72 research outputs found
A Study on the Optimization of Miller Cycle for Naval Vessel Diesel Engine
Since May 2005, all ocean-going vessels built after January 2000 have had to comply with the emission control regulations according to Annex โ
ฅ of the MARPOL 73/78 convention. Thesse regulations set limits on exhaust gas emissions for nitrogen oxides(NOx), sulphur oxides(SOx) and particulate matter(PM) from ships.
The air pollutants as NOx, SOx, PM etc are harmful things for human health. They can be obsorbed onto the lung and cause lung disease like a lung cancer.
And they are blamed as one of the major causes of photochemical smog and acid rains.
The NOx emission is related with engine combustion process as like high peak pressure, high compression ratio, high rate of fuel delivery. In other words, the
higher combustion temperature, the grater amount of NOx formation. Much of NOx emission can be decreased by the technology today. For example the fuel injection control by CR(Common Rail) and electronic control, EGR(Exhaust Gas Recirculation), SCR(Selective Catalytic Reduction) which using ammonia or urea, Miller Cycle and 2-stage turbocharging, etc.
Miller Cycle is one of the few measures that can be applied in an internal combustion engine to simultaneously reduce NOx emission and fuel consumption.
Since all engine builders strive to meet engine emission limits without any loss of efficiency, practically every modern engine is operated today with at least moderate Miller timing.
In this study, a performance simulation about naval vessel diesel engine carried out through a mathematical modeling techniques for flow analysis of the working
gas. And the simulation results were compared with measured data to evaluate reliability of simulation. Finally we obtained reliable simulation results.
The purpose of this study is to predict effect of miller cycle for naval vessel diesel engine. By changing the intake valve closing timing and boost pressure,
the engine performance is simulated. And we found the best valve timing and proper boost pressure.List of Tables โ
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List of Figures โ
ด
Abstract โ
ต
Nomenclature โ
ท
์ 1์ฅ ์ ๋ก 1
1.1 ์ฐ๊ตฌ ๋ฐฐ๊ฒฝ 1
1.2 ์ฐ๊ตฌ ๋ด์ฉ 3
์ 2์ฅ ์นํ๊ฒฝ ์์ง์ ์๊ตฌ์ ๋์ฑ
4
2.1 ์ ํด ๋ฐฐ๊ธฐ๊ฐ์ค ๋ฐฐ์ถ๊ท์ ๊ท์ 4
2.2 ์ ํด ๋ฐฐ๊ธฐ๊ฐ์ค ๊ฐ์ถ ๋์ฑ
9
2.2.1 ๋ฐฐ๊ธฐ๊ฐ์ค ์ฌ์ํ(EGR) ์ฅ์น 10
2.2.2 ์ ํ์ ์ด๋งค ํ์(SCR) ์ฅ์น 11
2.2.3 EGR ๋ฐ SCR ์ฅ์น ํจ์ ์ค์น ๊ฐ๋ฅ์ฑ ๊ณ ์ฐฐ 12
์ 3์ฅ ๋ฐ๋ฌ ์ฌ์ดํด(Miller Cycle) ํจ๊ณผ 15
3.1 ๋ฐ๋ฌ ์ฌ์ดํด์ ์๋ฆฌ 15
3.2 ๋ฐ๋ฌ ์ฌ์ดํด์ ์ดํจ์จ 17
3.3 ์์ง์ ๋ฐ๋ฌ ์ฌ์ดํดํ ์ฐ๊ตฌ ๋ฐ ์ ์ฉ์ฌ๋ก 21
์ 4์ฅ ๋์ ค๊ธฐ๊ด์ ์ฑ๋ฅ ์๋ฎฌ๋ ์ด์
ํ๋ก๊ทธ๋จ 23
4.1 ์ด๋ก ํด์์ ์ด์ฉ๋ ์ฃผ๋ ๊ฐ์ 23
4.2 ์ค๋ฆฐ๋ ๋ฐ ์ฉ๊ธฐ๋ด์ ์ํ ๋ณํ 25
4.2.1 ๊ฐ์ค ๊ตํ ๊ณผ์ 25
4.2.2 ์์ถ ํฝ์ฐฝ ๊ณผ์ 27
4.3 NO ์์ฑ๋ ๊ณ์ฐ๋ฐฉ๋ฒ 29
4.4 ๊ณผ๊ธ๊ธฐ ํจ์จ ๊ณ์ฐ๋ฐฉ๋ฒ 30
4.4.1 ์
๋ ฅ๋ฐ์ดํฐ ๋ฐ ๊ฐ์ 30
4.4.2 ๊ณผ๊ธ๊ธฐ ํจ์จ ๊ณ์ฐ๊ณผ์ 31
4.5 ์๋ฎฌ๋ ์ด์
๋์์์ง ๋ฐ ๊ณ์ฐ ๋ชจ๋ธ 32
4.5.1 ์๋ฎฌ๋ ์ด์
๋์์์ง 32
4.5.2 ๊ณ์ฐ๋ชจ๋ธ ๋ฐ ์กฐ๊ฑด 32
4.6 ์๋ฎฌ๋ ์ด์
๊ฒฐ๊ณผ ๊ณ ์ฐฐ 34
์ 5์ฅ ๋ฐ๋ฌ ์ฌ์ดํด ์ ์ฉ์ ์ฑ๋ฅ์์ธก 36
5.1 ๋ฐ๋ฌ ์ฌ์ดํด ์ ์ฉ 36
5.1.1 EIVC ์ ์ฉ 36
5.1.2 LIVC ์ ์ฉ 39
5.2 ๋ฐ๋ฌ ์ฌ์ดํด ์ ์ฉ ๊ฒฐ๊ณผ ๊ณ ์ฐฐ 39
5.2.1 25% ๋ถํ์กฐ๊ฑด 40
5.2.2 50% ๋ถํ์กฐ๊ฑด 44
5.2.3 75% ๋ถํ์กฐ๊ฑด 48
5.2.4 100% ๋ถํ์กฐ๊ฑด 52
์ 6์ฅ ๊ฒฐ๋ก 56
์ฐธ๊ณ ๋ฌธํ 57Maste
Epidemiology of HIV/AIDS in East Asia
