Maanshan Municipal Peoples Hospital
Maanshan Municipal Peoples Hospital
Wang Y.,Maanshan Municipal Peoples Hospital |
Li Y.,Shanghai Institute of Technology |
Chen Z.,Maanshan Municipal Peoples Hospital |
Wang T.,Sun Yat Sen University |
And 5 more authors.
Clinical Laboratory | Year: 2017
Background: DESMIN is a novel prognostic predictor and therapeutic target for colorectal cancer (CRC). En- zyme-linked immunosorbent assay (ELISA) and electrochemiluminescence (ELC) assays are large-scale and high- cost projects; therefore, it is necessary to develop a new, fast, and simple yet highly sensitive and specific method to detect DESMIN in serum. Semiconducting quantum dots (QDs) possess high fluorescence quantum yield, stability against photobleaching, and size-controlled luminescence properties, thus being utilized in photoeleetro- chemical tumor marker detection, especially in ameliorating the diagnostic value in complex biological ambient ionization. However, CdTe/CdS quantum dots (QDs) have not been applied in detecting DESMIN in serum. Methods: DESMIN in serum has been established using anti-DESMIN-conjugated CdTe/CdS quantum dots (QDs) and measurements. The assay sensitivity was determined by measurement of quenched fluorescence intensity of DESMIN at 0.1, 0.5, 1.0, 2.0, or 5.0 ng/mL in PBS or 0.25%, 0.5%, 1.0%, 2.0%, or 5% human serum diluted in PBS. The assay was optimized under different pH (7.00 - 7.40) for different reaction durations (10-60 minutes). The specificity of anti-DESMIN-QDs was determined by testing the interference of DESMIN activity with CEA, IgG, or AFP, each at I ng/mL. Results: Under the optimized incubation time (30 minutes) at room temperature and optimal pH 7.1 - 7.2, a correlation between the decreased fluorescence intensity of anti-DESMIN-conjugated CdTe/CdS QDs and the concentration of DESMIN in the range from 0.05 to 100 ng/mL, was established. The sensitivity for the detection of DESMIN in the range from 0.05 to 100 ng/mL, with a detection limit of 0.02 ng/mL. The assay presented a high specificity because the anti-DESMIN-conjugated CdTe/CdS QDs only reacted with ABR1B10 in the sera in the presence of CEA, IgG or AFP. Conclusions: The immunofluorescence assay to detect DESMIN in serum using anti-DEMSIN-conjugated CdTe/ CdS QDs was fast and simple yet presented high sensitivity and specificity. Our method provides a promising tool for early prediction of CRC risk.
Lu M.-Y.,Guilin Medical University |
Ren Y.,The 303rd Hospital of PLA |
Hu W.-Q.,Maanshan Municipal Peoples Hospital |
Gui Y.,Guilin Medical University |
Zhang L.-C.,The 303rd Hospital of PLA
Chinese Journal of Tissue Engineering Research | Year: 2014
BACKGROUND: The auditory ossicle chain reconstruction is still an important method to treat conductive deafness. Although a great variety of materials have been applied, the blood supply of otosteon after the implantation is ignored. Moreover, there is no real bone formed. OBJECTIVE: To observe the angiogenesis of vascular endothelial growth factor and collagen I modified β-tricalcium phosphate porous scaffold which is implanted into the otocyst of guinea pig. METHODS: Totally 60 guinea pigs were randomly divided into experimental group (vascular endothelial growth factor and collagen I modified β-tricalcium phosphate porous scaffold), collagen I control group (collagen I modified β-tricalcium phosphate porous scaffold) and blank control group (β-tricalcium phosphate porous scaffold). The guinea pigs were executed under anesthesia at weeks 1, 2, 3, 4 respectively. The surface of scaffolds was observed by scanning electron microscopy. The angiogenesis of scaffolds were observed by hematoxylin-eosin staining and CD34 immunohistochemistry staining, and then the microvascular density was counted. The osteogenesis of the scaffolds was observed by toluidine blue staining. RESULTS AND CONCLUSION: Endothelial cell proliferation and lumen formation could be observed after 1 week in the experimental group, and the angiogenesis reach the peak after 3 weeks with traffic branches formedbetween micropores. In the other two groups, the lumen formed at 2 weeks but no traffic branches were visible. The sprouting of new blood vessels in the pores were observed more in the experimental group than the other two groups (P < 0.05). The adherence and proliferation of cells could be examined in the surface and pores of the scaffold by scanning electron microscope. After 4 weeks, the osteogenesis could be observed by toluidine blue staining, especially in the experimental group. These findings suggest that the vascular endothelial growth factor and collagen I modified β-tricalcium phosphate porous scaffold can realize an effective vascularization in the environment of guinea pigs' middle ear. What's more, the scaffold also can promote bone formation.
