You M.,East China Normal University |
Yang S.,East China Normal University |
Jiao F.,East China Normal University |
Yang L.-Z.,Wenzhou Medical UniversityZhejiang |
And 2 more authors.
Electrochimica Acta | Year: 2016
A novel label-free electrochemical strategy was designed for multi-sites recognizing the guanine-rich DNA (G-rich DNA) with surface molecular imprinting polymer composite, in which the multi-walled carbon nanotubes (MWNCTs) were regarded as supporting material and the molecularly imprinted polymer (MIP) with guanine sites of DNA was applied as recognition element. Firstly, the vinyl groups were grafted onto the surface of carboxylic acid-functionalized MWNCTs (MWCNTs-COOH) through chemical modification. Then, the composite of MWCNTs-MIP was fabricated by the selective copolymerization of methacrylic acid, ethylene glycol dimethacrylate and guanine on the vinyl group-functionalized MWNTs surface. MWCNTs-MIP was characterized by different techniques, including Fourier transform infrared (FTIR) spectroscopy, scanning electronic microscopy (SEM), cyclic voltammogram (CV) and electrochemical impedance spectroscopy (EIS), showing that the MWCNTs-MIP composite was successfully prepared. Under the optimized conditions, the imprinting factor was nearly 5.68 according to the comparative slopes obtained on MWCNT-MIP and MWCNTs-non-imprinted polymer (MWCNTs-NIP), indicating that MWCNTs-MIP exhibited high selectivity for G-rich DNA. Moreover, the MWCNTs-MIP composite had a relatively wide linear range over G-rich DNA concentration of 0.05-1 μM and 5-30 μM with a detection limit of 7.52 nM (S/N = 3). Furthermore, the novel electrochemical strategy based on imprinted composite has very excellent performance in real samples of human serum and human urine. © 2016 Elsevier Ltd. All rights reserved. Source
Wu F.,Southern Medical University |
Wu F.,Wenzhou Medical UniversityZhejiang |
Lv T.,Huzhou Teachers College |
Chen G.,Wenzhou Medical UniversityZhejiang |
And 4 more authors.
Oncology Reports | Year: 2015
Dual-specificity phosphatase 9 (DUSP9) is a strong negative regulator of transcription factor activating kinases (ERK, JNK and p38) in the mitogen-activated protein kinase (MAPK) pathways. The aim of this study was to examine the CpG island methylation status of DUSP9 using bisulfite sequencing PCR (BSP) in gastric cancer (GC). The investigation was conducted on 30 clinical GC samples and selected corresponding tumor-free normal gastric mucosa tissues, using BSP for the determination of the promoter methylation status. The methylation status of the tumor samples was compared to the corresponding tumor-free samples. DUSP9 was silenced by promoter region hypermethylation and G2/M phase arrest was induced by DUSP9 in the MKN-1 GC cell line. MKN-1 proliferation was suppressed by DUSP9 by inhibiting c-Jun, which was induced by JNK signaling. The expression levels of CCND1, c-Jun, CDK4 and CDK6 were upregulated while p21 was downregulated by DUSP9 in MKN-1 cells. However, DUSP9-induced resulted in the regulation of the levels of cycle-related molecules, whivh were inhibited when the JNK inhibitor SP600125 was added. In conclusion, DUSP9 was frequently methylated in human GC and the expression of DUSP9 is silenced by promoter region hypermethylation. The results of this study, combined with previous studies, suggested that therapeutic intervention to increase the expression or activity of DUSP9 may enable the activation of anti-proliferation signals in malignant cells. © 2015, Spandidos Publications. All rights reserved. Source
Xu L.-J.,Wenzhou Medical UniversityZhejiang |
Nitter T.A.,YELEGESENTERET |
Liang Y.-B.,Wenzhou Medical UniversityZhejiang |
Jin Y.-N.,Fudan University |
And 3 more authors.
