鍼刺가 人體의 血漿 Atrial Natriuretic Peptide,Aldosterone, Cortisol 濃度 및 Renin 活性度에 미치는 影響

朴秀雄,李昊燮 圓光大學校 韓醫學硏究所 1991 원광한의학 Vol.1 No.1

The sources of body water are metabolically produced and ingested water. There are four sites from which water is lost to the external environment : skin, lungs, gastrointestinal tract, and kidneys. According to the theory of oriental medicine, the balance of body water is controlled by kidneys, lungs, Bee(脾), urinary bladder, and Sam Cho(三焦), the function of skin is controlled by lungs(肺主皮毛) The aim of the present study was to elucidate the effects of acupuncture in the meridian point Sam Cho Soo(B22), Bee Soo(B20), and Pye Soo(B13) on the renin-angiotensin aldosterone system and atrial natriuretic peptide(ANP). The results obtained were as follows: 1. Plasma atrial natriuretic peptide was decreased significantly after acupuncture in the meridian point Pye Soo(B13) 2. Plasma renin activity was decreased significantly after acupuncture in the meridian point Sam Cho Soo(B22). 3. Plasma renin activity was increased significantly after acupuncture in the meridian point Bee Soo(B20) 4. Plasma aldosterone concentration was decreased significantly after acupuncture in the meridian point Sam Cho Soo(B22) and Bee Soo(B20) 5. Plasma cortisol concentration was decreased significantly after acupuncture in the meridian point Bee Soo(B20). 6. Plasma ACTY concentration was decreased significantly after acupuncture in the meridian points Bee Soo(B20) and Pye Soo(B13) These results suggest that meridian points Sam Cho Soo(B22), Bee Soo(B22), and Pye Soo(B13) have regulatory function for the body water metabolism. The effects of acupuncture in the meridian points the Sam Cho Soo(B22) and Bee Soo(B20) were related with the changes of plasma levels of renin activity and aldosterone concentration, but the effects of acupuncture in the Pye Soo(B13) was related with the decreases of plasma levels of ANP and aldosterone.

FK506이 T 림프구 사멸에서 활성산소 생성에 미치는 영향

이호균(Ho Kyun Lee),정상영(Sang Young Chung),최수진나(Soo Jin Na Choi) 대한외과학회 2009 Annals of Surgical Treatment and Research(ASRT) Vol.77 No.5

Purpose: Tacrolimus (FK506) has been widely used as an immunosuppressant in organ transplanted recipients to suppress organ rejection phenomenon. We investigated the role of oxidative stress and heme oxygense-1 by FK506 on human Jurkat T cells. Methods: The cells viability was examined by DAPI stain, enzyme activity of caspase family proteins, and western blotting for Baks, PUMA, iNOS, HO-1. Cells were cultured in the absence or presence of CoPPIX or ZnPPIX and the fluorescence intensity was analyzed using a flow cytometry. Results: Treatment with FK506 increased the generation of reactive oxygen species (ROS), including hydrogen peroxide and superoxide anion, and NO in Jurkat cells in a dose-dependent manner. Immunohistochemistry and Western blot analysis data revealed the hemoxygenase-1 (HO-1) was induced by the addition of FK506 in Jurkat cells. Induction of CoPP, HO-1 inducer, resulted in decreased intracellular H₂O₂ and NO concentrations. Instead ZnPP, an HO-1 competitive inhibitor did it reversely. In addition, ZnPP regulates iNOS protein synthesis by inhibition of HO-1. Conclusion: Increase of HO-1 expression would induce to decrease the intracellular H₂O₂ and NO concentrations. Also, HO-1 would regulate iNOS protein synthesis. Consequently, we can expect the regulation of HO-1 expression with concomitants use of FK506 to suppress organ rejection phenomenon by enhancing apoptosis.

