Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes
The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely b...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Scott, Fraser W. [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
|---|
| Schlagwörter: |
|---|
| Umfang: |
16 |
|---|
| Übergeordnetes Werk: |
Enthalten in: Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties - Muthuraja, A. ELSEVIER, 2015, the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research, New York, NY |
|---|---|
| Übergeordnetes Werk: |
volume:179 ; year:2017 ; pages:183-198 ; extent:16 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.trsl.2016.09.001 |
|---|
| Katalog-ID: |
ELV035916591 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV035916591 | ||
| 003 | DE-627 | ||
| 005 | 20230625210031.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180603s2017 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.trsl.2016.09.001 |2 doi | |
| 028 | 5 | 2 | |a GBVA2017011000030.pica |
| 035 | |a (DE-627)ELV035916591 | ||
| 035 | |a (ELSEVIER)S1931-5244(16)30198-0 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | |a 610 | |
| 082 | 0 | 4 | |a 610 |q DE-600 |
| 082 | 0 | 4 | |a 530 |q VZ |
| 082 | 0 | 4 | |a 620 |q VZ |
| 082 | 0 | 4 | |a 670 |q VZ |
| 082 | 0 | 4 | |a 300 |q VZ |
| 084 | |a 70.00 |2 bkl | ||
| 084 | |a 71.00 |2 bkl | ||
| 100 | 1 | |a Scott, Fraser W. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes |
| 264 | 1 | |c 2017transfer abstract | |
| 300 | |a 16 | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. | ||
| 520 | |a The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. | ||
| 650 | 7 | |a CXCL9 |2 Elsevier | |
| 650 | 7 | |a CRAMP |2 Elsevier | |
| 650 | 7 | |a GWAS |2 Elsevier | |
| 650 | 7 | |a RNA |2 Elsevier | |
| 650 | 7 | |a T1D |2 Elsevier | |
| 650 | 7 | |a TEDDY |2 Elsevier | |
| 650 | 7 | |a MHC |2 Elsevier | |
| 650 | 7 | |a sMLN |2 Elsevier | |
| 650 | 7 | |a HO-1 |2 Elsevier | |
| 650 | 7 | |a PTPN22 |2 Elsevier | |
| 650 | 7 | |a EGFR |2 Elsevier | |
| 650 | 7 | |a LPS |2 Elsevier | |
| 650 | 7 | |a MLN |2 Elsevier | |
| 650 | 7 | |a BBdp |2 Elsevier | |
| 650 | 7 | |a PLN |2 Elsevier | |
| 650 | 7 | |a SNP |2 Elsevier | |
| 650 | 7 | |a GM-CSF |2 Elsevier | |
| 650 | 7 | |a CCL5 |2 Elsevier | |
| 650 | 7 | |a CCL3 |2 Elsevier | |
| 650 | 7 | |a CCL2 |2 Elsevier | |
| 650 | 7 | |a CTLA4 |2 Elsevier | |
| 650 | 7 | |a CD14 |2 Elsevier | |
| 650 | 7 | |a CAMP |2 Elsevier | |
| 650 | 7 | |a dsRNA |2 Elsevier | |
| 650 | 7 | |a CD163 |2 Elsevier | |
| 650 | 7 | |a cMLN |2 Elsevier | |
| 650 | 7 | |a NOD |2 Elsevier | |
| 650 | 7 | |a DIPP |2 Elsevier | |
| 650 | 7 | |a rRNA |2 Elsevier | |
| 650 | 7 | |a GAD |2 Elsevier | |
| 650 | 7 | |a IL-8 |2 Elsevier | |
| 650 | 7 | |a PBMC |2 Elsevier | |
| 650 | 7 | |a IL-6 |2 Elsevier | |
| 650 | 7 | |a IL-10 |2 Elsevier | |
| 650 | 7 | |a TRIGR |2 Elsevier | |
| 650 | 7 | |a CXCL10 |2 Elsevier | |
| 650 | 7 | |a IEL |2 Elsevier | |
| 650 | 7 | |a CXCL11 |2 Elsevier | |
| 650 | 7 | |a IL2RA |2 Elsevier | |
| 650 | 7 | |a HC |2 Elsevier | |
| 650 | 7 | |a HLA |2 Elsevier | |
| 650 | 7 | |a TLR4 |2 Elsevier | |
| 700 | 1 | |a Pound, Lynley D. |4 oth | |
| 700 | 1 | |a Patrick, Christopher |4 oth | |
| 700 | 1 | |a Eberhard, Chandra E. |4 oth | |
| 700 | 1 | |a Crookshank, Jennifer A. |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |a Muthuraja, A. ELSEVIER |t Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties |d 2015 |d the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research |g New York, NY |w (DE-627)ELV013179047 |
| 773 | 1 | 8 | |g volume:179 |g year:2017 |g pages:183-198 |g extent:16 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.trsl.2016.09.001 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 936 | b | k | |a 70.00 |j Sozialwissenschaften allgemein: Allgemeines |q VZ |
| 936 | b | k | |a 71.00 |j Soziologie: Allgemeines |q VZ |
| 951 | |a AR | ||
| 952 | |d 179 |j 2017 |h 183-198 |g 16 | ||
| 953 | |2 045F |a 610 | ||
| author_variant |
f w s fw fws |
|---|---|
| matchkey_str |
scottfraserwpoundlynleydpatrickchristoph:2017----:hrgnsetniomnitgaighrlogtuiacnetimnta |
| hierarchy_sort_str |
2017transfer abstract |
| bklnumber |
70.00 71.00 |
| publishDate |
2017 |
| allfields |
