Browsing by Author "Wang, Chih-Hong"

Now showing 1 - 10 of 10

A simulated model for cycle time reduction by acquiring optimal lot size in semiconductor manufacturing
(2007-10-01)
Wang, Chia-Nan
;
Wang, Chih-Hong
;
工業工程與管理學系
;
Department of Industrial Engineering and Management
Cycle time reduction is one of the most critical issues in gaining a competitive advantage in wafer fabrication. People widely recognize that lot size reduction can effectively shorten production cycle time. Due to the constraints of conventional equipment and technology, this concept has not been widely applied in wafer fabrication. However, because of the invention of new technology, restrictions on equipment and processes have been reduced in recent years. Wafer lot sizing policy thus becomes an alternative in reducing cycle time. This study develops a simulation model which can acquire optimal lot size to reduce cycle time under different bottleneck loading environments. Simulation experiments based on realistic data from a Taiwan semiconductor fabricator are conducted. Sensitivity analyses of lot sizing impact upon cycle time reduction in wafer fabrication are performed as well. Numerical results demonstrate that the proposed model is sound in acquiring the optimal lot size for cycle time reduction in different loading scenarios. The model can help fabrication managers obtain optimal lot sizes in different bottleneck situations to effectively reduce product cycle time.
Altered plasma acylcarnitine and amino acid profiles in type 2 diabetic kidney disease
(2016-06)
Chuang, Wen-Han
;
Arundhathi, Arivajiagane
;
Lu, Ching
;
Chen, Chang-Chiang
;
Wu, Wan-Chen
Introduction Dysregulation of acylcarnitines (AcylCNs) and amino acids metabolism have implicated in abnormality of fatty acid oxidation in type 2 diabetes (T2D). However, it is not well known whether altered plasma AcylCN, and amino acid profiles are associated with albuminuria or diabetic nephropathy (DN) in T2D. Objective The aim of this study was to elucidate alterations in plasma levels of AcylCNs and amino acids with respect to the T2D patients with various stages of albuminuria. Methods We recruited 52 healthy subjects as control, and 156 T2D patients which were divided into 52 normoalbuminuria, 52 microalbuminuria, and 52 macroalbuminuria. Plasma 37 AcylCNs and 12 amino acids were analyzed by tandem mass spectrometry. Results We found that T2D with normoalbuminuria and microalbuminuria had lower shot-, medium-, and long-chain AcylCNs, whereas T2D with macroalbuminuria had higher short-and medium-chain AcylCNs and lower long-chain AcylCNs than healthy subjects. Moreover, estimated glomerular filtration rate (eGFR) was a negative, independent and significant predictor of albumin to creatinine ratio (ACR) levels (beta = -0.376, P < 0.001), whereas plasma Low-density lipoprotein cholesterol (LDL-C) was significantly and positively associated with ACR levels (beta = 0.169, P = 0.049). Furthermore, multivariate ordinal logistic regression analysis revealed that isobutyrylcarnitine (C4) was a positive, independent, and significant predictor of ACR levels with higher odds of having T2D patients with progression normoalbuminuria to microalbuminuria [OR = 9.93, 95 % CI (3.51-28.05), P < 0.001]. Conclusions The findings suggest that plasma C4 may serve as a potential biomarker for the early stages of DN.
