• Journal of Chest Surgery
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• v.36 no.2
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• pp.63-72
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• 2003

Although a variety of synthetic vascular grafts are available in modern vascular surgery, no ideal prosthesis ha,4 yet been developed. Small-caliber vascular grafts with low flow, as used in the lower extremity, continue to become thrombosed at unacceptable rates. We have developed and evaluated the new antithrombogenic blood contacting surfaces in canine model. Material and Method: Two now antithrombogenic blood contacting surfaces(Polyvinylalcohol -Polyurethane(PVA-PU) blend and natural Graphite-polyurethane(G-PU) blend) have been developed and evaluated in canine model, using vascular grafts and patches. The luminal surfaces of the test vascular grafts(5 mm ID) were fabricated by dipping a glass rod in PVA-PU blend solution(50 % PVA) using phase separation method. Mongrel dogs of either sex weighing 18-22 kg were anesthetized by endotracheal intubation using halothane and their lungs were ventilated with a volume-cycled ventilator, Maintenance anesthesia with 0.5-1.0% halothane and supplemental oxygen was used. Two pairs were used for comparison in the bilateral femoral arteries for both vascular grafts(PVA-PU vs. PU) and vascular patches(G-PU vs. PU). Bilateral groin incisions were made and the arteries were exposed and clamped. After an excision of 1 cm of the artery between clamps, a grail of 2.5 cm in length was implanted end-to-end using 6-0 polypropylene suture. The vascular patch was implanted as a form of on-lay patch. Animals were sacrificed at 1, 2, 4, 6, 8 and 16 weeks for vascular grafts and 1, 2. 4 and 6 weeks for vascular patches. Result The vascular grafts of PVA-PU blends showed patent lumina in the 2 and 16 weeks animals, while those of PU showed a patent lumen in 2 weeks animal. PVA-PU graft of 16 weeks showed a fairly clean luminal surface. A light microscopic finding of this graft demonstrated good tissue infiltration through porosity, The animals with vascular patches showed patent arteries in both groups except 2 weeks animal. Scanning electron microscopy of the luminal surfaces of G-PU patches in 4 and 6 weeks animals showed endothelial cell covering with microvilli. PU patches showed qualitatively less endothelial cell covering. Conclusion: In conclusion, PVA-PU and G-PU blends can be a promising blood contacting surfaces for application in a synthetic vascualr graft. However, further animal study is needed to determine the real long-term effects of these methods of surface modifications.

• The Journal of Korean Medical History
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• v.18 no.2
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• pp.137-187
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• 2005

