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Article: Transient hemophagocytic activity in dengue immunopathogenesis.

Lei, Huan-Yao

Journal of the Formosan Medical Association = Taiwan yi zhi

2007 Volume 108, Issue 8, Page(s) 595–598

MeSH term(s)	Autoantibodies/immunology ; Dengue/complications ; Dengue/immunology ; Dengue Vaccines/adverse effects ; Humans ; Lymphohistiocytosis, Hemophagocytic/etiology
Chemical Substances	Autoantibodies ; Dengue Vaccines
Language	English
Publishing date	2007-11-05
Publishing country	Singapore
Document type	News ; Research Support, Non-U.S. Gov't
ZDB-ID	2096659-3
ISSN	1876-0821 ; 0929-6646
ISSN (online)	1876-0821
ISSN	0929-6646
DOI	10.1016/s0929-6646(09)60379-x
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Book: Dengue disease, 2008

Lei, Huan-Yao

2008

Author's details	editor, Huan-Yao Lei
Keywords	Dengue. ; Dengue viruses.
Language	English
Size	309 p. :, ill. ;, 22 cm.
Publisher	Research Signpost
Publishing place	Trivandrum
Document type	Book
ISBN	9788130802909 ; 8130802902
Database	NAL-Catalogue (AGRICOLA)

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Book: Dengue disease

Lei, Huan-Yao

2008

Author's details	editor, Huan-Yao Lei
MeSH term(s)	Dengue ; Dengue Virus/genetics
Language	English
Size	309 p. :, ill.
Publisher	Research Signpost
Publishing place	Kerala, India
Document type	Book
ISBN	9788130802909 ; 8130802902
Database	Catalogue of the US National Library of Medicine (NLM)

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Article ; Online: Lectin of Concanavalin A as an anti-hepatoma therapeutic agent.

Lei, Huan-Yao / Chang, Chih-Peng

Journal of biomedical science

2009 Volume 16, Page(s) 10

Abstract: Liver cancer is the predominant cause of cancer mortality in males of Southern China and Taiwan. The current therapy is not satisfactory, and more effective treatments are needed. In the search for new therapies for liver tumor, we found that ... ...

Abstract	Liver cancer is the predominant cause of cancer mortality in males of Southern China and Taiwan. The current therapy is not satisfactory, and more effective treatments are needed. In the search for new therapies for liver tumor, we found that Concanavalin A (Con A), a lectin from Jack bean seeds, can have a potent anti-hepatoma effect. Con A after binding to the mannose moiety on the cell membrane glycoprotein is internalized preferentially to the mitochondria. An autophagy is triggered which leads to cell death. Con A as a T cell mitogen subsequently activates the immune response in the liver and results in the eradication of the tumor in a murine in situ hepatoma model. The liver tumor nodule formation is inhibited by the CD8+ T cells, and a tumor antigen-specific immune memory is established during the hepatic inflammation. The dual properties (autophagic cytotoxicity and immunomodulation) via the specific carbohydrate binding let Con A exert a potent anti-hepatoma therapeutic effect. The novel mechanism of the Con A anti-hepatoma effect is discussed. The prototype of Con with an anti-hepatoma activity gives support to the search for other natural lectins as anti-cancer compounds.
MeSH term(s)	Animals ; Antigens, Neoplasm/metabolism ; Antineoplastic Agents/therapeutic use ; Autophagy/physiology ; Cancer Vaccines/therapeutic use ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/physiopathology ; Concanavalin A/therapeutic use ; Glycosylation ; Humans ; Liver Neoplasms/drug therapy ; Liver Neoplasms/physiopathology
Chemical Substances	Antigens, Neoplasm ; Antineoplastic Agents ; Cancer Vaccines ; Concanavalin A (11028-71-0)
Language	English
Publishing date	2009-01-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/1423-0127-16-10
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Article ; Online: Secretomic Analysis of Host-Pathogen Interactions Reveals That Elongation Factor-Tu Is a Potential Adherence Factor of Helicobacter pylori during Pathogenesis.

Chiu, Kuo-Hsun / Wang, Ling-Hui / Tsai, Tsung-Ting / Lei, Huan-Yao / Liao, Pao-Chi

Journal of proteome research

2017 Volume 16, Issue 1, Page(s) 264–273

Abstract: The secreted proteins of bacteria are usually accompanied by virulence factors, which can cause inflammation and damage host cells. Identifying the secretomes arising from the interactions of bacteria and host cells could therefore increase understanding ...

