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    Global gene expression profiling in congenital diaphragmatic hernia (CDH) patients
    (Springer Heidelberg, 2022) Gurunluoglu, Kubilay; Dundar, Muhammed; Unver, Turgay; Akpinar, Necmettin; Gokce, Ismail Kursad; Gurunluoglu, Semra; Demircan, Mehmet
    Congenital diaphragmatic hernia (CDH) is an anomaly characterized by a defect in the diaphragm, leading to the passage of intra-abdominal organs into the thoracic cavity. Herein, the presented work analyzes the global gene expression profiles in nine CDH and one healthy newborn. All of the patients had left posterolateral (Bochdalek) diaphragmatic hernia, operated via an abdominal approach, and stomach and bowels in the thorax cavity. Some patients also had additional anomalies. A total of 560 differentially regulated genes were measured. Among them, 11 genes showed significant changes in expression associated with lung tissue, vascular structure development, and vitamin A metabolism, which are typical ontologies related to CDH etiology. Among them, SLC25A24 and RAB3IL1 are involved in angiogenesis, HIF1A and FOXC2-AS1 are related with the alveolus, MAGI2-AS3 is associated with the diaphragm, LHX4 and DHH are linked with the lung, and BRINP1, FZD9, WNT4, and BLOC1S1-RDH5 are involved in retinol. Besides, the expression levels of some previously claimed genes with CDH etiology also showed diverse expression patterns in different patients. All these indicated that CDH is a complex, multigenic anomaly, requiring holistic approaches for its elucidation.
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    Global gene expression profiling in congenital diaphragmatic hernia (CDH) patients (vol 22, pg 359, 2022)
    (Springer Heidelberg, 2022) Gurunluoglu, Kubilay; Dundar, Muhammed; Unver, Turgay; Akpinar, Necmettin; Gokce, Ismail Kursad; Gurunluoglu, Semra; Demircan, Mehmet
    [Abstract Not Available]
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    Selenium deficiency is functionally linked with the molecular etiopathogenesis of necrotizing enterocolitis (NEC)
    (Springer Heidelberg, 2025) Gurunluoglu, Kubilay; Dundar, Muhammed; Unver, Turgay; Turgut, Hatice; Gurunluoglu, Semra; Akpinar, Necmettin; Ates, Hasan
    Necrotizing enterocolitis (NEC) is a severe and often catastrophic gastrointestinal emergency that predominantly affects neonates, especially those born prematurely, and is associated with high rates of morbidity and mortality. Despite its significant clinical impact, the precise etiology and molecular pathogenesis of NEC remain incompletely understood. In this study, we conducted global transcriptomic profiling using high-throughput RNA sequencing in 11 premature neonates diagnosed with NEC, following rigorous inclusion and exclusion criteria. Compared to healthy controls, we identified 1,204 differentially expressed genes (DEGs), including 636 upregulated and 568 downregulated transcripts. Notably, genes involved in hypoxia-induced apoptosis (e.g., HIF1 AAS3, HIF1 AAS1), the caspase cascade (BCL2, BCL6, CASP5, CASP7), and inflammation (IL1RAP, IL6ST, TNFAIP3, TNFRSF10 A, TLR6, TLR10) were significantly upregulated. In contrast, IL18, a key modulator of inflammatory responses, was downregulated. Interestingly, several genes encoding selenoproteins (GPX1, GPX4, SELENON, SELENOM, SELENOF, SELENOW, SELENOT) were also downregulated, suggesting molecular evidence of selenium deficiency. Gene ontology and pathway enrichment analyses revealed widespread dysregulation in pathways related to hypoxia response, systemic inflammation, coagulation, antimicrobial defense, mitochondrial function, autophagy, selenium metabolism, and apoptosis. Collectively, our findings provide novel insights into the molecular underpinnings of NEC in premature infants and suggest that systemic hypoxia, oxidative stress, selenium deficiency, and programmed cell death contribute significantly to its pathogenesis.