S100A8/A9 is an important host defence mediator in neuropathic foot ulcers in patients with type 2 diabetes mellitus
Chronic wounds and in particular diabetic foot ulcers (DFUs) are a growing clinical challenge, but the underlying molecular pathophysiological mechanisms are unclear. Recently, we reported reduced levels of the immunomodulating and antimicrobial S100A8/A9 in non-healing venous leg ulcers (VLUs), whi...
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| Veröffentlicht in: | Archives of Dermatological Research 2016-07, Vol.308 (5), p.347-355 |
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| description | Chronic wounds and in particular diabetic foot ulcers (DFUs) are a growing clinical challenge, but the underlying molecular pathophysiological mechanisms are unclear. Recently, we reported reduced levels of the immunomodulating and antimicrobial S100A8/A9 in non-healing venous leg ulcers (VLUs), while another study found increased S100A8/A9 in DFUs. To clarify these apparently contradictory findings, we compared S100A8/A9 as well as an inducer, lipopolysaccharide (LPS) and selected innate immune response mediators in wound fluids from non-healing DFUs and VLUs with healing wounds. Wound fluids were collected from neuropathic DFUs (
n
= 6) and VLUs (
n
= 9) of median 2-year duration, and split-thickness skin graft donor site wounds (
n
= 10) by standardized method. None of the patients had ischaemic extremities or clinically infected wounds. LPS was determined by limulus amoebocyte lysate test, and S100A8/A9, granulocyte colony-stimulating factor (G-CSF), interleukin (IL)-10 and vascular endothelial growth factor (VEGF) by immunospecific quantitative assays. LPS levels were median 8.7 (interquartile range 5.4–21.2) ng/ml in DFUs compared with 121 (22–2000) ng/ml in VLUs. S100A8/A9 was higher (
p
= 0.020) in DFUs [718 (634-811) µg/ml] than in VLUs [303 (252–533) µg/ml]. Neither G-CSF nor IL-10 wound fluid levels differed significantly between the chronic wound groups. VEGF levels correlated with LPS (
r
= 0.758,
p
= 0.011,
n
= 10) and were higher (
p
= 0.024) in VLU wound fluids. LPS (
p
|
| doi_str_mv | 10.1007/s00403-016-1646-7 |
| format | Article |
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n
= 6) and VLUs (
n
= 9) of median 2-year duration, and split-thickness skin graft donor site wounds (
n
= 10) by standardized method. None of the patients had ischaemic extremities or clinically infected wounds. LPS was determined by limulus amoebocyte lysate test, and S100A8/A9, granulocyte colony-stimulating factor (G-CSF), interleukin (IL)-10 and vascular endothelial growth factor (VEGF) by immunospecific quantitative assays. LPS levels were median 8.7 (interquartile range 5.4–21.2) ng/ml in DFUs compared with 121 (22–2000) ng/ml in VLUs. S100A8/A9 was higher (
p
= 0.020) in DFUs [718 (634-811) µg/ml] than in VLUs [303 (252–533) µg/ml]. Neither G-CSF nor IL-10 wound fluid levels differed significantly between the chronic wound groups. VEGF levels correlated with LPS (
r
= 0.758,
p
= 0.011,
n
= 10) and were higher (
p
= 0.024) in VLU wound fluids. LPS (
p
< 0.0001), S100A8/A9 (
p
= 0.005), G-CSF (
p
= 0.003), IL-10 (
p
= 0.003) and VEGF (
p
= 0.005) were increased in chronic wound fluids combined compared with the sterile donor site wound fluids. The protein alterations in the wounds were not reflected in the patients’ sera. Low S100A8/A9 levels may contribute to poor wound healing in colonized chronic wounds with striking difference between DFUs and VLUs.