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Article ; Online: Antenatal corticosteroid therapy in late preterm delivery: a nationwide population-based retrospective study in Taiwan.

Liang, F-W / Tsai, H-F / Kuo, P-L / Tsai, P-Y

BJOG : an international journal of obstetrics and gynaecology

2021 Volume 128, Issue 9, Page(s) 1497–1502

Abstract: Objective: To investigate whether antenatal corticosteroid therapy improves neonatal and maternal outcomes in late preterm delivery.: Design: Population-based retrospective study.: Setting: The linkages of Taiwan's National Health Insurance ... ...

Abstract	Objective: To investigate whether antenatal corticosteroid therapy improves neonatal and maternal outcomes in late preterm delivery. Design: Population-based retrospective study. Setting: The linkages of Taiwan's National Health Insurance Research Database, National Birth Reporting Database, and the Taiwan Maternal and Child Health Database. Population: All births at risk for late preterm deliveries in Taiwan between 2004 and 2011. Methods: For every birth at risk for late preterm delivery, five controls randomly matched by maternal and gestational ages and birthweight were included. A conditional logistic regression analysis was applied for risk estimation, with births without corticosteroids as the reference group. Odds ratios were adjusted for caesarean section, parity, sex, gestational hypertension and gestational diabetes mellitus. Main outcome measures: Neonatal outcomes, maternal outcomes and the utilisation of healthcare services. Results: The outcomes of 5745 women treated with corticosteroids between 34 Conclusions: Antenatal corticosteroid therapy in women at risk of late preterm delivery may significantly reduce the need for respiratory support and glucose supply, and respiratory complication risk in neonates. Tweetable abstract: Antenatal corticosteroids in late preterm delivery reduced the risk of neonatal respiratory complications in Taiwan.
MeSH term(s)	Adrenal Cortex Hormones/administration & dosage ; Adrenal Cortex Hormones/adverse effects ; Adult ; Case-Control Studies ; Databases, Factual ; Female ; Humans ; Infant, Newborn ; Male ; Neonatal Sepsis/epidemiology ; Pregnancy ; Premature Birth/drug therapy ; Premature Birth/epidemiology ; Respiratory Distress Syndrome, Newborn/epidemiology ; Respiratory Distress Syndrome, Newborn/prevention & control ; Retrospective Studies ; Risk Assessment ; Taiwan/epidemiology
Chemical Substances	Adrenal Cortex Hormones
Language	English
Publishing date	2021-03-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2000931-8
ISSN	1471-0528 ; 0306-5456 ; 1470-0328
ISSN (online)	1471-0528
ISSN	0306-5456 ; 1470-0328
DOI	10.1111/1471-0528.16677
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Article ; Online: TRAIL suppresses gut inflammation and inhibits colitogeic T-cell activation in experimental colitis via an apoptosis-independent pathway.

Chyuan, I T / Tsai, H F / Wu, C S / Hsu, P N

Mucosal immunology

2019 Volume 12, Issue 4, Page(s) 980–989

Abstract: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces cell apoptosis by transducing apoptosis signals. Recently, accumulating evidence demonstrated that TRAIL regulates autoimmune inflammation and immune cell homeostasis in several ... ...

