• The Korean Journal of Physiology and Pharmacology
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• v.22 no.4
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• pp.447-456
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• 2018

Angiotensin-(1-9) [Ang-(1-9)], generated from Ang I by Ang II converting enzyme 2, has been reported to have protective effects on cardiac and vascular remodeling. However, there is no report about the effect of Ang-(1-9) on pulmonary hypertension. The aim of the present study is to investigate whether Ang-(1-9) improves pulmonary vascular remodeling in monocrotaline (MCT)-induced pulmonary hypertensive rats. Sprague-Dawley rats received Ang-(1-9) ($576{\mu}g/kg/day$) or saline via osmotic mini-pumps for 3 weeks. Three days after implantation of osmotic mini-pumps, 50 mg/kg MCT or vehicle were subcutaneously injected. MCT caused increases in right ventricular weight and systolic pressure, which were reduced by co-administration of Ang-(1-9). Ang-(1-9) also attenuated endothelial damage and medial hypertrophy of pulmonary arterioles as well as pulmonary fibrosis induced by MCT. The protective effects of Ang-(1-9) against pulmonary hypertension were inhibited by Ang type 2 receptor ($AT_2R$) blocker, but not by Mas receptor blocker. Additionally, the levels of LDH and inflammatory cytokines, such as $TNF-{\alpha}$, MCP-1, $IL-1{\beta}$, and IL-6, in plasma were lower in Ang-(1-9) co-treated MCT group than in vehicle-treated MCT group. Changes in expressions of apoptosis-related proteins such as Bax, Bcl2, Caspase-3 and -9 in the lung tissue of MCT rats were attenuated by the treatment with Ang-(1-9). These results indicate that Ang-(1-9) improves MCT-induced pulmonary hypertension by decreasing apoptosis and inflammatory reaction via $AT_2R$.

• Journal of Chest Surgery
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• v.5 no.1
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• pp.13-18
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• 1972

In 1835,Schlesinger first described a case of subisthmlc lower thoracic aortic coarctation. Since Olim`s unsuccessful reconstructive surgery in 1949 and Beattie`s first successful resection with homograft replacement on such a lesion in 1951 were reported,about 20 cases of atypical aortic coarctation had been treated by definitive surgery until 1964. In Korea, only 2 cases of atypical aortic coarctation treated by bypass graft were reported until now. This is the third case-report treated by reconstructive surgery. The patient,11 year old girl who had 2 year history of headache, visual weakness, intermittent claudlcation, and general weakness, was first diagnosed of having the hypertension due to atypical coarctation by the findings of high blood pressure[170/110mmHg] at the upper extremity and weak pulsation on both femoral artery,murmur on the epigastrium, absence of aortic knob, and aorto graphy. Aortography demonstrated the isolated segmental narrowing[length 5cm, diameter 0.4cm] at the level of aortic hiatus 2cm above celiac arterial origin, the dilated right 9th, 10th, 11th intercostal arteries with multiple dimunitive collaterals and no associated abnormalities in the other arteries. Preoperatlve positive findings were strong positive mantoux test, high AST[720 units]. transient mild cardiomegaly with right lung infiltration on chest X-ray and suggestive left ventricular hypertrophy on ECG. On December 1970, through separate left thoracotomy and abdominal approach, bypass graft between descending thoracic aorta and abdominal aorta below renal artery was performed. The operation was first successful with satisfactory reduction of hypertension on the upper trunk[postoperatlve 130/80mmHg] and strong pulsation on the lower extremities[postop. O, postop. 140/100mmHg]. However,6 weeks after surgery, she expired of sudden hemoptysis and shock due to anastomotic leak within the thorax. Operative finding disclosed that the affected aorta was firm, with rich periaortic fibrosis and the outer diameter of stenotic site was not attenuated. Histopathology of the resected specimen was also compatible with primary arteritis.

