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Search Results: 1 - 10 of 132438 matches for " Yu-Huei Liu "
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Involvement of Prohibitin Upregulation in Abrin-Triggered Apoptosis
Yu-Huei Liu,Konan Peck,Jung-Yaw Lin
Evidence-Based Complementary and Alternative Medicine , 2012, DOI: 10.1155/2012/605154
Abstract: Abrin (ABR), a protein purified from the seeds of Abrus precatorius, induces apoptosis in various types of cancer cells. However, the detailed mechanism remains largely uncharacterized. By using a cDNA microarray platform, we determined that prohibitin (PHB), a tumor suppressor protein, is significantly upregulated in ABR-triggered apoptosis. ABR-induced upregulation of PHB is mediated by the stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/JNK) pathway, as demonstrated by chemical inhibitors. In addition, ABR significantly induced the expression of Bax as well as the activation of caspase-3 and poly(ADP-ribose) polymerase (PARP) in Jurkat T cells, whereas the reduction of PHB by specific RNA interference delayed ABR-triggered apoptosis through the proapoptotic genes examined. Moreover, our results also indicated that nuclear translocation of the PHB-p53 complex may play a role in the transcription of Bax. Collectively, our data show that PHB plays a role in ABR-induced apoptosis, which may be helpful for the development of diagnostic or therapeutic agents.
Association of IL12B polymorphisms with susceptibility to Graves ophthalmopathy in a Taiwan Chinese population
Liu Yu-Huei,Chen Ching-Chu,Liao Li-Ling,Wan Lei
Journal of Biomedical Science , 2012, DOI: 10.1186/1423-0127-19-97
Abstract: Background Interleukin 12B (IL12B) gene polymorphisms have been linked to several inflammatory diseases, but their role in the development of Graves ophthalmopathy (GO) in Graves disease (GD) patients is unclear. The purpose of this study was to investigate the disease association of IL12B single nucleotide polymorphisms (SNPs). Methods A Taiwan Chinese population comprising 200 GD patients with GO and 271 GD patients without GO was genotyped using an allele-specific extension and ligation method. Hardy-Weinberg equilibrium was estimated using the chi-square test. Allele and genotype frequencies were compared between GD patients with and without GO using the chi-square test. Results The genotype and allele frequencies of examined SNPs did not differ between GD patients with and without GO. Although the genotype distribution remained nonsignificant in the sex-stratified analyses, the frequency of the T allele at SNP rs1003199 was significantly higher in patients with GO in the male cohort (P = 6.00 × 10-3). In addition, haplotypes of IL12B may be used to predict the risk of GO (P = 1.70 × 10-2); however, we could not prove the statistical significance of analysis after applying the Bonferroni correction. Conclusions Our results provide new information that the examined IL12B gene polymorphisms may be associated with susceptibility to GO in the Taiwan Chinese population in a sex-specific manner. This conclusion requires further investigation.
Horizon news function and quasi-local energy-momentum flux near black hole
Yu-Huei Wu
Physics , 2007,
Abstract: From the 'quasi-local' definition of horizons, e.g. isolated horizon and dynamical horizon, the consequence quasi-local energy-momentum near horizons can be observed by using the idea of frame alignment. In particular, we find the horizon news function from the asymptotic expansion near horizons and use this to describe the gravitational flux and change of mass of a black hole.
Dual Effect of a Polymorphism in the Macrophage Migration Inhibitory Factor Gene Is Associated with New-Onset Graves Disease in a Taiwanese Chinese Population
Yu-Huei Liu, Ching-Chu Chen, Chen-Ming Yang, Yi-Ju Chen, Fuu-Jen Tsai
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0092849
Abstract: Graves disease (GD) is an autoimmune disease. Macrophage migration inhibitory factor (MIF) is a potent cytokine that plays an important role in the regulation of immune responses. Two polymorphisms in the promoter region of MIF, rs5844572 and rs755622, are known to affect MIF expression. The purpose of this study was to investigate the relationship between polymorphisms in the MIF gene promoter and the severity of GD. A total of 677 individuals, including 481 GD patients and 196 ethnically matched healthy controls, were genotyped to identify differences in the distribution of the MIF polymorphisms rs5844572 and rs755622. Although there were no significant differences in the allele or genotype distributions among patients with different grades of goiter in GD and healthy controls, the distribution of the C allele, especially C/C genotype, of the rs755622 single nucleotide polymorphism (SNP) in MIF, may be as a risk factor for goiter initiation whereas a protector against development of severe goiter in patients with untreated GD (p<0.05). A goiter-developmental model incorporating genetic (MIF SNP rs755622) and environmental risk factors (gender, radioiodine treatment, thyroid gland surgery and vitiligo) significantly increased the prediction accuracy. Further studies are required to address the role of MIF polymorphisms, as well as their association with other candidate genes, in GD.
