Publications by authors named "Ching-Ling Kuo"

3 Publications

  • Page 1 of 1

Oxidized low-density lipoproteins, autoantibodies against oxidized low-density lipoproteins and carotid intima media thickness in a clinically healthy population.

Cardiology 2008 12;110(4):252-9. Epub 2007 Dec 12.

Institute of Nutritional Science, Chung Shan Medical University, Taichung, Taiwan.

Background: Oxidized low-density lipoproteins (oxLDLs) play an important role in the progress of atherosclerosis. Autoantibodies (oxLDL Ab) against oxLDLs may reflect the extent of LDL oxidation in vivo. Our aim was to investigate the correlation between oxLDLs, oxLDL Ab and intima media thickness of the common carotid arteries (CCA-IMT) in a clinically healthy population.

Methods: Two hundred subjects were recruited, and demographic and clinical characteristics of the subjects were recorded. By use of tertile classification of plasma oxLDLs and oxLDL Ab, 9 groups including 4 extreme subject groups were generated. CCA-IMT was measured as an indicator of carotid atherosclerosis.

Results: Age and plasma LDL concentration contributed significantly to CCA-IMT (p < 0.05). Body mass index, smoking index and plasma LDL concentration were significantly positively related to the plasma oxLDLs concentration; by contrast, plasma oxLDL Ab were significantly negatively related to the plasma oxLDL concentration (p < 0.05). Subjects in the group with low oxLDL Ab/high oxLDLs had the greatest CCA-IMT and the highest level of LDL; by contrast, subjects in the group with high oxLDL Ab/low oxLDLs had the least CCA-IMT and the lowest level of LDL.

Conclusions: Both plasma oxLDLs and oxLDL Ab contribute, although in opposite ways, to the LDL metabolism and development of atherosclerosis. Immune response to oxLDLs may exert a protective role at an early stage of atherosclerosis.
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http://dx.doi.org/10.1159/000112409DOI Listing
July 2008

Attenuation of experimental subarachnoid hemorrhage-induced increases in circulating intercellular adhesion molecule-1 and cerebral vasospasm by the endothelin-converting enzyme inhibitor CGS 26303.

J Neurosurg 2007 Mar;106(3):442-8

Department of Neurosurgery, Kaohsiung Medical University, Kaohsiung, Taiwan.

Object: Adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin, are important mediators of inflammation, and their levels are elevated in the serum of patients following aneurysmal subarachnoid hemorrhage (SAH). The investigators previously found that CGS 26303 is effective in preventing and reversing arterial narrowing in a rabbit model of SAH. The purpose of the present study was to examine whether levels of adhesion molecules are altered after treatment with CGS 26303 in this animal model.

Methods: New Zealand White rabbits were each injected with 3 ml of autologous blood in the cisterna magna, and intravenous treatment with CGS 26303 (30 mg/kg) was initiated 1 hour later. The compound was subsequently administered at 12, 24, and 36 hours post-SAH. Blood samples were collected at 48 hours post-SAH to measure ICAM-1, VCAM-1, and E-selectin levels. After the rabbits had been killed by perfusion-fixation, the basilar arteries (BAs) were removed and sliced, and their cross-sectional areas were measured. Treatment with CGS 26303 attenuated arterial narrowing after SAH. Morphologically, corrugation of the internal elastic lamina of BAs was prominently observed in the SAH only and vehicle-treated SAH groups, but not in the CGS 26303-treated SAH group or in healthy controls. There were no significant differences in the levels of VCAM-1 among the four groups. The levels of E-selectin were increased in all animals subjected to SAH (those in the SAH only, SAH plus vehicle, and SAH plus CGS 26303 groups) compared with healthy controls (no SAH); however, the levels of ICAM-1 in the SAH only and SAH plus vehicle groups were significantly elevated (p < 0.001), and treatment with CGS 26303 reduced ICAM-1 to control levels following SAH.

Conclusions: These results show that ICAM-1 may play a role in mediating SAH-induced vasospasm and that a reduction of ICAM-1 levels after SAH may partly contribute to the antispastic effect of CGS 26303.
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http://dx.doi.org/10.3171/jns.2007.106.3.442DOI Listing
March 2007

Alteration of the copy number of mitochondrial DNA in leukocytes of patients with hyperlipidemia.

Ann N Y Acad Sci 2005 May;1042:70-5

Vascular and Genomic Research Center, Changhua Christian Hospital, Taiwan.

Lipid metabolism in leukocytes may be disturbed by mitochondrial dysfunction caused by depletion of mitochondrial DNA (mtDNA) in response to an increase of oxidative stress in blood circulation. It is possible that alteration in mtDNA copy number of the leukocyte is involved in the impairment of the scavenging of oxidatively modified plasma proteins such as oxidized low-density lipoprotein (oxLDL). To test this hypothesis, we recruited 91 healthy subjects and 63 patients with hyperlipidemia (LDL >130 mg/dL) for this study. The copy number of mtDNA in the leukocyte and the titer of oxLDL IgG autoantibody (oLAB) were determined as indices of the oxidative stress response of immune cells. The results revealed a significant higher level of plasma oxLDL, lower titer of oLAB, and decreased copy number of mtDNA in patients with hyperlipidemia (P <0.05). In the analysis of partial correlations under age control, we found that an increase in the copy number of mtDNA was positively correlated with an increase in the level of oLAB (P <0.005, r = 0.3002) and a decrease in the oxLDL level (P <0.05, r = -0.2654) in healthy subjects but not in patients. Based on the results obtained from this case-control study, we conclude that the increase of mtDNA copy number might provide the leukocyte an increased capability of scavenging oxLDL, possibly by enhanced generation of oLAB in healthy subjects, but not in hyperlipidemic patients who had lower mtDNA copy numbers in their leukocytes. Taken together, these findings suggest that an alteration of mtDNA copy number in the leukocyte may be one of the risk factors for hyperlipidemia.
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http://dx.doi.org/10.1196/annals.1338.008DOI Listing
May 2005