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대한내분비학회> Endocrinology and Metabolism(구 대한내분비학회지)> 의학논평 : 양성 갑상선 결절의 치료

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의학논평 : 양성 갑상선 결절의 치료

Editorial : Treatment of Benign Nodular Thyroid Disease

김원배(Won Bae Kim)
  • : 대한내분비학회
  • : Endocrinology and Metabolism(구 대한내분비학회지) 15권4호
  • : 연속간행물
  • : 2000년 12월
  • : 479-485(7pages)
Endocrinology and Metabolism(구 대한내분비학회지)

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UCI(KEPA)

I410-ECN-0102-2009-510-005279271

간행물정보

  • : 의약학분야  > 내과학
  • : KCI등재
  • : SCOPUS
  • : 격월
  • : 2093-596X
  • : 2093-5978
  • : 학술지
  • : 연속간행물
  • : 1986-2022
  • : 2677


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37권6호(2022년 12월) 수록논문
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1Prenatal Exposure to Per- and Polyfluoroalkyl Substances, Maternal Thyroid Dysfunction, and Child Autism Spectrum Disorder

저자 : Hyeong-moo Shin , Jiwon Oh , Rebecca J. Schmidt , Elizabeth N. Pearce

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 37권 6호 발행 연도 : 2022 페이지 : pp. 819-829 (11 pages)

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Autism spectrum disorder (ASD), with its high economic and societal costs, is a growing public health concern whose prevalence has risen steadily over the last two decades. Although actual increased incidence versus improved diagnosis remains controversial, the increased prevalence of ASD suggests non-inherited factors as likely contributors. There is increasing epidemiologic evidence that abnormal maternal thyroid function during pregnancy is associated with increased risk of child ASD and other neurodevelopmental disorders. Prenatal exposure to endocrine-disrupting chemicals such as per- and polyfluoroalkyl substances (PFAS) is known to disrupt thyroid function and can affect early brain development; thus, thyroid dysfunction is hypothesized to mediate this relationship. The concept of a potential pathway from prenatal PFAS exposure through thyroid dysfunction to ASD etiology is not new; however, the extant literature on this topic is scant. The aim of this review is to evaluate and summarize reports with regard to potential mechanisms in this pathway.

KCI등재 SCOPUS

2Preclinical Models of Follicular Cell-Derived Thyroid Cancer: An Overview from Cancer Cell Lines to Mouse Models

저자 : Min Ji Jeon , Bryan R. Haugen

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 37권 6호 발행 연도 : 2022 페이지 : pp. 830-838 (9 pages)

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The overall prognosis of thyroid cancer is excellent, but some patients have grossly invasive disease and distant metastases with limited responses to systemic therapies. Thus, relevant preclinical models are needed to investigate thyroid cancer biology and novel treatments. Different preclinical models have recently emerged with advances in thyroid cancer genetics, mouse modeling and new cell lines. Choosing the appropriate model according to the research question is crucial to studying thyroid cancer. This review will discuss the current preclinical models frequently used in thyroid cancer research, from cell lines to mouse models, and future perspectives on patient-derived and humanized preclinical models in this field.

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3Immune Checkpoint Inhibitors and Endocrine Disorders: A Position Statement from the Korean Endocrine Society

저자 : Hyemi Kwon , Eun Roh , Chang Ho Ahn , Hee Kyung Kim , Cheol Ryong Ku , Kyong Yeun Jung , Ju Hee Lee , Eun Heui Kim , Sunghwan Suh , Sangmo Hong , Jeonghoon Ha , Jun Sung Moon , Jin Hwa Kim , Mi-kyung Ki

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 37권 6호 발행 연도 : 2022 페이지 : pp. 839-850 (12 pages)

