[Corrigendum] Ginsenoside Rg1 inhibits inflammatory responses via modulation of the nuclear factor­κB pathway and inhibition of inflammasome activation in alcoholic hepatitis.

Following the publication of the above article, the authors drew to the attention of the Editorial Office that, after having reviewed all the figures and the data of their drawing software, they discovered that the pictures in the 'Control' and 'DEX' groups of Fig. 4D on p. 904 had been incorrectly imported into Fig. 6 on p. 905 when assembling this figure, effectively replacing the original and correctly placed images in Fig. 6D and E. The original (and correct) version of Fig. 6 is shown on the next page. All the authors agree with the publication of this Corrigendum, and express their gratitude to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 41: 899­907, 2018; DOI: 10.3892/ijmm.2017.3297].

Relationship between childhood trauma and non-suicidal self-injury in high school students: the mediating role of the stress perception and the moderating role of teacher-student relationship.

This study delves into the correlation between childhood trauma and non-suicidal self-injury (NSSI) behaviors among high school students. Additionally, it examines the mediating role of stress perception and the moderating role of the teacher-student relationship in this association. A questionnaire survey was administered to 1,329 high school students in Yunnan Province to assess childhood trauma, NSSI behaviors, and stress perception. Firstly, the survey revealed a 12% prevalence of NSSI, with girls exhibiting a higher occurrence compared to boys (OR = 0.413, 95% CI: 0.280-0.609). Secondly, childhood trauma emerged as a significant predictor of NSSI behavior, irrespective of gender or whether the individual was an only child (r = 0.17, P < 0.01). Thirdly, stress perception functioned as a mediator in the relationship between childhood trauma and NSSI among high school students (t = 4.65, P < 0.01). The mediation effect occupies 26.56% of the total effect. Furthermore, the teacher-student relationship moderated the mediating effect of stress perception on the link between childhood trauma and NSSI (ß = 0.0736, P < 0.01). Notably, individuals with strong teacher-student relationships exhibited a significant elevation in stress perception upon exposure to childhood trauma. The findings of this study support a moderated mediation model in the association between childhood trauma and NSSI, suggesting profound implications for the development of targeted interventions and prevention strategies among high school students.

The influence of parental autonomy support on cyberbullying victimization of high school students: A latent moderation analysis.

OBJECTIVE: To explore the relationship between parental autonomy support and cyberbullying victimization and the role of mobile phone addiction and teacher-student relationships. METHOD: Using the Perceived parental autonomy support scale, the Smartphone Addiction Scale, the Teacher-Student Relationship Questionnaire, and the Cyberbullying Victimization Scale, 1297 high school students were surveyed and a model based on latent moderated structural equation method was adopted. RESULTS: (1) Parental autonomy support can predict the level of cyberbullying victimization of high school students; (2) Mobile phone addiction plays a part of the mediating role between parental autonomy support and high school students' cyberbullying victimization; (3) With the increase of the level of teacher-student relationship, the predictive effect of parental autonomy support on mobile phone addiction gradually increases, and the predictive effect of parental autonomy support and mobile phone addiction on internet victimization becomes insignificant. CONCLUSION: A good teacher-student relationship helps to enhance the positive effect of parental autonomy support on high school students' mobile phone addiction and alleviate the negative effects of parental autonomy support as well as mobile phone addiction on increasing the risk of cyberbullying victimization among high school students.

In-depth investigations of the molecular basis underlying sex differences among middle-aged and elderly schizophrenia populations.

