• 대한한방내과학회지
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• 제38권2호
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• pp.264-269
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• 2017

CREST syndrome is a form of limited cutaneous scleroderma that occurs only in certain parts of the body, such as the skin of the hands and face. CREST refers to the five main features of the syndrome: calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia. Currently, there is no standard treatment for CREST syndrome, and there have been no studies of the use of traditional Korean medicine (TKM) for this disease. This study describes the effects of Keumsuyukun-jeon on CREST syndrome. The patient in this case had typical clinical symptoms of CREST syndrome. These symptoms improved within a relatively short period of receiving the TKM treatment. The results of Anti-centromere antibody (AI) and high sensitivity C-reactive protein (mg/L) also improved.

• 대한예방의학회:학술대회논문집
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• 대한예방의학회 2005년도 제57차 추계 학술대회 연제집
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• pp.299-299
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• 2005

• BMB Reports
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• 제48권8호
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• pp.454-460
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• 2015

Naturally occurring reoviruses are live replication-proficient viruses that specifically infect human cancer cells while sparing their normal counterpart. Since the discovery of reoviruses in 1950s, they have shown various degrees of safety and efficacy in pre-clinical or clinical applications for human anti-cancer therapeutics. I have recently discovered that cellular tumor suppressor genes are also important in determining reoviral tropism. Carcinogenesis is a multi-step process involving the accumulation of both oncogene and tumor suppressor gene abnormalities. Reoviruses can exploit abnormal cellular tumor suppressor signaling for their oncolytic specificity and efficacy. Many tumor suppressor genes such as p53, ataxia telangiectasia mutated (ATM), and retinoblastoma associated (RB) are known to play important roles in genomic fidelity/maintenance. Thus, a tumor suppressor gene abnormality could affect host genomic integrity and likely disrupt intact antiviral networks due to the accumulation of genetic defects which in turn could result in oncolytic reovirus susceptibility. This review outlines the discovery of oncolytic reovirus strains, recent progresses in elucidating the molecular connection between oncogene/tumor suppressor gene abnormalities and reoviral oncotropism, and their clinical implications. Future directions in the utility of reovirus virotherapy is also proposed in this review. [BMB Reports 2015; 48(8): 454-460]

• Tuberculosis and Respiratory Diseases
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• 제52권5호
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• pp.545-549
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• 2002

임신시에 발생한 폐동정맥기형은 드문 질환으로 유전성 출혈성 모세혈관확장증과 같이 유전적으로 동반되어 나타날 수 있는 질환이다. 저자들은 임신시에 발생한 호흡곤란과 흉부방사선촬영상의 종괴를 주소로 내원한 환자에서 발견된 폐동정맥기형 1예를 경험하였기에 문헌고찰과 함께 보고하는 바이다.

• Journal of Chest Surgery
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• 제16권3호
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• pp.362-367
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• 1983

Pulmonary arteriovenous fistula is a congenital malformation resulting from errant capillary development, with incomplete formation or disintegration of the vascular septa that normally divide the primitive connections between the venous and arterial plexuses. It generally occurs as part of the disorder known as hereditary hemorrhagic telangiectasia [Rendu-Osler-Weber disease]. The hereditary lesion is transmitted as a simple non-sex-linked dominant trait. It may be single or multiple, too small to see on plain chest films or large and easily recognized. One third of the lesions are multiple on plain chest film. The pathogenesis of its symptoms is that unoxygenated, desaturated arterial blood enters into the pulmonary venous system, directly. Recently we have experienced a case of the pulmonary arteriovenous fistula in 26 years old male soldier, which was confirmed by pulmonary angiography preoperatively. 2 thumb-tip sized, well circumscribed cystic masses filled with bright red colored blood were seen in subpleural and anterolateral portion of the right upper lobe. Right upper Iobectomy was performed due to close approximation of the fistula with pulmonary vein. Microscopically, it shows angiomatous dilatation of the abnormal vessels embedding in the parenchyma. Postoperative physiologic studies show nearly normal arterial oxygen saturation, hemoglobin and RBC count. There was good, uneventful postoperative course.

• Clinical Endoscopy
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• 제51권6호
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• pp.563-569
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• 2018

Background/Aims: To evaluate patients with portal hypertension (PH) of varied etiologies for portal hypertensive enteropathy (PHE) using the PillCam SB3 capsule endoscopy (CE) system. Methods: Consecutive patients with PH presenting with unexplained anemia and/or occult gastrointestinal bleeding were evaluated using the PillCam SB3 CE system. Abnormal findings were categorized as vascular or non-vascular. The patients with ongoing bleeding caused by PHE were treated. The correlation of the CE scores of PHE with the clinical, laboratory, and endoscopic features was determined. Results: Of the 43 patients included in the study, 41 (95.3%) showed PHE findings. These included varices (67.4%), red spots (60.5%), erythema (44.2%), villous edema (46.5%), telangiectasia (16.3%), and polyps (16.3%). The CE scores varied from 0 to 8 ($mean{\pm}standard$ deviation, $4.09{\pm}1.8$). Five patients (11.6%) showed evidence of ongoing or recent bleeding due to PHE. Three of these five patients underwent endotherapy, and one patient underwent radiological coil placement. Conclusions: The PillCam SB3 CE system revealed a high prevalence of PHE in the patients with PH. Using this system, evidence of bleeding due to PHE was found in a small but definite proportion of the patients.

