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1.
Biomedical and Environmental Sciences ; (12): 432-443, 2017.
Article in English | WPRIM | ID: wpr-311394

ABSTRACT

<p><b>OBJECTIVE</b>To investigate acrylamide (ACR)-induced subacute neurotoxic effects on the central nervous system (CNS) at the synapse level in rats.</p><p><b>METHODS</b>Thirty-six Sprague Dawley (SD) rats were randomized into three groups, (1) a 30 mg/kg ACR-treated group, (2) a 50 mg/kg ACR-treated group, and (3) a normal saline (NS)-treated control group. Body weight and neurological changes were recorded each day. At the end of the test, cerebral cortex and cerebellum tissues were harvested and viewed using light and electron microscopy. Additionally, the expression of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were investigated.</p><p><b>RESULTS</b>The 50 mg/kg ACR-treated rats showed a significant reduction in body weight compared with untreated individuals (P < 0.05). Rats exposed to ACR showed a significant increase in gait scores compared with the NS control group (P < 0.05). Histological examination indicated neuronal structural damage in the 50 mg/kg ACR treatment group. The active zone distance (AZD) and the nearest neighbor distance (NND) of synaptic vesicles in the cerebral cortex and cerebellum were increased in both the 30 mg/kg and 50 mg/kg ACR treatment groups. The ratio of the distribution of synaptic vesicles in the readily releasable pool (RRP) was decreased. Furthermore, the expression levels of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were decreased in both the 30 mg/kg and 50 mg/kg ACR treatment groups.</p><p><b>CONCLUSION</b>Subacute ACR exposure contributes to neuropathy in the rat CNS. Functional damage of synaptic proteins and vesicles may be a mechanism of ACR neurotoxicity.</p>


Subject(s)
Animals , Male , Rats , Acrylamide , Toxicity , Cerebellum , Cell Biology , Cerebral Cortex , Cell Biology , Drug Administration Schedule , Gait , Gene Expression Regulation , Neurons , Neurotoxicity Syndromes , Pathology , Rats, Sprague-Dawley , Synapses , Synapsins , Genetics , Metabolism , Synaptic Vesicles , Physiology , Weight Loss
2.
Journal of Veterinary Science ; : 71-78, 2016.
Article in English | WPRIM | ID: wpr-110763

ABSTRACT

Swine influenza viruses (SwIVs) cause considerable morbidity and mortality in domestic pigs, resulting in a significant economic burden. Moreover, pigs have been considered to be a possible mixing vessel in which novel strains loom. Here, we developed and evaluated a novel M2e-multiple antigenic peptide (M2e-MAP) as a supplemental antigen for inactivated H3N2 vaccine to provide cross-protection against two main subtypes of SwIVs, H1N1 and H3N2. The novel tetra-branched MAP was constructed by fusing four copies of M2e to one copy of foreign T helper cell epitopes. A high-yield reassortant H3N2 virus was generated by plasmid based reverse genetics. The efficacy of the novel H3N2 inactivated vaccines with or without M2e-MAP supplementation was evaluated in a mouse model. M2e-MAP conjugated vaccine induced strong antibody responses in mice. Complete protection against the heterologous swine H1N1 virus was observed in mice vaccinated with M2e-MAP combined vaccine. Moreover, this novel peptide confers protection against lethal challenge of A/Puerto Rico/8/34 (H1N1). Taken together, our results suggest the combined immunization of reassortant inactivated H3N2 vaccine and the novel M2e-MAP provided cross-protection against swine and human viruses and may serve as a promising approach for influenza vaccine development.


Subject(s)
Animals , Female , Mice , Antibodies, Viral/blood , Antigens, Viral/genetics , Body Weight , Cross Protection/immunology , Disease Models, Animal , Epitopes, T-Lymphocyte/genetics , Influenza A Virus, H3N2 Subtype/genetics , Influenza Vaccines/immunology , Mice, Inbred BALB C , Orthomyxoviridae Infections/immunology , Peptides/genetics , Random Allocation , Survival Analysis , Vaccines, Synthetic/immunology , Virus Replication
3.
Chinese Medical Journal ; (24): 2375-2378, 2010.
Article in English | WPRIM | ID: wpr-237446

ABSTRACT

<p><b>BACKGROUND</b>It has been shown that the β3-adrenergic receptor (β3-AR) gene Trp64Arg mutation was closely related to obesity and insulin resistance, and may be related to the prevalence of metabolic syndrome (MS). The aim of this study was to investigate the relationship between the β3-AR gene mutation and the prevalence of MS.</p><p><b>METHODS</b>A seven-year follow-up study was initiated in 2000, with 496 samples of simplex obese subjects (body mass index ≥ 25 kg/m(2)) and 248 normal-weight subjects. According to the β3-AR genotypes, the subjects were classified as Trp64 homozygote group and Arg64 carrier group and after 7 years the prevalence of MS was determined.</p><p><b>RESULTS</b>According to the baseline profile, there were no significant differences in the adiposity, blood pressure, lipid profile, fasting plasma glucose and fasting insulin between Trp64 homozygote group and Arg64 carrier group either in obesity or normal-weight subjects. The results of follow-up study indicated that in obese men the prevalence rate of MS was much higher in Arg64 carrier group than that in Trp64 homozygote group (54.76% vs. 40.85%, P < 0.05), but there was no statistical difference in women of the above groups. The prevalence rate of MS in obese men of both Trp64 homozygote group and Arg64 carrier obese group were obviously higher than that in women of the above groups (40.85% vs. 18.27% and 54.76% vs 21.28%, all P < 0.005). Differences were not statistically significant in the prevalence of MS for normal weight Trp64 homozygote group and normal weight Arg64 carrier group, either between men, between women, or between men and women. Comparison of populations indicated that no matter with the β3-AR gene mutation or not, the prevalence of MS in obese subjects was significantly higher than normal weight subjects (χ(2) = 28.240 and χ(2) = 15.586, all P < 0.005). Logistic analysis showed that the mutation of β3-AR gene was associated with the prevalence of MS in men.</p><p><b>CONCLUSION</b>The mutation of β3-AR gene is the independent risk factor for the prevalence of MS in men.</p>


Subject(s)
Adult , Female , Humans , Male , Middle Aged , Body Mass Index , Follow-Up Studies , Insulin Resistance , Logistic Models , Metabolic Syndrome , Genetics , Mutation , Receptors, Adrenergic, beta-3 , Genetics
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