Background:Recent predictions of catastrophic epidemic surge of HIV infection in East Asia concern experts and governmental organizations. As in many other areas, countries in East Asia show diversities in their HIV epidemics, both geographically and temporally. However, they have similar regional, cultural and racial characteristics which allow them to have certain common factors. Having a clear picture of the current extent and feature of HIV/AIDS in this region is a very difficult task largely due to the fast pacing of expending epidemic and difficulty in data-sharing among countries in the region. Hence, we decided to study the epidemiologic feature of HIV/AIDS in East Asia through East Asia Network on HIV (EAN-HIV).
Materials and Methods:The epidemiological patterns of HIV/AIDS in East Asian countries were investigated by collecting data through EAN-HIV.
Results:The HIV/AIDS epidemic in East Asia started relatively late at mid 1980s. Since then, the number of newly infected HIV/AIDS cases has been steadily increasing with stiffer escalation in recent years. In China and Taiwan, IDU plays an important part in the swiftly growing HIV epidemics; however, in other regions like Korea, Japan, and Hong Kong, MSM (men who have sex with men) seems to be more of a problem. The major subtypes of HIV in East Asia are subtype B, C, and CRF01_AE, and rapidly evolving circulating recombinant forms (CRF) between subtypes such as CRF07_BC give dynamic change to the current status.
Conclusion:The incidence of HIV/AIDS is rapidly increasing in East Asia. The epidemic pattern has undergone dynamic changes over time. China seems to be the leading source of HIV/AIDS epidemic in East Asia due to its large population and rapidly growing epidemics.ope
A Case of Brucellar Spondylitis with Multiple Spine Involvement
Brucellosis, a zoonosis with world wide distribution, is a systemic infection that affects several organs and has protean presentation. Although spondylitis is universally the most common complication of brucellosis and difficult to treat, there is no consensus on the preferred combination of antibiotics use. The authors report a case of a 58-year-old male patient with brucellar spondylitis involving several vertebrae. Diagnosis was made by positive blood culture and magnetic resonance imaging. The authors use a combination method of doxycycline, ciprofloxacin and streptomycin for a period of 3 months. The systemic symptoms were improved after treatment.ope
Prognosis Factors of Clostridium difficile Associated Diarrhea
Background:Clostridium difficile associated diarrhea (CDAD) has a wide range of clinical manifestations. The prognostic factors of CDAD are not fully understood.
Materialsand Methods:A retrospective cohort study of 115 patients with CDAD from Aug. 2002 to Dec. 2003 was conducted to evaluate prognostic factors of CDAD. Bacteriologic factors were determined by detecting the binary toxin gene, tcd A, tcd A rep and tcd B gene. Poor prognosis was defined as diarrhea more than 10 days even with classic treatment, recurrence, death, and moribund discharge.
Results:Approximately 79% of isolated strains were toxin A+/B+ strains and 21% were toxin A-/B+ strains. There was no difference in prognosis between toxin A+ and toxin A- strains. 39 (33.9%) cases showed poor prognosis and 76 (66.1%) cases showed good prognosis. Univariate analyses revealed that the poor prognostic factors were old age over 70 years old, male, the number of antibiotics used after onset of symptom, the administration of carbapenems, aminoglycosides, glycopeptides after onset of symptom, history of DM and stroke, and high Charlson comorbidity index. Multiple logistic regression analysis identified old age over 70 years old (odds ratio=3.378, P=0.009) and the administration of carbapenems after onset of symptom (odds ratio 7.210, P<0.001) as the independent poor prognostic factors.
