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조영석,권기현,이준철,나소영,이효진,홍우정,이유선,김군순,송민호,김영건,노흥규 충남대학교 의학연구소 2003 충남의대잡지 Vol.30 No.2
Prediction of thrapeutic response to radioiodine in Graves' disease is poorly understood. Although thyrotropin binding inhibitor immunoglobulin(TBII) level is a strong index for relapse after antithyroid drug medication, conflicting results are reported regarding its prognostic significance in Graves' disease treated with RAI. This study is dengned to evaluate possible relationship between post-treatment hypothyroidism and TBII in Graves' disease treated with RAI. Fourty two patient with Graves' disease after radioiodine treatment were studied retrospectively. The subject were divided into hypothyroid group and euthyroid or hyperthyroid group. We evaluated the association of hypothyroidism and TBII with radioiodine treatment dose. The mean age of hypothyroid group was 48±11 years and euthyroid or hyperthyroid group was 47±12 years. There was no difference in two groups. And there was no significant difference in post- treatment TBII between two groups(49.9±28.5%, 29.9±14.3%, p-value >0.05). The treatment-dose had no influence on post-treatment thyroid state. Euthyroid or hyperthyroid group was done with 13.6±6.9mCi and hypothyroid group was 17.0±10.4mCi(p-value > 0.05). TBII had no prognostic significance on long-term hypothyrodism in Graves' disease treated with radioiodine. And, treatment-dose had no influence on post-treatment thyroid state.
( Yoo Jin Lee ),( Yu Jin Ha ),( Yu Na Kang ),( Koo Jeong Kang ),( Woo Jin Chung ),( Jae Seok Hwang ),( Byoung Kuk Jang ) 대한간학회 2013 춘·추계 학술대회 (KASL) Vol.2013 No.1
Patients and methods: Expression of autophagy related markers (LC3 and Beclin 1) and ER stress related markers (GRP78 and CHOP) were analyzed by immunohistochemistry on tissues from completely resected specimens of 190 HCC patients. Their influence on clinicopathologic features and prognosis were evaluated using Chi-square test and Kaplan-Meier analysis. Correlations of each proteins were determined by Spearman`s correlation analysis. Results: Expression of LC3 was not correlated with TNM, BCLC stage or Edmonson-Steiner grading, whereas, had correlation with longer overall survival (OS) (P=0.039) and longer disease free survival (DFS) (P=0.068) by Kaplan-Meier analysis. Multivariate analysis indicated that LC3 expression was significantly independent prognostic factors of OS (OR, 0.379; 95% CI, 0.192-0.748; P-value=0.005) and DFS (OR, 0.520; 95% CI, 0.299-0.843; P-value=0.009). Positive correlation was not observed in the expression of autophagy related markers with ER stress related markers. Conclusions: Our study showed that expression of LC3 was correlated with overall survival and disease free survival regardless of tumor staging or liver function state. These results suggest that expression and extent of LC3 might be a strong prognostic factor of HCC.
( Na Jin Kang ),( Dong Hwan Koo ),( Gyeoung Jin Kang ),( Sang Chul Han ),( Bang Won Lee ),( Young Sang Koh ),( Jin Won Hyun ),( Nam Ho Lee ),( Mi Hee Ko ),( Hee Kyoung Kang ),( Eun Sook Yoo ) 한국응용약물학회 2015 Biomolecules & Therapeutics(구 응용약물학회지) Vol.23 No.3
Macrophage-derived chemokine, C-C motif chemokine 22 (MDC/CCL22), is one of the inflammatory chemokines that controls the movement of monocytes, monocyte-derived dendritic cells, and natural killer cells. Serum and skin MDC/CCL22 levels are elevated in atopic dermatitis, which suggests that the chemokines produced from keratinocytes are responsible for attracting inflammatory lymphocytes to the skin. A major signaling pathway in the interferon-γ (IFN-γ)-stimulated inflammation response involves the signal transducers and activators of transcription 1 (STAT1). In the present study, we investigated the anti-inflammatory effect of dieckol and its possible action mechanisms in the category of skin inflammation including atopic dermatitis. Dieckol inhibited MDC/CCL22 production induced by IFN-γ (10 ng/mL) in a dose dependent manner. Dieckol (5 and 10 μM) suppressed the phosphorylation and the nuclear translocation of STAT1. These results suggest that dieckol exhibits anti-inflammatory effect via the down-regulation of STAT1 activation.
( Yoo Jin Na ),( Eun Sang Yu ),( Dae Sik Kim ),( Dae-hee Lee ),( Sang Cheul Oh ),( Chul Won Choi ) 대한내과학회 2021 The Korean Journal of Internal Medicine Vol.36 No.0
Background/Aims: Nilotinib is used for treating patients with imatinib-sensitive or -resistant chronic myeloid leukemia (CML); however, nilotinib-resistant cases have been observed in recent years. In addition, a considerable number of patients receiving nilotinib developed diabetes. Metformin is a front-line drug for the treatment of type 2 diabetes, and several studies have shown that diabetes patients treated with metformin have reduced incidence of cancer. This study aimed to define the effect of metformin on CML cells to determine whether metformin overcomes nilotinib resistance, and to identify novel targets for the treatment of nilotinib resistance. Methods: We observed the effects of metformin and nilotinib on K562 and KU812 human CML cell lines. Nilotinib-resistant CML cell lines were generated by exposing cells to gradually increasing doses of nilotinib. Then, we investigated the driving force that makes resistance to nilotinib and the effect of metformin on the driving force. Results: Sub-toxic doses of metformin enhanced nilotinib efficacy by reducing Bcl-xL expression, which induces apoptosis in CML cells. Next, we generated nilotinib-resistant K562 and KU812 cell lines that overexpressed the c-Jun N-terminal kinase (JNK) gene. JNK silencing by a JNK inhibitor restored sensitivity to nilotinib. Furthermore, metformin was effective in decreasing phosphorylated JNK levels, restoring nilotinib sensitivity. Combined treatment with nilotinib and metformin was more effective than combined treatment with nilotinib and a JNK inhibitor in terms of cell proliferation inhibition. Conclusions: This study suggested that combination therapy with metformin and nilotinib may have clinical benefits of enhancing antileukemia efficacy and overcoming resistance to nilotinib.