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Park, D.W.,Kwak, D.S.,Park, Y.Y.,Chang, Y.,Huh, J.W.,Lim, C.M.,Koh, Y.,Song, D.K.,Hong, S.B. Grune Stratton 2014 Journal of critical care Vol.29 No.5
Purpose: The purpose of this study is to investigate the effect of serial lysophosphatidylcholine (LPC) measurement on 28-day mortality prediction in patients with severe sepsis or septic shock admitted to the medical intensive care unit (ICU). Methods: This is a prospective observational study of 74 ICU patients in a tertiary hospital. Serum LPC, white blood cell, C-reactive protein, and procalcitonin (PCT) levels were measured at baseline (day 1 of enrollment) and day 7. The LPC concentrations were compared with inflammatory markers using their absolute levels and relative changes. Results: The LPC concentration on day 7 was significantly lower in nonsurvivors than in survivors (68.45 +/- 42.36 μmol/L and 99.76 +/- 73.65 μmol/L; P = .04). A decreased LPC concentration on day 7 to its baseline as well as a sustained high concentration of PCT on day 7 at more than 50% of its baseline value was useful for predicting the 28-day mortality. Prognostic utility was substantially improved when combined LPC and PCT criteria were applied to 28-day mortality outcome predictions. Furthermore, LPC concentrations increased over time in patients with appropriate antibiotics but not in those with inappropriate antibiotics. Conclusions: Serial measurements of LPC help in the prediction of 28-day mortality in ICU patients with severe sepsis or septic shock.
Initiation and Discontinuation of Complementary Therapy Among Cancer Patients
Kim, Sung-Gyeong,Park, Eun-Cheol,Park, Jae-Hyun,Hahm, Myung-Il,Lim, Jin-Hwa,Choi, Kui-Son Grune & Stratton 2007 Journal of clinical oncology Vol.25 No.33
<B>Purpose</B><P>To identify the initiation or discontinuation of complementary therapy (CT) and determine the impact of sociodemographic and clinical factors on CT use among cancer patients.</P><B>Patients and Methods</B><P>Eligible patients were age 20 or older; newly diagnosed with stomach, liver, or colorectal cancer; and started their initial treatment at the National Cancer Center, Korea, between April 1, 2001, and April 30, 2003. In total, 541 cancer patients were surveyed in face-to-face interviews at baseline, and telephone follow-up interviews were performed every 3 months for 3 years.</P><B>Results</B><P>A total of 281 patients commenced CT after diagnosis; 164 patients stopped using CT during the follow-up period. The overall cumulative probability of starting CT at 1, 2, and 3 years was 50%, 54%, and 55%, respectively. In a Cox multivariate analysis, stomach and liver cancer were associated with an increased probability of initiating CT compared with colorectal cancer. Patients who were classified as stage I, II, or III at diagnosis were associated with a decreased probability of discontinuing CT compared with stage IV.</P><B>Conclusion</B><P>Most cancer patients started to use CT during the initial treatment period. Thus, physicians should communicate with cancer patients about CT at this phase. In particular, more attention should be paid to women and individuals with higher household incomes because these groups are more likely to start CT.</P>
PICOT Inhibits Cardiac Hypertrophy and Enhances Ventricular Function and Cardiomyocyte Contractility
Jeong, Dongtak,Cha, Hyeseon,Kim, Eunyoung,Kang, Misuk,Yang, Dong Kwon,Kim, Ji Myoung,Yoon, Pyoung Oh,Oh, Jae Gyun,Bernecker, Oliver Y.,Sakata, Susumu,Thu, Le Thi,Cui, Lei,Lee, Young-Hoon,Kim, Do Han,W Grune & Stratton 2006 Circulation research Vol.99 No.3
<P>Multiple signaling pathways involving protein kinase C (PKC) have been implicated in the development of cardiac hypertrophy. We observed that a putative PKC inhibitor, PICOT (PKC-Interacting Cousin Of Thioredoxin) was upregulated in response to hypertrophic stimuli both in vitro and in vivo. This suggested that PICOT may act as an endogenous negative feedback regulator of cardiac hypertrophy through its ability to inhibit PKC activity, which is elevated during cardiac hypertrophy. Adenovirus-mediated gene transfer of PICOT completely blocked the hypertrophic response of neonatal rat cardiomyocytes to enthothelin-1 and phenylephrine, as demonstrated by cell size, sarcomere rearrangement, atrial natriuretic factor expression, and rates of protein synthesis. Transgenic mice with cardiac-specific overexpression of PICOT showed that PICOT is a potent inhibitor of cardiac hypertrophy induced by pressure overload. In addition, PICOT overexpression dramatically increased the ventricular function and cardiomyocyte contractility as measured by ejection fraction and end-systolic pressure of transgenic hearts and peak shortening of isolated cardiomyocytes, respectively. Intracellular Ca(2+) handing analysis revealed that increases in myofilament Ca(2+) responsiveness, together with increased rate of sarcoplasmic reticulum Ca(2+) reuptake, are associated with the enhanced contractility in PICOT-overexpressing cardiomyocytes. The inhibition of cardiac remodeling by of PICOT with a concomitant increase in ventricular function and cardiomyocyte contractility suggests that PICOT may provide an efficient modality for treatment of cardiac hypertrophy and heart failure.</P>
Kim, Ki Mo,Pae, Hyun-Ock,Zheng, Min,Park, Raekil,Kim, Young-Myeong,Chung, Hun-Taeg Grune & Stratton 2007 Circulation research Vol.101 No.9
