http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
재조합 플라스미드 pSC3 에 단리된 효모 유전자 hom3 의 염색체 통합에 관한 연구
이호주,이우영,최승일 한국유전학회 1990 Genes & Genomics Vol.12 No.1
Aspartokinase (EC 2.7.2.4) is encoded by the HOM3 gene, a putative clone of which was previously isolated on a recombinant plasmid pSC3 (15.5 kbp) by its hom3 complementing ability in the yeast (Choi and Lea, 1988). The complementing sequence was further localized to the 2.15 kbp BamHI-Bg1II fragment by subcloning it from the pSC3. A replicating vector YRp7 to yield the plasmid pSC35. In an attempt to yield the integrative plasmid pSC351, the EcoRI fragment containing ARS-TRP1 was removed from pSC35. Mitotically stable integrative transformants were stable integrative transformants were selected upon introducing the linearized pSC351 into the original yeast recipient strain and crossed with an appropriate yeast strain for tetrad analysis. As a result, the integrated pSC351 DNA was positioned to, the expected genetic distance of 3.9 cM from the HIS1 locus on the right arm of yeast chromosome V, indicating that the 2.15 kbp fragment in pSC35 contains the entire functional HOM3 gene of the yeast, Saccharomyces cerevisiae.
( Young Jung Lee ),( Dong Young Choi ),( Im Seop Choi ),( Ki Ho Kim ),( Young Hee Kim ),( Hwan Mook Kim ),( K Iho Lee ),( Won Gil Cho ),( Lea Kyung Jung ),( Sang Bae Han ),( Jin Yi Han ),( Sang Yoon N 영남대학교 약품개발연구소 2012 영남대학교 약품개발연구소 연구업적집 Vol.22 No.0
BACKGROUND: Neuroinflammation is important in the pathogenesis and progression of Alzheimer disease (AD). Previously, we demonstrated that lipopolysaccharide (LPS)-induced neuroinflammationcaused memory impairments. In the present study, we investigated the possible preventive effects of 4-O-methylhonokiol, a constituent of Magnolia officinalis, on memory deficiency caused by LPS, along with the underlying mechanisms. METHODS: We investigated whether 4-O-methylhonokiol (0.5 and 1 mg/kg in 0.05% ethanol) preventsmemory dysfunction and amyloidogenesis on AD model mice by intraperitoneal LPS (250 μg/kg daily 7 times) injection. In addition, LPS-treated cultured astrocytes and microglial BV-2 cells were investigated for anti-neuroinflammatory and anti-amyloidogenic effect of 4-O-methylhonkiol (0.5, 1 and 2 μM). RESULTS: Oral administration of 4-O-methylhonokiol ameliorated LPS-induced memory impairment in a dose-dependent manner. In addition, 4-O-methylhonokiol prevented the LPS-induced expression of inflammatory proteins; inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) as well as activation of astrocytes (expression of glial fibrillary acidic protein; GFAP) in the brain. In in vitro study, we also found that 4-O-methylhonokiol suppressed the expression of iNOS and COX-2 as well as the production of reactive oxygen species, nitric oxide, prostaglandin E2, tumor necrosis factor-α, and interleukin-1β in the LPS-stimulated cultured astrocytes. 4-O-methylhonokiol also inhibited transcriptional and DNA binding activity of NF-κB via inhibition of IκB degradation as well as p50 and p65 translocation into nucleus of the brain and cultured astrocytes. Consistent with the inhibitory effecton neuroinflammation, 4-O-methylhonokiol inhibited LPS-induced Aβ1-42 generation, β- and γ-secretase activities, and expression of amyloid precursor protein (APP), BACE1 and C99 as well as activation of astrocytes and neuronal cell death in the brain, in cultured astrocytes and in microglial BV-2 cells. CONCLUSION: These results suggest that 4-O-methylhonokiol inhibits LPS-induced amyloidogenesisvia anti-inflammatory mechanisms. Thus, 4-O-methylhonokiol can be a useful agent againstneuroinflammation-associated development or the progression of AD.
