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Articles by H. C. Lee
Total Records ( 7 ) for H. C. Lee
  B. S Chen , C. H Chang and H. C. Lee

Motivation: Synthetic biology is to engineer artificial biological systems to investigate natural biological phenomena and for a variety of applications. However, the development of synthetic gene networks is still difficult and most newly created gene networks are non-functioning due to uncertain initial conditions and disturbances of extra-cellular environments on the host cell. At present, how to design a robust synthetic gene network to work properly under these uncertain factors is the most important topic of synthetic biology.

Results: A robust regulation design is proposed for a stochastic synthetic gene network to achieve the prescribed steady states under these uncertain factors from the minimax regulation perspective. This minimax regulation design problem can be transformed to an equivalent stochastic game problem. Since it is not easy to solve the robust regulation design problem of synthetic gene networks by non-linear stochastic game method directly, the Takagi–Sugeno (T–S) fuzzy model is proposed to approximate the non-linear synthetic gene network via the linear matrix inequality (LMI) technique through the Robust Control Toolbox in Matlab. Finally, an in silico example is given to illustrate the design procedure and to confirm the efficiency and efficacy of the proposed robust gene design method.

  T Lu , D. M Zhang , X. L Wang , T He , R. X Wang , Q Chai , Z. S Katusic and H. C. Lee

Rationale: The large conductance Ca2+-activated K+ (BK) channel, a key determinant of vascular tone, is regulated by angiotensin II (Ang II) type 1 receptor signaling. Upregulation of Ang II functions and downregulation of BK channel activities have been reported in diabetic vessels. However, the molecular mechanisms underlying Ang II-mediated BK channel modulation, especially in diabetes mellitus, have not been thoroughly examined.

Objectives: The aim in this study was to determine whether caveolae-targeting facilitates BK channel dysfunction in diabetic vessels.

Methods and Results: Using patch clamp techniques and molecular biological approaches, we found that BK channels, Ang II type 1 receptor, Gq/11 (G protein q/11 subunit), nonphagocytic NAD(P)H oxidases (NOX-1), and c-Src kinases (c-Src) were colocalized in the caveolae of rat arterial smooth muscle cells and the integrity of caveolae in smooth muscle cells was critical for Ang II-mediated BK channel regulation. Most importantly, membrane microdomain targeting of these proteins was upregulated in the caveolae of streptozotocin-induced rat diabetic vessels, leading to enhanced Ang II-induced redox-mediated BK channel modification and causing BK channel and coronary dysfunction. The absence of caveolae abolished the effects of Ang II on vascular BK channel activity and preserved BK channel function in diabetes.

Conclusions: These results identified a molecular scheme of receptor/enzyme/channel/caveolae microdomain complex that facilitates the development of vascular BK channel dysfunction in diabetes.

  S. E. Park , E. S. Kang , D. H. Kim , S. K. Kim , J. H. Lee , C. W. Ahn , H. C. Lee and B. S. Cha
  Aims To investigate the effect of two common ATP-binding cassette transporter 1 (ABCA1) polymorphisms (rs4149263 and rs2020927) on atherogenic dyslipidaemia in Korean Type 2 diabetic patients who were treated with rosiglitazone.

Patients and methods Two hundred and fifty-six patients with Type 2 diabetes who had never previously received peroxisome proliferator-activated receptor gamma (PPAR-γ) agonists or lipid-lowering treatment were treated with 4 mg of rosiglitazone daily for 12 weeks without any adjustment to their glucose-lowering regimen. The primary outcome was the change in atherogenic index of plasma (AIP), calculated as log [triglyceride (mmol/l)/high-density lipoprotein cholesterol (mmol/l)], before and after rosiglitazone treatment. The effect of rosiglitazone on the change in AIP was compared across the ABCA1 single nucleotide polymorphisms (SNPs) rs41429263 and rs2020927.

Results Before adjustment, the change in AIP at 12 weeks was significantly different across the rs4149263 genotypes [median (interquartile range): −0.05 (−0.21, 0.09) for TT; 0.02 (−0.09, 0.17) for TC; and 0.11 (0.03, 0.25) for CC; P = 0.003], but not across the rs2020927 [−0.04 (−0.18, 0.10) for TT; 0.03 (−0.17, 0.15) for TC; and −0.03 (−0.13, 0.10) for CC; P = 0.401]. After controlling for age, gender and duration of diabetes, the presence of the C-allele was significantly associated with an increase in AIP by 0.13 [95% confidence interval (CI), 0.04–0.21; P = 0.003]. This association did not change significantly when body mass index and pretreatment metabolic parameters were additionally controlled for (the change in AIP: 0.14; 95% CI, 0.04–0.24; P = 0.007).