10.1016/j.trsl.2016.09.001 doi GBVA2017011000030.pica (DE-627)ELV035916591 (ELSEVIER)S1931-5244(16)30198-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 530 VZ 620 VZ 670 VZ 300 VZ 70.00 bkl 71.00 bkl Scott, Fraser W. verfasserin aut Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes 2017transfer abstract 16 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. CXCL9 Elsevier CRAMP Elsevier GWAS Elsevier RNA Elsevier T1D Elsevier TEDDY Elsevier MHC Elsevier sMLN Elsevier HO-1 Elsevier PTPN22 Elsevier EGFR Elsevier LPS Elsevier MLN Elsevier BBdp Elsevier PLN Elsevier SNP Elsevier GM-CSF Elsevier CCL5 Elsevier CCL3 Elsevier CCL2 Elsevier CTLA4 Elsevier CD14 Elsevier CAMP Elsevier dsRNA Elsevier CD163 Elsevier cMLN Elsevier NOD Elsevier DIPP Elsevier rRNA Elsevier GAD Elsevier IL-8 Elsevier PBMC Elsevier IL-6 Elsevier IL-10 Elsevier TRIGR Elsevier CXCL10 Elsevier IEL Elsevier CXCL11 Elsevier IL2RA Elsevier HC Elsevier HLA Elsevier TLR4 Elsevier Pound, Lynley D. oth Patrick, Christopher oth Eberhard, Chandra E. oth Crookshank, Jennifer A. oth Enthalten in Elsevier Muthuraja, A. ELSEVIER Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties 2015 the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research New York, NY (DE-627)ELV013179047 volume:179 year:2017 pages:183-198 extent:16 https://doi.org/10.1016/j.trsl.2016.09.001 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 70.00 Sozialwissenschaften allgemein: Allgemeines VZ 71.00 Soziologie: Allgemeines VZ AR 179 2017 183-198 16 045F 610 |
| spelling |
10.1016/j.trsl.2016.09.001 doi GBVA2017011000030.pica (DE-627)ELV035916591 (ELSEVIER)S1931-5244(16)30198-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 530 VZ 620 VZ 670 VZ 300 VZ 70.00 bkl 71.00 bkl Scott, Fraser W. verfasserin aut Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes 2017transfer abstract 16 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. CXCL9 Elsevier CRAMP Elsevier GWAS Elsevier RNA Elsevier T1D Elsevier TEDDY Elsevier MHC Elsevier sMLN Elsevier HO-1 Elsevier PTPN22 Elsevier EGFR Elsevier LPS Elsevier MLN Elsevier BBdp Elsevier PLN Elsevier SNP Elsevier GM-CSF Elsevier CCL5 Elsevier CCL3 Elsevier CCL2 Elsevier CTLA4 Elsevier CD14 Elsevier CAMP Elsevier dsRNA Elsevier CD163 Elsevier cMLN Elsevier NOD Elsevier DIPP Elsevier rRNA Elsevier GAD Elsevier IL-8 Elsevier PBMC Elsevier IL-6 Elsevier IL-10 Elsevier TRIGR Elsevier CXCL10 Elsevier IEL Elsevier CXCL11 Elsevier IL2RA Elsevier HC Elsevier HLA Elsevier TLR4 Elsevier Pound, Lynley D. oth Patrick, Christopher oth Eberhard, Chandra E. oth Crookshank, Jennifer A. oth Enthalten in Elsevier Muthuraja, A. ELSEVIER Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties 2015 the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research New York, NY (DE-627)ELV013179047 volume:179 year:2017 pages:183-198 extent:16 https://doi.org/10.1016/j.trsl.2016.09.001 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 70.00 Sozialwissenschaften allgemein: Allgemeines VZ 71.00 Soziologie: Allgemeines VZ AR 179 2017 183-198 16 045F 610 |
| allfields_unstemmed |
10.1016/j.trsl.2016.09.001 doi GBVA2017011000030.pica (DE-627)ELV035916591 (ELSEVIER)S1931-5244(16)30198-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 530 VZ 620 VZ 670 VZ 300 VZ 70.00 bkl 71.00 bkl Scott, Fraser W. verfasserin aut Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes 2017transfer abstract 16 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. CXCL9 Elsevier CRAMP Elsevier GWAS Elsevier RNA Elsevier T1D Elsevier TEDDY Elsevier MHC Elsevier sMLN Elsevier HO-1 Elsevier PTPN22 Elsevier EGFR Elsevier LPS Elsevier MLN Elsevier BBdp Elsevier PLN Elsevier SNP Elsevier GM-CSF Elsevier CCL5 Elsevier CCL3 Elsevier CCL2 Elsevier CTLA4 Elsevier CD14 Elsevier CAMP Elsevier dsRNA Elsevier CD163 Elsevier cMLN Elsevier NOD Elsevier DIPP Elsevier rRNA Elsevier GAD Elsevier IL-8 Elsevier PBMC Elsevier IL-6 Elsevier IL-10 Elsevier TRIGR Elsevier CXCL10 Elsevier IEL Elsevier CXCL11 Elsevier IL2RA Elsevier HC Elsevier HLA Elsevier TLR4 Elsevier Pound, Lynley D. oth Patrick, Christopher oth Eberhard, Chandra E. oth Crookshank, Jennifer A. oth Enthalten in Elsevier Muthuraja, A. ELSEVIER Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties 2015 the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research New York, NY (DE-627)ELV013179047 volume:179 year:2017 pages:183-198 extent:16 https://doi.org/10.1016/j.trsl.2016.09.001 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 70.00 Sozialwissenschaften allgemein: Allgemeines VZ 71.00 Soziologie: Allgemeines VZ AR 179 2017 183-198 16 045F 610 |