This thesis study of the medical concept Qiu Zheng Lu (求正錄) is discussed in the Lei Jing Fu Yi (類經附翼), a book authored by Zhang Jie Bin (張介賓) a medical doctor during the Chinese Ming (明) dynasty (1368-1683). The meaning of Qiu Zheng Lu (求正錄) is "searching for the rightness." In his book Zhang Jie Bin (張介賓) intended to clarify Qiu Zheng Lu (求正錄) by delineating the concept into four categories. These are: Sanjiao Baoluo Mingmen Bian (三焦包絡命門 辨) the theory of the triple warmer, the Pericardium, the Gate of Life ; Da Bao Lun (大寶論) the theory of the great treasure of the human body; Zhen Yin Lun (眞陰論) the theory of true-yin fluid; and Shi Er Zang Mai Hou Bu Wei Lun (十二臟脈候部位論) the theory of the part of the pulse and its condition in regards to the twelve viscera. Sanjiao Baoluo Mingmen Bian (三焦包絡命門辨), the theory of the triple warmer, the Pericardium, the Gate of Life. The triple warmer (三焦: Sanjiao) is composed of three parts: the upper, middle, and lower. This concept is also connected with the functions and roles of the vital organs. The upper burner is related to the heart and lungs. The middle burner is related to the liver and spleen. Whereas, the lower burner is related to the kidneys. Bao-Luo (包絡) is the Pericardium, the envelope of the heart, serving as the protector of the heart. Ming-Men (命門) is the Gate of Life, reffering to the vitals of life. It functions as kidney-yang which is considered as the origin of yang-energy of the human body, and serves partly as the function of cortico-adrenal gland in modern medicine. Zhang Jie Bin (張介賓) discussed the Da Bao Lun (大寶論) as the most important function in the human body because the Da Bao (大寶/great treasure) is the true-yang (眞陽) which is the affective force for physiological functions, and as the source of energy for life activities. Moreover, true-yang (眞陽) functions both as a heater and thermometer that warms the human body and indicates vitality by levels of body warmth respectively. The Zhen Yin Lun (眞陰論) theory states that if true-yang (眞陽) is energy, then true-yin (眞陰) is the source of energy. This can be likened to a tree with roots which absorbs nutrients from the ground (source), and spreads the nutrients (energy) through its branches. Thus, true-yin (眞陰) is the root cause for later functional activities of true-yang (眞陽). In Shi Er Zang Mai Hou Bu Wei Lun (十二臟脈候部位論) the theory of the pulse (脈 /Mai) and its condition in regards to the twelve viscera, Zhang Jie Bin (張介賓) insisted that when a diagnoses by the pulse is made the five vital organs and the six viscera (五臟六腑) of a human body should be harmoniously arranged in accordance with its respective part of the pulse. Furthermore, Zhang Jie Bin (張介賓) supported his theory with evidence from earlier Chinese medical doctors. And, by stating that human beings must cultivate and preserve their true-yin (眞陰) and true-yang (眞陽) energies he therefore created four new prescriptions called: Zuoguiyin (左歸飮), Youguiyin (右歸飮), Zuoguiwan (左 歸丸), Youguiwan (右歸丸). To further clarify his theory Zhang Jie Bin (張介賓) considered that the function of true-yang (眞陽) and true-yin (眞陰) is expressed by Ming-Men (命門). This theory is that for humans to be spiritually and physically healthy they must live in accord with natural law. Also, within the framework of natural law, astronomical and geographical factors must be considered for complete, holistic, health. Thus, Ming-Men is the basis for healthy living in the modern world.

• Pediatric Infection and Vaccine
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• v.25 no.2
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• pp.82-90
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• 2018

Purpose: Survival after liver transplantation (LT) has improved over the years, but infection is still a major complication. We aimed to identify the characteristics of bacterial infections in pediatric LT recipients. Methods: This study is a retrospective review of 189 consecutive children undergoing LT between 2000 and 2015 at a single center. In this study, the incidence of infection was determined for the following periods: within 1 month, between 1-5 months, and between 6-12 months. Patients who underwent liver transplants more than once or multiple organ transplants were excluded. Results: All patients had received postoperative antibiotic for 3 days. Only the maintenance immunosuppression with oral tacrolimus and steroids were performed. As a result, 132 bacterial infections developed in 87 (46.0%) patients (0.70 events per person-year). Bacterial infections occurred most frequently within the first month (n=84, 63.6%) after LT. In the pathogens, Staphylococcus aureus (15.2%), Enterococcus species (15.2%), and Klebsiella species (13.6%) were most common. Regarding the organ infected, bloodstream was most common (n=39, 29.5%), followed by peritoneum (n=28, 21.2%), urinary tract (n=25, 18.9%), and lungs (n=20, 15.2%). We changed prophylactic antibiotics from ampicillin-sulbactam to piperacillin-tazobactam at 2011, October, there were no significant effects in the prevalence of antibiotics resistant bacterial infections. The 1-year mortality was 9.0% (n=17), in which 41.2% (n=7) was attributable to bacterial infection; septicemia (n=4), pneumonia (n=2), and peritonitis (n=1). Conclusions: The incidence and type of bacterial infectious complications after LT in pediatric patients were similar to those of previous studies. Bacterial complications affecting mortality occur within 6 months after transplantation, so proper prophylaxis and treatment in this period may improve the prognosis of LT.

