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Etiological research is necessary for understanding the occurrence and epidemiological patterns of diseases, and is also a prerequisite for the diagnosis, prevention and treatment of clinical diseases. Mendelian randomization(MR), a method of research that combines genetics and epidemiology, has the advantage of exploring the causal relationship between exposure and disease genetically as well as avoiding confounding factors and reverse causation. Thus, it has been extensively utilized in the etiological study of diseases. This paper reviews the implementation of MR in the research of ocular diseases and provides ideas and approaches for the investigation of related mechanisms as well as the development of intervention strategies.
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Objective To study the tumorigenesis mechanism in bone marrow mesenchyme stem cells (MSC). Methods The bone marrow MSC could be induced into turnout (F6 cells) in vitro. The difference between gene expression of F6 cells and MSC was distinguished by fluorescent differential display (FDD). Verification of the result was detected by Real time RT-PCR and Western blotting, and immunocytochemistry. Results FDD analysis confirmed that Nucleostemin (NS) was positively up-regulated in F6 cells compared with MSC. Similar results were obtained by PCR and Western blotting. The NS gene expression levels in MSC, F6, 176-4, F6-6 and F6-7 were significantly different(F =160, P <0.05). The NS gene expression level in F6 (0.0372±0.0019) was 18 folds higher than those of MSC(0.0021±0.0002,P <0.05). Expression levels in F6-4, F6-6 and F6-7 tissue were 0.0504±0.0083, 0.0995±0.0026 and 0.0614±0.0036, and were significantly higher than that in MSC(P <0.05). The expression of NS increased significantly with the accreting volume of turnour, and high-level protein expression of NS was confirmed by Western blotting and immunocytochemistry. Conclusion The expression level of NS might be one of the factors playing important roles during turnour genesis, especially in MSC mutation.
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<p><b>OBJECTIVE</b>To investigate the possible roles of MT1M gene on the cell cycle and signaling pathway of Hep-G2.</p><p><b>METHODS</b>Hep-G2 human hepatoma cells made by transfection with expressible MT1M gene, and the cell cycle was detected by flow cytometry, and the signaling pathway was measured by dual luciferase assay in Hep-G2 cells.</p><p><b>RESULTS</b>MT1M gene was able to induce changes of the cell cycle and the activation of NF-kappaB pathway in Hep-G2 cells.</p><p><b>CONCLUSION</b>MT1M gene may affect the cell cycle in Hep-G2 and activate the NF-kappaB-dependent transcription.</p>
Assuntos
Humanos , Linhagem Celular Tumoral , Citometria de Fluxo , Fase G2 , Fisiologia , Neoplasias Hepáticas , Patologia , Metalotioneína , Genética , NF-kappa B , Metabolismo , Plasmídeos , Genética , Transdução de Sinais , Fisiologia , TransfecçãoRESUMO
A Review The diseases caused by endotoxin have seriously affected human health. Previous studies have shown that p38 MAPK pathway is involved in the intracellular signal transduction induced by lipopolysaccharide (LPS), which plays an important role in the activation of inflammation-related cells to release inflammation mediator. Recently there have been some progresses in the isoforms distribution, substrate, molecular mechanism of regulating the release of inflammatory mediators, cellular specific activation and levels of p38 MAPK. [
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AIM: To investigate the effect of epigallocatechin-3-gallate (EGCG) on lipopolysaccharide (LPS)-induced p38 MAPK activation and tumor necrosis factor-? (TNF-?) secretion in macrophages. METHODS: Western blotting was used to detect the phosphorylation of p38 MAPK in mouse macrophages cultured in vitro. Enzyme linked immunosorbent assay was used to determine the secretion of TNF-? in macrophages. Electron microscopy was used to study the effect of EGCG on the structure of LPS. RESULTS: LPS caused activation of p38 MAPK and more production of TNF-?, EGCG inhibited LPS-induced phosphorylation of p38 MAPK and TNF-? production and had no effect on the structure of LPS. CONCLUSIONS: EGCG has no direct effect on LPS, but blocks cellular signal pathway. The inhibition of EGCG on LPS-induced TNF-? production is mediated, at least in part, through blocking of p38 MAPK pathway. [
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The structure, karyotype and behavior of synaptonemal complex (SC) in the spermatocytes of hedgehog (Erinaceus euroaaus dealbatus (insectivora)) were analyzed by light and electron microscopy with a modified surface spread preparation which involves the use of sodium dodecyl-sulphate (SDS) and silver staining. The lateral elements of the synaptonemal complex have a constant width of about 50 nm, the distance between the two lateral elements is about 100 nm. The relative length and arm rationale constant for each autosomal SC. The relative length and arm ratio constant for ea of the autosomal SCs are very similar to that of mitotic autosome.The X and Y chromosome axes have a clear morphological distinction from the autosomal SC. The axes of X and Y chromosome pair and form a SC of certain length at pachytene stage. The axes of unpaired X and Y chromosome are heteropycnotic and display various morphological complexities. But these differentiations in hedgehog are primary than in other mammalians, such as human and mice. At pachytene stage the X and Y chromosome display an extensive side-by-side pairing segment with decreasing length as meiotic prophase progressed.