Abstract	Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces cell apoptosis by transducing apoptosis signals. Recently, accumulating evidence demonstrated that TRAIL regulates autoimmune inflammation and immune cell homeostasis in several autoimmune animal models, suggesting a novel immunoregulatory role of TRAIL in autoimmune diseases. However, the impact of TRAIL in inflammatory bowel disease is yet undefined. This study is to address the therapeutic effects and immunoregulatory role of TRAIL in autoimmune gut inflammation. We demonstrated herein that TRAIL significantly suppressed gut inflammation and reduced the severity of colitis in a dextran sodium sulfate (DSS)-induced colitis model. Suppression of gut inflammation was not due to induction of apoptosis in colonic T cells, dendritic cells, or epithelium cells by TRAIL. In contrast, TRAIL directly inhibited activation of colitogenic T cells and development of gut inflammation in an adoptive transfer-induced colitis model. The anti-inflammatory effects of TRAIL on colitis were abolished when T cells from TRAIL receptor (TRAIL-R) knockout mice were adoptively transferred, suggesting that TRAIL regulates autoreactive colitogenic T-cell activation in the development of gut inflammation. Our results demonstrate that TRAIL effectively inhibited colonic T-cell activation and suppressed autoimmune colitis, suggesting a potential therapeutic application of TRAIL in human inflammatory bowel disease.
MeSH term(s)	Animals ; Apoptosis ; Autoimmunity ; Colitis/etiology ; Colitis/metabolism ; Colitis/pathology ; Cytokines/metabolism ; Dextran Sulfate ; Disease Models, Animal ; Humans ; Inflammation Mediators/metabolism ; Intestinal Mucosa/immunology ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/pathology ; Lymphocyte Activation/immunology ; Mice ; Mice, Knockout ; Signal Transduction ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; TNF-Related Apoptosis-Inducing Ligand/metabolism
Chemical Substances	Cytokines ; Inflammation Mediators ; TNF-Related Apoptosis-Inducing Ligand ; Dextran Sulfate (9042-14-2)
Language	English
Publishing date	2019-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2411370-0
ISSN	1935-3456 ; 1933-0219
ISSN (online)	1935-3456
ISSN	1933-0219
DOI	10.1038/s41385-019-0168-y
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Article ; Online: Helicobacter pylori sensitizes TNF-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis in human gastric epithelial cells through regulation of FLIP.

Lin, W-C / Tsai, H-F / Liao, H-J / Tang, C-H / Wu, Y-Y / Hsu, P-I / Cheng, A-L / Hsu, P-N

Cell death & disease

2014 Volume 5, Page(s) e1109

Abstract: Helicobacter pylori (H. pylori) infection is associated with chronic gastritis, peptic ulcer and gastric cancer. Apoptosis induced by microbial infections is implicated in the pathogenesis of H. pylori infection. Here we show that human gastric ... ...

Abstract	Helicobacter pylori (H. pylori) infection is associated with chronic gastritis, peptic ulcer and gastric cancer. Apoptosis induced by microbial infections is implicated in the pathogenesis of H. pylori infection. Here we show that human gastric epithelial cells sensitized to H. pylori confer susceptibility to TRAIL-mediated apoptosis via modulation of death receptor signaling. Human gastric epithelial cells are intrinsically resistant to TRAIL-mediated apoptosis. The induction of TRAIL sensitivity by H. pylori is dependent on the activation of caspase-8 and its downstream pathway. H. pylori induces caspase-8 activation via enhanced assembly of the TRAIL death-inducing signaling complex (DISC) through downregulation of cellular FLICE-inhibitory protein (FLIP). Overexpression of FLIP abolished the H. pylori-induced TRAIL sensitivity in human gastric epithelial cells. Our study thus demonstrates that H. pylori induces sensitivity to TRAIL apoptosis by regulation of FLIP and assembly of DISC, which initiates caspase activation, resulting in the breakdown of resistance to apoptosis, and provides insight into the pathogenesis of gastric damage in Helicobacter infection. Modulation of host apoptosis signaling by bacterial interaction adds a new dimension to the pathogenesis of Helicobacter.
MeSH term(s)	Apoptosis/drug effects ; BH3 Interacting Domain Death Agonist Protein/metabolism ; CASP8 and FADD-Like Apoptosis Regulating Protein/metabolism ; Caspase 8/metabolism ; Cell Line, Tumor ; Cytochromes c/metabolism ; Death Domain Receptor Signaling Adaptor Proteins/metabolism ; Dose-Response Relationship, Drug ; Enzyme Activation ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Epithelial Cells/microbiology ; Epithelial Cells/pathology ; Gastric Mucosa/metabolism ; Helicobacter Infections/microbiology ; Helicobacter pylori/pathogenicity ; Humans ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondria/pathology ; Recombinant Proteins/pharmacology ; Signal Transduction/drug effects ; Stomach/drug effects ; Stomach/microbiology ; Stomach/pathology ; TNF-Related Apoptosis-Inducing Ligand/pharmacology ; Time Factors
Chemical Substances	BH3 Interacting Domain Death Agonist Protein ; BID protein, human ; CASP8 and FADD-Like Apoptosis Regulating Protein ; CFLAR protein, human ; Death Domain Receptor Signaling Adaptor Proteins ; Recombinant Proteins ; TNF-Related Apoptosis-Inducing Ligand ; TNFSF10 protein, human ; Cytochromes c (9007-43-6) ; CASP8 protein, human (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-)
Language	English
Publishing date	2014-03-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2014.81
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Article: Molecular biology and evolution of the grass endophytes.