• Radiation Oncology Journal
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• v.13 no.4
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• pp.321-330
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• 1995

Purpose : To evaluate whether the early pulmonary irradiation can prevent or decrease the pulmonary damage and contribute to improve ultimate survival in paraquat lung. Materials and Methods : From Jun. 1987 to Aug. 1993, thirty patients with paraquat poisoning were evaluated. Fourteen of these patients were received pulmonary irradiation(RT). All of the patients were managed with aggressive supportive treatment such as gastric lavage, forced diuresis, antioxidant agents and antifibrosis agents. Ingested amounts of paraquat were estimated into three groups(A : minimal 50cc). Pulmonary irradiation was started within 24 hours after admission(from day 1 to day 11 after ingestion of paraquat). Both whole lungs were irradiated with AP/PA parallel opposing fields using Co-60 teletherapy machine. A total of 10Gy(2Gy/fr. x 5days) was delivered without correction of lung density. Results : In group A, all patients were alive regardless of pulmonary irradiation and in group C, all of the patients were died due to multi-organ failure, especially pulmonary fibrosis regardless of pulmonary irradiation. However, in group B, six of 7 patients($86{\%}$) with no RT were died due to respiratory failure, but 4 of 8 patients with RT were alive and 4 of 5 patients who were received pulmonary irradiation within 4 days after ingestion of paraquat were all alive though radiological pulmonary change. One patient who refused RT after 2Gy died due to pulmonary fibrosis. All 3 patients who were received pulmonary irradiation after 4 days after ingestion were died due to pulmonary fibrosis in spite of recovery from renal and hepatic toxicity Conclusion : It is difficult to find out the effect of pulmonary irradiation on the course of the paraquat lung because the precise plasma and urine paraquat concentration were not available between control and irradiation groups. But early pulmonary irradiation within 4 days after paraquat poisoning with aggresive supportive treatment appears to decrease Pulmonary toxicity and contribute survival in patients with mouthful ingestion of paraquat who are destined to have reversible renal and hepatic damage but irreversible pulmonary toxicity.

• Journal of Life Science
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• v.20 no.6
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• pp.845-852
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• 2010

Our previous study showed that lungs infected by Pseudomonas, a gram-negative bacteria, produce prostaglandin $D_2$ ($PGD_2$) and prostaglandin $E_2$ ($PGE_2$), the two major prostanoids generated by cyclooxygenase-2 (COX-2), and that the ratio of $PGD_2$ and $PGE_2$ can affect the outcome of the bacterial lung infection. In this study, we sought to uncover the mechanism that determines the ratio of $PGD_2$ and $PGE_2$ produced in lung inflammation. When treated with lipopolysaccharide (LPS), primary alveolar macrophages, extracted from mouse lung, more $PGE_2$ was produced than $PGD_2$, whereas MH-S, a murine alveolar macrophage cell line, produced more $PGD_2$ than $PGE_2$ in a similar experiment. Western blot analyses showed that the kinetics of COX-2 expression in both cell types is similar and epigenetic silencing of COX-2 expression did not affect expressions of lipocalin-PGD synthase (L-PGDS) and PGE synthase (mPGES-1), major enzymes synthesizing $PGD_2$ and $PGE_2$ in inflammation, respectively, indicating no effect of COX-2 on expressions of the two enzymes. Expressions of L-PGDS and mPGES-1 were also similar in both cell types, suggesting no effect of the two key enzymes in determining the ratio of $PGD_2$ and $PGE_2$ in these cells. A single intraperitoneal injection of LPS to C57BL/6 mice induced COX-2 expression and, similar to alveolar macrophages, produced more $PGE_2$ than $PGD_2$ in the lung. These results suggest that the differential expressions of $PGD_2$ and $PGE_2$ in the lung reflect those in alveolar macrophages and may not be directly determined by the enzymes responsible for $PGD_2$ and $PGE_2$ synthesis.

