• Journal of Welding and Joining
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• v.14 no.1
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• pp.38-46
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• 1996

High temperature low cycle fatigue crack growth behavior is investigated over a range of two temperatures and various frequencies in SUS 304 stainless steel. It is found that low frequency and temperature can enhance time-dependent crack growth. With high temperature, low frequency and long crack length, ${\Delta}J_c/{\Delta}J_ f$, the ratio of creep J integral range to fatigue J integral range is increased and time-dependent crack growth is accelerated. Interaction between ${\Delta}J_f$ and ${\Delta}J_c$ is occured at high frequency and low temparature and ${\Delta}J_c$, creep J integral range is fracture mechanical parameter on transition from cycle-dependent to time dependent crack growth in creep temperature region.

• Transactions of the Korean Society of Mechanical Engineers
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• v.9 no.5
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• pp.539-547
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• 1985

The low-cycle fatigue crack growth behavior of SUS 304 Stainless steel was investigated at 650.deg. C by the nonlinear fracture mechanics. Crack Propagation can be separated in to cycle-dependent and time-dependent, the former is correlated with .DELTA. $J_{f}$ , J-intergral range and the latter is correlated with J', modified J integral. Transition from cycle-dependent to time-dependent crack growth was successfully predicted using the .betha. hypothesis, which was proposed by the authors on the basis of an analysis on the interaction of elastic and creep strain. To investigate the reliability of .betha.-hypothesis, experimenting by the change of stress-level, stress rate and frequency, following conclusions were obtained. (1) High temperature fatigue crack propagation was separated into cycle-dependent and time-dependent. (2) Transition of crack propagation was predicted by .DELTA. $J_{c}$/.DELTA.$_{f}$ or .betha. (3) Lower limit in cycle-dependent crack propagation was obtained..

• BMB Reports
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• v.33 no.2
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• pp.103-111
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• 2000

Phosphorylation of the eukaryotic elongation factor 2 (eEF-2) blocks the elongation step of translation and stops overall protein synthesis. Although the overall rate of protein synthesis in mitosis reduces to 20% of that in S phase, it is unclear how the protein translation procedure is regulated during the cell cycle, especially in the stage of peptide elongation. To delineate the regulation of the elongation step through eEF-2 function, the changes in phosphorylation of eEF-2, and in activity of corresponding $Ca^{2+}$/calmodulin (CaM)-dependent protein kinase III (CaMK-III) during the cell cycle of NIH 3T3 cells, were determined. The in vivo level of phosphorylated eEF-2 showed an 80% and 40% increase in the cells arrested at G1 and M, respectively. The activity of CaMK-III also changed in a similar pattern, more than a 2-fold increase when arrested at G1 and M. The activity change of the kinase during one turn of the cell cycle also demonstrated the activation at G1 and M phases. The activity change of cAMP-dependent protein kinase (PKA) was reciprocal to that of CaMK-III. These results indicated: (1) the activity of CaMK-III was cell cycle-dependent and (2) the level of eEF-2 phosphorylation followed the kinase activity change. Therefore, the elongation step of protein synthesis might be cell cycle dependently regulated.

• Transactions of the Korean Society of Mechanical Engineers
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• v.18 no.3
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• pp.548-554
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• 1994

The high temperature fatigue crack growth behavior of SUS 304 stainless steel at $550^{\circ}C$ and $650^{\circ}C$ was investigated under various kinds of stress ratio and frequency in sinusoidal waveform on the basis of the non-linear fracture mechanics. The result arranging crack growth rate by modified J-integral J' showed influence of stress ratio and frequency. All the data obtained under the test at $550^{\circ}C$ were plotted within data band of da/dN-${\triangle}J_f$ relationship for cycle-dependent crack growth. On the basis of static creep and cycle-dependent data band; both time- and cycle-dependent crack growth behavior was observed under loading conditions at $650^{\circ}C$, but cycle-dependent crack growth behavior predominantly appeared and time-dependent crack growth behaviour was little observed under loading conditions at $550^{\circ}C$. Fractographic examinations for fracture surface indicated that the fracture mode was generally transgranular. The stripes were found on fracture surface and each stripe was accompanied by a crack tip blunting and an abrupt increase in the load-point displacement. The $J'_{an}$ had a validity in case of $650^{\circ}C, but scarcely had it in case of $550^{\circ}C$.

• YAKHAK HOEJI
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• v.46 no.1
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• pp.18-23
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• 2002

Ailanthus altissima has been used to settle an upset stomach, to alleviate a fever and as an insecticide. We reported that the water extract of A. altissima induced apoptotic cell death in Jurkat T-acute Iymphoblastic leukemia cells. Here, we showed the dose-dependent inhibitions of cell viability by the extract, as measured by cell morphology. The cell cycle control genes are considered to play important roles in tumorigenesis. The purpose of the present study is also to investigate the effect of A. altissima on cell cycle progression and its molecular mechanism in the cells. The level of p21 protein was increased after treatment of the extract, whereas both Bcl-2 and Bax protein levels were not changed. These results suggest that A. altissima induces apoptotic cell death via p21-dependent signaling pathway in Jurkat cells which delete wild type p53. Gl checkpoint related gene products tested (cyclin D3, cyclin dependent kinase 4, retinoblastoma, E2Fl) were decreased in their protein levels in a dose-dependent manner after treatment of the extract Taken together, these results indicate that the increase of apoptotic cell death by A. altissima may be due to the inhibition of cell cycle in Jurkat cells.

