Activity

5% and 99.99%, respectively. Conclusion The T-cell epitope-based peptide vaccine was designed for COVID-19 using the envelope protein as an immunogenic target. Nevertheless, the proposed vaccine rapidly needs to be validated clinically in order to ensure its safety and immunogenic profile to help stop this epidemic before it leads to devastating global outbreaks.Oxidative damage is closely involved in the development of doxorubicin- (DOX-) induced cardiotoxicity. It has been reported that tetrandrine can prevent the development of cardiac hypertrophy by suppressing reactive oxygen species- (ROS-) dependent signaling pathways in mice. However, whether tetrandrine could attenuate DOX-related cardiotoxicity remains unclear. To explore the protective effect of tetrandrine, mice were orally given a dose of tetrandrine (50 mg/kg) for 4 days beginning one day before DOX injection. To induce acute cardiac injury, the mice were exposed to a single intraperitoneal injection of DOX (15 mg/kg). The data in our study showed that tetrandrine prevented DOX-related whole-body wasting and heart atrophy, decreased markers of cardiac injury, and improved cardiac function in mice. Moreover, tetrandrine supplementation protected the mice against oxidative damage and myocardial apoptotic death. Tetrandrine supplementation also reduced ROS production and improved cell viability after DOX exposure in vitro. We also found that tetrandrine supplementation increased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) expression and activity in vivo and in vitro. The protection of tetrandrine supplementation was blocked by Nrf2 deficiency in mice. In conclusion, our study found that tetrandrine could improve cardiac function and prevent the development of DOX-related cardiac injury through activation of Nrf2.Purpose Parkinson’s disease (PD) is a neurodegenerative disorder with progressive motor defects. Therefore, the aim of the present investigation was to examine whether catalepsy, asymmetry, and nociceptive behaviors; the Nissl-body and neuron distribution; brain-derived neurotrophic factor (BDNF); malondialdehyde (MDA); total antioxidant capacity (TAC) levels; and the percentage of dopamine depletion of striatal neurons in the rat model of Parkinson’s disease (PD) can be affected by Toxoplasma gondii (TG) infection. Methods Fifty rats were divided into five groups control (intact rats), sham (rats which received an intrastriatal injection of artificial cerebrospinal fluid (ACSF)), PD control (induction of PD without TG infection), TG control (rats infected by TG without PD induction), and PD infected (third week after PD induction, infection by TG was done). PD was induced by the unilateral intrastriatal microinjection of 6-hydroxydopamine (6-OHDA) and ELISA quantified dopamine, BDNF, MDA, and TAC in the striociceptive and behaviors; the level of striatal dopamine release; BDNF levels; TAC; and MDA in PD rats.Methods circRNA expression was analysed in six cerebrospinal fluid (CSF) samples from three patients of the infectious and noninfectious phases using an Arraystar Human circRNA Array. Differentially altered circRNAs were validated by quantitative real-time polymerase chain reaction (qRT-PCR) in the 66 CSF samples of 33 patients of the infectious and noninfectious phases. H 89 in vitro t-test was used for statistical analysis. A bioinformatics analysis was employed to investigate the function mechanism of the circRNAs. Results Firstly, 142 circRNAs were found significantly different in 6 CSF samples of the infection and noninfection phases of 3 patients. Fourteen circRNAs with the top largest fold changes were chosen from the 142 circRNAs for PCR validation in the same 6 CSF samples of 3 patients. Three circRNAs were selected to be validated in 60 CSF samples of 30 patients using the PCR test. In infection CSF, an upregulated hsa_circRNA_402632 and downregulated hsa_circRNA_008636 and hsa_circRNA_405481 were confirmed by PCR test. A bioinformatics analysis was used to investigate the function mechanism of the 3 circRNAs. hsa_circRNA_402632 is enriched in the insulin resistance pathway, the FoxO and AMPK signaling pathways are the most important pathways for hsa_circRNA_008636 gene expression, and hsa_circRNA_405481 is enriched in the endometrial cancer signaling pathway, Fc epsilon RI signaling pathway, and TGF-beta signaling pathway. Conclusions hsa_circRNA_402632, hsa_circRNA_008636, and hsa_circRNA_405481 may be potential diagnostic markers for central nervous system infection after neurological surgery.Pancreatic cancer (PC) is a pernicious cancer of the digestive system which remains a high degree of malignancy. Increasing studies demonstrated that regulating the gut microbiome may become a brand new strategy to improve the therapeutic outcomes of PC. This study is aimed at obtaining the pathway in the microbial tumorigenesis of PC. Microarray datasets GSE27890, GSE46234, and GSE17610 were downloaded from the GEO (Gene Expression Omnibus) database. Differential analysis was performed for every single gene chip using the R software package (“Limma” package), and functional enrichment analyses were carried out by DAVID (Database for Annotation, Visualization and Integrated Discovery). The PPI (protein-protein interaction) network was constructed with the Search Tool for the Retrieval of Interacting Genes (STRING). The survival analysis was performed by GEPIA and USCS. A total of 84 differentially expressed genes (DEGs) were identified, and 3 of them were extracted (TUBB, TUBA4A, and TLR5). Biological process analysis revealed that these 3 genes were mainly enriched in pathogenic Escherichia coli (E. coli) infection. Survival analysis and pathway analysis revealed that TUBB (tubulin, beta class I) may be associated with the pathogenic E. coli infection, which may be involved in the carcinogenesis and progression of PC by activating the TUBB/Rho/ROCK signaling pathway. Elevated evidence indicated that a specific gut microbe could affect the progression of PC by suppressing immune response. However, little attention has been paid to the relationship and crosstalk between TUBB/Rho/ROCK signaling, microbes, and PC. This article is aimed at deducing that gut and tumor microbes are related to the development of PC by stimulating TUBB/Rho/ROCK signaling, while ablation of microbes by antibiotics cotreated with inhibitors of TUBB/Rho/ROCK signaling were identified as a novel target for PC therapy.