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Lee, Seungx2010,Hwan,Ha, Heex2010,Sung,Park, Youngx2010,Jun,Lee, Jinx2010,Hee,Yim, Hyeonx2010,Woo,Yoon, Kunx2010,Ho,Kang, Moo‐,Il,Lee, Wonx2010,Chul,Son, Hox2010,Young,Park, Yong Blackwell Publishing Ltd 2011 Clinical endocrinology Vol.75 No.4
<P><B>Summary</B></P><P><B>Objective </B> To investigate the prevalence and identify the phenotype of individuals suspected to be metabolically obese but normal weight (MONW).</P><P><B>Design and subjects </B> Eight thousand nine hundred and eighty‐seven nondiabetic subjects aged over 40 years were selected from the Chungju Metabolic disease Cohort study performed in 2003–2006 in Korea. Those within the highest quartile in the homeostasis model assessment of insulin resistance (HOMA‐IR) with a normal body mass index (BMI) between 18·5 and 23 kg/m<SUP>2</SUP> were classified as MONW.</P><P><B>Measurements </B> Data on anthropometry, lipid profiles and HOMA‐IR values were analysed.</P><P><B>Results </B> The prevalence of MONW was 14·2% for men and 12·9% for women amongst normal‐weight subjects. Multiple logistic regression analysis showed that total cholesterol (TC) levels over 5·17 m<SMALL>m</SMALL> (odds ratio, OR = 1·481; 95% confidence intervals, CI 1·086–2·021), triglyceride (TG) levels over 1·69 m<SMALL>m</SMALL> (OR = 1·507; 95% CI 1·093–2·077) and high‐density lipoprotein‐cholesterol levels lower than 1·03 m<SMALL>m</SMALL> (OR = 1·580; 95% CI 1·053–2·371) independently had higher odds of diagnosing MONW amongst men. For women, a BMI over 21·5 kg/m<SUP>2</SUP> (OR = 1·405; 95% CI 1·034–1·909), TC levels over 5·17 m<SMALL>m</SMALL> (OR = 1·524; 95% CI 1·112–2·090) and TG levels over 1·69 m<SMALL>m</SMALL> (OR = 1·799; 95% CI 1·302–2·487) were independently associated with a diagnosis of MONW.</P><P><B>Conclusions </B> More than 10% of normal‐weight subjects were classed as MONW in this cohort. Identification of these subjects based on lipid profiles could aid in the early detection of a high risk group of developing cardiometabolic diseases.</P>
Kim, Kyungx2010,Jin,Kim, Sangx2010,Hyun,Yoon, Young Won,Rha, Seungx2010,Woon,Hong, Soonx2010,Jun,Kwak, Choongx2010,Hwan,Kim, Weon,Nam, Changx2010,Wook,Rhee, Moo‐,Yong,Park, Taex201 John Wiley and Sons Inc. 2016 CARDIOVASCULAR THERAPEUTICS Vol.34 No.5
<P><B>Summary</B></P><P><B>Aim</B></P><P>We aimed to compare the effects of fixed‐dose combinations of ezetimibe plus rosuvastatin to rosuvastatin alone in patients with primary hypercholesterolemia, including a subgroup analysis of patients with diabetes mellitus (DM) or metabolic syndrome (MetS).</P><P><B>Method</B></P><P>This multicenter eight‐week randomized double‐blind phase III study evaluated the safety and efficacy of fixed‐dose combinations of ezetimibe 10 mg plus rosuvastatin, compared with rosuvastatin alone in patients with primary hypercholesterolemia. Four hundred and seven patients with primary hypercholesterolemia who required lipid‐lowering treatment according to the ATP III guideline were randomized to one of the following six treatments for 8 weeks: fixed‐dose combinations with ezetimibe 10 mg daily plus rosuvastatin (5, 10, or 20 mg daily) or rosuvastatin alone (5, 10, or 20 mg daily).</P><P><B>Results</B></P><P>Fixed‐dose combination of ezetimibe plus rosuvastatin significantly reduced LDL cholesterol, total cholesterol, and triglyceride levels compared with rosuvastatin alone. Depending on the rosuvastatin dose, these fixed‐dose combinations of ezetimibe plus rosuvastatin provided LDL cholesterol, total cholesterol, and triglyceride reductions of 56%–63%, 37%–43%, and 19%–24%, respectively. Moreover, the effect of combination treatment on cholesterol levels was more pronounced in patients with DM or MetS than in non‐DM or non‐MetS patients, respectively, whereas the effect of rosuvastatin alone did not differ between DM vs non‐DM or MetS vs non‐MetS patients.</P><P><B>Conclusion</B></P><P>Fixed‐dose combinations of ezetimibe and rosuvastatin provided significantly superior efficacy to rosuvastatin alone in lowering LDL cholesterol, total cholesterol, and triglyceride levels. Moreover, the reduction rate was greater in patients with DM or MetS.</P>
Hyun Lee, Choong,Yan, Bingchun,Yoo, Kix2010,Yeon,Choi, Jung Hoon,Kwon, Seungx2010,Hae,Her, Song,Sohn, Youdong,Hwang, In Koo,Cho, Jun Hwi,Kim, Youngx2010,Myeong,Won, Moo‐,Ho Wiley Subscription Services, Inc., A Wiley Company 2011 Journal of neuroscience research Vol.89 No.7