Sex can influence almost all aspects of schizophrenia. However, the molecular mechanisms underlying sex differences in schizophrenia remain poorly understood. In this project, the dataset GSE107638 containing neuronal RNA-seq data and age/sex information of individuals with or without schizophrenia were retrieved. Schizophrenia samples were divided into young male (M-1), young female (F-1), middle-aged and elderly male (M-2) and middle-aged and elderly female (F-2) groups. Next, green/yellow/turquoise modules related to the M-2 trait and turquoise module correlated with the F-2 trait were identified by weighted correlation network analysis (WGCNA) analysis (soft thresholding power: 13; min module size: 200). Crucial genes in the M-2 green, M-2 turquoise and F-2 turquoise modules were identified by WGCNA, gene significance/module membership, and protein-protein interaction (PPI) analysis. Moreover, 2067 and 934 differentially expressed genes (|log2 fold-change| ≥0.58 and P-value < 0.05) in M-2 and F-2 schizophrenia subgroups versus same-age and same-sex counterparts were identified, respectively. Additionally, 82 core genes in the M-2 turquoise module and 4 hub genes in the F-2 turquoise module were differentially expressed in M-2 and F-2 schizophrenia subgroups versus their counterparts, respectively. Among the 82 hub genes, 15 genes were found to be correlated with neuronal development by the Kyoto Encyclopedia of Genes and Genomes enrichment analysis. Also, 2 potential PPI networks related to neuronal development were identified. Taken together, multiple potential hub genes and 2 potential neurobiological networks related to schizophrenia sex differences and disease progression were identified among middle-aged and elderly schizophrenia populations.

Streptococcus mutans PrsA mediates AtlA secretion contributing to extracellular DNA release and biofilm formation in the pathogenesis of infective endocarditis.

The role of secretion chaperone-regulated virulence proteins in the pathogenesis of infective endocarditis (IE) induced by viridans streptococci such as Streptococcus mutans is unclear. In this study, we investigated the contribution of the foldase protein PrsA, a putative parvulin-type peptidyl-prolyl isomerase, to the pathogenesis of S. mutans-induced IE. We found that a prsA-deficient strain had reduced virulence in terms of formation of vegetation on damaged heart valves, as well as reduced autolysis activity, eDNA release and biofilm formation capacity. The secretion and surface exposure of AtlA in vitro was reduced in the prsA-deficient mutant strain, and complementation of recombinant AtlA in the culture medium restored a wild type biofilm phenotype of the prsA-deficient mutant strain. This result suggests that secretion and surface localization of AtlA is regulated by PrsA during biofilm formation. Together, these results demonstrate that S. mutans PrsA could regulate AtlA-mediated eDNA release to contribute to biofilm formation in the pathogenesis of IE.

Empathy alleviates the learning burnout of medical college students through enhancing resilience.

OBJECTIVE: The problem of learning burnout of medical students is becoming prominent, and empathy can play a good predictive role in learning burnout. The present study aimed to investigate the relationship between empathy and learning burnout, as well as the mediation effect of resilience in this relation. METHODS: Five hundred and eighty-eighth college students from a key medical university in Yunnan Province was investigated using the Basic Empathy Scale, Learning Burnout Scale, and Connor-Davidson Resilience Scale. All the measures showed good reliability and validity in the present study. Data were analyzed using SPSS 23.0 and Amos 22.0. RESULTS: Using structural equation modeling, we tested a conceptual model indicated that: (1) medical students' empathy negatively and significantly predicted learning burnout; (2) medical students' empathy positively predicts mental resilience; (3) resilience of medical students negatively predicts learning burnout; (4) resilience partially mediated the relationship between empathy and learning burnout of medical students, while also controlling for family socioeconomic status. CONCLUSION: These findings highlight the mediating role of resilience in the effect of empathy on learning burnout of medical college students. It may contribute to a better understanding of the effect of empathy. Moreover, it can also provide constructive suggestions for protecting and improve empathy and resilience of medical college students.

Relationship Between Family Socioeconomic Status and Learning Burnout of College Students: The Mediating Role of Subjective Well-Being and the Moderating Role of Resilience.