Abstract	The secreted proteins of bacteria are usually accompanied by virulence factors, which can cause inflammation and damage host cells. Identifying the secretomes arising from the interactions of bacteria and host cells could therefore increase understanding of the mechanisms during initial pathogenesis. The present study used a host-pathogen coculture system of Helicobacter pylori and monocytes (THP-1 cells) to investigate the secreted proteins associated with initial H. pylori pathogenesis. The secreted proteins from the conditioned media from H. pylori, THP-1 cells, and the coculture were collected and analyzed using SDS-PAGE and LC-MS/MS. Results indicated the presence of 15 overexpressed bands in the coculture. Thirty-one proteins were identified-11 were derived from THP-1 cells and 20 were derived from H. pylori. A potential adherence factor from H. pylori, elongation factor-Tu (EF-Tu), was selected for investigation of its biological function. Results from confocal microscopic and flow cytometric analyses indicated the contribution of EF-Tu to the binding ability of H. pylori in THP-1. The data demonstrated that fluorescence of EF-Tu on THP-1 cells increased after the addition of the H. pylori-conditioned medium. This study reports a novel secretory adherence factor in H. pylori, EF-Tu, and further elucidates mechanisms of H. pylori adaptation for host-pathogen interaction during pathogenesis.
MeSH term(s)	Amino Acid Sequence ; Bacterial Adhesion ; Bacterial Proteins/genetics ; Bacterial Proteins/secretion ; Cell Line ; Coculture Techniques ; Culture Media, Conditioned/chemistry ; Gene Expression Profiling ; Gene Expression Regulation ; Helicobacter pylori/genetics ; Helicobacter pylori/growth & development ; Helicobacter pylori/pathogenicity ; Host-Pathogen Interactions ; Humans ; Monocytes/metabolism ; Monocytes/microbiology ; Peptide Elongation Factor Tu/genetics ; Peptide Elongation Factor Tu/secretion ; Proteome/genetics ; Proteome/secretion ; Signal Transduction ; Virulence Factors/genetics ; Virulence Factors/metabolism
Chemical Substances	Bacterial Proteins ; Culture Media, Conditioned ; Proteome ; Virulence Factors ; Peptide Elongation Factor Tu (EC 3.6.1.-)
Language	English
Publishing date	2017-01-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2078618-9
ISSN	1535-3907 ; 1535-3893
ISSN (online)	1535-3907
ISSN	1535-3893
DOI	10.1021/acs.jproteome.6b00584
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Article: Secretomic Analysis of Host–Pathogen Interactions Reveals That Elongation Factor-Tu Is a Potential Adherence Factor of Helicobacter pylori during Pathogenesis

Chiu, Kuo-Hsun / Wang Ling-Hui / Tsai Tsung-Ting / Lei Huan-Yao / Liao Pao-Chi

Journal of Proteome Research. 2017 Jan. 06, v. 16, no. 1

2017

Abstract	The secreted proteins of bacteria are usually accompanied by virulence factors, which can cause inflammation and damage host cells. Identifying the secretomes arising from the interactions of bacteria and host cells could therefore increase understanding of the mechanisms during initial pathogenesis. The present study used a host–pathogen coculture system of Helicobacter pylori and monocytes (THP-1 cells) to investigate the secreted proteins associated with initial H. pylori pathogenesis. The secreted proteins from the conditioned media from H. pylori, THP-1 cells, and the coculture were collected and analyzed using SDS-PAGE and LC–MS/MS. Results indicated the presence of 15 overexpressed bands in the coculture. Thirty-one proteins were identified11 were derived from THP-1 cells and 20 were derived from H. pylori. A potential adherence factor from H. pylori, elongation factor-Tu (EF-Tu), was selected for investigation of its biological function. Results from confocal microscopic and flow cytometric analyses indicated the contribution of EF-Tu to the binding ability of H. pylori in THP-1. The data demonstrated that fluorescence of EF-Tu on THP-1 cells increased after the addition of the H. pylori-conditioned medium. This study reports a novel secretory adherence factor in H. pylori, EF-Tu, and further elucidates mechanisms of H. pylori adaptation for host–pathogen interaction during pathogenesis.
Keywords	Helicobacter pylori ; bacteria ; binding capacity ; coculture ; flow cytometry ; fluorescence ; host-pathogen relationships ; inflammation ; monocytes ; pathogenesis ; polyacrylamide gel electrophoresis ; protein secretion ; proteins ; proteome ; virulence
Language	English
Dates of publication	2017-0106
Size	p. 264-273.
Publishing place	American Chemical Society
Document type	Article
ZDB-ID	2078618-9
ISSN	1535-3907 ; 1535-3893
ISSN (online)	1535-3907
ISSN	1535-3893
DOI	10.1021%2Facs.jproteome.6b00584
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Cytokine immunopathogenesis of enterovirus 71 brain stem encephalitis.