Toll-like receptor gene polymorphisms are associated with susceptibility to graves' ophthalmopathy in Taiwan males
Wen-Ling Liao, Rong-Hsing Chen, Hui-Ju Lin, Yu-Huei Liu, Wen-Chi Chen, Yuhsin Tsai, Lei Wan, Fuu-Jen Tsai
BMC Medical Genetics , 2010, DOI: 10.1186/1471-2350-11-154
Abstract: 6 TLR-4 and 2 TLR-9 gene polymorphisms in 471 GD patients (200 patients with GO and 271 patients without GO) from a Taiwan Chinese population were evaluated.No statistically significant difference was observed in the genotypic and allelic frequencies of TLR-4 and TLR-9 gene polymorphisms between the GD patients with and without GO. However, sex-stratified analyses showed that the association between TLR-9 gene polymorphism and GO phenotype was more pronounced in the male patients. The odds ratios (ORs) was 2.11 (95% confidence interval [CI] = 1.14-3.91) for rs187084 AàG polymorphism and 1.97 (95% CI = 1.07-3.62) for rs352140 AàG polymorphism among the male patients. Increasing one G allele of rs287084 and one A allele of rs352140 increased the risk of GO (p values for trend tests were 0.0195 and 0.0345, respectively). Further, in haplotype analyses, the male patients carrying the GA haplotype had a higher risk of GO (odds ratio [OR] = 2.02, 95% confidence interval [CI] = 1.09-3.73) than those not carrying the GA haplotype.The present data suggest that TLR-9 gene polymorphisms were significantly associated with increased susceptibility of ophthalmopathy in male GD patients.Graves' disease (GD) is an organ-specific autoimmune thyroid disease, one of the manifestations of which is ophthalmopathy [1]. Graves' ophthalmopathy (GO) is characterized by inflammation and fat deposition in the eye muscles and the connective tissue surrounding the eye. It is known that multiple factors contribute to the etiology and severity of GD, including the host's genetic factors as well as environmental factors [2,3]. Female sex, old age, and smoking history are common risk factors for GD [4-8]. With regard to genetic factors, the classical major histocompatibility complex class II genes and cytotoxic T cell antigen-4 genes (CTLA-4) [9-11] have been consistently reported to be associated with GD. Also, there were published studies on association of GO and genes such as CD103 [12], CTLA-4
Association between copy number variation of complement component C4 and Graves' disease
Yu-Huei Liu, Lei Wan, Chwen-Tzuei Chang, Wen-Ling Liao, Wen-Chi Chen, Yuhsin Tsai, Chang-Hai Tsai, Fuu-Jen Tsai
Journal of Biomedical Science , 2011, DOI: 10.1186/1423-0127-18-71
Abstract: A case-control study including 624 patients with GD and 160 healthy individuals were enrolled. CNV of C4 isotypes (C4A and C4B) genes were performed by quantitative real-time polymerase chain reaction analysis. Statistical comparison and identification of CNV of total C4, C4 isotypes (C4A and C4B) and C4 polymorphisms were estimated according to the occurrence of GD and its associated clinical features.Individuals with 4, 2, and 2 copies of C4, C4A and C4B genes, especially those with A2B2 polymorphism may associate with the development of GD (p = 0.001, OR = 10.994, 95% CI: 6.277-19.255; p = 0.008, OR = 1.732, 95% CI: 1.190-2.520; p = 2.420 × 10-5, OR = 2.621, 95% CI: 1.791-3.835; and p = 1.395 × 10-4, OR = 2.671, 95% CI: 1.761-4.052, respectively). Although the distribution of copy number for total C4, C4 isotypes as well as C4 polymorphisms did not associate with the occurrence of goiter, nodular hyperplasia, GO and myxedema, <2 copies of C4A may associate with high risk toward vitiligo in patients with GD (p = 0.001, OR = 5.579, 95% CI: 1.659-18.763).These results may be further estimated for its clinical application on GD and the vitiligo in patients with GD.Graves' disease (GD) is an organ-specific autoimmune thyroid disease [1]. It has been known that multiple factors, including the host's genetic factors as well as environmental factors, contribute