• BMB Reports
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• v.36 no.1
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• pp.60-65
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• 2003

Cancer is frequently considered to be a disease of the cell cycle. As such, it is not surprising that the deregulation of the cell cycle is one of the most frequent alterations during tumor development. Cell cycle progression is a highly-ordered and tightly-regulated process that involves multiple checkpoints that assess extracellular growth signals, cell size, and DNA integrity. Cyclin-dependent kinases (CDKs) and their cyclin partners are positive regulators of accelerators that induce cell cycle progression; whereas, cyclin-dependent kinase inhibitors (CKIs) that act as brakes to stop cell cycle progression in response to regulatory signals are important negative regulators. Cancer originates from the abnormal expression of activation of positive regulators and functional suppression of negative regulators. Therefore, understanding the molecular mechanisms of the deregulation of cell cycle progression in cancer can provide important insights into how normal cells become tumorigenic, as well as how cancer treatment strategies can be designed.

• Journal of Ocean Engineering and Technology
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• v.9 no.2
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• pp.98-111
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• 1995

High temperature low cycle fatigue shows that cycle-dependent crack growth owing to cyclic plastic deformation occurred simultaneosly with time-dependent crack growth owing to intergranular deformation. Consequently, to estimate crack growth rate uniquely, many to investigators have proposed various kinds of parameters and theories but these could not produce satisfactory results. Therefore the goal of this study is focused on prediction of crack growth rate using predominant damage rule, linear cumulative damage rule and transitional parameter ${\Delta}J_c/{\Delta}J_f$. On the basis of these sinusoidal loading waveform at 600$^{\circ}C$ and 700$^{\circ}C$.

• BMB Reports
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• v.34 no.3
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• pp.212-218
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• 2001

Although the blockage of a cell cycle by specific inhibitors of $Ca^{2+}/$calmodulin-dependent protein kinase II (CaMK-II) is well known, the activity profile of CaMK-II during the cell cycle in the absence of any direct effectors of the enzyme is unclear. The activity of native CaMK-II in NIH 3T3 cells was examined by the use of cell cycle-specific arresting and synchronizing methods. The total catalytic activity of CaMK-II in arrested cells was decreased about 30% in the M phase, whereas the $Ca^{2+}$-independent autonomous activity increased about 1.5-fold in the M phase and decreased about 50% at the G1/S transition. The in vivo phosphorylation level of CaMK-II was lowest at G1/S and highest in M. The CaMK-II protein level was unchanged during the cell cycle. When the cells were synchronized, the autonomous activity was increased only in M. These results indicate that the physiologically relevant portion of CaMK-II is activated only in M, and that the net activation of CaMK-II is required in mitosis.

• The Korean Journal of Zoology
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• v.23 no.2
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• pp.61-68
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• 1980

Quantitative analysis of the activities of transport ATPases as well as alkaline phosphatase of the mouse uterus was carried out during the estrous cycle. Even though the proportional patterns of the enzyme activities were similar each another between the stages of estrous cycle, the absolute activities of the enzymes except $K^+$-dependent and $Na^+$, $K^+$-activated ATPases at the time of estrus were significantly (p<0.025) higher than that at any other time of the estrous cycle. That is, the activities of $K^+$-dependent and $Na^+$, $K^+$-activated ATPases were negligible during the period of time from diestrus to estrus while the little activities (0.04 $\\sim$ 0.05$\\mu$M/mg protein/hr in average, $6\\sim7$% of the total enzyme activity) of these enzymes appeared at the time of metaestrus. On the other hand, at the time of estrus, the activities of $Mg^++$-dependent phosphatase, transport ATPase and alkaline phosphatase were rapidly and tremendously increased to be 0.69 (35%), 0.42 (21%) and 1.58 (79%), respectively. The activity of alkaline phosphatase was in the range of 0.60 $\\sim$ 1.58 (79 $\\sim$ 90%) and predominant throughout the estrous cycle. The activity of $Mg^++$-dependent alkaline phosphatase was estimated as 12 $\\sim$ 16% of the total enzyme activity. Therefore, it is assumed likely that $K^+$-dependent and $Na^+$, $K^+$-activated ATPases are not the main factors to control the fluid accumulation at the time of estrus, but may be the factors to reabsorb the luminal fluid into the uterine epithelium at the time of metaestrus, and that $Mg^++$-dependent phosphatase, transport ATPase and alkaline phosphatase must be closely involved in the secretion of luminal fluid from the epithelial cells of the mouse uterus.

• Laboraroty Animal Research
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• v.34 no.4
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• pp.264-269
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• 2018

Cell cycle dysfunction can cause severe diseases, including neurodegenerative disease and cancer. Mutations in cyclin-dependent kinase inhibitors controlling the G1 phase of the cell cycle are prevalent in various cancers. Mice lacking the tumor suppressors $p16^{Ink4a}$ (Cdkn2a, cyclin-dependent kinase inhibitor 2a), $p19^{Arf}$ (an alternative reading frame product of Cdkn2a,), and $p27^{Kip1}$ (Cdkn1b, cyclin-dependent kinase inhibitor 1b) result in malignant progression of epithelial cancers, sarcomas, and melanomas, respectively. Here, we generated knockout mouse models for each of these three cyclin-dependent kinase inhibitors using engineered nucleases. The $p16^{Ink4a}$ and $p19^{Arf}$ knockout mice were generated via transcription activator-like effector nucleases (TALENs), and $p27^{Kip1}$ knockout mice via clustered regularly interspaced short palindromic repeats/CRISPR-associated nuclease 9 (CRISPR/Cas9). These gene editing technologies were targeted to the first exon of each gene, to induce frameshifts producing premature termination codons. Unlike preexisting embryonic stem cell-based knockout mice, our mouse models are free from selectable markers or other external gene insertions, permitting more precise study of cell cycle-related diseases without confounding influences of foreign DNA.