Browsing by Author "Lin, C. -S."

Now showing 1 - 9 of 9

ACE2 associated with pulmonary inflammation and MMPs activities in acute lung injury by bleomycin treatment
(2015-07-01)
Hsieh, W. -Y.
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Chuang, W. -H.
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Liu, F. -C.
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Lin, C. -S.
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生物科技學系
Angiotensin converting enzyme II deficiency accelerates the progression of COPD via irregular signaling STAT3 phosphorylation
(2015-07-01)
Hung, Y. -H.
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Hsieh, W. -Y.
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Hsieh, J. -S.
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Wu, C. -L.
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Lin, C. -S.
Detection of Escherichia coli O157 : H7 using An nanoparticles mediator on an electrochemical amperometric immunobiosensor
(2007)
Chen, S. -H.
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Lin, Y. -H.
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Chuang, Y. -C.
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Lin, Y. -R.
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Chang, C. A.
Detection of Escherichia coli O157 : H7 using Au nanoparticles mediator on an electrochemical amperometric immunobiosensor
(2007-01-01)
Chen, S. -H.
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Lin, Y. -H.
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Chuang, Y. -C.
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Lin, Y. -R.
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Chang, C. A.
Detection of Escherichia coli O157 : H7 using Au nanoparticles mediator on an electrochemical amperometric immunobiosensor
(2007)
Chen, S. -H.
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Lin, Y. -H.
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Chuang, Y. -C.
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Lin, Y. -R.
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Chang, C. A.
Estrogen receptor alpha-351 XbaI*G and -397 PvuII*C-related genotypes and alleles are associated with higher susceptibilities of endometriosis and leiomyoma
(2007-02-01)
Hsieh, Y. -Y.
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Wang, Y. -K.
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Chang, C. -C.
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Lin, C. -S.
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生物科技學系
Endometriosis and leiomyoma are both common estrogen-related gynaecological diseases. We aimed to elucidate the association of estrogen receptor alpha (ER alpha)-351 A > G (XbaI) and -397 T > C (PvuII) gene polymorphisms with endometriosis and leiomyoma. Women were divided into three groups: (i) severe endometriosis (n = 112), (ii) leiomyoma (n = 106) and (iii) normal controls (n = 110). Genomic DNA was obtained from peripheral leukocytes. ER alpha-351 A/G XbaI and -397 T/C PvuII polymorphisms were assayed by the method of PCR and restriction fragment length polymorphism (RFLP). Genotypes and allelic frequencies in each group were compared. The genotype/allele frequencies of ER alpha-351 and -397 polymorphisms in endometriosis or leiomyoma groups were different from those of normal controls. ER alpha mutant-related genotypes/alleles (-351G and -397C) presented higher percentages in the endometriosis/leiomyoma population compared with normal controls. Proportions of ER alpha-351 AA/AG/GG genotypes and A/G alleles in each group were (i) 26.8/57.1/16.1 and 55.4/44.6%; (ii) 19.8/52.8/27.4 and 46.2/53.8% and (iii) 33.6/64.6/1.8 and 65.9/34.1%. Proportions of ER alpha-397 TT/TC/CC genotypes and T/C alleles in each group were (i) 24.1/60.7/15.2 and 54.5/45.5%; (ii) 23.6/70.8/5.6 and 59/41% and (iii) 54.5/40/5.5 and 74.5/25.5%. We concluded that ER alpha-351 XbaI*G- and -397 PvuII*C-related genotypes/alleles were correlated with higher susceptibilities of endometriosis or leiomyoma, which might be associated with related pathogeneses.
Loss Of Angiotensin-Converting Enzyme 2 (ace2) Increases Pulmonary Inflammation And Gelatinase Activity In The Early Stages Of Chronic Obstructive Pulmonary Disease
(2014)
Hung, Y. -H.
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Hsieh, W. -Y.
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Liu, F. -C.
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Hsieh, J. -S.
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Yeh, F. -Y.
Mmp-2 And Mmp-9 Promoter Polymorphisms And Pleural Gelatinase Activity In The Patients With Pleural Effusions
(2014)
Liu, F. -C.
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Hsieh, W. -Y.
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Hung, Y. -H.
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Chen, M. -Y.
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Wu, C. -L.
Regulatory mechanisms of atrial fibrotic remodeling in atrial fibrillation
(2008-05-01)
Lin, C. -S.
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Pan, C. -H.
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生物科技學系
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Department of Biological Science and Technology
Electrical, contractile and structural remodeling have been characterized in atrial fibrillation (AF), and the latter is considered to be the major contributor to AF persistence. Recent data show that interstitial fibrosis can predispose to atrial conduction impairment and AF induction. The interplay between cardiac matrix metalloproteinases (MMPs) and their endogenous inhibitors, tissue inhibitors of MMPs (TIMPs), is thought to be critical in atrial extracellular matrix (ECM) metabolism. At the molecular level, angiotensin II, transforming growth factor-beta 1, inflammation and oxidative stress are particularly important for ECM dysregulation and atrial fibrotic remodeling in AF. Therefore, we review recent advances in the understanding of the atrial fibrotic process, the major downstream components in this remodeling process, and the expression and regulation of MMPs and TIMPs. We also describe the activation of bioactive molecules in both clinical studies and animal models to modulate MMPs and TIMPs and their effects on atrial fibrosis in AF.