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  • 1
    In: American Journal of Nephrology, S. Karger AG, Vol. 40, No. 4 ( 2014), p. 345-352
    Abstract: 〈 b 〉 〈 i 〉 Background/Aims: 〈 /i 〉 〈 /b 〉 Atrial fibrillation (AF) often coexists with acute myocardial infarction (AMI), and chronic kidney disease (CKD) is a major risk for AMI. However, the combined impact of CKD and AF on the mortality and morbidity in AMI population has not been determined. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Between January 2004 and December 2009, a total of 4,738 AMI patients were enrolled prospectively. Patients were divided into four groups according to the combined status of CKD and AF. The primary endpoint was a combination of 5-year major adverse cardiac and cerebrovascular events (MACCE). 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 The prevalence of AF was significantly higher in CKD patients than in non-CKD patients (6.76 vs. 3.31%, p 〈 0.001). The highest cumulative event rate of MACCE and death was observed in patients with both CKD and AF (68.5 and 64.0%), respectively. In multivariable analyses, compared with patients with neither AF nor CKD, hazard ratios (HR) for composite of MACCE were 1.66 (95% CI, 1.14-2.41), 1.24 (95% CI, 1.06-1.46), and 2.10 (95% CI, 1.42-3.13) for patients with AF only, those with CKD only, and those with both CKD and AF, respectively (p for interaction = 0.935). Patients with both CKD and AF had a greatest risk for all-cause mortality (HR 2.54; 95% CI, 1.60-4.53), and the significant synergistic interaction was observed between CKD and AF (p for interaction = 0.015). 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 The combined effect of AF and CKD on the risk of MACCE after an AMI is stronger than any separate condition, and it confers a synergistic effect on the all-cause mortality risk.
    Type of Medium: Online Resource
    ISSN: 0250-8095 , 1421-9670
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2014
    detail.hit.zdb_id: 1468523-1
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  • 2
    In: Respiration, S. Karger AG, Vol. 101, No. 5 ( 2022), p. 465-475
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Targeted therapies have broadened the available treatment options for patients with severe eosinophilic asthma (SEA). However, differences in the magnitude of treatment responses among patients indicate the presence of various underlying pathophysiological processes and patient subgroups. 〈 b 〉 〈 i 〉 Objectives: 〈 /i 〉 〈 /b 〉 We aimed to describe the characteristics of SEA and identify its patient subgroups. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Clinical data from the Cohort for Reality and Evolution of Adult Asthma in Korea were analyzed. Cluster analysis was performed among those with SEA using 5 variables, namely, prebronchodilator forced expiratory volume in 1 s, body mass index, age at symptom onset, smoking amount, and blood eosinophil counts. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Patients with SEA showed prevalent sensitization to aeroallergens, decreased lung function, and poor asthma control status. Cluster analysis revealed 3 distinctive subgroups among patients with SEA. Cluster 1 ( 〈 i 〉 n 〈 /i 〉 = 177) consisted of patients reporting the lowest blood eosinophils (median, 346.8 cells/μL) and modest severe asthma with preserved lung function during the 12-month treatment period. Cluster 2 ( 〈 i 〉 n 〈 /i 〉 = 42) predominantly included smoking males with severe persistent airway obstruction and moderate eosinophilia (median, 451.8 cells/μL). Lastly, cluster 3 ( 〈 i 〉 n 〈 /i 〉 = 95) included patients with the most severe asthma, the highest eosinophil levels (median, 817.5 cells/μL), and good treatment response in terms of improved lung function and control status. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Three subgroups were identified in SEA through the cluster analysis. The distinctive features of each cluster may help physicians predict patients who will respond to biologics with greater magnitude of clinical improvement. Further research regarding the underlying pathophysiology and clinical importance of each subgroup is warranted.
