Pateharvey7885
Clinical outcomes of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) showed enormous inter-individual and inter-population differences, possibly due to host genetics differences. Earlier studies identified single nucleotide polymorphisms (SNPs) associated with SARS-CoV-1 in Eastern Asian (EAS) populations. In this report, we aimed at exploring the frequency of a set of genetic polymorphisms that could affect SARS-CoV-2 susceptibility or severity, including those that were previously associated with SARS-CoV-1.
We extracted the list of SNPs that could potentially modulate SARS-CoV-2 from the genome wide association studies (GWAS) on SARS-CoV-1 and other viruses. We also collected the expression data of these SNPs from the expression quantitative trait loci (eQTLs) databases. Sequences from Qatar Genome Programme (QGP,
= 6,054) and 1000Genome project were used to calculate and compare allelic frequencies (AF).
A total of 74 SNPs, located ite these findings as well as to identify new genetic determinants linked to SARS-CoV-2.
Multiple genetic variants, which could potentially modulate SARS-CoV-2 infection, are significantly variable between populations, with the lowest frequency observed among Africans. Our results highlight the importance of exploring population genetics to understand and predict COVID-19 outcomes. Tamoxifen cost Indeed, further studies are needed to validate these findings as well as to identify new genetic determinants linked to SARS-CoV-2.
The aim of this study was to develop a comprehensive differential gene profile for hepatocellular carcinoma (HCC) patients treated with sorafenib.
The RNA sequencing data and miRNA sequencing data of 114 HCC patients treated with sorafenib only and 326 HCC control patients treated without any chemotherapeutic drugs were studied using differential expression, functional enrichment, and protein-protein interaction analysis.
Compared with HCC patients without any chemotherapy drugs, the sorafenib-treated patients develop 66 differentially expressed genes (DEGs), including 12 upregulated genes and 54 downregulated genes. Additionally, three differentially expressed miRNAs (DEMs) also show specific expression pattern. With further analysis, five primary genes including HTR2C, TRH, AGTR2, MCHR2, and SLC6A2 as well as three miRNAs (hsa-miR-4445, hsa-miR-466, and hsa-miR-2114) have been suggested as the potential targets for sorafenib. The specific gene expression of five genes has been validated in clinical HCC patients by ELISA method. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analyses indicate several significantly enriched biological processes (BPs), cellular components (CCs), and molecular functions (MFs).
Since sorafenib is becoming increasingly important in HCC treatment clinically, this study will help us understand the potential targets and eliminate diverse existing side effects of it as well as explore several potential clinical biomarkers with comprehensive analysis of differential gene expression profile.
Since sorafenib is becoming increasingly important in HCC treatment clinically, this study will help us understand the potential targets and eliminate diverse existing side effects of it as well as explore several potential clinical biomarkers with comprehensive analysis of differential gene expression profile.Familial hypercholesterolemia (FH) is one of the most common monogenic diseases, leading to an increased risk of premature atherosclerosis and its cardiovascular complications due to its effect on plasma cholesterol levels. Variants of three genes (LDL-R, APOB and PCSK9) are the major causes of FH, but in some probands, the FH phenotype is associated with variants of other genes. Alternatively, the typical clinical picture of FH can result from the accumulation of common cholesterol-increasing alleles (polygenic FH). Although the Czech Republic is one of the most successful countries with respect to FH detection, approximately 80% of FH patients remain undiagnosed. The opportunities for international collaboration and experience sharing within international programs (e.g., EAS FHSC, ScreenPro FH, etc.) will improve the detection of FH patients in the future and enable even more accessible and accurate genetic diagnostics.
Some lung diseases are cell type-specific. It is essential to study the cellular anatomy of the normal human lung for exploring the cellular origin of lung disease and the cell development trajectory.
We used the Seurat R package for data quality control. The principal component analysis (PCA) was used for linear dimensionality reduction. UMAP and tSNE were used for dimensionality reduction. Muonocle2 was used to extract lung epithelial cells to analyze the subtypes of epithelial cells further and to study the development of these cell subtypes.
We showed a total of 20154 high quality of cells from human normal lung tissue. They were initially divided into 17 clusters cells and then identified as seven types of cells, namely macrophages, monocytes, CD8 + T cells, epithelial cells, endothelial cells, adipocytes, and NK cells. 4240 epithelial cells were extracted for further analysis and they were divided into seven clusters. The seven cell clusters include alveolar cell, alveolar endothelial progenitor, ciliated cell, secretory cell, ionocyte cell, and a group of cells that are not clear at present. We show the development track of these subtypes of epithelial cells, in which we speculate that alveolar epithelial progenitor (AEP) is a kind of progenitor cells that can develop into alveolar cells, and find six essential genes that determine the cell fate, including AGER, RPL10, RPL9, RPS18, RPS27, and SFTPB.
We provide a transcription map of human lung cells, especially the in-depth study on the development of epithelial cell subtypes, which will help us to study lung cell biology and lung diseases.
We provide a transcription map of human lung cells, especially the in-depth study on the development of epithelial cell subtypes, which will help us to study lung cell biology and lung diseases.