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Molecular Mimicry: Infection Inducing Autoimmune Disease - Michael B. A. Oldstone
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Molecular Mimicry: Infection Inducing Autoimmune Disease - gebunden oder broschiert

2003, ISBN: 9783540255970

ID: 9783540255970

The purpose of this review is to examine the potential role of molecular mimicry in the pathogenesis of human T-lymphotropic virus type 1 ((HTLV- 1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP)). Comp- hensive reviews on the pathogenic mechanisms of HTLV-1-associated human diseases are available throughout the medical literature (Bangham 2000,, 2003 Barmak et al. 2003 Jacobson 2002 Levin and Jacobson 1997 Nagai and Osame 2003 Osame 2002). Approximately 25 years ago the rst human retrovirus, HTLV-1, was isolated (Poeisz et al. 1980). Subsequently, infection with HTLV-1 was shown to cause adult T-cell leukemia (ATL) and HAM/TSP (Gessain et al. 1985 McFarlin and Blattner 1991 Osame et al. 1986 Poeisz et al. 1980 Yoshida et al. 1987). HTLV-1 may infect up to 30% of people in endemic areas and 10 20 million people worldwide (Barmak et al. 2003 Edlich et al. 2000). However, only 1% 5% develop either ATL or HAM/TSP, the remainder being clinically asymptomatic carriers of HTLV-1 (Bangham 2000, 2003 Barmak et al. 2003 Jacobson 2002 Levin and Jacobson 1997 Nagai and Osame 2003 Osame 2002). Why infection with HTLV-1 causes ATL or HAM/TSP in some people while the vast majority of individuals are asymptomatic is largely - known. Some possible factors that may differentiate the asymptomatic from the diseased state include viral strain, human histocompatibility leukocyte antigen (HLA), viral load, and the immune response (Bangham 2000, 2003 Barmak et al. 2003 Jacobson 2002 Levin and Jacobson 1997 Nagai and Osame 2003 Nagai et al. 1998 Niewiesk et al. 1994 Osame 2002). Molecular Mimicry: Infection Inducing Autoimmune Disease: The purpose of this review is to examine the potential role of molecular mimicry in the pathogenesis of human T-lymphotropic virus type 1 ((HTLV- 1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP)). Comp- hensive reviews on the pathogenic mechanisms of HTLV-1-associated human diseases are available throughout the medical literature (Bangham 2000,, 2003 Barmak et al. 2003 Jacobson 2002 Levin and Jacobson 1997 Nagai and Osame 2003 Osame 2002). Approximately 25 years ago the rst human retrovirus, HTLV-1, was isolated (Poeisz et al. 1980). Subsequently, infection with HTLV-1 was shown to cause adult T-cell leukemia (ATL) and HAM/TSP (Gessain et al. 1985 McFarlin and Blattner 1991 Osame et al. 1986 Poeisz et al. 1980 Yoshida et al. 1987). HTLV-1 may infect up to 30% of people in endemic areas and 10 20 million people worldwide (Barmak et al. 2003 Edlich et al. 2000). However, only 1% 5% develop either ATL or HAM/TSP, the remainder being clinically asymptomatic carriers of HTLV-1 (Bangham 2000, 2003 Barmak et al. 2003 Jacobson 2002 Levin and Jacobson 1997 Nagai and Osame 2003 Osame 2002). Why infection with HTLV-1 causes ATL or HAM/TSP in some people while the vast majority of individuals are asymptomatic is largely - known. Some possible factors that may differentiate the asymptomatic from the diseased state include viral strain, human histocompatibility leukocyte antigen (HLA), viral load, and the immune response (Bangham 2000, 2003 Barmak et al. 2003 Jacobson 2002 Levin and Jacobson 1997 Nagai and Osame 2003 Nagai et al. 1998 Niewiesk et al. 1994 Osame 2002). Immunsystem - Immunologie - Immun - Autoimmunität Immunologie - Immun - Autoimmunität ( Immunsystem ) Immun - Autoimmunität ( Immunsystem - Immunologie ) Autoimmunität ( Immunsystem - Immunologie - Immun ) Infektion Biologie / Molekularbiologie Mole, Springer

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Molecular Mimicry: Infection Inducing Autoimmune Disease - Michael B. A. Oldstone
Vergriffenes Buch, derzeit bei uns nicht verfügbar.
(*)

Michael B. A. Oldstone:

