• Title/Summary/Keyword: Lung-heat

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Study on Epidemic Warm Diseases with dampness of "OnByeongJoByeon" ("온병조변(溫病條辨)" 습류온병(濕類溫病)에 대한 고찰)

  • Park, Mi Sun;Kim, Yeong Mok
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.26 no.6
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    • pp.803-811
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    • 2012
  • Oriental Medicine always attach great importance to the damp diseases. Dampness is related with many organs and many clinical diseases. The cause and the location of the damp disease, nature of the symptoms, combination with other pathogenic factors are very diverse. This article analyzed the concept, cause of disease, pathogenesis, characteristic of symptoms, treatment method and prescriptions of Epidemic Warm Diseases of dampness syndrome and cases of dampness-heat diseases based on the theories of Epidemic Warm Diseases and found that theories of Epidemic Warm Diseases have very wide area of application. Dampness is classified into cold-dampness and dampness-heat by combination of heat or cold. The dampness syndrome is related with organs such as lung, spleen, kidney, triple energizers and bladder, and affects liver and heart. The basic treatment methods are dispelling dampness turbidity and diffusing qi movement. The detail treatment methods are spreading lung qi with lightness and resolving dampness and excreting turbidity in upper energizer, opening and dipping down with pungent-bitter and diffusing qi movement and strengthening the spleen and stomach in the middle energizer, draining dampness with bland in the lower energizer. Warming Yang is the main method of treatment for cold-dampness and clearing heat is for dampness-heat with the assistant methods such as resolving dampness and promoting the flow of qi. 5. Acute fever, virus diseases, epidemic diseases among modern diseases are much related with the dampness-heat syndrome.

Study on the 'Diagnosis and Treatment of the Atrophy of lung.pulmonary abscess.Lung-distension' in Synopsis of Golden Chamber (금궤요략.폐위폐옹해수상기병맥증치제칠에 대한 연구)

  • Kim, Jong-Ho;Han, Sung-Kyu;Yeo, Sung-Won;Lee, Yun-Cheon;So, Yong-Sub;Ro, Seung-Jo;Jeong, Heon-Yeong
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.20 no.2
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    • pp.292-304
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    • 2006
  • The Atrophy of lung among chronic asthenia disease is a kind of tuberculosis. It is divided in two types. One is the Atrophy of lung with consumptive fever, the other is the Atrophy of lung with consumptive cold. Four prescriptions can be used treat this disease. Pulmonary abscess(肺癰) is infected by poisonous fatcors of wind and heat. It's symptoms like coughing, chest pain, fever and phlegm with pus after coughing are appeared generally, in case of serious condition, pyemia after coughing can be appeared. This disease is applicable to lung abscess, bronchiectasis, lung gangrene. Six prescriptions can be used to treat this disease. Coughing and congestion of the head(咳嗽上氣) is called Lung-distension(肺腸). Its symptom is dyspnea caused by more expiration rather than inspiration. This disease is divided into two types like chronic asthenia type and inflammatory type. Seven prescriptions can be used to treat this disease.

The effect of the occlusion of the left bronchial artery on the production of HSP70 in cat lung (고양이의 기관지 동맥의 결찰이 폐조직내 열단백질 70의 생성에 미치는 효과)

  • Yun, Sang Won;Rheu, Nam Soo;Cho, Dong Il;Nam, Hyun Jung;Sung, Back Kil;Na, Heung Sik;Hong, Seung Kil
    • Tuberculosis and Respiratory Diseases
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    • v.44 no.1
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    • pp.175-182
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    • 1997
  • Several stresses are known to induce synthesis of heat shock protein The present study was performed to see whether pulmonary ischemia, induced by the bronchial artery occlusion, produced HSP70 in cat lung. To This aim, we compared experimental and control groups of cats with respect to the HSP70 production in the lung. Experimental animals were subjected to 10-min bronchial artery occlusion followed by reperfusion. The interval between the end of the occlusion and the end of the reperfusion was 1 hour, 4 hours and 8 hours, whereas control animal was not subjected 10 any manipulation except anesthesia. According to the interval differences, experimental animals were divided into 1HR, 4HRs and 8HRs groups. To determine The induction of HSP70 in each group, total proteins of lung tissues were extracted and separated by PAGE electrophoresis. Immunoblotting with a mouse monoclonal anti -HSP70 IgG antibody revealed that HSP70 was not detected in the pulmonary tissues resected from control, 1HR or 4HRs groups. In contrast. HSP70 expression in 8HRs group was marked. These results suggest that pulmonary ischemia by the bronchial artery occlusion produces HSP70 in a delayed manner.

