Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA304981 | ENA |
REPOSITORIES: ENA
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Project description:Environmental enteric dysfunction includes a broad spectrum of inflammatory responses and epithelial repair processes.
| PRJNA301157 | ENA
Project description:Environmental enteric dysfunction (EED), a chronic diffuse inflammation of the small intestine, is associated with stunting in children in the developing world. The pathobiology of EED is poorly understood because of the lack of a method to elucidate the host response. This study utilized a novel microarray method to interrogate the host transcriptome in feces in Malawian children with EED. Our data showed that the children studied had a range of %L values, consistent a spectrum of EED from normal to severe. We identified 12 transcripts associated with the severity of EED, including chemokines that stimulate T-cell proliferation, Fc fragments of multiple immunoglobulin families, interferon-induced proteins, activators of neutrophils and B-cells, and mediators that dampen cellular responses to hormones. EED associated transcripts mapped to pathways related to cell adhesion, and responses to a broad spectrum of viral, bacterial and parasitic microbes and enhanced phagocytosis. Several mucins, regulatory factors and protein kinases associated with the maintenance of the mucous layer were expressed less in children with EED than normal children. In conclusion, EED represents the focused activation of elements of the immune system and is associated with widespread intestinal barrier disruption. The differentially expressed transcripts may be explored as potential biomarkers. In 259 children, EED was measured by lactulose permeability (%L) in the small intestine. After isolating low copy numbers of mRNA, the transcriptome was reliably and reproducibly profiled. mRNA copy number was correlated with %L using analyses of covariance. The transcripts identified were mapped to biological pathways and processes.
2016-03-01 | E-GEOD-74681 | biostudies-arrayexpress
Project description:Serum miRNA profiling by quantitative RT PCR [RT-PCR Array 1]
| PRJNA253724 | ENA
Project description:Serum miRNA profiling by quantitative RT PCR [RT-PCR Array 2]
| PRJNA253723 | ENA
Project description:Circadian clock is a highly conserved regulatory system which could coordinate many physiological processes with external stimuli, displaying oscillation with a periodicity of ~24 hour. Dysfunction of circadian clock has been involved in the pathogenesis of a broad spectrum of diseases such as metabolic diseases and chronic kidney disease. However the role of circadian clock in diabetic nephropathy remains largely unknown.
2023-05-04 | GSE217853 | GEO
Project description:Abstract Isorhynchophylline, a tetracyclic indole alkaloid, has anti-inflammatory and antioxidant activities against cardiovascular diseases and central nervous system disorders. Acute lung injury (ALI) is a manifestation of inflammation concentrated in the lungs and has a high incidence rate and mortality. Here, we established a mouse model of ALI and observed the effects of isorhynchophylline. Proteomic results showed that 5727 proteins were detected in mouse lung tissues, and 16 proteins were screened out. Isorhynchophylline could reverse the trend of these differential proteins. In addition, isorhynchophylline can act on integrin alpha M to reduce neutrophil recruitment and thereby produce anti-inflammatory effects and may suppress neutrophil migration through the leukocyte transendothelial migration pathway. TUNEL and RT-PCR experiments revealed that LPS-induced ALI in mice increases the apoptosis of lung tissues, damage to alveolar epithelial cells and levels of inflammatory factors. Treatment with isorhynchophylline can repair tissues, improve lung tissue pathology and reduce lung inflammation.
2024-06-23 | PXD050432 | Pride
Project description:Human rhinovirus (HRV), first isolated in 1956, belongs to the family Picornaviridae. HRV causes mild cold and severe respiratory disease. To date, no FDA-approved antiviral or anti-inflammatory drugs are available. TA25 is a phenolic amide derivative extracted from Nicotiana tabacum. To investigate the potential candidate for antiviral therapeutics, we evaluated the antiviral potency of TA25 for HRV and multiple zoonotic viruses. The antiviral and anti-inflammatory effects were evaluated using RT-qPCR and RNA-seq. Strand-specific RT-qPCR was performed to measure genomic and anti-genomic RNA expression after TA25 treatment. In addition, an AI-based docking test was conducted to investigate the binding affinity of TA25 with viral proteins. TA25 induced significant reduction in viral replication and suppressed the expression of pro-inflammatory genes. Inhibition of viral replication by TA25 treatment was confirmed by strand-specific RT-qPCR. TA25 showed broad-spectrum antiviral activity against multiple viruses, including HRV-1A, ZIKV, DENV, VACV, and IBV. Using AI-driven structure-based docking analysis, TA25 showed strongest binding affinity with HRV 2B protein. This study demonstrates that TA25 confers the broad antiviral and anti-inflammatory activity against HRV and multiple zoonotic viruses. These findings provide valuable insights into antiviral strategies of TA25 for a promising therapeutic candidate in response to emerging RNA and DNA viruses.