Molecular Mimicry: Infection Inducing Autoimmune Disease - neues Buch

2003, ISBN: 9783540255970

ID: 106551132

The purpose of this review is to examine the potential role of molecular mimicry in the pathogenesis of human T-lymphotropic virus type 1 ((HTLV- 1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP)). Comp- hensive reviews on the pathogenic mechanisms of HTLV-1-associated human diseases are available throughout the medical literature (Bangham 2000,, 2003; Barmak et al. 2003; Jacobson 2002; Levin and Jacobson 1997; Nagai and Osame 2003; Osame 2002). Approximately 25 years ago the ?rst human retrovirus, HTLV-1, was isolated (Poeisz et al. 1980). Subsequently, infection with HTLV-1 was shown to cause adult T-cell leukemia (ATL) and HAM/TSP (Gessain et al. 1985; McFarlin and Blattner 1991; Osame et al. 1986; Poeisz et al. 1980; Yoshida et al. 1987). HTLV-1 may infect up to 30% of people in endemic areas and 10 20 million people worldwide (Barmak et al. 2003; Edlich et al. 2000). However, only 1% 5% develop either ATL or HAM/TSP, the remainder being clinically asymptomatic carriers of HTLV-1 (Bangham 2000, 2003; Barmak et al. 2003; Jacobson 2002; Levin and Jacobson 1997; Nagai and Osame 2003; Osame 2002). Why infection with HTLV-1 causes ATL or HAM/TSP in some people while the vast majority of individuals are asymptomatic is largely - known. Some possible factors that may differentiate the asymptomatic from the diseased state include viral strain, human histocompatibility leukocyte antigen (HLA), viral load, and the immune response (Bangham 2000, 2003; Barmak et al. 2003; Jacobson 2002; Levin and Jacobson 1997; Nagai and Osame 2003; Nagai et al. 1998; Niewiesk et al. 1994; Osame 2002). Molecular Mimicry: Infection Inducing Autoimmune Disease Buch (fremdspr.) Bücher>Fremdsprachige Bücher>Englische Bücher, Springer

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Molecular Mimicry: Infection Inducing Autoimmune Disease - Michael B. A. Oldstone
Vergriffenes Buch, derzeit bei uns nicht verfügbar.
(*)
Michael B. A. Oldstone:
Molecular Mimicry: Infection Inducing Autoimmune Disease - neues Buch

2005

ISBN: 9783540255970

[ED: Buch], [PU: Springer], Neuware - The purpose of this review is to examine the potential role of molecular mimicry in the pathogenesis of human T-lymphotropic virus type 1 ((HTLV- 1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP)). Comp- hensive reviews on the pathogenic mechanisms of HTLV-1-associated human diseases are available throughout the medical literature (Bangham 2000,, 2003 Barmak et al. 2003 Jacobson 2002 Levin and Jacobson 1997 Nagai and Osame 2003 Osame 2002). Approximately 25 years ago the rst human retrovirus, HTLV-1, was isolated (Poeisz et al. 1980). Subsequently, infection with HTLV-1 was shown to cause adult T-cell leukemia (ATL) and HAM/TSP (Gessain et al. 1985 McFarlin and Blattner 1991 Osame et al. 1986 Poeisz et al. 1980 Yoshida et al. 1987). HTLV-1 may infect up to 30% of people in endemic areas and 10-20 million people worldwide (Barmak et al. 2003 Edlich et al. 2000). However, only 1%-5% develop either ATL or HAM/TSP, the remainder being clinically asymptomatic carriers of HTLV-1 (Bangham 2000, 2003 Barmak et al. 2003 Jacobson 2002 Levin and Jacobson 1997 Nagai and Osame 2003 Osame 2002). Why infection with HTLV-1 causes ATL or HAM/TSP in some people while the vast majority of individuals are asymptomatic is largely - known. Some possible factors that may differentiate the asymptomatic from the diseased state include viral strain, human histocompatibility leukocyte antigen (HLA), viral load, and the immune response (Bangham 2000, 2003 Barmak et al. 2003 Jacobson 2002 Levin and Jacobson 1997 Nagai and Osame 2003 Nagai et al. 1998 Niewiesk et al. 1994 Osame 2002)., [SC: 0.00]

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Molecular Mimicry: Infection Inducing Autoimmune Disease - Michael B. A. Oldstone
Vergriffenes Buch, derzeit bei uns nicht verfügbar.
(*)
Michael B. A. Oldstone:
Molecular Mimicry: Infection Inducing Autoimmune Disease - neues Buch