    Type of Medium: Online Resource
    ISSN: 0025-7931 , 1423-0356
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2022
    detail.hit.zdb_id: 1464419-8
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  • 3
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 159, No. 2 ( 2012), p. 187-193
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Obesity is a risk factor for asthma in the general population, but the effect of obesity on airway hyperresponsiveness (AFHR) or airway inflammation in asthma is not clear. This study evaluated the relationship between obesity and asthma, assessing aspects of symptoms, AHR, and severity. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 In total, 852 patients with asthma diagnosed by asthma specialists based on AHR as confirmed by a methacholine bronchial provocation test, were enrolled from the Cohort for Reality and Evolution of Adult Asthma in Korea (COREA) adult asthma cohort. The intensity of AHR was assessed by the concentration of methacholine needed to cause a 20% decrease in FEV 〈 sub 〉 1 〈 /sub 〉 (PC 〈 sub 〉 20 〈 /sub 〉 ). Patients were classified into four categories based on body mass index (BMI): underweight ( 〈 18.5), normal weight (18.5–24.9), overweight (25.0–29.9), and obese (≥30). 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 BMI was negatively correlated with FEV 〈 sub 〉 1 〈 /sub 〉 (l), FVC (l), and FEV 〈 sub 〉 1 〈 /sub 〉 /FVC (%) in lung function tests. The prevalence of wheezing increased with higher BMI after adjustment for age, sex, smoking, medication history, and PC 〈 sub 〉 20 〈 /sub 〉 (p 〈 0.0001). logPC 〈 sub 〉 20 〈 /sub 〉 was lower in the normal weight group compared with the overweight group (p = 0.003). The risk of moderate or severe AHR (PC 〈 sub 〉 20 〈 /sub 〉 ≤ 4 mg/ml) decreased with increased BMI after adjustment for age, sex, smoking, and medication history (p 〈 i 〉 = 〈 /i 〉 0.035). 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Obesity is a risk factor for asthma in the general population, but obesity in asthmatic patients is negatively correlated with the intensity of AHR and is not related to asthma severity. Obesity is positively related with the prevalence of wheezing but negatively related to AHR in asthmatic patients.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2012
    detail.hit.zdb_id: 1482722-0
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  • 4
    Online Resource
    Online Resource
    S. Karger AG ; 2011
    In:  International Archives of Allergy and Immunology Vol. 154, No. 2 ( 2011), p. 111-118
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 154, No. 2 ( 2011), p. 111-118
    Abstract: 〈 i 〉 Background: 〈 /i 〉 Sialic-acid-binding immunoglobulin-like lectins (Siglecs) are the best-characterized immunoglobulin-type lectins. There is a growing amount of data linking Siglec and autoimmune diseases. The recently identified Siglec-9 inhibits T cell receptor (TCR)-mediated signaling which has been demonstrated by site-directed mutagenesis. In human Siglec-9, at least 8 nonsynonymous SNPs have been detected without functional studies. This study examined the SNP(s) related to TCR-mediated signaling. 〈 i 〉 Methods: 〈 /i 〉 Since the functions of Siglecs are modulated by their interaction with sialic-acid-containing carbohydrate groups, a molecular modeling analysis of carbohydrate binding interactions and an RBC binding analysis were performed using the 8 SNPs. The TCR-mediated signaling was analyzed with the downstream signaling molecules ZAP-70 and IL-2. 〈 i 〉 Results: 〈 /i 〉 This study revealed that an A391C polymorphism is the only mutant related to the binding. Jurkat T cells transfected with the A391C mutant reduced the inhibition of ZAP-70 phosphorylation and IL-2 production compared to cells transfected with the wild type. 〈 i 〉 Conclusions: 〈 /i 〉 Siglec-9 A391C was the only polymorphism related to TCR-mediated signaling in human Siglec-9, resulting in less inhibition compared to the wild type.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2011