Comparative microarray analyses of mono(2-ethylhexyl)phthalate impacts on fat cell bioenergetics and adipokine network
(2017-12-01)
Chiang, Huai-Chih
;
Wang, Chih-Hong
;
Yeh, Szu-Ching
;
Lin, Yi-Hua
;
Kuo, Ya-Ting
Cellular accumulation of mono(2-ethylhexyl)phthalate (MEHP) has been recently demonstrated to disturb fat cell energy metabolism; however, the underlying mechanism remained unclear. The study aimed to determine how MEHP influenced fat cell transcriptome and how the changes might contribute to bioenergetics. Because of the pivotal role of PPAR gamma in energy metabolism of fat cells, comparative microarray analysis of gene expression in 3T3-L1 adipocytes treated with both MEHP and rosiglitazone was performed. Pathway enrichment analysis and gene ontology (GO) enrichment analysis revealed that both treatments caused up-regulation of genes involved in PPAR signaling/energy metabolism-related pathways and down-regulation of genes related to adipokine/inflammation signals. MEHP/rosiglitazone-treated adipocytes exhibited increased levels of lipolysis, glucose uptake, and glycolysis; the gene expression profiles provided molecular basis for the functional changes. Moreover, MEHP was shown to induce nuclear translocation and activation of PPAR gamma. The similarity in gene expression and functional changes in response to MEHP and rosiglitazone suggested that MEHP influenced bioenergetics and adipokine network mainly via PPAR gamma. Importantly, adipokine levels in C57BL/6J mice with di(2-ethylhexyl)phthalate (DEHP) treatments provided in vivo evidence for microarray results. On the basis of correlation between gene expression and functional assays, possible involvements of genes in bioenergetics of MEHP-treated adipocytes were proposed.
Enhancing Early Stage of Hepatocellular Carcinoma: Does Correlate to MicroRNA 122 and miR196a Interaction?
(2019-01-01)
Susanto, Hendra
;
Wang, Chih-Hong
;
Aulanni'am, Aulanni'am
;
Handaya, Adeodatus Yuda
;
生物科技學系
Hepatocellular carcinoma (HCC) is a representative of almost 85-90% of liver cancer in the recent global incidence. HCC is the second leading cause of mortality in subjects with cancer. The higher prevalence of this disease significantly increased in the Asia Pacific region in the last decades. Fatty liver (steatosis) linked cirrhosis showed a substantial contribution to the acceleration of HCC in patients. Importantly, another primary inducer of fatty liver, a short non-coding RNA miR-122, and miR196a are the essential miRNAs that predicted enhance the progression of HCC in the younger age. However, the lack of information about HCC related liver-derived hormone and miRNA remains. This study was conducted by using miR-122(+/-)-miR-196 (+) to generate miR-122(-/-)-miR 196 (+). In the current data, the significant morphological alteration of the liver with the early formation of nodule-like in the surface area was observed. Based on the histological section, the chronic portal inflammation also occurred in the liver of this double genetic modification mouse model. In summary, the interaction of miR-122 and miR196a may accelerate liver fibrosis due to chronic inflammation within the liver progress to cirrhosis in the early stage of hepatocellular carcinoma.
Higher serum betatrophin level in type 2 diabetes subjects is associated with urinary albumin excretion and renal function
(2016-01-07)
Chen, Chang-Chiang
;
Susanto, Hendra
;
Chuang, Wen-Han
;
Liu, Ta-Yu
;
Wang, Chih-Hong
Background: Betatrophin is a newly identified liver-derived hormone that is associated with glucose homeostasis and lipid metabolism. Although dysregulated lipid metabolism results in diabetic nephropathy (DN) development in patients with type 2 diabetes mellitus (T2DM), it is not understood whether betatrophin is associated with urinary albumin excretion and renal function. Methods: Based on albumin/creatinine ratio (ACR), 109 T2DM patients were divided into normoalbuminuria (ACR < 30 mg/g), microalbuminuria (ACR between 30 and 300 mg/g), and macroalbuminuria (ACR > 300 mg/g). Serum betatrophin levels of 109 T2DM patients and 32 healthy subjects were determined by enzyme-linked immunosorbent assay (ELISA). Results: Serum level of betatrophin was significantly increased in T2DM patients with normoalbuminuria, microalbuminuria, and macroalbuminuria as compared with healthy subjects (P < 0.001). Serum betatrophin level was positively correlated with sex, duration of diabetes, systolic blood pressure (SBP), body mass index (BMI), ACR, and triglyceride, whereas it was inversely correlated with estimated glomerular filtration rate (eGFR), total cholesterol, and high-density lipoprotein cholesterol (HDL-C) (P < 0.001). Furthermore, multivariate regression analysis showed the betatrophin was significantly and positively independent with triglyceride and low-density lipoprotein cholesterol (LDL-C) (P < 0.05), whereas it was inversely independent with eGFR, total cholesterol, and low-density lipoprotein cholesterol (HDL-C) (P < 0.05). In addition, the betatrophin had higher odds of having DN [odds ratio (OR) = 5.65, 95 % confidence interval (CI) 2.17-14.57, P < 0.001]. Conclusion: Betatrophin is significantly increased in T2DM patients with different stages of albuminuria. Betatrophin may be a novel endocrine regulator involved in DN development.