Conclusion:Old age over 70 and the administration of carbapenems after onset of symptom were the poor prognostic factors for CDAD caused by none-binary toxin producing strains.ope
ํ์๋ง์ฐ์ค์์ ์์ธ์ ์ ์กฐ์ฌํ ํํผ์์์ธํฌ์ ํ์์์ ์ ๊ฐ ๋ฏธ์น๋ ์ํฅ
์ํ๊ณผ/๋ฐ์ฌ[์๋ฌธ]
[ํ๊ธ]
์ธ์ฒด์ ์ ์ ํผ๋ถ์์ ์ฃผ๋ก ํํผ์ ์นจ์ฐฉ๋ ๋ฉ๋ผ๋์์์ ์นด๋กํฐ๋
ธ์ด๋์์ ๊ทธ๋ฆฌ๊ณ ์งํผ
ํ๊ด๋ด์ ํ์์๋ฑ์ ์ํด ์ํฅ์ ๋ฐ์ผ๋ ์ด์ค ํผ๋ถ์์ ๊ฐ์ฅ ์ค์ํ ์ํฅ์ ๋ฏธ์น๋ ๊ฒ
์ ๋ฉ๋ผ๋์์์ด๋ค. ํผ๋ถ์ ๋ฉ๋ผ๋์์ ์นจ์ฐฉ์ ๋๊ฐ์ง ๋ฒ์ฃผ๋ก ๊ตฌ๋ถํ ๋ ์ฒซ์งธ๋, ์์ธ์
์ด๋ ๋๋ ํ๊ฒฝ์์ธ์ ์ํฅ์์ด ์ ์ ์ ์ผ๋ก ๊ฒฐ์ ๋ ์์์ธํฌ์ ๊ธฐ๋ฅ์ ์ํด์๋ง ๋ฉ๋ผ๋์
์ ์นจ์ฐฉ์ด ํ์ฑ๋๋ ๊ณ ์ ์ ํผ๋ถ์ (constitutive skin color)๊ณผ ๋์งธ๋, ๊ณ ์ ํผ๋ถ์์
๋ํ์ฌ ์์ธ์ ์ด๋ ๊ทธ์ธ ๋ค๋ฅธ ํ๊ฒฝ์์ธ์ ์ํด ์ ๋ฐ๋๋ ์์์ ํผ๋ถ์ (facultative ski
n color)์ผ๋ก ๊ตฌ๋ณ๋ ์ ์๋ค.
์์ธ์ ์กฐ์ฌํ ์ ๋ฐ๋๋ ๋ฉ๋ผ๋์์์ ์ฆ๊ฐ๋ tyrosinaseํ์ฑํ ๋ฐ ํ๋์ฑ ์์์ธํฌ ์
์ ์ฆ๊ฐ์ ์ฐ๊ด์ด ์๋ ๊ฒ์ผ๋ก ๋ฐํ์ก์ผ๋ฉฐ, Rosdahl(1979)์ ์์ธ์ ์ด ์กฐ์ฌ๋์ง ์์ ์ค
ํ๋๋ฌผ์ ์์ธ์ ์ ์ผ์ ์ ๋ฐ๋ณต์กฐ์ฌํ ๊ฒฝ์ฐ DOPA์์ฑ ์์์ธํฌ์ ์์ ์ฆ๊ฐ๋ ์์ธ์ ์กฐ์ฌ
์ค๋จํ ์ฅ๊ธฐ๊ฐ ํ์ฑํ๋์ด ์ง์๋๋ ํ์์ ๋ณด๊ณ ํ์๋ค.
๋ณธ ์คํ์์ ์ ์๋ ์คํ๋๋ฌผ์ ์์ธ์ ์ ๋ฐ๋ณต์กฐ์ฌํ์ฌ ์์์ธํฌ ์์ ์ฆ๊ฐ์ ๋ฉ๋ผ๋
์์ฑ์ ์ ๋ฐ์ํจ ํ ์ฑ๋ถ์ด ๋ค๋ฅธ ํ์์์ ์ ๋ค์ ๋ํฌํ์ฌ ์๊ธฐ ์ ์ ๋ค์ด ํ์ง์ ์์์ธ
ํฌ์ ๋ฏธ์น๋ ์ํฅ์ ๊ด์ฐฐํ์๋ค.
์คํ๋๋ฌผ๋ก ์ฑ์๋ C57Bl ์
์ฑ๋ง์ฐ์ค 72๋ง๋ฆฌ๋ฅผ ์ฌ์ฉํ์์ผ๋ฉฐ ์ ์ฒด ๋ง์ฐ์ค์ ์์ชฝ ๊ท์
UV-B๋ฅผ 10์ผ๊ฐ ์กฐ์ฌํ์๋ค. UV-B์ ๊ด์์ผ๋ก YS UVB-400์ ์ฌ์ฉํ์์ผ๋ฉฐ ํ์ฅ์ 290โผ325
nm(์ฃผํ์ฅ, 301nm) ์ผ์ผ ์กฐ์ฌ๋์ 100mJ/ใ ์๋ค.
์์ธ์ ์กฐ์ฌ์๋ฃํ 72๋ง๋ฆฌ์ ๋ง์ฐ์ค๋ฅผ ๋ฌด์์๋ก 3๊ตฐ์ผ๋ก ๋๋์ด ๋ค์๊ณผ ๊ฐ์ด ์คํํ์
๋ค.
