Liu Z.,Boston University |
Liu Z.,Second Peoples Hospital of Shenzhen |
Zhu H.,Boston University |
Fang G.G.,Boston University |
And 6 more authors.
Journal of Alzheimer's Disease | Year: 2012
Sporadic Alzheimer's disease (AD) patients have low amyloid-β peptide (Aβ) clearance in the central nervous system. The peripheral Aβ clearance may also be important but its role in AD remains unclear. We aimed to study the Aβ degrading proteases including insulin degrading enzyme (IDE), angiotensin converting enzyme (ACE) and others in blood. Using the fluorogenic substrate V (a substrate of IDE and other metalloproteases), we showed that human serum degraded the substrate V, and the activity was inhibited by adding increasing dose of Aβ. The existence of IDE activity was demonstrated by the inhibition of insulin, amylin, or EDTA, and further confirmed by immunocapture of IDE using monoclonal antibodies. The involvement of ACE was indicated by the ability of the ACE inhibitor, lisinopril, to inhibit the substrate V degradation. To test the variations of substrate V degradation in humans, we used serum samples from a homebound elderly population with cognitive diagnoses. Compared with the elderly who had normal cognition, those with probable AD and amnestic mild cognitive impairment (amnestic MCI) had lower peptidase activities. Probable AD or amnestic MCI as an outcome remained negatively associated with serum substrate V degradation activity after adjusting for the confounders. The elderly with probable AD had lower serum substrate V degradation activity compared with those who had vascular dementia. The blood proteases mediating Aβ degradation may be important for the AD pathogenesis. More studies are needed to specify each Aβ degrading protease in blood as a useful biomarker and a possible treatment target for AD. © 2012-IOS Press and the authors. All rights reserved.
Huang X.-J.,Shanghai JiaoTong University |
Huang X.-J.,Second Peoples Hospital of Shenzhen |
Li W.-P.,Second Peoples Hospital of Shenzhen |
Lin Y.,Shanghai JiaoTong University |
And 4 more authors.
Journal of Neurotrauma | Year: 2014
Excessive active voltage-gated sodium channels are responsible for the cellular abnormalities associated with secondary brain injury following traumatic brain injury (TBI). We previously presented evidence that significant upregulation of Nav1.3 expression occurs in the rat cortex at 2 h and 12 h post-TBI and is correlated with TBI severity. In our current study, we tested the hypothesis that blocking upregulation of Nav1.3 expression in vivo in the acute stage post-TBI attenuates the secondary brain injury associated with TBI. We administered either antisense oligodeoxynucleotides (ODN) targeting Nav1.3 or artificial cerebrospinal fluid (aCSF) at 2 h, 4 h, 6 h, and 8 h following TBI. Control sham animals received aCSF administration at the same time points. At 12 h post-TBI, Nav1.3 messenger ribonucleic acid (mRNA) levels in bilateral hippocampi of the aCSF group were significantly elevated, compared with the sham and ODN groups (p<0.01). However, the Nav1.3 mRNA levels in the uninjured contralateral hippocampus of the ODN group were significantly lowered, compared with the sham group (p<0.01). Treatment with antisense ODN significantly decreased the number of degenerating neurons in the ipsilateral hippocampal CA3 and hilar region (p<0.01). A set of left-to-right ratio value analyzed by magnetic resonance imaging T2 image on one day, three days, and seven days post-TBI showed marked edema in the ipsilateral hemisphere of the aCSF group, compared with that of the ODN group (p<0.05). The Morris water maze memory retention test showed that both the aCSF and ODN groups took longer to find a hidden platform, compared with the sham group (p<0.01). However, latency in the aCSF group was significantly higher than in the ODN group (p<0.05). Our in vivo Nav1.3 inhibition studies suggest that therapeutic strategies to block upregulation of Nav1.3 expression in the brain may improve outcomes following TBI. © Copyright 2014, Mary Ann Liebert, Inc. 2014.
Liu L.-X.,Second Peoples Hospital of Shenzhen |
Lin C.,Jinjue Dental Institute of Jiamusi
Chinese Journal of Tissue Engineering Research | Year: 2014
BACKGROUND: Children teeth filled with glass ionomer cement are still susceptible with secondary caries, which is in close relationship with complex microbial community in dental plaque on the surface of glass ionomer cement. Traditional microbial methods are incapable of getting important information towards dental plaque microbes. OBJECTIVE: To analyze microbial community structure and numerical level of caries-induced microbes in dental plaque on the surface of glass ionomer cement for different caries-susceptible children. METHODS: Twenty-four children (age: 3-5 years) were divided into the caries-free, caries-positive, and caries-active children groups by the decayed, missing and filled index. With eight individuals in each group, their dental plaques were sampled for microbial community analysis. Denaturing gradient gel electrophoresis was employed to make clear the microbial community diversity and species identity in dental plaque of the caries-free, caries-positive, and caries-active children groups. Fluorescent in situ hybridization was used to investigate the numerical level of the caries-induced microbe Streptococcus spp. Quantitative PCR was carried out to analyze relative quantity of Streptococcus mutans in total bacteria. RESULTS AND CONCLUSION: Compared with the caries-positive and caries-active children groups, microbial community diversity among samples was significantly higher in the caries-free group. Microbes abound in the caries-positive and caries-active groups might act important roles in the development of caries. Streptococcus spp. and Actinomyces spp. might be important caries-induced microbes in the caries-active group. The ratios of Streptococcus spp. and Streptococcus mutans in total bacteria were significantly higher in the caries-free group than those in the caries-free and caries-positive groups. In summary, molecular ecology technologies can well reflect caries-related complex microbial community in dental plaque.
