• Journal of Yeungnam Medical Science
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• 제12권2호
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• pp.366-385
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• 1995

항산균 감염증의 예방 및 치료를 위하여는 역학적인 연구가 중요하다. 본 연구에서는 감염증의 분자역학적 연구를 위한 기법중 아직 항산균을 대상으로 pulsed-field gel electrophoresis (PFGE) 분석법을 확립하고자 하였다. PFGE분석에 적절한 제한효소는 DraI, AsnI 및 XbaI 등이었고 각 제한효소마다 최적의 PFGE조건은 서로 달랐다. DraI의 경우는 두단계로 나누어 전기영동을 시행하였다. 제1단계의 initial pulse는 10초 final pulse는 15초였으며 제2단계는 initial pulse는 60초 final pulse는 70초이었다. 전기영동시간은 각 단계마다 각각 14시간씩이었다. XbaI의 경우는 제2단계 없이 initial pulse가 3초 final pulse가 12초였고 전기영동시간은 22시간이었다. AsnI의 경우는 제2단계 없이 initial pulse가 5초 final pulse가 25초였고 전기영동시간은 22시간이었다. 모든 경우에 있어서 전압은 200V로 하였다. 표준균주로는 M. bovis BCG, M. tuberculosis 및 M. fortuitum등을 사용하였는데 PFGE분석상 동일균종내에서 표준균주들 간의 차이는 발견할 수 없었다. 임상에서 분리된 9주의 M. fortuitum 균주를 대상으로 AsnI 제한효소로 PFGE분석을 시행한 결과 2주만을 제외하고는 서로 간의 유전형 분류가 가능하였다. 균주간의 유전적 거리를 결정하기 위하여 cluster analysis를 시행한 결과 M. fortuitum 균주들은 크게 두 집단으로 나뉘었다. 제한효소 AsnI으로 동일 균종의 분류가 안되는 M. fortuitum 균주들은 XbaI 제한효소을 사용한 PFGE분석으로 유전형의 구분이 가능하였다. Cluster analysis를 시행한 결과 크게 두 집단으로 나뉘었던 M. fortuitum 균주들은 보다 복잡한 집단으로 분류되어 XbaI을 사용한 PFGE분석법이 M. fortuitum 균주분류를 위하여는 보다 적절함을 알 수 있었다. Cluster analysis에서 얻은 최대 % dissimilarity 값은 0.74(AsnI) 및 0.75(XbaI)로서 이 값은 arbitrarily primed polymerase chain reaction(AP-PCR)법보다는 높고 restriction fragment length polymorphism(RFLP) 법보다는 낮아 PFGE법이 RFLP를 보완하거나 대치할 수 있는 세균 유전형 분석법임을 알 수 있었다.

• 대한토목학회논문집
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• 제12권4_1호
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• pp.43-52
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• 1992

가로흐름에 같은 수심으로 그리고 직각으로 방류되는 ?흐름의 귀환현상이 차원해석과 수리실험을 통하여 해석된다. 운동량?의 경우 무차원귀환거리 $L/I_m$와 두께 $H/I_m$는 운동량특성길이와 방류구폭의 비 $I_m/W$, 부력?의 경우 무차원귀환거리 $L/I_b$는 부력특성길이와 운동량길특성의 비 $I_b/I_m$, 무차원온도분포 ${\Gamma}_m$은 무차원흐름방향거리 $x/I_b$의 영향을 받으며 이들은 모두 멱법칙으로 예측될 수 있다. 귀환의 발생여부는 속도비 R에 좌우되며 본 연구에서는 R>4.0때 귀환이 발생하지 않는 것으로 나타났다.

