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Search Results: 1 - 10 of 26211 matches for " Min-Jung Kwon "
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Weight Change as a Predictor of Incidence and Remission of Insulin Resistance
Yoosoo Chang, Eunju Sung, Kyung Eun Yun, Hyun-Suk Jung, Chan-Won Kim, Min-Jung Kwon, Sung-Il Cho, Seungho Ryu
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0063690
Abstract: Objective The objective of this study was to assess the longitudinal relationship of weight change on incidence and remission of insulin resistance (IR). Methods We performed a cohort study in apparently healthy Korean men, 30 to 59 years of age, who underwent a health checkup and were followed annually or biennially between 2002 and 2009. The computer model of homeostasis model assessment, HOMA2-IR, was obtained at each visit, and IR was defined as HOMA2-IR ≥75th percentile. Results For IR development, 1,755 of the 6,612 IR-free participants at baseline developed IR (rate 5.1 per 100 person-years) during 34,294.8 person-years of follow-up. The hazard ratios (95% confidence intervals) for incident IR with weight changes of <?0.9 kg, 0.6–2.1 kg and ≥2.2 kg from visit 1 to visit 2 (average 1.8 years) compared to weight change of ?0.9–0.5 kg (reference) were 0.78 (0.68–0.90), 1.19 (1.04–1.35) and 1.26 (1.11–1.44), respectively. This association persisted in normal-weight individuals or those without any metabolic syndrome traits and remained significant after introducing weight categories and confounders as time-dependent exposures (P-trend <0.001). For IR remission, 903 of 1,696 IR participants had no IR (remission rate 10.3 per 100 person-years) during 8,777.4 person-years of follow-up. IR remission decreased with increasing quartiles of weight change (P-trend <0.001) and this association persisted in normal-weight individuals. Conclusions Weight gain was associated with increased IR development and decreased IR remission regardless of baseline BMI status. Preventing weight gain, even in healthy and normal-weight individuals, is an important strategy for reducing IR and its associated consequences.
Higher Serum Direct Bilirubin Levels Were Associated with a Lower Risk of Incident Chronic Kidney Disease in Middle Aged Korean Men
Seungho Ryu, Yoosoo Chang, Yiyi Zhang, Hee-Yeon Woo, Min-Jung Kwon, Hyosoon Park, Kyu-Beck Lee, Hee Jung Son, Juhee Cho, Eliseo Guallar
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0075178
Abstract: Background The association between serum bilirubin levels and incident chronic kidney disease (CKD) in the general population is unknown. We aimed to examine the association between serum bilirubin concentration (total, direct, and indirect) and the risk of incident CKD. Methods and Findings Longitudinal cohort study of 12,823 Korean male workers 30 to 59 years old without CKD or proteinuria at baseline participating in medical health checkup program in a large worksite. Study participants were followed for incident CKD from 2002 through 2011. Estimated glomerular filtration rate (eGFR) was estimated by using the CKD-EPI equation. CKD was defined as eGFR <60 mL/min per 1.73 m2. Parametric Cox models and pooled logistic regression models were used to estimate adjusted hazard ratios for incident CKD. We observed 238 incident cases of CKD during 70,515.8 person-years of follow-up. In age-adjusted models, the hazard ratios for CKD comparing quartiles 2–4 vs. quartile 1 of serum direct bilirubin were 0.93 (95% CI 0.67–1.28), 0.88 (0.60–1.27) and 0.60 (0.42–0.88), respectively. In multivariable models, the adjusted hazard ratio for CKD comparing the highest to the lowest quartile of serum direct bilirubin levels was 0.60 (95% CI 0.41–0.87; P trend = 0.01). Neither serum total nor indirect bilirubin levels were significantly associated with the incidence of CKD. Conclusions Higher serum direct bilirubin levels were significantly associated with a lower risk of developing CKD, even adjusting for a variety of cardiometabolic parameters. Further research is needed to elucidate the mechanisms underlying this association and to establish the role of serum direct bilirubin as a marker for CKD risk.