• Tuberculosis and Respiratory Diseases
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• v.50 no.5
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• pp.615-623
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• 2001

Background : Pneumoconiosis is a parenchymal lung disease that results from the accumulation of coal dust in the lungs and the consequent tissue reaction. To evaluate the role of various personal factors in pneumoconiosis and the significance of some serologic markers for assessing the disease activity related to pneumoconiosis, the Rheumatoid Factor(RF), ${\alpha}_1$-AT, C-Reactive Protein(CRP), ceruloplasmin and fibrinogen levels were measured. Method : All the patients were males, 45-76 years old, and the mean duration of coal dust exposure was 23.2 years. 51 patients were classified as having Simple Pneumoconiosis (SP), 59 had Progressive Massive Fibrosis (PMF). Fifty eight men with ages ranging from 26-70 years were used as normal controls. The serum RF and CRP were titrated using an Autochemistry analyzer (HITACHI 7150 : Japan) and the ${\alpha}_1$-AT and ceruloplasmin levels were measured using a Nephelometer (Behring Nephelometer : Germany) and the fibrinogen levels were estimated by using an Autoanalyzer for hematologic coagulation. Result : There was a higher RF level in the SP, and PMF groups than in the control groups but there was no statistical difference. The CRP, ${\alpha}_1$-AT, and ceruloplasmin levels were also higher in the SP, and PMF groups. However, the fibrinogen concentration was within the normal ranges in both the SP and PMF groups. Conclusion : The CWP (Ed note : Define CWP) patients had significantly higher CRP, ${\alpha}_1$-AT, and ceruloplasmin levels compared to the control group. It is believed that these serologic changes could be used as a marker of the disease activity.

• Journal of Haehwa Medicine
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• v.9 no.2
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• pp.111-121
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• 2001

In order to evaluate the protective effect of Kamicheungkantang(KCKT) on hepatic damage induced by $CCl_4$, the study was done. The blood chemistry and histological study were done following oral administration with materials. The results were obtained as follows. 1. KCKT extracts didn't show cytotoxicity against BALB/C mouse lung fibroblast cell. 2. In the hepatotoxicity with $CCl_4$, serum alanine aminotransferase(ALT) was significantly decreased in KCKT treated group as compared with control group. 3. In the hepatotoxicity with $CCl_4$, serum aspartate aminotransferase (AST) was significantly decreased in KCKT treated group as compared with control group. 4. In the hepatotoxicity with $CCl_4$, serum alkaline phosphatase(ALP) was significantly decreased in KCKT treated group as compared with control group. 5. In the hepatotoxicity with $CCl_4$, serum lactate dehydrogenase(LDH> was insignificantly decreased in KCKT but insignificantly as compared with control group. 6. In the hepatotoxicity with $CCl_4$, serum cholestorol was significantly decreased in KCKT treated group as compared with control group. 7. In the hepatotoxicity with $CCl_4$, serum triglyceride was insignificantly decreased in KCKT treated groups as compared with data of control. 8. In the hepatotoxicity with $CCl_4$, serum total bilirubin, direct bilirubin, ${\gamma}$-GTP were not changed in KCKT treated groups as compared with data of control. 9. In histopathological changes, fatty changes, vacuole, nucleotic changes and fibrosis were observed in control group and degree of changes was increased over time. Whereas no differences were observed in KCKT treated group These results suggested that KCKT extracts might be usefully applied for treatment of hapatic disease and also it was necessary to do more studies about its mechanisms.

• Laboraroty Animal Research
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• v.33 no.2
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• pp.76-83
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• 2017

Chronic obstructive pulmonary diseases (COPD) is an important disease featured as intense inflammation, protease imbalance, and air flow limitation and mainly induced by cigarette smoke (CS). In present study, we explored the effects of $Pycnogenol^{(R)}$ (PYC, pine bark extract) on pulmonary fibrosis caused by CS+lipopolysaccharide (LPS) exposure. Mice were treated with LPS intranasally on day 12 and 26, followed by CS exposure for 1 h/day (8 cigarettes per day) for 4 weeks. One hour before CS exposure, 10 and 20 mg/kg of PYC were administered by oral gavage for 4 weeks. PYC effectively reduced the number of inflammatory cells and proinflammatory mediators caused by CS+LPS exposure in bronchoalveolar lavage fluid. PYC inhibited the collagen deposition on lung tissue caused by CS+LPS exposure, as evidenced by Masson's trichrome stain. Furthermore, transforming growth $factor-{\beta}1$ ($TGF-{\beta}1$) expression and Smad family member 2/3 (Smad 2/3) phosphorylation were effectively suppressed by PYC treatment. PYC markedly reduced the collagen deposition caused by CS+LPS exposure, which was closely involved in $TGF-{\beta}1$/Smad 2/3 signaling, which is associated with pulmonary fibrotic change. These findings suggest that treatment with PYC could be a therapeutic strategy for controlling COPD progression.