Schardl, C L / Tsai, H F

Natural toxins

1992 Volume 1, Issue 3, Page(s) 171–184

Abstract: Acremonium coenophialum Morgan-Jones et W. Gams is a maternally transmitted fungal symbiont (endophyte) of the important forage grass Festuca arundinacea Schreb. (tall fescue), and provides biological protection and enhanced fitness to its host, but its ... ...

Abstract	Acremonium coenophialum Morgan-Jones et W. Gams is a maternally transmitted fungal symbiont (endophyte) of the important forage grass Festuca arundinacea Schreb. (tall fescue), and provides biological protection and enhanced fitness to its host, but its anti-mammalian ergot alkaloids detract from the usefulness of tall fescue as forage for livestock. Molecular genetic techniques and materials are being developed in order to specifically eliminate the gene(s) encoding the first enzyme in ergot alkaloid biosynthesis. These techniques will also facilitate basic studies, such as host-fungus compatibility or biosynthesis of insecticidal alkaloids. Molecular phylogenetics indicate that endophytes related to A. coenophialum have evolved on multiple occasions from strains of Epichloë typhina (Ascomycotina, Clavicipitaceae), for which the sexual cycle is known. These studies also reveal significant diversity among seedborne endophytes in individual grass species. Thus, the endophytes are an important source of biochemical potential and genetic diversity in grass-fungus symbiota.
MeSH term(s)	Acremonium/genetics ; Base Sequence ; Biological Evolution ; DNA, Complementary/genetics ; Gene Library ; Molecular Sequence Data ; Poaceae/microbiology ; Symbiosis ; Transformation, Genetic
Chemical Substances	DNA, Complementary
Language	English
Publishing date	1992
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1141442-x
ISSN	1056-9014
ISSN	1056-9014
DOI	10.1002/nt.2620010305
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Article: The determinant step in ergot alkaloid biosynthesis by an endophyte of perennial ryegrass

Wang, J / Machado, C / Panaccione, D.G / Tsai, H.F / Schardl, C.L

Fungal genetics and biology : FG & B. 2004 Feb., v. 41, no. 2

2004

Language	English
Dates of publication	2004-02
Size	p. 189-198.
Document type	Article
ZDB-ID	1319820-8
ISSN	1096-0937 ; 1087-1845 ; 0147-5975
ISSN (online)	1096-0937
ISSN	1087-1845 ; 0147-5975
Database	NAL-Catalogue (AGRICOLA)

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Article: Genetic polymorphism in milk fat globule-EGF factor 8 (MFG-E8) is associated with systemic lupus erythematosus in human.

Hu, C Y / Wu, C S / Tsai, H F / Chang, S K / Tsai, W I / Hsu, P N

Lupus

2009 Volume 18, Issue 8, Page(s) 676–681

Abstract: Milk fat globule-EGF factor 8 (MFG-E8) is a molecule implicated in phagocytic clearance of apoptotic cells by bridging between macrophages and apoptotic cells. Defects in MFG-E8 cause lupus-like disease in murine models. The aim of our study is to ... ...