| allfieldsGer |
10.1016/j.trsl.2016.09.001 doi GBVA2017011000030.pica (DE-627)ELV035916591 (ELSEVIER)S1931-5244(16)30198-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 530 VZ 620 VZ 670 VZ 300 VZ 70.00 bkl 71.00 bkl Scott, Fraser W. verfasserin aut Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes 2017transfer abstract 16 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. CXCL9 Elsevier CRAMP Elsevier GWAS Elsevier RNA Elsevier T1D Elsevier TEDDY Elsevier MHC Elsevier sMLN Elsevier HO-1 Elsevier PTPN22 Elsevier EGFR Elsevier LPS Elsevier MLN Elsevier BBdp Elsevier PLN Elsevier SNP Elsevier GM-CSF Elsevier CCL5 Elsevier CCL3 Elsevier CCL2 Elsevier CTLA4 Elsevier CD14 Elsevier CAMP Elsevier dsRNA Elsevier CD163 Elsevier cMLN Elsevier NOD Elsevier DIPP Elsevier rRNA Elsevier GAD Elsevier IL-8 Elsevier PBMC Elsevier IL-6 Elsevier IL-10 Elsevier TRIGR Elsevier CXCL10 Elsevier IEL Elsevier CXCL11 Elsevier IL2RA Elsevier HC Elsevier HLA Elsevier TLR4 Elsevier Pound, Lynley D. oth Patrick, Christopher oth Eberhard, Chandra E. oth Crookshank, Jennifer A. oth Enthalten in Elsevier Muthuraja, A. ELSEVIER Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties 2015 the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research New York, NY (DE-627)ELV013179047 volume:179 year:2017 pages:183-198 extent:16 https://doi.org/10.1016/j.trsl.2016.09.001 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 70.00 Sozialwissenschaften allgemein: Allgemeines VZ 71.00 Soziologie: Allgemeines VZ AR 179 2017 183-198 16 045F 610 |
| allfieldsSound |
10.1016/j.trsl.2016.09.001 doi GBVA2017011000030.pica (DE-627)ELV035916591 (ELSEVIER)S1931-5244(16)30198-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 530 VZ 620 VZ 670 VZ 300 VZ 70.00 bkl 71.00 bkl Scott, Fraser W. verfasserin aut Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes 2017transfer abstract 16 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. CXCL9 Elsevier CRAMP Elsevier GWAS Elsevier RNA Elsevier T1D Elsevier TEDDY Elsevier MHC Elsevier sMLN Elsevier HO-1 Elsevier PTPN22 Elsevier EGFR Elsevier LPS Elsevier MLN Elsevier BBdp Elsevier PLN Elsevier SNP Elsevier GM-CSF Elsevier CCL5 Elsevier CCL3 Elsevier CCL2 Elsevier CTLA4 Elsevier CD14 Elsevier CAMP Elsevier dsRNA Elsevier CD163 Elsevier cMLN Elsevier NOD Elsevier DIPP Elsevier rRNA Elsevier GAD Elsevier IL-8 Elsevier PBMC Elsevier IL-6 Elsevier IL-10 Elsevier TRIGR Elsevier CXCL10 Elsevier IEL Elsevier CXCL11 Elsevier IL2RA Elsevier HC Elsevier HLA Elsevier TLR4 Elsevier Pound, Lynley D. oth Patrick, Christopher oth Eberhard, Chandra E. oth Crookshank, Jennifer A. oth Enthalten in Elsevier Muthuraja, A. ELSEVIER Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties 2015 the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research New York, NY (DE-627)ELV013179047 volume:179 year:2017 pages:183-198 extent:16 https://doi.org/10.1016/j.trsl.2016.09.001 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 70.00 Sozialwissenschaften allgemein: Allgemeines VZ 71.00 Soziologie: Allgemeines VZ AR 179 2017 183-198 16 045F 610 |
| language |
English |
| source |
Enthalten in Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties New York, NY volume:179 year:2017 pages:183-198 extent:16 |
| sourceStr |
Enthalten in Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties New York, NY volume:179 year:2017 pages:183-198 extent:16 |
| format_phy_str_mv |
Article |
| bklname |
Sozialwissenschaften allgemein: Allgemeines Soziologie: Allgemeines |
| institution |
findex.gbv.de |
| topic_facet |
CXCL9 CRAMP GWAS RNA T1D TEDDY MHC sMLN HO-1 PTPN22 EGFR LPS MLN BBdp PLN SNP GM-CSF CCL5 CCL3 CCL2 CTLA4 CD14 CAMP dsRNA CD163 cMLN NOD DIPP rRNA GAD IL-8 PBMC IL-6 IL-10 TRIGR CXCL10 IEL CXCL11 IL2RA HC HLA TLR4 |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties |
| authorswithroles_txt_mv |
Scott, Fraser W. @@aut@@ Pound, Lynley D. @@oth@@ Patrick, Christopher @@oth@@ Eberhard, Chandra E. @@oth@@ Crookshank, Jennifer A. @@oth@@ |
| publishDateDaySort_date |
2017-01-01T00:00:00Z |
| hierarchy_top_id |
ELV013179047 |
| dewey-sort |
3610 |
| id |