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Immune checkpoint inhibitors (ICIs) including an anti-cytotoxic T-lymphocyte-associated antigen 4 inhibitor, anti-programmed cell death protein 1 (PD-1) inhibitors, and anti-PD-ligand 1 inhibitors are representative therapeutics for various malignancies. In oncology, the application of ICIs is currently expanding to a wider range of malignancies due to their remarkable clinical outcomes. ICIs target immune checkpoints which suppress the activity of T-cells that are specific for tumor antigens, thereby allowing tumor cells to escape the immune response. However, immune checkpoints also play a crucial role in preventing autoimmune reactions. Therefore, ICIs targeting immune checkpoints can trigger various immune-related adverse events (irAEs), especially in endocrine organs. Considering the endocrine organs that are frequently involved, irAEs associated endocrinopathies are frequently life-threatening and have unfavorable clinical implications for patients. However, there are very limited data from large clinical trials that would inform the development of clinical guidelines for patients with irAEs associated endocrinopathies. Considering the current clinical situation, in which the scope and scale of the application of ICIs are increasing, position statements from clinical specialists play an essential role in providing the appropriate recommendations based on both medical evidence and clinical experience. As endocrinologists, we would like to present precautions and recommendations for the management of immune-related endocrine disorders, especially those involving the adrenal, thyroid, and pituitary glands caused by ICIs.

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4Forty Years Together, New Leap Forward! The 40th Anniversary of the Korean Endocrine Society

저자 : Jong Chul Won , Ki-hyun Baek

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 37권 6호 발행 연도 : 2022 페이지 : pp. 851-857 (7 pages)

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5DPP-4 Inhibitor in Type 2 Diabetes Mellitus Patient with Non-Alcoholic Fatty Liver Disease: Achieving Two Goals at Once?

저자 : Ji Cheol Bae

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 37권 6호 발행 연도 : 2022 페이지 : pp. 858-860 (3 pages)

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6Efficacy and Safety of Long-Term Methimazole versus Radioactive Iodine in the Treatment of Toxic Multinodular Goiter

저자 : Fereidoun Azizi , Navid Saadat , Mir Alireza Takyar , Hengameh Abdi , Ladan Mehran , Atieh Amouzegar

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 37권 6호 발행 연도 : 2022 페이지 : pp. 861-869 (9 pages)

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Background: This study compared the degree of sustained control of hyperthyroidism in patients with toxic multinodular goiter (TMNG) treated with long-term methimazole (LT-MMI) or radioactive iodine (RAI).
Methods: In this clinical trial, 130 untreated patients with TMNG were randomized to either LT-MMI or RAI treatment. Both groups were followed for 108 to 148 months, with median follow-up durations of 120 and 132 months in the LT-MMI and RAI groups, respectively. Both groups of patients were followed every 1 to 3 months in the first year and every 6 months thereafter.
Results: After excluding patients in whom the treatment modality was changed and those who were lost to follow-up, 53 patients in the LT-MMI group and 54 in the RAI group completed the study. At the end of the study period, 50 (96%) and 25 (46%) patients were euthyroid, and two (4%) and 25 (46%) were hypothyroid in LT-MMI and RAI groups, respectively. In the RAI group, four (8%) patients had subclinical hyperthyroidism. The mean time to euthyroidism was 4.3±1.3 months in LT-MMI patients and 16.3±15.0 months in RAI recipients (P<0.001). Patients treated with LT-MMI spent 95.8%±5.9% of the 12-year study period in a euthyroid state, whereas this proportion was 72.4%±14.8% in the RAI-treated patients (P<0.001). No major treatment-related adverse events were observed in either group.
Conclusion: In patients with TMNG, LT-MMI therapy is superior to RAI treatment, as shown by the earlier achievement of euthyroidism and the longer duration of sustained normal serum thyrotropin.

KCI등재 SCOPUS

7Identification of Mutations in the Thyroxine-Binding Globulin (TBG) Gene in Patients with TBG Deficiency in Korea

저자 : Jung Heo , Sang-mi Kim , Hyun Jin Ryu , Hyunju Park , Tae Hyuk Kim , Jae Hoon Chung , Hyung-doo Park , Sun Wook Kim

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 37권 6호 발행 연도 : 2022 페이지 : pp. 870-878 (9 pages)

