Objectives:To identify the key points for improving severe maternal morbidity by analyzing pregnancy-related ICU admissions in Beijing.Design:This was a retrospective, multicenter cohort study.Setting:Three ICUs in tertiary hospitals in Beijing.Patients:A total of 491 severe maternal cases in any trimester of pregnancy or within 42 days of delivery were reviewed between January 1, 2008, and December 31, 2016.Interventions:None.Measurements and Main Results:Among 491 obstetric ICU admissions (median Sequential Organ Failure Assessment score, 2) out of 87,850 hospital deliveries (a frequency of 5.6 admissions per 1,000 deliveries), the leading diagnoses were postpartum hemorrhage (170; 34.62%), hypertensive disorders of pregnancy (156; 31.77%), and cardio-cerebrovascular diseases (78; 15.9%). Comparing 2008–2011 to 2012–2016, the rates of maternal mortality (2.5% vs 1.9%; p = 0.991) and fetal loss (8.5% vs 8.6%; p = 0.977) did not decrease significantly, whereas the rates of ICU admission (3.05% vs 7.85%; p trends < 0.001) and postpartum hemorrhage (23% vs 38.5%; p = 0.002) increased. Hypertensive disorder (150/156; 96.2% transferred to the ICU postpartum, 24/28 women with fetal loss transferred from lower-level hospitals) was an independent maternal factor associated with fetal loss, and infections were the leading cause of maternal death (6/10) in the ICU.Conclusions:Our study highlights the increasing rate of intensive care admissions for postpartum hemorrhage. Improving prenatal care quality for pregnancy-induced hypertension and sepsis at lower-level hospitals may improve maternal and fetal outcomes. Specifically, providing more effective regional cooperation before transfer and shifting patients who require continuous surveillance but not necessarily intensive care to a transitional ward in a tertiary hospital would provide more ICU beds for more prenatal intensive care for the most complex medical conditions.
Background: Colorectal cancer (CRC) is the fourth most prevalent cancer in the world. However, the molecular mechanism underlying CRC is largely unknown. Objective: To explore the pathogenic mechanism of CRC and to facilitate better diagnosis and treatment of this disease. Methods: Differentially expressed miRNAs (DEMs) and genes (DEGs) in CRC vs. Control samples from the miRNA expression data in GSE115513 and the miRNA and mRNA expression data in TCGA-COAD dataset were screened, followed by the construction of miRNA-mRNA regulatory network. Functional and pathway enrichment analysis, protein-protein interaction (PPI) analysis, and survival analysis were then performed for these DEGs and DEMs. Results: We identified 64 DEMs from GSE115513 dataset and 265 DEMs and 2218 DEGs from TCGA-COAD dataset. miR-27a-3p was a hub DEM with the highest degree in miRNA-mRNA network, while GRIN2B and PCDH10 were hub DEGs targeted by multiple miRNAs, including miR-27a-3p. SNAP25 and GRIN2B were also hub DEGs with the highest degree of interactions in PPI network. These DEMs and DEGs were significantly enriched in multiple KEGG pathways, including proteoglycans expression and cAMP signaling pathway in cancer. Finally, seven DEGs, including FJX1 Dsc2, and hsa-miR-375, were revealed to be correlated with CRC prognosis. Conclusions: Aberrant expression of genes and miRNAs were involved in the pathogenesis of CRC probably by regulating proteoglycans expression and cAMP signaling. miR-27a-3p, PCDH10, GRIN2B, FJX1, Dsc2, and hsa-miR-375 were identified as potential targets for understanding the pathogenic mechanism of CRC. In addition, FJX1, Dsc2 and hsa-miR-375 were identified as potential predictive markers for CRC prognosis.
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