Adolescents’ Estimation of Energy Content of Standard Portion Size of Foods and Its Association with Body Mass Index  [PDF]
Mi-Kyeong Choi, Min-Jung Ko, Mi-Hyun Kim
Food and Nutrition Sciences (FNS) , 2012, DOI: 10.4236/fns.2012.310177
Abstract: The purpose of this study is to identify the adolescents’ knowledge of the energy content of the standard portion size of foods and to investigate the association between their knowledge and energy intake and also body mass index (BMI). A total of 251 middle school adolescents participated in this study. Participants’ knowledge was assessed based on their estimation of the energy content of the standard portion size of foods. To estimate the energy intake of the subjects, 24-hr recall was used. The percentage of participants who accurately estimated (that is within 20% of the true value) the energy content of the standard portion size was calculated for each of the 32 typical foods. The food for which the most participants revealed the accurate estimation was cooked rice (39.5%). The proportion of students who overestimated the energy contents was highest for vegetables (98%), and oils and sugar (90%). The female students were more likely than males to provide the accurate estimation of energy contents for standard portion size of foods. After adjusting for age and sex, the estimation level ([estimation value/true value] × 100) of the energy content of some foods had a significant positive relationship with BMI, but had no significant relationship with reported energy intake. From these results, we concluded that the knowledge of energy content of food was poor among middle-school adolescents, with some gender difference, and that their estimation of the calorie contents of foods increased along with their BMI.
Nevus-Like Appearance of Primary Malignant Melanoma of the Esophagus
Min-Jung Kang,Sun Young Yi
Gastroenterology Research and Practice , 2009, DOI: 10.1155/2009/285753
Abstract: The primary malignant melanoma of the esophagus (PMME) is a rare malignant disease, accounting for only 0.1–0.2% of all esophageal neoplasms, and the majority of the patients are diagnosed at advanced stages with poor prognosis. We present here a case of 56-year-old woman with epigastric pain and her endoscopic finding revealed several flat and black pigmented mucosal lesions within the distal portion of the esophagus which looked like flat nevus. The histopathology and immunohistochemical profile of the tissue specimens were diagnostic of malignant melanoma.
Spectrum of Cognitive Impairment in Korean ALS Patients without Known Genetic Mutations
Seong-il Oh, Aram Park, Hee-Jin Kim, Ki-Wook Oh, Hojin Choi, Min-Jung Kwon, Chang-Seok Ki, Hee-Tae Kim, Seung Hyun Kim
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0087163
Abstract: Background Cognitive impairment is associated with a negative prognosis in amyotrophic lateral sclerosis (ALS), as well as with clinical specificity. We investigate neuropsychological function in ALS patients without known genetic mutations in a Korean tertiary clinic. Methods Three hundred and eighteen patients were enrolled in a prospective longitudinal cohort from September 2008 to February 2012. At the time of diagnosis of sporadic ALS, we carried out genetic and comprehensive neuropsychological tests on all patients, and collected demographic and clinical characteristics. Six cognitive domains, namely executive function, attention, language, calculation, visuospatial function and memory were evaluated. ANOVA and t-tests were used to assess differences in clinical characteristics and neuropsychological parameters between sporadic ALS patients. The Kaplan-Meier method and Cox proportional hazard model were used for survival analysis. Results One hundred and sixty-six patients were categorized into five subtypes: normal cognition (ALS pure), cognitive impairment (ALSci), behavioral impairment (ALSbi), frontotemporal dementia (ALS-FTD), and other types of dementia. Seventy patients (70/166, 42.2%) were cognitively or behaviorally impaired. Among the impaired patients, eight (8/166, 4.8%) had FTD-type dementia and one (1/166, 0.6%) was Alzheimer's disease-type. The ALS patients with cognitive impairment (ALSci) and with FTD (ALS-FTD) were more severely impaired in executive function, attention, language and memory than the cognitively intact ALS patients (ALS pure). In a survival analysis, ALSci (β = 1.925, p = 0.025) and ALS-FTD groups (β = 4.150, p = 0.019) tended to have shorter survival than the ALS pure group. Conclusions About half of ALS patients without known genetic variation have cognitive or behavioral impairment. ALS patients with cognitive abnormalities, especially FTD, have a poorer prognosis than those without cognitive impairment. In neuropsychological profiling, executive tasks were effective in identifying cognitive impairment in the ALS patients. It would be useful for clinicians to classify ALS according to neuropsychological profiles, and screen for subtle cognitive impairment.