Combined Gene Therapy with Hypoxia-Inducible Factor-1α and Heme Oxygenase-1 for Therapeutic Angiogenesis

Bhang, Suk Ho,Kim, Ju Hee,Yang, Hee Seok,La, Wan-Geun,Lee, Tae-Jin,Kim, Ga Hee,Kim, Hyun Ah,Lee, Minhyung,Kim, Byung-Soo Mary Ann Liebert 2011 Tissue engineering. Part A Vol.17 No.7

<P>Transfection with either hypoxia-inducible factor-1α (HIF-1α) or heme oxygenase-1 (HO-1) gene can induce neovascularization in ischemic tissues. Although expression of transfected HIF-1α gene occurs rapidly, the expressed HIF-1α protein degrades quickly, limiting its therapeutic efficacy. Meanwhile, expressed HO-1 protein does not rapidly undergo degradation, but gene expression occurs a couple of days after transfection, resulting in apoptosis and a delay in angiogenesis in ischemic tissues at the incipient period of HO-1 gene transfection. We hypothesize that combined delivery of HIF-1α and HO-1 gene will enhance antiapoptosis and neovascularization in ischemic tissue compared with HIF-1α or HO-1 single-gene therapy. To test this hypothesis, ischemic mouse hindlimbs were treated with HIF-1α and/or HO-1 gene therapy. The combined gene therapy proved superior to both single-gene therapies, resulting in rapid expression of HIF-1α gene and long-term maintenance of expressed HO-1 protein. The apoptosis in the ischemic region was significantly less, and angiogenic growth factor secretion and angiogenesis were greater in the combined gene therapy than in either of the single-gene therapies. Our results suggest that a combined gene therapy of HIF-1α and HO-1 enhances the transfection of both genes and improves angiogenesis compared with either single-gene therapy.</P>

Hypoxia-Responsive MicroRNA-101 Promotes Angiogenesis <i>via</i> Heme Oxygenase-1/Vascular Endothelial Growth Factor Axis by Targeting Cullin 3

Kim, Ji-Hee,Lee, Kwang-Soon,Lee, Dong-Keon,Kim, Joohwan,Kwak, Su-Nam,Ha, Kwon-Soo,Choe, Jongseon,Won, Moo-Ho,Cho, Byung-Ryul,Jeoung, Dooil,Lee, Hansoo,Kwon, Young-Guen,Kim, Young-Myeong Mary Ann Liebert 2014 Antioxidants & redox signaling Vol.21 No.18

<P>Aims: Hypoxia induces expression of various genes and microRNAs (miRs) that regulate angiogenesis and vascular function. In this study, we investigated a new functional role of new hypoxia-responsive miR-101 in angiogenesis and its underlying mechanism for regulating heme oxygenase-1 (HO-1) and vascular endothelial growth factor (VEGF) expression. Results: We found that hypoxia induced miR-101, which binds to the 3 ' untranslated region of cullin 3 (Cul3) and stabilizes nuclear factor erythroid-derived 2-related factor 2 (Nrf2) via inhibition of the proteasomal degradation pathway. miR-101 overexpression promoted Nrf2 nuclear accumulation, which was accompanied with increases in HO-1 induction, VEGF expression, and endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) production. The elevated NO-induced S-nitrosylation of Kelch-like ECH-associated protein 1 and subsequent induction of Nrf2-dependent HO-1 lead to further elevation of VEGF production via a positive feedback loop between the Nrf2/HO-1 and VEGF/eNOS axes. Moreover, miR-101 promoted angiogenic signals and angiogenesis both in vitro and in vivo, and these events were attenuated by inhibiting the biological activity of HO-1, VEGF, or eNOS. Moreover, these effects were also observed in aortic rings from HO-1(+/-) and eNOS(-/-) mice. Local overexpression of miR-101 improved therapeutic angiogenesis and perfusion recovery in the ischemic mouse hindlimb, whereas antagomiR-101 diminished regional blood flow. Innovation: Hypoxia-responsive miR-101 stimulates angiogenesis by activating the HO-1/VEGF/eNOS axis via Cul3 targeting. Thus, miR-101 is a novel angiomir. Conclusion: Our results provide new mechanistic insights into a functional role of miR-101 as a potential therapeutic target in angiogenesis and vascular remodeling. Antioxid. Redox Signal. 21, 2469-2482.</P>

