• Tuberculosis and Respiratory Diseases
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• v.50 no.3
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• pp.367-372
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• 2001

Bacillus Calmette-Guerin(BCG) has been widely used for the prophylaxis of superficial bladder tumor recurrence and for the treatment of bladder carcinoma in situ. More than 95% of patients who receive BCG instillation tolerate the treatment well and side reactions have been reported in less than 5% of patients. Most side effects are minor and self-limiting. However, a rare occurrence of severe systemic reactions have been reported. Among the severe systemic reactions, hypersensitivity pneumonitis should be considered in patients with pneumonic complications after BCG instillation in cases where the culture for mycobacteria is negative in the sputwn, brochoalveolar lavage and blood specimen. In addition, a fiberoptic bronchoscopy with transbronchial lung biopsy demonstrates a fibrosis of the alveolar septums, where there is and an increased lymphocyte count with out tuberculous inflammatory changes, the and CD4 : CD8 ratio is increased and no symptomatic response to antituberculosis chemotherapy is observed. Here we report a 68 years old man with interstitial pneumonitis following intravesical BCG instillation.

• Proceedings of the Korean Society of Veterinary Pathology Conference
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• 2003.10a
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• pp.17-17
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• 2003

Accumulation of cholesterol may occur due to liver injury like hepatic steatosis and fibrosis as well as athrosclerosis and coronary heart disease. The aim of this study was search for protective effect of active ceramic water on experimental hepatic injury induced by high cholesterol diet(containing 1.0 ％ cholesterol and 0.3 ％ sodium cholate) in rats. (omitted)

• Journal of Chest Surgery
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• v.36 no.4
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• pp.277-279
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• 2003

A 15 year-old boy was referred to us because of mild dyspnea on exertion and incidentally found heart murmur. On echocardiography, a mass involving mainly interventricular septum and causing left ventricular outflow tract obstruction was detected. Cardiac catheterization demonstrated a transaortic pressure gradient of 20 mmHg. Partial excision of the septal mass was performed via aortotomy under cardiopulmonary bypass. The pathologic diagnosis revealed myocardial hamartoma. The lesion was mainly composed of mature, severely hypertrophic myocytes and intervening fibrosis. During the 5 year of follow-up after the surgery, no evidence of arrhythmia or tumor recurrence was documented.

• Journal of Korean Foot and Ankle Society
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• v.1 no.1
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• pp.30-37
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• 1997

Pilon fracture is an intraarticular fracture of distal tibia. It is high energy injury with significantly associated soft tissue damage, bone comminution, and articular surface disruption. Until recently, this treatment has followed the AO principles, Because the risk of complications outweighs potential benefits, the principle of a Pilon fracture treatment are changing. Newer techniques using articulated external fixation minimize disturbance of the soft tissue envelope and have decreased these complications. Series of 5 patients with Pilon fracture were treated by articulated external fixator and followed up more than 12 monthes at the Department of orthopaedic surgery, Kang Dong Sacred Heart Hospital, College of medicine, Hallym University. The results were as follows: 1. The type of fracture were type C2(3 cases),type C3(2 cases) according to AO-$M{\ddot{u}}ller$ classification. 2. The clinical results according to functional criteria by Mast and Teipner were good in 4 cases and poor in 1 case, which is an old fracture. 3. Techniques utilizing articulated external fixator were associated with satisfactory results and appeared to significantly decrease the incidence of soft tissue complication, post-traumatic arthritis, osteoporosis, and fibrosis of ankle joint.

• Korean Journal of Radiology
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• v.23 no.6
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• pp.581-597
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• 2022

Left ventricular (LV) wall thickening, or LV hypertrophy (LVH), is common and occurs in diverse conditions including hypertrophic cardiomyopathy (HCM), hypertensive heart disease, aortic valve stenosis, lysosomal storage disorders, cardiac amyloidosis, mitochondrial cardiomyopathy, sarcoidosis and athlete's heart. Cardiac magnetic resonance (CMR) imaging provides various tissue contrasts and characteristics that reflect histological changes in the myocardium, such as cellular hypertrophy, cardiomyocyte disarray, interstitial fibrosis, extracellular accumulation of insoluble proteins, intracellular accumulation of fat, and intracellular vacuolar changes. Therefore, CMR imaging may be beneficial in establishing a differential diagnosis of LVH. Although various diseases share LV wall thickening as a common feature, the histologic changes that underscore each disease are distinct. This review focuses on CMR multiparametric myocardial analysis, which may provide clues for the differentiation of thickened myocardium based on the histologic features of HCM and its phenocopies.

