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991.
J Jiang P Chen J Chen X Yu D Xie C Mei F Xiong W Shi W Zhou X Liu S Sun P Zhang X Yang Y Zhang Y Zhang X Liang Z Zhang Q Lin Y Yu T Miyata J Tian M Liang W Luo X Xu F Hou 《Atherosclerosis》2012,224(1):187-194
ObjectivesAccumulation of tissue advanced glycation end products (AGEs) is a marker of cumulative glycemic and/or oxidative stress. Cutaneous AGEs levels measured by skin autofluorescence correlate well with cardiovascular outcomes in diabetes and hemodialysis (HD) patients. The present study aimed to compare tissue AGEs levels with peritoneal dialysis (PD) and HD patients and to evaluate the relationship between skin autofluorescence and cardiovascular morbidity in patients on PD.MethodsA total of 2388 maintenance dialysis patients (613 PD and 1775 HD) were enrolled in this cross-sectional study. Skin autofluorescence was measured non-invasively with an autofluorescence reader. Cardiovascular morbidity was defined as clinically diagnosed ischemic heart disease, heart failure, stroke or peripheral vascular disease from initiation of dialysis.ResultsMore than 90% of patients on both PD and HD had met current dialysis adequacy targets. Compared to HD group, PD patients receiving conventional glucose-containing dialyzate had significantly higher skin autofluorescence values in each category of age and dialysis duration, irrespective of the presence or absence of diabetes. In PD patients, skin autofluorescence values were strongly correlated with the duration of PD and glucose exposure dose and independently associated with cardiovascular morbidity. Multivariate analysis revealed that glucose exposure dose and skin autofluorescence were the strongest risk factors for cardiovascular morbidity in PD patients after adjustment by age, gender, and other classic- or uremic-related risk factors.ConclusionsAccumulation of tissue AGEs provides a potential link between PD exposure of metabolic stress and progression of cardiovascular disease in patients on PD. 相似文献
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Huang ZM Chinen M Chang PJ Xie T Zhong L Demetriou S Patel MP Scherzer R Sviderskaya EV Bennett DC Millhauser GL Oh DH Cleaver JE Wei ML 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(2):553-558
Protein-trafficking pathways are targeted here in human melanoma cells using methods independent of oncogene mutational status, and the ability to up-regulate and down-regulate tumor treatment sensitivity is demonstrated. Sensitivity of melanoma cells to cis-diaminedichloroplatinum II (cDDP, cis-platin), carboplatin, dacarbazine, or temozolomide together with velaparib, an inhibitor of poly (ADP ribose) polymerase 1, is increased by up to 10-fold by targeting genes that regulate both protein trafficking and the formation of melanosomes, intracellular organelles unique to melanocytes and melanoma cells. Melanoma cells depleted of either of the protein-trafficking regulators vacuolar protein sorting 33A protein (VPS33A) or cappuccino protein (CNO) have increased nuclear localization of cDDP, increased nuclear DNA damage by platination, and increased apoptosis, resulting in increased treatment sensitivity. Depleted cells also exhibit a decreased proportion of intracellular, mature melanosomes compared with undepleted cells. Modulation of protein trafficking via cell-surface signaling by binding the melanocortin 1 receptor with the antagonist agouti-signaling protein decreased the proportion of mature melanosomes formed and increased cDDP sensitivity, whereas receptor binding with the agonist melanocyte-stimulating hormone resulted in an increased proportion of mature melanosomes formed and in decreased sensitivity (i.e., increased resistance) to cDDP. Mutation of the protein-trafficking gene Hps6, known to impair the formation of mature melanosomes, also increased cDDP sensitivity. Together, these results indicate that targeting protein-trafficking molecules markedly increases melanoma treatment sensitivity and influences the degree of melanosomes available for sequestration of therapeutic agents. 相似文献
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Background:
There are few recent data to delineate the beyond lipids‐decreased effect of statins and the effect of different doses of statins on endothelial‐derived microparticles (EMPs) and circulating endothelial progenitor cells (EPCs) in patients with ischemic cardiomyopathy (ICM).Hypothesis:
Statins might have the beyond lipids‐decreased effect and there were different effects between different doses of statins on EMPs and circulating EPCs in patients with ICM.Methods:
One hundred patients with ICM and 100 healthy examined people, who served as the normal control group, were recruited to this study. Patients were randomly divided into 2 groups: 10‐mg atorvastatin group (n = 50) and 40‐mg atorvastatin group (n = 50). All subjects were followed for 1 year. The levels of serum lipids, oxidized low‐density lipoprotein (oxLDL), high‐sensitivity C‐reactive protein (hsCRP), circulating EPCs, and EMPs were examined in all subjects. The incidences of adverse reactions in the 2 study groups were determined.Results:
At the beginning of this study, there were no significant differences in baseline characteristics between the 2 study groups. At the end of this study, the levels of total cholesterol, low‐density lipoprotein, serum hsCRP, oxLDL, and circulating EMPs were significantly decreased; circulating EPCs were significantly increased in the 40‐mg atorvastatin group compared to the 10‐mg atorvastatin group, P < 0.05. The multivariate linear regression analysis indicated that receiving only 40 mg of atorvastatin had a significant effect on the levels of circulating EPCs (β = 0.252,P = 0.014). There were no significant differences in the adverse reactions between the 2 groups.Conclusions:
Use of 40 mg of atorvastatin might decrease the levels of circulating EMPs and increase the number of circulating EPCs in patients with ICM in comparison with 10 mg of atorvastatin, and the effect might be independent of the decrease of lipids, oxLDL, and hsCRP. © 2012 Wiley Periodicals, Inc. This study was supported by the Bureau of Health of Guangzhou city (2009‐YB‐186). The authors have no other funding, financial relationships, or conflicts of interest to disclose. 相似文献999.
Zuo XR Zhang R Jiang X Li XL Zong F Xie WP Wang H Jing ZC 《The American journal of cardiology》2012,109(12):1801-1806
Although intravenous adenosine is recommended for acute vasodilator testing in patients with pulmonary hypertension, long-term outcomes in acute responders treated with calcium channel blockers (CCBs) who are identified by adenosine remain unknown. In this study, the value of adenosine for identifying long-term responders to CCBs was investigated in patients with idiopathic pulmonary arterial hypertension (IPAH). All acute responders were subsequently treated with high-dose CCB monotherapy, and 6-minute walk distances, hemodynamic data, and World Health Organization functional classifications were followed. Nine of 104 patients exhibited an acute response with intravenous adenosine (8.7%, 95% confidence interval 3.2 to 14.2). After 12 months of follow-up, all acute responders were still alive; however, only 6 patients showed sustained hemodynamic improvement (5.8%, 95% confidence interval 2 to 13). Three patients had failed CCB monotherapy and bosentan was added to their treatment. Mean tolerated dose of intravenous adenosine was 142 ± 49 μg/kg/min. No life-threatening adverse events were observed and only 2 patients of the nonresponders exhibited a 20% decrease in mean systemic arterial pressure. In nonresponders, 1- and 3-year survival rates were 89% and 75%, respectively. In conclusion, acute vasodilator testing with intravenous adenosine was safe and able to screen responders to CCB therapy in patients with IPAH. Long-term CCB responders accounted for about 5.8% of patients with IPAH. 相似文献
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