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Background: Thyroxine-binding globulin (TBG) is a major transporter protein for thyroid hormones. The serpin family A member 7 (SERPINA7) gene codes for TBG, and mutations of the SERPINA7 gene result in TBG deficiency. Although more than 40 mutations have been reported in several countries, only a few studies of TBG deficiency and SERPINA7 gene mutation have been performed in Korea. The aim of this study is to review the clinical presentations and laboratory findings of patients with TBG deficiency and to investigate the types of SERPINA7 gene mutation.
Methods: Five unrelated Korean adults with TBG deficiency attending endocrinology clinic underwent SERPINA7 gene sequencing. Four patients harbored a SERPINA7 gene mutation. Serum thyroid hormones, anti-microsomal antibodies, and TBG were measured. Genomic DNA was extracted from whole blood. All exons and intron-exon boundaries of the TBG gene were amplified and sequencing was performed.
Results: Two patients were heterozygous females, and the other two were hemizygous males. One heterozygous female had coexisting hypothyroidism. The other heterozygous female was erroneously prescribed levothyroxine at a local clinic. One hemizygous male harbored a novel mutation, p.Phe269Cysfs*18, which caused TBG partial deficiency. Three patients had the p.Leu372Phefs*23 mutation, which is known as TBG-complete deficiency Japan (TBG-CDJ) and was also presented in previous mutation analyses in Korea.
Conclusion: This study presents four patients diagnosed with TBG deficiency and provides the results of SERPINA7 gene sequencing. One novel mutation, p.Phe269Cysfs*18, causing TBD-partial deficiency and three cases of TBG-CDJ were demonstrated. It is necessary to identify TBG deficiency to prevent improper treatment. Also, sequencing of the SERPINA7 gene would provide valuable information about the TBG variants in Korea.

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8BRAFV600E Mutation Enhances Estrogen-Induced Metastatic Potential of Thyroid Cancer by Regulating the Expression of Estrogen Receptors

저자 : Minjun Kim , Su-jin Kim , Seong Yun Ha , Zhen Xu , Youngjin Han , Hyeon-gun Jee , Sun Wook Cho , Young Joo Park , Kyu Eun Lee

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 37권 6호 발행 연도 : 2022 페이지 : pp. 879-890 (12 pages)

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Background: Cross-talk between mitogen-activated protein kinase and estrogen has been reported; however, the role of BRAFV600E in the estrogen responsiveness of thyroid cancer is unknown. We elucidated the effect of BRAFV600E on the estrogen-induced increase in metastatic potential in thyroid cancer.
Methods: Using a pair of cell lines, human thyroid cell lines which harbor wild type BRAF gene (Nthy/WT) and Nthy/BRAFV600E (Nthy/V600E), the expression of estrogen receptors (ERs) and estrogen-induced metastatic phenotypes were evaluated. Susceptibility to ERα- and ERβ-selective agents was evaluated to confirm differential ER expression. ESR expression was analyzed according to BRAFV600E status and age (≤50 years vs. >50 years) using The Cancer Genome Atlas (TCGA) data.
Results: Estradiol increased the ERα/ERβ expression ratio in Nthy/V600E, whereas the decreased ERα/ERβ expression ratio was found in Nthy/WT. BRAFV600E-mutated cell lines showed a higher E2-induced increase in metastatic potential, including migration, invasion, and anchorage-independent growth compared with Nthy/WT. An ERα antagonist significantly inhibited migration in Nthy/V600E cells, whereas an ERβ agonist was more effective in Nthy/WT. In the BRAFV600E group, ESR1/ESR2 ratio was significantly higher in younger age group (≤50 years) compared with older age group (>50 years) by TCGA data analysis.
Conclusion: Our data show that BRAFV600E mutation plays a crucial role in the estrogen responsiveness of thyroid cancer by regulating ER expression. Therefore, BRAFV600E might be used as a biomarker when deciding future hormone therapies based on estrogen signaling in thyroid cancer patients.

