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Expression of Wnt Target Genes in Solid Pseudopapillary Tumor of the Pancreas: A Pilot Study
Kang, Chang Moo,Kim, Hyun Ki,Kim, Hoguen,Choi, Gi Hong,Kim, Kyung Sik,Choi, Jin Sub,Lee, Woo Jung Lippincott Williams Wilkins, Inc. 2009 PANCREAS Vol.38 No.2
OBJECTIVES:: Solid pseudopapillary tumor (SPT) of the pancreas is very rare. This study was performed to analyze the expression of Wnt signal target genes (matrix metalloproteinase-7 [MMP-7], cyclin-D1, and c-myc) and Ki-67 in resected SPTs to determine their clinicopathologic characteristics according to their expression. METHODS:: From January 1995 to December 2005, 23 patients underwent pancreatic resections for SPT of the pancreas. Among 23 formalin-fixed, paraffin-embedded tissues, 12 were evaluated as a pilot study. Immunohistochemistry was performed using various detection and antigen retrieval methods to detect MMP-7, cyclin-D1, c-myc, and Ki-67. The expression of Wnt target genes was correlated with clinicopathologic features of the patients. RESULTS:: Solid pseudopapillary tumors of the pancreas always showed cytoplasmic/nuclear accumulation of &bgr;-catenin, frequent expression of cyclin-D1, and low proliferation index. MMP-7, cyclin-D1, c-myc, and Ki-67 were not correlated with microscopic features suggesting malignant potential (P > 0.05). Tumor size was closely related to microscopic features of malignant potential and apparently has an inverse relationship with the expression of cyclin-D1 and Ki-67 (P < 0.05). CONCLUSIONS:: Low proliferative index and associated MMP-7 expression may cause an unpredictable clinical course in this tumor. Subtle changes in the intracellular environment, not pathologic (morphologic) changes, may elucidate the unpredictable clinical course of this tumor.
Yoo, Dae Young,Shin, Bich Na,Kim, In Hye,Kim, Woosuk,Kim, Dae Won,Yoo, Ki-Yeon,Choi, Jung Hoon,Lee, Choong Hyun,Yoon, Yeo Sung,Choi, Soo Young,Won, Moo-Ho,Hwang, In Koo Kluwer Academic/Plenum Publishers 2012 Neurochem Res Vol.37 No.2
<P>Oxidative stress is one of the most important factors in reducing adult hippocampal neurogenesis in the adult brain. In this study, we observed the effects of Cu,Zn-superoxide dismutase (SOD1) on lipid peroxidation, cell proliferation, and neuroblast differentiation in the mouse dentate gyrus using malondialdehyde (MDA), Ki67, and doublecortin (DCX), respectively. We constructed an expression vector, PEP-1, fused PEP-1 with SOD1, and generated PEP-1-SOD1 fusion protein. We administered PEP-1 and 100 or 500 관g PEP-1-SOD1 intraperitoneally once a day for 3 weeks and sacrificed at 30 min after the last administrations. PEP-1 administration did not change the MDA levels compared to those in the vehicle-treated group, while PEP-1-SOD1 treatment significantly reduced MDA levels compared to the vehicle-treated group. In the PEP-1-treated group, the number of Ki67-positive nuclei was similar to that in the vehicle-treated group. In the 100 관g PEP-1-SOD1-treated group, the number of Ki67-positive nuclei was slightly decreased; however, in the 500 관g PEP-1-SOD1-treated group, Ki67-positive nuclei were decreased to 78.5% of the vehicle-treated group. The number of DCX-positive neuroblasts in the PEP-1-treated group was similar to that in the vehicle-treated group. However, the arborization of DCX-positive neuroblasts was significantly decreased in both the 100 and 500 관g PEP-1-SOD1-treated groups compared to that in the vehicle-treated group. The number of DCX-positive neuroblasts with tertiary dendrites was markedly decreased in the 500 관g PEP-1-SOD1-treated group. These results suggest that a SOD1 supplement to healthy mice may not be necessary to modulate cell proliferation and neuroblast differentiation in the dentate gyrus.</P>