Wang, Shih-Min / Lei, Huan-Yao / Liu, Ching-Chuan

Clinical & developmental immunology

2012 Volume 2012, Page(s) 876241

Abstract: Enterovirus 71 (EV71) is one of the most important causes of herpangina and hand, foot, and mouth disease. It can also cause severe complications of the central nervous system (CNS). Brain stem encephalitis with pulmonary edema is the severe complication ...

Abstract	Enterovirus 71 (EV71) is one of the most important causes of herpangina and hand, foot, and mouth disease. It can also cause severe complications of the central nervous system (CNS). Brain stem encephalitis with pulmonary edema is the severe complication that can lead to death. EV71 replicates in leukocytes, endothelial cells, and dendritic cells resulting in the production of immune and inflammatory mediators that shape innate and acquired immune responses and the complications of disease. Cytokines, as a part of innate immunity, favor the development of antiviral and Th1 immune responses. Cytokines and chemokines play an important role in the pathogenesis EV71 brain stem encephalitis. Both the CNS and the systemic inflammatory responses to infection play important, but distinctly different, roles in the pathogenesis of EV71 pulmonary edema. Administration of intravenous immunoglobulin and milrinone, a phosphodiesterase inhibitor, has been shown to modulate inflammation, to reduce sympathetic overactivity, and to improve survival in patients with EV71 autonomic nervous system dysregulation and pulmonary edema.
MeSH term(s)	Brain Stem/pathology ; Brain Stem/virology ; Cytokines/blood ; Cytokines/cerebrospinal fluid ; Cytokines/metabolism ; Encephalitis, Viral/diagnosis ; Encephalitis, Viral/immunology ; Encephalitis, Viral/therapy ; Enterovirus A, Human/immunology ; Enterovirus A, Human/pathogenicity ; Enterovirus Infections/diagnosis ; Enterovirus Infections/immunology ; Enterovirus Infections/therapy ; Humans ; Immunoglobulins, Intravenous/therapeutic use ; Immunomodulation
Chemical Substances	Cytokines ; Immunoglobulins, Intravenous
Keywords	covid19
Language	English
Publishing date	2012-08-23
Publishing country	Egypt
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2119646-1
ISSN	1740-2530 ; 1740-2522
ISSN (online)	1740-2530
ISSN	1740-2522
DOI	10.1155/2012/876241
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Article ; Online: Lectin of Concanavalin A as an anti-hepatoma therapeutic agent

Lei Huan-Yao / Chang Chih-Peng

Journal of Biomedical Science, Vol 16, Iss 1, p

2009 Volume 10

Abstract: Abstract Liver cancer is the predominant cause of cancer mortality in males of Southern China and Taiwan. The current therapy is not satisfactory, and more effective treatments are needed. In the search for new therapies for liver tumor, we found that ... ...

Abstract	Abstract Liver cancer is the predominant cause of cancer mortality in males of Southern China and Taiwan. The current therapy is not satisfactory, and more effective treatments are needed. In the search for new therapies for liver tumor, we found that Concanavalin A (Con A), a lectin from Jack bean seeds, can have a potent anti-hepatoma effect. Con A after binding to the mannose moiety on the cell membrane glycoprotein is internalized preferentially to the mitochondria. An autophagy is triggered which leads to cell death. Con A as a T cell mitogen subsequently activates the immune response in the liver and results in the eradication of the tumor in a murine in situ hepatoma model. The liver tumor nodule formation is inhibited by the CD8 + T cells, and a tumor antigen-specific immune memory is established during the hepatic inflammation. The dual properties (autophagic cytotoxicity and immunomodulation) via the specific carbohydrate binding let Con A exert a potent anti-hepatoma therapeutic effect. The novel mechanism of the Con A anti-hepatoma effect is discussed. The prototype of Con with an anti-hepatoma activity gives support to the search for other natural lectins as anti-cancer compounds.
Keywords	Medicine ; R
Subject code	610
Language	English
Publishing date	2009-01-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Induction of autophagy by concanavalin A and its application in anti-tumor therapy.