Characterization and multicolor upconversion emission properties of BaMoO₄: Yb³⁺, Ln³⁺ (Ln = Tm, Ho, Tm/Ho) microcrystals

Ray, Schindra Kumar,Kshetri, Yuwaraj K.,Yamaguchi, Tokutaro,Kim, Tae-Ho,Lee, Soo Wohn Elsevier 2019 Journal of solid state chemistry Vol.272 No.-

<P><B>Abstract</B></P> <P>Hydrothermal process was employed to synthesize the Yb<SUP>3+</SUP>/Tm<SUP>3+</SUP>, Yb<SUP>3+</SUP>/Ho<SUP>3+</SUP> and Yb<SUP>3+</SUP>/Tm<SUP>3+</SUP>/Ho<SUP>3+</SUP> doped BaMoO<SUB>4</SUB> octahedron microcrystals (0.50–5.0 µm). The synthesized phosphors have scheelite tetragonal structure. The elemental mapping suggests the uniform distribution of elements in the samples. The oxidation state of samples were investigated by X-ray photoelectron spectroscopy (XPS) which indicates the existence of Ba<SUP>2+</SUP>, Mo<SUP>6+</SUP>, O, Yb<SUP>3+</SUP>, Tm<SUP>3+</SUP> and Ho<SUP>3+</SUP> in samples. The presence of rare earth ions was also verified by observation of specific absorption peaks in diffuse reflectance spectra (DRS). The tunable multicolor upconversion (UC) emissions were successfully obtained under 980 nm NIR excitation by precisely adjusting the concentration of rare earth ions. The as prepared sample exhibits blue, green and red emission as a result of energy transfer from the Yb<SUP>3+</SUP> to Tm<SUP>3+</SUP> and Ho<SUP>3+</SUP> ions. The power dependent UC emission spectra show the two photonic processes. The energy transfer mechanism from Yb<SUP>3+</SUP> to Tm<SUP>3+</SUP> and Ho<SUP>3+</SUP> was explained <I>via</I> an energy level analysis.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Synthesis of BaMoO<SUB>4</SUB>: Yb<SUP>3+</SUP>, Ln<SUP>3+</SUP> (Ln = Tm, Ho, Tm/Ho) by hydrothermal process. </LI> <LI> Investigation of upconversion luminescence of phosphors under 980 nm excitation. </LI> <LI> Obtaining the multicolor emission by adjusting doped rare-earth ions concentration. </LI> <LI> Explanation of photonic process and energy transfer mechanism. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>Multicolor upconversion emission properties of BaMoO<SUB>4</SUB>: Yb<SUP>3+</SUP>, Ln<SUP>3+</SUP> (Ln = Tm, Ho, Tm/Ho) octahedrons</P> <P>[DISPLAY OMISSION]</P>

Mycophenolic Acid에 의해 유도된 Jurkat 세포주 세포자멸사에서 Heme Oxygenase-1의 발현이 미치는 영향

이호균(Ho Kyun Lee),최수진나(Soo Jin Na Choi) 대한외과학회 2010 Annals of Surgical Treatment and Research(ASRT) Vol.78 No.6

Purpose: This study demonstrates that pharmacologic induction of heme oygenase-1 (HO-1) along with catalytic activation significantly modulated apoptosis of Jurkat cells induced by mycophenolic acid (MPA). Methods: Cells were cultured with the presence or absence of MPA. Flow cytometric analysis was performed after propidium iodide staining. Western blotting of HO-1, Bcl, and Bax was also performed. Cells were stained 4’-6-Diamidino-2-phenylindole (DAPI) and measured by flow cytometry in the absence or presence of CoPPIX. Results: Treatment of MPA decreased cell viability in a dose- and time-dependent manner. MPA-induced cell death was confirmed as apoptosis characterized by sub G0/G1 phase arrest. Expression of HO-1 assumes a pattern of decline after rising at the initial phase. CoPPIX, HO-1 inducer, significantly inhibited the cisplatin-induced apoptosis. Treatment of MPA resulted in reactive oxygen species (ROS) generation in Jurkat cells. CoPPIX attenuated ROS production in MPA-treated cells. Conclusion: This result suggests that the protective mechanism of HO-1 on MPA-induced cytotoxicity is associated with direct inhibition of ROS generation and mitochondrial permeability transition.