์ โ
๊ตฐ: ์ฐ๊ณ ๊ธฐ์ ๋ํฌ๊ตฐ(๋์กฐ๊ตฐ)โฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆ 24๋ง๋ฆฌ
์ โ
ก๊ตฐ: 20% monobenzylether of hydroquinone (MBEHQ) ๋ํฌ๊ตฐโฆโฆโฆโฆโฆโฆ24๋ง๋ฆฌ
์ โ
ข๊ตฐ: 20% azelaic acid(AZA) ๋ํฌ๊ตฐโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆ24๋ง๋ฆฌ
์๊ธฐ ํ์์์ ์ ๋ฅผ ๋ง์ฐ์ค์ ์์ชฝ ๊ท์ ๋งค์ผ ์ค์ ์คํ 2ํ์ฉ 6์ฃผ๊ฐ ๋ํฌํ์์ผ๋ฉฐ, DOP
A์ผ์๊ณผ ๊ดํํ๋ฏธ๊ฒฝ ๋ฐ ์ ์ํ๋ฏธ๊ฒฝ ๊ด์ฐฐ์ ์ํด ์คํ 6์ฃผ๋์ ๋งค์ฃผ ๊ฐ๊ตฐ๋น 4๋ง๋ฆฌ์ ๋ง์ฐ
์ค ์์ฆ ๊ท ๋ฐฐ๋ถ์์ ์๊ฒํ์๋ค.
์คํ๊ฒฐ๊ณผ๋ฅผ ์์ฝํ๋ฉด ๋ค์๊ณผ ๊ฐ๋ค.
1. 20% MBEHQ์ 20% AZA๋ํฌ๊ตฐ์ ๋์กฐ๊ตฐ์ ๋นํด DOPA์์ฑ ์์์ธํฌ์ ์์ ํฌ๊ธฐ, ๋๋
๊ธธ์ด ๋ฐ ๋ฉ๋ผ๋์์ ํ์ฑ์ ์ ์ํ ๊ฐ์๋ฅผ ๋ณด์ฌ ํ์์์ ์ ๋ก์ ์์์๋ ํจ๊ณผ๋ฅผ ๋ํ๋ด
์๋ค.
2. ๋ ์คํ๊ตฐ๊ฐ์ ๋น๊ต์์ AZA๋ํฌ๊ตฐ์ DOPA์์ฑ ์์์ธํฌ์๋ ๋ํฌ 6์ฃผ ํ์ MBEHQ
๋ํฌ๊ตฐ๋ณด๋ค ์์์๊ฒ ๊ฐ์๋์์ผ๋ฉฐ, hematoxylin-eosin ์ผ์์ MBEHQ๋ํฌ๊ตฐ์ AZA๋ํฌ๊ตฐ
์ ๋นํด ๋ํฌ 4์ฃผ ์ดํ๋ถํฐ ํํผ์ ํ์ ํ ๋นํ๋ฅผ ๋ํ๋ด์๋ค.
3. ์คํ์ฝ๋ฌผ์ด DOPA์์ฑ ์์์ธํฌ์ ํํ์ ๋ฏธ์น๋ ์ํฅ ์ค ํน์ดํ ํ์์ MBEHQ๋ํฌ๊ตฐ
์์ ๋ํฌ 3์ฃผ ํ์ ์์๋๊ธฐ๋ง ๊ฐ์๋๊ฑฐ๋ ์์ค๋ ๊ตฌํ์ ๋น์ ํ ์์์ธํฌ๊ฐ ๋ฐ๊ฒฌ๋ ๊ฒ
์ด๋ฉฐ, AZA๋ํฌ๊ตฐ์์๋ ์์์ธํฌ์ ์ธํฌ์ฒด์ ์์๋๊ธฐ๊ฐ ๋ชจ๋ ๋ํฌ๊ธฐ๊ฐ์ ๋น๋กํ์ฌ ๊ฐ์
๋๋ ์๊ฒฌ์ ๋ณด์๋ค.
4. ์ ์ํ๋ฏธ๊ฒฝ ์๊ฒฌ์, ๋์กฐ๊ตฐ์์ ์คํ ์ ๊ธฐ๊ฐ์ ๊ฑธ์ณ ๊ฐ์งํ์ฑ์ธํฌ ๋ด์ ์์์ธํฌ ๋ด
์ stage โ
ฃ์ ๋ฉ๋ผ๋์์ฒด๋ค์ด ๋ค์ ๊ด์ฐฐ๋์์ผ๋ฉฐ ์คํ๊ตฐ์์๋ ๋ํฌ 3์ฃผ ํ๋ถํฐ ๊ฐ์งํ
์ฑ์ธํฌ ๋ด์์ ๊ณตํฌ(vacuole)์ ๋ค์ด์๋ ์ ์๋ฐ๋๊ฐ ๋ฎ์ ์๋์ ๋ฉ๋ผ๋์์ฒด๋ค์ด ๊ด์ฐฐ๋
์๋ค. ์ด๋ฌํ ํ์์ MBEHQ๋ํฌ๊ตฐ์์ ๋ ํ์ ํ์๋ค. ๋ํฌ 5์ฃผ์ 6์ฃผ ํ์๋ ์คํ๊ตฐ์
๊ฐ์งํ์ฑ์ธํฌ ๋ฐ ์์์ธํฌ ๋ด์์ ๋ฉ๋ผ๋์์ฒด๊ฐ ์์ค๋์๊ฑฐ๋ ๋๋ฌผ๊ฒ ๊ด์ฐฐ๋์๋ค.
