Biography:
Antonio Drago has completed his PhD from Modena University and Postdoctoral studies from Bologna University. He has published more than 45 papers in reputed journals and has been serving as an Editorial Board Member of repute.
Abstract:
Objective. Psychotropic induced weight gain (PIWG) may lead to increased risk for cardiovascular diseases, metabolic disorders and, ultimately, treatment discontinuation. The hypothesis tested in the present contribution was that PIWG might be genetically driven. The analysis of complete molecular pathways may grant a sufficient power to tackle the biologic variance of PIWG. The identification of a genetic makeup at risk for PIWG could characterize the subjects at risk for this possible severe side effect, and helps move a step forward in the direction of personalized treatment in psychiatry.
Methods. A genetic sample from the CATIE trial (n=765; M=556, mean age = 40.93±11.03) treated with diverse antipsychotic drugs was investigated. A molecular pathway analysis was conducted in an R environment for the identification of the molecular pathways enriched in variations associated with PIWG.
Results. The developmental biology molecular pathway was found to be significantly (p.adj= 0.018) enriched in genetic variations significantly (p<0.01) associated with PIWG. 18 genes were identified and discussed. The developmental biology molecular pathway is involved in the regulation of beta-cell development, and the transcriptional regulation of white adipocyte differentiation. Interestingly, this finding was a result of an hypothesis – free approach.
Conclusion. Results from the current contribution correlates with previous evidence and it is consistent with our earlier result on the STAR*D sample. Furthermore, the involvement of the beta-cell development and the trasnscriptional regulation of white adipocyte differentiation pathways stresses the relevance of the peripheral tissue rearrangement, rather than increased food intake, in the biologic modifications that follow psychotropic treatment and may lead to PIWG. Further research is warranted.
Biography:
Prof. Sarantuya Jav graduated from Medical University of Sankt Petersburg (Leningrad), Russia with a bachelor’s degree in medicine, as a pediatrician. In 1998, she held master’s degree at the Medical University of Mongolia. In 2004, she received her PhD degree in Medicine at the School of Medicine, Kagoshima University, Japan. She became associate professor of HSUM in 2009 and professor of MNUMS in 2014.
From 1988 – 1999, she worked at Department of infantry and department of reanimation of National Center for Child and Maternity Health. 1999 – 2004, she was a doctorate and assistant teacher at the Pediatric department. 2004 to present, she is working at the Dept. of Molecular biology and Genetics, School of Pharmacy and Biomedicine, Mongolian National University of Medical Sciences as a lecturer, senior lecturer, Ass. Professor and Professor. Now prof. Sarantuya is a head of Dept. of Molecular Biology and Genetics.
Prof. Sarantuya Jav teaches Molecular Biology, Biotechnology and Applied molecular biology and diagnostics for undergraduate, graduate and postgraduate students.
Abstract:
Age-related macular degeneration (AMD) is an eye condition, that occurs people aged above 50, leads to gradual loss of the vision because of damage in the macula, which is located in the center of the retina. Several polymorphisms in different genes have been proposed as factors that increase the disease susceptibility. Therefore, we investigated the association between rs833061 polymorphism of VEGF-A gene and rs10490924 polymorphism of ARMS2 gene and AMD. This case-control study was conducted on 74 AMD patients and 32 unaffected age- and gender-matched control individuals. Genomic DNA was extracted from the peripheral venous blood. The single nucleotide polymorphisms were identified by restriction fragment length polymorphism (RFLP) method and results confirmed by gel electrophoresis. No significant differences were observed for С allele and СС genotype frequency of rs833061 polymorphism of VEGF-A gene between patients and controls. However, analysis of rs10490924 polymorphism of ARMS2 gene shows that T allele (OR=2.72, 95% CI, 1.47 – 5.02, p=0.001), TT genotype (OR=4.54, 95% CI, 1.49 – 13.87,p=0.019) were significantly associated with AMD risk. Haplotype analysis of these SNPs showed that C+T haplotype was statistically significantly different (OR=5.23, 95% CI, 1.76-15.54, p=0.002) between patients and controls. As shown by results, rs10490924 polymorphism of ARMS2 gene show that T allele, TT genotype and C+T haplotype were significantly associated with AMD risk.
Biography:
Abstract:
Background: Garcinol, a polyisoprenylated benzophenone isolated from fruiting bodies of Garcinia indica, and possessing anti-inflammatory, antioxidant, acetyltransferase inhibitory and anticancer activities. our perviously work has demonstrated α7-nAChR drives the progression and recurrence of HCC through JAK2/STAT3 signaling, which has been linked with proliferation, survival, invasion and angiogenesis, and might be a novel target for anti-HCC therapy. Thus, novel agents that can suppress α7-nAChR activation have potential for both prevention and treatment of HCC. Here we report, garcinol, could suppress α7-nAChR and downregulated JAK2/STAT3 axis in vitro and in vivo model of HCC.
Methods: Two HCC cell lines have been treated with garcinol and the inhibition of expression of α7-nAChR have been checked by immunoblotting, immuno-fluorescence, and RT-PCR. Xenografted tumor model has been generated in nude mice using HCC cell line and effect of garcinol in the inhibition of tumor growth has been investigated.