    detail.hit.zdb_id: 1482722-0
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  • 5
    Online Resource
    Online Resource
    S. Karger AG ; 2008
    In:  Microbial Physiology Vol. 15, No. 2-3 ( 2008), p. 152-171
    In: Microbial Physiology, S. Karger AG, Vol. 15, No. 2-3 ( 2008), p. 152-171
    Abstract: Polychlorinated dibenzo- 〈 i 〉 p 〈 /i 〉 -dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs), commonly known as dioxins (PCDD/Fs), are toxic environmental pollutants formed from various sources. Elimination of these pollutants from the environment is a difficult task due to their persistent and ubiquitous nature. Removal of dioxins by biological degradation (biodegradation) is considered a feasible method as an alternative to other expensive physicochemical approaches. Biodegradation of dioxins has been extensively studied in several microorganisms, and details concerning biodiversity, biodegradation, biochemistry and molecular biology of this process have accumulated during the last three decades. There are several microbial mechanisms responsible for biodegradation of dioxins, including oxidative degradation by dioxygenase-containing aerobic bacteria, bacterial and fungal cytochrome P-450, fungal lignolytic enzymes, reductive dechlorination by anaerobic bacteria, and direct ether ring cleavage by fungi containing etherase-like enzymes. Many attempts have been made to bioremediate PCDD/Fs using this basic knowledge of microbial dioxin degradation. This review emphasizes the present knowledge and recent advancements in the microbial biotransformation, biodegradation and bioremediation of dioxins.
    Type of Medium: Online Resource
    ISSN: 2673-1665 , 2673-1673
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2008
    detail.hit.zdb_id: 3042601-7
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  • 6
    In: Cardiorenal Medicine, S. Karger AG, Vol. 5, No. 1 ( 2015), p. 61-68
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Considering that contrast medium is excreted through the whole kidney in a similar manner to drug excretion, the use of raw estimated glomerular filtration rate (eGFR) rather than body surface area (BSA)-normalized eGFR is thought to be more appropriate for evaluating the risk of contrast-induced acute kidney injury (CI-AKI). 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 This study included 2,189 myocardial infarction patients treated with percutaneous coronary intervention. Logistic regression analysis was performed to identify the independent risk factors. We used receiver-operating characteristic (ROC) curves to compare the ratios of contrast volume (CV) to eGFR with and without BSA normalization in predicting CI-AKI. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 The area under the curve (AUC) of the ROC curve for the model including all the significant variables such as diabetes mellitus, left ventricular ejection fraction, preprocedural glucose, and the CV/raw modification of diet in renal disease (MDRD) eGFR ratio was 0.768 [95% confidence interval (CI), 0.720-0.816; p 〈 0.001]. When the CV/raw MDRD eGFR ratio was used as a single risk value, the AUC of the ROC curve was 0.650 (95% CI, 0.590-0.711; p 〈 0.001). When the CV/MDRD eGFR ratio with BSA normalization ratio was used, the AUC of the ROC curve further decreased to 0.635 (95% CI, 0.574-0.696; p 〈 0.001). The difference between the two AUCs was significant (p = 0.002). 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Raw eGFR is a better predictor for CI-AKI than BSA-normalized eGFR.