• Toxicological Research
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• v.33 no.1
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• pp.7-14
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• 2017

Didecyldimethylammonium chloride (DDAC) is used in many types of biocidal products including tableware, carpets, humidifiers, and swimming pools, etc. In spite of increased chances of DDAC exposure through inhalation, studies on the inhalation toxicity of DDAC are not common even though the toxicity of DDAC might be significantly higher if it were to be administered through routes other than the respiratory system. DDAC aerosols were exposed to Sprague-Dawley rats in whole body exposure chambers for a duration of 13 weeks. The Mass Median Aerodynamic Diameters of the DDAC aerosol were $0.63{\mu}m$, $0.81{\mu}m$, and $1.65{\mu}m$, and the geometric standard deviations were 1.62, 1.65, and 1.65 in the low ($0.11{\pm}0.06mg/m^3$), the middle ($0.36{\pm}0.20mg/m^3$) and the high ($1.41{\pm}0.71mg/m^3$) exposure groups, respectively. Body weight was confirmed to be clearly influenced by exposure to DDAC and mean body weight was approximately 35% lower in the high ($1.41{\pm}0.71mg/m^3$) male group and 15% lower in the high ($1.41{\pm}0.71mg/m^3$) female group compared to that of the control group. In the bronchoalveolar lavage fluid assay, the levels of albumin and lactate dehydrogenase had no effect on DDAC exposure. The lung weight increased for the middle ($0.36{\pm}0.20mg/m^3$) and the high ($1.41{\pm}0.71mg/m^3$) concentrations of the DDAC exposure group, and inflammatory cell infiltration and interstitial pneumonia were partially observed in the lungs of the middle ($0.36{\pm}0.20mg/m^3$) and the high ($1.41{\pm}0.71mg/m^3$) exposure groups. However, severe histopathological symptoms, including proteinosis and/or fibrosis, were not found. Based on the results of the changes in the body weight and lung weight, it is considered that the NOAEL (no-observed adverse effect) level for the 13-week exposure duration is $0.11mg/m^3$.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.23
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• pp.10209-10215
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• 2015

To assess the contribution of tumor necrosis factor $(TNF){\beta}$ +252 polymorphisms to risk and prognosis of hepatocellular carcinoma (HCC), we enrolled 150 pairs of sex- and age-matched patients with HCC, patients with cirrhosis alone, and unrelated healthy controls. $TNF{\beta}$ +252 genotypes were determined by polymerase chain reaction with restriction fragment length polymorphism. Multivariate analysis indicated that $TNF{\beta}$ G/G genotype [odds ratio (OR), 3.64; 95%CI, 1.49-8.91], hepatitis B surface antigen (OR, 16.38; 95%CI, 8.30-32.33), and antibodies to hepatitis C virus (HCV) (OR, 39.11; 95%CI, 14.83-103.14) were independent risk factors for HCC. There was an additive interaction between $TNF{\beta}$ G/G genotype and chronic hepatitis B virus (HBV)/HCV infection (synergy index=1.15). Multivariate analysis indicated that factors associated with $TNF{\beta}$ G/G genotype included cirrhosis with Child-Pugh C (OR, 4.06; 95%CI, 1.34-12.29), thrombocytopenia (OR, 6.55; 95%CI, 1.46-29.43), and higher serum ${\alpha}$-fetoprotein concentration (OR, 2.53; 95%CI, 1.14-5.62). Patients with $TNF{\beta}$ G/G genotype had poor cumulative survival (p=0.005). Cox proportional hazard model indicated that $TNF{\beta}$ G/G genotype was a biomarker for poor HCC survival (hazard ratio, 1.70; 95%CI, 1.07-2.69). In conclusion, there are independent and additive effects between $TNF{\beta}$ G/G genotype and chronic HBV/HCV infection on risk for HCC. It is a biomarker for poor HCC survival. Carriage of this genotype correlates with disease severity and advanced hepatic fibrosis, which may contribute to a higher risk and poor survival of HCC. Chronic HBV/HCV infected subjects with this genotype should receive more intensive surveillance for early detection of HCC.

