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  • Ovid Technologies (Wolters Kluwer Health)  (65)
  • 1
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 9, No. 21 ( 2020-11-03)
    Abstract: Inflammation levels are lower in East Asians than in Western people. We studied the association between high‐sensitivity hs‐CRP (C‐reactive protein) and adverse outcomes in Korean patients with chronic kidney disease. Methods and Results We included 2018 participants from the KNOW‐CKD (Korean Cohort Study for Outcome in Patients With Chronic Kidney Disease) between April 2011 and February 2016. The primary outcome was a composite of extended major cardiovascular events (eMACE) or all‐cause mortality. The secondary end points were separate outcomes of eMACE, all‐cause death, and adverse kidney outcome. We also evaluated predictive ability of hs‐CRP for the primary outcome. The median hs‐CRP level was 0.60 mg/L. During the mean follow‐up of 3.9 years, there were 125 (6.2%) eMACEs and 80 (4.0%) deaths. In multivariable Cox analysis after adjustment of confounders, there was a graded association of hs‐CRP with the primary outcome. The hazard ratios for hs‐CRPs of 1.0 to 2.99 and ≥3.0 mg/L were 1.33 (95% CI, 0.87–2.03) and 2.08 (95% CI, 1.30–3.33) compared with the hs‐CRP of 〈 1.0 mg/L. In secondary outcomes, this association was consistent for eMACE and all‐cause death; however, hs‐CRP was not associated with adverse kidney outcomes. Finally, prediction models failed to show improvement of predictive performance of hs‐CRP compared with conventional factors. Conclusions In Korean patients with chronic kidney disease, the hs‐CRP level was low and significantly associated with higher risks of eMACEs and mortality. However, hs‐CRP did not associate with adverse kidney outcome, and the predictive performance of hs‐CRP was not strong. Registration URL: http://www.clinicaltrials.gov ; Unique identifier: NCT01630486.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2653953-6
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  • 2
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 100, No. 17 ( 2021-04-30), p. e25640-
    Type of Medium: Online Resource
    ISSN: 0025-7974 , 1536-5964
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2049818-4
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  • 3
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Liver Transplantation Vol. 18, No. 10 ( 2012-10), p. 1237-1243
    In: Liver Transplantation, Ovid Technologies (Wolters Kluwer Health), Vol. 18, No. 10 ( 2012-10), p. 1237-1243
    Type of Medium: Online Resource
    ISSN: 1527-6465
    URL: Issue
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2002186-0
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  • 4
    In: Critical Care Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 45, No. 1 ( 2017-01), p. 47-57
    Abstract: Severe acute kidney injury requiring continuous renal replacement therapy is associated with a high risk of early mortality. Our objectives were to identify a cohort of early survivors and to follow their renal progress and long-term mortality. Design: Multicenter, observational, retrospective cohort study. Setting: ICUs in tertiary academic hospitals in Korea. Patients: From 2009 to 2013, we identified 1,764 severe acute kidney injury patients who were started on continuous renal replacement therapy at four hospitals. Of these, we identified 331 survivors for whom we could identify renal function at baseline and at 3 months. Interventions: None. Measurements and Main Results: The 331 patients were separated into two groups based on their renal function at 3 months after the start of continuous renal replacement therapy. Those who displayed significant deterioration in renal function compared to baseline, defined as greater than or equal to 50% increase in serum creatinine or greater than or equal to 35% decrease in the estimated glomerular filtration rate, or those who continued to receive renal replacement therapy were designated as a “3-month chronic kidney disease progression” group. Those with a return to baseline, less than 50% increase in serum creatinine or less than 35% decrease in the estimated glomerular filtration rate, were designated as a “3-month chronic kidney disease nonprogression” group. The acute kidney injury patients requiring continuous renal replacement therapy showed a higher risk of progression to end-stage renal disease compared to that of stage 3 chronic kidney disease patients who did not undergo an acute kidney injury episode, even if the acute kidney injury was recovered at 3 months after continuous renal replacement therapy initiation. Furthermore, “3-month chronic kidney disease progression” was associated with a high risk of progression to end-stage renal disease and long-term mortality over a median follow-up period of 12.7 (3.8–33.2) and 20.4 (7.5–39.7) months, respectively. Older age, higher baseline serum creatinine levels, and higher blood urea nitrogen concentrations at continuous renal replacement therapy initiation, and lower 24-hour urine output after continuous renal replacement therapy initiation are associated with an increased risk of “3-month chronic kidney disease progression.” Conclusions: Renal functional assessment at 3 months after continuous renal replacement therapy initiation can be useful in predicting progression to end-stage renal disease and long-term mortality. Furthermore, continuous close monitoring and management of acute kidney injury patients requiring continuous renal replacement therapy are required, even in those with recovered renal function.