    Type of Medium: Online Resource
    ISSN: 1664-3828 , 1664-5502
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 2595659-0
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  • 7
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 184, No. 9 ( 2023), p. 893-902
    Abstract: 〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 Eotaxin-2 and -3 of the C-C chemokine subfamily function as potent chemoattractant factors for eosinophil recruitment and various immune responses in allergic and inflammatory airway diseases. Mucin 5AC (MUC5AC), a major gel-forming secretory mucin, is overexpressed in airway inflammation. However, the association between mucin secretion and eotaxin-2/3 expression in the upper and lower airway epithelial cells has not been fully elucidated. Therefore, in this study, we investigated the effects of eotaxin-2/3 on 〈 i 〉 MUC5AC 〈 /i 〉 expression and its potential signaling mediators. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 We analyzed the effects of eotaxin-2 and -3 on NCI-H292 human airway epithelial cells and primary human nasal epithelial cells (HNEpCs) via reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay, and western blotting. Along with immunoblot analyses with specific inhibitors and small interfering RNA (siRNA), we explored the signaling pathway involved in MUC5AC expression following eotaxin-2/3 treatment. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 In HCI-H292 cells, eotaxin-2/3 activated the mRNA expression and protein production of MUC5AC. A specific inhibitor of C-C motif chemokine receptor 3 (CCR3), SB328437, suppressed eotaxin-2/3-induced 〈 i 〉 MUC5AC 〈 /i 〉 expression at both the mRNA and protein levels. Eotaxin-2/3 induced the phosphorylation of extracellular signal-regulated kinase (ERK)-1/2 and p38, whereas pretreatment with a CCR3 inhibitor significantly attenuated this effect. Induction of 〈 i 〉 MUC5AC 〈 /i 〉 expression with eotaxin-2/3 was decreased by U0126 and SB203580, specific inhibitors of ERK1/2 and p38 mitogen-activated protein kinase (MAPK), respectively. In addition, cell transfection with ERK1/2 and p38 siRNAs inhibited eotaxin-2/3-induced 〈 i 〉 MUC5AC 〈 /i 〉 expression. Moreover, specific inhibitors (SB328437, U0126, and SB203580) attenuated eotaxin-2/3-induced 〈 i 〉 MUC5AC 〈 /i 〉 expression in HNEpCs. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 Our results imply that 〈 i 〉 CCR3 〈 /i 〉 -mediated ERK1/2 and p38 MAPK are involved in the signal transduction of eotaxin-2/3-induced 〈 i 〉 MUC5AC 〈 /i 〉 overexpression.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2023
    detail.hit.zdb_id: 1482722-0
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  • 8
    In: Cardiorenal Medicine, S. Karger AG, Vol. 8, No. 3 ( 2018), p. 228-236
    Abstract: 〈 b 〉 〈 i 〉 Aim: 〈 /i 〉 〈 /b 〉 The aim of this study was to assess the combined effects of chronic kidney disease (CKD) and diabetes on the extent and developmental pattern of coronary artery disease (CAD). 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 A total of 3,017 self-referred asymptomatic individuals without known CAD who underwent 64-channel dual-source coronary computed tomography angiography between 2006 and 2010 were enrolled. The patients were divided into six groups based on their diabetes status (nondiabetic or diabetic) and estimated glomerular filtration rate (eGFR) (eGFR & #x3e; 90 mL/min/1.73 m 〈 sup 〉 2 〈 /sup 〉 , normal renal function; eGFR 60–89, mild CKD; or eGFR 30–59, moderate CKD). We compared the coronary artery calcium score (CACS), segment stenosis score (SSS), and ≥50% obstructive CAD among the groups. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 In nondiabetics, whereas SSS and ≥50% obstructive CAD were not different as renal function deteriorated, after adjusting for cardiovascular risk factors, CACS showed a unique developmental pattern: no CACS increase until mild CKD, but abrupt increase from the stage of moderate CKD (moderate vs. normal renal function, adjusted OR 5.118, 95% CI 1.293–20.262, 〈 i 〉 p 〈 /i 〉 = 0.020). In diabetics, patients from the stage of mild CKD were more likely to have ≥50% obstructive CAD ( 〈 i 〉 p 〈 /i 〉 = 0.004), higher CACS ( 〈 i 〉 p 〈 /i 〉 = 0.020), and SSS ( 〈 i 〉 p 〈 /i 〉 = 0.001) in multivariable analysis. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 The presence of CKD did not have a significant impact on the development of coronary atherosclerosis, but affected the progression of coronary calcification more markedly from the stage of moderate CKD in nondiabetics. However, in diabetics, the deterioration of renal function was significantly associated with the development of coronary atherosclerosis and calcification from the stage of mild CKD.