ELV035916591 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV035916591</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625210031.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.trsl.2016.09.001</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2017011000030.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV035916591</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1931-5244(16)30198-0</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">530</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">620</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">670</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">300</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">70.00</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">71.00</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Scott, Fraser W.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">16</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CXCL9</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CRAMP</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">GWAS</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">RNA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">T1D</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TEDDY</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">MHC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">sMLN</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">HO-1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PTPN22</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">EGFR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">LPS</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">MLN</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">BBdp</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PLN</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">SNP</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">GM-CSF</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CCL5</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CCL3</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CCL2</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CTLA4</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CD14</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CAMP</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">dsRNA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CD163</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">cMLN</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NOD</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">DIPP</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">rRNA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">GAD</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IL-8</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PBMC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IL-6</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IL-10</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TRIGR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CXCL10</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IEL</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CXCL11</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IL2RA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">HC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">HLA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TLR4</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pound, Lynley D.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Patrick, Christopher</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Eberhard, Chandra E.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Crookshank, Jennifer A.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Muthuraja, A. ELSEVIER</subfield><subfield code="t">Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties</subfield><subfield code="d">2015</subfield><subfield code="d">the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research</subfield><subfield code="g">New York, NY</subfield><subfield code="w">(DE-627)ELV013179047</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:179</subfield><subfield code="g">year:2017</subfield><subfield code="g">pages:183-198</subfield><subfield code="g">extent:16</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.trsl.2016.09.001</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">70.00</subfield><subfield code="j">Sozialwissenschaften allgemein: Allgemeines</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">71.00</subfield><subfield code="j">Soziologie: Allgemeines</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">179</subfield><subfield code="j">2017</subfield><subfield code="h">183-198</subfield><subfield code="g">16</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| author |