<P>Carbon monoxide (CO), a reaction product of the cytoprotective heme oxygenase (HO)-1, is antiapoptotic in a variety of models of cellular injury, but the precise mechanisms remain to be established. In human umbilical vein endothelial cells, exogenous CO activated Nrf2 through the phosphorylation of protein kinase R-like endoplasmic reticulum kinase (PERK), resulting in HO-1 expression. CO-induced activation of PERK was followed by the phosphorylation of eukaryotic translation initiation factor 2alpha and the expression of activating transcription factor 4. However, CO fails to induce X-box binding protein-1 expression and activating transcription factor 6 cleavage. CO had no significant effect on synthesis of endoplasmic reticulum (ER) chaperone proteins such as the 78-kDa glucose-regulated protein 78 and 94. Instead, CO prevented X-box binding protein 1 expression and activating transcription factor 6 cleavage induced by ER-stress inducers such as thapsigargin, tunicamycin and homocysteine. CO also prevented endothelial apoptosis triggered by these ER inducers through suppression of C/EBP homologous protein expression, which was associated with its activation of p38 mitogen-activated protein kinase. Similarly, endogenous CO produced from endothelial HO-1 induced by either exogenous CO or a pharmacological inducer was also cytoprotective against ER stress through C/EBP homologous protein suppression. Our findings suggest that CO renders endothelial cells resistant to ER stress not only by downregulating C/EBP homologous protein expression via p38 mitogen-activated protein kinase activation but also by upregulating Nrf2-dependent HO-1 expression via PERK activation. Thus, the HO-1/CO system might be potential therapeutics in vascular diseases associated with ER stress.</P>
Shin, Dong Wook,Kim, So Young,Cho, Juhee,Sanson-Fisher, Robert W,Guallar, Eliseo,Chai, Gyu Young,Kim, Hak-Soon,Park, Bo Ram,Park, Eun-Cheol,Park, Jong-Hyock Grune Stratton ; American Society of Clinical Onco 2011 Journal of clinical oncology Vol.29 No.33
<P>Identification of supportive care needs in patients with cancer is essential for planning appropriate interventions. We aimed to determine patient-physician concordance in perceived supportive care needs in cancer care and to explore the predictors and potential consequences of patient-physician concordance.</P>
Yun, Young Ho,Lee, Myung Kyung,Park, Sohee,Lee, Jung Lim,Park, Jeanno,Choi, Youn Seon,Lim, Yeun Keun,Kim, Sam Yong,Jeong, Hyun Sik,Kang, Jung Hun,Oh, Ho-Suk,Park, Ji Chan,Kim, Si-Young,Song, Hong Suk Grune Stratton ; American Society of Clinical Onco 2011 Journal of clinical oncology Vol.29 No.36
<P>We tested whether a decision aid explaining how to discuss the approach of death with a family member with cancer would help family caregivers decide to discuss a terminal prognosis.</P>
Oh, H.J.,Shin, D.H.,Lee, M.J.,Koo, H.M.,Doh, F.M.,Kim, H.R.,Han, J.H.,Park, J.T.,Han, S.H.,Yoo, T.H.,Choi, K.H.,Kang, S.W. Grune Stratton 2012 Journal of critical care Vol.27 No.6
Purpose: The definition of ''early'' in terms of continuous renal replacement therapy (CRRT) initiation has not been uniformly used. Therefore, we tried to elucidate whether the timing of CRRT application, based on the interval between the start time of vasopressors infusion and CRRT initiation, was an independent predictor of mortality in the patients with septic acute kidney injury (AKI). Materials and Methods: Progressive septic AKI patients, in whom the infusion doses of vasopressors were increased compared with the initial dose during the first 6 hours of vasopressor treatment and CRRT was performed, between 2009 and 2011, were collected and divided into 2 groups based on the median interval between the 2 points. Results: A total of 210 patients were included. The mean age was 62.4 years, and 126 patients (60.0%) were male. The most common comorbid disease was malignancy (53.8%), followed by hypertension (35.7%) and diabetes mellitus (29.0%). The median interval between the start time of vasopressor infusion and CRRT commencement was 2.0 days. During the study period, 156 patients (74.3%) died within 28 days of CRRT application. The interval between 2 points was significantly shorter in the survivor compared with the death group (P < .001). Moreover, 28-day overall mortality rates in the early CRRT group were significantly lower than those in the late CRRT group (P = .034). Furthermore, early CRRT treatment was independently associated with a lower mortality rate even after adjustment for age, sex, causative organisms, and infection sites (P = .032). Conclusions: This retrospective cohort study suggests that early initiation of CRRT may be of benefit. Given the complex nature of this intervention, the ongoing controversies regarding early vs late initiation of therapy in acute and chronic situation, there is an urgent need to develop well-designed clinical trials to answer the question definitely.
Kang, Sokbom,Kang, Woo Dae,Chung, Hyun Hoon,Jeong, Dae Hoon,Seo, Sang-Soo,Lee, Jong-Min,Lee, Jae-Kwan,Kim, Jae Weon,Kim, Seok-Mo,Park, Sang-Yoon,Kim, Ki Tae Grune Stratton ; American Society of Clinical Onco 2012 Journal of clinical oncology Vol.30 No.12
<P>The aim of this study was to develop a preoperative risk prediction model for lymph node metastasis in patients with endometrial cancer and to identify a low-risk group before surgery.</P>