• Title/Summary/Keyword: Telangiectasia

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A Pilot Study to Evaluate the Efficacy and Safety of Treatment with Botulinum Toxin in Patients with Recalcitrant and Persistent Erythematotelangiectatic Rosacea

  • Park, Kui Young;Kwon, Hyun Jung;Kim, Jae Min;Jeong, Guk Jin;Kim, Beom Joon;Seo, Seong Jun;Kim, Myeong Nam
    • Annals of dermatology
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    • v.30 no.6
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    • pp.688-693
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    • 2018
  • Background: There are few pharmacologic options to reduce erythema and flushing in patients with recalcitrant erythematotelangiectatic rosacea (ETR). We previously reported two cases of refractory flushing and erythema of rosacea that were successfully treated with intradermal botulinum toxin injection, and additional research is needed to prove the efficacy and safety of this treatment. Objective: To report the efficacy and safety of botulinum toxin injection as an aid in persistent erythema of rosacea patients. Methods: A total of 20 Korean patients with recalcitrant ETR were enrolled to receive treatment by injection of botulinum toxin. Patients received one treatment of intradermal botulinum toxin injection and were assessed 1, 2, 4, and 8 weeks after treatment. The severity of erythema and telangiectasia was investigated by a non-treating physician, and the Erythema Index (EI) was assessed by mexameter at each visit. Patient satisfaction and any adverse events were also assessed at each visit. Results: 17 patients completed all follow-up visits and were included in the analysis. Intradermal injection of botulinum toxin significantly reduced erythema severity and EI in ETR patients. Patients reported a satisfaction score of $2.94{\pm}0.56$ at 8 weeks after treatment. Except for three patients who discontinued the study early due to inconvenience of facial muscle paralysis, 17 patients participating in the final analysis did not report side effects except injection pain at the time of the procedure. Conclusion: Intradermal injection of botulinum toxin can be used as an effective and relatively safe adjuvant agent for recalcitrant and persistent erythema of ETR patients.

Ginsenoside compound K reduces the progression of Huntington's disease via the inhibition of oxidative stress and overactivation of the ATM/AMPK pathway

  • Hua, Kuo-Feng;Chao, A-Ching;Lin, Ting-Yu;Chen, Wan-Tze;Lee, Yu-Chieh;Hsu, Wan-Han;Lee, Sheau-Long;Wang, Hsin-Min;Yang, Ding-I.;Ju, Tz-Chuen
    • Journal of Ginseng Research
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    • v.46 no.4
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    • pp.572-584
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    • 2022
  • Background: Huntington's disease (HD) is a neurodegenerative disorder caused by the expansion of trinucleotide CAG repeat in the Huntingtin (Htt) gene. The major pathogenic pathways underlying HD involve the impairment of cellular energy homeostasis and DNA damage in the brain. The protein kinase ataxia-telangiectasia mutated (ATM) is an important regulator of the DNA damage response. ATM is involved in the phosphorylation of AMP-activated protein kinase (AMPK), suggesting that AMPK plays a critical role in response to DNA damage. Herein, we demonstrated that expression of polyQ-expanded mutant Htt (mHtt) enhanced the phosphorylation of ATM. Ginsenoside is the main and most effective component of Panax ginseng. However, the protective effect of a ginsenoside (compound K, CK) in HD remains unclear and warrants further investigation. Methods: This study used the R6/2 transgenic mouse model of HD and performed behavioral tests, survival rate, histological analyses, and immunoblot assays. Results: The systematic administration of CK into R6/2 mice suppressed the activation of ATM/AMPK and reduced neuronal toxicity and mHTT aggregation. Most importantly, CK increased neuronal density and lifespan and improved motor dysfunction in R6/2 mice. Conversely, CK enhanced the expression of Bcl2 protected striatal cells from the toxicity induced by the overactivation of mHtt and AMPK. Conclusions: Thus, the oral administration of CK reduced the disease progression and markedly enhanced lifespan in the transgenic mouse model (R6/2) of HD.

Adaptive Response to ionizing Radiation Induced by Low Doses of Gamma Rays in Human Lymphoblastoid Cell Lines (인체임파양세포에서 저선량의 감마선에 의해서 유도되는 적응 반응)