to the etiology and severity of GD [2,3]. However, other forms of variation that might affect gene expression should also be considered.A new paradigm in human genetics is high frequencies of interindividual variation in the copy number (CN) of specific genomic DNA segments. Copy number variation (CNV) loci often contain genes engaged in host-environment interactions, including those involved in immune functions, which results in susceptibility or resistance to autoimmune diseases [4-7], however, no significant association has been found between CNV and GD [6].Complement component C4 (C4), located on chromosome 6q
Effects of a Chinese Herbal Medicine, Guan-Jen-Huang (Aeginetia indica Linn.), on Renal Cancer Cell Growth and Metastasis
Yu-Huei Liu,Meng-Luen Li,Meng-Yu Hsu,Ya-Yueh Pang,I-Ling Chen,Ching-Kuei Chen,Sai-Wen Tang,Hsuan-Yuan Lin,Jung-Yaw Lin
Evidence-Based Complementary and Alternative Medicine , 2012, DOI: 10.1155/2012/935860
Abstract: Aeginetia indica Linn. (Guan-Jen-Huang, GJH), a traditional Chinese herb, has the potential to be an immunomodulatory agent. The purpose of this study was to explore the effect of GJH in the treatment of renal cancer. Concentration-effect curves for the influence of GJH on cellular proliferation showed a biphasic shape. Besides, GJH had a synergistic effect on cytotoxicity when combined with 5-fluorouracil (5-FU)which may be due to the alternation of the chemotherapeutic agent resistance-related genes and due to the synergistic effects on apoptosis. In addition, treatment with GJH extract markedly reduced 786-O cell adherence to human umbilical vein endothelial cells (HUVECs) and decreased 786-O cell migration and invasion. In a xenograft animal model, GJH extract had an inhibitory effect on tumor cell-induced metastasis. Moreover, western blot analysis showed that the expression of intercellular adhesion molecule-1 (ICAM-1) in 786-O cells was significantly decreased by treatment with GJH extract through inactivation of nuclear factor-κB (NF--κB). These results suggest that GJH extract has a synergistic effect on apoptosis induced by chemotherapeutic agents and an inhibitory effect on cell adhesion, migration, and invasion, providing evidence for the use of water-based extracts of GJH as novel alternative therapeutic agents in the treatment of human renal cancer.
Aqueous Extract of Paeonia suffruticosa Inhibits Migration and Metastasis of Renal Cell Carcinoma Cells via Suppressing VEGFR-3 Pathway
Shih-Chin Wang,Sai-Wen Tang,Sio-Hong Lam,Chung-Chieh Wang,Yu-Huei Liu,Hsuan-Yuan Lin,Shoei-Sheng Lee,Jung-Yaw Lin
Evidence-Based Complementary and Alternative Medicine , 2012, DOI: 10.1155/2012/409823
Abstract: Renal cell carcinoma (RCC) cells are characterized by strong drug resistance and high metastatic incidence. In this study, the effects of ten kinds of Chinese herbs on RCC cell migration and proliferation were examined. Aqueous extract of Paeonia suffruticosa (PS-A) exerted strong inhibitory effects on cancer cell migration, mobility, and invasion. The results of mouse xenograft experiments showed that the treatment of PS-A significantly suppressed tumor growth and pulmonary metastasis. We further found that PS-A markedly decreased expression of VEGF receptor-3 (VEGFR-3) and phosphorylation of FAK in RCC cells. Moreover, the activation of Rac-1, a modulator of cytoskeletal dynamics, was remarkably reduced by PS-A. Additionally, PS-A suppressed polymerization of actin filament as demonstrated by confocal microscopy analysis and decreased the ratio of F-actin to G-actin in RCC cells, suggesting that PS-A inhibits RCC cell migration through modulating VEGFR-3/FAK/Rac-1 pathway to disrupt actin filament polymerization. In conclusion, this research elucidates the effects and molecular mechanism for antimigration of PS-A on RCC cells and suggests PS-A to be a therapeutic or adjuvant strategy for the patients with aggressive RCC.
