2.Lipoprotein-Associated Phospholipase A2 Is Related to Plaque Stability and Is a Potential Biomarker for Acute Coronary Syndrome.
Hyemoon CHUNG ; Hyuck Moon KWON ; Jong Youn KIM ; Young Won YOON ; Jihyuk RHEE ; Eui Young CHOI ; Pil Ki MIN ; Bum Kee HONG ; Se Joong RIM ; Ji Hyun YOON ; Sung Joo LEE ; Jong Kwan PARK ; Myung Hyun KIM ; Minhee JO ; Jeong Hee YANG ; Byoung Kwon LEE
Yonsei Medical Journal 2014;55(6):1507-1515
PURPOSE: Plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) binds to low-density lipoprotein. The levels of Lp-PLA2 reflect the plaque burden, and are upregulated in acute coronary syndrome (ACS). We investigated the diagnostic value of Lp-PLA2 levels and found that it might be a potential biomarker for ACS. MATERIALS AND METHODS: We classified 226 study participants into three groups: patients without significant stenosis (control group), patients with significant stenosis with stable angina (SA group), and patients with ACS (ACS group). RESULTS: Lp-PLA2 and high-sensitivity C-reactive protein (hs-CRP) levels were significantly greater in the ACS group than in the SA group (p=0.044 and p=0.029, respectively). Multivariate logistic regression analysis revealed that Lp-PLA2 levels are significantly associated with ACS (odds ratio=1.047, p=0.013). The addition of Lp-PLA2 to the ACS model significantly increased the global chi2 value over traditional risk factors (28.14 to 35.602, p=0.006). The area under the receiver operating characteristic curve for Lp-PLA2 was 0.624 (p=0.004). The addition of Lp-PLA2 level to serum hs-CRP concentration yielded an integrated discrimination improvement of 0.0368 (p=0.0093, standard error: 0.0142) and improved the ability to diagnose ACS. CONCLUSION: Lp-PLA2 levels are related to plaque stability and might be a diagnostic biomarker for ACS.
1-Alkyl-2-acetylglycerophosphocholine Esterase/*blood
;
Acute Coronary Syndrome/*blood/physiopathology
;
Aged
;
Aged, 80 and over
;
Angina Pectoris
;
Biological Markers/blood
;
C-Reactive Protein/*metabolism
;
Coronary Angiography
;
Female
;
Humans
;
Lipoproteins, LDL/*blood
;
Logistic Models
;
Male
;
Middle Aged
;
Multivariate Analysis
;
Plaque, Atherosclerotic/blood
;
ROC Curve
;
Risk Factors
3.Ascorbic acid insufficiency induces the severe defect on bone formation via the down-regulation of osteocalcin production.
Won KIM ; Seyeon BAE ; Hyemin KIM ; Yejin KIM ; Jiwon CHOI ; Sun Young LIM ; Hei Jin LEE ; Jihyuk LEE ; Jiyea CHOI ; Mirim JANG ; Kyoung Eun LEE ; Sun G CHUNG ; Young Il HWANG ; Jae Seung KANG ; Wang Jae LEE
Anatomy & Cell Biology 2013;46(4):254-261
The L-gulono-gamma-lactone oxidase gene (Gulo) encodes an essential enzyme in the synthesis of ascorbic acid from glucose. On the basis of previous findings of bone abnormalities in Gulo-/- mice under conditions of ascorbic acid insufficiency, we investigated the effect of ascorbic acid insufficiency on factors related to bone metabolism in Gulo-/- mice. Four groups of mice were raised for 4 weeks under differing conditions of ascorbic acid insufficiency, namely, wild type; ascorbic acid-sufficient Gulo-/- mice, 3-week ascorbic acid-insufficient Gulo-/- mice, and 4-week ascorbic acid-insufficient Gulo-/- mice. Four weeks of ascorbic acid insufficiency resulted in significant weight loss in Gulo-/- mice. Interestingly, average plasma osteocalcin levels were significantly decreased in Gulo-/- mice after 3 weeks of ascorbic acid insufficiency. In addition, the tibia weight in ascorbic acid-sufficient Gulo-/- mice was significantly higher than that in the other three groups. Moreover, significant decreases in trabecular bone volume near to the growth plate, as well as in trabecular bone attachment to the growth plate, were evident in 3- or 4-week ascorbic acid-insufficient Gulo-/-. In summary, ascorbic acid insufficiency in Gulo-/- mice results in severe defects in normal bone formation, which are closely related to a decrease in plasma osteocalcin levels.
Animals
;
Ascorbic Acid*
;
Down-Regulation*
;
Glucose
;
Growth Plate
;
L-Gulonolactone Oxidase
;
Metabolism
;
Mice
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Osteocalcin*
;
Osteogenesis*
;
Plasma
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Tibia
;
Weight Loss

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