KCI등재 SCOPUS

9Metabolite Changes during the Transition from Hyperthyroidism to Euthyroidism in Patients with Graves' Disease

저자 : Ho Yeop Lee , Byeong Chang Sim , Ha Thi Nga , Ji Sun Moon , Jingwen Tian , Nguyen Thi Linh , Sang Hyeon Ju , Dong Wook Choi , Daiki Setoyama , Hyon-seung Yi

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 37권 6호 발행 연도 : 2022 페이지 : pp. 891-900 (10 pages)

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Background: An excess of thyroid hormones in Graves' disease (GD) has profound effects on systemic energy metabolism that are currently partially understood. In this study, we aimed to provide a comprehensive understanding of the metabolite changes that occur when patients with GD transition from hyperthyroidism to euthyroidism with methimazole treatment.
Methods: Eighteen patients (mean age, 38.6±14.7 years; 66.7% female) with newly diagnosed or relapsed GD attending the endocrinology outpatient clinics in a single institution were recruited between January 2019 and July 2020. All subjects were treated with methimazole to achieve euthyroidism. We explored metabolomics by performing liquid chromatography-mass spectrometry analysis of plasma samples of these patients and then performed multivariate statistical analysis of the metabolomics data.
Results: Two hundred metabolites were measured before and after 12 weeks of methimazole treatment in patients with GD. The levels of 61 metabolites, including palmitic acid (C16:0) and oleic acid (C18:1), were elevated in methimazole-naïve patients with GD, and these levels were decreased by methimazole treatment. The levels of another 15 metabolites, including glycine and creatinine, were increased after recovery of euthyroidism upon methimazole treatment in patients with GD. Pathway analysis of metabolomics data showed that hyperthyroidism was closely related to aminoacyl-transfer ribonucleic acid biosynthesis and branched-chain amino acid biosynthesis pathways.
Conclusion: In this study, significant variations of plasma metabolomic patterns that occur during the transition from hyperthyroidism to euthyroidism were detected in patients with GD via untargeted metabolomics analysis.

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10Inhibition of miR-146a-5p and miR-8114 in Insulin-Secreting Cells Contributes to the Protection of Melatonin against Stearic Acid-Induced Cellular Senescence by Targeting Mafa

저자 : Shenghan Su , Qingrui Zhao , Lingfeng Dan , Yuqing Lin , Xuebei Li , Yunjin Zhang , Chunxiao Yang , Yimeng Dong , Xiaohan Li , Romano Regazzi , Changhao Sun , Xia Chu , Huimin Lu

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 37권 6호 발행 연도 : 2022 페이지 : pp. 901-917 (17 pages)

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Background: Chronic exposure to elevated levels of saturated fatty acids results in pancreatic β-cell senescence. However, targets and effective agents for preventing stearic acid-induced β-cell senescence are still lacking. Although melatonin administration can protect β-cells against lipotoxicity through anti-senescence processes, the precise underlying mechanisms still need to be explored. Therefore, we investigated the anti-senescence effect of melatonin on stearic acid-treated mouse β-cells and elucidated the possible role of microRNAs in this process.
Methods: β-Cell senescence was identified by measuring the expression of senescence-related genes and senescence-associated β-galactosidase staining. Gain- and loss-of-function approaches were used to investigate the involvement of microRNAs in stearic acid-evoked β-cell senescence and dysfunction. Bioinformatics analyses and luciferase reporter activity assays were applied to predict the direct targets of microRNAs.
Results: Long-term exposure to a high concentration of stearic acid-induced senescence and upregulated miR-146a-5p and miR-8114 expression in both mouse islets and β-TC6 cell lines. Melatonin effectively suppressed this process and reduced the levels of these two miRNAs. A remarkable reversibility of stearic acid-induced β-cell senescence and dysfunction was observed after silencing miR-146a-5p and miR-8114. Moreover, V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (Mafa) was verified as a direct target of miR-146a-5p and miR-8114. Melatonin also significantly ameliorated senescence and dysfunction in miR-146a-5p- and miR-8114-transfected β-cells.
Conclusion: These data demonstrate that melatonin protects against stearic acid-induced β-cell senescence by inhibiting miR-146a-5p and miR-8114 and upregulating Mafa expression. This not only provides novel targets for preventing stearic acid-induced β-cell dysfunction, but also points to melatonin as a promising drug to combat type 2 diabetes progression.

