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Background: Anembryonic pregnancy (AP) is the most severe dysmorphogenesis of human embryo development and a frequent presentation of early pregnancy loss (EPL). Studies have analyzed the association between assisted reproductive technologies (ART) and EPL. However, the specific relationship between ART and AP has not been fully elucidated. Several studies suggested that non-genomic anomalies might be related to AP and ART might increase the risk of epigenetic changes, thus possibly detecting some associations between ART and AP. Our study aims to find out any possible risk factors of AP in ART treatments, and translate the results into clinical practice. Methods: A retrospective cohort study was conducted in Nanfang Hospital. Data from 1,765 singleton pregnancies following fresh or frozen-thawed embryo transfer from January 2014 to December 2017 were collated with the inclusion of EPLs and normal live births (NLB). Participants were divided into three groups: NLB (full-term birth with normal body weight infants), EPL (spontaneous pregnancy loss prior to 13 weeks gestation) with embryos (EE), and APs (embryonic pole was invisible in two consecutive ultrasound examinations). The basic characteristics of the patients and the association between ART-related variables and AP were analyzed using one-way analysis of variance (ANOVA) and multivariable logistic regression model, respectively. Products of conception (POC) from AP and EE patients received karyotype analysis using multiplex ligation-dependent probe amplification (MLPA). Results: Blastocyst culture of non-top-quality cleavage stage embryos almost doubled the percentage of AP in EPL (45.9% vs. 24.4%, P=0.037), and the normal euploid rate was significantly higher in the AP group (50.5% vs. 32.3%, P=0.003). Using multivariable logistic regression model, we found that blastocyst transfer and advanced maternal age might be risk factors for AP (OR >1, P<0.05). Deceased ß-HCG level might indicate its occurrence (OR <1, P<0.001) while CoQ10 supplementation might be a protective factor (OR <1, P<0.001). Conclusions: The occurrence of AP may be due to epigenetic abnormalities associated with advanced maternal age and extended in vitro embryo culture, while CoQ10 supplementation may be a potential method in preventing AP. Future multi-center prospective cohort studies should be conducted to verify these results.

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Oxidative stress and mitochondrial dysfunction are hallmarks of heart failure (HF). Coenzyme Q10 (CoQ10) is a vitamin-like organic compound widely expressed in humans as ubiquinol (reduced form) and ubiquinone (oxidized form). CoQ10 plays a key role in electron transport in oxidative phosphorylation of mitochondria. CoQ10 acts as a potent antioxidant, membrane stabilizer and cofactor in the production of adenosine triphosphate by oxidative phosphorylation, inhibiting the oxidation of proteins and DNA. Patients with HF showed CoQ10 deficiency; therefore, a number of clinical trials investigating the effects of CoQ10 supplementation in HF have been conducted. CoQ10 supplementation may confer potential prognostic advantages in HF patients with no adverse hemodynamic profile or safety issues. The latest evidence on the clinical effects of CoQ10 supplementation in HF was reviewed.

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BACKGROUND: The aim of the study was to determine the effects of coenzyme Q10 (CoQ10) supplementation on biomarkers of inflammation and oxidative stress among diabetic hemodialysis (HD) patients. METHODS: Sixty diabetic HD patients participated in the randomized, double blind, placebo-controlled clinical trial. They were randomly assigned into two groups to intake either 60 mg CoQ10 supplements (n = 30) or placebo (n = 30) twice a day for 12 weeks. RESULTS: After 12 weeks of intervention, CoQ10 supplementation significantly increased total antioxidant (TAC) (54.921 ± 26.437 vs. -126.781 ± 26.437, P < 0.001) and nitric oxide (NO) levels (4.121 ± 1.314 vs. -1.427 ± 1.314, P = 0.006) and decreased C-reactive protein (CRP) (-1.302 ± 0.583 vs. 0.345 ± 0.583, 0.042) levels compared with the placebo. We did not observe any significant effect of CoQ10 supplementation on malondialdehyde (MDA) and glutathione (GSH) levels compared with the placebo. CONCLUSIONS: Overall, our study showed that CoQ10 supplementation to diabetic HD patients for 12 weeks was associated with increased levels of TAC and NO levels and decreased level of high-sensitivity CRP (hs-CRP) levels, but did not have any beneficial effects on MDA and GSH.