• Journal of Acupuncture Research
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• v.22 no.3
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• pp.185-200
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• 2005

Objective : The aim of this study was to investigate the asthma-suppressive and immune-regulatory effect of AHCR-HA(ASARI HERBA CUM RADICE Herbal-acupuncture) at Pyesu(BLl3) on OVA(ovalbumin)-induced asthma in mice. Methods : C57BL/6 mice out of all the experimental groups, except the Normal group and the AHCR-HA group, were sensitized and challenged with OVA The mice in the AHCR-HA group and the OVA-AHCR-HA group were treated with AHCR-HA(1%) at Pyesu(BL13). The mice in the OVA-Saline group were injected with saline at Pyesu(BL13). The mice in the OVA-Needle-Prick group were treated with a single prick with an injection needle at Pyesu(BL13). AHCR-HA saline injection and needle prick were administered for 8 weeks, three times a week. Result : 1. The populations of granulocytes, CD3e-/CCR3+ cells, CD69+/CD3e+ cells, CD4+ cells and CD23+/B220+ cells in the OVA-induced asthmatic mouse lungs decreased significantly by AHCR-HA. 2. The lung weight, total cells in lung, total leukocytes in BALF, eosinophils in BALF, collagen accumulation in the lung sections of the OVA-AHCR-HA group decreased significantly. 3.The concentrations of IL-4, IL-5, IL-13, IgE in BALF and serum of the OVA-AHCR-HA group decreased significantly. 4. The numbers of Gr-1+/CD11b+, CCR3+, CD3e+, CD19+, CD3e+/CD69+cells in the OVA-AHCR-HA group decreased significantly. 5. The mRAN expressions of $TNF-{\alpha}$, IL-5, IL-4 and IL-13 in lung of the OVA-AHCR-HA group decreased significantly. 6. The AHCR-HA group didn't show any considerable difference from the Normal group. The OVA-saline group and the OVA-Needle prick group showed suppressive effects on OVA-induced asthma however they were not statistically significant. Conclusion : These results suggest that AHCR-HA at Pyesu(BL13) is considered to be effective in treating asthma and to be put to practical use in the future asthma clinic.

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.835-845
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• 1998

Background: Silica-induced lung diseases is characterized by the accumulation of inflammatory cells at early stage and fibrosis in pulmonary parenchyma and interstitium at late stage. As a consequence of inflammation, silicosis is accompanied with the expansion of interstitial collagen and the formation of fibrotic nodule. In this process, several kinds of lung cells produce cytokines which can amplify and modulate pulmonary fibrosis. The alveolar macrophage is a potent source of proflammatory cytokines and growth factor. But in the process of silicotic inflammation and fibrosis, there are many changes of the kinetics in cytokine network. And the sources of cytokines in each phase are not well known. Method: 2.5 mg of silica was instillated into the lung of C57BL/6J mice. After intratracheal instillation of silica, the lungs were removed for imunohistochemical stain at 1, 2, 7 day, 2, 4, 8, 12 week, respectively. We investigated the expression of IL-1$\beta$, IL-6, TNF-$\alpha$ and TGF-$\beta$ in lung tissue. Results: 1) The expression of IL-6 increased from 1 day after exposure to 8 weeks in vascular endothelium. Also peribronchial area were stained for IL-6 from 7 days and reached the peak level for 4 weeks. 2) The IL-1 $\beta$ was expressed weakly at the alveolar and peribronchial area through 12 weeks. 3) The TNF-$\alpha$ expressed strongly at alveolar and bronchial epithelia during early stage and maintained for 12 weeks. 4) TGF-$\beta$ was expressed strongly at bronchial epithelia and peribronchial area after 1 week and the strongest at 8 weeks. Conclusion: The results above suggests IL-6, TNF-$\alpha$ appear to be a early inflammatory response in silica induced lung fibrosis and TGF-$\beta$ play a major role in the maintenance and modulation of fibrosis in lung tissue. And the regulation of TNF-$\alpha$ production will be a key role in modultion of silica-induced fibrosis.