<P><B>Abstract</B></P><P>Glucagon‐like peptide‐1 receptor (GLP‐1R) protects against neuronal damages in the brain. In the present study, ischemia‐induced changes in GLP‐1R immunoreactivity in the gerbil hippocampal CA1 region were evaluated after transient cerebral ischemia; in addition, the neuroprotective effect of the GLP‐1R agonist exendin‐4 (EX‐4) against ischemic damage was studied. GLP‐1R immunoreactivity and its protein levels in the ischemic CA1 region were highest at 1 day after ischemia/reperfusion (I/R). At 4 days after I/R, GLP‐1R immunoreactivity was hardly detected in CA1 pyramidal neurons, and its protein level was lowest. GLP‐1R protein level was increased again at 10 days after I/R, and GLP‐1R immunoreactivity was found in astrocytes and GABAergic interneurons. In addition, EX‐4 treatment attenuated ischemia‐induced hyperactivity, neuronal damage, and microglial activation in the ischemic CA1 region in a dose‐dependent manner. EX‐4 treatment also induced the elevation of GLP‐1R immunoreactivity and protein levels in the ischemic CA1 region. These results indicate that GLP‐1R is altered in the ischemic region after an ischemic insult and that EX‐4 protects against ischemia‐induced neuronal death possibly by increasing GLP‐1R expression and attenuating microglial activation against transient cerebral ischemic damage. © 2011 Wiley‐Liss, Inc.</P>
REDD‐1 aggravates endotoxin‐induced inflammation <i>VIA</i> atypical NF‐κB activation
Lee, Dongx2010,Keon,Kim, Jix2010,Hee,Kim, Joohwan,Choi, Seunghwan,Park, MinSik,Park, Wonjin,Kim, Suji,Lee, Kyux2010,Sun,Kim, Taesam,Jung, Jiwon,Choi, Yoon Kyung,Ha, Kwonx2010,Soo,Won, Moo Federation of American Society for Experimental Bi 2018 The FASEB Journal Vol.32 No.8
Yi, Gihwan,Choi, Junx2010,Ho,Lee, Jongx2010,Hee,Jeong, Unggi,Nam, Minx2010,Hee,Yun, Dohx2010,Won,Eun, Moo‐,Young Taylor Francis 2005 Preparative biochemistry & biotechnology Vol.35 No.3
<P>We describe a rapid and simple procedure for homogenizing leaf samples suitable for mini/midi‐scale DNA preparation in rice. The methods used tungsten carbide beads and general vortexer for homogenizing leaf samples. In general, two samples can be ground completely within 11.3±1.5 sec at one time. Up to 20 samples can be ground at a time using a vortexer attachment. The yields of the DNA ranged from 2.2 to 7.6 µg from 25–150 mg of young fresh leaf tissue. The quality and quantity of DNA was compatible for most of PCR work and RFLP analysis.</P>
Yoo, Dae Young,Kim, Woosuk,Yoo, Kix2010,Yeon,Nam, Sung Min,Chung, Jin Young,Yoon, Yeo Sung,Won, Moo‐,Ho,Hwang, In Koo Wiley Subscription Services, Inc., A Wiley Company 2012 JOURNAL OF NEUROSCIENCE RESEARCH - Vol.90 No.8
<P><B>Abstract</B></P><P>In this study, we challenged pyridoxine to mice fed a high‐fat diet (HFD) and investigated the effects of pyridoxine on HFD‐induced phenotypes such as blood glucose, reduction of cell proliferation and neuroblast differentiation in the dentate gyrus using Ki67 and doublecortin (DCX), respectively. Mice were fed a commercially available low‐fat diet (LFD) as control diet or HFD (60% fat) for 8 weeks. After 5 weeks of LFD or HFD treatment, 350 mg/kg pyridoxine was administered for 3 weeks. The administration of pyridoxine significantly decreased body weight in the HFD‐treated group. In addition, there were no significant differences in hepatic histology and pancreatic insulin‐immunoreactive (‐ir) and glucagon‐ir cells of the HFD‐treated group after pyridoxine treatment. In the HFD‐fed group, Ki67‐positive nuclei and DCX‐ir neuroblasts were significantly decreased in the dentate gyrus compared with those in the LFD‐fed mice. However, the administration of pyridoxine significantly increased Ki67‐positive nuclei and DCX‐ir neuroblasts in the dentate gyrus in both LFD‐ and HFD‐fed mice. In addition, the administration of pyridoxine significantly increased the protein levels of glutamic acid decarboxylase 67 (GAD67) and brain‐derived neurotrophic factor (BDNF) and the immunoreactivity of phosphorylated cyclic AMP response element binding protein (pCREB) compared with the vehicle‐treated LFD‐ and HFD‐fed mice. In contrast, the administration of pyridoxine significantly decreased HFD‐induced malondialdehyde (MDA) levels in the hippocampus. These results showed that pyridoxine supplement reduced the HFD‐induced reduction of cell proliferation and neuroblast differentiation in the dentate gyrus via controlling the levels of GAD67, pCREB, BDNF, and MDA. © 2012 Wiley Periodicals, Inc.</P>