Project description:Carbapenem-resistant Klebsiella pneumoniae (CRKP), particularly the K64 serotype, poses a severe clinical threat due to its high virulence and multidrug resistance. In this study, we investigated the gene expression profiles of host lung tissues to understand the pathogenesis of K64-CRKP infection and the therapeutic mechanism of Dep44, a capsule-degrading depolymerase. An acute pneumonia mouse model was established via intranasal infection with K64-CRKP. We performed high-throughput RNA sequencing (RNA-seq) on lung tissues from four experimental groups: the negative control group (healthy mice), the positive control group (K64-CRKP infected model), the treatment group (infected mice treated with Dep44), and the drug control group (healthy mice treated with Dep44). The analysis aims to elucidate the host immune response to K64-CRKP infection and evaluate how Dep44 treatment modulates these transcriptomic changes to exert its therapeutic effect.
Project description:We performed shallow whole genome sequencing (WGS) on circulating free (cf)DNA extracted from plasma or cerebrospinal fluid (CSF), and shallow WGS on the tissue DNA extracted from the biopsy in order to evaluate the correlation between the two biomaterials. After library construction and sequencing (Hiseq3000 or Ion Proton), copy number variations were called with WisecondorX.
Project description:Whole genome sequencing (WGS) of tongue cancer samples and cell line was performed to identify the fusion gene translocation breakpoint. WGS raw data was aligned to human reference genome (GRCh38.p12) using BWA-MEM (v0.7.17). The BAM files generated were further analysed using SvABA (v1.1.3) tool to identify translocation breakpoints. The translocation breakpoints were annotated using custom scripts, using the reference GENCODE GTF (v30). The fusion breakpoints identified in the SvABA analysis were additionally confirmed using MANTA tool (v1.6.0).
Project description:Detailed exploration was performed on the T cell and B cell transcriptional profiles when comparing moderate and severe patients to healthy donors, identifying candidate gene signatures. Furthermore, we analyzed the properties of cytotoxicity and exhaustion within T cell subgroups derived from CRKP samples.