Conclusions The ABCA1 SNP rs4149263 may be associated with the change in atherogenic lipid profile in Type 2 diabetes treated with rosiglitazone.

  J. S. Nam , J. Y. Nam , J. S. Yoo , M. Cho , J. S. Park , C. W. Ahn , B. S. Cha , E. J. Lee , S. K. Lim , K. R. Kim and H. C. Lee
  Aim We examined the effect of rosiglitazone on insulin sensitivity, abdominal fat and mid-thigh intramuscular fat distribution, and plasma concentrations of adipocytokines in patients with Type 2 diabetes.
Methods Rosiglitazone was administered at a daily dose of 4 mg to 42 Type 2 diabetes patients [age 32–70 years, body mass index (BMI) 17.5–32.6 kg/m2, 15 women, 27 men] for 12 weeks. Various anthropometric and metabolic profiles, plasma adiponectin, leptin, and resistin levels were measured, and insulin resistance was calculated from the short insulin tolerance test. Body fat composition was assessed by computed tomography.
Results Twelve weeks' rosiglitazone treatment resulted in improved insulin resistance despite increases in body weight and BMI. There was a significant decrease in abdominal visceral adipose tissue area (145 ± 65.6 vs. 129 ± 73.1 cm2, P = 0.049). Mid-thigh low-density muscle area (TLDMA) increased from 23 ± 9.6 to 26 ± 8.2 cm2 (P = 0.009). There were significant changes in plasma adipocytokines, but they were not significantly correlated with changes in insulin resistance.
Conclusions Rosiglitazone treatment resulted in an improvement of insulin responsiveness in Type 2 diabetic subjects, which was associated with the redistribution of visceral and subcutaneous adipose tissue, an increase in TLDMA, and changes in serum adipocytokine levels. Further studies are needed to elucidate the insulin sensitizing mechanism of rosiglitazone on peripheral skeletal muscles.
  H. K. Won , K. J. Kim , B.W. Lee , E. S. Kang , B. S. Cha and H. C. Lee
  Aim To investigate whether the change in glycated albumin 3 weeks after initiating anti-diabetes treatment (oral hypoglycaemic agent or insulin) could predict the corresponding change in HbA1c 3 months later in Korean patients with Type 2 diabetes. Methods A total of 140 patients were enrolled into two groups: group I (insulin-based; n = 100) and group II (oral hypoglycaemic agent-based; n = 40). Both glycated albumin and HbA1c levels were measured as ‘glucose control markers’ during hospitalization. Glycated albumin was measured again at 3 weeks (first visit) after the initial measurement, and HbA1c was measured at 3 months (second visit) after the initial measurement.. The change in glucose control marker was defined as 100 x (follow-up glucose control marker − hospital glucose control marker)/hospital glucose control marker. Results In both groups, the change in glycated albumin at the first visit and in HbA1c at the second visit showed a moderate linear relationship (r = 0.735; P < 0.01). In group II (r = 0.778; P < 0.01), a slightly stronger linear relationship was demonstrated than in group I (r = 0.738; P < 0.001); however, there was no statistically significant difference between the two groups. A correlation coefficient between the change in glycated albumin and HbA1c was not affected by sex, age, BMI, haemoglobin, serum creatinine or albumin. Conclusion The reduction in glycated albumin 3 weeks after the initiation of treatment corresponded with the reduction in HbA1c 3 months after starting treatment in both the group treated with a oral hypoglycaemic agent and the insulin-treated group of Korean patients with Type 2 diabetes.
  H. C Lin , C. H Tang and H. C. Lee

Using a nationwide population-based dataset, the aim of the present study was to investigate the association between paternal schizophrenia and the risk of low birthweight (LBW). This study linked the 2001 Taiwan National Health Insurance Research Dataset with Taiwan's birth and death certificate registries. In total, 220 465 singleton live births were included. The key dependent variable was whether or not an infant's father was diagnosed with schizophrenia, while the independent variable of interest was whether an infant had LBW. Multivariate logistic regression analysis was performed to explore the relationship between paternal schizophrenia and the risk of LBW, after adjusting for the infant and parents’ characteristics. The results show that infants whose fathers had schizophrenia were more likely to have LBW than those whose fathers did not (12.6% vs 8.0%). Infants whose fathers had schizophrenia were found to be 1.58 (95% confidence interval = 1.10–2.52, P < .05) times more likely to have LBW than their counterparts whose fathers did not have schizophrenia, following adjustment for gestational week at birth, parity, paternal age and highest educational level, family monthly incomes, and marital status. We conclude that the offspring whose fathers had a diagnosis of schizophrenia had increased risk of LBW compared with those whose fathers had no schizophrenia. This finding paves the way for further studies and suggests that there may be potential benefit to early intervention to prevent LBW in pregnant women with husbands with schizophrenia.

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