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[ Last edited by cheungsober on 2009-12-9 at 10:11 ]

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goodtimega

Ìú¸Ëľ³æ (ÖøÃûдÊÖ)

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cheungsober(½ð±Ò+20,VIP+0):лл£¬°ïÖú 12-9 11:34
Fluoride poisoning presents a serious public health problem in many regions. The prevention and treatment of endemic diseases has been the national thrust. Endemic fluorosis to fluoride elements in the abnormal accumulation of bone tissue leads to increased bone turnover characterized mainly for dental fluorosis and fluoride bone disease. Currently, the pathogenesis of skeletal fluorosis is not fully understood.
2Â¥2009-12-09 10:25:19
ÒÑÔÄ   »Ø¸´´ËÂ¥   ¹Ø×¢TA ¸øTA·¢ÏûÏ¢ ËÍTAºì»¨ TAµÄ»ØÌû

goodtimega

Ìú¸Ëľ³æ (ÖøÃûдÊÖ)

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cheungsober(½ð±Ò+30,VIP+0):лл£¬ÄãµÄÓ¢ÓïÊÇÔõôÁ·³öÀ´µÄ 12-9 11:36
MCM3 proteins involve in cell division cycle and cell proliferation is sensitive to molecular signature [1]. Low doses of laser irradiation can result in vitro rat osteoblast MC3T3-E1 in the increase of the expression of MCM3 mRNA and the Ershi DNA replication [2]. Researchers [3-6] have found that osteoblasts exposed to fluoride endoplasmic reticulum swelling are resistant to protein synthesis. Local scholars have found that by using proteomics technology osteoblasts exposed to fluoride are closely related to protein folding and molecular chaperones such as heat shock protein 70 (HSP70) and protein disulfide isomerase (PDI) with increased expression [7]. They are related to the oxidation of intracellular protein folding, an endoplasmic reticulum stress response (endoplastic reticulum stress, ERS) of the signal molecule. Within the endoplasmic reticulum stress the endoplasmic reticulum molecular chaperone (BIP, also known as GRP78) and other expression increase.  The endoplasmic reticulum stress-specific transcription factor CHOP (also known as GADDl53) notably up-regulates expression of the main features [8]. In this regard, Hamamura et al [9] indicated that endoplasmic reticulum stress on osteoblast bi-directional stimulus.  Short period of time can promote osteoblast proliferation and the promotion of runx2/osterix with increased expression of collagen ¢ñ.  As the long one inhibits osteoblast cell growth, osteoblasts runx2/osterix decrease expression of collagen I.  Obviously in MCM3, endoplasmic reticulum stress can regulate osteoblast growth. Active function of osteoblasts (bone cell proliferation, hypertrophy, and active osteoblasts) in the skeletal fluorosis is a disease than happens at early stage, and plays an important role in the link [10].
3Â¥2009-12-09 10:32:46
ÒÑÔÄ   »Ø¸´´ËÂ¥   ¹Ø×¢TA ¸øTA·¢ÏûÏ¢ ËÍTAºì»¨ TAµÄ»ØÌû

goodtimega

Ìú¸Ëľ³æ (ÖøÃûдÊÖ)

cheungsober(½ð±Ò+1,VIP+0):лл£¬°¦£¬ÏòÄúѧϰ 12-9 11:36
cheungsober(½ð±Ò+1,VIP+0):ºÜÃ÷ÏÔÊÇÈí¼þ·­ÒëµÄ 12-9 11:39
zap65535(½ð±Ò-2,VIP+0):¾Ý˵Äú¾­³£Éó¸å...... 12-23 10:02
Using fluorescence quantitative PCR and immunohistochemical method, Near-Jie Zhong et al [11,12] showed that fluoride acts on osteoblastic cells that can affect the MCM3 gene expression.  For MCM3 in osteogenic cells fluorine can promote an increasingly essential role and is of diagnostic importantce, for which protein levels need to be verified. Based on these studies and the associated assumptions, osteoblasts exposed to fluoride after the endoplasmic reticulum stress may be correlated to MCM3 through a common regulation of osteoblast proliferation. Currently it is capable of separating the mechanism for the fluoride osteoblasts endoplasmic reticulum stress that has not been reported. In the present study, fluoride in vitro is proposed to verify the simultaneous detection of the MCM3 endoplasmic reticulum stress-related genes Bip, Xbp-1, CHOP, and MCM3.  For genes in bone cells and protein expression, primary investigation has been conducted for the relationship between the two characteristics.
4Â¥2009-12-09 10:39:15
ÒÑÔÄ   »Ø¸´´ËÂ¥   ¹Ø×¢TA ¸øTA·¢ÏûÏ¢ ËÍTAºì»¨ TAµÄ»ØÌû
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