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Guo Y.,Chinese PLA General Hospital | Zhang Z.,Chinese PLA General Hospital | Zhou B.,Chinese PLA General Hospital | Wang P.,Chinese PLA General Hospital | And 7 more authors.
Neuroscience Bulletin | Year: 2014

Specific patterns of brain atrophy may be helpful in the diagnosis of Alzheimer's disease (AD). In the present study, we set out to evaluate the utility of grey-matter volume in the classification of AD and amnestic mild cognitive impairment (aMCI) compared to normal control (NC) individuals. Voxel-based morphometric analyses were performed on structural MRIs from 35 AD patients, 27 aMCI patients, and 27 NC participants. A two-sample two-tailed t-test was computed between the NC and AD groups to create a map of abnormal grey matter in AD. The brain areas with significant differences were extracted as regions of interest (ROIs), and the grey-matter volumes in the ROIs of the aMCI patients were included to evaluate the patterns of change across different disease severities. Next, correlation analyses between the grey-matter volumes in the ROIs and all clinical variables were performed in aMCI and AD patients to determine whether they varied with disease progression. The results revealed significantly decreased grey matter in the bilateral hippocampus/ parahippocampus, the bilateral superior/middle temporal gyri, and the right precuneus in AD patients. The grey-matter volumes were positively correlated with clinical variables. Finally, we performed exploratory linear discriminative analyses to assess the classifying capacity of grey-matter volumes in the bilateral hippocampus and parahippocampus among AD, aMCI, and NC. Leave-one-out crossvalidation analyses demonstrated that grey-matter volumes in hippocampus and parahippocampus accurately distinguished AD from NC. These findings indicate that grey-matter volumes are useful in the classification of AD. © 2014 Shanghai Institutes for Biological Sciences, CAS and Springer-Verlag. Source

Fang F.,Shandong University | Huang R.-L.,Shanghai JiaoTong University | Zheng Y.,Peoples Hospital of Jimo | Liu M.,Peoples Hospital of Jimo | Huo R.,Shandong University
Journal of Dermatological Science | Year: 2016

Background: Hypertrophic scars and keloids, characterized by over-proliferation of fibroblasts and aberrant formation of the extracellular matrix (ECM), are considered fibrotic diseases. Accumulating evidence indicates that mesenchymal stem cells (MSCs) promote scar-free wound healing and inhibit fibrotic tissue formation, making them a potentially effective therapeutic treatment for hypertrophic scars and keloids. Objective: To investigate the paracrine effects of bone marrow derived MSCs (BMSCs) on the biological behavior of hypertrophic scar fibroblasts (HSFs) and keloid fibroblasts (KFs). Methods: Proliferative and profibrotic phenotype changes of the fibroblasts were analyzed by immunofluorescence staining, in-cell western blot, and real-time PCR. Results: BMSC-conditioned medium inhibited HSF and KF proliferation and migration, but did not induce apoptosis. Interestingly, normal skin fibroblast-conditioned medium exhibited no inhibitory effects on HSF or KF proliferation and migration. Furthermore, BMSC-conditioned medium significantly decreased expression of profibrotic genes, including connective tissue growth factor, plasminogen activator inhibitor-1, transforming growth factor-β1, and transforming growth factor-β2, in HSFs and KFs at both transcriptional and translational levels. In contrast, the expression of antifibrotic genes, such as transforming growth factor-β3 and decorin, was substantially enhanced under the same culture conditions. Finally, we observed that BMSC-conditioned medium suppressed the ECM synthesis in HSFs and KFs, as indicated by decreased expression of collagen I and fibronectin and low levels of hydroxyproline in cell culture supernatant. Conclusion: These findings suggest that BMSCs attenuate the proliferative and profibrotic phenotype associated with HSFs and KFs and inhibit ECM synthesis through a paracrine signaling mechanism. © 2016. Source

Ren L.-J.,Peoples Hospital of Jimo | Li B.,Jiaozhou Central Hospital of Qingdao | Zhu X.-D.,Peoples Hospital of Jimo
Chinese Journal of Cancer Prevention and Treatment | Year: 2010

