• Tuberculosis and Respiratory Diseases
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• v.51 no.2
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• pp.166-172
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• 2001

Silicone fluid is a biomaterial widely used in modern cosmetic procedures because there are few side effects, considerable chemical stability and predictable physical properties. However, many local and systemic adverse reactions have reported. In particular some serious pulmonary complications have been reported such as pulmonary thromboembolism, acute respiratory distress syndrome with some cases leading to mortality. Most of the serious complicated cases were induced by an illegal silicone fluid injection. We experienced two cases of acute respiratory distress syndrome with pulmonary hemorrhage induced by an illegal silicone fluid injection. The patients were 41 & 51 year old women, who complained of dyspnea. The chest X-ray and HRCT scan findings showed a bilateral ground glass attenuation on the bilateral dependent portion of the upper and middle lung zone. The patients clinical symptoms and the radiologic and other laboratory findings were compatible with acute respiratory distress syndrome induced by the silicon fluid injection. Here we report two cases of acute respiratory distress syndrome with pulmonary hemorrhage induced by an illegal silicone injection with a review of the relevant literature.

• ALGAE
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• v.38 no.4
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• pp.295-306
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• 2023

Human coronavirus diseases, particularly severe acute respiratory syndrome coronavirus 2, still remain a persistent public health issue, and many recent studies are focusing on the quest for new leads against coronaviruses. To contribute to this growing pool of knowledge and explore the available marine natural products against coronaviruses, this study investigated the antiviral effects of fucoxanthin isolated from Sargassum siliquastrum-a brown alga found on Jeju Island, South Korea. The antiviral effects of fucoxanthin were confirmed in severe acute respiratory syndrome coronavirus 2-infected Vero cells, and its structural characteristics were verified in silico using molecular docking and molecular dynamic simulations and in vitro colorimetric method. Fucoxanthin inhibited the infection in a concentration-dependent manner, without showing cytotoxicity. Molecular docking simulations revealed that fucoxanthin binds to the angiotensinconverting enzyme 2-spike protein (binding energy -318.306 kcal mol^-1) and main protease (binding energy -205.118 kcal mol^-1). Moreover, molecular dynamic simulations showed that fucoxanthin remains docked to angiotensin-converting enzyme 2-spike protein for 20 ns, whereas it breaks away from main protease after 3 ns. Also, the in silico prediction of the fucoxanthin was verified through the in vitro colorimetric method by inhibiting the binding between angiotensinconverting enzyme 2 and spike protein in a concentration-dependent manner. These results indicate that fucoxanthin exhibits antiviral effects against severe acute respiratory syndrome coronavirus 2 by blocking the entry of the virus. Therefore, fucoxanthin from S. siliquastrum can be a potential candidate for treating coronavirus infection.

• Tuberculosis and Respiratory Diseases
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• v.80 no.3
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• pp.311-312
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• 2017

• Tuberculosis and Respiratory Diseases
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• v.51 no.1
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• pp.5-16
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• 2001

• Tuberculosis and Respiratory Diseases
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• v.50 no.5
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• pp.525-539
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• 2001

• Clinical and Experimental Pediatrics
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• v.63 no.4
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• pp.119-124
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• 2020

A cluster of severe pneumonia of unknown etiology in Wuhan City, Hubei province in China emerged in December 2019. A novel coronavirus named severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) was isolated from lower respiratory tract sample as the causative agent. The current outbreak of infections with SARS-CoV-2 is termed Coronavirus Disease 2019 (COVID-19) by the World Health Organization (WHO). COVID-19 rapidly spread into at least 114 countries and killed more than 4,000 people by March 11 2020. WHO officially declared COVID-19 a pandemic on March 11, 2020. There have been 2 novel coronavirus outbreaks in the past 2 decades. The outbreak of severe acute respiratory syndrome (SARS) in 2002-2003 caused by SARS-CoV had a case fatality rate of around 10% (8,098 confirmed cases and 774 deaths), while Middle East respiratory syndrome (MERS) caused by MERS-CoV killed 861 people out of a total 2,502 confirmed cases between 2012 and 2019. The purpose of this review is to summarize known-to-date information about SARS-CoV-2, transmission of SARS-CoV-2, and clinical features.

• Childhood Kidney Diseases
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• v.25 no.2
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• pp.122-127
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• 2021

C1q nephropathy is a rare glomerulopathy that typically presents with nephrotic syndrome in children. Treatment with immunosuppressive agents renders patients vulnerable to infection and its complications. Gastroenteritis is common in children, and rotavirus is a leading cause. Extraintestinal manifestations of rotavirus have recently been reported; however, there is a paucity of cases exploring the involvement of a rotavirus on the respiratory system. Acute respiratory distress syndrome (ARDS) is a rapid onset respiratory failure characterized by noncardiogenic pulmonary edema and hypoxemia. Causes of ARDS include sepsis, pneumonia, pancreatitis, aspiration, and trauma. In this paper, we report a case of ARDS after rotavirus infection in a child with C1q nephropathy who had been treated with immunosuppressive agents.