Chang L.,Nanjing Southeast University |
Wu P.,Jiangsu Jiankang Vocational College |
Senthilkumar R.,Nanjing Southeast University |
Tian X.,Nanjing Southeast University |
And 4 more authors.
Journal of Cancer Research and Clinical Oncology | Year: 2016
Purpose: Altered cellular metabolism has received increased attention as an important hallmark of cancer. Activation of FASN has been found to be involved in many human tumors. Despite extensive research in FASN function on cancer, the underlying mechanism is not entirely understood yet. Methods: Cerulenin was used to suppress the FASN expression in human colorectal cancer cell lines (HT29 and LoVo). Expression of PI3K, Akt, p-Akt, mTOR, p-mTOR, FASN, and AZGP1 was measured using western blotting and qPCR. ATP and lactic acid were assessed to investigate the activation of energy metabolism. Cell cytotoxicity assay was studied by cell counting kit-8 assay. The capacity of cell proliferation and migration was investigated by clonogenic and invasion assay. Analysis of apoptosis and the cell cycle was detected by flow cytometry. Results: We found that the expression of FASN was down-regulated, while the expression of PI3K, p-Akt, p-mTOR, and AZGP1 was down-regulated in HT29 and LoVo cells treated with FASN inhibitor. Proliferation was reduced in FASN inhibitor-treated cells, which is consistent with an increased apoptosis rate. Furthermore, the migration of FASN inhibitor-treated cells was decreased and the content of ATP and lactic acid was also dropped. Conclusion: These findings suggest that inhibited FASN suppresses the malignant phenotype of colorectal cancer cells by down-regulating energy metabolism and mTOR signaling pathway. The results have paved the way to understand the relations of FASN, mTOR signaling pathway, and energy metabolism in colorectal cancer cells. © 2015, Springer-Verlag Berlin Heidelberg.
PubMed | Maanshan Municipal Peoples Hospital, Jiangsu Jiankang Vocational College and Nanjing Southeast University
Type: Journal Article | Journal: Journal of cancer research and clinical oncology | Year: 2016
Altered cellular metabolism has received increased attention as an important hallmark of cancer. Activation of FASN has been found to be involved in many human tumors. Despite extensive research in FASN function on cancer, the underlying mechanism is not entirely understood yet.Cerulenin was used to suppress the FASN expression in human colorectal cancer cell lines (HT29 and LoVo). Expression of PI3K, Akt, p-Akt, mTOR, p-mTOR, FASN, and AZGP1 was measured using western blotting and qPCR. ATP and lactic acid were assessed to investigate the activation of energy metabolism. Cell cytotoxicity assay was studied by cell counting kit-8 assay. The capacity of cell proliferation and migration was investigated by clonogenic and invasion assay. Analysis of apoptosis and the cell cycle was detected by flow cytometry.We found that the expression of FASN was down-regulated, while the expression of PI3K, p-Akt, p-mTOR, and AZGP1 was down-regulated in HT29 and LoVo cells treated with FASN inhibitor. Proliferation was reduced in FASN inhibitor-treated cells, which is consistent with an increased apoptosis rate. Furthermore, the migration of FASN inhibitor-treated cells was decreased and the content of ATP and lactic acid was also dropped.These findings suggest that inhibited FASN suppresses the malignant phenotype of colorectal cancer cells by down-regulating energy metabolism and mTOR signaling pathway. The results have paved the way to understand the relations of FASN, mTOR signaling pathway, and energy metabolism in colorectal cancer cells.
Shi R.,Nanjing University |
Shi R.,Maanshan Municipal Peoples Hospital |
Yuan K.,Southern Medical University |
Hu B.,Maanshan Municipal Peoples Hospital |
And 12 more authors.
