Similar Datasets
Project description:PM2.5 can harm various systems in the human body. However, due to the limitations of epidemiology and toxicology, the disease types, shared and specific pathogenic mechanisms induced by PM2.5 in various human systems are not comprehensive and in-depth revealed. Thus, this study conducted an analysis on the aforementioned issues in respiratory, circulatory, endocrine, female, and male urogenital systems. According to this study, PM2.5 was more likely to induce pulmonary emphysema, reperfusion injury, malignant neoplasm of thyroid, endometriosis of ovary, nephritis in above each system respectively. FOS, extracellular matrix, urogenital system development, extracellular matrix structural constituent conferring tensile strength, and ferroptosis was the most important co-existing gene, cellular component, biological process, molecular function, and pathway in five systems targeted by PM2.5. Furthermore, BTG2, BIRC5, NFE2L2, TBK1, and STAT1 were significantly uniquely targeted by PM2.5 in each system respectively. Important disease related cellular component, biological process, and molecular function were highly specially induced by PM2.5, such as response to wounding, blood vessel morphogenesis, body morphogenesis, negative regulation of response to endoplasmic reticulum stress, and response to type I interferon were the top 1 uq-existing biological processes in each system respectively. PM2.5 highly specially acted on the key disease related pathway, such as PD-L1 expression and PD-1 checkpoint pathway in cancer (respiratory), cell cycle (circulatory), apoptosis (endocrine), antigen processing and presentation (female), and neuroactive ligand-receptor interaction (male). This study provides a new analysis method to clarify PM2.5-related disease types, which is an important supplement to epidemiological investigation. Furthermore, this study has clarified the risks of PM2.5 exposure, elucidated the pathogenic mechanisms, and provided scientific support for promoting precise prevention and treatment of PM2.5-related diseases.
2025-12-31 | GSE252421 | GEO
Project description:PM2.5 can harm various systems in the human body. However, due to the limitations of epidemiology and toxicology, the disease types, shared and specific pathogenic mechanisms induced by PM2.5 in various human systems are not comprehensive and in-depth revealed. Thus, this study conducted an analysis on the aforementioned issues in respiratory, circulatory, endocrine, female, and male urogenital systems. According to this study, PM2.5 was more likely to induce pulmonary emphysema, reperfusion injury, malignant neoplasm of thyroid, endometriosis of ovary, nephritis in above each system respectively. FOS, extracellular matrix, urogenital system development, extracellular matrix structural constituent conferring tensile strength, and ferroptosis was the most important co-existing gene, cellular component, biological process, molecular function, and pathway in five systems targeted by PM2.5. Furthermore, BTG2, BIRC5, NFE2L2, TBK1, and STAT1 were significantly uniquely targeted by PM2.5 in each system respectively. Important disease related cellular component, biological process, and molecular function were highly specially induced by PM2.5, such as response to wounding, blood vessel morphogenesis, body morphogenesis, negative regulation of response to endoplasmic reticulum stress, and response to type I interferon were the top 1 uq-existing biological processes in each system respectively. PM2.5 highly specially acted on the key disease related pathway, such as PD-L1 expression and PD-1 checkpoint pathway in cancer (respiratory), cell cycle (circulatory), apoptosis (endocrine), antigen processing and presentation (female), and neuroactive ligand-receptor interaction (male). This study provides a new analysis method to clarify PM2.5-related disease types, which is an important supplement to epidemiological investigation. Furthermore, this study has clarified the risks of PM2.5 exposure, elucidated the pathogenic mechanisms, and provided scientific support for promoting precise prevention and treatment of PM2.5-related diseases.
2024-12-08 | GSE252420 | GEO
Project description:PM2.5 can harm various systems in the human body. However, due to the limitations of epidemiology and toxicology, the disease types, shared and specific pathogenic mechanisms induced by PM2.5 in various human systems are not comprehensive and in-depth revealed. Thus, this study conducted an analysis on the aforementioned issues in respiratory, circulatory, endocrine, female, and male urogenital systems. According to this study, PM2.5 was more likely to induce pulmonary emphysema, reperfusion injury, malignant neoplasm of thyroid, endometriosis of ovary, nephritis in above each system respectively. FOS, extracellular matrix, urogenital system development, extracellular matrix structural constituent conferring tensile strength, and ferroptosis was the most important co-existing gene, cellular component, biological process, molecular function, and pathway in five systems targeted by PM2.5. Furthermore, BTG2, BIRC5, NFE2L2, TBK1, and STAT1 were significantly uniquely targeted by PM2.5 in each system respectively. Important disease related cellular component, biological process, and molecular function were highly specially induced by PM2.5, such as response to wounding, blood vessel morphogenesis, body morphogenesis, negative regulation of response to endoplasmic reticulum stress, and response to type I interferon were the top 1 uq-existing biological processes in each system respectively. PM2.5 highly specially acted on the key disease related pathway, such as PD-L1 expression and PD-1 checkpoint pathway in cancer (respiratory), cell cycle (circulatory), apoptosis (endocrine), antigen processing and presentation (female), and neuroactive ligand-receptor interaction (male). This study provides a new analysis method to clarify PM2.5-related disease types, which is an important supplement to epidemiological investigation. Furthermore, this study has clarified the risks of PM2.5 exposure, elucidated the pathogenic mechanisms, and provided scientific support for promoting precise prevention and treatment of PM2.5-related diseases.
