• Journal of Acupuncture Research
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• v.22 no.3
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• pp.253-270
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• 2005

Objective : The purpose of this study is to establish a category for acupuncture therapy by appropriate etiological analysis and differenciation of edema. Methods : We arrange Huang Di Nei Jing and thirty four kinds of literature about edema. Results : 1. The cause of Edema is functional disorder of lung, spleen, kidney, bladder and tri-energizer by six kinds of natural factors, internal injury and loss of nutritions. 2. Edema compartmentalize into the water of five zang organs, several kinds of edema(e,g. 5, 10, 12, 24) and yang & yin edema. 3. An ultimate cause of edema pathogenesis is the disturbance of Qi function in kidney. 4. In view of the results so far achived,'GV26(水淸)' is a vitally important acupoint in acupuncture treatment of edema.'GV26(水淸)' and 'CV9(水分)' are very useful acupoints in moxibustion. 5. In the acupuncture and moxibustion treatment of yang edema, we can use acupoints as like 'GV26(水溝)', 'S36(足三里)', 'B20(脾兪)' and 'SP9(陰陵泉)' by purgation and reduction for expelling wind, reducing fever and eliminating dampness. In an instance of yin edema, we can use acupoints as like 'CV9(水分)' 'S36(足三里)', 'CV6(氣海)', 'B20(脾兪)', 'B23(腎兪)' and 'K3(太谿)' by reinforcement for tonifying spleen yang-middle energizer-, qi-transmission and water promoting.

• Tuberculosis and Respiratory Diseases
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• v.42 no.4
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• pp.522-534
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• 1995

Background: In the pathogenesis of acute lung injury induced by lipopolysaccharide(LPS), oxygen radiclls are known to be involved in one part. Superoxide dismutase(SOD) protects oxygen radical-induced tissue damage by dismutating superoxide to hydrogen peroxide. In eukaryotic cells, two forms of SOD exist intracellularly as a cytosolic, dimeric copper/zinc-containing SOD(CuZnSOD) and a mitochondrial, tetrameric manganese-containing SOD(MnSOD). But there has been little information about SOD gene expression and its regulation in pulmonary alveolar macrophages(PAMs). The objective of this study is to evaluate the SOD gene expression induced by LPS and its regulation in PAMs of rat. Method: In Sprague-Dawley rats, PAMs obtained by broncholaveolar lavage were purified by adherence to plastic plate. To study the effect of LPS on the SOD gene expression of PAMs, they were stimulated with different doses of LPS($0.01{\mu}g/ml{\sim}10{\mu}g/ml$) and for different intervals(0, 2, 4, 8, 24hrs). Also for evaluating the level of SOD gene regulation actinomycin D(AD) or cycloheximide(CHX) were added respectively. To assess whether LPS altered SOD mRNA stability, the rate of mRNA decay was determined in control group and LPS-treated group. Total cellular RNA extraction by guanidinium thiocyanate/phenolfchlorofonn method and Northern blot analysis by using a $^{32}P$-labelled rat MnSOD and CuZnSOD cDNAs were performed. Results: The expression of mRNA in MnSOD increased dose-dependently, but not in CuZnSOD. MnSOD mRNA expression peaked at 8 hours after LPS treatment. Upregulation of MnSOD mRNA expression induced by LPS was suppressed by adding AD or CHX respectively. MnSOD mRNA stability was not altered by LPS. Conclusion: These findings show that PAMs of rat could be an important source of SOD in response to LPS, and suggest that their MnSOD mRNA expression may be regulated transcriptionally and require de novo protein synthesis without affecting mRNA stability.

• Tuberculosis and Respiratory Diseases
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• v.45 no.2
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• pp.369-379
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• 1998

Background: Platelet-activating factor(PAF) might play an important role in the development of acute respiratory distress syndrome. Since PAF induced lung injury is similar to changes of acute respiratory distress gyndrome, and abnormalities in surfactant function have been described in acute respiratory distress syndrome, the authors investigated the effects of PAF on the regulation of surfactant protein A, B and C mRNA accumulation Method: The effects of PAF on gene expression of surfactant protein A, B and C in 24 hours after intratracheal injection of PAF in rats. Surfactant protein A, B and C mRNAs were measured by filter hybridization. Results: The accumulation of SP-A mRNA in PAF treated group was significantly decreased by 37.1 % and 41.6%, respectively compared to the control group and the group treated with Lyso-PAF(p<0.025, p<0.01). The accumulation of SP-B mRNA in PAF treated group was decreased by 18.7% and 32.2 %, respectively compared to the control group and the group treated with Lyso-PAF but statistically not significant. The accumulation of SP-C mRNA in PAF treated group was significantly decreased by 30.7% and 38.5%, respectively compared to the control group and the group treated with Lyso-PAF(p<0.l, p<0.01). Conclusion: These findings represent a marked inhibitory effects of platelet-activating factor on surfactant proteins expression in vivo. This supports, in turn, 'platelet-activating factor might be related to pathogenesis of acute respiratory distress syndrome.