    Type of Medium: Online Resource
    ISSN: 0090-3493
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2034247-0
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  • 5
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 78, No. 5 ( 2021-11), p. 1355-1364
    Abstract: Studies on the longitudinal temporal trend of blood pressure (BP) and its impact on kidney function are scarce. Here, we evaluated the association of dynamic changes in systolic blood pressure (SBP) over time with adverse kidney outcomes. We analyzed 1837 participants from the KNOW-CKD (Korean Cohort Study for Outcomes in Patients With Chronic Kidney Disease). The main exposure was 3 distinct SBP trajectories determined by the latent class mixed model (decreasing, stable, and increasing) using 3 SBP measurements at 0, 6, and 12 months. The primary outcome was CKD progression, defined as a composite of halving estimated glomerular filtration rate from baseline value or onset of end-stage kidney disease. SBP declined from 144 to 120 mm Hg in the decreasing SBP trajectory group and rose from 114 to 136 mm Hg in the increasing trajectory group within 1 year. During 6576 person-years of follow-up (median, 3.7 years), the composite outcome occurred in 521 (28.4%) participants. There were fewer primary outcome events in the decreasing (30.6%) and stable (26.5%) SBP trajectory groups than in the increasing trajectory group (33.0%). In the multivariable-adjusted cause-specific hazards model, increasing SBP trajectory was associated with a 1.28-fold higher risk for adverse kidney outcome compared with stable SBP trajectory. However, the risk for the primary outcome did not differ between the decreasing and stable SBP trajectory groups. In this longitudinal CKD cohort study, compared with stable SBP trajectory, increasing SBP trajectory was associated with higher risk for adverse kidney outcome, whereas decreasing SBP trajectory showed similar risk.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2094210-2
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  • 6
    In: Journal of the American Society of Nephrology, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. 9 ( 2022-09), p. 1726-1741
    Abstract: Mutations in ciliogenesis-associated kinase 1 ( CILK1 ) cause ciliopathies. However, the pathogenesis of the ciliary defect in the CILK1-deficient kidney remains unknown. We found that CILK1 deficiency in a mouse model leads to polycystic kidney disease (PKD) with abnormal ciliary trafficking and that kinesin light chain–3 (KLC3), a novel ciliary regulator, interacts with CILK1. Furthermore, KLC3 localizes at cilia bases, where it promotes ciliary trafficking of the IFT-EGFR complex, which contributes to cyst progression. KLC3 knockdown restored abnormal ciliary trafficking and cyst progression caused by CILK1 deficiency. Identifying KLC3 as a ciliary regulator involved in cystogenesis provides insights into the pathogenesis of CILK1 deficiency–related PKD. Background Ciliogenesis-associated kinase 1 ( CILK1 ) is a ciliary gene that localizes in primary cilia and regulates ciliary transport. Mutations in CILK1 cause various ciliopathies. However, the pathogenesis of CILK1-deficient kidney disease is unknown. Methods To examine whether CILK1 deficiency causes PKD accompanied by abnormal cilia, we generated mice with deletion of Cilk1 in cells of the renal collecting duct. A yeast two-hybrid system and coimmunoprecipitation (co-IP) were used to identify a novel regulator, kinesin light chain–3 (KLC3), of ciliary trafficking and cyst progression in the Cilk1 -deficient model. Immunocytochemistry and co-IP were used to examine the effect of KLC3 on ciliary trafficking of the IFT-B complex and EGFR. We evaluated the effects of these genes on ciliary trafficking and cyst progression by modulating CILK1 and KLC3 expression levels. Results CILK1 deficiency leads to PKD accompanied by abnormal ciliary trafficking. KLC3 interacts with CILK1 at cilia bases and is increased in cyst-lining cells of CILK1-deficient mice. KLC3 overexpression promotes ciliary recruitment of IFT-B and EGFR in the CILK1 deficiency condition, which contributes to the ciliary defect in cystogenesis. Reduction in KLC3 rescued the ciliary defects and inhibited cyst progression caused by CILK1 deficiency. Conclusions Our findings suggest that CILK1 deficiency in renal collecting ducts leads to PKD and promotes ciliary trafficking via increased KLC3.
    Type of Medium: Online Resource
    ISSN: 1046-6673 , 1533-3450
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2029124-3
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  • 7
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 100, No. 18 ( 2021-05-07), p. e25900-
    Abstract: Aged population with comorbidities demonstrated high mortality rate and severe clinical outcome in the patients with coronavirus disease 2019 (COVID-19). However, whether age-adjusted Charlson comorbidity index score (CCIS) predict fatal outcomes remains uncertain. This retrospective, nationwide cohort study was performed to evaluate patient mortality and clinical outcome according to CCIS among the hospitalized patients with COVID-19 infection. We included 5621 patients who had been discharged from isolation or had died from COVID-19 by April 30, 2020. The primary outcome was composites of death, admission to intensive care unit, use of mechanical ventilator or extracorporeal membrane oxygenation. The secondary outcome was mortality. Multivariate Cox proportional hazard model was used to evaluate CCIS as the independent risk factor for death. Among 5621 patients, the high CCIS (≥ 3) group showed higher proportion of elderly population and lower plasma hemoglobin and lower lymphocyte and platelet counts. The high CCIS group was an independent risk factor for composite outcome (HR 3.63, 95% CI 2.45–5.37, P   〈  .001) and patient mortality (HR 22.96, 95% CI 7.20–73.24, P   〈  .001). The nomogram showed that CCIS was the most important factor contributing to the prognosis followed by the presence of dyspnea (hazard ratio [HR] 2.88, 95% confidence interval [CI] 2.16–3.83), low body mass index  〈  18.5 kg/m 2 (HR 2.36, CI 1.49–3.75), lymphopenia ( 〈 0.8 x10 9 /L) (HR 2.15, CI 1.59–2.91), thrombocytopenia ( 〈 150.0 x10 9 /L) (HR 1.29, CI 0.94–1.78), anemia ( 〈 12.0 g/dL) (HR 1.80, CI 1.33–2.43), and male sex (HR 1.76, CI 1.32–2.34). The nomogram demonstrated that the CCIS was the most potent predictive factor for patient mortality. The predictive nomogram using CCIS for the hospitalized patients with COVID-19 may help clinicians to triage the high-risk population and to concentrate limited resources to manage them.