• Korean Journal of Radiology
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• v.22 no.3
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• pp.324-333
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• 2021

Objective: The clinical course of an individual patient with heart failure is unpredictable with left ventricle ejection fraction (LVEF) only. We aimed to evaluate the prognostic value of cardiac magnetic resonance (CMR)-derived myocardial fibrosis extent and to determine the cutoff value for event-free survival in patients with non-ischemic cardiomyopathy (NICM) who had severely reduced LVEF. Materials and Methods: Our prospective cohort study included 78 NICM patients with significantly reduced LV systolic function (LVEF < 35%). CMR images were analyzed for the presence and extent of late gadolinium enhancement (LGE). The primary outcome was major adverse cardiac events (MACEs), defined as a composite of cardiac death, heart transplantation, implantable cardioverter-defibrillator discharge for major arrhythmia, and hospitalization for congestive heart failure within 5 years after enrollment. Results: A total of 80.8% (n = 63) of enrolled patients had LGE, with the median LVEF of 25.4% (19.8-32.4%). The extent of myocardial scarring was significantly higher in patients who experienced MACE than in those without any cardiac events (22.0 [5.5-46.1] %LV vs. 6.7 [0-17.1] %LV, respectively, p = 0.008). During follow-up, 51.4% of patients with LGE ≥ 12.0 %LV experienced MACE, along with 20.9% of those with LGE ≤ 12.0 %LV (log-rank p = 0.001). According to multivariate analysis, LGE extent more than 12.0 %LV was independently associated with MACE (adjusted hazard ratio, 6.71; 95% confidence interval, 2.54-17.74; p < 0.001). Conclusion: In NICM patients with significantly reduced LV systolic function, the extent of LGE is a strong predictor for long-term adverse cardiac outcomes. Event-free survival was well discriminated with an LGE cutoff value of 12.0 %LV in these patients.

• Molecules and Cells
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• v.40 no.1
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• pp.66-72
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• 2017

Pathological hypertrophy of the heart is closely associated with endoplasmic reticulum stress (ERS), leading to maladaptations such as myocardial fibrosis, induction of apoptosis, and cardiac dysfunctions. Salubrinal is a known selective inhibitor of protein phosphatase 1 (PP1) complex involving dephosphorylation of phospho-eukaryotic translation initiation factor 2 subunit $(p-eIF2)-{\alpha}$, the key signaling process in the ERS pathway. In this study, the effects of salubrinal were examined on cardiac hypertrophy using the mouse model of transverse aortic constriction (TAC) and cell model of neonatal rat ventricular myocytes (NRVMs). Treatment of TAC-induced mice with salubrinal ($0.5mg{\cdot}kg^{-1}{\cdot}day^{-1}$) alleviated cardiac hypertrophy and tissue fibrosis. Salubrinal also alleviated hypertrophic growth in endothelin 1 (ET1)-treated NRVMs. Therefore, the present results suggest that salubrinal may be a potentially efficacious drug for treating pathological cardiac remodeling.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.6
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• pp.511-518
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• 2022

Sepsis-associated myocardial injury, an invertible myocardial depression, is a common complication of sepsis. Neogambogic acid is an active compound in garcinia and exerts anthelmintic, anti-inflammatory, and detoxification properties. The role of neogambogic acid in sepsis-associated myocardial injury was assessed. Firstly, mice were pretreated with neogambogic acid and then subjected to lipopolysaccharide treatment to induce sepsis. Results showed that lipopolysaccharide treatment induced up-regulation of biomarkers involved in cardiac injury, including lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and troponin I (cTnI). However, pretreatment with neogambogic acid reduced levels of LDH, CK-MB, and cTnI, and ameliorated histopathological changes in the heart tissues of septic mice. Secondly, neogambogic acid also improved cardiac function in septic mice through reduction in left ventricular end-diastolic pressure, and enhancement of ejection fraction, fractional shortening, and left ventricular systolic mean pressure. Moreover, neogambogic acid suppressed cardiac apoptosis and inflammation in septic mice and reduced cardiac fibrosis. Lastly, protein expression of p-p38, p-JNK, and p-NF-κB in septic mice was decreased by neogambogic acid. In conclusion, neogambogic acid exerted anti-apoptotic, anti-fibrotic, and anti-inflammatory effects in septic mice through the inactivation of MAPK/NF-κB pathway.