    Type of Medium: Online Resource
    ISSN: 1664-3828 , 1664-5502
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 2595659-0
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  • 9
    In: Neuroendocrinology, S. Karger AG, Vol. 111, No. 8 ( 2021), p. 794-804
    Abstract: 〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 The prognostic factors of pancreatic neuroendocrine tumor (PNET) are unclear, and the treatment guidelines are insufficient. This study aimed to suggest a treatment algorithm for PNET based on risk factors for recurrence in a large cohort. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Data of 918 patients who underwent curative intent surgery for PNET were collected from 14 tertiary centers. Risk factors for recurrence and survival analyses were performed. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 The 5-year disease-free survival (DFS) rate was 86.5%. Risk factors for recurrence included margin status (R1, hazard ratio [HR] 2.438; R2, HR 3.721), 2010 WHO grade (G2, HR 3.864; G3, HR 7.352), and N category (N1, HR 2.273). A size of 2 cm was significant in the univariate analysis (HR 8.511) but not in the multivariate analysis ( 〈 i 〉 p 〈 /i 〉 = 0.407). Tumor size was not a risk factor for recurrence, but strongly reflected 2010 WHO grade and lymph node (LN) status. Tumors ≤2 cm had lower 2010 WHO grade, less LN metastasis ( 〈 i 〉 p 〈 /i 〉 & #x3c; 0.001), and significantly longer 5-year DFS (77.9 vs. 98.2%, 〈 i 〉 p 〈 /i 〉 & #x3c; 0.001) than tumors & #x3e;2 cm. The clinicopathologic features of tumors & #x3c;1 and 1-2 cm were similar. However, the LN metastasis rate was 10.3% in 1-2-cm sized tumors and recurrence occurred in 3.0%. Tumors & #x3c;1 cm in size did not have any LN metastasis or recurrence. 〈 b 〉 〈 i 〉 Discussion/Conclusion: 〈 /i 〉 〈 /b 〉 Radical surgery is needed in suspected LN metastasis or G3 PNET or tumors & #x3e;2 cm. Surveillance for & #x3c;1-cm PNETs should be sufficient. Tumors sized 1-2 cm require limited surgery with LN resection, but should be converted to radical surgery in cases of doubtful margins or LN metastasis.
    Type of Medium: Online Resource
    ISSN: 0028-3835 , 1423-0194
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2021
    detail.hit.zdb_id: 1483028-0
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  • 10
    In: Digestive Surgery, S. Karger AG, Vol. 36, No. 1 ( 2019), p. 1-6
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Despite the increasing number of reports on the favorable outcomes of laparoscopic surgery for gallbladder cancer (GBC), there is no consensus regarding this surgical procedure. 〈 b 〉 〈 i 〉 Objective: 〈 /i 〉 〈 /b 〉 The study aimed to develop a consensus statement on the application of laparoscopic surgery for GBC based on expert opinions. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 A consensus meeting among experts was held on September 10, 2016, in Seoul, Korea. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Early concerns regarding port site/peritoneal metastasis after laparoscopic surgery have been abated by improved preoperative recognition of GBC and careful manipulation to avoid bile spillage. There is no evidence that laparoscopic surgery is associated with decreased survival compared with open surgery in patients with early-stage GBC if definitive resection during/after laparoscopic cholecystectomy is performed. Although experience with laparoscopic extended cholecystectomy for GBC has been limited to a few experts, the postoperative and survival outcomes were similar between laparoscopic and open surgeries. Laparoscopic reoperation for postoperatively diagnosed GBC is technically challenging, but its feasibility has been demonstrated by a few experts. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Laparoscopic surgery for GBC is still in the early phase of the adoption curve, and more evidence is required to assess this procedure.
    Type of Medium: Online Resource
    ISSN: 0253-4886 , 1421-9883
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2019
    detail.hit.zdb_id: 1468560-7
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