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Du Z.,Southern Medical University | Du Z.,Key Laboratory for Organ Failure Research | Zeng Q.,Southern Medical University | Zeng Q.,Key Laboratory for Organ Failure Research | And 8 more authors.
Experimental and Clinical Cardiology

Background/Objective: Metabolomics studies have demonstrated that the serum and urine metabolic profiles of patients with chronic heart failure are different from those of patients with normal heart function. However, it is difficult to eliminate irrelevant factors, such as metabolic diseases, diet, activity status and other factors that can affect patient metabolic profiles. Therefore, we used a rat model with coronary artery ligation to mimic the pathogenesis of ischemic heart failure and subsequent chromatography/mass spectroscopy (GC/MS) analysis to determine whether the observed differences in serum metabolic profiles were caused by heart failure. Methods: Fifty-one male SD rats (SPF) were randomized into the sham group and the surgery group. The rat model of chronic ischemic heart failure was prepared by coronary artery ligation. Venous blood from the inferior vena cava was collected after ligation for 4 weeks and the plasma was extracted for serum metabolomics analysis. Results: PCA score plot data revealed significant metabolic differences between the severe heart failure group and the control group, but no significant differences were observed between the slight heart failure group and the control group. A stable and reliable OPLS-DA model was created and used to filter out 44 types of metabolite differences. The levels of free fatty acids, glucose, and lactate were significantly elevated in rats with severe heart failure. Conclusions: The serum metabolic profiles of rats with severe heart failure were markedly different from those of sham rats. A total of 44 metabolites exhibited differences between the severe heart failure and control groups. Source

Xu F.-T.,Gannan Medical University | Li H.-M.,Guangxi Medical University | Yin Q.-S.,Guangzhou General Hospital of PLA | Liu D.-L.,Southern Medical University | And 3 more authors.
Cellular Physiology and Biochemistry

Background: The main complication of autologous free fat tissue transplantation is fat resorption and calcification due to the ischemic necrosis of fat. The promotion of transplant neovascularization soon after autologous free fat grafts may reduce these outcomes. In adulthood, stromal cell-derived factor-1 (SDF-1) and its membrane receptor C-X-C chemokine receptor type 4 (CXCR4) are involved in the homing and migration of multiple stem cell types, neovascularization, and cell proliferation. We hypothesized that CXCR4 may improve the long-term survival of free fat tissue transplants by recruiting endothelial progenitor cells (EPCs) and may therefore improve graft revascularization. In this study, we aimed to determine the effect of human breast adipose-derived stem cells (HBASCs) transfected with the CXCR4 gene on the survival rate of human autologous free fat transplants in nude mice. Methods: Human breast adipose-derived stem cells (HBASCs) were expanded ex vivo for 3 passages, labeled with green fluorescent protein (GFP) and transfected with CXCR4 or left untransfected. Autologous fat tissues were mixed with the GFP-labeled, CXCR4-transfected HBASCs (group A), GFP-labeled HBASCs (group B), the known vascularization-promoting agent VEGF (group C), or medium (group D) and then injected subcutaneously into 32 nude mice at 4 spots in a random fashion. Six months later, the transplanted tissue volume and histology were evaluated, and neo-vascularization was quantified by counting the capillaries. CXCR4 and SDF-1α mRNA expression in the transplants was determined using real-time quantitative PCR analysis (qPCR). Results: The data revealed that the control (group D) transplant volume survival was 28.3 ± 4.5%. Mixing CXCR4-transfected (group A) and untransfected (group B) HBASCs significantly increased transplant volume survival (79.5 ± 8.3% and 67.2 ± 5.9%, respectively), whereas VEGF-transfected HBASCs (group C) were less effective (41.2 ± 5.1%). Histological analysis revealed that both types of HBASCs-treated transplants consisted predominantly of adipose tissue, unlike the control transplants, and also presented significantly less fat necrosis and fibrosis. The CXCR4-transfected HBASCs-treated transplants had a significantly higher capillary density than did the other transplants and showed GFP and CD31 double-positive cells (i.e., ASCs-derived endothelial cells). The mRNA expression of CXCR4 and SDF-1α was much higher in the CXCR4-transfected HBASCs transplants than in the other three transplants. Conclusions: Our data demonstrated that HBASCs can enhance the survival and quality of transplanted free fat tissues. Moreover, CXCR4 transfection of these HBASCs could augment this effect. Stimulation of angiogenesis and decreased fat cell apoptosis due to the recruitment of endothelial progenitor cells (EPCs) and an increase in graft revascularization are potential mechanisms underlying the improved long-term survival of free fat transplants following CXCR4-transfected HBASCs treatment. © 2015 S. Karger AG, Basel. Source

Xu F.-T.,Gannan Medical University | Li H.-M.,Guangxi Medical University | Yin Q.-S.,Guangzhou General Hospital of PLA | Liang Z.-J.,Guangxi Medical University | And 5 more authors.
American Journal of Translational Research