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1Uncoupling Protein ( UCP ) 이란 ?

저자 : 최웅환(Woong Hwan Choi)

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 15권 4호 발행 연도 : 2000 페이지 : pp. 453-462 (10 pages)

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2DNA Chip

저자 : 박종훈(Jong Hoon Park)

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 15권 4호 발행 연도 : 2000 페이지 : pp. 463-467 (5 pages)

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3혈관내분비학 (血管內分泌學) - 내분비학의 새로운 분야 발전을 위한 논술 -

저자 : 유형준(Hyung Joon Yoo)

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 15권 4호 발행 연도 : 2000 페이지 : pp. 468-478 (11 pages)

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4의학논평 : 양성 갑상선 결절의 치료

저자 : 김원배(Won Bae Kim)

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 15권 4호 발행 연도 : 2000 페이지 : pp. 479-485 (7 pages)

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5포도당과 이소프로테레놀에 의한 시상하부의 소마토스타틴 분비가 갑상선자극호르몬방출호르몬에 의한 갑상선자극호르몬에 미치는 효과

저자 : 박철영(Cheol Young Park) , 양인명(In Myung Yang) , 오승준(Seung Joon Oh) , 김덕윤(Deog Yoon Kim) , 우정택(Jeong Taek Woo) , 김성운(Sung Woon Kim) , 김진우(Jin Woo Kim) , 김영설(Young Seol Kim) , 최영길(Young Kil Choi)

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 15권 4호 발행 연도 : 2000 페이지 : pp. 486-492 (7 pages)

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Background: Acute hyperglycemia stimulates somatostatin (SRIH) release from the hypothalamus, and which in turn suppress growth hormone (GH) secretion and thyroid stimulating hormone (TSH) from the anterior pituitary gland. Beta-adrenergic pathway is known to stimulate the hypothalamus SRIH release. Recently, We demonstrated that isoproterenol, a beta-adrenergic agonist, had an additional suppressive effect on the suppression by glucose of GHRH-stimulated GH response. Therefore, the present study aimed to determine whether isoproterenol has an additional suppressive effect on the suppression by glucose of TRH-stimulated TSH response. Methods: Seven healthy young men, aged 24 to 27 years, were studied. Four different TRH stimulation tests were carried out. (Test 1) TRH (Hoechst AG, Germany), 200 μg bolus, was given intravenously at 0 minute. (Test 2) Glucose, 100 g, was given orally 30 min before TRH administration. (Test 3) Isoproterenol(Isuprel, Sanofi Winthrop, USA), 0.012 pg/kg, was infused continuously for 120 min after TRH administration. (Test 4) After pretreatment with glucose as Test 2, isoproterenol and TRH were administered as Test 3. Results: Oral glucose ingestion significantly suppressed the TRH-stimulated TSH secretion. Isoproterenol infusion significantly suppressed the TRH-stimulated TSH secretion. Glucose-induced suppression of the TSH response was significantly greater than that by isoproterenol. 1soproterenol infusion after glucose pretreatment did not show any additional suppressive effect on the glucose-induced suppression of TSH response to TRH. Conclusion: The results suggest that isoproterenol infusion in addition to glucose pretreatment before the TRH stimulation test is not necessary for the development of stronger stimulation test for the hypothalamic somatostatin secretion (J Kor Soc Endocrinol l5:486-492, 2000).

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6성장호르몬 결핍증 환아에서 성장호르몬 치료가 혈청 leptin 농도에 미치는 영향

저자 : 오진희(Jin Hee Oh) , 이병철(Byung Churl Lee)

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 15권 4호 발행 연도 : 2000 페이지 : pp. 493-501 (9 pages)