KIM, Il Yong,HWANG, In Koo,CHOI, Ji Won,YOO, Ki-Yeon,KIM, Yo Na,YI, Sun Shin,WON, Moo-Ho,LEE, In Se,YOON, Yeo Sung,SEONG, Je Kyung Japanese Society of Veterinary Science 2009 The Journal of veterinary medical science Vol.71 No.6
<P>In this study, we observed and compared the effects of a high cholesterol diet (HCD) on cell proliferation and differentiation in the subgranular zone of the dentate gyrus of C57BL/6N (B6, susceptible strain) and C3H/HeN (C3H, resistant strain) mice. Ki67 (a marker for cell proliferation) positive cells) were significantly decreased in HCD-fed B6 mice compared to those in B6 (49.7%) and C3H mice fed a low cholesterol diet (LCD). In addition, doublecortin (DCX, a marker for cell differentiation or neuroblasts)-immunoreactive cells in HCD-fed B6 mice were significantly decreased compared to those in LCD-fed B6 and C3H mice. These results suggest that B6 strains are sensitive to HCD, which impairs cell proliferation and differentiation.</P>
Depth Jump 시 하지 관절 상해에 관한 운동역학적 분석
소재무,김윤지,이종희,서진희,정연옥,김광기 한국운동역학회 2005 한국운동역학회지 Vol.15 No.1
J. M. SO, Y. J. KIM, J. H. LEE, H. J. SEO, Y. O. CHUNG ? K. K. KIM. The analysis of lower extremities injury on depth jump. Korean Journal of Sport Biomechanics, Vol. 15, No. 1, pp. 127-142, 2005. The purpose of this study was to analysis biomechanics of the lower extremities injury the heights(40cm, 60cm, 80cm) of jump box as performed depth jump motion by 6 females aerobic athletes and 6 non-experience females students. The event of depth jump were set to be drop, landing and jump. The depth jump motions on the force plate were filmed using a digital video cameras, and data were collected through the cinematography and force plate. On the basis of the results analyzed, the conclusions were drawn as follows: 1. The landing time of skill group was shorter than unskill group at 40cm, 60cm drop height during drop-landing-jump phase especially. The landing time of 60cm drop height was significant between two group(p<.05). 2. The peak GRF of sagittal and frontal direction following drop height improve was variety pattern and the peak vertical force of 40cm drop height was significantly(p<.05). 3. The magnitude of peak passive force was not increase to change the drop height. 4. The peak passive forces was significant at 40cm drop height between two groups(p<.05)
Yoo, Dae Young,Kim, Woosuk,Yoo, Ki‐,Yeon,Nam, Sung Min,Chung, Jin Young,Yoon, Yeo Sung,Won, Moo‐,Ho,Hwang, In Koo Wiley Subscription Services, Inc., A Wiley Company 2012 JOURNAL OF NEUROSCIENCE RESEARCH - Vol.90 No.8