Zhang Y.,Sun Yat Sen University |
Zhang Y.,Southern Medical University |
Huang H.,Sun Yat Sen University |
Zhou H.,Sun Yat Sen University |
And 8 more authors.
Cancer | Year: 2014
BACKGROUND: Nuclear factor jB (NFκB) signaling is strongly associated with tumor progression, and studies have shown that SHANK-associated RH domain interacting protein (SHARPIN) is crucial for NFκB pathway activation. However, the expression and functions of SHARPIN in prostate cancer (PCa) have not yet been defined.METHODS: The expression of SHARPIN in PCa cell lines and tissues was evaluated with western blotting, quantitative real-time polymerase chain reaction, and immunohistochemistry. After SHARPIN was silenced in the PCa cell lines, western blots were used to confirm that SHARPIN physically associated with components of the NFκB pathway and the downstream targets (survivin and livin). The functions of SHARPIN in cell proliferation, migration, and invasion in vitro were measured with 5-(3-carboxymethoxyphenyl)-2-(4,5-dimenthylthiazoly)-3-(4-sulfophenyl)tetrazolium, inner salt (MTS), Transwell, and invasion assays, respectively. Flow cytometry was employed to evaluate cell apoptosis. Furthermore, tumorigenesis in vivo was examined with tumorigenicity assays.RESULTS: SHARPIN expression was upregulated in PCa cell lines and tissues. The knockdown of SHARPIN or incubation with Bay 11-7082 (an NFκB inhibitor) led to dramatically decreased levels of phosphorylated IjBa and phosphorylated p65 in comparison with the control group. Downregulation of survivin and livin due to SHARPIN inhibition was attributable to transcriptional repression (P<.05). Decreases in cell viability, migration, invasion, and survival with a higher sensitivity to docetaxel in vitro and with repressed tumorigenesis in vivo were observed upon SHARPIN silencing, and this was consistent with the results from inhibition of the NFκB pathway and its downstream targets.CONCLUSION: The current study demonstrates that overexpression of SHARPIN promotes activation of the NFκB pathway and downstream targets survivin and livin, which potentially contributes to PCa development. © 2014 American Cancer Society.
Wang C.,University of Jinan |
Fang M.,Guangzhou University |
Zhang M.,Second Peoples Hospital of Shenzhen |
Li W.,Second Peoples Hospital of Shenzhen |
And 4 more authors.
Neuropathology | Year: 2013
The relationship between DJ-1 and β-catenin, and its impact on the prognosis for glioma patients has not been fully understood. This study determined the effect of DJ-1 on β-catenin and the prognostic significance of this interaction in glioma patients. We collected tumor specimens from 88 glioma patients and determined the expression of DJ-1, β-catenin and PTEN by using immunohistochemical staining. The involvement of DJ-1 and β-catenin in glioma cell lines was evaluated by immunohistochemistry and Western blotting. High DJ-1 expression (37.5%) and high β-catenin expression (34.1%) in glioma specimens were significantly associated with high grade and poor prognosis in glioma patients. However, only high levels of DJ-1 (P=0.014) was a strong independent prognostic factor, correlated with a reduced overall survival time. In vitroDJ-1 expression was positively correlated with the expression levels of β-catenin and p-Akt, and negatively correlated with PTEN expression in U87, U251 MG, SWO-38 and SHG44 human glioma cell lines. After the knockdown of DJ-1, Akt, p-Akt or β-catenin expression levels were not affected in the PTEN-null cell lines (U87 and U251 MG). However, in the SWO-38 cell line, which has wild-type PTEN protein, the level of PTEN increased while Akt/p-Akt and β-catenin levels were reduced. Furthermore, β-catenin staining weakened in SWO-38 cells after DJ-1 levels decreased according to immunocytochemical analysis. In conclusion, DJ-1 and β-catenin may contribute to the development and recurrence of glioma and are valuable prognostic factors for glioma patients. DJ-1 may regulate β-catenin expression via PTEN and p-Akt. © 2013 Japanese Society of Neuropathology.