  • Seong, Jin-Sil;Suh, Chang-Ok;Kim, Gwi-Eon
    • Radiation Oncology Journal
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    • v.12 no.1
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    • pp.1-8
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    • 1994
  • When cells are exposed to low doses of a mutagenic or clastogenic agents. they often become less sensitive to the effects of a higher dose administered subsequently. Such adaptive responses were first described in Escherichia coli and mammalian cells to low doses of an alkylating agent. Since most of the studies have been carried out with human lymphocytes, it is urgently necessary to study this effect in different cellular systems. Its relation with inherent cellular radiosensitivity and underlying mechanism also remain to be answered. In this study, adaptive response by 1 cGy of gamma rays was investigated in three human lymphoblastoid cell lines which were derived from ataxia telangiectasia homozygote, ataxia telangiectasia heterozygote, and normal individual. Experiments were carried out by delivering 1 cGy followed by 50 cGy of gamma radiation and chromatid breaks were scored as an endpoint. The results indicate that prior exposure to 1 cGy of gamma rays reduces the number of chromatid breaks induced by subsequent higher dose (50 cGy), The expression of this adaptive response was similar among three cell lines despite of their different radiosensitivity. When 3-aminobenzamide, an inhibitor of poly (ADP-ribose) polymerase, was added after 50 cGy, adaptive responses were abolished in all the tested cell lines. Therefore it is suggested that the adaptive response can be observed in human lymphoblastoid cell lines, which was first documented through this study. The expression of adaptive response was similar among the cell lines regardless of their radiosensitivity. The elimination of the adaptive response by 3-aminobenzamide is consistent with the proposal that this adaptive response is the result of the induction of a certain chromosomal repair mechanism.

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Pulmonary Arteriovenous Fistula -One Case Report- (폐동정맥루)

  • 최영호
    • Journal of Chest Surgery
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    • v.15 no.2
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    • pp.183-187
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    • 1982
  • Pulmonary arteriovenous fistula is a congenital vascular malformation In the lung, various synonyms including Pulmonary cavernous vascular malformation, Pulmonary arteriovenous aneurysm, Cavernous hemangioma of the lung0 Pulmonary telangiectasia, Pulmonary hamartoma, etc. The pathogenesis of its symptoms is that unoxygenated, desaturated arterial blood enters into the pulmonary venous system directly. Recently we have experienced one case of the pulmonary arteriovenous fistula which was diagnosed as the pulmonary cystic lesion of the lung preoperatively in 20 years old, 61 kg, male patient. Operation was revealed well circumscribed cystic lesion filled with blood, subpleural and anterior mediobasal location, and bright red colored aspirates on two times needle aspirations. Microscopic finding shows ill circumscribed vascular lesion composed of varying sized blood vessels with irregular thickening of wall and final pathological diagnosis is Pulmonary Arteriovenous Fistula. Basal segmentectomy was done and the patient shows good postoperative course.

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Acquired Pulmonary Arteriovenous Fistula -A Case Report- (후천성 폐 동정맥루 -1례 보고-)

  • 김남혁
    • Journal of Chest Surgery
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    • v.28 no.5
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    • pp.495-498
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    • 1995
  • Pulmonary arteriovenous fistula can be either congenital or acquired. The vast majority are congenital, and about 60% have been associated with hereditary hemorrhagic telangiectasia [Rendu-Osler-Weber disease . Secondary or acquired pulmonary arteriovenous fistula occurs with trauma, schistosomiasis, long-standing hepatic cirrhosis, metastatic carcinoma, and actinomycosis. Pulmonary hemorrhage secondary to acquired pulmonary arteriovenous fistula is a rare event associated with mortality. We have experienced 64 year-old female patient with the hemoptysis secondary to acquired pulmonary arteriovenous fistula due to the infection of pulmonary parasite. The chest PA and CT scan was showed calcified nodule to the distal portion of lateral segmental bronchus of RML. The bronchial angiogram was demonstrated slightly hypertrophied bronchial artery supplying RML bronchus and the presence of hypervascularization around the calcified nodule, rapid A-V shunting is noted by fluoroscopy. The patient was successfully treated by the right middle lobectomy.

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Delayed Radionecrosis of the Larynx (지연성 후두방사선괴사에 대한 고찰)

  • 홍기환;김연우;전희석;양윤수
    • Korean Journal of Bronchoesophagology
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    • v.8 no.1
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    • pp.75-80
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    • 2002
  • Radiation therapy is an effective treatment modality for malignant disease of the head and neck, but it is not without risk and complication. Response of the larynx to radiotherapy varies from mild erythema to severe inflammation with edema and induration. possibly leading to necrosis of cartilage. These changes are due to an inflammatory reaction characterized by infiltration of polymorphonuclear leukocytes, vascular thrombosis, and obliteration of lymphatic channels. Late changes consist of telangiectasia of the skin, alopecia, loss of subcutaneous fat, degenerative changes in the connective tissues. But, radiation necrosis of laryngeal cartilage is an uncommon complication and it is a devastating process for which further necessitates surgical treatment. It is generally agreed that the only treatment for patient not responding to conservative measures is a total laryngectomy. We experienced 4 cases of delayed radionecrosis of the larynx who underwent radiation therapy for glottic cancer and hypopharyngeal cancer. We report these cases with review of literature.

