Dalian Medical University is a university in Dalian, Liaoning, China under the provincial government. It was founded in 1947 in the southern part of Dalian city, China by Mao Ze Dong.. In October 2007, it moved to the new campus in Lushunkou District, Dalian, which is across Lushun South Road from Dalian University of Foreign Languages' new campus.The school through its Dalian Medical University Plastination Co. subsidiary is the source of the cadavers which have undergone plastination to appear worldwide in the BODIES... The Exhibition. Wikipedia.
Tang Y.,CAS Shanghai Institutes for Biological Sciences |
Le W.,Dalian Medical University
Molecular Neurobiology | Year: 2016
One of the most striking hallmarks shared by various neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis, is microglia-mediated neuroinflammation. Increasing evidence indicates that microglial activation in the central nervous system is heterogeneous, which can be categorized into two opposite types: M1 phenotype and M2 phenotype. Depending on the phenotypes activated, microglia can produce either cytotoxic or neuroprotective effects. In this review, we focus on the potential role of M1 and M2 microglia and the dynamic changes of M1/M2 phenotypes that are critically associated with the neurodegenerative diseases. Generally, M1 microglia predominate at the injury site at the end stage of disease, when the immunoresolution and repair process of M2 microglia are dampened. This phenotype transformation is very complicated in AD due to the phagocytosis of regionally distributed β-amyloid (Aβ) plaque and tangles that are released into the extracellular space. The endogenous stimuli including aggregated α-synuclein, mutated superoxide dismutase, Aβ, and tau oligomers exist in the milieu that may persistently activate M1 pro-inflammatory responses and finally lead to irreversible neuron loss. The changes of microglial phenotypes depend on the disease stages and severity; mastering the stage-specific switching of M1/M2 phenotypes within appropriate time windows may provide better therapeutic benefit. © 2015, Springer Science+Business Media New York.
Xu L.,Dalian University |
He D.,Dalian Medical University |
Bai Y.,Dalian University
Molecular Neurobiology | Year: 2016
Microglia are the main effectors in the inflammatory process of the central nervous system. As the first line of defense, microglia play an important role in the inflammatory reaction. When there is pathogen invasion or cell debris, microglia will be activated rapidly and remove it, while releasing the inflammatory cytokines to mediate inflammatory reaction. Activated microglia were found surrounding lesions of various neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, muscular amyotrophic lateral sclerosis, and multiple sclerosis. Microglia, the effectors of neuronal degeneration and necrosis, are involved in the removal of necrotic neurons. But over activated microglia may accelerate the process of some neurodegenerative diseases. Activated microglia can release cytotoxic factor and cytokines. Some of them may cause further damage to neuron, and some of them can regulate inflammatory cells to gather to the lesion. Microglia-mediated inflammation was considered to be the possible mechanism for the occurrence or deterioration of neurodegenerative diseases. Therefore, inhibiting the activity of microglia appropriately may be an effective way for the treatment of neurodegenerative diseases. © 2015, Springer Science+Business Media New York.
Wang H.,Dalian Medical University
OncoTargets and Therapy | Year: 2014
Lapatinib is an oral, small-molecule, reversible inhibitor of both epidermal growth factor receptor and human epidermal growth factor receptor-2 (HER2) tyrosine kinases. In March2007, the US Food and Drug Administration approved lapatinib for use in combination with capecitabine for the treatment of women with HER2-overexpressing, advanced or metastatic breast cancer. This review discusses the available information of lapatinib in Chinese breast cancer patients, focusing on its effectiveness and clinical application against advanced or metastatic breast cancer. In pivotal phase III trials, a combination of lapatinib and capecitabine significantly decreased the risk of disease progression compared to capecitabine alone in women with HER2-positive advanced or metastatic breast cancer. Other trials were used to evaluate lapatinib in combination with hormone therapy, in combination with trastuzumab, and as an adjunct to adjuvant therapy for early-stage disease. Preclinical data have revealed that lapatinib is active in trastuzumab-resistant cell lines as well as synergistic with trastuzumab. In clinical trials, lapatinib has not been associated with serious or symptomatic cardiotoxicity. Further, it can cross the blood-brain barrier and may therefore have a role in preventing cancer progression in the central nervous system. Thus, lapatinib warrants further evaluation in HER2-positive metastatic and early-stage breast cancer patients. © 2014 Wang.
