• BMB Reports
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• v.45 no.4
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• pp.207-212
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• 2012

Retroviruses have often been used for gene therapy because of their capacity for the long-term expression of transgenes via stable integration into the host genome. However, retroviral integration can also result in the transformation of normal cells into cancer cells, as demonstrated by the incidence of leukemia in a recent retroviral gene therapy trial in Europe. This unfortunate outcome has led to the rapid initiation of studies examining various biological and pathological aspects of retroviral integration. This review summarizes recent findings from these studies, including the global integration patterns of various types of retroviruses, viral and cellular determinants of integration, implications of integration for gene therapy and retrovirus-mediated infectious diseases, and strategies to shift integration to safe host genomic loci. A more comprehensive and mechanistic understanding of retroviral integration processes will eventually make it possible to generate safer retroviral vector platforms in the near future.

• Journal of Mechanical Science and Technology
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• v.17 no.7
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• pp.1016-1025
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• 2003

The rupture of blood vessels in the human brain results in serious pathological and medical problems. In particular, brain hemorrhage and hematomas resulting from impact to the head are a major cause of death. As such, investigating the tensile behavior and rupture of blood vessels in the brain is very important from a medical point of view. In the present study, the tensile characteristics of the blood vessels in the human brain were analyzed using a quasi-static uniaxial tensile test, and the properties of the arteries and veins compared. In addition, to compare the tensile behavior and demonstrate the validity of the experimental results, blood vessels from the legs of pigs were also tested and analyzed. The overall results were in accordance with the histological structures and previous medical reports.

• BMB Reports
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• v.49 no.8
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• pp.424-430
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• 2016

Autophagy, an evolutionarily conserved cellular degradation pathway of the lysosome, is associated with many physiological and pathological processes. The hallmark of autophagy is the formation of the autophagosome that engulfs and degrades cytosolic components via its fusion with the lysosome, in either a selective or a non-selective manner. Autophagy is tightly regulated by proteins encoded by autophagy-related (atg) genes. Among these proteins, ATG8/LC3 is essential for autophagosome biogenesis/maturation and it also functions as an adaptor protein for selective autophagy. In mammalian cells, several homologs of yeast Atg8 such as MAP1LC3, GABARAP, and GABARAPL 1/2 have been identified. However, the biological relevance of this gene diversity in higher eukaryotes, and their specific roles, are largely unknown. In this review, we describe the mammalian ATG8/LC3 family and discuss recent advancements in understanding their roles in the autophagic process.

• BMB Reports
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• v.51 no.2
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• pp.65-72
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• 2018

The endothelial to mesenchymal transition (EndMT) is a newly recognized, fundamental biological process involved in development and tissue regeneration, as well as pathological processes such as the complications of diabetes, fibrosis and pulmonary arterial hypertension. The EndMT process is tightly controlled by diverse signaling networks, similar to the epithelial to mesenchymal transition. Accumulating evidence suggests that microRNAs (miRNAs) are key regulators of this network, with the capacity to target multiple messenger RNAs involved in the EndMT process as well as in the regulation of disease progression. Thus, it is highly important to understand the molecular basis of miRNA control of EndMT. This review highlights the current fund of knowledge regarding the known links between miRNAs and the EndMT process, with a focus on the mechanism that regulates associated signaling pathways and discusses the potential for the EndMT as a therapeutic target to treat many diseases.

• Journal of Life Science
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• v.12 no.2
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• pp.57-60
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• 2002

Apoptosis of vascular smooth muscle cell is observed in the vascular diseases such as atherosclerosis and restenosis. The death of vascular smooth muscle cells can be induced by cytokines and activation of Fas-pathways. It is widely accepted that apoptosis occurs without inflammation. There are, however, reports that apoptosis is not silent. Vascular smooth muscle cells dying by Fas-pathway secreted inflammatory cytokines including monocyte chemoattractant protein-1. This study have investigated whether apoptosis is associated with potent inflammatory cytokine tumor tumor necrosis factor (TNF)-${\alpha}$. The cells which undergo apoptosis by expressing FADD in the absence of tetracycline expressed and secreted TNF-${\alpha}$. When the level of TNF-${\alpha}$ transcript was investigated, dying smooth muscle cells exhibited transcriptional activation of TNF-${\alpha}$. The data indicate that dying vascular smooth muscle cells contribute to inflammation by expressing inflammatory cytokines. The present study suggests that apoptosis could not be silent in certain pathological situations.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.21 no.3
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• pp.209-213
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• 2018