Jin A.,Second Peoples Hospital of Shenzhen |
Chen H.,Second Peoples Hospital of Shenzhen |
Chen H.,Chinese University of Hong Kong |
Wang C.,Chinese University of Hong Kong |
And 5 more authors.
Fertility and Sterility | Year: 2014
Objective To examine the expression of CD147 in 60 human endometriosis lesions and how CD147 regulates migration and apoptosis in human uterine epithelial (HESs) cells. Design Experimental clinical study and laboratory-based investigation. Setting Hospital and academic research center. Patient(s) Sixty women with chocolate cysts and 16 control women without endometriosis. Intervention(s) Human uterine epithelial cells were treated with anti-CD147 antibody. Main Outcome Measure(s) Real-time polymerase chain reaction for detecting CD147 expression in 60 human endometriosis lesions; migration assay and CellTiter 96 AQueous One Solution Cell Proliferation Assay (MTS) assay for cell functional investigation; Western blot for detecting protein levels; gelatin zymography for evaluating the activity of matrix metalloproteinase-2 (MMP-2) in cultured cells. Result(s) Expression of CD147 was significantly higher in ectopic endometrial tissues from patients with endometriosis than in normal endometrial tissues. Interference with CD147 function led to decreased migration and cell viability in HESs cells. Surprisingly, MMP-2 expression and activity were not changed after treating HESs cells with anti-CD147 antibody. Further examination revealed that immunodepletion of CD147 induced apoptosis in HESs cells, leading to the activation of caspase 3 and poly(ADP-ribose) polymerase. Conclusion(s) The results of the present study suggest that abnormally high expression of CD147 in ovarian endometriosis lesions with enhanced cell survival (reduced apoptosis) and migration, in an MMP-2-independent manner, may underlie the progression of endometriosis in humans. Copyright © 2014 American Society for Reproductive Medicine, Published by Elsevier Inc.
Liu J.F.,Shantou University |
Chen B.,Second Peoples Hospital of Shenzhen |
Ni Y.,Second Peoples Hospital of Shenzhen |
Zhan Y.Q.,Second Peoples Hospital of Shenzhen |
Gao H.B.,Second Peoples Hospital of Shenzhen
Chinese Medical Journal | Year: 2014
Background The operating microscopes have been applied to modern surgery for nearly a century. However, generations of microsurgeons have to flex their necks and fix their eyes on the eyepieces of a microscope continually that leads to physical and mental fatigue during a long operation. Stereoscopic three-dimensional (3D) media provides more ergonomic working environment, subsequently, resulting better performance in tasks and more accurate judgment. In this study, an alternative method of magnification was analyzed using a three-dimensional microsurgical video system and compared with the traditional method under microscopy to evaluate the availability and feasibility of a 3D microsurgical video system for microvascular anastomosis. Methods Forty Sprague-Dawley rats were randomly divided into four groups with each of 10. In 20 rats, 10 femoral artery anastomoses with a conventional microscope (arterial microscope group) were compared with that of 10 femoral artery anastomoses with a 3D microsurgical video system (arterial 3D group). For the other 20 rats, 10 femoral vein anastomoses using a conventional microscope (venous microscope group) were compared with that of 10 femoral vein anastomoses using a 3D microsurgical video system (venous 3D group). The arterial and venous microscope groups were considered to be the control groups. The arterial and venous 3D groups were the experimental groups. The examined criteria were as follows: anastomotic time, patency right after the procedure and 10 days later, number of sutures, vessel caliber, and pathological features. Results There were no differences between the operating equipment with respect to vessel caliber, anastomotic time, patency rate, number of sutures, and pathological changes in either the small arteries or veins. The average arterial anastomotic time of the arterial microscope group and arterial 3D group was 34.21 and 33.87 minutes, respectively (P >0.05). The average venous anastomotic time of the venous microscope group and venous 3D group was 29.95 and 31.50 minutes, respectively (P >0.05). Conclusions A small vessel anastomosis can be performed successfully with the help of a 3D display system. Although the vascular anastomotic time did not demonstrate a significant difference between the groups, the 3D microsurgical video system offers another option to improve the working environment for surgeons. Further development of our 3D monitoring system should focus on a higher resolution and better flexibility.