Results: Garcinol inhibit α7-nAChR and downstream JAK2/STAT-3 expression in Mahlavu and Hep-J5 cancer cell lines and was also found to inhibit cell proliferation, invasion, migration and lower the tumor’s sphere-formation ability. Western blot and real-time PCR further evaluated the expression of α7-nAChR. These results is consist with our previously work on inhibition of α7-nAChR via siRNA. We further verified in vivo using human HCC xenograft tumors in nude mice, where administration of garcinol significantly inhibited tumor growth, improved overall survival, and western blot analysis of remnant tumor lysates showed reduced α7-nAChR expression and activation.
Conclusion: Together, these study suggested garcinol exerts its anti-proliferative and pro-apoptotic effects through suppression of α7-nAChR and downregulated JAK2/STAT3 signaling in HCC both in vitro and in vivo.
Keywords: Garcinol, α7-nAChR, nicotine receptor, JAK2, Hepatocellular carcinoma
Biography:
Abstract:
The ketamine-treated sample included 191 unrelated subjects with major depressive disorder (MDD) or bipolar disorder (BD). Changes in depression rating scale score at Day 1 (24 hours post-treatment) were considered the primary outcome, as assessed via the Montgomery-Asberg Depression Rating Scale (MADRS) or the 17-item Hamilton Depression Rating Scale (HAM-D) Ketamine is an antagonist of the glutamate NMDA receptor. Ketamine is thought to work by blocking NMDA receptors on inhibitory GABA-containing interneurons, ultimately promoting glutamate release. We conducted a GWAS analysis, using imputed genotype data. Polygenic risk score analysis was conducted (Ketamine and Scopolamine), below are our preliminary results.
The ketamine-treated sample included 157 unrelated European subjects with major MDD or bipolar disorder (BD). The scopolamine-treated sample comprised 37 unrelated European subjects diagnosed with either MDD or BD who had a current Major Depressive Episode (MDE), and had failed at least two adequate treatment trials for depression. Change in Montgomery–Asberg Depression Rating Scale (MADRS) or the 17-item Hamilton Depression Rating Scale (HAM-D) scale scores at day 1 (24h post-treatment) was considered the primary outcome. Here, we conduct a pilot GWAS analysis to identify potential markers of ketamine response and dissociative side effects. Polygenic risk score analysis of SNPs ranked by the strength of their association with ketamine response was then calculated in order to assess whether common genetic markers from the ketamine study could predict response to scopolamine. Findings require replication in larger samples in light of low power of analyses of these small samples. Nevertheless, our data indicate a promising illustration of our future potential to identify genetic variants underlying rapid treatment response in mood disorders.
Biography:
Abstract:
Schizophrenia is inheritance mental disease that caused by genetic susceptibility and socio-environmental factors. We believe the identification of genetic risk factors for schizophrenia susceptibility, it may improve a diagnostic management of schizophrenia. Recent studies have reported that SNPs of NRG1 and 5-HT2AR genes may have influence on schizophrenia. We investigated the association of rs3924999 and rs6311 SNPs of NRG1 and 5-HT2AR genes with schizophrenia. 105 patients with schizophrenia and 150 healthy volunteers were randomly involved in case-control study. SNPs were identified by PCR-RFLP analysis. No significant differences were observed for allele frequencies of SNPs, between case and control groups. CT genotype of SNP rs3924999 (OR=1.19, 95% CI, 0.72-1.98, p=0.48) and AG genotype of SNP rs6311 (OR=1.46, 95% CI, 0.88-2.41, p=0.137) were more frequent in schizophrenia patients than controls. The results suggesting that rs3924999, rs6311 SNPs of NRG1 and 5-HT2AR genes were not associated with schizophrenia susceptibility.
Biography:
Antonio Drago has completed his PhD from Modena University and Postdoctoral studies from Bologna University. He has published more than 45 papers in reputed journals and has been serving as an Editorial Board Member of repute.
Abstract:
Objective. Psychotropic induced weight gain (PIWG) may lead to increased risk for cardiovascular diseases, metabolic disorders and, ultimately, treatment discontinuation. The hypothesis tested in the present contribution was that PIWG might be genetically driven. The analysis of complete molecular pathways may grant a sufficient power to tackle the biologic variance of PIWG. The identification of a genetic makeup at risk for PIWG could characterize the subjects at risk for this possible severe side effect, and helps move a step forward in the direction of personalized treatment in psychiatry.
Methods. A genetic sample from the CATIE trial (n=765; M=556, mean age = 40.93±11.03) treated with diverse antipsychotic drugs was investigated. A molecular pathway analysis was conducted in an R environment for the identification of the molecular pathways enriched in variations associated with PIWG.
Results. The developmental biology molecular pathway was found to be significantly (p.adj= 0.018) enriched in genetic variations significantly (p<0.01) associated with PIWG. 18 genes were identified and discussed. The developmental biology molecular pathway is involved in the regulation of beta-cell development, and the transcriptional regulation of white adipocyte differentiation. Interestingly, this finding was a result of an hypothesis – free approach.
Conclusion. Results from the current contribution correlates with previous evidence and it is consistent with our earlier result on the STAR*D sample. Furthermore, the involvement of the beta-cell development and the trasnscriptional regulation of white adipocyte differentiation pathways stresses the relevance of the peripheral tissue rearrangement, rather than increased food intake, in the biologic modifications that follow psychotropic treatment and may lead to PIWG. Further research is warranted.