Aagesensingh2869

Aim To investigate the mechanism of small nucleolar RNA host gene 1 (SNHG1) in cervical cancer (CC). Methods The expression of SNHG1, miR-194 and human cervical cancer oncogene (HCCR) in CC tissues and cells was detected using qRT-PCR and western blot. The interaction among the three molecules was measured using dual-luciferase reporter assay and RNA immunoprecipitation assay. The function of SNHG1 in CC cells was detected by CKK-8 assay and flow cytometry analysis. Results SNHG1 was highly expressed in CC tissues and CC cell lines. Knockdown of SNHG1 inhibited CC cell proliferation and enhanced the ability of cell apoptosis. Mechanism investigation revealed that SNHG1 modulated HCCR expression via acting as a competing endogenous RNA of miR-194. Moreover, miR-194 inhibitor changed the effects of si-SNHG1 on CC cells growth. In vivo experiment, silencing of SNHG1 suppressed CC tumor growth by modulating miR-194/HCCR axis. Conclusion Knockdown of SNHG1 inhibited CC progression by targeting HCCR via sponging with miR-194.Objectives To add to the growing evidence on SARS-CoV-2 infection during pregnancy, so as to better inform clinical decision making and optimize patient outcomes. Methods A systematic search of relevant databases was perfomed on 25 March 2020 and a repeat search, on 10 April 2020. Reports of pregnant patients with SARS-CoV-2 infection at any time during their pregnancy were reviewed and summarized . Results We summarized the outcomes of a total of 155 pregnant women and 118 neonates. Bcl-xL protein The evidence suggests a similar rate of severe COVID-19 cases in pregnant women and the general population. The frequency of cesarean deliveries is high, against guidelines recommendations. Conclusion Limited data on COVID-19 during preganacy, associated with a wide variation in the methodology make accurate data interpretation difficult.Objectives To evaluate the effect of using progesterone due to early vaginal bleeding on aneuploidy screening markers in the first trimester.Material and methods This case control study includes the pregnant women who applied to our clinic in order to have a screening test for Down syndrome in the weeks of 11°/7-136/7. The patients were divided into three groups. Self reported vaginal bleeding with progesterone therapy (Bl+, Prg+, n70), Self reported vaginal bleeding without progesterone therapy (Bl+, Prg-, n70) and as a control group pregnant women who had no vaginal bleeding. (NoBl, NoPrg, n70). In all patients, free beta-human chorionic gonadotrophin (β-hCG), pregnancy associated plasma protein-A (PAPP-A) levels and nuchal translucency (NT) thickness were analyzed. Mean MoMs of the markers were compared between three groups.Results In the two groups with vaginal bleeding (Bl+, Prg + and Bl+, Prg-) the free β-Hcg MoM values were statistically higher (1.22 ± 0.72, 0.98 ± 0.45, respectively) compared to the No Bleeding/No Progesterone group (0.81 ± 0.52) (p ≤ 0.001, p ≤ .01, respectively). However, no significant difference was found between the free β-hCG MoM value of women with Bl+, Prg + group (1.22 ± 0.72) and Bl+, Prg - group (0.98 ± 0.45). (p .053, significance level limitation with Bonferroni correction p .017). PAPP-A and NT thickness did not differ significantly between the groups.Conclusion Our data did not find an association between the use of oral progesterone and any alternations in first trimester screening parameters. Regardless of the progesterone usage, vaginal bleeding in the first trimester pregnancies increased the free β-hCG MoM values compared to pregnancies without vaginal bleeding during pregnancy.Although self-control consistently emerges as one of the most robust correlates of delinquent behavior, limited empirical attempts have been made to explore the contextual variability of the relationship between self-control and delinquency outside of Western societies. Using data collected from 587 seventh- to ninth-grade students across 10 middle schools in a rural county of Southeast China, we examine self-control's efficacy in explaining juvenile delinquency in the presence of external environmental factors, and investigate relative strength of self-control and contextual factors in predicting delinquent behaviors. Our results confirm that self-control is an important predictor of delinquent behavior in a non-Western cultural context. However, certain environmental factors rooted in family, school, and peer groups are also shown to be the predictors of delinquent behavior where strength seems to exceed that of self-control. These findings shed more nuanced insights on the nexus between self-control, external situations, and delinquency, and in a broader sense, contribute to the elaboration of a more comprehensive understanding of self-control theory.Background and aims Inflammatory Bowel Disease (IBD) with colonic involvement increases colorectal cancer risk. However, the distinction between IBD related and sporadic dysplasia in IBD patients is difficult. Some data favors the importance of abnormal DNA methylation in IBD-related carcinogenesis. We aimed to define methylation patterns in patients with colonic cancer or dysplasia diagnosis following an IBD diagnosis.Methods Multicentric cross-sectional study-91 samples from colonic mucosa with/without dysplasia from 9 patients with IBD-related dysplasia/cancer and 26 patients with IBD and sporadic dysplasia/cancer were included. Methylation patterns of CpG islands in the promoter regions of 67 genes were studied by Methylation-specific Multiplex Ligation-dependent Probe Amplification.Results Mean age at IBD diagnosis 42 ± 16 years;at dysplasia diagnosis 56 ± 14 years. Twenty-ninepatients had ulcerative colitis. Twenty-five