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Spatially Resolved Integrative Analysis of Transcriptomic and Metabolomic Changes in Tissue Injury Studies
No full textRecent developments in spatially resolved -omics have enabled the joint study of gene expression, metabolite levels and tissue morphology, offering greater insights into biological pathways. Integrating these modalities from matched tissue sections to probe spatially-coordinated processes, however, remains challenging. Here we introduce MAGPIE, a framework for co-registering spatially resolved transcriptomics, metabolomics, and tissue morphology from the same or consecutive sections. We show MAGPIE\u27s generalisability and scalability on spatial multi-omics data from multiple tissues, combining Visium with MALDI and DESI mass spectrometry imaging. MAGPIE was also applied to new multi-modal datasets generated with a specialised sampling strategy to characterise the metabolic and transcriptomic landscape in an in vivo model of drug-induced pulmonary fibrosis and to link small-molecule co-detection with endogenous lung responses. MAGPIE demonstrates the refined resolution and enhanced interpretability that spatial multi-modal analyses provide for studying tissue injury especially in pharmacological contexts, and delivers a modular, accessible workflow for data integration
Journal Publishing on Digital Commons
No full textHave you visited Digital Commons@TMC, the institutional repository before?Take your research to the next level and learn about the basics of how you can publish your open access student-led (faculty advisor needed) or professional journal on this platform and the steps getting started. DigitalCommons@TMC is viewed by 165+ countries, 2500+ institutions, with more than 120k downloads monthly
Enhancing Visibility and Impact: Author Profiles & Citation Tracking
No full textAccurate profiles improve discoverability, citation metrics inform funding, promotion, and collaboration. Today we will talk about how to manage author profiles (Orcid, Scopus author id, Web of Science/Publons, Google Scholar profile, LinkedIn, ResearchGate) and track citations to support research visibility and evaluation
Maternal Myo-Inositol Intake and Congenital Heart Defects in Offspring: A Population-Based Case-Control Study
No full textObjective: To investigate associations between maternal periconceptional (three months prior through the third pregnancy month) myo-inositol intake and the odds of selected congenital heart defects in offspring.
Design: A population-based case-control study using the National Birth Defects Prevention Study (NBDPS) database.
Setting: United States.
Population or sample: Women with singleton live births without major birth defects (controls) and women with singleton live births, stillbirths, or terminations with selected nonsyndromic congenital heart defects (CHD; cases).
Methods: Descriptive analyses, logistic regression models, ascertainment of myo-inositol intake from supplements and food using a shortened food frequency questionnaire and survey.
Main outcome measures: Odds of CHD.
Results: 11 752 cases and 11 415 controls were included. Compared to women not taking myo-inositol supplements, women with any supplemental intake were less likely to have a pregnancy with the selected congenital heart defects as a group (adjusted odds ratio [aOR] = 0.79; 95% confidence interval [CI] 0.66-0.94) or with septal defects alone (aOR = 0.61; 95% CI 0.46-0.81). Compared to women with low total myo-inositol intake from food or supplements, women with high total myo-inositol intake (≥ 500 mg/day) were less likely to have a pregnancy with the selected CHD as a group (aOR = 0.88; 95% CI 0.84-0.93) or conotruncal defects (aOR = 0.87; 95% CI 0.79-0.96); left ventricular outflow tract defects (aOR = 0.87; 95% CI 0.78-0.96); right ventricular outflow tract defects (aOR = 0.85; 95% CI 0.77-0.95); or atrial septal defects (aOR = 0.91; 95% CI 0.83-0.99).
Conclusions: An inverse association was observed between maternal myo-inositol intake during the periconceptional period and the odds of selected CHDs in offspring
KDM4A Promotes NEPC Progression Through Regulation of MYC Expression
No full textNeuroendocrine prostate cancer (NEPC) is a highly aggressive and lethal subtype of prostate cancer (PCa) that often emerges in response to androgen receptor pathway inhibitors (ARPIs), which are widely used in treating metastatic castration-resistant and hormone-sensitive prostate cancer. The incidence of NEPC is increasing, yet effective therapeutic strategies remain limited due to an incomplete understanding of its molecular drivers. Through transcriptomic analyses of human prostate tumor samples, we identified the histone lysine demethylase KDM4A as uniquely overexpressed in human and mouse NEPC compared to prostate adenocarcinoma. Functional validation demonstrated that KDM4A is a key regulator of NEPC progression and a promising therapeutic target, as knockdown or knockout of KDM4A suppresses NEPC cell proliferation in vitro and tumor growth in vivo. Mechanistically, we found that KDM4A directly regulates the transcription of the oncogene MYC, which we show is essential for NEPC cell growth through knockdown and inhibitor studies. Importantly, pharmacologic inhibition of KDM4A using QC6352, a potent pan-KDM4 inhibitor, significantly reduced NEPC cell proliferation in vitro and tumor growth in vivo, providing proof-of-concept for therapeutic targeting. Collectively, our findings establish KDM4A as a critical epigenetic driver of NEPC through MYC regulation and demonstrate its therapeutic potential for this lethal disease that currently lacks effective treatments