Scott, Fraser W. |
| spellingShingle |
Scott, Fraser W. ddc 610 ddc 530 ddc 620 ddc 670 ddc 300 bkl 70.00 bkl 71.00 Elsevier CXCL9 Elsevier CRAMP Elsevier GWAS Elsevier RNA Elsevier T1D Elsevier TEDDY Elsevier MHC Elsevier sMLN Elsevier HO-1 Elsevier PTPN22 Elsevier EGFR Elsevier LPS Elsevier MLN Elsevier BBdp Elsevier PLN Elsevier SNP Elsevier GM-CSF Elsevier CCL5 Elsevier CCL3 Elsevier CCL2 Elsevier CTLA4 Elsevier CD14 Elsevier CAMP Elsevier dsRNA Elsevier CD163 Elsevier cMLN Elsevier NOD Elsevier DIPP Elsevier rRNA Elsevier GAD Elsevier IL-8 Elsevier PBMC Elsevier IL-6 Elsevier IL-10 Elsevier TRIGR Elsevier CXCL10 Elsevier IEL Elsevier CXCL11 Elsevier IL2RA Elsevier HC Elsevier HLA Elsevier TLR4 Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes |
| authorStr |
Scott, Fraser W. |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV013179047 |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health 530 - Physics 620 - Engineering & allied operations 670 - Manufacturing 300 - Social sciences |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 610 DE-600 530 VZ 620 VZ 670 VZ 300 VZ 70.00 bkl 71.00 bkl Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes CXCL9 Elsevier CRAMP Elsevier GWAS Elsevier RNA Elsevier T1D Elsevier TEDDY Elsevier MHC Elsevier sMLN Elsevier HO-1 Elsevier PTPN22 Elsevier EGFR Elsevier LPS Elsevier MLN Elsevier BBdp Elsevier PLN Elsevier SNP Elsevier GM-CSF Elsevier CCL5 Elsevier CCL3 Elsevier CCL2 Elsevier CTLA4 Elsevier CD14 Elsevier CAMP Elsevier dsRNA Elsevier CD163 Elsevier cMLN Elsevier NOD Elsevier DIPP Elsevier rRNA Elsevier GAD Elsevier IL-8 Elsevier PBMC Elsevier IL-6 Elsevier IL-10 Elsevier TRIGR Elsevier CXCL10 Elsevier IEL Elsevier CXCL11 Elsevier IL2RA Elsevier HC Elsevier HLA Elsevier TLR4 Elsevier |
| topic |
ddc 610 ddc 530 ddc 620 ddc 670 ddc 300 bkl 70.00 bkl 71.00 Elsevier CXCL9 Elsevier CRAMP Elsevier GWAS Elsevier RNA Elsevier T1D Elsevier TEDDY Elsevier MHC Elsevier sMLN Elsevier HO-1 Elsevier PTPN22 Elsevier EGFR Elsevier LPS Elsevier MLN Elsevier BBdp Elsevier PLN Elsevier SNP Elsevier GM-CSF Elsevier CCL5 Elsevier CCL3 Elsevier CCL2 Elsevier CTLA4 Elsevier CD14 Elsevier CAMP Elsevier dsRNA Elsevier CD163 Elsevier cMLN Elsevier NOD Elsevier DIPP Elsevier rRNA Elsevier GAD Elsevier IL-8 Elsevier PBMC Elsevier IL-6 Elsevier IL-10 Elsevier TRIGR Elsevier CXCL10 Elsevier IEL Elsevier CXCL11 Elsevier IL2RA Elsevier HC Elsevier HLA Elsevier TLR4 |
| topic_unstemmed |
ddc 610 ddc 530 ddc 620 ddc 670 ddc 300 bkl 70.00 bkl 71.00 Elsevier CXCL9 Elsevier CRAMP Elsevier GWAS Elsevier RNA Elsevier T1D Elsevier TEDDY Elsevier MHC Elsevier sMLN Elsevier HO-1 Elsevier PTPN22 Elsevier EGFR Elsevier LPS Elsevier MLN Elsevier BBdp Elsevier PLN Elsevier SNP Elsevier GM-CSF Elsevier CCL5 Elsevier CCL3 Elsevier CCL2 Elsevier CTLA4 Elsevier CD14 Elsevier CAMP Elsevier dsRNA Elsevier CD163 Elsevier cMLN Elsevier NOD Elsevier DIPP Elsevier rRNA Elsevier GAD Elsevier IL-8 Elsevier PBMC Elsevier IL-6 Elsevier IL-10 Elsevier TRIGR Elsevier CXCL10 Elsevier IEL Elsevier CXCL11 Elsevier IL2RA Elsevier HC Elsevier HLA Elsevier TLR4 |
| topic_browse |
ddc 610 ddc 530 ddc 620 ddc 670 ddc 300 bkl 70.00 bkl 71.00 Elsevier CXCL9 Elsevier CRAMP Elsevier GWAS Elsevier RNA Elsevier T1D Elsevier TEDDY Elsevier MHC Elsevier sMLN Elsevier HO-1 Elsevier PTPN22 Elsevier EGFR Elsevier LPS Elsevier MLN Elsevier BBdp Elsevier PLN Elsevier SNP Elsevier GM-CSF Elsevier CCL5 Elsevier CCL3 Elsevier CCL2 Elsevier CTLA4 Elsevier CD14 Elsevier CAMP Elsevier dsRNA Elsevier CD163 Elsevier cMLN Elsevier NOD Elsevier DIPP Elsevier rRNA Elsevier GAD Elsevier IL-8 Elsevier PBMC Elsevier IL-6 Elsevier IL-10 Elsevier TRIGR Elsevier CXCL10 Elsevier IEL Elsevier CXCL11 Elsevier IL2RA Elsevier HC Elsevier HLA Elsevier TLR4 |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
l d p ld ldp c p cp c e e ce cee j a c ja jac |
| hierarchy_parent_title |
Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties |
| hierarchy_parent_id |
ELV013179047 |
| dewey-tens |
610 - Medicine & health 530 - Physics 620 - Engineering 670 - Manufacturing 300 - Social sciences, sociology & anthropology |
| hierarchy_top_title |
Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV013179047 |
| title |
Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes |
| ctrlnum |
(DE-627)ELV035916591 (ELSEVIER)S1931-5244(16)30198-0 |
| title_full |
Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes |
| author_sort |
Scott, Fraser W. |
| journal |
Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties |
| journalStr |
Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology 500 - Science 300 - Social sciences |
| recordtype |
marc |
| publishDateSort |
2017 |
| contenttype_str_mv |
zzz |
| container_start_page |
183 |
| author_browse |
Scott, Fraser W. |
| container_volume |
179 |
| physical |
16 |
| class |
610 610 DE-600 530 VZ 620 VZ 670 VZ 300 VZ 70.00 bkl 71.00 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Scott, Fraser W. |
| doi_str_mv |
10.1016/j.trsl.2016.09.001 |
| dewey-full |
610 530 620 670 300 |
| title_sort |
where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes |
| title_auth |
Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes |
| abstract |
The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. |
| abstractGer |
The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. |
| abstract_unstemmed |
The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U |
| title_short |
Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes |
| url |
https://doi.org/10.1016/j.trsl.2016.09.001 |
| remote_bool |
true |
| author2 |
Pound, Lynley D. Patrick, Christopher Eberhard, Chandra E. Crookshank, Jennifer A. |
| author2Str |
Pound, Lynley D. Patrick, Christopher Eberhard, Chandra E. Crookshank, Jennifer A. |
| ppnlink |
ELV013179047 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth |
| doi_str |
10.1016/j.trsl.2016.09.001 |
| up_date |
2024-07-06T18:48:56.764Z |
| _version_ |
1803856628170096640 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV035916591</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625210031.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.trsl.2016.09.001</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2017011000030.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV035916591</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1931-5244(16)30198-0</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">530</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">620</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">670</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">300</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">70.00</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">71.00</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Scott, Fraser W.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Where genes meet environment—integrating the role of gut luminal contents, immunity and pancreas in type 1 diabetes</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">16</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The rise in new cases of type 1 diabetes (T1D) in genetically susceptible individuals over the past half century has been attributed to numerous environmental “triggers” or promoters such as enteroviruses, diet, and most recently, gut bacteria. No single cause has been identified in humans, likely because there are several pathways by which one can develop T1D. There is renewed attention to the role of the gut and its immune system in T1D pathogenesis based largely on recent animal studies demonstrating that altering the gut microbiota affects diabetes incidence. Although T1D patients display dysbiosis in the gut microbiome, it is unclear whether this is cause or effect. The heart of this question involves several moving parts including numerous risk genes, diet, viruses, gut microbiota, timing, and loss of immune tolerance to β-cells. Most clinical trials have addressed only one aspect of this puzzle using some form of immune suppression, without much success. The key location where our genes meet and deal with the environment is the gastrointestinal tract. The influence of all of its major contents, including microbes, diet, and immune system, must be understood as part of the integrative biology of T1D before we can develop durable means of preventing, treating, or curing this disease. In the present review, we expand our previous gut-centric model based on recent developments in the field.