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( Sangmi Jang ),( Gwang Hyeon Choi ),( Sung-ho Hwang ),( Jaewon Park ),( Won Joon Choi ),( Woo Jin Jung ),( Eun Sun Jang ),( Jin-wook Kim ),( Sook-hyang Jeong ) 대한간학회 2020 춘·추계 학술대회 (KASL) Vol.2020 No.1
Aims: Alpha-fetoprotein (AFP) is a well-known biomarker of liver cancer and liver injury. However, apparently healthy individuals having AFP elevation on heath check-ups were encountered in clinics. Their clinical features and cause of AFP elevation were not clear. Thus, we aim to investigate the clinical characteristics of the patients with an “elevated AFP level” (>7 ng/ mL cutoff), and its relation with body fat deposition in terms of hepatic steatosis and visceral adiposity. Methods: Patients having a diagnostic code of “elevated AFP level” (R772) were searched from 2009 to 2018 in a tertiary hospital. After excluding patients with any malignancies, liver cirrhosis, or viral hepatitis, 146 patients were included in the case group. As a control group, age and sex-matched 146 hepatic hemangioma (<3cm) patients were selected. Among the subgroup of case (n=49) and controls (n=49) who underwent liver CT, hepatic fat and visceral fat were measured using the pre-contrast CT image. Results: The case group showed a mean age of 48.7 years, male proportion of 64.4%, and a higher mean serum AFP level (12.76 ng/mL) than the control (2.85 ng/mL). The case group showed a higher prevalence of dyslipidemia (21.2 vs 3.4%, P<0.001) and hypertension (11.6 vs 4.8%, P=0.033), but a lower body mass index (BMI) (22.68 vs 23.85 kg/m2, P=0.003) than the control. Total-bilirubin level was higher in the case group (0.8 vs 0.5 mg/dL, P<0.001), but other laboratory results were similar to the control group. Hepatic fat measured by Hounsfield units of 8 regions of liver segments and visceral adiposity index in the subgroups of case and control were not different (59.40 vs 61.76, P=0.158 and 28.53 vs 27.32 ㎠/㎡, P=0.788, respectively). Conclusions: Asymptomatic patients with an elevated AFP level showed a higher prevalence of hypertension and dyslipidemia despite lower BMI than controls. Its relationship with abnormal fat metabolism warrants further study.
( Woo Jin Jung ),( Jin-wook Kim ),( Sangmi Jang ),( Won Joon Choi ),( Jaewon Park ),( Gwang Hyeon Choi ),( Eun Sun Jang ),( Sook-hyang Jeong ) 대한간학회 2020 춘·추계 학술대회 (KASL) Vol.2020 No.1
Aims: Metformin has received attention in cancer prevention strategy because of its potential for biological specificity. Retrospective studies and meta-analyses have reported that metformin reduced the risk of developing hepatocellular carcinoma (HCC) in cirrhotic patients with diabetes. Moreover, in vitro data suggested that metformin may enhance anticancer effect of cytotoxic drugs and radiotherapy in hepatoma cells. Therefore, this study aimed to assess whether metformin enhances therapeutic efficacy of transcatheter arterial chemoembolization (TACE) in HCC. Methods: This retrospective analysis included all consecutive HCC patients who underwent TACE in our institute between April 2003 and February 2020. Study population was limited to treatment-naïve patients who had single nodular HCC without vascular or ductal or extrahepatic invasion. Treatment response was assessed according the modified Response Evaluation Criteria in Solid Tumors criteria. Logistic regression analysis was used to determine predictors of tumor response by TACE. Results: Among the 709 patients with single nodular HCC who received TACE, 105 were diabetics on metformin, 74 diabetics without metformin and 530 were control without diabetes. The overall response rate was 61.5% for complete response and 72.5% for objective response rate (ORR; complete response + partial response). In univariate analysis, metformin use increased ORR compared to diabetics without metformin (odds ratio [OR] = 2.3, 95% confidence interval [CI] = 1.34 - 4.1, P<0.001), along with small tumor size (< 3 cm) (OR = 2.47, 95% CI = 1.76 - 3.46, P<0.001). Multivariate analysis confirmed the independent associations between metformin use and ORR (OR = 4.1, CI = 2.0 - 8.4, P<0.001), along with tumor size < 3cm (OR = 2.6, CI=1.8 - 3.7, P<0.001) and absence of diabetes (OR = 1.8, CI = 1.1 - 3.0, P=0.029). Conclusions: Metformin use enhances tumor response of TACE for single nodular HCC.