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Background: Leptin the ob gene product is secreted by adipocytes and binds to specific receptors in the central nervous system regulating energe intake and expenditure. Correlation between fat mass and leptin level is well established. However, data on the hormonal regulation of the leptin in human are scarce. Growth hormone (GH) has lypolytic action and patients with growth hormone deficiency (GHD) have showed higher leptin levels than expected for the obesity We investigated the changes in serum leptin levels and body mass index in children with GHD during GH therapy. Methods: Thirty children with GHD participated. All subjects were 5~13 years old and in prepubertal stage. The causes of GHD were idiopathic in 15 and organic in 15 children. Patients received GH 0.6.7 IU/kg/week subcutaneously, in 67 divided doses and investigated at baseline and after 6 and 12 months of GH treatment. Serum leptin levels were determined with a human leptin and IGF-1 radioimmunoassay (Linco Research and Nichols Institute, USA). Results: The height velocity was increased significantly after 12 months of GH treatment. Serum leptin concentrations were significantly reduced after 6 and 12 months of treatment but revealed no significant differences in the sex and the causes of GHD. Body mass indices were significantly reduced after treatment. Serum leptin levels positively correlated with body mass index at baseline and after 6 and 12 months of GH treatment. The serum IGF-1 level were increased significantly after GH treatment and did not significantly correlated with leptin levels at baseline and after treatment. Conclusion: This study demonstrated that serum leptin and body mass index were decreased with significant positive correlation during GH treatment in children with GHD (J Kor Soc Endocrinol 15:493-501, 2000).

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7유전성 비만 마우스 ( ob / ob ) 에서 Retrovirus 를 이용한 Leptin 유전자의 전입 및 발현

저자 : 변용준(Young Jun Byun) , 정인철(In Cheol Jeong) , 오상환(Sang Hwan Oh) , 조무연(Moo Youn Cho)

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 15권 4호 발행 연도 : 2000 페이지 : pp. 502-512 (11 pages)

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Background: Leptin gene is known to be related to obesity in human and animals and complete genetic defect of the gene in ob/ob mouse has been identified. Therefore, ob/ob mouse is widely used as an animal model for the study of etiology and therapy of obesity. The main biological function of leptin was thought to involve in the regulation of food intake and weight gain, however, the regulatory mechanisms by which leptin functions in the weight reduction and lowering the blood glucose level are uncertain. In the present study, retroviral-mediated leptin gene transduction into ob/ob mouse was attempted for the correction of biochemical parameters of obesity. Methods: Leptin cDNA was inserted into pLXSN retroviral vector (pLXSN-lep) and recombinant leptin expressing retrovirus particles (3 X10 CFU/mL) were produced in Ψ2 ecotropic packaging cells and subsequent transfection into PA317 amphotropic packaging cells. The leptin expressing recombinant viruses (LER) were transduced into NIH3T3 mouse fibroblasts and insertion of leptin cDNA into chromosomal DNA of PA317 and MH3T3 mouse fibroblasts was confirmed by Southern blot hybridizations. Leptin mRNA and its protein expressed in the cells were identified by Northern blot hybridization and Western blot immunodetection method, respectively. LER were injected I. P. into ob/ob mice, and body weight, food intake, serum leptin level and blood glucose level were measured. Results: Expression of leptin was identified in PA317 and NIH3T3 mouse fibroblasts transduced with LER. Leptin content in sera of mice transfused with LER was drastically increased after 1 week and decreased to the almost basal level at 3 weeks after the transfusion. The body weight as well as food intake of ob/ob mouse transduced by LER decreased for the first 3 weeks and slightly increased thereafter. The reduction of both body weight and food intake in ob/ob mice transduced with LER was observed with the concomitant increase of serum leptin level, indicating that retroviral-mediated transduction of leptin gene in ob/ob mouse in vivo produced a biologically active leptin protein and released it into blood circulation. Conclusion: A transient expression of leptin cDNA in ob/ob mice by a retroviral-mediated transduction was performed and further studies are required for long term expression of the gene in vivo (J Kor Soc Endocrinol 15:502-512, 2000).