Oxidative Medicine and Cellular Longevity | Year: 2016
Diabetes mellitus (DM) substantially increases the risk of ischemic stroke and reduces the tolerance to ischemic insults. Tissue kallikrein (TK) has been demonstrated to protect neurons from ischemia/reperfusion (I/R) injury in orthoglycemic model by activating the bradykinin B2 receptor (B2R). Considering the differential effects of B2R or bradykinin B1 receptor (B1R) on cardioprotection and neuroprotection in I/R with or without diabetes, this study was designed to investigate the role of TK during cerebral I/R injury in streptozotocin-induced diabetic rats. Intravenous injection of TK inhibited apoptosis in neurons, alleviated edema and inflammatory reactions after focal cerebral I/R, significantly reduced the infarct volume, and improved functional recovery. These beneficial effects were accompanied by activation of the extracellular signal-regulated kinase 1/2 (ERK1/2), cAMP response element-binding (CREB), and Bcl-2 signal proteins. Inhibition of the B2R or ERK1/2 pathway abated the effects of TK, whereas an antagonist of B1R enhanced the effects. These findings reveal that the neuroprotective effect of TK against cerebral I/R injury in streptozotocin-induced diabetic rats mainly involves the enhancement of B2R and ERK1/2-CREB-Bcl-2 signaling pathway activity. © 2016 Ruifeng Shi et al.
Wu H.,Nanjing Medical University |
Wu H.,Maanshan Municipal Peoples Hospital |
Han Z.-L.,Nanjing Medical University |
Cao Y.-S.,Nanjing Medical University |
And 3 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2014
Objective: The Ras homolog enriched in brain gene (Rheb) is a center player within the insulin/Rheb/Mammalian Target of Rapamycin (mTOR) pathway, and plays a critical role in regulating cellular growth. Rheb-/- embryos have been reported to die around midgestation, due to the defects of the development of the cardiovascular system. Recent studies from ours and another group consistently showed that Rheb1 was indispensable for the cardiac hypertrophic growth after early postnatal period. Besides that, we also found that Rheb1 a-MHC-Cre (cKO) mice exhibited ventricular tachycardia. However, the precise mechanism by which Rheb1 knockout causes ventricular arrhythmia in these mice is still unclear. Methods: Mouse cardiomyocytes were isolated using 10 days suckling Rheb1 cKO and wide type mice using Collagenase Type II. Sodium currents and L-type calcium currents were recorded using the whole-cell patch clamping technique. Results: The sodium current density of ventricular cardiomyocytes from Rheb1 cKO mice was decreased by about 60%. Significant left shift but no slope altered was observed in activation curve with V1/2 values of -35.35 ± 1.12 mV for Rheb1 cKO group and -40.72 ± 1.18 mV for the controls. In addition, the area of window current, which refers the overlap of normalized activation and inactivation, was larger in Rheb1 cKO mice. Moreover, the sodium current, in general, was recovered much slower in Rheb1 cKO mice than that of the controls. However, L-type calcium currents were preserved in Rheb1 cKO mice. Conclusion: Sodium currents are decreased in Rheb1 cKO mice, which might be responsible for the phenotype of arrhythima in Rheb1 cKO mice. Understanding the molecular composition of sodium ion channel complexes in the heart of these Rheb1 cKO mice will be critical to develop innovative and effective therapies for the treatment of cardiac arrhythmia.
Yin Z.,Nanjing Medical University |
Yang X.,Nanjing Medical University |
Jiang Y.,Nanjing Medical University |
Xing L.,Maanshan Municipal Peoples Hospital |
And 5 more authors.
Journal of Biomaterials Applications | Year: 2014
Objective: The purpose of this study was to determine whether the platelet-rich plasma-agarose gel scaffold could be a bioactive scaffold capable of growth factors release for cartilage repair. Methods: Porcine chondrocytes were seeded in agarose gel and platelet-rich plasma-agarose gel. During the 28-days culture, microstructure of hydrogels and morphologies of chondrocytes seeded in the hydrogels were observed using scanning electron microscope; viability of chondrocytes in gels was examined by live/dead assay; qualitative and quantitative analysis of glycosaminoglycan, collagen and DNA were assessed by histological, immunohistochemcial staining and biochemical assay; gene expression was measured by real-time polymerase chain reaction. In vitro cartilage ring models were used to evaluate the integration of the scaffolds, and the integration strength was analyzed by mechanical push-out tests. Results: Scanning electron microscope revealed both scaffolds had highly uniform porous structure. Live/dead scaffolds showed 100% cells alive in both groups. After 28-days culture, glycosaminoglycan, collagen, DNA content and chondrocyte- related genes expression in platelet-rich plasma-agarose gel were significantly higher than pure agarose gel. Integration strength in platelet-rich plasma-agarose gel was also higher compared to pure agarose gel. Conclusion: Platelet-rich plasma showed a positive effect on chondrocytes proliferation, differentiation and integration between native cartilage and engineered tissue when combined with agarose gel. Our findings suggest that platelet-rich plasma-agarose gel scaffold is a promising bioactive scaffold for future cartilage tissue engineering and future clinical works.© 2013 The Author(s).