</description><identifier>ISSN: 0340-3696</identifier><identifier>EISSN: 1432-069X</identifier><identifier>DOI: 10.1007/s00403-016-1646-7</identifier><identifier>PMID: 27084691</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Chronic Disease ; Dermatology ; Diabetes Mellitus, Type 2 - complications ; Diabetic Foot - immunology ; Diabetic Foot - metabolism ; Diabetic Neuropathies - immunology ; Diabetic Neuropathies - metabolism ; Female ; Granulocyte Colony-Stimulating Factor - metabolism ; Humans ; Immunity, Innate ; Interleukin-10 - metabolism ; Leukocyte L1 Antigen Complex - immunology ; Leukocyte L1 Antigen Complex - metabolism ; Limulus ; Limulus Test ; Lipopolysaccharides - metabolism ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Original Paper ; Varicose Ulcer - immunology ; Varicose Ulcer - metabolism ; Vascular Endothelial Growth Factor A - metabolism ; Wound Healing - immunology</subject><ispartof>Archives of Dermatological Research, 2016-07, Vol.308 (5), p.347-355</ispartof><rights>Springer-Verlag Berlin Heidelberg 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-5dd8bc0bec1f3290e90cbedf83ec11d65b74ce67a31e3f61197011d0cd971bc03</citedby><cites>FETCH-LOGICAL-c405t-5dd8bc0bec1f3290e90cbedf83ec11d65b74ce67a31e3f61197011d0cd971bc03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00403-016-1646-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00403-016-1646-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27084691$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Trøstrup, Hannah</creatorcontrib><creatorcontrib>Holstein, Per</creatorcontrib><creatorcontrib>Christophersen, Lars</creatorcontrib><creatorcontrib>Jørgensen, Bo</creatorcontrib><creatorcontrib>Karlsmark, Tonny</creatorcontrib><creatorcontrib>Høiby, Niels</creatorcontrib><creatorcontrib>Moser, Claus</creatorcontrib><creatorcontrib>Ågren, Magnus S.</creatorcontrib><title>S100A8/A9 is an important host defence mediator in neuropathic foot ulcers in patients with type 2 diabetes mellitus</title><title>Archives of Dermatological Research</title><addtitle>Arch Dermatol Res</addtitle><addtitle>Arch Dermatol Res</addtitle><description>Chronic wounds and in particular diabetic foot ulcers (DFUs) are a growing clinical challenge, but the underlying molecular pathophysiological mechanisms are unclear. Recently, we reported reduced levels of the immunomodulating and antimicrobial S100A8/A9 in non-healing venous leg ulcers (VLUs), while another study found increased S100A8/A9 in DFUs. To clarify these apparently contradictory findings, we compared S100A8/A9 as well as an inducer, lipopolysaccharide (LPS) and selected innate immune response mediators in wound fluids from non-healing DFUs and VLUs with healing wounds. Wound fluids were collected from neuropathic DFUs (
n
= 6) and VLUs (
n
= 9) of median 2-year duration, and split-thickness skin graft donor site wounds (
n
= 10) by standardized method. None of the patients had ischaemic extremities or clinically infected wounds. LPS was determined by limulus amoebocyte lysate test, and S100A8/A9, granulocyte colony-stimulating factor (G-CSF), interleukin (IL)-10 and vascular endothelial growth factor (VEGF) by immunospecific quantitative assays. LPS levels were median 8.7 (interquartile range 5.4–21.2) ng/ml in DFUs compared with 121 (22–2000) ng/ml in VLUs. S100A8/A9 was higher (
p
= 0.020) in DFUs [718 (634-811) µg/ml] than in VLUs [303 (252–533) µg/ml]. Neither G-CSF nor IL-10 wound fluid levels differed significantly between the chronic wound groups. VEGF levels correlated with LPS (
r
= 0.758,
p
= 0.011,
n
= 10) and were higher (
p
= 0.024) in VLU wound fluids. LPS (
p
< 0.0001), S100A8/A9 (
p
= 0.005), G-CSF (
p
= 0.003), IL-10 (
p
= 0.003) and VEGF (
p