์ด์์ ๊ฒฐ๊ณผ๋ฅผ ์ข
ํฉํ๋ฉด, MBEHQ์ AZA๊ฐ ํ์์์ ์ ๋ก์ ์์ฉํ๋ ๊ธฐ์ ์ ์๊ธฐ ์ฝ์ ๋ชจ
๋ ํํผ์์์ธํฌ์ ์์ฉํ์ฌ ํ์์ ํจ๊ณผ๋ฅผ ๋ํ๋ด๋ ๊ฒ์ผ๋ก ์ฌ๋ฃ๋๋ฉฐ MBEHQ๋ ์ฅ๊ธฐ๊ฐ ๋
ํฌ์ ๋ง์ฐ์ค ํผ๋ถ์ ์๊ทนํ์์ ์ ๋ฐํ๋ ๊ฒ์ผ๋ก ๊ด์ฐฐ๋์๋ค.
The Effect of Depigmenting Agents on Epidermal Melanocytes in UV-irradiated Mice
Young Keun Kim
Department of Medical Science The Graduate School, Yonsei University
(Directed by Professor Yoon-Kee Park, M.D.)
Normal human skin colors are produced by four skin pigments: in the epidermis,
carotenoids and melanin; and in the dermis, oxygenated and reduced hemoglobin. Of
these pigments, the major color determinant is melanin. Melanin pigmentation of the
skin can be divided into two categories. The first, constitutive skin color
designates the amount of cutaneous melanin pigmentation generated in accordance
with cellular genetic programs in the absence of direct influences by radiations.
The second, facultative (inducible) skin color characterizes the increase in
melanin pigmentation above the constitutive level and arises from the complex
interplay of solar radiation and other environmental factors upon the genetically
endowed melanogenesis of the individual.
Published reports regarding the increased melanin pigmentation following
ultraviolet radiation suggest that an increase in tyrosinase activitr and a
numerical increase of functioning melanocytes are responsib1e for enhanced pigment
production.
In this experiment, we induced activation of melanocytes and melanin pigmentation
in the epidermis of C 57 B1 mice by UV-B irradiation. Aftar UV-B irradiation we
observed the effect of the two different kinds of depigmenting agents on the
epidermal melanocytes in UV-irradiated mice.
A total of 72 mice had both their ears irradiated by UV-B daily for 10 days. The
light source was YS UVB-400 with a wave length spectrum of 290โผ325nm(peak out-put
at 301). The lamp to target distance was 30ใ and daily dose was 100 mJ/ใ . After
irradiation, 72 mice were divided into 3 groups in random sampling and the
application of depigmenting agents on each group is as follows.
Group โ
: cream base(control)โฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆ24
Group โ
ก: 20% monobenzylether of hydroquinone (MBEHQ)โฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆ24
Group โ
ข: 20% azelaic acid(AZA)โฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆโฆ24
The application of the depigmenting agents was done twice a day on both ears of
mice for 6 weeks and four mice in each group were sacrificed by the end of the 1st,
2nd, 3rd, 4th, 5th, and 6th week of the application. Both ears of the mouse were
cut at the base for split-dopa preparation and for light microscopic and electron
microscopic preparation. The results are summarized as follows:
1. Both of MBEHQ and AZA showed significant diminution in the size,
circumference, and number of dopa-positive melanocytes in C 57 Bl mouse skin.
2. As compared with the two experimental groups, the number of dopa-positive
melanocytes tended to be of smaller quantity in AZA treated group by the end of the
6th week of the application. In areas treated with MBEHQ, the vertical sections
stained with hematoxylin-eosin showed marked epidermal thickening after the 4
weeks' application.
3. In areas treated with MBEHQ, many of the remaining melanocytes were abnormal
in shape having lost their dendrites so that they appeared as round bodies after
the 3 weeks' application. In areas treated with AZA, there were no abnormal
morphologic changes such as round bodies throughout the period of experiment.
4. On electron microscopic findings, there were many melanosomes of stage โ
ฃ in
the keartinocytes and melanocytes during the experimental period in the control
group. In the experimental groups, a small amount of melanosomes surrounded by
vacuoles in the cytoplasm of keratinocytes was a prominent feature after the 3
weeks' application especially in MBEHQ treated group. By the end of the 5th and 6th
week of the application in the experimental groups, there was a small amount or no
melanosomes in the epidermis.
