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OBJECTIVE: To observe the effects of bone marrow mesenchymal stem cells( BMSCs) on the treatment of pulmonary fibrosis in silicosis mice. METHODS: Specific pathogen free healthy male C57BL/6 mice were randomly divided into control group,silicosis group and treatment group with 10 mice in each group. The mice of the control group were given one intra-tracheal injection of 20. 0 μL 0. 90% sodium chloride solution. The silicosis group and treatment group received one 20. 0 μL( mass concentration 250 g/L) of silica dust suspension. After 4 weeks,mice in treatment group were injected with 250. 0 μL of BMSCs suspension( cell density 2 × 10~9/L) by tail vein and silicosis group injected with 250. 0 μL of 0. 90% sodium chloride solution instead,once a week with continuous treatment for 4 weeks. Control group was not given any treatment. Mice were euthanized two weeks after the last treatment. Pathological sections were observed,pulmonary fibrosis score( Ashcroft scores) was marked. Lung coefficient was measured. Lung tissue hydroxyproline( HYP) level and serum transforming growth factor β1( TGF-β1) level were measured. The level of pulmonary fibrosis was scored and the percentages of T helper cell 17( Th17 cell) and regulatory T cell( Treg cell) of spleen and hilar lymph node( HLN) were measured by flow cytometry. RESULTS: The results of lung histopathological examination showed that the pulmonary fibrosis was severe in silicosis group. Massive collagen fiber accumulation and silicotic nodule were found. In treatment group,fibrosis was mild,little collagen fiber accumulation and silicotic nodule were found. The lung coefficient,Aschcroft scores,lung tissue HYP level,serum TGF-β level and the percentage of Th17 cell of spleen and HLN in silicosis group were higher than that of control group( P < 0. 05),while the above indexes of treatment group were lower than that of silicosis group( P < 0. 01). The percentage of Treg cell of spleen and HLN in silicosis group were lower than that of control group( P < 0. 05),while those indexes of treatment group were higher than that of silicosis group( P < 0. 01).CONCLUSION: BMSCs could effectively alleviate the pulmonary fibrosis in silicosis mice and correct the imbalance of Th17/Treg.
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OBJECTIVE: To explore the repair effects of bone marrow mesenchymal stem cells( BMSCs) on hematopoietic injury induced by benzene poisoning in mice. METHODS: Five specific pathogen free healthy male Kunming mice were selected to obtain BMSCs through bone marrow attachment culturing method. The Kunming mice were randomly divided into poisoning group and BMSCs transplantation group,18 mice in each group,after the benzene poisoning model was established by subcutaneous multi-point injection of benzene and oil mixture 3 times/week,10 weeks continuously. Each group was injected through tail vein with 250. 0 μL 0. 9% sodium chloride solution or 250. 0 μL BMSCs suspension( cell density 2 × 109/L) once per week for 4 weeks,respectively. The control group( 10 mice) was not given any treatment.Mice were euthanized 2 weeks after treatment. The blood routine examination was conducted. Nucleated cells in bone marrow were observed after Giemsa staining. The clones of hemopoietic progenitor cells were counted and the levels of serum interferon-γ( IFN-γ) were examined using enzyme-linked immune sorbent assay. RESULTS: The mouse model of chronic benzene poisoning was established successfully. After the BMSCs transplantation treatment,the white blood cell count,platelet count,red blood cell count,hemoglobin level and bone marrow nucleated cell as well as granulocyte-macrophage colony forming unit( CFU-GM) in benzene poisoning group were significantly decreased compared with control group( P <0. 01),while those indexes of BMSCs treatment group were higher than that of benzene poisoning group( P < 0. 05). The counts of platelet,red blood cell,bone marrow nucleated cell and CFU-GM in BMSCs treatment group were significantly lower than that of control group( P < 0. 05). The level of serum IFN-γ in benzene poisoning group was higher than that of control group( P < 0. 01),and serum IFN-γ level in BMSCs treatment group was lower than that of benzene poisoning group( P < 0. 01). There was no significant difference of IFN-γ level in BMSCs treatment group compared with control group( P > 0. 05). CONCLUSION: BMSCs have repair effects on hematopoietic system injury caused by benzene poisoning.
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The culture of umbilical cord-derived mesenchymal stem cells is extremely important for studies on umbilical cord mesenchymal stem cells. Optimization of cellculture technology is crucial for clinical application of mesenchymal stem cells and even celltherapy. Meanwhile, the labeling and tracer technique of umbilical cord-derived mesenchymal stem cells is a hotspot in stem celltransplantation. OBJECTIVE:To review the research and development of the cellmarkers and tracer methods of umbilical cord-derived mesenchymal stem cells. METHODS:A computer-based search of VIP, CNKI, Medline, Highwire and Foreign Journals Integration System databases was performed for articles concerning culture and labeling of umbilical cord-derived mesenchymal stem cells published from January 2001 to October 2013. The keywords were“stem cells, mesenchymal stem cells, umbilical cord-derived mesenchymalstem cells, cellculture, labeling methods”in Chinese and English, respectively. Final y, 35 articles were included in result analysis. RESULTS AND CONCLUSION:Umbilical cord-derived mesenchymal stem cells have not yet been widely used, mainly because of the immature isolation, culture and staining techniques of umbilical cord-derived mesenchymal stem cells. These techniques are worthy of further optimization studies. Although in recent years, cellmarkers and tracer technology of umbilical cord-derived mesenchymal stem cell s have made great progress, there are stil many problems need to be solved.
