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Tai Hee Lee  (Lee TH) 9 Articles
Platelet Aggregability in Type 2 Diabetics.
Chang Hun Lee, Nam Il Cheon, Yeon Sang Lee, Dong Hyeok Cho, Hyun Ho Shin, Jung Min Kim, Dae Ho Lee, Dong Jin Chung, Min Young Chung, Tai Hee Lee
Korean Diabetes J. 2000;24(3):300-309.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Increased platelet aggregability is known to be one of the important risk factors for diabetic vascular complications. The relationship between platelet aggregability and diabetic macrovascular complications, varying severity of diabetic microvascular complications and other possible factors was evaluated in Korean adults. METHODS: Platelet aggregability was measured with platelet rich plasma by addition of adenosine diphosphate (ADP) in 45 cases. Normal control group (n=15) was compared with diabetics without macrovascular complications (n=15), diabetics with macrovascular complications (n=15) and several groups divided accoring to the severity of microvascular complications. RESULTS: 1) The mean maximum value of platelet aggregation was 70.3+/-5.3% in control group, and 80.0+/-7.3% in diabetics (p<0.005). 2) The mean maximum value of platelet aggregation was 78.0+/-5.5% in diabetics without macrovascular complications and 83.5+/-7.1% in diabetics with macrovascular complications (p=0.093). 3) The mean maximum value of platelet aggregation was 77.0+/-5.1% in normoproteinuria group, 78.1+/-7.3% in microproteinuria group, and 82.9+/-6.2% in overt proteinuria group (p=0.083). 4) The mean maximum value of platelet aggregation was 77.2+/-6.8% in diabetes without neuropathy group and 82.9+/-6.2% in diabetes with neuropathy group (p=0.114). 5) The mean maximum value of platelet aggregation was 79.3+/-4.9% in diabetes with normal funduscopic findings, 80.2+/-7.3% in diabetes with background retinopathy and 81.6+/-7.9% in diabetes with proliferative retinopathy (p=0.852). 6) Blood glucose showed positive correlations with the mean maximum platelet aggregation ( =0.529, p<0.005). CONCLUSION: The elevated mean maximum value of platelet aggregation was found in diabetics and there were no significant differences between macrovascular complications and between varying severity of retinopathy, neuropathy and proteinuria. Blood glucose showed positive correlations with mean maximum platelet aggregation. Hyperglycemia was a major risk factor affecting platelet aggregation in diabetics and its control may play an important role in prevention of diabetic vascular complications.
Protective Mechanism of Glucose against Alloxan-Indeved HIT-T15 Cell Damage.
Tai Hee Lee, Tae Sun Park, Hyung Rho Kim
Korean Diabetes J. 1999;23(4):530-540.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Glucose prevents the development of alloxan-induced diabetes, but the precise protective mechanism of glucose is not yet clearly known. METHODS: The protective mechanism of glucose on alloxan-induced B-cell damage as investigated using a Syrian hamster transformed B-cell line,HIT-T15 cells. RESULTS: Alloxan caused cell death, inhibition of insulin release, elevation of cytosolic free Ca, DNA fragmentation and decrease of cellular NAD+and ATP. However, pretreatment of HIT-T15 ce]ls with glucose significantly blocked DNA fragmentation, depletion of intracellular NAD+,ATP and cell viability induced by alloxan, but did not affect the increase of cytosolic free Ca2+.The result indicate that glucose acts between Ca2+ influx and DNA fragmentation on a chain of reactions in the diabetogenesis of alloxan. CONCLUSION: These protective effects of glucose on alloxan-induced B-cell damage werepletely abolished by pretreatment with inhibitors of glucose-6-phosphate dehydrogenase, dehydroepian- drosterone (DHEA) and epiandrosterone (EPI), suggesting that a metabolic intermediate, such as NADPH, produced from glucose through pentose phosphate pathway plays an important role in the protection of B-cell damage by alloxan.
Lipoprotein (a) Level and Vascular Complications in NIDDM.