Objective: Learning burnout affects the positive development of college students. The present study aimed to investigate the relationship between family socioeconomic status (FSES) and learning burnout, as well as the mediation effect of subjective well-being and the moderation effect of resilience in this relation. Methods: A total of 550 Chinese college students from Yunnan completed a questionnaire measuring the research variables in this study. Results: (1) After controlling for participants' gender and age, FSES negatively, and significantly predicted learning burnout; (2) subjective well-being partially mediated the relationship between FSES and learning burnout; and (3) the direct effect of FSES on learning burnout and the mediation effect of subjective well-being was moderated by resilience. The level of learning burnout of individuals with low resilience increased significantly with the decrease of FSES, and the level of learning burnout of individuals with high resilience decreased significantly with the increase in subjective well-being. Conclusion: The present findings support the moderated mediation model underlying the relationship between FSES and learning burnout. This also has significant implications for formulating prevention and intervention measures on learning burnout among college students. Limitations: First of all, this study used the cross-sectional study design, which cannot make a causal inference. In addition, the sample in this study is university students from Kunming, which may affect the popularity of the results.

The Mobile Phone Addiction and Depression Among High School Students: The Roles of Cyberbullying Victimization, Perpetration, and Gender.

Objective: To examine the relation between mobile phone addiction and high school students' depression, and its inner mechanism-the sequential mediating roles of the cyberbullying victimization and the cyberbullying perpetration in this relationship. Methods: 1297 high school students were recruited to complete the Smartphone Addiction Scale, European Cyberbullying Intervention Project Questionnaire and the Center for Epidemiological Studies Depression Scale. Results: (1) Mobile phone addiction was positively correlated with and high school students' depression; (2) cyberbullying victimization and the cyberbullying perpetration significantly mediated the relation between mobile phone addiction and high school students' depression, which contained tow mediating paths-the independent mediating effects of cyberbullying victimization and the sequential mediating effect of cyberbullying victimization and the cyberbullying perpetration; (3) there are gender differences in the sequential mediation model, and boys who are victims of cyberbullying are more likely to develop into cyberbullying perpetrators than girls. Conclusion: The results of this study indicate that depression among high school students with mobile phone addiction can be eliminated through the development of cyberbullying victimization and the cyberbullying perpetration.

Eczema is a shared risk factor for anxiety and depression: A meta-analysis and systematic review.

Globally, anxiety and depression are the most common psychiatric disorders that add large burdens to individuals and society; however, the mechanisms underlying these disorders are unclear. Several studies have found that eczema is a shared risk factor for both these conditions. We identified and evaluated eligible observational studies from EMBASE and PubMed. In total, 20 relevant cohort and case-control studies comprising 141,910 patients with eczema and 4,736,222 control participants fulfilled our established criteria. Information extracted included study design, location, sample size, sex distribution of cases and controls or reference cohorts, measurements of outcomes, odds ratio (OR) with 95% confidence interval (CI), and adjusted factors for exposure associated with outcome risk. The meta-analysis was performed by calculating the pooled OR with 95% CI, and heterogeneity was assessed using Cochrane Q and I2 statistics. The pooled effect showed a positive association (n = 4,896,099, OR = 1.63, 95% CI [1.42-1.88], p<0.001) between eczema and depression or anxiety, with positive associations also observed in the depression (n = 4,878,746, OR = 1.64, 95% CI [1.39-1.94], p<0.001) and anxiety (n = 4,607,597, OR = 1.68, 95% CI [1.27-2.21], p<0.001) groups. Subgroup and sensitivity analyses confirmed that these findings were stable and reliable. This study suggests that eczema is associated with an increased risk of developing depression and anxiety, which may assist clinicians in the prevention or treatment of these disorders.

Relationship Between Medical Students' Empathy and Occupation Expectation: Mediating Roles of Resilience and Subjective Well-Being.