• Molecules and Cells
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• 제42권3호
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• pp.210-217
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• 2019

The maintenance of mitochondrial function is closely linked to the control of senescence. In our previous study, we uncovered a novel mechanism in which senescence amelioration in normal aging cells is mediated by the recovered mitochondrial function upon Ataxia telangiectasia mutated (ATM) inhibition. However, it remains elusive whether this mechanism is also applicable to senescence amelioration in accelerated aging cells. In this study, we examined the role of ATM inhibition on mitochondrial function in Hutchinson-Gilford progeria syndrome (HGPS) and Werner syndrome (WS) cells. We found that ATM inhibition induced mitochondrial functional recovery accompanied by metabolic reprogramming, which has been known to be a prerequisite for senescence alleviation in normal aging cells. Indeed, the induced mitochondrial metabolic reprogramming was coupled with senescence amelioration in accelerated aging cells. Furthermore, the therapeutic effect via ATM inhibition was observed in HGPS as evidenced by reduced progerin accumulation with concomitant decrease of abnormal nuclear morphology. Taken together, our data indicate that the mitochondrial functional recovery by ATM inhibition might represent a promising strategy to ameliorate the accelerated aging phenotypes and to treat age-related disease.

• 대한상부위장관⦁헬리코박터학회지
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• 제18권3호
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• pp.209-212
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• 2018

We report a rare case of systemic amyloidosis with gastrointestinal and lymph node involvement. A 64-year-old woman was admitted to our hospital with dyspepsia and weight loss. Initial esophagogastroduodenoscopy (EGD) revealed nonspecific findings, and abdominal computed tomography showed necrotizing lymphadenopathy at the porta hepatis. Laparoscopic lymph node biopsy was performed under suspicion of tuberculous lymphadenopathy, but a definite diagnosis was not established. Follow-up EGD performed 6 months later revealed multiple telangiectasia-like lesions at the gastric body, and endoscopic biopsy revealed amyloid deposition. Through additional blood and urine protein electrophoresis, the patient was finally diagnosed with systemic amyloidosis associated with multiple myeloma. She was treated with dexamethasone, thalidomide, and bortezomib; however, she died 3 months after diagnosis because of pneumonia and multiple organ failure.

• BMB Reports
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• 제56권3호
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• pp.166-171
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• 2023

Monocytes are peripheral leukocytes that function in innate immunity. Excessive triglyceride (TG) accumulation causes monocyte death and thus can compromise innate immunity. However, the mechanisms by which TG mediates monocyte death remain unclear to date. Thus, this study aimed to elucidate the mechanisms by which TG induces monocyte death. Results showed that TG induced monocyte death by activating caspase-3/7 and promoting poly (ADP-ribose) polymerase (PARP) cleavage. In addition, TG induced DNA damage and activated the ataxia telangiectasia mutated (ATM)/checkpoint kinase 2 and ATM-and Rad3-related (ATR)/checkpoint kinase 1 pathways, leading to the cell death. Furthermore, TG-induced DNA damage and monocyte death were mediated by caspase-2 and -8, and caspase-8 acted as an upstream molecule of caspase-2. Taken together, these results suggest that TG-induced monocyte death is mediated via the caspase-8/caspase-2/DNA damage/executioner caspase/PARP pathways.

• BMB Reports
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• 제56권10호
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• pp.557-562
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• 2023

Dysregulation of the E3 ubiquitin ligase Parkin has been linked to various human cancers, indicating that Parkin is a tumor suppressor protein. However, the mechanisms of action of Parkin remain unclear to date. Thus, we aimed to elucidate the mechanisms of action of Parkin as a tumor suppressor in human lung and colorectal cancer cells. Results showed that Parkin overexpression reduced the viability of A549 human lung cancer cells by inducing G2/M cell cycle arrest. In addition, Parkin caused DNA damage and ATM (Ataxia telangiectasia mutated) activation, which subsequently led to p53 activation. It also induced the p53-mediated upregulation of p21 and downregulation of cyclin B1. Moreover, Parkin suppressed the proliferation of HCT-15 human colorectal cancer cells by a mechanism similar to that in A549 lung cancer cells. Taken together, our results suggest that the tumor-suppressive effects of Parkin on lung and colorectal cancer cells are mediated by DNA damage/p53 activation/cyclin B1 reduction/cell cycle arrest.