• Journal of Korean Physical Therapy Science
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• v.8 no.2
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• pp.997-1003
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• 2001

The purpose of this study is to know the average of pint range of motion and difference according to the aging for the elderly, This study consisted of elder male(n=75) and elder female(n=l09), The result of assessment and analysis in shoulder pint range of motion are as follows: 1) The average shoulder flexion pint range of motion in 60-69(from sixty to sixty-nine)years old are 163.04(Left-Male), 162.91(Right-Male), 158.74 (Left-Female), 158.74 (Right-Female). 70-79years old are 149.40(L-M), 152.38(R-M), 153,37(L-F), 153.37(R-F). 80-89 years old are 149.57(L-M), 147.93(R-M), 151.17(L-F), 150.33(R-F). There was no significant difference among group, 2) The average shoulder extension pint range of motion in 60-69years old are 48.15(L-M), 47.20(R-M), 45.16(L-F), 44.23(R-F), 70-79years old are 37.l1(L-M), 38.70(R-M), 35.17(L-F), 36.71(R-F), 80-89 years old are 34.46(L-M). 36.71(R-M), 33.90(L-F), 33.09(R-F). There was significant difference among group(p<.05). 3) The average shoulder abduction pint range of motion in 60-69years old are 164.22(L-M), 165.96(R-M), 159.34(L-F), 159.97(R-F), 70-79years old are 152.27(L-M), 155.05(R-M), 152.32(L-F), 53.66(R-F), 80-89 years old are 152.17(L-M), 153.76(R-M), 147.53(L-F), 147.37(R-F). There was significant difference in right shoulder abduction among group(p<05). 4) The average shoulder internal rotation pint range of motion in 60-69years old are 63.52(L-M), 65.70(R-M), 64.16(L-F), 64.61(R-F), 70-79years old are 64.50(L-M), 65.81(R-M) 61.10(L-F), 61.83(R-F). 80-89 years old are 61.60(L-M), 61.66(R-M), 57.53(L-F), 57.53(R-F). There was no significant difference among group. 5) The average shoulder external rotation pint range of motion in 60-69years old are 50.87(L-M), 50.22(R-M), 51.03(L-F), 50.42(R-F), 70-79years old are 50.91(L-M), 50.20(R-M) 48.37(L-F), 50.20(R-F). 80-89 years old are 46.83(L-M), 47.93(R-M), 43.43(L-F), 43.72(R-F).There was significant difference in left shoulder external rotation among group(p<.05).

• Kyungpook Mathematical Journal
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• v.53 no.1
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• pp.117-124
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• 2013

We show that for 1 < $p$ < ${\infty}$, $k$, $m{\in}\mathbb{N}$, $n^{(k)}(l_p)=inf\{n^{(k)}(l^m_p):m{\in}\mathbb{N}\}$ and that for any positive measure ${\mu}$, $n^{(k)}(L_p({\mu})){\geq}n^{(k)}(l_p)$. We also prove that for every $Q{\in}P(^kl_p:l_p)$ (1 < $p$ < ${\infty}$), if $v(Q)=0$, then ${\parallel}Q{\parallel}=0$.

• Journal of the Korean Chemical Society
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• v.53 no.1
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• pp.90-94
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• 2009

• Animal cells and systems
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• v.8 no.3
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• pp.205-212
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• 2004

The tumor suppressor protein p53 is stabilized by the herpes-virus-associated ubiquitin-specific protease (HAUSP), a deubiquitinating enzyme. We previously isolated and characterized a mouse orthologue of HAUSP, mHAUSP. mHAUSP cDNA consisted of 3,312 bp encodes 1,103 amino acids with a molecular weight of approximately 135 kDa containing highly conserved Cys, Asp (I), His, and Asn/Asp (II) domains. In this study, we carried out site-directed mutagenesis of 6 conserved amino acids (Cys224, Gln231, Asp296, His457, His465, and Asp482) in Cys box, QQD box, and His box. Interestingly, the conserved Gln 231 was not essential for the catalytic activity of mHAUSP. However, the other conserved amino acids were required for deubiquitinating activity of mHAUSP. We performed isopeptidase assay and confirmed that mHAUSP is able to remove ubiquitin from ubiquitinated substrates. In addition, we observed that mHAUSP induces apoptosis in HeLa cells.