patients had at least 1 lesion endoscopically described as adenoma-like, 4 at least 1 non-adenoma like, 3 had cancer and 3 had dysplasia in flat mucosa. No patient had both adenoma-like and non-adenoma-like lesions. Patients with an IBD-related lesion were significantly younger at IBD diagnosis (p = .003) and at dysplasia/cancer diagnosis (p = .039). Promoter methylation of IGF2, RARB, ESR1, CHFR, CDH13, WT1, GATA5, WIF1genes was significantly associated to dysplasia/cancer; methylation of MSH6, TIMP3 was significantly associated to IBD-related dysplasia/cancer. Promoter methylation of MSH6, MSH3, RUNX3, CRABP1, TP73, RARB, CDH13, PAX5, WT1, THBS1, TP53, SFRP1, WIF1, APAF1, BCL2 genes was significantly associated to active IBD.Conclusions Methylation analysis, namely of MSH6, may contribute to the classification of dysplastic lesions in IBD- to be further tested in prospective studies.This study aimed to investigate the effect of Cordyceps militaris extract on the proliferation and apoptosis of non-small cell lung cancer (NSCLC) cells and determine the underlying mechanisms. We performed a CCK-8 assay to detect cell proliferation, detection of morphological changes through transmission electron microscopy (TEM), annexin V-FITC/PI double staining to analyze apoptosis, and immunoblotting to measure the protein expression of apoptosis and hedgehog signaling-related proteins, with C militaris treated NSCLC cells. In this study, we first found that C militaris reduced the viability and induced morphological disruption in NSCLC cells. The gene expression profiles indicated a reprogramming pattern of genes and transcription factors associated with the action of TCTN3 on NSCLC cells. We also confirmed that the C militaris-induced inhibition of TCTN3 expression affected the hedgehog signaling pathway. Immunoblotting indicated that C militaris-mediated TCTN3 downregulation induced apoptosis in NSCLC cells, involved in the serial activation of caspases. Moreover, we demonstrated that the C militaris negatively modulated GLI1 transcriptional activity by suppressing SMO/PTCH1 signaling, which affects the intrinsic apoptotic pathway. When hedgehog binds to the PTCH1, SMO dissociates from PTCH1 inhibition at cilia. As a result, the active GLI1 translocates to the nucleus. C militaris clearly suppressed GLI1 nuclear translocation, leading to Bcl-2 and Bcl-xL down-regulation. These results suggested that C militaris induced NSCLC cell apoptosis, possibly through the downregulation of SMO/PTCH1 signaling and GLI1 activation via inhibition of TCTN3. Taken together, our findings provide new insights into the treatment of NSCLC using C militaris.The 12th International Society for the Study of Xenobiotics (ISSX) meeting, held in Portland, OR, USA from July 28 to 31, 2019, was attended by diverse members of the pharmaceutical sciences community. The ISSX New Investigators Group provides learning and professional growth opportunities for student and early career members of ISSX. To share meeting content with those who were unable to attend, the ISSX New Investigators herein elected to highlight the "Advances in the Study of Drug Metabolism" symposium, as it engaged attendees with diverse backgrounds. This session covered a wide range of current topics in drug metabolism research including predicting sites and routes of metabolism, metabolite identification, ligand docking, and medicinal and natural products chemistry, and highlighted approaches complemented by computational modeling. In silico tools have been increasingly applied in both academic and industrial settings, alongside traditional and evolving in vitro techniques, to strengthen and streamline pharmaceutical research. Approaches such as quantum mechanics simulations facilitate understanding of reaction energetics toward prediction of routes and sites of drug metabolism. Furthermore, in tandem with crystallographic and orthogonal wet lab techniques for structural validation of drug metabolizing enzymes, in silico models can aid understanding of substrate recognition by particular enzymes, identify metabolic soft spots and predict toxic metabolites for improved molecular design. Of note, integration of chemical synthesis and biosynthesis using natural products remains an important approach for identifying new chemical scaffolds in drug discovery. These subjects, compiled by the symposium organizers, presenters, and the ISSX New Investigators Group, are discussed in this review.Introduction Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease. Early referral and treatment are key to the effective management of the disease. This makes imperative the identification of biomarkers and of pathobiological endotypes. Areas covered This review describes recent efforts to integrate large-scale datasets for the identification of disease endotypes for precision medicine in early, seropositive RA. We conducted a search for systems and multi-omics papers in early RA patients through to 1 January 2020. We reviewed investigations of multiple technologies such as transcriptomic, proteomic and metabolomic platforms as well as extensive clinical datasets. We outline progress made and describe some of the advantages and limitations of current computational and statistical methods. Expert opinion The search for pathobiological endotypes in early RA is rapidly developing. While currently, studies tend to be small, reliant upon new technologies and unproven analytical tools, as the technology becomes cheaper and more reliable, and the properties of analytical tools for the integration of cross-platform biology become better understood, it seems likely that better biomarkers of disease, remission and response to individual therapies will emerge.