Background: The occupation expectation of medical students can predict the possibility of their future employment in the medical industry, and empathy is the special ability of medical students in their study and career, which affects the development of their occupation expectation. Objective: To explore the relationship between resilience and subjective well-being between medical students' empathy and occupation expectation and their internal mechanisms. Design: Data were collected from October 2020 to March 2021 using a paper questionnaire survey. Subjective: 586 medical students at a key medical university in Yunnan Province were invited to complete the survey. Main Measures: The Basic Empathy Scale, Connor-Davidson Resilience Scale, Subjective Well-Being Questionnaire, and Occupation Expectation Scale. Key Results: The empathy is intended to affect the occupation expectation of medical students through four paths. The direct path effect value is 0.073 (95% CI: 0.007∼0.217), the indirect path 1 effect value is 0.078 (95% CI: 0.022∼0.134), indirect path 2 effect value is 0.010 (95% CI: 0.005∼0.022), indirect path 3 effect value is 0.022 (95% CI: 0.0604∼0.039), all the confidence intervals do not contain 0, and the mediated effect ratio is 60.109%. Conclusion: Empathy has an impact on occupation expectation of medical students through the sequential mediating effects of resilience and subjective well-being. Medical colleges should fully consider the role of protective factors when cultivating and enhancing the occupation expectation of clinical medical students. Strengthening the intervention of emotional factors (empathy), self-regulating ability (psychological toughness) and cognitive factors (subjective well-being) is an important way to effectively establish professional values, improve occupation expectation of medical students and reduce the turnover rate of medical students.

SEMA3B-AS1-inhibited osteogenic differentiation of human mesenchymal stem cells revealed by quantitative proteomics analysis.

Human mesenchymal stem cells (hMSCs) are fibroblastoid multipotent adult stem cells with capacities of differentiation into osteoblasts and chondrocytes and show great potential in new bone formation and bone repair-related clinical settings, such as osteoporosis. Long noncoding RNAs (lncRNAs) have been demonstrated to play important roles in various biological processes. Here, we report an antisense lncRNA SEMA3B-AS1 regulating hMSCs osteogenesis. SEMA3B-AS1 is proximal to a member of the semaphorin family Sema3b. Overexpression of SEMA3B-AS1 using the lentivirus system markedly inhibits the proliferation of hMSCs and meanwhile reduces osteogenic differentiation. Using a comprehensive proteomic technique named isobaric tag for relative and absolute quantitation, we found that SEMA3B-AS1 significantly alters the process of osteogenesis through downregulating the expression of proteins involved in actin cytoskeleton, focal adhesion, and extracellular matrix-receptor interaction, while increasing the expression of proteins in the spliceosome. Collectively, we find that SEMA3B-AS1 is a target for controlling osteogenesis of hMSCs.

HERV-W env regulates calcium influx via activating TRPC3 channel together with depressing DISC1 in human neuroblastoma cells.

The activation and involvement of human endogenous retroviruses W family envelope gene (HERV-W env, also called ERVWE1) have been reported in several neuropsychiatric disorders, including schizophrenia, as well as in multiple sclerosis (MS). Dysregulation of intracellular calcium content is also involved in the pathogenesis of these diseases. Our previous studies showed that HERV-W env overexpression results in activation of small conductance Ca2+-activated K+ channel protein 3 (SK3), a potential risk factor for schizophrenia. In the present study, we aimed to elucidate the relationship between HERV-W env and calcium signaling in schizophrenia. Our results showed that HERV-W env could induce Ca2+ influx in two human neuroblastoma cell lines and upregulate the expression and activation of TRPC3 in cells. The abnormal increase in intracellular Ca2+ concentration was inhibited by addition of the TRPC3 channel blocker pyr3, demonstrating that the Ca2+ influx induced by HERV-W env was TRPC3-dependent. Further experiments showed that HERV-W env overexpression downregulated DISC1, while knockdown of DISC1 promoted activation of TRPC3 without affecting TRPC3 expression. In conclusion, HERV-W env induced Ca2+ influx in human neuroblastoma cells by activating the TRPC3 channel through directly regulating its expression or downregulating DISC1, which could also increase TRPC3 activation without affecting TRPC3 expression. These findings provide new insights into how HERV-W env affects neuronal activity and contributes to the pathogenesis of schizophrenia.

Ginsenoside Rg1 ameliorates liver fibrosis via suppressing epithelial to mesenchymal transition and reactive oxygen species production in vitro and in vivo.