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Developing Pattern Identification Questionnaire of Allergic Rhinitis (알레르기 비염의 변증을 위한 설문문항 개발)

  • Kim, Min-Hee;Yun, Young-Hee;Ahn, Jin-Hyang;Ko, Seoung-Gyu;Choi, In-Hwa
    • The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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    • v.30 no.2
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    • pp.112-125
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    • 2017
  • Objectives : The prevalence of allergic rhinitis (AR) is 10-40% worldwide and there are many demands for Traditionl Medicine (TM) treatment for AR. Pattern identification (PI) is essential process in diagnosis and treatment of TM, however, objective assessment measurement for PI of AR in TM is lacked. Methods : PI questionnaire for AR was developed in 2008 by specialists in the department of Otolaryngology of TM, based on systemic and nasal symptoms and signs. However, that questionnaire had many problems in application to clinical practice and has since been revised based on several studies and delphi method. Consequently, the PI questionnaire for AR version 3.0 has been developed. Results & Conclusions : This questionnaire classifies patients with AR as possessing lung-heat, lung-cold, or spleen qi deficiency based on nasal symptoms and general conditions of AR patients. This is first questionnaire for pattern identification of AR. We plan to conduct a validation and reliability study, and revise the questionnaire based on the results of this study.

A Study on Chief Lung-Disorder Diseases of Yeong-Chu Gyeong-maek Chapter (${\ulcorner}$靈樞 經脈編${\Ircorner}$) and Dongui-Bogam (${\ulcorner}$東醫寶鑑${\Ircorner}$) on the Relationship of Sasang Constitutional Diseases ("영추(靈樞).경맥편(經脈編)${\Ircorner}$ 및 주요 폐병증(肺病證)과 사상체질병증(四象體質病證)의 비교.고찰)

  • Kim, Oh-Young;Kim, Il-Hwan;Park, Hye-Sun;Kim, Hyo-Soo;Cho, Jae-Seung;Yim, Chi-Hye
    • Journal of Sasang Constitutional Medicine
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    • v.18 no.2
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    • pp.1-14
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    • 2006
  • 1. Objectives This study is purposed to classify deficiency syndrome(虛證) and Excess syndrome(實證) of chief lung-disorder diseases. 2. Methods It was researched on the comparative and literal study about the relation to Yeong-Chu Gyeong-maek Chapter (${\ulcorner}$靈樞 經脈編${\Ircorner}$) and Dongui-Bogam (${\ulcorner}$東醫寶鑑${\Ircorner}$) and Dongui-Susebowon (${\ulcorner}$東醫壽世保元${\Ircorner}$) in chief lung-disorder symptoms or diseases. 3. Results and Conclusions (1) The chief lung-disorder diseases of Yeong-Chu Gyeong-maek Chapter (${\ulcorner}$靈樞 經脈編${\Ircorner}$), Dongui-Bogam (${\ulcorner}$東醫寶鑑${\Ircorner}$) and Dongui-Susebowon (${\ulcorner}$東醫壽世保元${\Ircorner}$) are asthma(喘), coughing(咳), fullness in the chest(胸滿), sweating symptoms(汗出), cold-heat symptoms(寒熱), dysphoria(煩躁) and sneezing. (2) Asthma symptom(喘) was shown to Soeumin's 4 exterior deficiency diseases, Taeumin's 1 exterior deficiency disease and 1 interior excess disease, and Soyangin's 1 interior excess disease. (3) Coughing symptom(咳) was shown to Soeumin's 1 extrerior deficiency disease and Taeumin's 1 interior excess disease. (4) Fullness in the chest(胸滿) was shown co Soyangin's 4 exterior excess diseases. (5) Sweating symptoms(汗出) was shown to Soeumin's 10 exterior deficiency diseases, Taeumins's 1 exterior deficiency disease, and Soyangin's 1 exterior defecieny disease. (6) Cold-heat symptoms(寒熱) was shown to Soyangin's 4 exterior excess diseases. (7) Dysphoria(煩躁) was shown co Soeumin's 1 exterior deficiency disease and 8 interior deficiency diseases, Taeumin's 1 interior excess disease, and Soyangin's 4 exterior excess and interior excess diseases. (8) Sneezing symptom was shown to Taeumin's 1 exterior excess disease.