Association of phospholipase A2 receptor 1 polymorphisms with idiopathic membranous nephropathy in Chinese patients in Taiwan
Yu-Huei Liu, Cheng-Hsu Chen, Shih-Yin Chen, Ying-Ju Lin, Wen-Ling Liao, Chang-Hai Tsai, Lei Wan, Fuu-Jen Tsai
Journal of Biomedical Science , 2010, DOI: 10.1186/1423-0127-17-81
Abstract: Taiwanese-Chinese individuals (129 patients with IMN and 106 healthy controls) were enrolled in this study. The selected single nucleotide polymorphisms (SNPs) in PLA2R1 were genotyped by real-time polymerase chain reaction using TaqMan fluorescent probes, and were further confirmed by polymerase chain reaction-restriction fragment length polymorphism. The roles of the SNPs in disease progression were analyzed.Genotype distribution was significantly different between patients with IMN and controls for PLA2R1 SNP rs35771982 (p = 0.015). The frequency of G allele at rs35771982 was significantly higher in patients with IMN as compared with controls (p = 0.005). In addition, haplotypes of PLA2R1 may be used to predict the risk of IMN (p = 0.004). Haplotype H1 plays a role in an increased risk of IMN while haplotype H3 plays a protective role against this disease. None of these polymorphisms showed a significant and independent influence on the progression of IMN and the risk of end-stage renal failure and death (ESRF/death). High disease progression in patients having C/T genotype at rs6757188 and C/G genotype at rs35771982 were associated with a low rate of remission.Our results provide new evidence that genetic polymorphisms of PLA2R1 may be the underlying cause of IMN, and the polymorphisms revealed by this study warrant further investigation.Podocytes are highly specialized cells that play a crucial role in the glomerular filtration barrier [1,2]. Alterations in surface molecules of podocytes lead to the accumulation of antipodocytic antibodies on podocytes within the kidney, which leads to autoimmune response and cell damage [3]. When damage occurs, the interaction between immune-related factors and damaged cells can lead to foot process retraction, proteinuria, destruction of the filtration barrier, nephritis, and subsequently induction of end-stage renal failure and death (ESRF/death) [4,5].Accumulating evidence suggests that podocytes are the primary target of i
Folate Deficiency Triggers an Oxidative-Nitrosative Stress-Mediated Apoptotic Cell Death and Impedes Insulin Biosynthesis in RINm5F Pancreatic Islet β–Cells: Relevant to the Pathogenesis of Diabetes
Hung-Chih Hsu, Jeng-Fong Chiou, Yu-Huei Wang, Chia-Hui Chen, Shin-Yi Mau, Chun-Te Ho, Pey-Jium Chang, Tsan-Zon Liu, Ching-Hsein Chen
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0077931
Abstract: It has been postulated that folic acid (folate) deficiency (FD) may be a risk factor for the pathogenesis of a variety of oxidative stress-triggered chronic degenerative diseases including diabetes, however, the direct evidence to lend support to this hypothesis is scanty. For this reason, we set out to study if FD can trigger the apoptotic events in an insulin-producing pancreatic RINm5F islet β cells. When these cells were cultivated under FD condition, a time-dependent growth impediment was observed and the demise of these cells was demonstrated to be apoptotic in nature proceeding through a mitochondria-dependent pathway. In addition to evoke oxidative stress, FD condition could also trigger nitrosative stress through a NF-κB-dependent iNOS-mediated overproduction of nitric oxide (NO). The latter compound could then trigger depletion of endoplasmic reticulum (ER) calcium (Ca2+) store leading to cytosolic Ca2+ overload and caused ER stress as evidence by the activation of CHOP expression. Furthermore, FD-induced apoptosis of RINm5F cells was found to be correlated with a time-dependent depletion of intracellular gluthathione (GSH) and a severe down-regulation of Bcl-2 expression. Along the same vein, we also demonstrated that FD could severely impede RINm5F cells to synthesize insulin and their abilities to secret insulin in response to glucose stimulation were appreciably hampered. Even more importantly, we found that folate replenishment could not restore the ability of RINm5F cells to resynthesize insulin. Taken together, our data provide strong evidence to support the hypothesis that FD is a legitimate risk factor for the pathogenesis of diabetes.
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