## 2016 Vol. 29, No. 11

Select articles
2016, 29(11): 773-781. doi: 10.3967/bes2016.104
Objective In this study, the ameliorative effects of gold nanoparticles (gold NP) on the renal tissue damage in Schistosoma mansoni (S. mansoni)-infected mice was investigated.
Methods High-resolution transmission electron microscopy was used for the characterization of NP. The gold NP at concentrations of 250, 500, and 1000 μg/kg body weight were inoculated into S. mansoni-infected mice.
Results The parasite caused alterations in the histological architecture. Furthermore, it induced a significant reduction in the renal glutathione levels; however, the levels of nitric oxide and malondialdehyde were significantly elevated. The parasite also managed to downregulate KIM-1, NGAL, MCP-1, and TGF-βmRNA expression in infected animals. Notably, gold NP treatment in mice reduced the extent of histological impairment and renal oxidative damage. Gold NP were able to regulate gene expression impaired by S. Mansoni infection.
Conclusion The curative effect of gold NP against renal toxicity in S. mansoni-infected mice is associated with their role as free radical scavengers.
2016, 29(11): 782-789. doi: 10.3967/bes2016.105
Objective To explore the role of RAS/PI3K pathway in the impairment of long-term potentiation (LTP) induced by acute aluminum (Al) treatment in rats in vivo.
Methods First, different dosages of aluminum-maltolate complex [Al(mal)3] were given to rats via acute intracerebroventricular (i.c.v.) injection. Following Al exposure, the RAS activity of rat hippocampus were detected by ELISA assay after the hippocampal LTP recording by field potentiation technique in vivo. Second, the antagonism on the aluminum-induced suppression of hippocampal LTP was observed after the treatment of the RAS activator epidermal growth factor (EGF). Finally, the antagonism on the downstream molecules (PKB activity and the phosphorylation of GluR1 S831 and S845) were tested by ELISA and West-blot assays at the same time.
Results With the increasing aluminum dosage, a gradually decreasing in RAS activity of the rat hippocampus was produced after a gradually suppressing on LTP. The aluminum-induced early suppression of hippocampal LTP was antagonized by the RAS activator epidermal growth factor (EGF). And the EGF treatment produced changes similar to those observed for LTP between the groups on PKB activity as well as the phosphorylation of GluR1 S831 and S845.
Conclusion The RAS→PI3K/PKB→GluR1 S831 and S845 signal transduction pathway may be involved in the inhibition of hippocampal LTP by aluminum exposure in rats. However, the mechanisms underlying this observation need further investigation.
2016, 29(11): 790-801. doi: 10.3967/bes2016.106
Objective To determine the hepatitis B immunoprophylactic failure rate in infants born to hepatitis B virus (HBV) infected mothers and to characterize HBV genes.
Methods HBV-serological testing was conducted for pregnant women and infants. The complete genomes of 30 HBV isolates were sequenced, and genetic characteristics were analyzed using MEGA 5 software.
Results The immunoprophylactic failure rate for infants who had completed the scheduled hepatitis B vaccination program was 5.76%(32/556). High sequence homology (99.8%-100%) was observed in 8 of the 10 mother-infant pairs. We identified 19 subgenotype C2 strains, 9 subgenotype B2 strains, and 2 subgenotype C1 strains. Three serotypes were detected:adr (19/30), adw (9/30), and ayw (2/30). The frequency of amino acid mutation of the‘a’ determinant region was 16.67%(5/30), including that of Q129H, F134Y, S136Y, and G145E. We detected 67 amino acid mutations in the basal core promoter, precore, and core regions of the genome.
Conclusion The immunoprophylactic failure rate in infants born to HBV-infected mothers is low in the regions of China examined during this study. Moreover, HBV mutation in the ‘a’ determinant region could not account for immunoprophylactic failure for all infants.
2016, 29(11): 802-813. doi: 10.3967/bes2016.107
Objective To reduce health-related threats of heat waves, interventions have been implemented in many parts of the world. However, there is a lack of higher-level evidence concerning the intervention efficacy. This study aimed to determine the efficacy of an intervention to reduce the number of heat-related illnesses.
Methods A quasi-experimental design was employed by two cross-sectional surveys in the year 2014 and 2015, including 2,240 participants and 2,356 participants, respectively. Each survey was designed to include one control group and one intervention group, which conducted in Licheng, China. A representative sample was selected using a multistage sampling method. Data, collected from questionnaires about heat waves in 2014 and 2015, were analyzed using a difference-in-difference analysis and cost effectiveness analysis. Outcomes included changes in the prevalence of heat-related illnesses and cost-effectiveness variables.
Results Relative to the control participants, the prevalence of heat-related illness in the intervention participants decreased to a greater extent in rural areas than in urban areas (OR=0.495 vs. OR=1.281). Moreover, the cost-effectiveness ratio in the intervention group was less than that in the control group (US$15.06 vs. US$15.69 per participant). Furthermore, to avoid one additional patient, the incremental cost-effectiveness ratio showed that an additional US\$14.47 would be needed for the intervention compared to when no intervention was applied.
Conclusion The intervention program may be considered a worthwhile investment for rural areas that are more likely to experience heat waves. Meanwhile, corresponding improving measures should be presented towards urban areas. Future research should examine whether the intervention strategies could be spread out in other domestic or international regions where heat waves are usually experienced.
2016, 29(11): 814-817. doi: 10.3967/bes2016.108
2016, 29(11): 818-824. doi: 10.3967/bes2016.109
2016, 29(11): 825-828. doi: 10.3967/bes2016.110
2016, 29(11): 829-833. doi: 10.3967/bes2016.111
2016, 29(11): 834-839. doi: 10.3967/bes2016.112
2016, 29(11): 840-847. doi: 10.3967/bes2016.113