• 한국식품영양과학회지
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• 제28권3호
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• pp.670-676
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• 1999

The effect of exercise and/or high fat diet on carnitine status and carnitine palmitoyltransferase I(CPT I) level were investigated in Weanling Sprague Dawley rats. The rats were fed an AIN 76 diet or a modified high fat AIN diet, supplemented with 35% corn oil, for 31 days. During the 31 day period half of the animals in each dietary group were exercised on a treadmill for 90 minutes per day. Carnitine concentrations were determined in plasma and liver and CPT I mRNA levels were measured by Northern blot analysis with CPT I cDNA probe in livers of rats. Exercise rats gained less weight than non exercised rats during the study for high fat diet group. Exercise rats had a higher plasma acid soluble acylcarnitine and acid insoluble acylcarnitine concnetrations than non exercised rats for normal diet group. Exercise or high fat diet increased liver carnitine concentration, but a mixed effect was not shown. In exercised rats, CPT I mRNA levels increased significantly relative to those of nonexercised rats. CPT I mRNA levels also increased when compared high fat fed rats with those of normal diet fed rats. These data suggest that there is a correlation between carnitine concen trations and CPT I mRNA levels and that CPT I can be regulated at the transcriptional level by exercise and/or high fat diet.

• 미생물학회지
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• 제40권3호
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• pp.199-204
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• 2004

Pseudomonas rhodesiae H5가 생성하는 parathion hydrolase를 $(NH_{4})_{2}SO_{4}$침전, DEAE-Toyopearl 650M ion exchange chromatography, Sephadex gel filtration의 단계로 정제한 결과, 이 균주가 생성하는 parathion hydrolase는 두 종류의 효소였으며, 이를 각각 OPH $I_1$과 OPH $I_2$라 명명하였다. OPH $I_1$과 OPH $I_2$의 최적 pH와 온도는 각각 pH7.2, $30^{\circ}C$와 PH7.6, $37^{\circ}C$이었다. OPH $I_1$의 Parathion을 가수분해하는 활성화 에너지는 $4^{\circ}C$-$30^{\circ}C$에서 3.01㎉/㏖ 이었으며 Km값은 69.2${\mu}M$이었다. 반면, OPH $I_2$의 활성화에너지는 $4^{\circ}C$-$37^{\circ}C$에서 4.07kcal/㏖이었으며 Km값은 150.9${\mu}M$이었다. OPH $I_1$은 1 mM의 $Mg^2+$, $Cu^2+$, $Ca^2+$, $Ni^2+$에 의해서 효소활성이 완전 저해되었으나 OPH $I_2$는 저해를 덜 받는 것으로 확인되었다.

• 대한수학회지
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• 제52권6호
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• pp.1253-1270
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• 2015

Let (R, m) be a commutative Noetherian local domain, M a non-zero finitely generated R-module of dimension n > 0 and I be an ideal of R. In this paper it is shown that if $x_1,{\ldots },x_t$ ($1{\leq}t{\leq}n$) be a sub-set of a system of parameters for M, then the R-module $H^t_{(x_1,{\ldots },x_t)}$(R) is faithful, i.e., Ann $H^t_{(x_1,{\ldots },x_t)}$(R) = 0. Also, it is shown that, if $H^i_I$ (R) = 0 for all i > dim R - dim R/I, then the R-module $H^{dimR-dimR/I}_I(R)$ is faithful. These results provide some partially affirmative answers to the Lynch's conjecture in [10]. Moreover, for an ideal I of an arbitrary Noetherian ring R, we calculate the annihilator of the top local cohomology module $H^1_I(M)$, when $H^i_I(M)=0$ for all integers i > 1. Also, for such ideals we show that the finitely generated R-algebra $D_I(R)$ is a flat R-algebra.

• The Korean Journal of Physiology and Pharmacology
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• 제8권6호
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• pp.313-317
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• 2004