= 0.005) were increased in chronic wound fluids combined compared with the sterile donor site wound fluids. The protein alterations in the wounds were not reflected in the patients’ sera. Low S100A8/A9 levels may contribute to poor wound healing in colonized chronic wounds with striking difference between DFUs and VLUs.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Chronic Disease</subject><subject>Dermatology</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetic Foot - immunology</subject><subject>Diabetic Foot - metabolism</subject><subject>Diabetic Neuropathies - immunology</subject><subject>Diabetic Neuropathies - metabolism</subject><subject>Female</subject><subject>Granulocyte Colony-Stimulating Factor - metabolism</subject><subject>Humans</subject><subject>Immunity, Innate</subject><subject>Interleukin-10 - metabolism</subject><subject>Leukocyte L1 Antigen Complex - immunology</subject><subject>Leukocyte L1 Antigen Complex - metabolism</subject><subject>Limulus</subject><subject>Limulus Test</subject><subject>Lipopolysaccharides - metabolism</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Original Paper</subject><subject>Varicose Ulcer - immunology</subject><subject>Varicose Ulcer - metabolism</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>Wound Healing - immunology</subject><issn>0340-3696</issn><issn>1432-069X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkU1r3DAQhkVpSZY0PyCXIMglFycjS6uP4xKSthDooS30Jmx53FXYlRxJpuTfV-6mIRRKdRHMPPPOx0vIGYMrBqCuM4AA3gCTDZNCNuoNWTHB2wak-f6WrIALaLg08pic5vwA9SkQLagjctwq0EIatiLlSxXb6OuNoT7TLlC_n2IqXSh0G3OhA44YHNI9Dr4rMVEfaMA5xakrW-_oGGOh885hykuqRj2GkulPX7a0PE1IW1oreyyYq8hu58uc35N3Y7fLePr8n5Bvd7dfbz42958_fLrZ3DdOwLo062HQvYMeHRt5awANuB6HUfMaYYNc90o4lKrjDPkoGTMKahzcYBSrhfyEXB50pxQfZ8zF7n12dYguYJyzZRq0bKXS6v-oMmut601FRS_-Qh_inEJd5DclmZTt0psdKJdizglHOyW_79KTZWAXA-3BQFsNtIuBdhni_Fl57uvBXyr-2FWB9gDkmgo_ML1q_U_VX6qqpMY</recordid><startdate>20160701</startdate><enddate>20160701</enddate><creator>Trøstrup, Hannah</creator><creator>Holstein, Per</creator><creator>Christophersen, Lars</creator><creator>Jørgensen, Bo</creator><creator>Karlsmark, Tonny</creator><creator>Høiby, Niels</creator><creator>Moser, Claus</creator><creator>Ågren, Magnus S.</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20160701</creationdate><title>S100A8/A9 is an important host defence mediator in neuropathic foot ulcers in patients with type 2 diabetes mellitus</title><author>Trøstrup, Hannah ; Holstein, Per ; Christophersen, Lars ; Jørgensen, Bo ; Karlsmark, Tonny ; Høiby, Niels ; Moser, Claus ; Ågren, Magnus S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-5dd8bc0bec1f3290e90cbedf83ec11d65b74ce67a31e3f61197011d0cd971bc03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Chronic Disease</topic><topic>Dermatology</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetic Foot - immunology</topic><topic>Diabetic Foot - metabolism</topic><topic>Diabetic Neuropathies - immunology</topic><topic>Diabetic Neuropathies - metabolism</topic><topic>Female</topic><topic>Granulocyte Colony-Stimulating Factor - metabolism</topic><topic>Humans</topic><topic>Immunity, Innate</topic><topic>Interleukin-10 - metabolism</topic><topic>Leukocyte L1 Antigen Complex - immunology</topic><topic>Leukocyte L1 Antigen Complex - metabolism</topic><topic>Limulus</topic><topic>Limulus Test</topic><topic>Lipopolysaccharides - metabolism</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Original Paper</topic><topic>Varicose Ulcer - immunology</topic><topic>Varicose Ulcer - metabolism</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>Wound Healing - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Trøstrup, Hannah</creatorcontrib><creatorcontrib>Holstein, Per</creatorcontrib><creatorcontrib>Christophersen, Lars</creatorcontrib><creatorcontrib>Jørgensen, Bo</creatorcontrib><creatorcontrib>Karlsmark, Tonny</creatorcontrib><creatorcontrib>Høiby, Niels</creatorcontrib><creatorcontrib>Moser, Claus</creatorcontrib><creatorcontrib>Ågren, Magnus S.