Carbon monoxide prevents TNF-α-induced eNOS downregulation by inhibiting NF-κB-responsive miR-155-5p biogenesis

Choi, Seunghwan,Kim, Joohwan,Kim, Ji-Hee,Lee, Dong-Keon,Park, Wonjin,Park, Minsik,Kim, Suji,Hwang, Jong Yun,Won, Moo-Ho,Choi, Yoon Kyung,Ryoo, Sungwoo,Ha, Kwon-Soo,Kwon, Young-Guen,Kim, Young-Myeong Nature Publishing Group 2017 Experimental and molecular medicine Vol.49 No.11

<P>Heme oxygenase-1-derived carbon monoxide prevents inflammatory vascular disorders. To date, there is no clear evidence that HO-1/CO prevents endothelial dysfunction associated with the downregulation of endothelial NO synthesis in human endothelial cells stimulated with TNF-α. Here, we found that the CO-releasing compound CORM-2 prevented TNF-α-mediated decreases in eNOS expression and NO/cGMP production, without affecting eNOS promoter activity, by maintaining the functional activity of the <I>eNOS</I> mRNA 3′-untranslated region. By contrast, CORM-2 inhibited MIR155HG expression and miR-155-5p biogenesis in TNF-α-stimulated endothelial cells, resulting in recovery of the 3′-UTR activity of <I>eNOS</I> mRNA, a target of miR-155-5p. The beneficial effect of CORM-2 was blocked by an NF-κB inhibitor, a miR-155-5p mimic, a HO-1 inhibitor and siRNA against HO-1, indicating that CO rescues TNF-α-induced eNOS downregulation through NF-κB-responsive miR-155-5p expression via HO-1 induction; similar protective effects of ectopic HO-1 expression and bilirubin were observed in endothelial cells treated with TNF-α. Moreover, heme degradation products, except iron and <I>N</I>-acetylcysteine prevented H<SUB>2</SUB>O<SUB>2</SUB>-mediated miR-155-5p biogenesis and eNOS downregulation. These data demonstrate that CO prevents TNF-α-mediated eNOS downregulation by inhibiting redox-sensitive miR-155-5p biogenesis through a positive forward circuit between CO and HO-1 induction. This circuit may play an important preventive role in inflammatory endothelial dysfunction associated with human vascular diseases.</P>

공정제어에의 應用을 위한 마이크로 콤퓨터 시스템의 개발

李秀東,禹治水,李泰鎬,朴源深,黃德浩 울산대학교 1978 연구논문집 Vol.9 No.2

마이크로 프로세서를 이용한 디지탈 공정제어 수단이 고찰되었다. 관심의 초점은 분산-종합제어에 적합한 단말제어 프로세서에 두었다. 시험 제작된 프로세서는 8개의 제어 루우프를 운전하는 독립된 제어장치이며 동시에 종합제어를 위하여 상위 전산기와 데이타 교환이 가능하도록 설계 되었다. 주기적 샘플링에 의한 비례-적분-미분(PID)제어방식을 기본으로 하고 있으며 파라메터 값에 의하여 PI,PD등으로 축소될 수 있도록 하였다. 시험 장치에서는 주기를 2초로 하였는데 A/D변환기의 적절한 선정에 의하여 0.2초정도 까지는 쉽게 단축할 수 있다. 조작자용의 프로세서에 대한 고찰은 최소한의 기능을 가진 것에 한정하였으며 이는 실제 적용 현장과 관련하여 기능이 확장되어야 할 것이다. 사용된 마이크로 프로세서는 범용의 것으로 단말용에는 M6800계통을, 조작자용에는 SC/MP계통을 사용하였다. A microprocessor based digital process controller has been studied. The objective was to develope a stand-alone terminal processor for distributed on-line control systems. The prototype terminal proposed in this paper has the capability of handling eight independent control loops under the supervisory control of main computer and/or operator console. The control algorithm follows analog PID action based on periodically sampled data. The control action can also be reduced to PI,PD and so forth through parameter assignment. Availability of A/D converters to the authors limited sampling period to 2 seconds, but it could easily be reduced to 0.2 sec. employing appropriate A/D devices. The number of operational functions of console processor is kept minimum in this study, the expansion of which should be done for particular application. Hardware implementation was done with general purpose microprocessors; M6800 system for terminal and SC/MP system for console.