The present study were designed to characterize the action mechanisms of acetylcholine (ACh)-induced endothelium-dependent relaxation in arteries precontracted with high $K^+$(70 mM). For this, we simultaneously measured both muscle tension and cytosolic free $Ca^{2+}$ concentration $([Ca^{2+}]_i)$, using fura-2, in endothelium-intact, rabbit carotid arterial strips. In the artery with endothelium, high $K^+$ increased both $[Ca^{2+}]_i$ and muscle tension whereas ACh $(10{\mu}M)$ significantly relaxed the muscle and increased $[Ca^{2+}]_i$. In the presence of $N^G$-nitro-L-arginine (L-NAME, 0.1 mM), ACh increased $[Ca^{2+}]_i$ without relaxing the muscle. In the artery without endothelium, high $K^+$ increased both $[Ca^{2+}]_i$ and muscle tension although ACh was ineffective. 4-DAMP (10 nM) or atropine $(0.1{\mu}M)$ abolished ACh-induced increase in $[Ca^{2+}]_i$ and relaxation. The increase of $[Ca^{2+}]_i$ and vasorelaxation by ACh was siginificantly reduced by either $3{\mu}M$ gadolinium, $10{\mu}M$ lanthanum, or by $10{\mu}M$ SKF 96365. These results suggest that in rabbit carotid artery, ACh-evoked relaxation of 70 mM $K^+$-induced contractions appears to be mediated by the release of NO. ACh-evoked vasorelaxation is mediated via the $M_3$ subtype, and activation of the $M_3$ subtype is suggested to stimulate nonselective cation channels, leading to increase of $[Ca^{2+}]_i$ in endothelial cells.

• 대한수학회보
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• 제60권3호
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• pp.637-647
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• 2023

Let R be a commutative Noetherian ring, 𝔞 an ideal of R, M an arbitrary R-module and X a finite R-module. We prove a characterization for Hⁱ_𝔞(M) and Hⁱ_𝔞(X, M) to be 𝔞-weakly cofinite for all i, whenever one of the following cases holds: (a) ara(𝔞) ≤ 1, (b) dim R/𝔞 ≤ 1 or (c) dim R ≤ 2. We also prove that, if M is a weakly Laskerian R-module, then Hⁱ_𝔞(X, M) is 𝔞-weakly cofinite for all i, whenever dim X ≤ 2 or dim M ≤ 2 (resp. (R, m) a local ring and dim X ≤ 3 or dim M ≤ 3). Let d = dim M < ∞, we prove an equivalent condition for top local cohomology module H^d_𝔞(M) to be weakly Artinian.

• The Korean Journal of Physiology and Pharmacology
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• 제10권1호
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• pp.25-30
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• 2006

Lysophosphatidylcholine (LPC), which accumulates in atherosclerotic arteries, has been reported to inhibit endothelium-dependent relaxation (EDR) in many different species. However, the underlying mechanism of LPC-induced inhibition of EDR is still uncertain. In the present study, we measured simultaneously both isometric tension and cytosolic free $Ca^{2+}$ ($[Ca^{2+}]_i$) in rabbit carotid strips, and examined the effect of LPC on tension and $[Ca^{2+}]_i$. In carotid strips with intact-endothelium, high $K^+$ (70 mM) increased both tension and $[Ca^{2+}]_i$, and cumulative addition of acetylcholine (ACh) from 0.1 to $10{\mu}M$ induced dose dependent increase of $[Ca^{2+}]_i$ with concomitant relaxation. In the presence of L-NAME (0.1 mM), ACh increased $[Ca^{2+}]_i$ without affecting the amplitude of high $K^+-induced$ tension. These ACh-induced change of $[Ca^{2+}]_i$ and tension was abolished by removal of endothelium or 10 nM 4-DAMP (muscarinic receptor antagonist) pretreatment. Pretreatment of LPC ($10{\mu}M$) inhibited ACh ($10{\mu}M$)-induced change of tension and $[Ca^{2+}]_i$ in endothelium-intact carotid artery. On the other hand, LPC had no effect on ACh-induced change of tension and $[Ca^{2+}]_i$ in endothelium denuded artery. In $Ca^{2+}$-free external solution, ACh transiently increased $[Ca^{2+}]_i$, and pretreatment of LPC significantly inhibited ACh-induced transient $[Ca^{2+}]_i$ change. Based on the above results, it may be concluded that LPC inhibits the ACh-induced $[Ca^{2+}]_i$ change through inhibition of $Ca^{2+}$ mobilization in vascular endothelial cells, resulting in decreased production of NO and concomitant inhibition of endotheliumdependent vascular relaxation.