Ock, Sangmi,Lee, Wang Soo,Kim, Hyun Min,Park, Kyu-Sang,Kim, Young-Kook,Kook, Hyun,Park, Woo Jin,Lee, Tae Jin,Abel, E.D.,Kim, Jaetaek Elsevier 2018 Biochimica et biophysica acta Vol.1864 No.4
<P><B>Abstract</B></P> <P>While deletion of <I>Akt1</I> results in a smaller heart size and <I>Akt2</I> <SUP>−/−</SUP> mice are mildly insulin resistant, <I>Akt1</I> <SUP>−/−</SUP>/<I>Akt2</I> <SUP>−/−</SUP> mice exhibit perinatal lethality, indicating a large degree of functional overlap between the isoforms of the serine/threonine kinase Akt. The present study aimed to determine the cooperative contribution of Akt1 and Akt2 on the structure and contractile function of adult hearts. To generate an inducible, cardiomyocyte-restricted Akt2 knockout (KO) model, <I>Akt2</I> <SUP>flox/flox</SUP> mice were crossed with tamoxifen-inducible MerCreMer transgenic (MCM) mice and germline <I>Akt1</I> <SUP>−/−</SUP> mice to generate the following genotypes:<I>Akt1</I> <SUP>+/+</SUP>; <I>Akt2</I> <SUP>flox/flox</SUP> (WT), <I>Akt2</I> <SUP>flox/flox</SUP>; α-MHC-MCM (<I>iAkt2</I> KO), <I>Akt1</I> <SUP>−/−</SUP>, and <I>Akt1</I> <SUP>−/−</SUP>; <I>Akt2</I> <SUP>flox/flox</SUP>; α-MHC-MCM mice (<I>Akt1</I> <SUP>−/−</SUP>/<I>iAkt2</I> KO). At 28 days after the first tamoxifen injection, <I>Akt1</I> <SUP>−/−</SUP>/<I>iAkt2</I> KO mice developed contractile dysfunction paralleling increased atrial and brain natriuretic peptide (ANP and BNP) levels, and repressed mitochondrial gene expression. Neither cardiac fibrosis nor apoptosis were detected in <I>Akt1</I> <SUP>−/−</SUP>/<I>iAkt2</I> KO hearts. To explore potential molecular mechanisms for contractile dysfunction, we investigated myocardial microstructure before the onset of heart failure. At 3 days after the first tamoxifen injection, <I>Akt1</I> <SUP>−/−</SUP>/<I>iAkt2</I> KO hearts showed decreased expression of connexin43 (Cx43) and connexin-interacting protein zonula occludens-1 (ZO-1). Furthermore, Akt1/2 silencing significantly decreased both Cx43 and ZO-1 expression in cultured neonatal rat cardiomyocytes in concert with reduced beating frequency. Akt1 and Akt2 are required to maintain cardiac contraction. Loss of Akt signaling disrupts gap junction protein, which might precipitate early contractile dysfunction prior to heart failure in the absence of myocardial remodeling, such as hypertrophy, fibrosis, or cell death.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Cardiac <I>Akt1</I> <SUP>-/-</SUP>/<I>iAkt2</I> KO in mice reduces cardiac size and induces contractile dysfunction without myocardial remodeling. </LI> <LI> <I>Akt1</I> <SUP>-/-</SUP>/<I>iAkt2</I> KO hearts revealed decreased expression of Cx43 and connexin-interacting protein ZO-1. </LI> <LI> Akt isoforms may play important roles to maintain cardiac contractile function through gap junction protein stability. </LI> </UL> </P>