• Tuberculosis and Respiratory Diseases
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• v.57 no.1
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• pp.37-46
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• 2004

Background : Lung pericytes are important constituent cells of blood-air barrier in pulmonary microvasculature. These cells take part in the control of vascular contractility and permeability. In this study, it was hypothesized that change of lung pericytes might be attributable to pathologic change in microvasculature in acute lung injury. The purpose of this study was how hypoxia change proliferation and genetic expression in lung pericytes. Methods : From the lungs of several Sprague-Dawley rats, performed the primary culture of lung pericytes and subculture. Characteristics of lung pericytes were confirmed with stellate shape in light microscopy and immunocytochemistry. 2% concentration of oxygen and $200{\mu}M$ $CoCl_2$ were treated to cells. Tryphan blue method and reverse transcription-polymerase chain reaction were done. Results : 1. We established methodology for primary culture of lung pericytes. 2. Hypoxia inhibited cellular proliferation in pericytes. 3. Hypoxia could markedly induce vascular endothelial growth factor(VEGF) and smad-2. 4. Hypoxia-inducible factor-$1{\alpha}$(HIF-$1{\alpha}$) was also induced by 2% oxygen. Conclusion : Viability of lung pericytes are inhibited by hypoxia. Hypoxia can stimulate expression of hypoxia-responsive genes. Pericytic change may be contributed to dysfunction of alveolar-capillary barrier in various pulmonary disorders.

• Tuberculosis and Respiratory Diseases
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• v.81 no.1
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• pp.42-48
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• 2018

Background: The diffusing capacity of the lung is influenced by multiple factors such as age, sex, height, weight, ethnicity and smoking status. Although a prediction equation for the diffusing capacity of Korea was proposed in the mid-1980s, this equation is not used currently. The aim of this study was to develop a new prediction equation for the diffusing capacity for Koreans. Methods: Using the data of the Korean National Health and Nutrition Examination Survey, a total of 140 nonsmokers with normal chest X-rays were enrolled in this study. Results: Using linear regression analysis, a new predicting equation for diffusing capacity was developed. For men, the following new equations were developed: carbon monoxide diffusing capacity (DLco)=-10.4433-0.1434${\times}$age (year)+0.2482${\times}$heights (cm); DLco/alveolar volume (VA)=6.01507-0.02374${\times}$age (year)-0.00233${\times}$heights (cm). For women the prediction equations were described as followed: DLco=-12.8895-0.0532${\times}$age (year)+0.2145${\times}$heights (cm) and DLco/VA=7.69516-0.02219${\times}$age (year)-0.01377${\times}$heights (cm). All equations were internally validated by k-fold cross validation method. Conclusion: In this study, we developed new prediction equations for the diffusing capacity of the lungs of Koreans. A further study is needed to validate the new predicting equation for diffusing capacity.

• Tuberculosis and Respiratory Diseases
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• v.39 no.6
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• pp.474-483
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• 1992

Background: Regardless of its causes, acute lung injury is characterized pathophysiologically by increased pulmonary arterial pressure and the protein-rich edema. Many inflammatory mediators are known to be involved in the pathogenesis of acute lung injury, including oxygen free radicals (OFR). But the changes in pulmonary capillary pressure in the OFR-induced acute lung injury is not clear. While the pulmonary edema characterized by the movement of fluid and solutes is dependent on the pressure gradient and the alveolar-capillary permeability, the role of pulmonary capillary pressure in the development of pulmonary edema is also not well understood. Method: Male Sprague-Dawley rats were divided into 5 groups: normal control (n=5), xanthine/xanthine oxidase (X/XO)-treated group (n=7), catalase-pretreated group (n=5), papaverine-pretreated group (n=7), and indomethacin-pretreated group (n=5). In isolated perfused rat lungs, the sequential changes in pulmonary arterial pressure, pulmonary capillary pressure by double occlusion method, and lung weight as a parameter of pulmonary edema were determined. Results: Pulmonary arterial pressure and pulmonary capillary pressure were increased by X/XO. This increase was significantly attenuated by catalase and papaverine, but indomethacin did not prevent the X/XO-induced increase. Lung weight gain was also observed by X/XO perfusion. It was prevented by catalase. Papaverine did not completely block the increase, but significantly delayed the onset. Indomethacin had no effect on the increase in lung weight. Conclusion: These data suggest that increased pulmonary capillary pressure by OFR may aggravate pulmonary edema in the presence of increased alveolar-capillary permeability and this may not be mediated by cyclooxygenase metabolites.