Quantification of Trace-Level DNA by Real-Time Whole Genome Amplification
Min-Jung Kang,Hannah Yu,Sook-Kyung Kim,Sang-Ryoul Park,Inchul Yang
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0028661
Abstract: Quantification of trace amounts of DNA is a challenge in analytical applications where the concentration of a target DNA is very low or only limited amounts of samples are available for analysis. PCR-based methods including real-time PCR are highly sensitive and widely used for quantification of low-level DNA samples. However, ordinary PCR methods require at least one copy of a specific gene sequence for amplification and may not work for a sub-genomic amount of DNA. We suggest a real-time whole genome amplification method adopting the degenerate oligonucleotide primed PCR (DOP-PCR) for quantification of sub-genomic amounts of DNA. This approach enabled quantification of sub-picogram amounts of DNA independently of their sequences. When the method was applied to the human placental DNA of which amount was accurately determined by inductively coupled plasma-optical emission spectroscopy (ICP-OES), an accurate and stable quantification capability for DNA samples ranging from 80 fg to 8 ng was obtained. In blind tests of laboratory-prepared DNA samples, measurement accuracies of 7.4%, ?2.1%, and ?13.9% with analytical precisions around 15% were achieved for 400-pg, 4-pg, and 400-fg DNA samples, respectively. A similar quantification capability was also observed for other DNA species from calf, E. coli, and lambda phage. Therefore, when provided with an appropriate standard DNA, the suggested real-time DOP-PCR method can be used as a universal method for quantification of trace amounts of DNA.
SPIN90 Phosphorylation Modulates Spine Structure and Synaptic Function
In Ha Cho, Dae Hwan Kim, Min-Jung Lee, Jeomil Bae, Kun Ho Lee, Woo Keun Song
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0054276
Abstract: The correct rearrangement of postsynaptic components in dendritic spines is important for driving changes of spine structure and synaptic function. SPIN90 plays an essential role in many cellular processes including actin polymerization, endocytosis, growth cone formation and dendritic spine morphogenesis. Here, we demonstrate that SPIN90, which is a binding partner of PSD95 and Shank in spines, is targeted to synapses and leads to enhanced synaptic activity in neurons. We show, using in vitro and in vivo kinase assays, that SPIN90 is tyrosine phosphorylated by Src kinase. SPIN90 that was tyrosine-phosphorylated by Src was targeted to dendritic spines in cultured hippocampal neurons. Moreover, a SPIN90 phospho-deficient mutant was unable to accumulate at dendritic spines whereas SPIN90 WT and a phospho-mimicking mutant were localized at spines and bound PSD95 and Shank with increased efficiency. Consistent with these findings, hippocampal neurons that overexpressed SPIN90 WT or a phospho-mimicking mutant had enlarged spine heads, leading to enhanced postsynaptic function in terms of both amplitude and frequency. Together, our findings show that SPIN90 modulates synaptic activity in neurons as a result of its phosphorylation.
Ihh and Runx2/Runx3 Signaling Interact to Coordinate Early Chondrogenesis: A Mouse Model
Eun-Jung Kim, Sung-Won Cho, Jeong-Oh Shin, Min-Jung Lee, Kye-Seong Kim, Han-Sung Jung
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0055296
Abstract: Endochondral bone formation begins with the development of a cartilage intermediate that is subsequently replaced by calcified bone. The mechanisms occurring during early chondrogenesis that control both mesenchymal cell differentiation into chondrocytes and cell proliferation are not clearly understood in vertebrates. Indian hedgehog (Ihh), one of the hedgehog signaling molecules, is known to control both the hypertrophy of chondrocytes and bone replacement; these processes are particularly important in postnatal endochondral bone formation rather than in early chondrogenesis. In this study, we utilized the maternal transfer of 5E1 to E12.5 in mouse embryos, a process that leads to an attenuation of Ihh activity. As a result, mouse limb bud chondrogenesis was inhibited, and an exogenous recombinant IHH protein enhanced the proliferation and differentiation of mesenchymal cells. Analysis of the genetic relationships in the limb buds suggested a more extensive role for Ihh and Runx genes in early chondrogenesis. The transfer of 5E1 decreased the expression of Runx2 and Runx3, whereas an exogenous recombinant IHH protein increased Runx2 and Runx3 expression. Moreover, a transcription factor Gli1 in hedgehog pathway enhances the direct induction of both Runx2 and Runx3 transcription. These findings suggested that Ihh signaling plays an important role in chondrocyte proliferation and differentiation via interactions with Runx2 and Runx3.