2025-12-31 | GSE252423 | GEO
Project description:Disease type and Pathogenic Mechanism induced by PM2.5 in five Human Systems using omics and Human Disease Database
| PRJNA1060619 | ENA
Project description:Disease type and Pathogenic Mechanism induced by PM2.5 in five Human Systems using omics and Human Disease Database [Sertoli]
| PRJNA1060617 | ENA
Project description:Disease type and Pathogenic Mechanism induced by PM2.5 in five Human Systems using omics and Human Disease Database [EA.hy926]
| PRJNA1060618 | ENA
Project description:Disease type and Pathogenic Mechanism induced by PM2.5 in five Human Systems using omics and Human Disease Database [IOSE+Nthy]
| PRJNA1060625 | ENA
Project description:Multi-omics has helped elucidate the gene expression patterns and genomic variations closely associated with economically significant traits in geese. Despite the substantial genomic data generated through extensive goose studies, a unified platform for integrating these datasets is lacking. To address this gap, we introduced the Goose Multi-omics Database (GMD), which is accessible at http://goosedb.com/. The GMD is a comprehensive resource enabling streamlined search, analysis, and visualization of genetic information through a unified interface, providing insights into phenotypic traits, gene sequences, structures, expression profiles, genomic variations, gene families, homology, and collinearity. Equipped with robust analytical tools such as GBrowse and BLAST, the GMD facilitates rapid access to target gene information, significantly enhancing the efficiency and productivity of genomic research. By serving as a versatile and intuitive online repository, the GMD offers transformative potential for advancing goose biology, fostering multi-omics investigations, and integrating cutting-edge methodologies such as deep learning to accelerate discoveries in goose genomics.
| S-EPMC11810826 | biostudies-literature
Project description:The pathogenic mechanisms of many diseases are well understood at the molecular level, but there are prevalent syndromes associated with pathogenic signaling, such as diabetes and chronic inflammation, where our understanding is more limited. Here we report that pathogenic signaling suppresses the mobility of a spectrum of proteins that play essential roles in cellular functions known to be dysregulated in these chronic diseases. The reduced protein mobility, which we call proteolethargy, was linked to cysteine residues in the affected proteins and signaling-related increases in excess reactive oxygen species. Diverse pathogenic stimuli, including hyperglycemia, dyslipidemia and inflammation, produce similar reduced protein mobility phenotypes. We propose that proteolethargy is an overlooked cellular mechanism that may account for various pathogenic features of diverse chronic diseases.
2025-01-15 | GSE273733 | GEO
Project description:Hirschsprung's disease (HSCR) is a severe congenital anomaly of the enteric nervous system (ENS) characterized by functional intestinal obstruction due to a lack of intrinsic innervation in the distal bowel. Distal innervation deficiency results from incomplete colonization of the bowel by enteric neural crest cells (eNCCs), the ENS precursors. Here, we report the generation of a mouse model for HSCR--named Holstein--that contains an untargeted transgenic insertion upstream of the collagen-6?4 (Col6a4) gene. This insertion induces eNCC-specific upregulation of Col6a4 expression that increases total collagen VI protein levels in the extracellular matrix (ECM) surrounding both the developing and the postnatal ENS. Increased collagen VI levels during development mainly result in slower migration of eNCCs. This appears to be due to the fact that collagen VI is a poor substratum for supporting eNCC migration and can even interfere with the migration-promoting effects of fibronectin. Importantly, for a majority of patients in a HSCR cohort, the myenteric ganglia from the ganglionated region are also specifically surrounded by abundant collagen VI microfibrils, an outcome accentuated by Down syndrome. Collectively, our data thus unveil a clinically relevant pathogenic mechanism for HSCR that involves cell-autonomous changes in ECM composition surrounding eNCCs. Moreover, as COL6A1 and COL6A2 are on human Chr.21q, this mechanism is highly relevant to the predisposition of patients with Down syndrome to HSCR.
| S-EPMC4665793 | biostudies-other