Lei, Huan-Yao / Chang, Chih-Peng

Autophagy

2007 Volume 3, Issue 4, Page(s) 402–404

Abstract: Concanavalin A (Con A), a lectin from Jack bean seeds that, once bound to the mannose moiety on the cell membrane glycoprotein, is internalized preferentially to the mitochondria. A BNIP3-mediated mitochondria autophagy is then induced, and causes the ... ...

Abstract	Concanavalin A (Con A), a lectin from Jack bean seeds that, once bound to the mannose moiety on the cell membrane glycoprotein, is internalized preferentially to the mitochondria. A BNIP3-mediated mitochondria autophagy is then induced, and causes the tumor cells to undergo autophagic cell death. Con A is also a T cell mitogen that can induce autoimmune hepatitis in mice. Because of the dual properties (autophagic cytotoxicity and immunomodulation) via the specific mannose binding, Con A can exert a potent anti-hepatoma therapeutic effect by inhibiting tumor nodule formation in the liver and prolonging the survival of the tumor-bearing mice. The anti-tumor effect is primarily mediated by activated CD8(+) T cells, and will also establish a tumor antigen-specific immune memory during the hepatic inflammation. This finding provides a novel mechanism in which Con A can be used as an anti-hepatoma agent, and also gives support for the search for natural lectins as anti-cancer compounds.
MeSH term(s)	Animals ; Autophagy/drug effects ; Carcinoma, Hepatocellular/drug therapy ; Concanavalin A/pharmacology ; Concanavalin A/therapeutic use ; Liver Neoplasms/drug therapy ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mitogens/pharmacology ; Mitogens/therapeutic use
Chemical Substances	Mitogens ; Concanavalin A (11028-71-0)
Language	English
Publishing date	2007-07-13
Publishing country	United States
Document type	Comment ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.4161/auto.4280
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Article ; Online: Concanavalin A/IFN-gamma triggers autophagy-related necrotic hepatocyte death through IRGM1-mediated lysosomal membrane disruption.

Chang, Chih-Peng / Yang, Ming-Chen / Lei, Huan-Yao

PloS one

2011 Volume 6, Issue 12, Page(s) e28323

Abstract: Interferon-gamma (IFN-γ), a potent Th1 cytokine with multiple biological functions, can induce autophagy to enhance the clearance of the invading microorganism or cause cell death. We have reported that Concanavalin A (Con A) can cause autophagic cell ... ...

Abstract	Interferon-gamma (IFN-γ), a potent Th1 cytokine with multiple biological functions, can induce autophagy to enhance the clearance of the invading microorganism or cause cell death. We have reported that Concanavalin A (Con A) can cause autophagic cell death in hepatocytes and induce both T cell-dependent and -independent acute hepatitis in immunocompetent and immunodeficient mice, respectively. Although IFN-γ is known to enhance liver injury in Con A-induced hepatitis, its role in autophagy-related hepatocyte death is not clear. In this study we report that IFN-γ can enhance Con A-induced autophagic flux and cell death in hepatoma cell lines. A necrotic cell death with increased lysosomal membrane permeabilization (LMP) is observed in Con A-treated hepatoma cells in the presence of IFN-γ. Cathepsin B and L were released from lysosomes to cause cell death. Furthermore, IFN-γ induces immunity related GTPase family M member 1(IRGM1) translocation to lysosomes and prolongs its activity in Con A-treated hepatoma cells. Knockdown of IRGM1 inhibits the IFN-γ/Con A-induced LMP change and cell death. Furthermore, IFN-γ(-/-) mice are resistant to Con A-induced autophagy-associated necrotic hepatocyte death. We conclude that IFN-γ enhances Con A-induced autophagic flux and causes an IRGM1-dependent lysosome-mediated necrotic cell death in hepatocytes.
MeSH term(s)	Animals ; Autophagy ; Carcinoma, Hepatocellular/metabolism ; Cathepsin B/metabolism ; Cathepsin L/metabolism ; Cell Line, Tumor ; Cell Membrane/metabolism ; Concanavalin A/metabolism ; Endocytosis ; GTP-Binding Proteins/metabolism ; Hep G2 Cells ; Hepatocytes/cytology ; Humans ; Interferon-gamma/metabolism ; Liver Neoplasms/metabolism ; Lysosomes/metabolism ; Mice ; Mice, Inbred BALB C ; Necrosis ; Permeability
Chemical Substances	Ifi1 protein, mouse ; Concanavalin A (11028-71-0) ; Interferon-gamma (82115-62-6) ; Cathepsin B (EC 3.4.22.1) ; Cathepsin L (EC 3.4.22.15) ; GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2011-12-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0028323
Database	MEDical Literature Analysis and Retrieval System OnLINE

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