High-Throughput Screening for the Identification of New Therapeutic Options for Metastatic Pheochromocytoma and Paraganglioma
Alessio Giubellino, Uma Shankavaram, Petra Bullova, Jan Schovanek, Yaqin Zhang, Min Shen, Nikita Patel, Abdel Elkahloun, Min-Jung Lee, Jane Trepel, Marc Ferrer, Karel Pacak
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0090458
Abstract: Drug repurposing or repositioning is an important part of drug discovery that has been growing in the last few years for the development of therapeutic options in oncology. We applied this paradigm in a screening of a library of about 3,800 compounds (including FDA-approved drugs and pharmacologically active compounds) employing a model of metastatic pheochromocytoma, the most common tumor of the adrenal medulla in children and adults. The collection of approved drugs was screened in quantitative mode, testing the compounds in compound-titration series (dose-response curves). Analysis of the dose-response screening data facilitated the selection of 50 molecules with potential bioactivity in pheochromocytoma cells. These drugs were classified based on molecular/cellular targets and signaling pathways affected, and selected drugs were further validated in a proliferation assay and by flow cytometric cell death analysis. Using meta-analysis information from molecular targets of the top drugs identified by our screening with gene expression data from human and murine microarrays, we identified potential drugs to be used as single drugs or in combination. An example of a combination with a synergistic effect is presented. Our study exemplifies a promising model to identify potential drugs from a group of clinically approved compounds that can more rapidly be implemented into clinical trials in patients with metastatic pheochromocytoma or paraganglioma.
In Vitro and Ex Vivo Analysis of CHRNA3 and CHRNA5 Haplotype Expression
Glenn A. Doyle, Min-Jung Wang, Andrew D. Chou, John U. Oleynick, Steven E. Arnold, Russell J. Buono, Thomas N. Ferraro, Wade H. Berrettini
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0023373
Abstract: Genome-wide association studies implicate variations in CHRNA5 and CHRNA3 as being associated with nicotine addiction (NA). Multiple common haplotypes (“risk”, “mixed” and “protective”) exist in Europeans; however, high linkage disequilibrium between variations in CHRNA5 and CHRNA3 makes assigning causative allele(s) for NA difficult through genotyping experiments alone. We investigated whether CHRNA5 or CHRNA3 promoter haplotypes, associated previously with NA, might influence allelic expression levels. For in vitro analyses, promoter haplotypes were sub-cloned into a luciferase reporter vector. When assessed in BE(2)-C cells, luciferase expression was equivalent among CHRNA3 haplotypes, but the combination of deletion at rs3841324 and variation at rs503464 decreased CHRNA5 promoter-derived luciferase activity, possibly due to loss of an SP-1 and other site(s). Variation within the CHRNA5 5’UTR at rs55853698 and rs55781567 also altered luciferase expression in BE(2)-C cells. Allelic expression imbalance (AEI) from the “risk” or “protective” haplotypes was assessed in post-mortem brain tissue from individuals heterozygous at coding polymorphisms in CHRNA3 (rs1051730) or CHRNA5 (rs16969968). In most cases, equivalent allelic expression was observed; however, one individual showed CHRNA5 AEI that favored the “protective” allele and that was concordant with heterozygosity at polymorphisms ~13.5 kb upstream of the CHRNA5 transcription start site. Putative enhancer activity from these distal promoter elements was assessed using heterologous promoter constructs. We observed no differences in promoter activity from the two distal promoter haplotypes examined, but found that the distal promoter region strongly repressed transcription. We conclude that CHRNA5 promoter variants may affect relative risk for NA in some heterozygous individuals.
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