2026-02-11 | GSE319110 | GEO
Project description:Background: Neonatal sepsis-associated acute lung injury (ALI) is a therapeutic challenge. This study evaluated the efficacy of CQMUH-011, a novel small-molecule compound, against lipopolysaccharide (LPS)-induced ALI in neonatal rabbits. Methods: Neonatal rabbits at postnatal age 5-7 days were intraperitoneally injected with LPS (50 mg/kg) to induce ALI, and subsequently treated with CQMUH-011 at 675 μg/kg at 0.5 hour. Outcomes within 10-hour of observation were assessed through survival analysis, neurobehavioral assessment, blood gas, histopathological scoring, alveolar phospholipid quantification in bronchoalveolar lavage fluid, RT-PCR for inflammatory mediators and surfactant proteins, and gene expression profiles through transcriptomic analysis. Results: LPS administration induced severe ALI characterized by metabolic acidosis, hypoxemia, lung inflammatory injury, neuromotor dysfunction, and mortality. CQMUH-011 improved neurological deficits, restored blood gas balance, enriched phospholipid pool, reduced lung injury scores, diminished leukocyte infiltration and improved alveolar expansion. RT-PCR results showed significantly mitigated mRNA expressions of proinflammatory cytokines and enhanced surfactant proteins and phospholipid synthesis-associated enzymes. Transcriptomic analysis revealed the dual mechanism of CQMUH-011 by downregulating multiple inflammatory pathways, including cytokine-cytokine receptor interaction, T-helper 17 cell differentiation, interleukin-17 and nuclear transcription factor-kappa B, tumor necrosis factor-α, concurrent with activation of phosphatidylinositol 3-kinase/protein kinase B-dependent cytoprotection, cytoskeletal remodeling, and intercellular junction reinforcement. Conclusions: CQMUH-011 exerts potent anti-inflammatory and lung-protective effects in neonatal ALI by modulating critical inflammatory and repair pathways, making it a promising therapeutic candidate for sepsis-associated ALI.
2026-06-18 | GSE312949 | GEO
Project description:To determine whether NRF2-mediated anti-inflammatory differentiation and its downstream consequences on tumor immunology are intrinsic macrophage processes, we conducted a series of in vitro studies. First, we performed scRNA-seq studies of WT, Keap1 KO, and Nrf2 KO BMDMs after short-term culture with GM-CSF for 5 days to capture a broad spectrum of differentiation and polarization states across the macrophage lineage trajectory.
2025-10-10 | GSE290431 | GEO
Project description:The p53 transcription factor is a regulator of key cellular processes including DNA repair, cell cycle arrest, and apoptosis. In this theoretical study, we investigate how the complex circuitry of the p53 network allows for stochastic yet unambiguous cell fate decision-making. The proposed Markov chain model consists of the regulatory core and two subordinated bistable modules responsible for cell cycle arrest and apoptosis. The regulatory core is controlled by two negative feedback loops (regulated by Mdm2 and Wip1) responsible for oscillations, and two antagonistic positive feedback loops (regulated by phosphatases Wip1 and PTEN) responsible for bistability. By means of bifurcation analysis of the deterministic approximation we capture the recurrent solutions (i.e., steady states and limit cycles) that delineate temporal responses of the stochastic system. Direct switching from the limit-cycle oscillations to the "apoptotic" steady state is enabled by the existence of a subcritical Neimark-Sacker bifurcation in which the limit cycle loses its stability by merging with an unstable invariant torus. Our analysis provides an explanation why cancer cell lines known to have vastly diverse expression levels of Wip1 and PTEN exhibit a broad spectrum of responses to DNA damage: from a fast transition to a high level of p53 killer (a p53 phosphoform which promotes commitment to apoptosis) in cells characterized by high PTEN and low Wip1 levels to long-lasting p53 level oscillations in cells having PTEN promoter methylated (as in, e.g., MCF-7 cell line).
2024-09-02 | BIOMD0000000943 | BioModels