Wang Y.,Dalian Medical University |
Wang Y.,University of North Carolina at Chapel Hill |
Wang Z.,University of North Carolina at Chapel Hill
RNA | Year: 2015
While the human transcriptome contains a large number of circular RNAs (circRNAs), the functions of most circRNAs remain unclear. Sequence annotation suggests that most circRNAs are generated from splicing in reversed orders across exons. However, the mechanisms of this backsplicing are largely unknown. Here we constructed a single exon minigene containing split GFP, and found that the pre-mRNA indeed produces circRNA through efficient backsplicing in human and Drosophila cells. The backsplicing is enhanced by complementary introns that form double-stranded RNA structure to bring splice sites in proximity, but such structure is not required. Moreover, backsplicing is regulated by general splicing factors and cis-elements, but with regulatory rules distinct from canonical splicing. The resulting circRNA can be translated to generate functional proteins. Unlike linear mRNA, poly-adenosine or poly-thymidine in 3' UTR can inhibit circular mRNA translation. This study revealed that backsplicing can occur efficiently in diverse eukaryotes to generate circular mRNAs. © 2015 Wang and Wang
Wang L.,Dalian Medical University
Circulation | Year: 2016
BACKGROUND—: The recruitment of leukocytes to the vascular wall is a key step in hypertension development. Chemokine receptor CXCR2 mediates inflammatory cell chemotaxis in several diseases, however, the role of CXCR2 in hypertension development and the underlying mechanisms remain unknown. METHODS—: Angiotensin II (490 ng·kg·min) or DOCA-salt-induced mouse hypertensive models in genetic ablation, pharmacological inhibition of CXCR2 and adoptive bone marrow transfer mice were used to determine the role of CXCR2 in hypertension (measured by radiotelemetry and tail-cuff system), inflammation (verified by flow cytometry and quantitative real-time PCR analysis), vascular remodeling (studied by haematoxylin and eosin (H&E) and Massonʼs trichrome staining), vascular dysfunction (assessed by aortic ring), and oxidative stress (indicated by NADPH oxidase activity, DHE staining and quantitative real-time PCR analysis). Moreover, the blood CXCR2 cells in normotensive controls and hypertension patients were analyzed by flow cytometry. RESULTS—: Angiotensin II significantly up-regulated the expression of CXCR2 mRNA and protein, and increased the number of CD45 CXCR2 cells in mouse aorta (n=8 per group). Selective CXCR2 knockout (CXCR2) or pharmacological inhibition of CXCR2 markedly reduced angiotensin II- or DOCA-salt-induced blood pressure elevation, aortic thickness and collagen deposition, accumulation of pro-inflammatory cells into the vascular wall, and the expression of cytokines (n=8 per group). CXCR2 inhibition also ameliorated angiotensin II-induced vascular dysfunction and reduced vascular superoxide formation, NADPH activity and the expression of NADPH oxidase subunits (n=6 per group). Bone marrow reconstitution of wild-type (WT) mice with CXCR2 bone marrow cells also significantly abolished angiotensin II-induced responses (n=6 per group). Importantly, CXCR2 blockade reversed established hypertension induced by angiotensin II or DOCA-salt challenge (n=10 per group). Furthermore, we demonstrated that CXCR2 pro-inflammatory cells were higher in hypertensive patients (n=30) compared with normotensive individuals (n=20). CONCLUSIONS—: Infiltration of CXCR2 cells plays a pathogenic role in arterial hypertension and vascular dysfunction. Inhibition of CXCR2 pathway may represent a novel therapeutic approach to treat hypertension.Circulation is published on behalf of the American Heart Association, Inc., by Wolters Kluwer. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDervis License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made. © 2016 by the American College of Cardiology Foundation and the American Heart Association, Inc.
Le W.,Dalian Medical University |
Sayana P.,Gandhi Medical College |
Jankovic J.,Baylor College of Medicine
Neurotherapeutics | Year: 2014
Parkinson's disease (PD) is a progressive, neurodegenerative disorder of unknown etiology, although a complex interaction between environmental and genetic factors has been implicated as a pathogenic mechanism of selected neuronal loss. A better understanding of the etiology, pathogenesis, and molecular mechanisms underlying the disease process may be gained from research on animal models. While cell and tissue models are helpful in unraveling involved molecular pathways, animal models are much better suited to study the pathogenesis and potential treatment strategies. The animal models most relevant to PD include those generated by neurotoxic chemicals that selectively disrupt the catecholaminergic system such as 6-hydroxydopamine; 1-methyl-1,2,3,6-tetrahydropiridine; agricultural pesticide toxins, such as rotenone and paraquat; the ubiquitin proteasome system inhibitors; inflammatory modulators; and several genetically manipulated models, such as α-synuclein, DJ-1, PINK1, Parkin, and leucine-rich repeat kinase 2 transgenic or knock-out animals. Genetic and nongenetic animal models have their own unique advantages and limitations, which must be considered when they are employed in the study of pathogenesis or treatment approaches. This review provides a summary and a critical review of our current knowledge about various in vivo models of PD used to test novel therapeutic strategies. © 2013 The American Society for Experimental NeuroTherapeutics, Inc.
