• The Bulletin of The Korean Astronomical Society
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• v.24 no.2
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• pp.38-38
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• 1999

• Proceedings of the Korea Society of Design Studies Conference
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• 2001.10a
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• pp.38.2-38
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• 2001

• The Bulletin of The Korean Astronomical Society
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• v.23
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• pp.38-38
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• 1998

• Proceedings of the Materials Research Society of Korea Conference
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• 2008.05a
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• pp.38.2-38.2
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• 2008

• Journal of Biomedical Engineering Research
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• v.38 no.5
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• pp.232-236
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• 2017

In this study, We investigated the effect of foot cooling on the reduction of body temperature after hard exercise at the high temperature of $40^{\circ}C$. We performed a total of 30 subjects, and the subjects performed treadmill exercise for 30 minutes. We produced the cooling device to cool the foot using Peltier module. After the end of the exercise, We performed normal recovery method and cooling recovery method(one foot, both feet) for 1 hour on the same indoor environmental conditions and confirmed the change of body temperature of subjects. The results of deep body temperature measurement showed average $38.78{\pm}0.22^{\circ}C$ to $38.54{\pm}0.15^{\circ}C$ when the normal recovery method was performed. Cooling recovery method on one foot showed average $38.69{\pm}0.14^{\circ}C$ to average $38.06{\pm}0.17^{\circ}C$ and Cooling recovery method on both feet showed average $38.69{\pm}0.15^{\circ}C$ to average $37.84{\pm}0.21^{\circ}C$. There was a significant difference between the normal recovery method and the one foot cooling recovery method(p < .05), there was a significant difference between the normal recovery method and the both feet cooling recovery method(p < .05) and there was a significant difference between the one foot cooling recovery method and the both feet cooling recovery method(p < .05). Body temperature showed the lowest decrease rate when the normal recovery method was performed, and body temperature showed the highest decrease rate when the both feet cooling recovery method was performed. Therefore, recovery of cooling on the foot after hard exercise have decreased body temperature, delay fatigue in the body, and will be contributed to improvement of athlete performance.

• Korean Journal of Microbiology
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• v.39 no.2
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• pp.83-88
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• 2003

We cloned a gene encoding acetyl xylan esterase(axeA) of Streptomyces coelicolor A3(2) and studied its expression pattern in Escherichia coli. The full sequence of axeA was amplified by PCR. Sequence analysis of the PCR product revealed an open reading frame of 1,008 nucleotides encoding a protein consisted of 335 amino acid residues, with a calculated molecular mass of about 38 kDa. The base sequence showed 98% homology to the same gene of Streptomyces lividans. Two different kinds of acetyl xylan esterases were produced in Escherichia coli(pLacI) by IPTG induction; their molecular weights were 38 kDa and 34 kDa, respectively. Of these, 38 kDa protein seemed to be a total protein holding N-terminal signal peptide region, whereas 34 kDa protein seemed to be a matured protein without signal peptide which was produced by peptide bond cleavage between two amino acid residues of alanine 41 and alanine 42.

• Molecules and Cells
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• v.23 no.1
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• pp.30-38
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• 2007

Dipyrithione (2, 2'-dithiobispyridine-1, 1'-dioxide, PTS2), a pyrithione derivate, is highly bactericidal and fungicidal. In this study we examined its apoptotic effect on HeLa cells. PTS2 induced HeLa cell death in a dose and time dependent manner. ERK1/2 and p38 were markedly activated, but little JNK1/2 activation was detected. Suppression of p38 activation by SB203580 reduced the extent of apoptosis of the HeLa cells and also prevented induction of p21, release of cytochrome c, and cleavage of caspase-3 and PARP. Inhibition of ERK1/2 with PD98059 increased apoptosis, indicating that ERK1/2 activation has an anti-apoptotic effect on PTS2-induced HeLa cell apoptosis. PTS2 also inhibited murine sarcoma 180 and hepatoma 22 tumor growth in an animal tumor model. Our findings indicate that PTS2 possesses anti-tumor activity, that caspase-3 and poly (ADP-ribose) polymerase (PARP) are involved in PTS2-induced HeLa cell apoptosis and that ERK1/2 and p38 have opposing effects on this apoptosis.