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CXCL9</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CRAMP</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">GWAS</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">RNA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">T1D</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TEDDY</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">MHC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">sMLN</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">HO-1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PTPN22</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">EGFR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">LPS</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">MLN</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">BBdp</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PLN</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">SNP</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">GM-CSF</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CCL5</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CCL3</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CCL2</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CTLA4</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CD14</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CAMP</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">dsRNA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CD163</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">cMLN</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NOD</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">DIPP</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">rRNA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">GAD</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IL-8</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PBMC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IL-6</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IL-10</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TRIGR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CXCL10</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IEL</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CXCL11</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IL2RA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">HC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">HLA</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TLR4</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pound, Lynley D.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Patrick, Christopher</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Eberhard, Chandra E.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Crookshank, Jennifer A.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Muthuraja, A. ELSEVIER</subfield><subfield code="t">Growth of organic benzimidazole (BMZ) single crystal by vertical Bridgman technique and its structural, spectral, thermal, optical, mechanical and dielectric properties</subfield><subfield code="d">2015</subfield><subfield code="d">the journal of laboratory and clinical medicine : the official publication of the Central Society for Clinical Research</subfield><subfield code="g">New York, NY</subfield><subfield code="w">(DE-627)ELV013179047</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:179</subfield><subfield code="g">year:2017</subfield><subfield code="g">pages:183-198</subfield><subfield code="g">extent:16</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.trsl.2016.09.001</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">70.00</subfield><subfield code="j">Sozialwissenschaften allgemein: Allgemeines</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">71.00</subfield><subfield code="j">Soziologie: Allgemeines</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">179</subfield><subfield code="j">2017</subfield><subfield code="h">183-198</subfield><subfield code="g">16</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| score |
7.4018383 |