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8갑상선 여포선암 진단시 HBME - 1 면역염색법의 유용성

저자 : 신영구(Young Goo Shin) , 이기범(Kyi Bum Lee) , 정윤석(Yoon Sok Chung) , 김현만(Hyeon Man Kim)

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 15권 4호 발행 연도 : 2000 페이지 : pp. 513-521 (9 pages)

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Background: Leptin gene is known to be related to obesity in human and animals and complete genetic defect of the gene in ob/ob mouse has been identified. Therefore, ob/ob mouse is widely used as an animal model for the study of etiology and therapy of obesity. The main biological function of leptin was thought to involve in the regulation of food intake and weight gain, however, the regulatory mechanisms by which leptin functions in the weight reduction and lowering the blood glucose level are uncertain. In the present study, retroviral-mediated leptin gene transduction into ob/ob mouse was attempted for the correction of biochemical parameters of obesity. Methods: Leptin cDNA was inserted into pLXSN retroviral vector (pLXSN-lep) and recombinant leptin expressing retrovirus particles (3 X10 CFU/mL) were produced in Ψ2 ecotropic packaging cells and subsequent transfection into PA317 amphotropic packaging cells. The leptin expressing recombinant viruses (LER) were transduced into NIH3T3 mouse fibroblasts and insertion of leptin cDNA into chromosomal DNA of PA317 and MH3T3 mouse fibroblasts was confirmed by Southern blot hybridizations. Leptin mRNA and its protein expressed in the cells were identified by Northern blot hybridization and Westen blot immunodetection method, respectively. LER were injected I. P. into ob/ob mice, and body weight, food intake, serum leptin level and blood glucose level were measured. Results: Expression of leptin was identified in PA317 and NIH3T3 mouse fibroblasts transduced with LER. Leptin content in sera of mice transfused with LER was drastically increased after 1 week and decreased to the almost basal level at 3 weeks after the transfusion. The body weight as well as food intake of ob/ob mouse transduced by LER decreased for the first 3 weeks and slightly increased thereafter. The reduction of both body weight and food intake in ob/ob mice transduced with LER was observed with the concomitant increase of serum leptin level, indicating that retroviral-mediated transduction of leptin gene in ob/ob mouse in vivo produced a biologically active leptin protein and released it into blood circulation. Conclusion: A transient expression of leptin cDNA in ob/ob mice by a retroviral-mediated transduction was performed and further studies are required for long term expression of the gene in vivo (J Kor Soc Endocrinol 15:502-512, 2000).

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9갑상선암 세포주에서 아데노바이러스 - hNIS ( Ad - hNIS ) 유전자 이입에 의한 방사성 요오드 포획 증진 효과

저자 : 박건구(Kun Koo Park) , 진정선(Jung Sun Jin) , 이성진(Seong Jin Lee) , 박정윤(Jung Yoon Park) , 이희란(Heui Ran Lee) , 문대혁(Dae Hyuk Moon) , 안일민(Il Min Ahn) , 장혜숙(Hye Sook Chang)

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 15권 4호 발행 연도 : 2000 페이지 : pp. 522-531 (10 pages)

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Background: The sodium-iodide-symporter (NIS) is a plasma membrane glycoprotein with 13 putative transmembrane domains, which is responsible for concentrating iodide into the thyroid by an active transport and provides the mechanism for radioactive-iodine (RAI) therapy for thyroid cancer. However, undifferentiated thyroid cancers and about 2050% of differentiated thyroid cancers do not take up the RAI at therapeutic dose. The NIS has been cloned from rat and human (hNIS) and characterized recently. In an attempt to develop a new therapeutic strategy using hNIS gene for improving the efficacy of RAI therapy in thyroid cancers, we have constructed a recombinant adenovirus encoding the hNIS (Ad-hNIS) and tested its function by an iodide uptake by infecting human thyroid cancer cells. Methods: RT-PCR was performed to measure an intrinsic hNIS expression in thyroid cancer cell lines, such as NPA, FRO and ARO. To generate the hNIS adenovirus, hNIS cDNA was isolated and ligated into Swa I site of cosmid shuttle vector (pAxCAwt). We have produced recombinant adenovirus by co-transfecting the cosmid with DNA-TPC to 293 cell line. Adenovirus that express (β-Galactosidase (LacZ) was also prepared by the similar strategy. Adenovirus infection efficiency was measured in three thyroid cancer cell lines. Finally, 24 hours after infection of ad-hNIS into the cells, I125-uptake was measured. Results: Endogenous hNIS expression was detected only in FRO cells but not in NPA, ARO and Hela cells by RT-PCR. X-Gal staining after infection of Ad-LacZ to thyroid cancer cell (NPA, ARO, FRO) showed that an infection rate in ARO cells was 98.5+0.5%, 97.0+0.2% in FRO cells and 75.5+5.0% in NPA cells. We selected ARO cells for the infection of Ad-hNIS due to the highest infection efficiency and the absence of endogenous hNIS expression. When ARO cells were infected with the ad-hNIS, I125 uptake was increased 504+6.4%. Conclusion: Overexpression of hNIS gene in thyroid cancer cells elicited over 5 fold increase in I-uptake, suggesting that the Ad-hNIS infection to the thyroid cancer cells may improve the efficiency of radioactive iodine therapy (J Kor Soc Endocrinol 15:522-53l, 2000).