Wei Z.,Anhui University of Technology |
Yu X.,Anhui University of Technology |
Xu X.,Anhui University of Technology |
Chen X.,Maanshan Municipal Peoples Hospital
Computer Methods and Programs in Biomedicine | Year: 2014
In this paper, a new method involving an experiment in vivo and hydro-mechanical coupling simulations was proposed to investigate the biomechanical property of human periodontal ligament (PDL). Teeth were loaded and their displacements were measured in vivo. The finite element model of the experiment was built and hydro-mechanical coupling simulations were conducted to test some PDL's constitutive models. In the simulations, the linear elastic model, the hyperfoam model, and the Ogden model were assumed for the solid phase of the PDL coupled with a model of the fluid phase of the PDL. The displacements of the teeth derived from the simulations were compared with the experimental data to validate these constitutive models. The study shows that a proposed constitutive model of the PDL can be reliably tested by this method. Furthermore, the influence of species, areas, and the fluid volume ratio on PDL's mechanical property should be considered in the modeling and simulation of the mechanical property of the PDL. © 2013 Elsevier Ireland Ltd.
Wang X.-Z.,Nanjing Medical University |
Yang Z.-J.,Nanjing Medical University |
Wang Y.-S.,Maanshan Municipal Peoples Hospital |
Zhang P.,Maanshan Municipal Peoples Hospital |
And 2 more authors.
Acta Academiae Medicinae Sinicae | Year: 2011
Objective: To evaluate the role of intracoronary electrocardiogram (IcECG) in examining early myocardial injury during percutaneous coronary intervention (PCI). Methods: Eight-six patients who had undergone elective PCI for their coronary heart disease were enrolled in the study. The IcECG both at baseline and after procedure were recorded with an incoronary guidewire and the serum levels of cardiac troponin T (cTnT) and creatine kinase-myoglobin were measured at baseline and 8 and 24 hours after intervention. Myocardial damage was defined as serum levels of cTnT increase above the upper normal value after intervention. Cardiac events after intervention was followed up. Results: Of all these 86 patients with normal serum levels of cardiac markers before the procedure, significant shift at ST-segment in IcECG during PCI was observed in 30 patients (35%, abnormal group) and no shift in the remaining 56 patients (65%, control group). All the procedures were successful. Serum levels of cTnT and creatine kinase-myoglobin were significantly higher in abnormal group than in control group after intervention (P < 0.01). The intracoronary ST-segment shift had a sensitivity of 77% and a specificity of 94% in predicting myocardial injury, with positive and negative predictive values of 90% and 86%, respectively. More cardiac events were observed in abnormal group than those in control group at a 4-week follow-up after intervention (P < 0.05) and major coronary event-free survival was significantly lower in those with post-procedural ST-segment shift in the IcECG (P < 0.05). Conclusion: IcECG may be a useful method for predicting myocardial injuries during PCI.
Zhao H.-L.,Maanshan Municipal Peoples Hospital |
Tao G.-C.,Maanshan Municipal Peoples Hospital |
Fei X.-Q.,Maanshan Municipal Peoples Hospital
International Journal of Ophthalmology | Year: 2012
AIM: To detect the incidence and mechanism of high intraocular pressure (IOP) at the early stage after small incision non-phacoemulsification cataract surgery. METHODS: Totally 116 patients (116 eyes) who had undergone small incision non-phacoemulsification cataract surgery in our hospital in the first half of 2011 were retrospectively analysed. RESULTS: Among the 116 eyes, postoperative IOP elevation occurred in 35 eyes (about 30.2%). The IOP reached the peak mostly 6 to 24 hours after the surgery, up to 56mmHg (1mmHg=0.133kPa). 88.6% of high IOP occurred at the same time. And in this period the incidence of IOP elevation were significantly higher than in other periods (P<0.01). 62.9% of high IOP rose slightly, less than 30mmHg. CONCLUSION: The incidence of higy IOP at the early stage after small incision non-phacoemulsification cataract surgery is high, but most of the IOP rose slightly. The most common reason is that some substances blocked the trabecular meshwork. These substances were residual viscoelastic agent, residual cortex, denatured red blood cells, macrophages and pigment particle. These substances blocked the trabecular meshwork, and aqueous humor outflow was obstructed, and then the IOP rose. Other reasons also included IOL subluxation, endophthalmitis, etc.