Higher serum betatrophin level in type 2 diabetes subjects is associated with urinary albumin excretion and renal function (vol 15, pg 3, 2016)
(2017-04-26)
Chen, Chang-Chiang
;
Susanto, Hendra
;
Chuang, Wen-Han
;
Liu, Ta-Yu
;
Arundhathi, Arivajiagane
In vitro and in vivo imaging of peroxynitrite by a ratiometric boronatebased fluorescent probe
(2017-05-15)
Palanisamy, Sathyadevi
;
Wu, Pei-Yu
;
Wu, Shou-Cheng
;
Chen, Yu-Jen
;
Tzou, Shey-Cherng
Peroxynitrite (ONOO-) is an important species involved in many physiopathological processes. Progresses have been made in developing novel fluorescent probes to detect peroxynitrite with relatively high sensitivity and specificity. Herein, we report the synthesis, characterization and biological applications of a new boronate-based fluorescent probe, 4-MB. The studies showed that 4-MB exhibits a dual ratiometric and calorimetric response toward peroxynitrite due to ONOO--triggered oxidative reaction. A possible mechanism of the oxidation reaction was proposed and the reaction product was isolated and characterized using different spectroscopic methods. We have thoroughly demonstrated the utility of 4-MB for intracellular peroxynitrite imaging. Further, we showed that 4-MB can be potentially employed to visualize exogenous and endogenous peroxynitrite in RAW264.7 macrophages, EAhy926 cells, zebrafish and in live tissues from a high-fat diet-induced obese mouse model.
Increased serum levels of betatrophin in pancreatic cancer-associated diabetes
(2016-07-05)
Susanto, Hendra
;
Liu, Ta-Yu
;
Chen, Chang-Chiang
;
Purnomo, Jerry D. T.
;
Chen, Shu-Fan
Long-standing diabetes or glucose intolerance is recognized as a crucial event in the process of pancreatic cancer. Betatrophin, a novel liver-derived hormone, promotes beta-cell proliferation and improves glucose intolerance. However, the relationship between betatrophin and PDAC-associated diabetes is not fully understood. To evaluate the serum betatrophin levels in PDAC-associated diabetes, a total 105 Taiwanese subjects including 15 healthy subjects, and 12 patients having PDAC with normal glucose tolerance (PDAC-NGT), 12 patients having PC with impaired glucose tolerance (PDAC-IGT), and 66 patients having PC with diabetes mellitus (PDAC-DM) were enrolled for this study. Serum betatrophin and carbohydrate antigen 19-9 (CA19-9) levels were analyzed by enzyme-linked immunosorbent assay (ELISA). Compared to healthy subjects, PDAC patients had higher levels of betatrophin and CA19-9. Consistently, betatrophin protein was significantly expressed in pancreatic ductal of PDAC-associated DM patients using immunohistochemistry (IHC) method. Furthermore, multivariate regression analysis showed the betatrophin was significantly and positively independent with T category (beta = 0.605, P=0.010), serum albumin (beta = 0. 423, P=0.021), lipase (beta = 0.292, P=0.039), and blood urea nitrogen (BUN) (beta = 0.303, P=0.040). Further, the betatrophin was three folds of having PDAC-associated diabetes with the highest odds ratio [OR=3.39; 95% CI (1.20-9.57); P=0.021) and receiver operating characteristic (ROC) curve analysis showed that AUC value of betarophin was 0.853 which is slightly larger than AUC value of CA19-9 (0.792) in PDAC-DM patients. Interestingly, AUC value of betarophin plus CA19-9 was 0.988 in PDAC-DM patients. Therefore, betatrophin combined CA19-9 may serve as a potential biomarker for PDAC-associated diabetes.