Liver fibrosis remains a major cause of morbidity and mortality with a complicated etiology and notorious complications, but there is a lack of efficacious therapeutics. Epithelial to mesenchymal transition (EMT) has a central role in the course of liver fibrosis, and thus, prevention of the development of EMT may control and even reverse liver fibrosis. This study aimed to examine the beneficial effect of ginsenoside Rg1, a phrenological active component isolated from Ginseng, and interrogate the mechanism in vitro and in vivo, with a focus on transforming growth factor-ß (TGF-ß)/Smad and Nrf2-mediated signaling pathways. We employed a TGF-ß-induced EMT model in HSC-T6 cells and CCl4 -induced liver fibrosis in animal. We found that ginsenoside Rg1 significantly reduced cell proliferation and reversed transforming growth factor-ß (TGF-ß)-induced EMT in HSC-T6 cells; and ginsenoside Rg1 induced cell apoptosis, Ginsenoside Rg1 decreased the cellular level of collagen I and III in HSC-T6 cells, indicating the amelioration of fibrosis. We showed that ginsenoside Rg1 reduced cellular reactive oxygen species (ROS). We also observed similar beneficial effects of ginsenoside Rg1 in vivo. The data showed that ginsenoside Rg1 decreased the level of alanine aminotransferase and aspartate aminotransferase, and collage type IV (IV-C), hyaluronic acid, and laminin in carbon tetrachloride (CCl4)-induced liver fibrotic model. Mechanistically, we showed that ginsenoside Rg1 tuned down the TGF-ß/Smad and stimulated Nrf-2 nuclear translocation, which could explain the beneficial effects. In aggregate, our results demonstrate that ginsenoside Rg1 exhibits a protective effect on liver fibrosis via suppressing EMT and cellular ROS level. © 2018 BioFactors, 2018.

Ginsenoside Rg1 inhibits inflammatory responses via modulation of the nuclear factor­κB pathway and inhibition of inflammasome activation in alcoholic hepatitis.

Ginsenoside Rg1 (G­Rg1) is an active ingredient of Panax ginseng, which has previously been reported to attenuate alcohol­induced hepatic damage; however, the underlying mechanisms remain largely unknown. The present study aimed to investigate the protective effects of G­Rg1 on alcohol­induced cell injury in vitro and on a rat model of alcoholic hepatitis in vivo. For the in vitro model, L­O2 cells were incubated with ethanol in the presence or absence of G­Rg1. For the in vivo model, rats were administered ethanol by intragastric injection and were treated with G­Rg1, or dexamethasone as a control. The results indicated that serum biochemical parameters, including alanine aminotransferase, aspartate aminotransferase and total bilirubin, as well as the expression of nuclear factor (NF)­κB pathway­associated inflammatory cytokines, including interleukin (IL)­6, tumor necrosis factor­α and IL­1ß, were elevated in response to alcohol; however, they were significantly decreased by G­Rg1 treatment. Furthermore, NF­κB pathway activation was reduced by treatment with G­Rg1. G­Rg1 also decreased oxidative stress by inhibiting cytochrome P450 2E1 expression and reactive oxygen species production, and promoting glutathione peroxidase expression. Furthermore, G­Rg1 inhibited the expression levels of caspase­3 and ­8, which may be associated with decreased hepatocyte apoptosis. These data suggested that G­Rg1 may protect hepatocytes against alcohol­induced injury, through preventing excessive inflammation and hepatocellular apoptosis.

Aberrant regulation of Wnt signaling in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the most lethal malignancies in the world. Several signaling pathways, including the wingless/int-1 (Wnt) signaling pathway, have been shown to be commonly activated in HCC. The Wnt signaling pathway can be triggered via both catenin ß1 (CTNNB1)-dependent (also known as "canonical") and CTNNB1-independent (often referred to as "non-canonical") pathways. Specifically, the canonical Wnt pathway is one of those most frequently reported in HCC. Aberrant regulation from three complexes (the cell-surface receptor complex, the cytoplasmic destruction complex and the nuclear CTNNB1/T-cell-specific transcription factor/lymphoid enhancer binding factor transcriptional complex) are all involved in HCC. Although the non-canonical Wnt pathway is rarely reported, two main non-canonical pathways, Wnt/planar cell polarity pathway and Wnt/Ca(2+) pathway, participate in the regulation of hepatocarcinogenesis. Interestingly, the canonical Wnt pathway is antagonized by non-canonical Wnt signaling in HCC. Moreover, other signaling cascades have also been demonstrated to regulate the Wnt pathway through crosstalk in HCC pathogenesis. This review provides a perspective on the emerging evidence that the aberrant regulation of Wnt signaling is a critical mechanism for the development of HCC. Furthermore, crosstalk between different signaling pathways might be conducive to the development of novel molecular targets of HCC.