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PURPOSE: The current study was conducted to determine the effects of coenzyme Q10 (CoQ10) supplementation on glycemic control and markers of lipid profiles risk in diabetic hemodialysis (HD) patients. METHODS: This randomized, double blind, placebo-controlled clinical trial was performed among 60 diabetic HD patients. Subjects were randomly allocated into two groups to take either 120 mg/day of CoQ10 supplements or placebo (n = 30 each group) for 12 weeks. RESULTS: After 12 weeks of intervention, CoQ10 supplementation, compared with the placebo, resulted in a significant decrease in serum insulin concentrations (- 2.5 ± 4.0 vs. + 2.8 ± 5.3 µIU/mL, P < 0.001), homeostasis model of assessment-estimated insulin resistance (- 0.9 ± 2.1 vs. + 1.2 ± 3.0, P = 0.002), and significant increase in the quantitative insulin sensitivity check index (+ 0.009 ± 0.01 vs. - 0.02 ± 0.05, P = 0.003). In addition, a trend toward a greater decrease in serum triglycerides (- 5 ± 53 vs. + 17 ± 44, P = 0.078) and VLDL-cholesterol levels (- 0.9 ± 10 vs. + 3 ± 9, P = 0.078) was observed in the CoQ10 group compared to the placebo group. We did not observe any significant effect of CoQ10 supplementation on fasting glucose, HbA1c and other lipid profiles compared with the placebo. CONCLUSIONS: Overall, our study supported that CoQ10 supplementation to diabetic HD patients for 12 weeks had beneficial effects on markers of insulin metabolism, but did not affect fasting glucose, HbA1c, and lipid profiles. Clinical registration http://www.irct.ir : IRCT2016081811763N30.

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OBJECTIVE: Data on the effects of coenzyme Q10 (CoQ10) supplementation on glucose metabolism, lipid profiles, inflammation, and oxidative stress in subjects with diabetic nephropathy (DN) are scarce. This research was done to determine the effects of CoQ10 supplementation on metabolic status in subjects with DN. METHODS: This randomized double-blind placebo-controlled clinical trial was done in 50 subjects with DN. Participants were randomly assigned into two groups to intake either 100 mg/day CoQ10 supplements (n = 25) or placebo (n = 25) for 12 weeks. Fasting blood samples were obtained at first and after 12-week intervention to quantify metabolic profiles. RESULTS: After 12 weeks of treatment, compared with the placebo, CoQ10 supplementation resulted in significant decreases in serum insulin levels (-3.4 ± 6.8 vs +0.8 ± 6.4 µIU/mL, p = 0.02), homeostasis model of assessment-estimated insulin resistance (-1.0 ± 2.0 vs +0.2 ± 1.8, p = 0.03), homeostasis model of assessment-estimated B cell function (-12.3 ± 26.3 vs +3.5 ± 23.1, p = 0.02) and HbA1c (-1.1 ± 1.0 vs -0.1 ± 0.2%, p < 0.001), and a significant improvement in quantitative insulin sensitivity check index (+0.009 ± 0.01 vs -0.006 ± 0.01, p = 0.01). In addition, CoQ10 supplementation significantly decreased plasma malondialdehyde (MDA) (-0.6 ± 0.5 vs +0.5 ± 1.0 µmol/L, p < 0.001) and advanced glycation end products levels (AGEs) (-316.4 ± 380.9 vs +318.6 ± 732.0 AU, p < 0.001) compared with the placebo. Supplementation with CoQ10had no significant impacts on fasting plasma glucose (FPG), lipid profiles, and matrix metalloproteinase-2 (MMP-2) compared with the placebo. CONCLUSIONS: Taken together, our study demonstrated that CoQ10 supplementation for 12 weeks among DN patients had favorable effects on glucose metabolism, MDA, and AGEs levels, but unchanged FPG, lipid profiles, and MMP-2 concentrations.

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BACKGROUND: It has been reported that higher levels of oxidative stress and inflammation play a key role in the progression of hepatocellular carcinoma (HCC) after surgery. Coenzyme Q10 is an endogenous lipid-soluble antioxidant. To date, no intervention study has investigated coenzyme Q10 supplementation in HCC patients after surgery. The purpose of this study was to investigate oxidative stress, antioxidant enzymes activity, and inflammation levels in HCC patients after surgery following administration of coenzyme Q10 (300 mg/day). METHODS: This study was designed as a single-blinded, randomized, parallel, placebo-controlled study. Patients who were diagnosed with primary HCC (n = 41) and were randomly assign to a placebo (n = 20) or coenzyme Q10 (300 mg/day, n = 21) group after surgery. The intervention lasted for 12 weeks. Plasma coenzyme Q10, vitamin E, oxidative stress antioxidant enzymes activity and inflammatory markers levels were measured. RESULTS: The oxidative stress (p = 0.04) and inflammatory markers (hs-CRP and IL-6, p < 0.01) levels were significantly decreased, and the antioxidant enzymes activity was significantly increased (p < 0.01) after 12 weeks of coenzyme Q10 supplementation. In addition, the coenzyme Q10 level was significantly negatively correlated with the oxidative stress (p = 0.01), and positively correlated with antioxidant enzymes activity (SOD, p = 0.01; CAT, p < 0.05; GPx, p = 0.04) and vitamin E level (p = 0.01) after supplementation. CONCLUSION: In conclusion, we demonstrated that a dose of 300 mg/d of coenzyme Q10 supplementation significantly increased the antioxidant capacity and reduced the oxidative stress and inflammation levels in HCC patients after surgery. TRIAL REGISTRATION: Clinical Trials.gov Identifier: NCT01964001.

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