Prorenin receptor acts as a potential molecular target for pancreatic ductal adenocarcinoma diagnosis
(2016-08-23)
Arundhathi, Arivajiagane
;
Chuang, Wen-Han
;
Chen, Jen-Kun
;
Wang, Shin-E
;
Shyr, Yi-Ming
Recent studies have implicated the prorenin receptor (PRR) is associated with pancreatic tumorigenesis. We therefore investigated the role of PRR in pancreatic tumorigenesis and assessed whether PRR can serve as a target for imaging diagnosis at early stages of PDAC. Here we show that aberrant expression of PRR in premalignant PanIN lesions, and human PDAC samples, and PDAC cell lines, particularly in Panc-1 cells. Interestingly, PRR expression was positively associated with PDAC progression. Moreover, overexpression of human PRR resulted in increased cell proliferation and decreased apoptosis, while knockdown of human PRR caused decreased cell proliferation and enhanced apoptosis in pancreatic cancer cells. We also observed that overexpression of human PRR enhanced MAPK and PI3K/Akt signaling pathways in PDAC cells, while knockdown of human PRR suppressed both of pathways. The confocal imaging analysis showed that human PRR was highly expressed in Panc-1, ASPC, and Miapaca cells, whereas BXPC-3, and HPAC cells had a significantly lower fluorescent signals. Consistently, the single-photon emission computed tomography (SPET/CT) showed that the uptake of anti-PRR labelled with I-125 was higher in Panc-1 and ASPC tumors-bearing mice after 96 hours injection. Importantly, tumors in pancreas of Pdx1-cre; LSL-Kras(G12D) mice had a significant increased PRR expression and accumulation of radioactivity at 96 h after injection. These data suggest that I-125-anti-PRR can detect the orthotopic tumors in Pdx1-cre; LSL-Kras(G12D) mice. Therefore, anti-PRR labelled with I-125 is a promising radiotracer for imaging diagnosis at early stages of pancreatic cancer.
The nonalcoholic fatty liver disease-like phenotype and lowered serum VLDL are associated with decreased expression and DNA hypermethylation of hepatic ApoB in male offspring of ApoE deficient mothers fed a with Western diet
(2020-03-01)
Chen, Hsiao-Chien
;
Chen, Yi-Zhen
;
Wang, Chih-Hong
;
Lin, Fu-Jung
;
生物科技學系
Increasing evidence indicates that the intra-uterine environment has consequences for later life. However, the mechanisms of this fetal programming remain unclear. We aimed to investigate the impact of diet-induced maternal hypercholesterolemia on the predisposition of offspring to nonalcoholic fatty liver diseases (NAFLD) and metabolic diseases and its underlying mechanisms. Female apolipoprotein (Apo) E-deficient mice were fed a control diet (CD) or high fat/high cholesterol Western-type diet (WD) before and throughout pregnancy and lactation, and their offspring were weaned onto a CD postnatally. Strikingly, male offspring of WD-fed dams developed glucose intolerance and decreased peripheral insulin sensitivity and exhibited hepatic steatosis. Hepatic steatosis could be attributed, at least in part, to increased hepatic lipogenesis in E18.5 embryos and decreased serum VLDL levels in adulthood. In addition, males born to WD-fed dams had lower serum ApoB levels and hepatic ApoB gene expression compared with males born to CD-fed dams. DNA methylation analysis revealed increased methylation of CpG dinucleotides on the promoter region of the ApoB genes in the livers of male offspring of WD-fed dams. Our findings suggest that maternal WD intake can exacerbate the development of NAFLD in male offspring potentially by affecting ApoB gene expression through epigenetic alterations. (C) 2019 Elsevier Inc. All rights reserved.