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10양성 갑상선 결절에서 티록신 억제 요법의 효과

저자 : 윤석기(Seog Ki Yun) , 김철희(Chul Hee Kim) , 김영선(Young Sun Kim) , 변동원(Dong Won Byun) , 서교일(Kyo Il Suh) , 유명희(Myung Hi Yoo)

발행기관 : 대한내분비학회 간행물 : Endocrinology and Metabolism(구 대한내분비학회지) 15권 4호 발행 연도 : 2000 페이지 : pp. 532-541 (10 pages)

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Background: Benign pathologic findings are shown in 800% of thyroid nodules by fine needle aspiration cytology (FNAC) or needle biopsy. About half of these benign nodules are follicular lesions which are presented only as thyroid follicles or thyroid cell clumps. Differential diagnosis of follicular adenoma, follicular carcinoma and adenomatous goiter is impossible by FNAC or needle biopsy. Thyroxine suppression therapy has been performed traditionally in order to discriminate malignant nodules, but few studies are available which confirmed the efficacy of thyroxine suppression therapy in thyroid nodules of those the initial pathologic findings were follicular lesions. So we tried to evaluate the efficacy of thyroxine suppression therapy in benign thyroid nodules and also the incidence of thyroid cancer of the thyroid nosules which were not decreased on thyroxine suppression therapy after surgical resection. Methods: Total 1027 patients with thyroid nodules were evaluated by FNAC or needle biopsy at Soonchunhyang university hospital from 1990 to 1996. Among 1027 patients, 507 patients showed follicular lesions in FNAC or needle biopsy and they received thyroxine suppression therapy. Thyroid nodule volume was measured before and after thyroxine suppression therapy using ultrasonography. We studied 184 patients who were followed up for more than 1 year. Serial changes of thyroid function tests, thyroid nodule volume, serum thyroglubulin (Tg) level before and after therapy were analyzed. Results: l. In 80 (43.5%) of the 184 patients, nodule volumes decreased more than 50 percent after thyroxine suppression therapy. 2. There was no significant difference in serum T3, T4, TSH levels before and after thyroxine suppression therapy between group I (nodule volume decreased less than 50%) and group II (nodule volume decreased more than 50%). 3. In group II patients, thyroid nodule volumes were decreased continuously at 12 month, 18 month and 30 month after thyroxine suppression (p<0.05). 4. There was no significant difference between the group I and group II in the frequency of multiple thyroid nodules on ultrasonography. 5. Among 37 patients who underwent thyroidectomy, 19 cases (51.4%) were revealed as malignant thyroid nodules (papillary cancer 4 cases, follicular cancer 15 cases). Eighteen cases (48.6%) were revealed as benign thyroid nodules (follicular adenoma 10 cases, adenomatous goiter 8 cases). 6. There was no significant difference in the frequency of multiple nodules on ultrasonography between benign and malignant nodules. Conclusion: Our data suggested thyroxine suppression therapy was effective in discriminating malignant thyroid nodules from benign nodules, especially in selecting follicular carcinoma from follicular lesion by FNAC or biopsy (J Kor Soc Endocrinol 15:532-541, 2000).

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