Guo Y.-J.,General Hospital of Beijing Military Region |
Liu J.-X.,Second Peoples Hospital of Shenzhen |
Guan Y.-W.,General Hospital of Beijing Military Region
European Review for Medical and Pharmacological Sciences | Year: 2016
OBJECTIVE: Previous studies reported that NDRG2 might be a tumor suppressor of prostate cancer. In this study, we investigated the hypoxia-induced expression change of miR-301a/b in prostate cancer cells and explored its regulation on NDRG2 in autophagy and viability of prostate cancer cells. MATERIALS AND METHODS: MiR-301a/b expression in hypoxia and normoxia cultured prostate cancer cells was measured. Its regulation on autophagy was measured by quantifying expression change of LC3B and p62. The direct binding between miR-301a/b and 3'UTR of NDRG2 was verified using dual luciferase, qRT-PCR and Western blot assay. The influence of miR-301a/b-NDRG2 axis on autophagy, viability and apoptosis of prostate cancer cells was further investigated. RESULTS: Hypoxia induced a significant upregulation of miR-301a/b in prostate cancer cells. Enhanced miR-301a/b expression significantly weakened autophagy of prostate cancer cells. Both miR-301a and miR-301b could directly target 3'UTR of NDRG2 and decrease its expression. Decreased NDRG2 expression directly resulted in increased autophagy and cell viability and reduced cell apoptosis. CONCLUSIONS: Taken together, we demonstrated that miR-301a/b-NDRG2 might be an important axis modulating autophagy and viability of prostate cancer cells under hypoxia.
Liu L.-X.,Second Peoples Hospital Of Shenzhen |
Chen L.,Jiamusi Jinjue Institute for Dentistry
Chinese Journal of Tissue Engineering Research | Year: 2014
BACKGROUND: Glass ionomer cements have been gradually employed in many aspects of dental clinical field. However, low mechanical strength and antibacterial effect restrict its further applications. OBJECTIVE: To proportionally explore the effects of titanium dioxide nanoparticles on the mechanical strength and antibacterial effect of traditional glass ionomer cements. METHODS: Base on different mass fractions of titanium dioxide nanoparticles in glass ionomer cements, all the glass ionomer cement samples were divided into control group (no titanium dioxide nanoparticles), low titanium dioxide group (containing 3% titanium dioxide nanoparticles), medium titanium dioxide group (containing 6% titanium dioxide nanoparticles), and high titanium dioxide group (containing 9% titanium dioxide nanoparticles). A universal material testing machine and a hardness tester were used to examine flexural strength, compressive strength, and surface hardness of glass ionomer cement samples, respectively. Glass ionomer cement samples were immerged into the artificial saliva, and fluoride release was measured by using a fluoride ion selective electrode. The direct contact test was used to investigate antibacterial effect of glass ionomer cement samples towards Streptococcus mutans. RESULTS AND CONCLUSION: Compared with the control group, few titanium dioxide nanoparticles (low and medium titanium dioxide group) could significantly improve flexural strength, compressive strength and surface hardness of glass ionomer cement samples (P < 0.05), and high titanium dioxide nanoparticles (high titanium dioxide group) significantly decreased flexural strength, compressive strength and surface hardness (P < 0.05). The introduction of titanium dioxide nanoparticles had little effect on fluorine release behavior of glass ionomer cement samples, and greatly improved antibacterial effect of glass ionomer cement samples towards Streptococcus mutans. © 2014, Journal of Clinical Rehabilitative Tissue Engineering Research. All rights reserved.
Li H.-Y.,Second Peoples Hospital of Shenzhen |
Luo G.-C.,Second Peoples Hospital of Shenzhen |
Guo J.,Second Peoples Hospital of Shenzhen |
Liang Z.,Second Peoples Hospital of Shenzhen
International Journal of Ophthalmology | Year: 2010
AIM: To evaluate the effects of glycemic control on refraction in diabetic patients. METHODS: Twenty newly diagnosed diabetic patients were included in this study. The random blood glucose, HbA1c levels, fasting C-peptide and postprandial 2h C-peptide were measured before treatment. The patients with random blood glucose higher than 12.0mmol/L and HbA1c level higher than 10.0% were selected. Refraction, intraocular pressure, radius of the anterior corneal curvature, depth of the anterior chamber, lens thickness, vitreous length, and axial length were measured on admission and at the end of week 1, 2, 3 and 4 during glycemic control. RESULTS: A transient hyperopic change occurred in all the patients receiving glycemic control. The maximum hyperopic change was 1.60D (range 0.50 ± 3.20D). Recovery of the previous refraction occurred between two and four weeks after insulin treatment. There was a positive correlation between the maximum hyperopic changes and the HbA1c levels on admission (r =0.84, P <0.05). There was a positive correlation between the maximum hyperopic changes and the daily rate of blood glucose reduction over the first 7 days of the treatment (r =0.53,p <0.05). During transient hyperopia, no significant changes were observed in the intraocular pressure, radius of the anterior corneal curvature, depth of the anterior chamber, lens thickness, vitreous length and axial length. CONCLUSION: Transient hyperopic changes occur after glycemic control in diabetic patients with severe hyperglycemia. The degrees of transient hyperopia are highly dependent on HbA1c levels before treatment and the rate of reduction of the blood glucose level. Copyright © IJO Press Co., Limited.