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Effect of BIS depletion on HSF1-dependent transcriptional activation in A549 non-small cell lung cancer cells

  • Yun, Hye Hyeon;Baek, Ji-Ye;Seo, Gwanwoo;Kim, Yong Sam;Ko, Jeong-Heon;Lee, Jeong-Hwa
    • The Korean Journal of Physiology and Pharmacology
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    • v.22 no.4
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    • pp.457-465
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    • 2018
  • The expression of BCL-2 interacting cell death suppressor (BIS), an anti-stress or anti-apoptotic protein, has been shown to be regulated at the transcriptional level by heat shock factor 1 (HSF1) upon various stresses. Recently, HSF1 was also shown to bind to BIS, but the significance of these protein-protein interactions on HSF1 activity has not been fully defined. In the present study, we observed that complete depletion of BIS using a CRISPR/Cas9 system in A549 non-small cell lung cancer did not affect the induction of heat shock protein (HSP) 70 and HSP27 mRNAs under various stress conditions such as heat shock, proteotoxic stress, and oxidative stress. The lack of a functional association of BIS with HSF1 activity was also demonstrated by transient downregulation of BIS by siRNA in A549 and U87 glioblastoma cells. Endogenous BIS mRNA levels were significantly suppressed in BIS knockout (KO) A549 cells compared to BIS wild type (WT) A549 cells at the constitutive and inducible levels. The promoter activities of BIS and HSP70 as well as the degradation rate of BIS mRNA were not influenced by depletion of BIS. In addition, the expression levels of the mutant BIS construct, in which 14 bp were deleted as in BIS-KO A549 cells, were not different from those of the WT BIS construct, indicating that mRNA stability was not the mechanism for autoregulation of BIS. Our results suggested that BIS was not required for HSF1 activity, but was required for its own expression, which involved an HSF1-independent pathway.

Heat Dissipation Designs for LED Backlight System; Simulation and Experiment

  • Chiu, Tien-Lung;Tseng, Wet-Yang;Chien, Chin-Cheng;Lo, Wei-Yu;Ting, Chu-Chi;Chang, Chia-Yuan;Chang, Chao-Jen;Sun, Oliver
    • 한국정보디스플레이학회:학술대회논문집
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    • 2005.07a
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    • pp.522-524
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    • 2005
  • The LED light source has many excellent advantages for the application of LCD backlight module. As we know, the operational temperature can significantly influence the characteristics of LEDs. Heat can damage the LED 's quality, and decrease its lifetime and output light intensity. In this paper, we perform computer software, Flomerics CFD (Computational Fluid Dynamics), to simulate heat distribution of the 20.1" LED backlight module we designing, and realize how the different heat sinks can solve the serious heat problem in practice.

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A study on the theory of "Pyong-Yeol-Byong (評熱病論)" in 33th chapter of "SoMon (素問)" Yellow Emperor's Nei-Ching (黃帝內經) (황제내경(黃帝內經) 소문(素問) 평열병론(評熱病論)에 대(對)한 연구(硏究))