• Journal of Chest Surgery
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• v.44 no.5
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• pp.348-354
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• 2011

Background: Traumatic rupture of the diaphragm is an unusual type of trauma. In addition, it is difficult to diagnose because it can be accompanied by injuries to other organs. If it is not detected early, the mortality rate can increase due to serious complications. Diaphragmatic rupture is an important indicator of the severity of the trauma. The aim of this study was to investigate the factors affecting the incidence of complications and mortality in patients who had surgery to treat traumatic rupture of the diaphragm. Materials and Methods: The subjects were patients who had undergone a diaphragmatic rupture by blunt trauma or stab wounds except patients who were transferred to other hospitals within 3 days of hospitalization, from January 2000 to December 2007. This study was a retrospective study. 43 patients were hospitalized, and 40 patients were included during the study period. Among them, 28 were male, 12 were female, and the average age was 42 (from 18 to 80). Outcome predictive factors including hypoxia, ventilator application days, revised trauma score (RTS), injury severity score (ISS), age, herniated organs, complications, and the mortality rate were investigated. Results: Causes of trauma included motor vehicle crashes for 20 patients (50%), falls for 10 (25%), stab wounds for 8 (20%), and agricultural machinery accidents for 2 (5%). Most of the patients (36 patients; 90%) had wound sites on the left. Diagnosis was performed within 12 hours for most patients. The diaphragmatic rupture was diagnosed preoperatively in 27 patients (70%) and in 12 patients (30%) during other surgeries. For surgical treatment, thoracotomy was performed in 14 patients (35%), laparotomy in 11 (27.5%), and a surgery combining thoracotomy and laparotomy in 15 patients (37.5%). Herniated organs in the thoracic cavity included the stomach for 23 patients (57.5%), the omentum for 15 patients (37.5%), the colon for 10 patients (25%), and the spleen for 6 patients (15%). Accompanying surgeries included splenectomy for 13 patients (32.5%), lung suture for 6 patients (15%), and liver suture for 5 patients (12.5%). The average hospital stay was $47.80{\pm}56.72$ days, and the period of ventilation was $3.90{\pm}5.8$ days. The average ISS was $35.90{\pm}16.81$ (11~75), and the average RTS was $6.46{\pm}1.88$ (1.02~7.84). The mortality rate was 17.5% (7 patients). Factors affecting complications were stomach hernia and age. Factors affecting the mortality rate were ISS and RTS. Conclusion: There are no typical symptoms of the traumatic rupture of the diaphragm by blunt trauma. Nor are there any special methods of diagnosis; in fact, it is difficult to diagnose because it accompanies injuries to other organs. Stab wounds are also not easy to diagnose, though they are relatively easy to diagnose compared to blunt trauma because the accompanying injuries are more limited. Suture of the diaphragm can be performed through the chest, the abdomen, or the thoracoabdomen. These surgical methods are chosen based on accompanying organ injuries. When there are many organ injuries, there are a great number of complications. Significant factors affecting the complication rate were stomach hernia and age. ISS and RTS were significant as factors affecting the mortality rate. In the case of severe trauma such as pelvic fractures, frequent physical examinations and chest X-rays are necessary to confirm traumatic rupture of the diaphragm because it does not have specific symptoms, and there are no clear diagnosis methods. Complications and the mortality rate should be reduced with early diagnosis and with treatment by confirming diaphragmatic rupture in the thoracic cavity and the abdomen during surgery.

