Background:The 3 minutes increment of dobutamine dose protocol is most commonly used method in dobutamine stress echocardiography(DSE). But the precise hemodynamic response to dobutamine dosage and its difference by extending stage duration have not been well elucidated. Materials and Method:Nineteen healthy voluntary subjects with a mean age of 23.9±4.7 years were included. All subjects underwent 3minutes incremental and 5-minnutes incremental protocol of DSE at random order in a same day. Heart rate, blood pressure, stroke volume, fractional shortening, rate-pressure product and cardiac output were measured every 3 minutes in 3-min protocol of DSE. In 5-min protocol, same variables were measured at 3 minutes of each stage as well as at 5 minutes. Results:1) Heart rate did not increase until 10 μg/kg/min dose and increased thereafter by increment of dobutamine dose 2) Fractional shortening and stroke volume increased markedly from the 5 μg/kg/min until 20 μg/kg/min dose and showed slow increase or plateau at a higher dobutamine dose. 3) Systolic blood pressure, cardiac output and rate-pressure product increased continuously from initial dose to maximal dose. 4) Although by extending stage duration to 5 minute in 5-min protocol produced greater hemodynamic effects than those measured at 3 minutes of each stage, there were no significant difference in the results of 3-min and 5-min protocol of DSE. Conclusion:The increase of cardiac contractility most contributed to increase of cardiac output until 20μg/kg/min dose and the increase of herat rate contributed dominantly thereafter, thus the hemodynamic variables showed different responses to increment of dobutamine dose. There were no significant difference in hemodynamic effects between the two protocols. So it is considered that 3-min protocol of DSE gives similar hemodynamic information as 5-min protocol and is more time-saving method. (Korean Circulation J 1998;28(8):1244-1252) KEY WORD:Dobutamine stress echocardiography. 논문접수일:1998년 9월 23일 심사완료일:1998년 9월 25일 교신저자:심완주, 136-075 성북구 안암동 5가 고려대학교 의과대학 내과학교실 전화:(02) 920-5445·전송:(02) 927-1478
<p>Figure S1: Significant concordance between silence of Hippo signature and YAP1 expression in human hepatocellular carcinoma (HCC); Figure S2: Venn diagram of gene lists from two different gene expression signatures; Table S1: Genes in the SOH signature; Table S2: Functional categories of genes in the SOH signature; Table S3: Canonical Pathways enriched in the SOH signature; Table S4: Significant association between the SOH subtype and YAP1 protein expression in HCC; Table S5: Univariate and multivariate Cox regression analyses of recurrence-free survival with continuous SOH probability; Table S6: Univariate and multivariate Cox regression analyses of overall survival; Table S7: Univariate and multivariate Cox regression analyses of overall survival with continuous SOH probability; Table S8: Drop in concordance index in multivariable analysis; Table S9: Concordance of silence of Hippo signature with other prognostic HCC gene expression signatures in the NCI cohort; Table S10: Characteristics of HCC patients in the MSH cohort, stratified by SOH signature.</p>
We aimed to develop an easy‐to‐use risk score with a limited number of genes that can predict the prognosis of hepatocellular carcinoma (HCC) patients. In 139 patients, we identified 65 genes whose expression patterns were significantly associated with overall survival and recurrence in two independent HCC cohorts. The risk score was developed by using Cox coefficient values for the 65 genes from the training set. The risk score was a highly significant predictor of both overall survival and recurrence in the test cohort. The risk score also predicted the prognosis of 65‐base invasion. High‐risk HCC was characterized by activation of IGFR (P = 2.2 × 10–4) and AKT (P = 0.003), whereas low‐risk disease was associated with active mutations of CTNNB1 (P= 0.05). Our new risk score can identify two clinically distinct HCC subtypes in a simple and highly reproducible manner across multiple data sets.
Abstract ESR1 is one of the most important oncogenes and therapeutic targets in breast cancer. By applying systems-level re-analysis of publicly available gene expression data, we uncovered potential regulator of ESR1. We demonstrated that orphan nuclear receptor NR2E3 regulates ESR1 via direct binding to the ESR1 promoter with concomitant recruitment of PIAS3 to promoter in breast cancer cells, and is essential for physiological cellular activity of ESR1 in estrogen receptor (ER)-positive breast cancer cells. Moreover, expression of NR2E3 was significantly associated with recurrence-free survival and favorable response to tamoxifen treatment in women with ER-positive breast cancer. Our results provide mechanistic insight into how ESR1 is regulated by NR2E3 and clinical relevance of NR2E3 in breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 356. doi:10.1158/1538-7445.AM2011-356
Ursolic acid (UA) possesses various pharmacological activities, such as antitumorigenic and anti-inflammatory effects. In the present study, we investigated the mechanisms underlying the effects of UA against esophageal squamous cell carcinoma (ESCC) (TE-8 cells and TE-12 cells). The cell viability assay showed that UA decreased the viability of ESCC in a dose-dependent manner. In the soft agar colony formation assay, the colony numbers and size were reduced in a dose-dependent manner after UA treatment. UA caused the accumulation of vacuoles and LC3 puncta, a marker of autophagosome, in a dose-dependent manner. Autophagy induction was confirmed by measuring the expression levels of LC3 and p62 protein in ESCC cells. UA increased LC3-II protein levels and decreased p62 levels in ESCC cells. When autophagy was hampered using 3-methyladenine (3-MA), the effect of UA on cell viability was reversed. UA also significantly inhibited protein kinase B (Akt) activation and increased p-Akt expression in a dose-dependent manner in ESCC cells. Accumulated LC3 puncta by UA was reversed after wortmannin treatment. LC3-II protein levels were also decreased after treatment with Akt inhibitor and wortmannin. Moreover, UA treatment increased cellular reactive oxygen species (ROS) levels in ESCC in a time- and dose-dependent manner. Diphenyleneiodonium (an ROS production inhibitor) blocked the ROS and UA induced accumulation of LC3-II levels in ESCC cells, suggesting that UA-induced cell death and autophagy are mediated by ROS. Therefore, our data indicate that UA inhibits the growth of ESCC cells by inducing ROS-dependent autophagy.
Background
Despite many attempts to establish pre-treatment prognostic markers to understand the clinical biology of esophageal adenocarcinoma (EAC), validated clinical biomarkers or parameters remain elusive. We generated and analyzed tumor transcriptome to develop a practical biomarker prognostic signature in EAC.
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