  • Moon, Hee-Seork;Hong, Won-Sik
    • Journal of Korean Medical classics
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    • v.3
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    • pp.399-443
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    • 1989
  • In this thesis, I intend to study the translational and clinical interpretation through the syndrom of "Pyong-Yeol-Byong", and reached the following conclusions. 1. Eum-Yang-Kyo (陰陽交)' 1) Meaning: "Eum" means "Essential and vital energy" "Yang" means "Evil factor affecting health" and "Kyo" means "cross-struggle." 2) Location of disease: Heat evil enter Hyeol-Bun (血分) 3) Pathogenesis: Heat evil invade Eum-Bun (陰分) and struggles with Health energy, therefore Eum-Chung (陰精) is exhausted and Heat-evil doesn't disapper, it damage Eum and exhaust fluid. Reach fever, rapid pulse raving and unable to take meal, not controled by sweating and sceach death. 4) Particularity of Syndrome: Heat enter Hyol-Bun, and Evil factor is enough and Health energy is insufficient, so that reveal the symptoms of high fever, delirium with coma, unable to take meals. 5) Therapy: It clears Gi-Bun heat evil (氣分熱邪) by Gypsum, Rhizoma Anemarrhenae, Flos Lonicerae, Fructus Forsythiae, Fructus Gardeniae, Radix Scutellanae Rhizoma Coptidis, and cools Blood by Cornu Rhinoceri Asiatici, Radix Rehmanniae, Cortex Moutan Radicis, Dae-Chung-Yob (大靑葉) Radix Arnebiae Seu Lithospermi. 2. Poong Gweol (風厥) 1) Meaning: Poong means wind-evil, Gweol means reversing up. 2) Location of disease: Disease complexes with TaeYang (太陽) in outer part, and with So-Eum (少陰) in inner part. 3) Pathogenesis: Tae-Yang-Gyeong (太陽經) accept wind-evil and So-Eum-Gyeong (少陽經) Kidney Energy reverse up so that fidgetiness not resolves by sweating. 4) Particularity of Syndrome: There are outer symptoms of fever, hydrosis with inner symptoms of fidgetinessis. 5) Therapy: Reduce Jok-Tae-Yang (足太陽) and Supply Jok-So-Eum (足少陰) by accupuncture, so cure Poong Gweol and make balance between Yeong (營) and Wi (衛). 3. Scrofula coused by wind-evil (勞風) 1) Meaning: It means accepting wind evil rest less. 2) Location of Disease: It locates lung 3) Pathogenesis: Because of accepting wind-evil restless, he take scrofula with damaging lung. 4) Particularity of disease: It is lung disease of aversion to wind and shiver, nape-stiffiness, dim eyesight, cough, disphea, vomitting sputum, if one camnot vomit sputum, he died by damage of lung. 5) Therapy: The period of therapy is different by age or strength of health energy, so I think must prevent Eum deficiency and clear fever no reduced in lung. 4. Shin-Poong (腎風) 1) Meaning: It means taking edema by accepting wind-evil, because the kidney controls water. 2) Location of Disease: It is that wind-evil envade kidney. 3) Pathogenesis : Water evil of kidney with wind-heat rises up to face, reach edema, puffines s of the lower eyelid, floating pulse, bombus, yellowish urine, hydrosis and hand-heating, drymouth and excessive thirsty, walkless by heaviness, menstrual disfunction, restless and unable to take meals, unable to lie flat, heavy cough if lie flat, and accepting wind-evil by deficiency of kidney function, so the function of dredging the water passage is not smooth, symptom of water and symptom of wind reveal together. 4) Therapy: Remove wind-heat, promote diuresis to eliminate tile wetness-evil, supplement the dificiency of kidney's Eum. Finally, we can know that later Fever Disease Medicime (溫病學) is affected to the theory of "Pyong Yeol Byong" in 33th Chapter of SoMoon (素問).

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Pool Boiling Heat Transfer Coefficients Upto Critical Heat flux (임계 열유속 근방까지의 풀 비등 열전달계수)

  • Park, Ki-Jung;Jung, Dong-Soo
    • Korean Journal of Air-Conditioning and Refrigeration Engineering
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    • v.20 no.9
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    • pp.571-580
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    • 2008
  • In this work, pool boiling heat transfer coefficients(HTCs) of 5 refrigerants of differing vapor pressure are measured on horizontal smooth square surface of 9.52 mm length. Tested refrigerants are R123, R152a, R134a, R22, and R32 and HTCs are taken from $10\;kW/m^2$ to critical heat flux of each refrigerant. Wall and fluid temperatures are measured directly by thermocouples located underneath the test surface and by thermocouples in the liquid pool. Test results show that pool boiling HTCs of refrigerants increase as the heat flux and vapor pressure increase. This typical trend is maintained even at high heat fluxes above $200\;kW/m^2$. Zuber's prediction equation for critical heat flux is quite accurate showing a maximum deviation of 21% for all refrigerants tested. For all refrigerant data up to the critical heat flux, Stephan and Abdelsalam's well known correlation underpredicted the data with an average deviation of 21.3% while Cooper's correlation overpredicted the data with an average deviation of 14.2%. On the other hand, Gorenflo's and lung et al.'s correlation showed only 5.8% and 6.4% deviations respectively in the entire nucleate boiling range.

