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Background/Aims: Ovarian cancer (OC) is a malignant neoplasm of the female reproductive system with a high mortality rate. Identifying useful biomarkers and clarifying the molecular pathogenesis of OC are critical for early diagnosis and treatment. The aim of the study was to identify candidate biomarkers and explore metabolic changes of OC. Methods: A two-stage design was used in our study, with a discovery cohort of OC cases (n = 30) and controls (n = 30) and an independent cohort of cases (n = 17) and controls (n = 18) for validation. The serum metabolic profiling was investigated by ultra-performance liquid chromatography and quadrupole time-of-fight mass spectrometry with positive electrospray ionization. Results: A total of 18 metabolites closely related to OC were identified in the discovery stage, of which 12 were confirmed in the validation cohort. Metabolic pathways in OC related to these biomarkers included fatty acid β-oxidation, phospholipid metabolism, and bile acid metabolism, which are closely related to the proliferation, invasion, and metastasis of cancer cells. Multiple logistic regression analysis of these metabolites showed that 2-piperidinone and 1-heptadecanoylglycerophosphoethanolamine were potential biomarkers of OC, with high sensitivity (96.7%), specificity (66.7%), and area under the receiver operating characteristic curve value (0.894). Conclusion: These findings provide insight into the pathogenesis pathogenesis of OC and may be useful for clinical diagnosis and treatment.

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Therapeutic hypercapnia has the potential for neuroprotection after global cerebral ischemia. Here we further investigated the effects of different degrees of acute systemic hypoxia in combination with hypercapnia on brain damage in a rat model of hypoxia and ischemia. Adult wistar rats underwent unilateral common carotid artery (CCA) ligation for 60 min followed by ventilation with normoxic or systemic hypoxic gas containing 11%O2,13%O2,15%O2 and 18%O2 (targeted to PaO2 30–39 mmHg, 40–49 mmHg, 50–59 mmHg, and 60–69 mmHg, respectively) or systemic hypoxic gas containing 8% carbon dioxide (targeted to PaCO2 60–80 mmHg) for 180 min. The mean artery pressure (MAP), blood gas, and cerebral blood flow (CBF) were evaluated. The cortical vascular permeability and brain edema were examined. The ipsilateral cortex damage and the percentage of hippocampal apoptotic neurons were evaluated by Nissl staining and terminal deoxynucleotidyl transferase-mediated 2′-deoxyuridine 5′-triphosphate-biotin nick end labeling (TUNEL) assay as well as flow cytometry, respectively. Immunofluorescence and western blotting were performed to determine aquaporin-4 (AQP4) expression. In rats treated with severe hypoxia (PaO2 < 50 mmHg), hypercapnia augmented the decline of MAP with cortical CBF and damaged blood–brain barrier permeability (p < 0.05). In contrast, in rats treated with mild to moderate hypoxia (PaO2 > 50 mmHg), hypercapnia protected against these pathophysiological changes. Moreover, hypercapnia treatment significantly reduced brain damage in the ischemic ipsilateral cortex and decreased the percentage of apoptotic neurons in the hippocampus after the CCA ligated rats were exposed to mild or moderate hypoxemia (PaO2 > 50 mmHg); especially under mild hypoxemia (PaO2 > 60 mmHg), hypercapnia significantly attenuated the expression of AQP4 protein with brain edema (p < 0.05). Hypercapnia exerts beneficial effects under mild to moderate hypoxemia and augments detrimental effects under severe hypoxemia on brain damage in a rat model of hypoxia-ischemia.

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