혼합기 회전수와 용적에 따른 고성능 콘크리트의 성능에 대한 연구
최해영(Choi, Hae Young),김용권(Kim, Yong Kwon),김정훈(Kim, Jung Hoon),노홍래(Lo, Hong Lea),손영준(Son, Young Jun) 한국콘크리트학회 2021 한국콘크리트학회 학술대회 논문집 Vol.33 No.2
본 연구에서는 콘크리트 혼합기의 혼합인자(회전수, 혼합용량)에 따른 고성능 콘크리트의 물성변화에 대해 검토하였다. 물리적 성능(슬럼프플로우, V-lot, T-500) 시험결과, 혼합회전수(RPM)는 30, 혼합용량은 30L이 적정 수준인 것으로 판단된다. The purpose of this study is to evaluate the physical variation in high performance concrete as the RPM(revolutions per minute) and the amount of batch. The proper conditions of mixing RPM and volume was 30 and 30 liters
Subcloning and Chromosomal Integration of the Yeast Threonine Synthase Gene THR4
Sohn, Young Doug,Lea, Ho Zoo,Lea, Woo Young,Choi, Seoung Il 한국유전학회 1990 Genes & Genomics Vol.12 No.4
The yeast gene THR4 encodes the threonine synthase (E.C. 4.2.99.2) which catalyses the last step of the threonine biosynthesis pathway. A recombinant plasmid pYL1 (22.0 kbp, vector YCp50) has been cloned into E. coli HB101 from a yeast genomic library through its complementing activity of the thr4 mutation in a yeast recipient strain M21-59. When subcloned into pYL12 (12.4 kbp, vector YCp50) and pYL121 (10.0 kbp, vector YIp5), the ClaI - ClaI fragment (4.4 kbp) of pYL1 insert was positive in threonine complementing activity in M21-59. The KpnI linearized pYL121 was introduced into the original recipient yeast strain and mitotically stable chromosomal integrants were identified among transformants. Through the tetrad analysis, the integration site of pYL121 was localized to the region of THR4 structural gene at the expected right arm of yeast chromosome III. Thus, it was also genetically proved that the cloned ClaI fragment contains the yeast THR4 structural gene.
Choi, Jae-Seok,Lee, Young-Jun,Kim, Tae-Hyung,Lim, Hyun-Jung,Ahn, Mee-Young,Kwack, Seung-Jun,Kang, Tae-Seok,Park, Kui-Lea,Lee, Jae-Won,Kim, Nam-Deuk,Jeong, Tae-Cheon,Kim, Sang-Geum,Jeong, Hye-Gwang,Lee Korean Society of ToxicologyKorea Environmental Mu 2011 Toxicological Research Vol.28 No.2
Brominated flame retardants (BFRs) are present in many consumer products ranging from fabrics to plastics and electronics. Wide use of flame retardants can pose an environmental hazard, which makes it important to determine the mechanism of their toxicity. In the present study, dose-dependent toxicity of tetrabromobisphenol A (TBBPA), a flame retardant, was examined in male prepubertal rats (postnatal day 18) treated orally with TBBPA at 0, 125, 250 or 500 mg/kg for 30 days. There were no differences in body weight gain between the control and TBBPA-treated groups. However, absolute and relative liver weights were significantly increased in high dose of TBBPA-treated groups. TBBPA treatment led to significant induction of CYP2B1 and constitutive androstane receptor (CAR) expression in the liver. In addition, serum thyroxin (T4) concentration was significantly reduced in the TBBPA treated group. These results indicate that repeated exposure to TBBPA induces drug-metabolising enzymes in rats through the CAR signaling pathway. In particular, TBBPA efficiently produced reactive oxygen species (ROS) through CYP2B1 induction in rats. We measured 8-hydroxy-2'-deoxyguanosine (8-OHdG), a biomarker of DNA oxidative damage, in the kidney, liver and testes of rats following TBBPA treatment. As expected, TBBPA strongly induced the production of 8-OHdG in the testis and kidney. These observations suggest that TBBPA-induced target organ toxicity may be due to ROS produced by metabolism of TBBPA in Sprague-Dawley rats.