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Archives of Dermatological Research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Trøstrup, Hannah</au><au>Holstein, Per</au><au>Christophersen, Lars</au><au>Jørgensen, Bo</au><au>Karlsmark, Tonny</au><au>Høiby, Niels</au><au>Moser, Claus</au><au>Ågren, Magnus S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>S100A8/A9 is an important host defence mediator in neuropathic foot ulcers in patients with type 2 diabetes mellitus</atitle><jtitle>Archives of Dermatological Research</jtitle><stitle>Arch Dermatol Res</stitle><addtitle>Arch Dermatol Res</addtitle><date>2016-07-01</date><risdate>2016</risdate><volume>308</volume><issue>5</issue><spage>347</spage><epage>355</epage><pages>347-355</pages><issn>0340-3696</issn><eissn>1432-069X</eissn><abstract>Chronic wounds and in particular diabetic foot ulcers (DFUs) are a growing clinical challenge, but the underlying molecular pathophysiological mechanisms are unclear. Recently, we reported reduced levels of the immunomodulating and antimicrobial S100A8/A9 in non-healing venous leg ulcers (VLUs), while another study found increased S100A8/A9 in DFUs. To clarify these apparently contradictory findings, we compared S100A8/A9 as well as an inducer, lipopolysaccharide (LPS) and selected innate immune response mediators in wound fluids from non-healing DFUs and VLUs with healing wounds. Wound fluids were collected from neuropathic DFUs (
n
= 6) and VLUs (
n
= 9) of median 2-year duration, and split-thickness skin graft donor site wounds (
n
= 10) by standardized method. None of the patients had ischaemic extremities or clinically infected wounds. LPS was determined by limulus amoebocyte lysate test, and S100A8/A9, granulocyte colony-stimulating factor (G-CSF), interleukin (IL)-10 and vascular endothelial growth factor (VEGF) by immunospecific quantitative assays. LPS levels were median 8.7 (interquartile range 5.4–21.2) ng/ml in DFUs compared with 121 (22–2000) ng/ml in VLUs. S100A8/A9 was higher (
p
= 0.020) in DFUs [718 (634-811) µg/ml] than in VLUs [303 (252–533) µg/ml]. Neither G-CSF nor IL-10 wound fluid levels differed significantly between the chronic wound groups. VEGF levels correlated with LPS (
r
= 0.758,
p
= 0.011,
n
= 10) and were higher (
p
= 0.024) in VLU wound fluids. LPS (
p
< 0.0001), S100A8/A9 (
p
= 0.005), G-CSF (
p
= 0.003), IL-10 (
p
= 0.003) and VEGF (
p
= 0.005) were increased in chronic wound fluids combined compared with the sterile donor site wound fluids. The protein alterations in the wounds were not reflected in the patients’ sera. Low S100A8/A9 levels may contribute to poor wound healing in colonized chronic wounds with striking difference between DFUs and VLUs.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>27084691</pmid><doi>10.1007/s00403-016-1646-7</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Archives of Dermatological Research, 2016-07, Vol.308 (5), p.347-355 |
| issn | 0340-3696 1432-069X |
| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Adult Aged Aged, 80 and over Chronic Disease Dermatology Diabetes Mellitus, Type 2 - complications Diabetic Foot - immunology Diabetic Foot - metabolism Diabetic Neuropathies - immunology Diabetic Neuropathies - metabolism Female Granulocyte Colony-Stimulating Factor - metabolism Humans Immunity, Innate Interleukin-10 - metabolism Leukocyte L1 Antigen Complex - immunology Leukocyte L1 Antigen Complex - metabolism Limulus Limulus Test Lipopolysaccharides - metabolism Male Medicine Medicine & Public Health Middle Aged Original Paper Varicose Ulcer - immunology Varicose Ulcer - metabolism Vascular Endothelial Growth Factor A - metabolism Wound Healing - immunology |
| title | S100A8/A9 is an important host defence mediator in neuropathic foot ulcers in patients with type 2 diabetes mellitus |
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