• Journal of applied mathematics & informatics
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• 제26권3_4호
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• pp.457-469
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• 2008

In this paper, we study the existence of positive solutions for the following nonlinear m-point boundary value problem with p-Laplacian: $\{{{{(\phi_p(u'))'\;+\;f(t,u(t))=0, \;0<t<1,} \atop u'(0)={\sum}{^{m-2}_{i=1}}\;a_iu'(\xi_i),} \atop u(1)={\sum}{^k_{i=1}}\;b_iu(\xi_i)\;-\;{\sum}{^s_{i=k+1}}\;b_iu(\xi_i)\;-\;{\sum}{^{m-2}_{i=s+1}}\;b_iu'(xi_i),}$ where ${\phi}_p(s)$ is p-Laplacian operator, i.e., ${\phi}_p(s)=\mid s\mid^{p-2}s$, p>1, ${\phi}_q\;=\;({\phi}_p)^{-1}$, $\frac{1}{p}+\frac{1}{q}=1$, $1\;{\leq}\;k\;{\leq}\;s\;{\leq}m\;-\;2$, $b_i\;{\in}\;(0,+{\infty})$ with $0\;<\;{\sum}{^k_{k=1}}\;b_i\;-\;{\sum}{^s_{i=k+1}}\;b_i\;<\;1$, $0\;<\;{\sum}{^{m-2}_{i=1}}\la_i\;<\;1$, $0\;<\;{\xi}_1\;<\;{\xi}_2\;<\;{\cdots}\;<\;{\xi}_{m-2}\;<\;1$, $f\;{\in}\;C([0,\;1]\;{\times}\;[0,\;+{\infty}),\;[0,\;+{\infty}))$. We show that there exists one or two positive solutions by using fixed-point theorem for operator on a cone. The conclusions in this paper essentially extend and improve the known results.

• Archives of Pharmacal Research
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• 제27권7호
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• pp.769-775
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• 2004

Hepatic ischemia and reperfusion (l/R) predisposes the liver to secondary stresses such as endotoxemia, possibly via dysregulation of the hepatic microcirculation secondary to an imbalanced regulation of the vascular stress genes. In this study, the effect of hepatic I/R on the hepatic vasoregulatory gene expression in response to endotoxin was determined. Rats were subjected to 90 min of hepatic ischemia and 6 h of reperfusion. Lipopolysaccharide (LPS, 1 mg/kg) was injected intraperitoneally after reperfusion. Plasma and liver samples were obtained 6 h after reperfusion for serum aminotransferase assays and RT-PCR analysis of the mRNA for the genes of interest： endothelin-1 (ET-1), its receptors $ET_A$ and $ET_B$, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), heme oxygenase-1 (HO-1), cyciooxygenase-2 (COX-2), and tumor necrosis factor-a (TNF-${\alpha}$). The activities of serum aminotransferases were significantly increased in the I/R group. This increase was markedly potentiated by LPS treatment. The ET-1 mRNA was increased by LPS alone, and this increase was significantly greater in both the I/R alone and I/R ＋ LPS groups compared to the sham. There were no significant differences in ETA receptor mRNA levels among any of the experimental groups. $ET_B$ mRNA was increased by both LPS alone and I/R alone, with no significant difference between the I/R alone and I/R ＋ LPS groups. The eN OS and HO-1 transcripts were increased by I/R alone and further increased by I/R ＋ LPS. The iNOS mRNA levels were increased by I/R alone, but increased significantly more by both LPS alone and I/R ＋ LPS compared to I/R alone. The TNF-${\alpha}$ mRNA levels showed no change with I/R alone, but were increased by both LPS alone and I/R ＋ LPS. The COX-2 expression was increased significantly by I/R alone and significantly more by I/R ＋ LPS. Taken collectively, significantly greater induction of the vasodilator genes over the constriction forces was observed with I/R ＋ LPS. These results may partly explain the increased susceptibility of ischemic livers to injury as a result of endotoxemia.