Abstract	Milk fat globule-EGF factor 8 (MFG-E8) is a molecule implicated in phagocytic clearance of apoptotic cells by bridging between macrophages and apoptotic cells. Defects in MFG-E8 cause lupus-like disease in murine models. The aim of our study is to determine whether genetic variation in MFG-E8 predisposes human to systemic lupus erythematosus (SLE). A case-control study of MFG-E8 genetic polymorphism was performed on 147 SLE patients and 146 non-lupus control subjects. Single nucleotide polymorphisms (SNPs) in the coding sequence of human MFG-E8 gene were investigated. SNPs on MFG-E8 residues 3 (3(Arg or Ser)) and 76 (76(Leu or Met)) did not show genetic linkage. Genetic polymorphism on MFG-E8 residue 76 correlated significantly to SLE. The MFG-E8-76(Met) allele predisposed subjects to SLE in a recessive mode (odds ratio: 2.1, P = 0.020), while carriage of MFG-E8-76(Leu) were negatively associated with SLE. The MFG-E8 genotypic combinations with 3(Ser) and 76(Leu) showed the most pronounced protective effect on SLE when compared to the most predisposing genotype 3(Arg/Arg)-76(Met/Met) (OR: 0.29, P = 0.007). According to our result, MFG-E8 is associated with SLE predisposition in Taiwanese. Our study implicates that the impairment of phagocytic clearance of apoptotic cells through phosphotidylserine-dependent MFG-E8 system may lead to the development of human SLE.
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Animals ; Antigens, Surface/genetics ; Base Sequence ; Case-Control Studies ; DNA Mutational Analysis ; Female ; Genetic Predisposition to Disease ; Genotype ; Humans ; Lupus Erythematosus, Systemic/genetics ; Male ; Middle Aged ; Milk Proteins/genetics ; Molecular Sequence Data ; Phagocytes/metabolism ; Polymorphism, Genetic ; Young Adult
Chemical Substances	Antigens, Surface ; MFGE8 protein, human ; Milk Proteins
Language	English
Publishing date	2009-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1154407-7
ISSN	0961-2033
ISSN	0961-2033
DOI	10.1177/0961203309103027
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Article ; Online: Elevated serum decoy receptor 3 with enhanced T cell activation in systemic lupus erythematosus.

Lee, C-S / Hu, C-Y / Tsai, H-F / Wu, C-S / Hsieh, S-L / Liu, L-C / Hsu, P-N

Clinical and experimental immunology

2008 Volume 151, Issue 3, Page(s) 383–390

Abstract: Decoy receptor 3 (DcR3/TR6) is a decoy receptor for the Fas ligand (FasL) and can inhibit FasL-induced apoptosis. It has been reported recently that DcR3 can induce T cell activation via co-stimulation of T cells, suggesting that DcR3 may be involved in ... ...

Abstract	Decoy receptor 3 (DcR3/TR6) is a decoy receptor for the Fas ligand (FasL) and can inhibit FasL-induced apoptosis. It has been reported recently that DcR3 can induce T cell activation via co-stimulation of T cells, suggesting that DcR3 may be involved in the pathophysiology of autoimmune diseases. This study aims to analyse the serum DcR3 in patients with systemic lupus erythematosus (SLE) and to investigate the role of DcR3 in the pathogenesis of SLE. Significantly elevated serum DcR3 was observed in SLE patients, and the mean serum DcR3 level was significantly higher for those with active disease [SLE disease activity index (SLEDAI) >/= 10] compared with that in patients with inactive disease (SLEDAI < 10). In addition to reducing activation-induced cell death in activated T cells via neutralization of the FasL, soluble DcR3-Fc enhanced T cell proliferation and increased interleukin-2 and interferon-gamma production via co-stimulation of T cells. Moreover, enhanced T cell reactivity to DcR3-induced co-stimulation was demonstrated in lymphocytes from patients with SLE, suggesting the elevated serum DcR3 may associate with enhanced T cell activation in vivo. These findings are the first to demonstrate that serum DcR3 concentrations are increased in SLE patients, and this may imply a possible role of DcR3 in the pathogenesis of SLE via enhanced T cell hyperreactivity and reduced apoptosis in activated T cells.
MeSH term(s)	Adult ; Apoptosis/immunology ; Cell Proliferation ; Cells, Cultured ; Female ; Humans ; Lupus Erythematosus, Systemic/immunology ; Lymphocyte Activation/immunology ; Male ; Middle Aged ; Receptors, Tumor Necrosis Factor, Member 6b/blood ; Severity of Illness Index ; T-Lymphocytes/immunology
Chemical Substances	Receptors, Tumor Necrosis Factor, Member 6b ; TNFRSF6B protein, human
Language	English
Publishing date	2008-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218531-3
ISSN	1365-2249 ; 0009-9104 ; 0964-2536
ISSN (online)	1365-2249
ISSN	0009-9104 ; 0964-2536
DOI	10.1111/j.1365-2249.2007.03579.x
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Article: Elevated serum decoy receptor 3 with enhanced T cell activation in systemic lupus erythematosus

Lee, C.-S / Hu, C.-Y / Tsai, H.-F / Wu, C.-S / Hsieh, S.-L / Liu, L.-C / Hsu, P.-N