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BACKGROUND:There are less studies addressing whether bone marrow mesenchymal stem cells from systemic lupus erythematosus patients are different from healthy people. OBJECTIVE:To compare the multi-differentiation capacity of bone marrow mesenchymal stem cells isolated from systemic lupus erythematosus model mice and normal control mice. METHODS:Bone marrow mesenchymal stem cells of systemic lupus erythematosus model mice and C57BL mice were isolated and cultured fol owed by osteogenic and adipogenic differentiations, respectively. Differentiation abilities of two kinds of mouse bone marrow mesenchymal stem cells were observed. RESULTS AND CONCLUSION:Passaged bone marrow mesenchymal stem cells from C57BL mice were long spindle-shaped and evenly distributed, while bone marrow mesenchymal stem cells from systemic lupus erythematosus model mice showed slow growth and were relatively smal er than those from C57BL mice. After osteogenic induction, the amount of calcium salt and calcium nodules were significantly less in the bone marrow mesenchymal stem cells from systemic lupus erythematosus model mice than from normal control mice. PCR detection showed that expressions of Runx2, alkaline phosphatase and osteocalcin were also significantly decreased in the bone marrow mesenchymal stem cells from systemic lupus erythematosus model mice. After adipogenic induction, the number of lipid droplets in the bone marrow mesenchymal stem cells from systemic lupus erythematosus model mice was significantly less than the control group, and PCR detection also showed significantly decreased expression of adipogenic genes, including PPARγ2 and lipoprotein lipase. These findings suggest that the bone marrow mesenchymal stem cells from systemic lupus erythematosus model mice exhibit lower osteogenic and adipogenic capacities than those from normal C57BL mice, and also have the impaired multi-differentiation ability.
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BACKGROUND:Metabolic syndrome is based on sugar, fat and other metabolic disorders and central obesity, hypertension as features in a series of syndrome. The traditional treatment is not yet possible to fundamental y improve and cure metabolic syndrome. OBJECTIVE:To provide an overview of the research progress of stem celltransplantation in the treatment of metabolic syndrome. METHODS:The first author retrieved PubMed database and CNKI database for articles regarding basic research on progress of stem celltransplantation in the treatment of metabolic syndrome, insulin resistance, diabetes, hyperlipidemia and hypertension published from 2002 to 2012. The key words were“stem cells, metabolic syndrome, insulin resistance, diabetes, hyperlipidemia, hypertension, stem cells transplantation”in English and Chinese, respectively. Outdated and repetitive studies were excluded, and 43 literatures were included for summarization. RESULTS AND CONCLUSION:Stem cells are the origin of the body cells, and have self-replicating, highly value-added and differentiation capacity. Stem celltherapy can promote a variety of damage repair and renew aging or death of cells, so as to improve the structure and function of tissues and organs, and to promote the utilization and excretion of metabolites. Studies have shown that stem cells can treat lipid metabolism, insulin resistance, hypertension, hyperglycemia, atherosclerosis and other hazards of metabolic syndrome disorders through a variety of mechanisms. There are many problems to be solved in the treatment of metabolic syndrome with stem celltransplantation. But the existing research data have been confirmed, and stem celltransplantation in the treatment of the metabolic syndrome is a promising new approach.
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ET-CT demonstrated that VX2 tumor tissues could uptake 18F-FDG more than normal tissue, which made the basis for further study of VX2 tumor model.
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To investigate the role of H-fas oncogene in the early stages of human breast carcinogenesis. Methods Thirty cases of human breast cancer, 36 epithelial hyperplasia of usual type and 31 atypical hyperplasia were employed to detect H-ras gene codon 12 mutations by PCR-RFLP and PCR-SSCP assays, and to detect the expression of H-ras protein by immunohistochemistry method. ResultsExpression of H-ras protein were found in 73.3 % (22/30) of breast cancer and 48.4 % (15/31 ) of atypical hyperplasia. No H-ras protein expression was observed in hyperplasia of usual type. All tested sarnples of breast cancer and hyperplsia showed no mutations of H-ras gene codon 12. ConclusionOverexpression of H-ras protein is involved in early stages of breast carcinogenesis, but mutations of H-ras gene codon 12 is rarely present in the stage.