Li L.,Dalian Medical University
Expert review of proteomics | Year: 2012
miRNAs are a family of 17- to 23-nucleotide noncoding small RNAs that primarily function as gene expression fine regulators. A number of studies have shown that miRNAs play an important role in breast tumorigenesis, metastasis, proliferation and differentiation of breast cancer stem cells. This short review summarizes the progression of miRNA-mediated breast tumorigenesis and metastasis through various signaling pathways associated with drug resistance.
Ji J.J.,Dalian Medical University
African journal of traditional, complementary, and alternative medicines : AJTCAM / African Networks on Ethnomedicines | Year: 2013
Rheumatoid arthritis (RA) is the rheumatism mainly manifested as disabling joint disease and mainly involves hands, wrists, feet and other small joints. Recurrent arthritis attacks, synovial cell hypertrophy and hyperplasia and bone and cartilage damages eventually lead to joint dysfunction and other complications, and there is no cure. Quercetin (QU) is a kind of natural flavonoids, with lipid-lowering, anti-inflammatory and other pharmacological activities, and minor toxic side effects. Thus, we assume that QU may be an adjuvant natural drug for treatment of RA. The possible mechanism is through regulation of NF-κB, to inhibit the transcription of joint synovitis factors, hinder the generation of inflammatory factors, and inhibit the inflammatory reaction; through inhibiting the activities of VEGF, bFGF, MMP-2 and other cytokines, to inhibit angiogenesis in multiple links and inhibit synovial pannus formation. QU may be an adjuvant natural drug for treatment of RA.
Sun Y.,Dalian Medical University |
Liu J.,Dalian Medical University
Clinical Therapeutics | Year: 2014
Background: Exosomes are 30- to 100-nm, membrane-bound vesicles that are released by most types of cells, including tumor cells. Exosomes contain a great variety of bioactive molecules, including signal peptides, microRNA, lipids, and DNA. In cancer, tumor cells aberrantly secrete large quantities of exosomes to transport paracrine signals or to contribute to tumor-environment interaction at a distance. Objective: The goal of this review was to discuss the recent advances on the mechanism of cancer-derived exosomes in tumor regulation. Methods: Pertinent articles and abstracts were identified through searches of PubMed for literature published from 1983 to December 2013. Search terms included exosome, tumor, cancer, diagnosis, and therapy. Results: All of the exposed evidence points to communication between cancer cells and their surroundings, either mediated by cancer cell-derived exosomes or by stromal cell-derived exosomes. This communication probably supports tumor proliferation, motility, invasion, angiogenesis, and premeta-static niche preparation. In addition, recent research implies that cancer cell-derived exosomes play a suppressive role in cancer-directed immune response. Conclusions: The biomarkers detected in bodily fluid- derived exosomes imply a potential for exosomes in cancer diagnosis. Also, exosomes could be used as a vehicle to selectively deliver therapeutic nucleic-acid drugs or conventional drugs for tumor therapy. The tolerability and feasibility of cancer exosomes in diagnosis and therapy need to be further evaluated. © 2014 Elsevier HS Journals, Inc.
Li J.-N.,Dalian Medical University
Synthesis and Reactivity in Inorganic, Metal-Organic and Nano-Metal Chemistry | Year: 2013
Coordination compounds of cobalt(II) and zinc(II) with Schiff bases 4-chloro-2-[(2-ethylaminoethylimino)methyl]phenol and 4-chloro-2-[(2-piperazin- 1-ylethylimino)methyl]phenol, respectively, were synthesized. The characterization of the newly formed compounds was done by elemental analysis, IR spectra, molar electric conductibility, and single crystal X-ray determination. The Co atom in the cobalt complex is in an octahedral coordination, and the Zn atom in the zinc complex is in a tetrahedral coordination. The Schiff bases and the two complexes have been evaluated for their antibacterial activity against four gram-positive bacteria, Stereptococcus pyogenes, Stereptococcus agalactiae, Staphylococcus aureus, and Bacillus anthracis, and two gram-negative bacteria, Klebsiella pneumonia and Pseudomonas aeruginosa. © 2013 Copyright Taylor and Francis Group, LLC.