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Zbigniew Gronostajski,Marek Hawryluk,Marcin Kaszuba,Paweł Widomski,Jacek Ziemba 한국자동차공학회 2017 International journal of automotive technology Vol.18 No.4
This study is focused on tools used in the industrial hot forging process of a front wheel forging (eventually – gear wheel) manufactured for the automotive industry. Four different variants were applied for the tools: 2 die inserts were coated with two different hybrid layers (GN + PVD type), i.e. AlCrTiN and AlCrTiSiN, one insert was only nitrided, and one was pad welded, to improve tool durability. The tool wear was analysed and represented by the material degradation on the working surface, based on the 3D scanning and the material growth of the periodically collected forgings. Additionally, the scanned tools were divided into two areas, in which it was found, based on the reliminary analysis, that various degradation mechanisms are predominant. Microstructural and hardness measurements of the analyzed tools were also performed. Based on the results, it was found that, in the central part of the die insert (area A), thermo-mechanical fatigue and wear occurred, while in the area of the bridge insert (area B), only abrasive wear could be observed. For these areas (A and B), the loss of material was determined separately. In area A for the inserts with hybrid layer GN+AlCrTiSiN and gas nitrided, an intensive increase of wear took place, which was not observed for the pad welded and GN+AlCrTiN layer insert, for which, together with the increase of the forging number, a proportional growth of the loss of material occurred. In area B the weakest results were obtained for the insert with GN+AlCrTiSiN layer, while wear of other die inserts grew similar and proportional.
상아모세포 분화과정에서 nuclear factor I - C 의 역할
배현숙,김홍중,정문진,박민주,안성민,Gronostajski RM2,박주철 대한구강악안면병리학회 2005 대한구강악안면병리학회지 Vol.29 No.2
Nuclear factor 1 (NFI) was discovered as a protein required for adenovirus DNA replication in vitro, but it is now clear that NFI protein plays an important role in the expression of many cellular genes. NFI-C null mice demonstrated aberrant odontoblast differentiation, abnormal dentin formation, and thus molar lacking roots while other tissues/or gans in the body, including ameloblasts appear to be unaffected and normal. However, little is known about the mechanism of NFI -C function in odontoblast differentiation and dentin formation. In this study, in order to elucidate the molecular mechanisms of odntoblast differentiation, we examined morphological characteristics of the aberrant odontoblast in NFI-C null mice. we also evaluate the expression of dentin sialophosphoprotein (DSPP) and bone sialoprotein (BSP) mRNAs in the MDPC-23 cells by northern analysis after over-expression and inactiγation of NFI -C into mouse MDPC-23 cells Odontoblasts of the NFI-C null mouse were round in shape, lost their polarity, organized as a sheet of cells, and trapped in osteodentin-like mineralized tissue. Abnormal odontoblasts of NFI-C null mouse revealed the absence of an intercellular junctional complex known as the t erminal webs. MDPC-23 cells started to express DSPP mRNA beginning from the postnatal day of 14 and showed a steady increase as differentiating into odontoblasts. Over-expression of NFI -C increased the expression of DSPP mRNA. Inactivation of NFI - C induced BSP mRNA expression. These results suggest that NFI-C plays an important role in odontoblast differentiation in a cell-type specific manner and thus in dentin formation
Lee, Tae-Yeon,Lee, Dong-Seol,Kim, Hyun-Man,Ko, Jea Seung,Gronostajski, Richard M.,Cho, Moon-Il,Son, Ho-Hyun,Park, Joo-Cheol SAGE Publications 2009 The Journal of histochemistry and cytochemistry Vol.57 No.5
<P>We reported previously that Nfic-deficient mice exhibit short and abnormal molar roots and severely deformed incisors. The objective of this study is to address the mechanisms responsible for these changes using morphological, IHC, and RT-PCR analysis. Nfic-deficient mice exhibited aberrant odontoblasts and abnormal dentin formation in molar roots and the labial crown analog of incisors. The most striking changes observed in these aberrant odontoblasts were the loss of intercellular junctions and the decreased expression of ZO-1 and occludin. As a result, they became dissociated, had a round shape, and lost their cellular polarity and arrangement as a sheet of cells. Furthermore, the dissociated odontoblasts became trapped in dentin-like mineralized tissue, resembling osteodentin in the overall morphology. These findings suggest that loss of the Nfic gene interferes with the formation of intercellular junctions that causes aberrant odontoblast differentiation and abnormal dentin formation. Collectively, these changes in odontoblasts contributed to development of molars with short and abnormal roots in Nfic-deficient mice.</P>
Lee, Dong-Seol,Park, Jong-Tae,Kim, Hyun-Man,Ko, Jea Seung,Son, Ho-Hyun,Gronostajski, Richard M,Cho, Moon-Il,Choung, Pill-Hoon,Park, Joo-Cheol American Society for Biochemistry and Molecular Bi 2009 The Journal of biological chemistry Vol.284 No.25
<P>Our previous studies have demonstrated that nuclear factor I-C (NFI-C) null mice developed short molar roots that contain aberrant odontoblasts and abnormal dentin formation. Based on these findings, we performed studies to elucidate the function of NFI-C in odontoblasts. Initial studies demonstrated that aberrant odontoblasts become dissociated and trapped in an osteodentin-like mineralized tissue. Abnormal odontoblasts exhibit strong bone sialoprotein expression but a decreased level of dentin sialophosphoprotein expression when compared with wild type odontoblasts. Loss of Nfic results in an increase in p-Smad2/3 expression in aberrant odontoblasts and pulp cells in the subodontoblastic layer in vivo and primary pulp cells from Nfic-deficient mice in vitro. Cell proliferation analysis of both cervical loop and ectomesenchymal cells of the Nfic-deficient mice revealed significantly decreased proliferative activity compared with wild type mice. In addition, Nfic-deficient primary pulp cells showed increased expression of p21 and p16 but decreased expression of cyclin D1 and cyclin B1, strongly suggesting cell growth arrest caused by a lack of Nfic activity. Analysis of the pulp and abnormal dentin in Nfic-deficient mice revealed an increase in apoptotic activity. Further, Nfic-deficient primary pulp cells exhibited an increase in caspase-8 and -3 activation, whereas the cleaved form of Bid was hardly detected. These results indicate that the loss of Nfic leads to the suppression of odontogenic cell proliferation and differentiation and induces apoptosis of aberrant odontoblasts during root formation, thereby contributing to the formation of short roots.</P>