continued presence of pathogenic factors, human umbilical cord-derived mesenchymal stem cel transplantation cannot reverse liver fibrosis or cirrhosis, and only delay the process of liver fibrosis or cirrhosis.

Different antiepileptic drugs (AEDs) may cause similar adverse effects, one of which is diplopia. However, the AEDs causing diplopia and the dose-response effect of each drug remains uncertain. In this study, we compared several second-generation AEDs to find out whether they would contribute to the risk of diplopia and their effect-causing dose. A meta-analysis was performed on 19 studies in agreement with our inclusion criteria. The results showed that eight commonly used second-generation AEDs (gabapentin, levetiracetam, oxcarbazepine, lamotrigine, pregabalin, topiramate, vigabatrin and zonisamide) could cause diplopia. The reported odds ratios (ORs) ranged from 1.406 to 7.996. Ranking risks from the highest to the lowest ORs of the eight AEDs of any dose resulted in the following order: use of oxcarbazepine (7.996), levetiracetam (7.472), lamotrigine (5.258), vigabatrin (3.562), pregabalin (3.048), topiramate (2.660), gabapentin (1.966), zonisamide (1.406). Taking into account the ORs above, we can conclude that second-generation AEDs of any dose may cause diplopia. However, the levetiracetam-caused diplopia needs to be further studied according to the data (OR, 7.472; 95% confidence interval, 0.375-148.772). These findings ask for better concerns about patients' quality of life when giving antiepileptic treatments.

Different antiepileptic drugs (AEDs) may cause similar adverse effects, one of which is diplopia. However, the AEDs causing diplopia and the dose-response effect of each drug remains uncertain. In this study, we compared several second-generation AEDs to find out whether they would contribute to the risk of diplopia and their effect-causing dose. A meta-analysis was performed on 19 studies in agreement with our inclusion criteria. The results showed that eight commonly used second-generation AEDs (gabapentin, levetiracetam, oxcarbazepine, lamotrigine, pregabalin, topiramate, vigabatrin and zonisamide) could cause diplopia. The reported odds ratios (ORs) ranged from 1.406 to 7.996. Ranking risks from the highest to the lowest ORs of the eight AEDs of any dose resulted in the following order: use of oxcarbazepine (7.996), levetiracetam (7.472), lamotrigine (5.258), vigabatrin (3.562), pregabalin (3.048), topiramate (2.660), gabapentin (1.966), zonisamide (1.406). Taking into account the ORs above, we can conclude that second-generation AEDs of any dose may cause diplopia. However, the levetiracetam-caused diplopia needs to be further studied according to the data (OR, 7.472; 95% confidence interval, 0.375-148.772). These findings ask for better concerns about patients' quality of life when giving antiepileptic treatments.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Anticonvulsants ; therapeutic use ; Child ; Diplopia ; drug therapy ; Humans ; Middle Aged ; Placebo Effect ; Young Adult

Talents are the core driving force to promote the high-quality development of public hospitals,and the talent team building is an important factor for hospitals to get sustainable development and improve comprehensive competitiveness.In view of the shortage of high-level talents,the imperfect talent reserve system,and the lagging personnel management mechanism of public hospitals and the resulting unreasonable talent team structure and talent gap,public hospitals should take talent team building as the starting point,pay equal attention to the introduction and training of talents,interact with discipline construction and talent construction,vigorously promote the construction of personnel management system and mechanism innovation,form a standardized,scientific,refined and efficient modern hospital management system,so that the effectiveness of talents can be max-imized,and provide intellectual support for the high-quality development of public hospitals.