    Type of Medium: Online Resource
    ISSN: 0025-7974 , 1536-5964
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2049818-4
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  • 8
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 10, No. 1 ( 2021-01-05)
    Abstract: This study sought to investigate the safety of 3‐month dual antiplatelet therapy (DAPT) in patients receiving ultrathin sirolimus‐eluting stents with biodegradable polymer (Orsiro). Methods and Results The SMART‐CHOICE (Smart Angioplasty Research Team: Comparison Between P2Y12 Antagonist Monotherapy vs Dual Anti‐ platelet Therapy in Patients Undergoing Implantation of Coronary Drug‐Eluting Stents) randomized trial compared 3‐month DAPT followed by P2Y12 inhibitor monotherapy with 12‐month DAPT in 2993 patients undergoing percutaneous coronary intervention. The present analysis was a prespecified subgroup analysis for patients receiving Orsiro stents. As a post hoc analysis, comparisons between Orsiro and everolimus‐eluting stents were also done among patients receiving 3‐month DAPT. Of 972 patients receiving Orsiro stents, 481 patients were randomly assigned to 3‐month DAPT and 491 to 12‐month DAPT. At 12 months, the target vessel failure, defined as a composite of cardiac death, target vessel–related myocardial infarction, or target vessel revascularization, occurred in 8 patients (1.7%) in the 3‐month DAPT group and in 14 patients (2.9%) in the 12‐month DAPT group (hazard ratio [HR], 0.58; 95% CI, 0.24–1.39; P =0.22). In whole population who were randomly assigned to receive 3‐month DAPT (n=1495), there was no significant difference in the target vessel failure between the Orsiro group and the everolimus‐eluting stent group (n=1014) (1.7% versus 1.8%; HR, 0.96; 95% CI, 0.41–2.22; P =0.92). Conclusions In patients receiving Orsiro stents, clinical outcomes at 1 year were similar between the 3‐month DAPT followed by P2Y12 inhibitor monotherapy and 12‐month DAPT strategies. With 3‐month DAPT, there was no significant difference in target vessel failure between Orsiro and everolimus‐eluting stents. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02079194.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2653953-6
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  • 9
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  American Journal of Surgical Pathology Vol. 32, No. 1 ( 2008-01), p. 103-112
    In: American Journal of Surgical Pathology, Ovid Technologies (Wolters Kluwer Health), Vol. 32, No. 1 ( 2008-01), p. 103-112
    Type of Medium: Online Resource
    ISSN: 0147-5185
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 2029143-7
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  • 10
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 96, No. 11 ( 2005-06-10), p. 1200-1207
    Abstract: Increased oxidative stress in vascular cells plays a key role in the development of endothelial dysfunction and atherosclerosis. Uncoupling protein 2 (UCP2) is an important regulator of intracellular reactive oxygen species (ROS) production. This study was undertaken to test the hypothesis that, UCP2 functions as an inhibitor of the atherosclerotic process in endothelial cells. Adenovirus-mediated UCP2 (Ad-UCP2) overexpression led to a significant increase in endothelial nitric oxide synthase (eNOS) and decrease in endothelin-1 mRNA expression in human aortic endothelial cells (HAECs). Moreover, UCP2 inhibited the increase in ROS production and NF-κB activation, and apoptosis of HAECs induced by lysophophatidylcholine (LPC) and linoleic acid. LPC and linoleic acid caused mitochondrial calcium accumulation and transient mitochondrial membrane hyperpolarization, which was followed by depolarization. UCP2 overexpression prevented these processes. In isolated rat aorta, Ad-UCP2 infection markedly improved impaired vascular relaxation induced by LPC. The data collectively suggest that UCP2, functions as a physiologic regulator of ROS generation in endothelial cells. Thus, measures to increase UCP2 expression in vascular endothelial cells may aid in preventing the development and progression of atherosclerosis in patients with metabolic syndrome.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
    detail.hit.zdb_id: 1467838-X
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