• Tuberculosis and Respiratory Diseases
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• v.59 no.1
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• pp.97-103
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• 2005

Hypereosinophilic syndrome (HES) is characterized by a sustained eosinophilia of $1,500/mm^3$ or more in the absence of any known causes or the signs and symptoms of organ involvement. We report a 64-year-old man with HES initially presenting with involvement of the liver and bone marrow. Despite controlling the eosinophilia by corticosteroid, he developed a cerebral infarction and later progressive interstitial pneumonia. Brain angiography revealed a severe stenosis of the proximal right internal carotid artery (ICA) and a complete obstruction of the intracranial ICA. An open lung biopsy revealed fibrosis and lymphoplasma cell infiltration without eosinophils, which were consistent with nonspecific interstitial pneumonia.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.5
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• pp.2717-2722
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• 2013

Background: The objective of this research is the computed axial tomography (CT) imaging grading of radiation induced pneumonitis (RP) and its correlation with clinical and radiotherapeutic parameters. Materials and Methods: The chest CT films of 20 patients with non-small cell lung cancer who have undergone threedimensional conformal radiation therapy were reviewed. The proposed CT grading of RP is supported on solely radiological diagnosis criteria and distinguishes five grades. The manifestation of RP was also correlated with any positive pre-existing chronic obstructive pulmonary disease (COPD) history, smoking history, the FEV1 value, and the dosimetric variable V20. Results: The CT grading of RP was as follows: 3 patients (15%) presented with ground glass opacity (grade 1), 9 patients (45%) were classified as grade 2, 7 patients (35%) presented with focal consolidation, with or without elements of fibrosis (grade 3), and only one patient (5%) presented with opacity with accompanying atelectasis and loss of pulmonary volume (grade 4). Both univariate and multivariate analysis revealed as prognostic factors for the radiological grading of RP the reduction of FEV1 and the V20 (P=0.026 and P=0.003, respectively). There was also a significant (P<0.001) correlation of radiological grading of RP with FEV1 and V20 (spearman rho 0.92 and 0.93, respectively). Conclusions: The high correlation of the proposed radiological grading with the FEV1 and the V20 is giving a satisfactory clinical validity. Although the proposed grading scale seems relevant to clinical practice, further studies are needed for the confirmation of its validity and reliability.

• Journal of Veterinary Science
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• v.23 no.1
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• pp.2.1-2.18
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• 2022

Background: Co-infections of the porcine reproductive and respiratory syndrome virus (PRRSV) and the Haemophilus parasuis (HPS) are severe in Chinese pigs, but the immune response genes against co-infected with 2 pathogens in the lungs have not been reported. Objectives: To understand the effect of PRRSV and/or HPS infection on the genes expression associated with lung immune function. Methods: The expression of the immune-related genes was analyzed using RNA-sequencing and bioinformatics. Differentially expressed genes (DEGs) were detected and identified by quantitative real-time polymerase chain reaction (qRT-PCR), immunohistochemistry (IHC) and western blotting assays. Results: All experimental pigs showed clinical symptoms and lung lesions. RNA-seq analysis showed that 922 DEGs in co-challenged pigs were more than in the HPS group (709 DEGs) and the PRRSV group (676 DEGs). Eleven DEGs validated by qRT-PCR were consistent with the RNA sequencing results. Eleven common Kyoto Encyclopedia of Genes and Genomes pathways related to infection and immune were found in single-infected and co-challenged pigs, including autophagy, cytokine-cytokine receptor interaction, and antigen processing and presentation, involving different DEGs. A model of immune response to infection with PRRSV and HPS was predicted among the DEGs in the co-challenged pigs. Dual oxidase 1 (DUOX1) and interleukin-21 (IL21) were detected by IHC and western blot and showed significant differences between the co-challenged pigs and the controls. Conclusions: These findings elucidated the transcriptome changes in the lungs after PRRSV and/or HPS infections, providing ideas for further study to inhibit ROS production and promote pulmonary fibrosis caused by co-challenging with PRRSV and HPS.