• Korean Journal of Food Science and Technology
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• v.22 no.4
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• pp.411-414
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• 1990

Antithiamin activities of BHA, BHT PG and TBHQ of synthetic phenolic antioxidants at various pH's and temperatures were studied. All antioxidants had little antithiamin activity as is the case with control group at pH 4 and $38^{\circ}C$, but antithiamin activity was stronger at $60^{\circ}C$ than at $38^{\circ}C$ under the same pH. Meanwhile, the destruction of thiamin incubated at $38^{\circ}C$ was more rapid at pH 7 than at pH 4, and the destruction of thiamin at pH 7 was much more rapid at $60^{\circ}C$ than at $38^{\circ}C$. BHA and BHT had little, or extremely slight antithiamin activity. Antithiamin activity of PG was comparatively strong, but TBHQ had the strongest antithiamin activity among synthetic phenolic antioxidants examined.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1183-1186
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• 2012

Objective: To observe the effect of insulin-like growth factor-1 (IGF-1) on bone morphogenetic protein (BMP)-2 expression in hepatocellular carcinoma SMMC7721 cells. Methods: Cells were divided into blank control, IGF-1, IGF-1 + SB203580, and SB203580 groups. SB203580 was used to block the p38 MAPK signaling pathway. Changes in the expression of BMP-2, p38 MAPK, and phosphorylated p38, MERK, ERK and JNK were determined using reverse transcription polymerase chain reactions (RT-PCR) and Western blot analysis. Results: Protein expression of phosphorylated BMP-2, MERK, ERK, and JNK was significantly up-regulated by IGF-1 compared with the control group ($1.138{\pm}0.065$ vs. $0.606{\pm}0.013$, $0.292{\pm}0.005$ vs. $0.150{\pm}0.081$, $0.378{\pm}0.006$ vs. $0.606{\pm}0.013$, and $0.299{\pm}0.015$ vs. $0.196{\pm}0.017$, respectively; P<0.05). Levels of BMP-2 and phosphorylated MERK and JNK were significantly reduced after blocking of the p38MAPK signaling pathway ($0.494{\pm}0.052$ vs. $0.165{\pm}0.017$, $0.073{\pm}0.07$ vs. $0.150{\pm}0.081$, and $0.018{\pm}0.008$ vs. $0.196{\pm}0.017$, respectively; P<0.05), but such a significant difference was not observed for phosphorylated ERK protein expression ($0.173{\pm}0.07$ vs. $0.150{\pm}0.081$, P>0.05). Conclusion: IGF-1 can up-regulate BMP-2 expression, and p38 MAPK signaling pathway blockage can noticeably reduce the up-regulated expression. We can conclude that the up-regulatory effect of IGF-1 on BMP-2 expression is realized through the p38 MAPK signaling pathway.

• Bulletin of the Korean Chemical Society
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• v.22 no.12
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• pp.1361-1365
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• 2001

Recombinant immunotoxins are hybrid cytotoxic proteins designed to selectively kill cancer cells. A divalent immunotoxins, [B3(FabH1)-PE38]2, was constructed by recombining Fab domain of B3 antibody as a cell-targeting domain and Pseudo monas exotoxin A (PE) as a cytotoxic domain. Monoclonal antibody, B3, is the murine antibody (IgG1k) directed against Lewis Y-related carbohydrate antigens, which are abundant on the surface of many carcinomas. Fab fragment of this antibody was used in this study with the modified hinge sequence where last two cysteines out of three were mutated to serine. PE is a 66 kDa bacterial toxin that kills eukaryotic cells by inhibiting protein synthesis with ADP ribosylation of ribosomal elongation factor 2 (EF2). Fc region of B3 antibody was substituted with the truncated form of PE (38 kDa, PE38) on DNA level. [B3(FabH1)-PE38]2 was formed by disulfide bond between cysteines in the modified hinge region of B3(FabH1)-PE38. Each polypeptide for recombinant immunotoxins was overexpressed in Escherichia coli and collected as inclusion bodies. Each inclusion body was solubilized and refolded, and cytotoxic effects were measured. Divalent immunotoxins, [B3(FabH1)-PE38]2, had ID50 values of about 10 ng/mL on A431 cell lines and about 4 ng/mL on CRL1739 cell lines. Control immunotoxins, B3(scFv)-PE40, had ID50 values of about 28 ng/mL on A431 cell lines and about 41 ng/mL on CRL1739 cell lines. Divalent immunotoxins, [B3(FabH1)-PE38]2, had higher cytotoxic effects than B3(scFv)-PE40 control immunotoxins.