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Journal: International Journal of Biological Sciences
Article Title: Molecular Mechanisms of Ischemia/Reperfusion Injury and Graft Dysfunction in Liver Transplantation: Insights from Multi-Omics Studies in Rodent Animal Models
doi: 10.7150/ijbs.109449
Figure Lengend Snippet: Main features of studies with omics application in rodent ischemia and reperfusion injury model
Article Snippet: Hua, China, 2022 , C57BL6 mice/ male/ 8-10 wks/ 6 vs. 6 , 70% WI (left+middle lobe) , IPC/none , Liver/at the end of each treatment ,
Techniques: Control, Sampling, Comparison, Biomarker Discovery, Microarray, Ubiquitin Proteomics, Functional Assay, Expressing, Protein-Protein interactions, Gene Expression, Migration, Activation Assay, TUNEL Assay, Infection, Construct, Sequencing
Journal: Biomedicines
Article Title: Generation of Transcript Length Variants and Reprogramming of mRNA Splicing During Atherosclerosis Progression in ApoE-Deficient Mice
doi: 10.3390/biomedicines12122703
Figure Lengend Snippet: Pipeline of the experimental approach followed. Female ApoE -/- mice were treated twice weekly for 16 weeks (arrowheads) with an intraperitoneal administration of 50 μg of an αCD40 siRNA (treatment group, T) or 50 μg of a scrambled sequence siRNA (control group, C). Aortic tissue was extracted at weeks 8 (basal) and 10 and 24 for both experimental groups (C10, C24, T10 and T24). Total RNA was extracted and used for a microarray experiment in which expression data were normalized to the basal levels at week 8. Only downregulated transcripts of the C and T groups were used in this analysis of length dynamics (see text). In parenthesis is the number of transcripts from each group. Transcripts simultaneously expressed in two experimental conditions (C10/C24 and T10/T24) were identified and used for bioinformatic analysis of the mechanisms regulating transcript length variation.
Article Snippet: In this work, we used the
Techniques: Sequencing, Control, Microarray, Expressing
Journal: Cellular and Molecular Life Sciences: CMLS
Article Title: Long noncoding RNA AK144717 exacerbates pathological cardiac hypertrophy through modulating the cellular distribution of HMGB1 and subsequent DNA damage response
doi: 10.1007/s00018-024-05464-0
Figure Lengend Snippet: Establishment of cardiac failure model and identification of altered lncRNAs. A–C . Echocardiography and quantitative analysis ( n = 6–7). D–E . Representative images of hematoxylin and eosin (H&E) staining (upper) and wheat germ agglutinin (WGA) staining ( n = 6–7). Scale bar: 100 μm. F . Quantitative analysis of the heart weight (HW)/body weight (BW) ratio ( n = 6–7). G . qPCR analysis of ANP and BNP mRNA expressions ( n = 6–7). H . Heat map of the top 20 altered lncRNAs in the heart. The lncRNAs with raw intensities over 20 in the microarray sequencing report are framed in red. I . qPCR analysis of lncRNAs in the samples applied for microarray sequencing ( n = 3). J . qPCR validation of LncRNA AK144717 and Gm4316 (ENSMUST00000212411) in all the mice of sham and TAC group ( n = 6–7). K. qPCR analysis of LncRNA AK144717 expression in the TAC models of different time ( n = 6). * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001; NS means not significant between groups
Article Snippet: The ventricular samples from 3 mice operated by TAC for 6 weeks and 3 mice with sham surgery were sent to Shanghai KangChen Bio-tech Company to detect the differentially expressed lncRNAs by using
Techniques: Staining, Microarray, Sequencing, Biomarker Discovery, Expressing