<P><B>Abstract</B></P><P>In this study, we challenged pyridoxine to mice fed a high‐fat diet (HFD) and investigated the effects of pyridoxine on HFD‐induced phenotypes such as blood glucose, reduction of cell proliferation and neuroblast differentiation in the dentate gyrus using Ki67 and doublecortin (DCX), respectively. Mice were fed a commercially available low‐fat diet (LFD) as control diet or HFD (60% fat) for 8 weeks. After 5 weeks of LFD or HFD treatment, 350 mg/kg pyridoxine was administered for 3 weeks. The administration of pyridoxine significantly decreased body weight in the HFD‐treated group. In addition, there were no significant differences in hepatic histology and pancreatic insulin‐immunoreactive (‐ir) and glucagon‐ir cells of the HFD‐treated group after pyridoxine treatment. In the HFD‐fed group, Ki67‐positive nuclei and DCX‐ir neuroblasts were significantly decreased in the dentate gyrus compared with those in the LFD‐fed mice. However, the administration of pyridoxine significantly increased Ki67‐positive nuclei and DCX‐ir neuroblasts in the dentate gyrus in both LFD‐ and HFD‐fed mice. In addition, the administration of pyridoxine significantly increased the protein levels of glutamic acid decarboxylase 67 (GAD67) and brain‐derived neurotrophic factor (BDNF) and the immunoreactivity of phosphorylated cyclic AMP response element binding protein (pCREB) compared with the vehicle‐treated LFD‐ and HFD‐fed mice. In contrast, the administration of pyridoxine significantly decreased HFD‐induced malondialdehyde (MDA) levels in the hippocampus. These results showed that pyridoxine supplement reduced the HFD‐induced reduction of cell proliferation and neuroblast differentiation in the dentate gyrus via controlling the levels of GAD67, pCREB, BDNF, and MDA. © 2012 Wiley Periodicals, Inc.</P>
Bing Chun Yan,In Hye Kim,Joon Ha Park,Ji Hyeon Ahn,Jeong-Hwi Cho,Bai Hui Chen,Jae-Chul Lee,Jung Hoon Choi,Ki-Yeon Yoo,Choong Hyun Lee,Jun Hwi Cho,Jong-Dai Kim,Moo-Ho Won 한국실험동물학회 2013 Laboratory Animal Research Vol.29 No.3
In the present study, we investigated the effect of Tetaus toxin (TeT) on cell proliferation and neuroblast differentiation using specific markers: 5-bromo-2-deoxyuridine (BrdU) as an exogenous marker for cell proliferation, Ki-67 as an endogenous marker for cell proliferation and doublecortin (DCX) as a marker for neuroblasts in the mouse hippocampal dentate gyrus (DG) after TeT treatment. Mice were intraperitoneally administered 2.5 and 10 ng/kg TeT and sacrificed 15 days after the treatment. In both the TeT-treated groups, no neuronal death occurred in any layers of the DG using neuronal nuclei (NeuN, a neuron nuclei maker) and Fluoro-Jade B (F-J B, a high-affinity fluorescent marker for the localization of neuronal degeneration). In addition, no significant change in glial activation in both the 2.5 and 10 ng/kg TeT-treated-groups was found by GFAP (a marker for astrocytes) and Iba-1 (a marker for microglia) immunohistochemistry. However, in the 2.5 ng/kg TeT-treated-group, the mean number of BrdU, Ki-67 and DCX immunoreactive cells, respectively, were apparently decreased compared to the control group, and the mean number of each in the 10 ng/kg TeT-treated-group was much more decreased. In addition, processes of DCX-immunoreactive cells, which projected into the molecular layer, were short compared to those in the control group. In brief, our present results show that low dosage (10 ng/kg) TeT treatment apparently decreased cell proliferation and neuroblast differentiation in the mouse hippocampal DG without distinct gliosis as well as any loss of adult neurons.