The objective of this study was to compare the clinical effect of treating multiple osseous metastasis between 89SrCl2 and the association of 89SrCl2 and zoledronic acid. Eighty cases of multiple osseous metastasis were divided into two groups randomly, the group A was solely applied adionuclide 89SrCl2 and the group B was used the association of 89SrCl2 and zoledronic acid, and the condition of remission of bone ache and quality of life after the treatment were observed to compare the changing of bone metabolism of metastatic lesion and the reaction of hematological toxicity. The effective rate of relieving pain of group A was 72. 5% (29/40), the effective rate of relieving pain of group B was 77. 5%(31/40, χ2 =4. 24, P<0. 05). The effective rate of improving of group A was 65. 0%(26/40). The effective rate of improving of group B was 82. 5%(33/40, χ2 =7. 49, P<0. 01). The effective rates of bone metabolism of metastatic lesion after treatment were 45. 0% and 67. 5% (P0. 05). Applying the association of 89SrCl2, and zoledronic acid in the treatment of multiple osseous metastasis can increase the analgesic effect and improve of the quality of life furthermore, but not adding toxic and side reactions, so it is a better method of associated treatment. Source

Zhao Y.-B.,Peoples Hospital of Jimo | Zhang S.-H.,Peoples Hospital of Jimo | Lu J.,Peoples Hospital of Jimo
Journal of Practical Oncology | Year: 2012

To investigate the effects of retrovirus-mediated siRNA targeting EphA2 on the breast cancer cell line MCF-7.Methods The recombinant retroviral vector expressing EphA2 short interference RNA (siRNA) was constructed and transfected into the MCF-7 cells, and then stable transfectants were isolated by puromycin and were cultured. The EphA2 protein in transfected MCF-7 cells was detected by Western blot. Compared with cells transfected with empty retroviral vector and untransfected cells, the level of EphA2 protein expression was greatly decreased in MCF-7 cells transfected by the recombinant retroviral vector with Western blot techniques. EphA2 protein expression in MCF-7 cell line is successfully suppressed by using the recombinant retrovirus-mediated RNAi technique, indicating that this may contributes to the study of the changes of malignant biological activity of breast cancer cell lines by transfection of siRNA retrviral vectors and provide a new solution for EphA2-targeting therapeutic intervention of breast carcinoma. Source

Fan Q.,Shandong University | Hu Y.,Peoples Hospital of Jimo | Pang H.,Peoples Hospital of Jimo | Sun J.,Peoples Hospital of Jimo | And 2 more authors.
Molecular Medicine Reports | Year: 2014

The aim of the present study was to explore the pro-apoptotic effect and specific mechanism of action of melittin (MEL) in humans. The effects of MEL on apoptosis in osteosarcoma and fetal osteoblast cells were investigated, and the mechanism that induced MG63 cell growth was also explored. The effects of MEL on cell proliferation were detected by a 2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl) -2H-tetrazolium-5-carboxanilide analysis. Apoptosis was detected by flow cytometric analysis. MEL protein, inositol-requiring protein-1 (IRE- α), phosphorylated-protein kinase R-like endoplasmic reticulum (ER) kinase, spliced X-box-1 (XBP1), eukaryotic translation initiation factor-2α, cleaved activating transcription factor-6, caspase-12 and C/EBP homology protein (CHOP) were detected in three groups and two cell lines by western blot analysis. The results indicated that the expression or incubation of MEL in the MG63 cells triggered apoptosis and the inhibition of proliferation. One protein from the ER stress unfolded protein response pathway, IRE-α, was involved in the MEL-induced apoptosis in MG63 cells. Furthermore, spliced XBP1 protein was significantly increased in the MEL peptide incubated and MEL expressing groups of MG63 cells. Furthermore, CHOP protein expression was activated in MG63 cells following being incubated with or expressing MEL. In conclusion, MEL serves as an effective factor that inhibits the proliferation of MG63 cells via activating the ER stress-mediated apoptosis pathway. This activation is triggered by the IRE-α pathway mediated by inducing CHOP protein expression. Source

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