Ophthalmology in China | Year: 2015
Objective: To evaluate the diagnostic value of retinal ganglion cell complex (GCC) thickness in open angle glaucoma by comparing with peripapillary retinal nerve fiber layer thickness (pRNFL) and their combinations. Design: Diagnostic method evaluation. Participants: 66 patients with primary open angle glaucoma (POAG) and 40 healthy controls who came to yelegesenteret during October 2013 to March 2014 were included in this study. According to the Hodapp-Anderson-Parrish (HAP) grading scale, POAG patients were classified into two subgroups, which were an early group (EG) and a moderate-to-advanced group (AG). By HAP criteria, 34 eyes were included in EG, whereas 32 eyes were in AG. Methods: All subjects underwent SD-OCT (iVue 100) imaging: GCC parameters and ONH parameters were measured in each participant. By comparing the area under the receiver operator characteristic curves, the diagnostic abilities of the parameters were evaluated. Main Outcome Measures: Thickness of GCC and pRNFL. Results: The total GCC thickness showed strong correlation with corresponding pRNFL. Both the total thickness of GCC (EG 81.03±6.37 μm, AG 76.28±9.39 μm) and corresponding pRNFL (EG 80.47±9.02 μm, AG 69.84± 11.74 μm) appeared significant reduction in glaucoma group comparing with the normal group (GCC 92.90±6.07 μm, pRNFL 96.98 ±8.09 μm). The parameter with the best diagnostic ability in EG compared with in normal subjects after adjusting age was the superior GCC thickness (AUC=0.929). The parameter with the best diagnostic ability in AG compared with in normal subjects after adjusting age was the total pRNFL thickness (AUC=0.988). In EG, the combination of total GCC thickness and total pRNFL thickness by statistical regressive method may improve diagnostic ability, but without statistical significance. In AG, the parallel combination of total GCC thickness and total pRNFL thickness may significantly improve sensitivity by comparing with sole total pRNFL thickness. Conclusions: Imaging of GCC using SD-OCT (iVue 100) has strong diagnostic ability and was comparable to pRNFL measurement in distinguishing POAG patients from healthy subjects irrespective the severity of POAG. The parallel combination of these two parameters may improve sensitivity in AG. Copyright © 2015 by the Editorial Board of OPHTHALMOLOGY IN CHINA. Source
Feng X.,Emory University |
Zhang Y.,Wenzhou Medical UniversityZhejiang |
Zhang Y.,Emory University |
Shao N.,Wenzhou Medical UniversityZhejiang |
And 14 more authors.
American Journal of Physiology - Renal Physiology | Year: 2015
Thiazide-sensitive sodium chloride cotransporter (NCC) plays an important role in maintaining blood pressure. Aldosterone is known to modulate NCC abundance. Previous studies reported that dietary salts modulated NCC abundance through either WNK4 [with no lysine (k) kinase 4]-SPAK (Ste20- related proline alanine-rich kinase) or WNK4-extracellular signalregulated kinase-1 and -2 (ERK1/2) signaling pathways. To exclude the influence of SPAK signaling pathway on the role of the aldosterone- mediated ERK1/2 pathway in NCC regulation, we investigated the effects of dietary salt changes and aldosterone on NCC abundance in SPAK knockout (KO) mice. We found that in SPAK KO mice low-salt diet significantly increased total NCC abundance while reducing ERK1/2 phosphorylation, whereas high-salt diet decreased total NCC while increasing ERK1/2 phosphorylation. Importantly, exogenous aldosterone administration increased total NCC abundance in SPAK KO mice while increasing DUSP6 expression, an ERK1/2- specific phosphatase, and led to decreasing ERK1/2 phosphorylation without changing the ratio of phospho-T53-NCC/total NCC. In mouse distal convoluted tubule (mDCT) cells, aldosterone increased DUSP6 expression while reducing ERK1/2 phosphorylation. DUSP6 Knockdown increased ERK1/2 phosphorylation while reducing total NCC expression. Inhibition of DUSP6 by (E)-2-benzylidene-3-(cyclohexylamino)- 2,3-dihydro-1H-inden-1-one increased ERK1/2 phosphorylation and reversed the aldosterone-mediated increments of NCC partly by increasing NCC ubiquitination. Therefore, these data suggest that aldosterone modulates NCC abundance via altering NCC ubiquitination through a DUSP6-dependent ERK1/2 signal pathway in SPAK KO mice and part of the effects of dietary salt changes may be mediated by aldosterone in the DCTs. © 2015 the American Physiological Society. Source