• Environmental Mutagens and Carcinogens
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• v.24 no.3
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• pp.113-120
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• 2004

Chromium compounds are known human and animal carcinogens. In this study, the effects of sodium chromate on apoptosis and cell cycle were investigated in order to unveil the elements of early cellular responses to the metal. Using Chinese hamster ovary cells(CHO-K1-BH4), we found taht chromium (VI) treatment induced apoptosis in these cells, as signified by nuclear fragmentation, DNA laddering on agarose gel electrophoresis, and an increased proportionof cells with hypodiploid DNA. Preceding these changes, chromium (VI) treatment increased caspase 3 pritease activity and also increased expression of p53 protein, while the level of bcl2 protein was not changed. Coincubation with caspase inhibitor, Z-DEVD-FMK, inhibited chromium-induced apoptosis. In the flow cytometric analysis using propidium iodide fluorescence, an increase of cell population in G2/M phase was shown in cells exposed to at least 160 $\mu\textrm{m}$ of sodium chromate for 72h, form 9.8% for 0$\mu\textrm{m}$ chromium (VI) to 26.4% for 320$\mu\textrm{m}$ chromium(VI). Taken together, these findings suggest that chromium(VI)-induced apoptosis is accompanied by G2/M cell cycle arrest, and that p53-mediated pathway may be involved in positive regulation of G2/M arrest and a concurred apoptosis in CHO cells.

• Bulletin of the Korean Mathematical Society
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• v.53 no.6
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• pp.1909-1911
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• 2016

In this note we point out some mistakes in a recent paper by M. Nunokawa et al. [Bull. Korean Math. Soc. 53 (2016), no. 1, 215-225].

• Biomedical Science Letters
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• v.14 no.3
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• pp.157-165
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• 2008

Recently, the number of patients with prostate cancer has been increased gradually by both the change of living environment and the increase of aged population. In this study the serum prostate specific antigen (PSA) level was compared to the Gleason score known as a prognostic factor for the prostate cancer. In the Gleason score 6 and $9{\sim}10$, the average age was 69.68 years old and 69.52 years old, respectively and there was no statistically difference in both of age and Gleason score. the PSA serum consistency appeared <4 ng/mL as example 1, $4{\sim}20ng/mL$ as example 17 and ${\geq}20ng/mL$ as example 4 in the Gleason score 6, and In the Gleason score $9{\sim}10$, it appeared <4 ng/mL as example 1, $4{\sim}20ng/mL$ as example 6 and ${\geq}20ng/mL$ as example 15. PSA serum consistency in the Gleason score $9{\sim}10$ showed higher value than those of Gleason score 6 (P<0.05). Next, expression ratios of bcl-2, Ki-67 and p53 were examined in the Gleason score 6 and $9{\sim}10$. the p53 expression ratio, a tumor suppression gene, appeared the significance statistically by the classification of the Gleason score as example 7 (28%) in the Gleason score 6 and as example 16 (64%) in the Gleason score $9{\sim}10$ (P<0.05). but not different in the expression ratios of the Ki-67 and bcl-2. The expression ratio of p53 by the expression ratio of bcl-2 and the expression ratio of Ki-67 by the expression ratio of p53 had a positive relationship in all of the Gleason score 6 and the Gleason score $9{\sim}10$ (P<0.05). However, the expression ratio of Ki-67 by the expression ratio of bcl-2 did not show any significance in the Gleason score $9{\sim}10$ (P<0.05). Therefore, the results suggested that p53 expression could be used as an independent prognostic factor.