In summary, the present study suggests that both of MBEHQ and AZA inhibit melanin
pigmentation by the action on epidermal melanocytes either by destroying or
inactivating melanocytes and the skin treated with MBEHQ skewed marked epidermal
thickening comparing to the skin treated with AZA.restrictio
์ด์ข ๊ธฐ์ ์ฆ๊ธฐ ์ฆ์ฐฉ ์คํฉ์ ์ด์ฉํ ๊ณ ๋ถ์์นด๋ณธ ๋๋ ธํ๋ธ ์ ์กฐ
Thesis(master`s)--์์ธ๋ํ๊ต ๋ํ์ :์์ฉํํ๋ถ,2005.Maste
๋ผ๋์นผ๋ฐ์์ ์ด์ฉํ ์ฐ์๊ณ ๋ฆฌํํฉ๋ฌผ์ ํฉ์ฑ
Thesis (master`s)--์์ธ๋ํ๊ต ๋ํ์ :ํํ๊ณผ ์ ๊ธฐํํ์ ๊ณต,1996.Maste
Chloroquine resistance and analysis of single-nucleotide polymorphisms of pvmdr1 gene in Korean vivax malaria
์ํ๊ณผ/๋ฐ์ฌ[ํ๊ธ]
๋ฐฐ๊ฒฝ: 1997๋
์ดํ ๋น๋ฌด์ฅ์ง๋ ๊ทผ์ฒ ๋ง๋ผ๋ฆฌ์ ์ํ์ง์ญ์ ์ค์ฌ์ผ๋ก ์์ํ ํ๊ตญ๊ตฐ์ ๋ง๋ผ๋ฆฌ์์ ๋ํ hydroxychloroquine/primaquine ์๋ฐฉ์๋ฒ์ ๋ง๋ผ๋ฆฌ์ ๋ฐ์์จ ๊ฐ์์ ๊ธฐ์ฌํ๊ณ ์์ผ๋, chloroquine ๋ด์ฑ ๋ง๋ผ๋ฆฌ์ ์ถํ์ ์ํ์ฑ์ด ์๋ค. ์ด์ ์ฐ๊ตฌ์๋ ์๋ฐฉ์ฝ์ ์ ์ ํ ๋ณต์ฉํ์์์๋ ๋ถ๊ตฌํ๊ณ ๋ฐ์ํ ๋ง๋ผ๋ฆฌ์์ ๋น๋ ๋ฐ chloroquine ๋ด์ฑ๊ฐ์๋ฅผ ์ํํ์๊ณ , pvmdr1 ์ ์ ์ ๋จ์ผ๊ธฐ๋ณ์ด์ chloroquine ๋ด์ฑ๊ณผ์ ์ฐ๊ด์ฑ์ ์กฐ์ฌํ์๋ค.๋ฐฉ๋ฒ: ๋ง๋ผ๋ฆฌ์ ๋ฐ์ ์ํ์ง์ญ์ ํ๊ตญ๊ตฐ์ ๋์์ผ๋ก ์๋ฐฉ์ ์ํ์ฌ 2006๋
5์๋ถํฐ hydroxychloroquine sulfate 400 mg์ด ๋ง๋ผ๋ฆฌ์ ์ ํ๊ธฐ์ 1์ฃผ๋ง๋ค ํฌ์ฌ๋์๋ค. 2006๋
6์๋ถํฐ 9์๊น์ง ๋น๋ฌด์ฅ์ง๋ ๊ทผ์ฒ์ ๊ฒฝ๊ธฐ๋์ ์ฃผ๋ํ ํ๊ตญ๊ตฐ์์ ๋ฐ์ํ 102๋ช
์ ํ์๋ฅผ ๋์์ผ๋ก ๋ง๋ผ๋ฆฌ์ ๋ฐ์ ์ด์ ์ ์๋ฐฉ์๋ฒ์ ์ ์ ์ฑ์ ์กฐ์ฌํ์๋ค. ์ด ์ค 85๋ช
์ ํ์๋ฅผ ๋์์ผ๋ก 28์ผ๊ฐ chloroquine ์น๋ฃ ๋ด์ฑ ๊ฐ์๋ฅผ ์ํํ์์ผ๋ฉฐ ์ด๋ค ํ์๋ก๋ถํฐ ๋ถ๋ฆฌ๋ Plasmodium vivax๋ก๋ถํฐ pvmdr1 ์ ์ ์์ ๋จ์ผ๊ธฐ๋ณ์ด๋ฅผ ๋ถ์ํ์๋ค.๊ฒฐ๊ณผ: 102๋ช
์ ํ์ ์ค ์๋ฐฉ์๋ฒ์ด ์ ์ ํ์๋ ํ์๋ 66๋ช
(64.7%) ์ด์๊ณ , ๋ถ๊ท์นํ ๋ณต์ฉ 11๋ช
(10.8%), ์๋ฐฉ์ฝ์ ์ ํ ๋ณต์ฉํ์ง ์์๋ ํ์๋ 25๋ช
(24.5%)์ด์๋ค. Chloroquine ์น๋ฃ ๋ด์ฑ ๊ฐ์๋ฅผ ์ํํ ๋ชจ๋ ํ์์์ chloroquine ํ์ค์น๋ฃ 3์ผ ์ดํ์ ๋ง์ดํ์ก๋๋ง๊ฒ์ฌ์์ ๋ง๋ผ๋ฆฌ์ ์์ถฉ์ ๊ด์ฐฐ๋์ง ์์๋ค. pvmdr1 ์ ์ ์ ๋ถ์์ ์ํํ 78์ ๋ชจ๋์์ F1076L ๋ณ์ด๊ฐ ๊ด์ฐฐ๋์๋ค.๊ฒฐ๋ก : ์ฐ๊ตฌ ๋์ ๋ง๋ผ๋ฆฌ์ ๋ฐ์ ํ์ ์ค 2/3๊ฐ ์ ์ ํ ์๋ฐฉ์ฝ์ ๋ณต์ฉํ๊ณ ์์๋ค. Chloroquine์ ์น๋ฃ์คํจ๋ ์์์ผ๋, pvmdr1 ์ ์ ์์ F1076L ๋ณ์ด๊ฐ chloroquine ์๋ฐฉ์คํจ์ ๊ด๋ จ ์์ ๊ฒ์ผ๋ก ์๊ฐ๋๋ค.