YOO, Dae Young,NAM, YoonYi,KIM, Woosuk,YOO, Ki-Yeon,PARK, Jaeil,LEE, Choong Hyun,CHOI, Jung Hoon,YOON, Yeo Sung,KIM, Dong-Woo,WON, Moo-Ho,HWANG, In Koo Japanese Society of Veterinary Science 2011 The Journal of veterinary medical science Vol.73 No.1
<P><I>Ginkgo biloba </I>leaf extract (Gb) has been known to improve blood flow and preclude the tissue from free radical damage. Effects of Gb were examined by using Ki67, a specific proliferative marker for cellular proliferation, and doublecortin (DCX), a marker for immature neurons, indicating degree of neuroblast differentiation in the hippocampal dentate gyrus (DG) of adult C57BL/6 mice. The mice were fed with Gb at 40 and 100 mg/kg once daily for 28 days. The increase of Ki67- and DCX-immunoreactive cells in the DG was increased in a dose-dependent manner. Especially, the group having 100 mg/kg Gb showed a significant increase of DCX-immunoreactive neuroblasts with well-developed tertiary dendrites. Expression of DCX protein in the Gb groups was also significantly increased upon compared with the vehicle group. The results suggested that repeated intake of Gb would enhance cell proliferation and neuroblast differentiation in the mouse DG.</P>
흰쥐에 있어서 납과 카드뮴이 Hepatic Microsomal Electron Transport System 활성도에 미치는 영향
김주봉,장성근,김기웅,송용범,김무호 순천향대학교 1994 논문집 Vol.17 No.3
In rats treated with lead nitrate and cadmium chloride we observed a change of he level of hepatic microsomal protein, cytochrome P-450 and ??, and electron transport system for P-450 dependent reaction. The contents of microsomal protein, P-450 and b5, and activity of NADPH-cytochrome C(P-450) reductase were decreased according to the dosage of lead nitrate and cadmium chloride. On the other hand, the activity of NADH-cytochrome ?? reductase was increased according to the dosage of lead nitrate and cadmium chloride. These results suggest that the content and activity of cytochrome dependent mono-oxygenase may be dependent on specificity of substrates, and electron transport occurred through two pathway, that is, NADPH-cytochrome C(P-450) reductase and ?? reductase but NADH-cytochrome ?? reductase was mainly act as a mobile carrier so-called second electron carrier.
MgCl₂溶液內에서 STS 304 HP Stainless Steel 熔接部의 破壞擧動에 對한 硏究
金永奭,丁太權,朴昌彦,洪錫柱,梁仁榮,金基玉,朴煥奎,李茂錫,曺圭宰,鄭在康 조선대학교 생산기술연구소 1983 生産技術硏究 Vol.1983 No.-
This paper is based on an experiment analysing the stress corrosion cracking behaviour of welding specimens compared to that of non-welding specimens of STS 304 HP stainless steel in corrosion solution. As a corrosion condition, stainless steel has been known to be the most fragile in a solution of 42% MgCl₂heated to the boiling point, therefore the experiment was carried out in this condition. The experiment was carried out with argon gas TIG welding specimens and non-welding ones made of stainless steel plates, thickness 2mm, by tensile force. At this time, the tensile force was taken to be the value of the yield strength of the tensile test specimens divided by the safety factor of 3.0 to 3.5, 4.0, 4.5, and 5.0. In this paper, the relations between Time of Initial Crack, Time of Failure, Time of Final Fracture and Crack Propagation Length were investigated and then plotted. Furthermore, the relations between Stress Intensity Factor K proposed by Irwin and the Time of Initial Crack, the Time of Failure, the Time of Final Fracture were calculated and plotted. At the last, all the relations plotted were expressed to normal equations by computer, and the equations were used to analyse the data obtained in the experiment. The conclusions obtained in this study are as follows: 1. Welding materials, compared with non-welding ones, as the Time of Initial Crack, the Time of Failure, and the Time of Final Fracture were generally very fast, appeared to be a phenomenon of unstable brittleness fracture. 2. Non-welding materials, compared with welding ones, as the safety factor was larger or the working stress was smaller, appeared to be a phenomenon that the longer had had greater durability. Therefor, welding materials must be considered enough to be used in heate affected and stress corrosion atmosphere. 3. The normal equations of the Time of Initial Crack and the variation rate to the same Stress Intensity Factor K are as follows: (A) Non-welding T =259702.4-5451.2 K+28.386 K² T = -5451.2+28.386 K (B) Welding T= -332.693+28.043 K-0.211 K² T' =28.043-0.211 K here, T; Time of Initial Crack, T'; Variation Rate of Time of Initial Crack to Stress Intensity Factor K, K ; Stress Intensity Factor.