• Journal of the Korean Mathematical Society
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• v.53 no.2
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• pp.403-414
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• 2016

Let R be a ring, and let M be a left R-module. If M is Rad-supplementing, then every direct summand of M is Rad-supplementing, but not each factor module of M. Any finite direct sum of Rad-supplementing modules is Rad-supplementing. Every module with composition series is (Rad-)supplementing. M has a Rad-supplement in its injective envelope if and only if M has a Rad-supplement in every essential extension. R is left perfect if and only if R is semilocal, reduced and the free left R-module $(_RR)^{({\mathbb{N})}$ is Rad-supplementing if and only if R is reduced and the free left R-module $(_RR)^{({\mathbb{N})}$ is ample Rad-supplementing. M is ample Rad-supplementing if and only if every submodule of M is Rad-supplementing. Every left R-module is (ample) Rad-supplementing if and only if R/P(R) is left perfect, where P(R) is the sum of all left ideals I of R such that Rad I = I.

• Journal of Ginseng Research
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• v.40 no.1
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• pp.47-54
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• 2016

Background: The roots of Panax ginseng contain noble tetracyclic triterpenoid saponins derived from dammarenediol-II. Dammarene-type ginsenosides are classified into the protopanaxadiol (PPD) and protopanaxatriol (PPT) groups based on their triterpene aglycone structures. Two cytochrome P450 (CYP) genes (CYP716A47 and CYP716A53v2) are critical for the production of PPD and PPT aglycones, respectively. CYP716A53v2 is a protopanaxadiol 6-hydroxylase that catalyzes PPT production from PPD in P. ginseng. Methods: We constructed transgenic P. ginseng lines overexpressing or silencing (via RNA interference) the CYP716A53v2 gene and analyzed changes in their ginsenoside profiles. Result: Overexpression of CYP716A53v2 led to increased accumulation of CYP716A53v2 mRNA in all transgenic roots compared to nontransgenic roots. Conversely, silencing of CYP716A53v2 mRNA in RNAi transgenic roots resulted in reduced CYP716A53v2 transcription. HPLC analysis revealed that transgenic roots overexpressing CYP716A53v2 contained higher levels of PPT-group ginsenosides ($Rg_1$, Re, and Rf) but lower levels of PPD-group ginsenosides (Rb1, Rc, $Rb_2$, and Rd). By contrast, RNAi transgenic roots contained lower levels of PPT-group compounds and higher levels of PPD-group compounds. Conclusion: The production of PPD- and PPT-group ginsenosides can be altered by changing the expression of CYP716A53v2 in transgenic P. ginseng. The biological activities of PPD-group ginsenosides are known to differ from those of the PPT group. Thus, increasing or decreasing the levels of PPT-group ginsenosides in transgenic P. ginseng may yield new medicinal uses for transgenic P. ginseng.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.9
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• pp.4101-4107
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• 2014

Protein phosphatase 1 (PP1) is a major serine/threonine phosphatase that controls gene expression and cell cycle progression. The active mutant IPP5 ($8-60hIPP5^m$), the latest member of the inhibitory molecules for PP1, has been shown to inhibit the growth of human cervix carcinoma cells (HeLa). In order to elucidate the underlying mechanisms, the present study assessed overexpression of $8-60hIPP5^m$ in HeLa cells. Flow cytometric and biochemical analyses showed that overexpression of $8-60hIPP5^m$ induced G2/M-phase arrest, which was accompanied by the upregulation of cyclin B1 and phosphorylation of G2/M-phase proteins ATM, p53, $p21^{cip1/waf1}$ and Cdc2, suggesting that $8-60hIPP5^m$ induces G2/M arrest through activation of the ATM/p53/$p21^{cip1/waf1}$/Cdc2/cyclin B1 pathways. We further showed that overexpression of $8-60hIPP5^m$ led to delayed nuclear translocation of cyclin B1. $8-60hIPP5^m$ also could translocate to the nucleus in G2/M phase and interact with $pp1{\alpha}$ and Cdc2 as demonstrated by co-precipitation assay. Taken together, our data demonstrate a novel role for $8-60hIPP5^m$ in regulation of cell cycle in HeLa cells, possibly contributing to the development of new therapeutic strategies for cervix carcinoma.