[์๋ฌธ]
Background: Chemoprophylaxis with chloroquine (CQ) and primaquine has been used in the Republic of Korea (ROK) Army since 1997 to reduce the number of the malaria cases. It has contributed, in part, to the decrease in the number of malaria cases among military personnel. However, chemoprophylaxis may facilitate the development of CQ-resistant strains of Plasmodium vivax. We investigated the breakthrough malaria infection and the therapeutic efficacy of CQ in P. vivax in ROK. And the pvmdr1 gene polymorphisms and its relevance to CQ-resistance in P. vivax were evaluated.Methods: Chemoprophylaxis with hydroxychloroquine sulfate (400 mg, once per week) was started in May and continued throughout the transmission season. From June to September 2006, 102 soldiers with vivax malaria near the demilitarized zone in Gyeonggi-do, ROK, were enrolled. Breakthrough malaria was defined when a patient had taken all prophylactic doses every week prior to infection. The status of chemoprophylaxis was determined by the interview. In 85 patients, therapeutic efficacy was monitored during 28 days after standard CQ treatment. The single nucleotide polymorphisms of pvmdr1 in the isolates from these patients were analyzed.Results: Among 102 malaria cases occurring during study period, breakthrough malaria was observed in 66 patients (64.7%) who had complete compliance. Incomplete compliance was 11 cases (10.8%) and no compliance was 25 cases (24.5%). In all patients enrolled in therapeutic efficacy monitoring, parasitemia had not been observed since 3 days after standard CQ treatment. Nucleotide polymorphism at 1 codon (F1076L) was found in all analyzed isolates.Conclusion: Breakthrough malaria was observed in about two thirds of malaria cases occurring in the area on chemoprophylaxis. Although there was no treatment failure, it was likely that the F1076L mutation of the pvmdr1 gene might contribute to CQ-prophylaxis failure in P. vivax.ope
Effect of tuberculosis on the course of HIV infection
์ํ๊ณผ/์์ฌ[ํ๊ธ]
์ฌ๋๋ฉด์ญ๊ฒฐํ๋ฐ์ด๋ฌ์ค(human immunodeficiency virus; HIV) ๊ฐ์ผ์์์ ๋ฐ์ํ๋ ๊ธฐํ๊ฐ์ผ ์ค ๊ฒฐํต์ ๊ตญ๋ด๋ฟ๋ง ์๋๋ผ ์ธ๊ณ์ ์ผ๋ก ๊ฐ์ฅ ํํ ํ์ฒ์ฑ ๋ฉด์ญ๊ฒฐํ์ฆ(acquired immunodeficiency syndrome; AIDS) ์ ์ ์งํ์ด๋ฉด์ HIV ๊ฐ์ผ์์ ์ฃผ์ ์ฌ๋ง ์์ธ์ด๋ค. ๊ฒฐํต์ด HIV์ ๋ณต์ ๋ฅผ ์ฆ๊ฐ์ํจ๋ค๊ณ ์๋ ค์ ธ ์์ง๋ง ์์์ ์ผ๋ก HIV ๊ฐ์ผ์ ์ง๋ณ๊ฒฝ๊ณผ๋ฅผ ์
ํ์ํฌ ์ ์๋์ง์ ๋ํ์ฌ๋ ๋
ผ๋์ด ๋ง์ ๊ตญ๋ด์์์ ๊ฒฐํต์ด HIV ๊ฐ์ผ์ ์ง๋ณ๊ฒฝ๊ณผ์ ๋ฏธ์น๋ ์ํฅ์ ์กฐ์ฌํ์๋ค.์ฐ์ธ๋ํ๊ต ์๊ณผ๋ํ ์ธ๋ธ๋์ค๋ณ์์์ 1992๋
๋ถํฐ 2004๋