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.861-869
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• 1998

Backgrounds: The injury of a tissue results in the infalmmation, and the imflammed tissue is replaced by the normal parenchymal cells during the process of repair. But, constitutional or repetitive damage of a tissue causes the deposition of collagen resulting in the loss of its function. These lesions are found in the lung of patients with idiopathic pulmonary fibrosis, complicated fibrosis after diffuse alveolar damage (DAD) and inorganic dust-induced lung fibrosis. The tissue from lungs of patients undergoing episodes of active and/or end-stage pulmonary fibrosis shows the accumulation of inflammatory cells, such as mononuclear cells, neutrophils, mast cells and eosinophils, and fibroblast hyperplasia. In this regard, it appears that the inflammation triggers fibroblast activation and proliferation with enhanced matrix synthesis, stimulated by inflammatory mediators such as interleukin-1 (IL-1) and/or tumor necrosis factor (TNF). It has been well known that TGF-$\beta$ enhance the proliferation of fibroblasts and the production of collagen and fibronectin, and inhibit the degradation of collagen. In this regard, It is likely that TGF-$\beta$ undergoes important roles in the pathogenesis of pulmonary fibrosis. Nevertheless, this single cytokine is not the sole regulator of the pulmonary fibrotic response. It is likely that the balance of many cytokines including TGF-$\beta$, IL-1, IL-6 and TNF-$\alpha$ regulates the pathogenesis of pulmonary fibrosis. In this study, we investigate the interaction of TGF-$\beta$, IL-1$\beta$, IL-6 and TNF-$\alpha$ and their effect on the proliferation of fibroblasts. Methods: We used a human fibroblast cell line, MRC-5 (ATCC). The culture of MRC-5 was confirmed by immunofluorecent staining. First, we determined the concentration of serum in cuture medium, in which the proliferation of MRC-5 is supressed but the survival of MRC-5 is retained. Second, we measured optical density after staining the cytokine-stimulated cells with 0.5% naphthol blue black in order to detect the effect of cytokines on the proliferation of MRC-5. Result: In the medium containing 0.5% fetal calf serum, the proliferation of MRC-5 increased by 50%, and it was maintained for 6 days. IL-1$\beta$, TNF-$\alpha$ and IL-6 induced the proliferation of MRC-5 by 45%, 160% and 120%, respectively. IL-1$\beta$ and TNF-$\alpha$ enhanced TGF-$\beta$-induced proliferation of MRC-5 by 64% and 159%, but IL-6 did not affect the TGF-$\beta$-induced proliferation. And lNF-$\alpha$-induced proliferation of MRC-5 was reduced by IL-1$\beta$ in 50%. TGF-$\beta$, TNF-$\alpha$ and both induced the proliferation of MRC-5 to 89%, 135% and 222%, respectively. Conclusions: TNF-$\alpha$, TGF-$\beta$ and IL-1$\beta$, in the order of the effectiveness, showed the induction of MRC-5 proliferation of MRC-5. TNF-$\alpha$ and IL-1$\beta$ enhance the TGF-$\beta$-induced proliferation of MRC-5, but IL-6 did not have any effect TNF-$\alpha$-induced proliferation of MRC-5 is diminished by IL-1, and TNF-$\alpha$ and TGF-$\beta$ showed a additive effect.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1252-1264
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• 1998

Background : Patients with established ARDS have a mortality rate that exceeds 50 percent despite of intensive care including artificial ventilation modality, Mortality has been associated with sepsis and organ failure preceding or following ARDS ; APACHE II score ; old age and predisposing factors. Revised ventilator strategy over last 10 years especially at ARDS appeared to improve the mortality of it. We retrospectively investigated 40 ARDS patients of respiratory-care unit to examine how these factors influence outcome. Methods : A retrospective investigation of 40 ARDS patients in respiratory-care unit with ventilator management over 46 months was performed. We investigated the clinical characteristics such as a risk factor, cause of death and mortality, and also parameters such as APACHE II score, number of organ dysfunction, and hypoxia score (HS, $PaO_2/FIO_2$) at day 1, 3, 7 of severe acute lung injury, and simultaneously the PEEP level and tidal volume. Results : Clinical conditions associated with ARDS were sepsis 50%, pneumonia 30%, aspiration pneumonia 20%, and mortality rate based on the etiology of ARDS was sepsis 50%, pneumonia 67%(p<0.01 vs sepsis), aspiration pneumonia 38%. Overall mortality rate was 60%. In 28 day-nonsurvivors, leading cause of death was severe sepsis(42.9%) followed by MOF(28.6%), respiratory failure(19.1 %), and others(9.5%). There were no differences in variables of age, sex, APACHE II score, HS, and numbers of organ dysfunction at day 1 of ARDS between 28-days survivor and nonsurvivors. In view of categorized variables of age(>70), APACHE II score(>26), HS(<150) at day 1 of ARDS, there were significant differences between 28-days survivor and nonsurvivors(p<0.05). After day 1 of ARDS, the survivors have improved their APACHE II score, HS, numbers of organ dysfunction over the first 3d to 7d, but nonsurvivors did not improve over a seven-day course. There were significant differences in APACHE II score and numbers of organ dysfunction of day 3, 7 of ARDS, and HS of day 7 of ARDS between survivors and nonsurvivors(p<0.05). Fatality rate of ARDS has been declined from 68% to less than 40% between 1995 and 1998. There were no differences in APACHE II score, HS, numbers of organ dysfunction, old age at presentation of ARDS. In last years, mean PEEP level was significantly higher and mean tidal volume was significantly lower than previous years during seven days of ARDS(p<0.01). Conclusions : Improvement of HS, APACHE II score, organ dysfunction over the first 3d to 7d is associated with increased survival Decline in ARDS fatality rates between 1995 and 1998 seems that this trend must be attributed to improved supportive therapy including at least high PEEP instead of conventional-least PEEP approach in ventilator management of acute respiratory distress syndrome.