Ji Youn Kim, Mung Su Kim, Joung Min Kim, Jai Hong Park, Joung Hun Lee, Seung Won Yang, Dong Jin Chung, Min Young Chung, Tai Hee Lee
Korean Diabetes J. 1998;22(1):65-73.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
The risk of atherosclerosis is increased in subjects with diabetes mellitus. Lipoprotein(a) [Lp(a)] is an independent risk factor for atherosclerotic vascular disease in subjects without diabetes. The contribution of Lp(a) to the increased risk for atherosclerosis and diabetic complications in subjects with diabetes is not well known. In this report we examined the relationship between Lp(a) levels and development of vascular (macro- and microvascular) complications, and the relationship between Lp(a) and other risk factors for vascular complications in subjects with non-insulin-dependent diabetes mellitus(NIDDM), METHODS: For this study we evaluated 152 patients with NIDDM(72 women and 80 men). Lp(a) level was measured with N-Latex Lp(a) Reagent. Electrocardiography, coronary angiography, brain CT/MRI, doppler velocimetry and peripheral angiography were done for diagnosis of macravascular complieations, and fundus camera, nerve conduction velocity, BBV (beat to beat variation), VPT(vibration perception threshold) and 24-hour urine protein amount were examined for diagnosis of microvascular complications. RESULTS: Lp(a) levels in subjects with ischemic heart disease, cerebrovascular disease and diabetic retinopathy were significantly higher than those in subjects without above mentioned diseases. ApoB/ApoA1 ratio and LDL-cholesterol levels in subjects with Lp(a) level>30mg/dL were significantly higher than those in subjects with Lp(a) level 30mg/dL, and Lp(a) has a positive correlation with ApoB/ApoA1 ratio and LDL-cholesterol in NIDDM patients with vasculopathy. CONCLUSION: These results suggest that high Lp(a) levels seem to be associated with macrovascular and microvascular(especially with retinopathy) complications in subjects with NIDDM and Lp(a) level should be measured in the NIDDM with high level of ApoB/ApoA1 ratio and/or LDL-eholesterol.
Effect of clisapride on gastric emptying in patients with diabetic gastroparesis.
Jae Soo Ahn, Hyun Ju Chang, Eun Jin Choi, Sang Sun Park, Dai Ho Lee, Jae Hyun Cho, Ho Chul Kang, Min Young Chung, Tai Hee Lee
Korean Diabetes J. 1993;17(2):217-223.   Published online January 1, 2001
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  • 18 Download
AbstractAbstract PDF
No abstract available.
Action mechanism of diabetogenic agents.
Tai Hee Lee
Korean Diabetes J. 1993;17(1):1-15.   Published online January 1, 2001
  • 786 View
  • 21 Download
AbstractAbstract PDF
No abstract available.
Clinical study of cilostazol in diabetic patients with peripheralvascular disease.
Tai Hee Lee, Young Kil Choi, Kap Bum Huh, Soon Hyun Shin, Hong Kyu Lee, Ho Young Son, Young Seol Kim, Hyun Chul Lee, Min Young Chung
Korean Diabetes J. 1992;16(4):325-334.   Published online January 1, 2001
  • 1,176 View
  • 24 Download
AbstractAbstract PDF
No abstract available.
A case of NIDDM complicated by acute mediastinitis.
Dae Ho Lee, Ho Cheol Kang, Jae Soo An, Hyun Joo Jang, Eun Jin Choi, Sang Seon Park, Jae Hyun Jho, Min Young Chung, Tai Hee Lee
Korean Diabetes J. 1992;16(3):237-240.   Published online January 1, 2001
  • 1,120 View
  • 17 Download
AbstractAbstract PDF
No abstract available.
An electron microscopic study of superior mesenteric ganglion of vacor-induced diabetic mongolian gerbil.
Won Sup Lim, Tai Hee Lee, Jae Rhyong Yoon, Sun Hun Kim
Korean Diabetes J. 1992;16(1):9-16.   Published online January 1, 2001
  • 763 View
  • 19 Download
AbstractAbstract PDF
No abstract available.
Glomerulopathy in vacor-induced diabetic mongolian gerbil.
Phil Woo Chung, Min Young Chung, Tai Hee Lee, Sun Hun Kim, Jae Rhyong Yoon
Korean Diabetes J. 1991;15(1):79-83.   Published online January 1, 2001
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  • 19 Download
AbstractAbstract PDF
No abstract available.

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