• Journal of Ginseng Research
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• v.47 no.2
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• pp.218-227
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• 2023

Background: Myocardial fibrosis (MF) is an advanced pathological manifestation of many cardiovascular diseases, which can induce heart failure and malignant arrhythmias. However, the current treatment of MF lacks specific drugs. Ginsenoside Re has anti-MF effect in rat, but its mechanism is still not clear. Therefore, we investigated the anti-MF effect of ginsenoside Re by constructing mouse acute myocardial infarction (AMI) model and AngII induced cardiac fibroblasts (CFs) model. Methods: The anti-MF effect of miR-489 was investigated by transfection of miR-489 mimic and inhibitor in CFs. Effect of ginsenoside Re on MF and its related mechanisms were investigated by ultrasonographic, ELISA, histopathologic staining, transwell test, immunofluorescence, Western blot and qPCR in the mouse model of AMI and the AngII-induced CFs model. Results: MiR-489 decreased the expression of α-SMA, collagenI, collagen III and myd88, and inhibited the phosphorylation of NF-κB p65 in normal CFs and CFs treated with AngII. Ginsenoside Re could improve cardiac function, inhibit collagen deposition and CFs migration, promote the transcription of miR-489, and reduce the expression of myd88 and the phosphorylation of NF-κB p65. Conclusion: MiR-489 can effectively inhibit the pathological process of MF, and the mechanism is at least partly related to the regulation of myd88/NF-κB pathway. Ginsenoside Re can ameliorate AMI and AngII induced MF, and the mechanism is at least partially related to the regulation of miR-489/myd88/NF-κB signaling pathway. Therefore, miR-489 may be a potential target of anti-MF and ginsenoside Re may be an effective drug for the treatment of MF.

• Korean Circulation Journal
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• v.53 no.12
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• pp.795-810
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• 2023

Background and Objectives: Myocarditis is a potentially fatal disease, but curative treatments have not yet been established. Myocardial inflammation is an important pathogenesis of this disease, and immunosuppressants such as methylprednisolone and immunoglobulin have been used for treatment; however, the effectiveness needs to be improved. Thalidomide and dipeptidyl peptidase (DPP) 4 inhibitors were recently investigated regarding their immunomodulatory properties. This study aimed to test whether thalidomide or a DPP4 inhibitor (evogliptin) can improve the effectiveness of myocarditis treatment using a rat model of experimental autoimmune myocarditis (EAM). Methods: Rats with or without myocarditis were administered thalidomide at 100 mg/kg/day and DPP4 inhibitor at 10 mg/kg/day orally. Measurement of echocardiography, serum inflammatory cytokines, myocardial histopathological examination, and immunohistochemical staining for leukocytes, macrophages, CD4+ T cells, and cytoskeleton were performed after 3 weeks, and the fibrosis area was measured after 3 and 6 weeks. Results: Thalidomide and DPP4 inhibitor did not reduce the severity of myocarditis compared with the EAM without treatment rats by comparing the echocardiographic data, myocardial CD4⁺, macrophages, neutrophil infiltrations, and the heart weight/body weight ratio in 3 weeks. The levels of inflammatory cytokines were not lower in the thalidomide and DPP4 inhibitor-treated group than in the untreated group in 3 weeks. In 6 weeks, thalidomide and DPP4 inhibitors did not reduce the fibrosis area compared to untreated groups. Conclusions: Although thalidomide and the DPP4 inhibitor had an immunomodulatory effect and are used against inflammatory diseases, they did not ameliorate myocardial inflammation and fibrosis in this rat model of EAM.