Lung Injury Indices Depending on Tumor Necrosis Factor-$\alpha$ Level and Novel 35 kDa Protein Synthesis in Lipopolysaccharide-Treated Rat (내독소처치 흰쥐에서 Tumor Necrosis Factor-$\alpha$치 상승에 따른 폐손상 악화 및 35 kDa 단백질 합성)

  • Choi, Young-Mee;Kim, Young-Kyoon;Kwon, Soon-Seog;Kim, Kwan-Hyoung;Moon, Hwa-Sik;Song, Jeong-Sup;Park, Sung-Hak
    • Tuberculosis and Respiratory Diseases
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    • v.45 no.6
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    • pp.1236-1251
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    • 1998
  • Background : TNF-$\alpha$ appears to be a central mediator of the host response to sepsis. While TNF-$\alpha$ is mainly considered a proinflammatory cytokine, it can also act as a direct cytotoxic cytokine. However, there are not so many studies about the relationship bet ween TNF-$\alpha$ level and lung injury severity in ALI, particularly regarding the case of ALI caused by direct lung injury such as diffuse pulmonary infection. Recently, a natural defense mechanism, known as the stress response or the heat shock response, has been reported in cellular or tissue injury reaction. There are a number of reports examining the protective role of pre-induced heat stress proteins on subsequent LPS-induced TNF-$\alpha$ release from monocyte or macrophage and also on subsequent LPS-induced ALI in animals. However it is not well established whether the stress protein synthesis such as HSP can be induced from rat alveolar macrophages by in vitro or in vivo LPS stimulation. Methods : We measured the level of TNF-$\alpha$, the percentage of inflammatory cells in bronchoalveolar lavage fluid, protein synthesis in alveolar macrophages isolated from rats at 1, 2, 3, 4, 6, 12, and 24 hours after intratracheal LPS instillation. We performed histologic examination and also obtained histologic lung injury index score in lungs from other rats at 1, 2, 3, 4, 6, 12, 24 h after intratracheal LPS instillation. Isolated non-stimulated macrophages were incubated for 2 h with different concentration of LPS (0, 1, 10, 100 ng/ml, 1, or 10 ${\mu}g/ml$). Other non-stimulated macrophages were exposed at $43^{\circ}C$ for 15 min, then returned to at $37^{\circ}C$ in 5% CO2-95% for 1 hour, and then incubated for 2 h with LPS (0, 1, 10, 100ng/ml, 1, or 10 ${\mu}g/ml$). Results : TNF-$\alpha$ levels began to increase significantly at 1 h, reached a peak at 3 h (P<0.0001), began to decrease at 6 h, and returned to control level at 12 h after LPS instillation. The percentage of inflammatory cells (neutrophils and alveolar macrophages) began to change significantly at 2 h, reached a peak at 6 h, began to recover but still showed significant change at 12 h, and showed insignificant change at 24 h after LPS instillation compared with the normal control. After LPS instillation, the score of histologic lung injury index reached a maximum value at 6 h and remained steady for 24 hours. 35 kDa protein band was newly synthesized in alveolar macrophage from 1 hour on for 24 hours after LPS instillation. Inducible heat stress protein 72 was not found in any alveolar macrophages obtained from rats after LPS instillation. TNF-$\alpha$ levels in supernatants of LPS-stimulated macro phages were significantly higher than those of non-stimulated macrophages(p<0.05). Following LPS stimulation, TNF-$\alpha$ levels in supernatants were significantly lower after heat treatment than in those without heat treatment (p<0.05). The inducible heat stress protein 72 was not found at any concentrations of LPS stimulation. Whereas the 35 kDa protein band was exclusively found at dose of LPS of 10 ${\mu}g/ml$. Conclusion : TNF-$\alpha$ has a direct or indirect close relationship with lung injury severity in acute lung injury or acute respiratory distress syndrome. In vivo and in vitro LPS stimulation dose not induce heat stress protein 72 in alveolar macrophages. It is likely that 35 kDa protein, synthesized by alveolar macrophage after LPS instillation, does not have a defense role in acute lung injury.

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