단결정 Si(111) 위에 형성된 Ti-실리사이드에 대한 RBS 및 XRD 분석

이중환,권오준,최치규,박동수,김건호,이상환,이의완,곽호원 濟州大學校 基礎科學硏究所 1991 基礎科學硏究 Vol.4 No.1

초고진공 상태에서 p형 Si(111)기판에 Ti을 증착한 후 고진공에서 열처리하여 Ti-실리사이드를 형성시켰으며, Ti-실리사이드의 상전이 및 형성운동학은 2 MeV⁴He? 이온 후방산란과 x-선 회절방법으로 규명하였다. 형성된 TiSi₂는 결정학적으로 C49(ZrSi₂)와 C54 구조의 두 종류로 확인되었다. C49 TiSi₂상은 열처리온도가 700℃이하의 저온에서 형성되었고, 700℃ 이상의 고온에서는 C54 TiSi₂상으로 나타났다. 본 연구에서 확인된 C54 TiSi₂전이온도(??)는 700℃ 였고, TiSi₂형성온도 영역내에서 TiSi₂ 층두께(χ)와 열처리시간(t)의 관계는 저온(700℃ 이하)일 경우 ??이고, 고온(750℃ 이상)에서는 χ=ct+d 의 관계식이 만족됨을 알 수 있었다. 이것은 700℃ 이하에서 TiSi₂ 형성기구가 Si 확산에 의해 제어되며, 750℃ 이상에서는 핵형성 제어에 의하여 계면반응하는 것으로 나타났다. Titanium silicides were prepared by depositing titanium film on p-type Si(111) followed by annealing in ultra high vacuum. The growth kinetics of Ti-silicide has been studied by using ion backscattering spectrometry and x-ray diffractometry. Two crystallographic structures of Ti-silicide were identified the (ZrSi₂)structure and C54. The C49 TiSi₂ phase was formed at low annealing temperature(<700℃),and it transformed to the C54 phase over 700℃. The relation between the thickness of TiSi₂ layer(χ) and the annealing time(t) was ?? when annealing temperature was under 700℃ and χ=ct+d when that was over 750℃. The former implied that the formation of TiSi₂ was controlled by diffusion and the latter by nucleation of at the Ti/Si(111) interface.

휴대폰 카메라용 자동초점 구동기의 충격해석

이성민,김봉석,송준호,이수훈,이혜진,이문구,송준엽,이창우 한국공작기계학회 2008 한국공작기계학회 춘계학술대회논문집 Vol.2008 No.-

Recently, the robustness against daily impact is important according to portablization and downsizing of mobile electronics. Especially, almost parts of cellular phone should undergo drop test when they fall 1.5 m above ground. This test simulates the case when cellular phone slips through user's fingers while he is talking on the phone. This paper studies a drop test of auto focusing (AF) actuator for camera module in cellular phone. This component is composed of voice coil motor (VCM) as an actuator and leaf spring as a guide and suspension. The leaf spring's deformation is essential for the test because its permanent distortion disables the focusing, and then, a high quality photograph cannot be obtained. Up to now the drop test has been carried out after fabricating real AF actuator. We propose a dropt test model which simulates the drop test based on finite element analysis. This model makes us enable investigate the stress acting on the clamping and curved parts of leaf spring. Stress over Von Mises criterion lets the spring deformed permanently, and then AF actuator malfunctioned, It helps us to design and modify AF actuator without manufacturing the real product. And also, it saves the time and cost for the development of new products.