Most solitary gastrointestinal (GI) polyps in children are either inflammatory or hamartomatous. Solitary hyperplastic polyp, sentinel polyp and solitary adenomatous polyp have been occasionally diagnosed in adults, but very rarely reported in Korean children. We recently came across a case with adenomatous polyp in the colon, a case with hyperplastic polyp beneath the gastroesophageal junction, a case with hyperplastic polyp in the prepyloric area, and a case with sentinel polyp in the distal esophagus, which are unusual pathologic types in children. These mucosal lesions were diagnosed incidentally during elective endoscopic examinations for GI symptoms. Most polyps do not cause significant symptoms, so the diagnosis might be delayed, especially in children, in whom GI endoscopy is not commonly performed for screening purpose as in the adults.

• Journal of Trauma and Injury
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• v.26 no.1
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• pp.34-37
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• 2013

Although a majority of patients with splenic rupture present acutely, up to 15% present with a delayed rupture days to weeks following a substantial abdominal injury. The mortality for patients presenting with acute splenic rupture is approximately 1% whereas that associated with delayed rupture approaches 15%. Although many cases of delayed splenic rupture have been reported, the majority of those reports present delayed splenic rupture associated with an underlying systemic disorder such as liver or kidney disease, or another hematologic disorder. We found a delayed splenic rupture case that documented the normal spleens of young healthy soldiers after trivial abdominal trauma, and we have had successful treatment experience with delayed rupture of a normal spleen after trivial trauma. Therefore, we want to review the literature and discuss the phenomenon of delayed rupture of the spleen following trivial trauma.

• Journal of Chest Surgery
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• v.22 no.2
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• pp.297-304
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• 1989

A 45-year old woman with congestive heart failure due to left atrial tumor was operated on. Three tumor masses arising from posterior wall, atrial septum, anterior portion of mitral valve were resected. Pathological diagnosis was malignant fibrous histiocytoma [MFH]. Above one case and sixteen previous reports are reviewed. Eleven cases out of 17 were females. The tumors all originated primarily in the left atrium and 8 had distant metastases. The metastatic sites are lung [4 cases], brain [2 cases], liver, jejunum, cervix and pleura etc. Careful pathologic study is necessary to differentiate the uniformly fatal MFH of the heart from the more common benign atrial myxoma. The treatment modalities are surgical resection, chemotherapy, and radiation therapy & the prognosis of intracardiac MFH is poor. We underwent partial resection of left atrial MFH and obtained symptom relief and patient still alive 7 months post-operatively in state of NYHA class II.

• BMB Reports
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• v.44 no.6
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• pp.359-368
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• 2011

Polycystic kidney disease (PKD) is a common genetic disorder in which extensive epithelial-lined cysts develop in the kidneys. In previous studies, abnormalities of polycystin protein and its interacting proteins, as well as primary cilia, have been suggested to play critical roles in the development of renal cysts. However, although several therapeutic targets for PKD have been suggested, no early diagnosis or effective treatments are currently available. Current developments are active for treatment of PKD including inhibitors or antagonists of PPAR-${\gamma}$, TNF-${\alpha}$, CDK and VEGF. These drugs are potential therapeutic targets in PKD, and need to be determined about pathological functions in human PKD. It has recently been reported that the alteration of epigenetic regulation, as well as gene mutations, may affect the pathogenesis of PKD. In this review, we will discuss recent approaches to PKD therapy. It provides important information regarding potential targets for PKD.

• BMB Reports
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• v.48 no.10
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• pp.541-548
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• 2015

Cardiomyopathy is an inherited or acquired disease of the myocardium, which can result in severe ventricular dysfunction. Mitochondrial dysfunction is involved in the pathological process of cardiomyopathy. Many dysfunctions in cardiac mitochondria are consequences of mutations in nuclear or mitochondrial DNA followed by alterations in transcriptional regulation, mitochondrial protein function, and mitochondrial dynamics and energetics, presenting with associated multisystem mitochondrial disorders. To ensure correct diagnosis and optimal management of mitochondrial dysfunction in cardiomyopathy caused by multiple pathogenesis, multidisciplinary approaches are required, and to integrate between clinical and basic sciences, ideal translational models are needed. In this review, we will focus on experimental models to provide insights into basic mitochondrial physiology and detailed underlying mechanisms of cardiomyopathy and current mitochondria-targeted therapies for cardiomyopathy.