Clinical and experimental immunology. 2008 Mar., v. 151, no. 3

2008

Abstract	Decoy receptor 3 (DcR3/TR6) is a decoy receptor for the Fas ligand (FasL) and can inhibit FasL-induced apoptosis. It has been reported recently that DcR3 can induce T cell activation via co-stimulation of T cells, suggesting that DcR3 may be involved in the pathophysiology of autoimmune diseases. This study aims to analyse the serum DcR3 in patients with systemic lupus erythematosus (SLE) and to investigate the role of DcR3 in the pathogenesis of SLE. Significantly elevated serum DcR3 was observed in SLE patients, and the mean serum DcR3 level was significantly higher for those with active disease [SLE disease activity index (SLEDAI) >= 10] compared with that in patients with inactive disease (SLEDAI < 10). In addition to reducing activation-induced cell death in activated T cells via neutralization of the FasL, soluble DcR3-Fc enhanced T cell proliferation and increased interleukin-2 and interferon-γ production via co-stimulation of T cells. Moreover, enhanced T cell reactivity to DcR3-induced co-stimulation was demonstrated in lymphocytes from patients with SLE, suggesting the elevated serum DcR3 may associate with enhanced T cell activation in vivo. These findings are the first to demonstrate that serum DcR3 concentrations are increased in SLE patients, and this may imply a possible role of DcR3 in the pathogenesis of SLE via enhanced T cell hyperreactivity and reduced apoptosis in activated T cells.
Keywords	apoptosis
Language	English
Dates of publication	2008-03
Size	p. 383-390.
Publisher	Blackwell Publishing Ltd
Publishing place	Oxford, UK
Document type	Article
ZDB-ID	218531-3
ISSN	1365-2249 ; 0009-9104 ; 0964-2536
ISSN (online)	1365-2249
ISSN	0009-9104 ; 0964-2536
DOI	10.1111/j.1365-2249.2007.03579.x
Database	NAL-Catalogue (AGRICOLA)

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Article: Molecular biology and evolution of the grass endophytes

Schardl, C.L / Tsai, H.F

Natural toxins. 1992. v. 1 (3)

1992

Abstract	Acremonium coenophialum Morgan-Jones et W. Gams is a maternally transmitted fungal symbiont (endophyte) of the important forage grass Festuca arundinacea Schreb. (tall fescue), and provides biological protection and enhanced fitness to its host, but its anti-mammalian ergot alkaloids detract from the usefulness of tall fescue as forage for livestock. Molecular genetic techniques and materials are being developed in order to specifically eliminate the gene(s) encoding the first enzyme in ergot alkaloid biosynthesis. These techniques will also facilitate basic studies, such as host-fungus compatibility or biosynthesis of insecticidal alkaloids. Molecular phylogenetics indicate that endophytes related to A. coenophialum have evolved on multiple occasions from strains of Epichloe typhina (Ascomycotina, Clavicipitaceae), for which the sexual cycle is known. These studies also reveal significant diversity among seedborne endophytes in individual grass species. Thus, the endophytes are an important source of biochemical potential and genetic diversity in grass-fungus symbiota.
Keywords	Festuca arundinacea ; Neotyphodium coenophialum ; endophytes ; ergot alkaloids ; molecular biology ; genetic transformation ; phylogeny
Language	English
Size	p. 171-184.
Document type	Article
ZDB-ID	1141442-x
ISSN	1056-9014
ISSN	1056-9014
Database	NAL-Catalogue (AGRICOLA)

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Article: Genome sizes of Epichloe species and anamorphic hybrids

Kuldau, G.A / Tsai, H.F / Schardl, C.L

Mycologia. Sept/Oct 1999. v. 91 (5)

1999

Keywords	Deuteromycotina ; Neotyphodium coenophialum ; Epichloe ; interspecific hybridization ; hybrids ; karyotyping ; genomics ; Acremonium lolii
Language	English
Dates of publication	1999-09
Size	p. 776-782.
Document type	Article
ZDB-ID	281335-x
ISSN	1557-2536 ; 0027-5514
ISSN (online)	1557-2536
ISSN	0027-5514
Database	NAL-Catalogue (AGRICOLA)

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