3, ISBN: 9783540255970

[ED: Buch], [PU: Springer], Neuware - The purpose of this review is to examine the potential role of molecular mimicry in the pathogenesis of human T-lymphotropic virus type 1 ((HTLV- 1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP)). Comp- hensive reviews on the pathogenic mechanisms of HTLV-1-associated human diseases are available throughout the medical literature (Bangham 2000,, 2003 Barmak et al. 2003 Jacobson 2002 Levin and Jacobson 1997 Nagai and Osame 2003 Osame 2002). Approximately 25 years ago the rst human retrovirus, HTLV-1, was isolated (Poeisz et al. 1980). Subsequently, infection with HTLV-1 was shown to cause adult T-cell leukemia (ATL) and HAM/TSP (Gessain et al. 1985 McFarlin and Blattner 1991 Osame et al. 1986 Poeisz et al. 1980 Yoshida et al. 1987). HTLV-1 may infect up to 30% of people in endemic areas and 10-20 million people worldwide (Barmak et al. 2003 Edlich et al. 2000). However, only 1%-5% develop either ATL or HAM/TSP, the remainder being clinically asymptomatic carriers of HTLV-1 (Bangham 2000, 2003 Barmak et al. 2003 Jacobson 2002 Levin and Jacobson 1997 Nagai and Osame 2003 Osame 2002). Why infection with HTLV-1 causes ATL or HAM/TSP in some people while the vast majority of individuals are asymptomatic is largely - known. Some possible factors that may differentiate the asymptomatic from the diseased state include viral strain, human histocompatibility leukocyte antigen (HLA), viral load, and the immune response (Bangham 2000, 2003 Barmak et al. 2003 Jacobson 2002 Levin and Jacobson 1997 Nagai and Osame 2003 Nagai et al. 1998 Niewiesk et al. 1994 Osame 2002)., [SC: 1.40]

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Molecular Mimicry: Infection Inducing Autoimmune Disease - Michael B. A. Oldstone
Vergriffenes Buch, derzeit bei uns nicht verfügbar.
(*)
Michael B. A. Oldstone:
Molecular Mimicry: Infection Inducing Autoimmune Disease - neues Buch

ISBN: 9783540255970

[ED: Buch], [PU: Springer], Neuware - The conceptual basis for molecular mimicry was first defined in the early 1980s when monoclonal antibodies against viruses were also shown to react with non-viral host protein in this case, measles virus phosphoprotein cross-reacted with host cell cytokeratin, herpes simplex virus type 1 with host-cell vimentin and vaccinia virus with host-cell intermediate filaments. Following this discovery, others emerged, again at the clonal level, that T cell clones against proteins from a variety of infectious agents also reacted with host antigenic determinants. The clonal distinction was imperative for the initial definition of mimicry. At least 30 years prior to our initial description of molecular mimicry involving cross-reactions between numerous microbes, on the polyclonal antibody level, streptococcus was believed to react with renal glomeruli, heart and basal ganglia to account for the glomerulonephritis, heart and valvular disease and chorea, respectively. However, subsequent research showed that the nephritis was caused by immune complex deposits and the tissue damage they produced. Later, in 1990, the cross-reactivity of streptococcal antigen with myocardial antigens on a clonal level was uncovered. Hence, for both historical reasons and mechanistic understanding, it is best to provide evidence for cross-reactivity at the clonal level to prove that molecular mimicry exists., [SC: 1.40]

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Details zum Buch
Molecular Mimicry: Infection Inducing Autoimmune Disease
Autor:

Michael B. A. Oldstone

Titel:

Molecular Mimicry: Infection Inducing Autoimmune Disease

ISBN-Nummer:

9783540255970

The conceptual basis for molecular mimicry was first defined in the early 1980s when monoclonal antibodies against viruses were also shown to react with non-viral host protein; in this case, measles virus phosphoprotein cross-reacted with host cell cytokeratin, herpes simplex virus type 1 with host-cell vimentin and vaccinia virus with host-cell intermediate filaments. Following this discovery, others emerged, again at the clonal level, that T cell clones against proteins from a variety of infectious agents also reacted with host antigenic determinants. The clonal distinction was imperative for the initial definition of mimicry. At least 30 years prior to our initial description of molecular mimicry involving cross-reactions between numerous microbes, on the polyclonal antibody level, streptococcus was believed to react with renal glomeruli, heart and basal ganglia to account for the glomerulonephritis, heart and valvular disease and chorea, respectively. However, subsequent research showed that the nephritis was caused by immune complex deposits and the tissue damage they produced. Later, in 1990, the cross-reactivity of streptococcal antigen with myocardial antigens on a clonal level was uncovered. Hence, for both historical reasons and mechanistic understanding, it is best to provide evidence for cross-reactivity at the clonal level to prove that molecular mimicry exists.

Detailangaben zum Buch - Molecular Mimicry: Infection Inducing Autoimmune Disease


EAN (ISBN-13): 9783540255970
ISBN (ISBN-10): 3540255974
Gebundene Ausgabe
Erscheinungsjahr: 2005
Herausgeber: Springer-Verlag GmbH
168 Seiten
Gewicht: 0,471 kg
Sprache: eng/Englisch

Buch in der Datenbank seit 04.06.2007 21:14:56
Buch zuletzt gefunden am 09.03.2016 16:51:32
ISBN/EAN: 9783540255970

ISBN - alternative Schreibweisen:
3-540-25597-4, 978-3-540-25597-0

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