To investigate whether activated autologous platelet-rich plasma (PRP) can promote proliferation and osteogenic differentiation of human adipose-derived stem cells (hASCs) in vitro. hASCs were isolated from lipo-aspirates, and characterized by specific cell markers and multilineage differentiation capacity after culturing to the 3 rd passage. PRP was collected and activated from human peripheral blood of the same patient. Cultured hASCs were treated with normal osteogenic inductive media alone (group A, control) or osteogenic inductive media plus 5%, 10%, 20%, 40%PRP (group B, C, D, E, respectively). Cell proliferation was assessed by CCK-8 assay. mRNA expression of osteogenic marker genes including alkaline phosphatase (ALP), osteopontin (OPN), osteocalcin (OCN) and core binding factor alpha 1 (Cbfa1) were determined by Real-Time Quantitative PCR Analysis (qPCR). Data revealed that different concentrations of activated autologous PRP significantly promoted hASCs growth in the proliferation phase compared to the without PRP group and resulted in a dose-response relationship. At 7-d and 14-d time point of the osteogenic induced stage, ALP activity in PRP groups gradually increased with the increasing of concentrations of PRP and showed that dose-response relationship. At 21-d time point of the osteogenic induced stage, PRP groups make much more mineralization and mRNA relative expression of ALP, OPN, OCN and Cbfa1 than that without PRP groups and show that dose-response relationship. This study indicated that different concentrations of activated autologous PRP can promote cell proliferation at earlier stage and promote osteogenic differentiation at later stage of hASCs in vitro. Moreover, it displayed a dose-dependent effect of activated autologous PRP on cell proliferation and osteogenic differentiation of hASCs in vitro. © 2015, E-Century Publishing Corporation. All right reserved. Source

Chen L.,Chinese PLA General Hospital | Li L.,Guangzhou General Hospital of PLA | Wang Y.,Fuzhou General Hospital of Nanjing Command | Li P.,Chinese PLA General Hospital | And 4 more authors.
Cancer Causes and Control

Purpose: C-peptide, a hormone secreted by the pancreas, is a marker for insulin production and hyperinsulinemia. Epidemiological studies have suggested an association between circulating C-peptide level and colorectal neoplasia risk; however, the results were not always consistent. Herein, we conducted a systematic review and meta-analysis study to evaluate the association between circulating C-peptide level and the colorectal neoplasia risk. Methods: The PubMed database was searched for the eligibility studies updated to May 2013, which prospectively evaluated the association between circulating C-peptide level and colorectal neoplasia risk. The summary estimates and 95 % confidential intervals (95 % CIs) for those with the highest quantile C-peptide level in contrast to the lowest quantile were estimated with the random-effects model. Heterogeneity between the studies was assessed with the Q test and the I 2 statistic. Potential publication bias was evaluated with the Egger's test. Results: We identified 9 nested case-control studies that have recruited a total of 3,109 cases and 4,285 controls met the criteria. From the meta-analysis, we found that subjects with high circulating C-peptide were associated with a 37 % increased colorectal neoplasia risk [pooled odds ratios (OR) 1.37, 95 % CI 1.09-1.72] under the random-effects model. In the stratification studies, we found the association was more prominent in the men (pooled OR 2.34, 95 % CI 1.36-4.04) compared to women (pooled OR 1.41, 95 % CI 0.89-2.25). Significant association between circulating C-peptide level and colon cancer risk was found (pooled OR 1.72, 95 % CI 1.26-2.36), but not for rectal cancer (pooled OR 1.14, 95 % CI 0.75-1.73). No significant publication bias was found for any meta-analysis study. Conclusion: In conclusion, the results of the meta-analysis studies suggested that higher circulating C-peptide could be a predictive factor for higher colorectal neoplasia susceptibility. © 2013 Springer Science+Business Media Dordrecht. Source

Du Z.,Southern Medical University | Du Z.,Key Laboratory for Organ Failure Research | Shen A.,Southern Medical University | Huang Y.,Southern Medical University | And 15 more authors.

Objective: Elevated myocardial energy expenditure (MEE) is related with reduced left ventricular ejection fraction, and has also been documented as an independent predictor of cardiovascular mortality. However, the serum small-molecule metabolite profiles and pathophysiological mechanisms of elevated MEE in heart failure (HF) are still lacking. Herein, we used 1H-NMR-based metabolomics analysis to screen for potential biomarkers of MEE in HF. Methods: A total of 61 subjects were enrolled, including 46 patients with heart failure and 15 age-matched controls. Venous serum samples were collected from subjects after an 8-hour fast. An INOVA 600 MHz nuclear magnetic resonance spectrometer with Carr-Purcell-Melboom-Gill (CPMG) pulse sequence was employed for the metabolomics analysis and MEE was calculated using colored Doppler echocardiography. Metabolomics data were processed using orthogonal signal correction and regression analysis was performed using the partial least squares method. Results: The mean MEE levels of HF patients and controls were 139.61±58.18 cal/min and 61.09±23.54 cal/min, respectively. Serum metabolomics varied with MEE changed, and 3-hydroxybutyrate, acetone and succinate were significantly elevated with the increasing MEE. Importantly, these three metabolites were independent of administration of angiotensin converting enzyme inhibitor, β-receptor blockers, diuretics and statins (P>0.05). Conclusions: These results suggested that in patients with heart failure, MEE elevation was associated with significant changes in serum metabolomics profiles, especially the concentration of 3-hydroxybutyrate, acetone and succinate. These compounds could be used as potential serum biomarkers to study myocardial energy mechanism in HF patients. © 2014 Du et al. Source

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