๊น์ง HIV ๊ฐ์ผ์์ค ๊ฒฐํต์ผ๋ก ์ง๋จ ๋ฐ์ 44์์ ํ์๊ตฐ๊ณผ ํ์๊ตฐ๊ณผ ๋น์ทํ CD4+ T์ธํฌ์ (ยฑ25/ใ)์ ๋์ํ๋ ๊ฒฐํต ๋ฐ๋ณ์ด ์์๋ HIV ๊ฐ์ผ์ 44์์ ๋์กฐ๊ตฐ์ ํํฅ์ ์ฝํธํธ ์ฐ๊ตฌ๋ฐฉ๋ฒ์ผ๋ก viral load, ๊ด์ฐฐ ์์ ํ AIDS ์ ์ ์งํ์ ๋ฐ์ ๋น๋, ์์กด์จ์ ๋น๊ตํ์ฌ ๊ฒฐํต์ด HIV ๊ฐ์ผ์ ์ง๋ณ๊ฒฝ๊ณผ์ ๋ฏธ์น๋ ์ํฅ์ ์กฐ์ฌํ์๋ค.ํ์๊ตฐ๊ณผ ๋์กฐ๊ตฐ ๊ฐ์ ์ฐ๋ น, ์ฑ๋ณ, ๊ฐ๋ ฅํ ํญ๋ ํธ๋ก๋ฐ์ด๋ฌ์ค ์น๋ฃ(highly active anti-retroviral therapy; HAART) ์ ๋ฌด์ ์ฐจ์ด๋ ์์๋ค. ํ๊ท CD4+ T์ธํฌ์๋ ํ์๊ตฐ 84.5๊ฐ/ใ, ๋์กฐ๊ตฐ 84.0๊ฐ/ใ๋ก ์ฐจ์ด๊ฐ ์์๋ค. ํ๊ท viral load๋ ํ์๊ตฐ 6.2ร105 copies/ใ, ๋์กฐ๊ตฐ 2.9ร105 copies/ใ๋ก ํ์๊ตฐ์์ ๋๊ฒ ๋ํ๋ฌ์ผ๋ฉฐ(p=0.001), ๊ด์ฐฐ ์์ ํ AIDS ์ ์ ์งํ์ ๋ฐ์ ๋น๋๋ ํ์๊ตฐ 2.9/100 person-months, ๋์กฐ๊ตฐ 1.2/100 person-months๋ก ๋์กฐ๊ตฐ์ ๋นํ์ฌ ํ์๊ตฐ์ด 2.43(95% CI: 1.02-5.14)๋ฐฐ ๋์๋ค. ํ์๊ตฐ์ ์ฌ๋ง๋ฅ ๋ํ ๋์กฐ๊ตฐ๋ณด๋ค ๋์์ผ๋ฉฐ(p=0.025, log rank), ๊ฒฐํต์ด HIV ๊ฐ์ผ์์ ์ฌ๋ง์ ๋ฏธ์น๋ ๊ธฐ์ฌ ์ํ๋๋ 2.09(95% CI: 1.07-4.08)์๋ค.์๊ธฐ์ ๊ฒฐ๊ณผ๋ฅผ ํตํ์ฌ HIV ๊ฐ์ผ์์๊ฒ ๊ฒฐํต์ด ๋ฐ์ํ๋ฉด viral load๊ฐ ์ฆ๊ฐํ์ฌ ๋ฉด์ญ ์ ํ๋ฅผ ์ฆ๊ฐ์ํด์ผ๋ก ๊ธฐํ ๊ฐ์ผ์ ๋น๋๋ฅผ ๋์ด๊ณ ๊ฒฐ๊ตญ ์ฌ๋ง์ ์ํฅ์ ์ค ์ ์์ด ๊ฒฐํต์ด HIV ๊ฐ์ผ์์ ์ง๋ณ ๊ฒฝ๊ณผ๋ฅผ ์
ํ์ํจ๋ค๋ ๊ฒ์ ์ ์ ์์๋ค.
[์๋ฌธ]Background: In Korea, endemic area of Mycobacterium tuberculosis (TB) infection, the incidence of new HIV infection has been persistently increasing each year and HIV/TB coinfected patients are common. Several studies suggested that TB enhanced the replication of HIV and could accelerate the course of HIV infection. So, we investigated the effect of tuberculosis on the course of HIV infection in Korea.Methods: In an observational study of retrospective cohorts at Severance Hospital, Yonsei University College of Medicine, Seoul, Korea from 1992 to 2004, the evolution of 44 HIV-infected patients with TB (cases) was compared with that of the absolute CD4+ T cell count matched(ยฑ25 cells/ใ) 44 HIV-infected patients without TB (control subjects). To determine the effect of tuberculosis on the course of HIV infection, the incidence rate of opportunistic diseases and the mortality were evaluated.Results: There were no significant differences between the cohorts for age, sex and antiretroviral therapy including highly active antiretroviral therapy. The mean CD4+ T cell counts were similar between cases and control subjects (84.5 cells/ใ versus 84.0 cells/ใ, respectively). The mean viral load was much higher in cases than that of control subjects (6.2ร105 copies/ใ versus 2.9ร105 copies/ใ, respectively, p=0.001). The incidence rate of new subsequent AIDS-defining opportunistic diseases in cases was 2.9 infections per 100 person-months compared with 1.2 infections per 100 person-months in control subjects for an incidence rate density ratio of 2.43 (95% CI: 1.02-5.14). Cases also had a shorter overall survival than did control subjects (p = 0.025, log rank test). Tuberculosis in HIV-infected patients was associated with an increased risk for death (hazard ratio = 2.09, 95% CI: 1.07-4.08).Conclusion: Tuberculosis in HIV-infected patients was related to more frequent AIDS-defining opportunistic diseases and shorter survival.ope
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