Elevation of Ser9 phosphorylation of GSK3ß is required for HERV-W env-mediated BDNF signaling in human U251 cells.

Human endogenous retrovirus W family (HERV-W) envelope (env) is known to be associated with neurological and psychiatric disorders, such as multiple sclerosis and schizophrenia. Previous studies showed that overexpression of HERV-W env could induce brain-derived neurotrophic factor (BDNF) gene expression. In human and rat cells, BDNF-mediated signal transduction might be modulated by glycogen synthase kinase 3ß (GSK3ß). Both BDNF and GSK3ß are schizophrenia-related genes. In this paper, we investigated whether GSK3ß was involved in the HERV-W env-induced expression of BDNF. We found that HERV-W env increased phosphorylation of GSK3ß at Ser9 (p-GSK3ß (Ser9)) and the ratio of p-GSK3ß (Ser9) to total GSK3ß (p<0.05) in U251 cells. Overexpression of HERV-W env led to a 36.2% reduction in GSK3ß activity compared to control (p<0.05). The levels of ß-catenin, cyclin D1 and TSC2 mRNAs were upregulated (p<0.05). These data suggested that overexpression of HERV-W env might activate the GSK3ß signaling pathway in U251 cells. Further, knockdown of GSK3ß reduced the expression of total GSK3ß, p-GSK3ß (Ser9), and the ratio of p-GSK3ß (Ser9) to total GSK3ß by 28.6%, 50.4%, and 30.2%, respectively (p<0.05). Levels of ß-catenin, cyclin D1 and TSC2 mRNAs were also reduced (p<0.05). Interestingly, GSK3ß activity increased (p<0.05). Knockdown of GSK3ß also decreased mRNA and protein expression of BDNF by 49.9% and 48.5% respectively (p<0.05). These results indicated that phosphorylation of GSK3ß at Ser9 might be involved in HERV-W env-induced BDNF expression, and will hopefully improve our understanding of the role of HERV-W env in neurological and psychiatric diseases (schizophrenia, etc).

Activation of elements in HERV-W family by caffeine and aspirin.

Caffeine and aspirin have been suggested to be involved in neurologic diseases, such as schizophrenia, and previous data have revealed that abnormal expression of HERV-W elements may be an important factor in the etiopathogenesis of those diseases. In this article, we reported that caffeine and aspirin contributed to the expression of HERV-W env and gag in Human SH-SY5Y neuroblastoma cells. Semi-quantitative RT-PCR and quantitative Real-time PCR were used to detect the mRNA of HERV-W env and gag in cells exposed to caffeine or aspirin. Western blotting was used to detect the protein of HERV-W env. Luciferase activity assay was employed to detect the activity of HERV-W env promoter. It was found that both caffeine and aspirin could increase the expression of HERV-W env and gag in human SH-SY5Y neuroblastoma cells. Caffeine could activate the HERV-W env promoter, while aspirin could not. With previous studies we can conjecture that HERVs might play a bridging role between environmental factors, such as drugs and neurologic diseases.

ATP13A2 variability in Taiwanese Parkinson's disease.