• Tuberculosis and Respiratory Diseases
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• v.41 no.5
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• pp.452-461
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• 1994

Background: Tumor necrosis factor(TNF)-$\alpha$ and Interleukin(lL)-$1{\beta}$ are thought to play a major role in the pathogenesis of the septic syndrome, which is frequently associated with adult respiratory distress syndrome(ARDS). In spite of many reports for the role of TNF-$\alpha$ in the pathogenesis of ARDS, including human studies, it has been reported that TNF-$\alpha$ is not sensitive and specific marker for impending ARDS. But there is a possibility that the results were affected by the diversity of pathogenetic mechanisms leading to the ARDS because of various underlying disorders of the study group in the previous reports. The purpose of the present study was to evaluate the roles of TNF-$\alpha$ and IL-$1{\beta}$ as a predictable marker for development of ARDS in the patients with septic syndrome, in which the pathogenesis is believed to be mainly cytokine-mediated. Methods: Thirty-six patients of the septic syndrome hospitalized in the intensive care units of the Asan Medical Center were studied. Sixteens suffered from ARDS, whereas the remaining 20 were at the risk of developing ARDS(acute hypoxemic respiratory failure, AHRF). In all patients venous blood samples were collected in heparin-coated tubes at the time of enrollment, at 24 and 72 h thereafter. TNF-$\alpha$ and IL-$1{\beta}$ was measured by an enzyme-linked immunosorbent assay (ELISA). All data are expressed as median with interquartile range. Results: 1) Plama TNF-$\alpha$ levels: Plasma TNF-$\beta$ levels were less than 10pg/mL, which is lowest detection value of the kit used in this study within the range of the $mean{\pm}2SD$, in all of the normal controls, 8 of 16 subjects of ARDS and in 8 in 20 subjects of AHRF. Plasma TNF-$\alpha$ levels from patients with ARDS were 10.26pg/mL(median; <10-16.99pg/mL, interquartile range) and not different from those of patients at AHRF(10.82, <10-20.38pg/mL). There was also no significant difference between pre-ARDS(<10, <10-15.32pg/mL) and ARDS(<10, <10-10.22pg/mL). TNF-$\alpha$ levels were significantly greater in the patients with shock than the patients without shock(12.53pg/mL vs. <10pg/mL) (p<0.01). There was no statistical significance between survivors(<10, <10-12.92pg/mL) and nonsurvivors(11.80, <10-20.8pg/mL) (P=0.28) in the plasma TNF-$\alpha$ levels. 2) Plasma IL-$1{\beta}$ levels: Plasma IL-$1{\beta}$ levels were less than 0.3ng/mL, which is the lowest detection value of the kit used in this study, in one of each patients group. There was no significant difference in IL-$1{\beta}$ levels of the ARDS(2.22, 1.37-8.01ng/mL) and of the AHRF(2.13, 0.83-5.29ng/mL). There was also no significant difference between pre-ARDS(2.53, <0.3-8.34ngfmL) and ARDS(5.35, 0.66-11.51ng/mL), and between patients with septic shock and patients without shock (2.51, 1.28-8.34 vs 1.46, 0.15-2.13ng/mL). Plasma IL-$1{\beta}$ levels were significantly different between survivors(1.37, 0.4-2.36ng/mL) and nonsurvivors(2.84, 1.46-8.34ng/mL). Conclusion: Plasma TNF-$\alpha$ and IL-$1{\beta}$ level are not a predictable marker for development of ARDS. But TNF-$\alpha$ is a marker for shock in septic syndrome. These result could not exclude a possibility of pathophysiologic roles of TNF-$\alpha$ and IL-$1{\beta}$ in acute lung injury because these cytokine could be locally produced and exert its effects within the lungs.