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Differences of SRE (Serum Responsive Element) Activity and Gene Expression between AT5BIVA and LM217 Cells

  • Park, Eun-Kyung;Kim, You-Jin;Rhee, Yun-Hee;Hyesook Chang;Park, Kun-Koo
    • Proceedings of the Korean Biophysical Society Conference
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    • 1999.06a
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    • pp.69-69
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    • 1999
  • The human genetic disorder ataxia-telangiectasia (A-T) is a multisystem disease characterized by extreme radiosensitivity. The recent identification of the gene mutated in A-T, ATM, and the demonstration that it encodes a homologous of phosphatidylinositol 3-kinase (PI3-K), the catalytic subunit of an enzyme involved in transmitting signals from the cell surface to the nucleus, provides support for a role for this gene in signal transduction.(omitted)

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Effect of Protein Kinase C Inhibitor (PKCI) on Radiation Sensitivity and c-fos Transcription Activity (Protein Kinase C Inhibitor (PKCI)에 의한 방사선 민감도 변화와 c-fos Proto-oncogene의 전사 조절)

  • Choi Eun Kyung;Chang Hyesook;Rhee Yun-Hee;Park Kun-Koo
    • Radiation Oncology Journal
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    • v.17 no.4
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    • pp.299-306
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    • 1999
  • Purpose : The human genetic disorder ataxia-telangiectasia (AT) is a multisystem disease characterized by extreme radiosensitivity. The recent identification of the gene mutated in AT, ATM, and the demonstration that it encodes a homologous domain of phosphatidylinositol 3-kinase (PI3-K), the catalytic subunit of an enzyme involved in transmitting signals from the cell surface to the nucleus, provide support for a role of this gene in signal transduction. Although ionizing radiation was known to induce c-fos transcription, nothing is known about how ATM or PKCI mediated signal transduction pathway modulates the c-fos gene transcription and gene expression. Here we have studied the effect of PKCI on radiation sensitivity and c-fos transcription in normal and AT cells. Materials and Methods: Normal (LM217) and AT (AT5BIVA) cells were transfected with PKCI expression plasmid and the overexpression and integration of PKCI was evaluated by northern blotting and polymerase chain reaction, respectively. 5 Gy of radiation was exposed to LM and AT cells transfected with PKCI expression plasmid and cells were harvested 48 hours after radiation and investigated apoptosis with TUNEL method. The c-fos transcription activity was studied by performing CAT assay of reporter gene after transfection of c-fos CAT plasmid into AT and LM cells. Results: Our results demonstrate for the first time a role of PKCI on the radiation sensitivity and c-fos expression in LM and AT cells. PKCI increased radiation induced apoptosis in LM cells but reduced apoptosis in AT cells. The basal c-fos transcription activity is 70 times lower in AT cells than that in LM cells. The c-fos transcription activity was repressed by overexpression of PKCI in LM cells but not in AT cells. After induction of c-fos by Ras protein, overexpression of PKCI repressed c-fos transcription in LM cells but not in AT cells Conclusion: Overexpression of PKCI increased radiation sensitivity and repressed c-fos transcription in LM cells but not in AT cells. The results may be a. reason of increased radiation sensitivity of AT cells. PKCI may be involved in an ionizing radiation induced signal transduction pathway responsible for radiation sensitivity and c-fos transcription. The data also provided evidence for novel transcriptional difference between LM and AT cells.

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Survival and Histological Changes in Gill of the Rockfish, Sebastes schlegeli Following Exposure to Naphthalene (나프탈렌에 노출된 조피볼락의 생존 및 아가미의 조직학적 변화)

  • Cho, Jae Kwon;Kim, Tae Ik;Son, Maeng Hyun;Kim, Kyong Min;Jin, Young Guk
    • Korean Journal of Ichthyology
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    • v.25 no.1
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    • pp.1-8
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    • 2013
  • Rockfish, Sebastes schlegeli (total length; $10.36{\pm}0.49cm$, total weight; $16.28{\pm}1.86g$, N; 290) were exposed to various concentrations of naphthalene for 28 days. Exposure concentrations of naphthalene established control, ethanol (solvent) control, 0.5, 1.0, 1.5 and 2.0 mg Nap $L^{-1}$. After exposure, We observed survival rate, and degree of tissue change (DTC) in gill under optical microscopy. Survival rate of the rockfish was more than 90% in control, ethanol control, 0.5 and 1.0 mg Nap $L^{-1}$, whereas it decreased in 1.5 and 2.0 mg Nap $L^{-1}$ (respectively 80%, 62.2%). In histological observation of gill, hyperplasia of epithelial cells observed in all exposure groups. But no showed increase of DTC which was related to concentration. Whereas, DTC at fusion of gill lamellar, lamellar telangiectasia, stasis, aneurysm and necrosis showed dose dependent increase. Especially, fusion of gill lamellar, lamellar telangiectasia and stasis observed at more 1.0 mg Nap $L^{-1}$, and aneurysm and necrosis at more 1.5 mg Nap $L^{-1}$. These results showed naphthalene caused survival and severe change to the gill of the rockfish which was related to exposure concentration.

The Effect of Traditional Korean Medicine Treatment on CREST Syndrome: A Case Report

  • Joung, Jin-yong;Seo, Hyun-sik;Son, Chang-gue;Lee, Nam-hun;Cho, Jung-hyo
    • The Journal of Internal Korean Medicine
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    • v.38 no.2
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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.