Mutations in ATP13A2 have been reported to associate with Parkinson's disease (PD). This study investigates the contribution of genetic variants in ATP13A2 to Taiwanese PD. ATP13A2 cDNA fragments from 65 early onset PD (onset <50 years) were sequenced. The identified variants were validated in a cohort of PD (n = 493) and ethnically matched controls (n = 585). A novel heterozygous G1014S, located at the conserved seventh transmembrane domain of ATP13A2 protein, was identified in an early onset PD patient, which was absent in 585 normal controls. Additionally, a reported heterozygous A746T was found in two PD patients and four controls. The clinical features and 99mTc-TRODAT-1 single photon emission computed tomography (SPECT) image of the patients carrying G1014S and A746T were similar to that of idiopathic PD. One normal control with A746T showed an asymmetric reduction of 99mT TRODAT-1 uptake in the right striatum. Under oxidative stress or apoptotic stimulus, lymphoblastoid cells carrying either A764T or G1014S showed increased caspase 3 activity compared with the controls. The rates of decay for G1014S and A746T proteins were more or less reduced in cycloheximide chase experiment. In silico modeling of G1014S exhibited a more stable feature than wild-type, and G1014S is mislocalized mainly in the intralysosomal space, which is coherent with the prediction of prohibiting N-myristoylation and membrane association. We therefore hypothesize that rare variants of ATP13A2 may contribute to PD susceptibility in Taiwan. The role played by ATP13A2 variants in PD remains to be clarified.

[Changes of spleen cytokines in mice immunized with recombinant Bb-Eg95-EgA31 vaccine against Echinococcus granulosus].

OBJECTIVE: To investigate the level of cytokines in spleen from mice immunized with recombinant Bifidobacteria bifidum(Bb)-Eg95-EgA31 vaccine of Echinococcus granulosus (Eg) and challenged with Eg protoscoleces. METHODS: 56 female BALB/c mice were randomly divided into 7 groups: Recombinant Bb-Eg9S-95-EgA31 vaccine subcutaneous injection (group A), intramuscular injection (B), intranasal immunization (C), oral administration (D), blank vector control (E), Bb control (F) and MRS control (G). Mice in all groups were challenged with 50 Eg protoscoleces on the 8th week after vaccination and sacrificed on the 25th week after infection. Spleens were collected to prepare splenocytes, which were cultured under activation of crude Eg antigen (EgAg), with concanavalin A (ConA) or lipopolysaccharide (LPS) stimulation and non-stimulation as control. The splenocyte supernatants were collected to determine the levels of interferon-gamma (IFN-gamma), interleukin-12 (IL-12), tumour necrosis factor-alpha (TNF-alpha) and IL-10 by ELISA. RESULTS: The level of IFN-gamma in groups A [(137.5 +/- 23.2) pg/ml], B [(162.5 +/- 23.2) pg/ml], C [(250.0 +/- 53.5) pg/ml] and D [(215.0 +/- 37.4) pg/ml] was higher than that of group G [(50.0 +/- 10.7) pg/ml] (P < 0.01). The level of IL-12 in groups A [(27.5 +/- 4.6) pg/ml], B [(32.5 +/- 4.6) pg/ml], C [(45.0 +/- 5.4) pg/ml] and D [(35.0 +/- 5.4) pg/ml] was higher than that of group G [(15.0 +/- 5.4) pg/ml] (P < 0.01). The level of TNF-alpha in groups A [(275.0 +/- 46.3) pg/ml], B [(325.0 +/- 46.3) pg/ml], C [(450.0 +/- 53.5) pg/ml] and D [(350.0 +/- 53.5) pg/ml] was higher than that of group G [(150.0 +/- 53.5) pg/ml] (P < 0.01). The level of IL-10 in groups A [(37.5 +/- 4.6) pg/ml], B [(35.0 +/- 5.4) pg/ml], C [(25.0 +/- 5.4) pg/ml] and D [(32.5 +/- 4.6) pg/ml] was lower than that of group G [(45.0 +/- 5.4) pg/ml] (P < 0.05 or P < 0.01). CONCLUSION: The recombinant Bb-Eg95-EgA31 vaccine can induce a protective Th1 type immune response in mice

[Research status on DNA vaccine against Cysticercus cellulosae infection].

DNA vaccine against Cysticercus cellulosae infection is a newly emerging vaccine in recent years. It can induce not only humoral immune response, but also a high level cellular immune response. The DNA vaccine displays prominent advantages in the prevention on cysticercosis. This article reviews the current situation on several DNA vaccines.