• Tuberculosis and Respiratory Diseases
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• v.48 no.4
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• pp.513-521
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• 2000

Background : TNF may play an important role(central mediator) in the development of an acute respiratory distress syndrome. Since TNF induced lung injury in the acute respiratory distress syndrome and abnormalities in surfactant function have been described in acute respiratory distress syndrome, the authors investigated the effects of TNF on the regulation of surfactant protein A, B and C mRNA accumulation. Methods : The effects of TNF on gene expression of surfactant protein A, B, and C were analyzed using filter hybridization, 12 and 24 hours after intravenous injection of TNF in rats. Results : 1. The accumulation of SP-A mRNA in the TNF treated group (12 and 24 hours after TNF injection) was significantly decreased by 22.9% and 27.4%, respectively, compared to the control group (P<.025, P<.025). 2. The accumulation of SP-B mRNA in 24 hours after TNF treated group was significantly decreased by 20.5% compared to that of the control group(P<.01). 3. The accumulation of SP-C mRNA in 12 hours after TNF treated group was significantly decreased by 31% the compared to that of the control group(P<.01). Conclusions : These findings indicate the marked inhibitory effects of tumor necrosis factor on surfactant proteins expression in vivo. This finding. in turn, supports the idea of inhibitory effects of tumor necrosis factor on surfactant proteins expression as it relates to pathogenesis of acute respiratory distress syndrome.

• Journal of Preventive Medicine and Public Health
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• v.53 no.2
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• pp.82-88
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• 2020

Objectives: The objective of this study was to identify individual and institutional factors associated with the prescription of systemic steroids in patients with acute respiratory infections and to investigate the role of a policy measure aimed to reduce inappropriate prescriptions. Methods: We used data from the National Health Insurance Service-National Sample Cohort from 2006 to 2015 and focused on episodes of acute respiratory infection. Descriptive analysis and multiple logistic regression analysis were performed to identify individual-level and institution-level factors associated with the prescription of systemic steroids. In addition, steroid prescription rates were compared with antibiotic prescription rates to assess their serial trends in relation to Health Insurance Review and Assessment Service (HIRA) Prescription Appropriateness Evaluation policy. Results: Among a total of 9 460 552 episodes of respiratory infection, the steroid prescription rate was 6.8%. Defined daily doses/1000 persons/d of steroid increased gradually until 2009, but rose sharply since 2010. The steroid prescription rate was higher among ear, nose and throat specialties (13.0%) than other specialties, and in hospitals (8.0%) than in tertiary hospitals (3.0%) and other types of institutions. Following a prolonged reduction in the steroid prescription rate, this rate increased since the HIRA Prescription Appropriateness Evaluation dropped steroids from its list of evaluation items in 2009. Such a trend reversal was not observed for the prescription rate of antibiotics, which continue to be on the HIRA Prescription Appropriateness Evaluation list. Conclusions: Specialty and type of institution are important correlates of steroid prescriptions in cases of acute respiratory infection. Steroid prescriptions can also be influenced by policy measures, such as the HIRA Prescription Appropriateness Evaluation policy.

• Tuberculosis and Respiratory Diseases
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• v.68 no.6
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• pp.334-344
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• 2010

Background: Based on the known immunoregulatory functions of moxifloxacin on phagocytes, the therapeutic effect of moxifloxacin on oleic acid (OA)-induced acute lung injury (ALI) was investigated. Methods: Moxifloxacin (10 mg/kg) was given to male Sprague-Dawley rats that had been given oleic acid (OA, $30{\mu}L$) intravenously. Five hours after OA injection, parameters demonstrating ALI were assessed to measure the effects of moxifloxacin on acute lung injury. Results: The pathological findings of OA-induced ALI's was diminished by moxifloxacin. Through ultrastructural and $CeCl_3$ EM histochemistry, moxifloxacin was confirmed to be effective in decreasing oxidative stress in the lung as well. Indices of ALI, such as lung weight/body weight ratio, protein content in bronchoalveolar lavage fluid, and lung myeloperoxidase were decreased by moxifloxacin. In diaminobenzidine immunohistochemistry, fluorescent immunohistochemistry, and Western blotting of the lung, moxifloxacin had decreased the enhanced expression of secretory phospholipase $A_2$ ($sPLA_2$) by OA. Conclusion: We concluded that moxifloxacin was effective in lessening acute inflammatory pulmonary edema caused by OA, by inhibiting the neutrophilic respiratory burst, which was initiated by the activation of $sPLA_2$.