Project description:Porcine alveolar macrophages (PAMs) play impoartant role in innate immunity. Haemophilus parasuis is the etiological agent of Glasser’s disease in pigs. We used microarrays to study the transcriptome of PAMs infection with Haemophilus parasuis.
Project description:Porcine alveolar macrophages (PAMs) play impoartant role in innate immunity. Haemophilus parasuis is the etiological agent of Glasser’s disease in pigs. Haemophilus parasuis is the etiological agent of Glasser’s disease in pigs. We used microarrays to study the transcriptome of PAMs infection with HPS4.
Project description:To understand the mechanism of the adaptations, global gene expression profiles of the cecropin B--resistant strains of Haemophilus parasuis, The development of cecropin B (CB) resistance in H. parasuis SH0165 by exposing SH0165 using various concentrations of CB was investigated. One colony of bacterial cultures grown on TSA containing 30M-NM-<g/mL CB was named CBR30, CBR30 cultured in TSA without CB for 50 passages was named CBR30-50. we used microarray technology to analyze the variation of the H. parasuis SH0165 transcriptional profile in CBR30 and CBR30-50. Our analysis to identify several genes whose system could be involved in inorganic ion transport, amino acid transport, and metabolism. Quantitative PCR was used to validate the differential expression of selected genes. The H. parasuis SH0165 control group was normal culture with no tilmicosin at OD600 >0.3 (12 h). The H. parasuis CBR30 was normal culture with 30M-NM-<g/mL cecropin B at OD600 >0.3 (20 h). The H. parasuis CBR30-50 was normal culture with no cecropin B at OD600 >0.3 (12 h). Three independent experiments were performed on each group using a different sample for each experiment.
Project description:LncRNAs play a crucial role in regulating the progression of NSCLC, making them potential targets for cancer diagnosis and treatment. Therefore, identifying new lncRNAs as therapeutic target and comprehending their underlying regulatory mechanisms are crucial for treating NSCLC. In this study, we found that glioblastoma down-regulated RNA (GLIDR) was increased in non-response NSCLC patients with the primary treatment, and GLIDR was also highly expressed in NSCLC patients. We used bioinformatic analysis and luciferase assays to identify that microRNA-342-5p (miR-342-5p) directly targets GLIDR. MiR-342-5p overexpression inhibits NSCLC cell proliferation, migration, and invasion, whereas miR-342-5p inhibition promotes NSCLC malignancy, which can be rescued by suppressing GLIDR. Peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PPARGC1A) was identified as a downstream target of miR-342-5p. PPARGC1A inhibition significantly suppresses NSCLC malignancy, whereas overexpression promotes it. The results also revealed that GLIDR overexpression reduced PPARGC1A inhibition by miR-342-5p, and increased PPARGC1A expression reversed the inhibition of NSCLC malignancies caused by decreased GLIDR. To the best of our knowledge, we are the first to discover that GLIDR promotes NSCLC progression by sponging miR-342-5p to regulate PPARGC1A expression, presenting that GLIDR act as a potential therapeutic target in NSCLC.
Project description:To understand the mechanism of the adaptations, global gene expression profiles of the cecropin B--resistant strains of Haemophilus parasuis, The development of cecropin B (CB) resistance in H. parasuis SH0165 by exposing SH0165 using various concentrations of CB was investigated. One colony of bacterial cultures grown on TSA containing 30μg/mL CB was named CBR30, CBR30 cultured in TSA without CB for 50 passages was named CBR30-50. we used microarray technology to analyze the variation of the H. parasuis SH0165 transcriptional profile in CBR30 and CBR30-50. Our analysis to identify several genes whose system could be involved in inorganic ion transport, amino acid transport, and metabolism. Quantitative PCR was used to validate the differential expression of selected genes.
