Biological Responses at Artificial Surfaces and Recent Progress in Extracorporeal Circulation View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1992

AUTHORS

Takehisa Matsuda

ABSTRACT

The activation of body defence mechanisms during extracorporeal circulation often causes local and systemic adverse effects on the body. The former is exemplified as thrombus formation at the blood-material interfaces, and the latter as peripheral circulation failure associated with microemboli and granulocyte aggregation, resulting in symptoms such as systemic hypertension and peripheral hypotension. Understanding the biological responses at the blood-material interface of extracorporeal devices, such as a hemodialysis, plasmapheresis and artificial oxygenator, is very important for upgrading the biocompatibility of a device under development. The body defence mechanisms associated with thrombus formation and immunological alterations include many biological systems, including the coagulation, complement and cellular systems. As schematically shown in Fig. 1, the multiple activations of these biological systems occur as blood comes in contact with a foreign surface. The characteristic feature of body defence mechanisms leading to thrombus formation is that, although they are independently activated at blood-material surfaces, there exists a positive feed-back mechanism in which an activated form also activates other biological systems. For instance, the activated form (Factor XIIa) of the coagulation system can activate the third component of the complement system, and the activated complement factor (C5a) is a potent aggregation activator of granulocytes. Besides participation in thrombus formation, immunological alterations are involved in humoral and cellular activation. Therefore, the understanding of molecular events at a blood-material interface is of particular importance for the logical surface design of blood-contacting material, particularly that used in extracorporeal devices. More... »

PAGES

169-176

Book

TITLE

Hemostasis and Circulation

ISBN

978-4-431-70096-8
978-4-431-66925-8

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-4-431-66925-8_28

DOI

http://dx.doi.org/10.1007/978-4-431-66925-8_28

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1050275112


Indexing Status Check whether this publication has been indexed by Scopus and Web Of Science using the SN Indexing Status Tool
Incoming Citations Browse incoming citations for this publication using opencitations.net

JSON-LD is the canonical representation for SciGraph data.

TIP: You can open this SciGraph record using an external JSON-LD service: JSON-LD Playground Google SDTT

[
  {
    "@context": "https://springernature.github.io/scigraph/jsonld/sgcontext.json", 
    "about": [
      {
        "id": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/0903", 
        "inDefinedTermSet": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/", 
        "name": "Biomedical Engineering", 
        "type": "DefinedTerm"
      }, 
      {
        "id": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/09", 
        "inDefinedTermSet": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/", 
        "name": "Engineering", 
        "type": "DefinedTerm"
      }
    ], 
    "author": [
      {
        "affiliation": {
          "alternateName": "National Cerebral and Cardiovascular Center", 
          "id": "https://www.grid.ac/institutes/grid.410796.d", 
          "name": [
            "Dept. of Bioengineering, National Cardiovascular Center Research Institute, 5\u20137\u20131 Fujishirodai, Suita, Osaka, Japan"
          ], 
          "type": "Organization"
        }, 
        "familyName": "Matsuda", 
        "givenName": "Takehisa", 
        "id": "sg:person.016364747632.42", 
        "sameAs": [
          "https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.016364747632.42"
        ], 
        "type": "Person"
      }
    ], 
    "datePublished": "1992", 
    "datePublishedReg": "1992-01-01", 
    "description": "The activation of body defence mechanisms during extracorporeal circulation often causes local and systemic adverse effects on the body. The former is exemplified as thrombus formation at the blood-material interfaces, and the latter as peripheral circulation failure associated with microemboli and granulocyte aggregation, resulting in symptoms such as systemic hypertension and peripheral hypotension. Understanding the biological responses at the blood-material interface of extracorporeal devices, such as a hemodialysis, plasmapheresis and artificial oxygenator, is very important for upgrading the biocompatibility of a device under development. The body defence mechanisms associated with thrombus formation and immunological alterations include many biological systems, including the coagulation, complement and cellular systems. As schematically shown in Fig. 1, the multiple activations of these biological systems occur as blood comes in contact with a foreign surface. The characteristic feature of body defence mechanisms leading to thrombus formation is that, although they are independently activated at blood-material surfaces, there exists a positive feed-back mechanism in which an activated form also activates other biological systems. For instance, the activated form (Factor XIIa) of the coagulation system can activate the third component of the complement system, and the activated complement factor (C5a) is a potent aggregation activator of granulocytes. Besides participation in thrombus formation, immunological alterations are involved in humoral and cellular activation. Therefore, the understanding of molecular events at a blood-material interface is of particular importance for the logical surface design of blood-contacting material, particularly that used in extracorporeal devices.", 
    "editor": [
      {
        "familyName": "Takada", 
        "givenName": "A.", 
        "type": "Person"
      }, 
      {
        "familyName": "Budzynski", 
        "givenName": "A. Z.", 
        "type": "Person"
      }
    ], 
    "genre": "chapter", 
    "id": "sg:pub.10.1007/978-4-431-66925-8_28", 
    "inLanguage": [
      "en"
    ], 
    "isAccessibleForFree": false, 
    "isPartOf": {
      "isbn": [
        "978-4-431-70096-8", 
        "978-4-431-66925-8"
      ], 
      "name": "Hemostasis and Circulation", 
      "type": "Book"
    }, 
    "name": "Biological Responses at Artificial Surfaces and Recent Progress in Extracorporeal Circulation", 
    "pagination": "169-176", 
    "productId": [
      {
        "name": "doi", 
        "type": "PropertyValue", 
        "value": [
          "10.1007/978-4-431-66925-8_28"
        ]
      }, 
      {
        "name": "readcube_id", 
        "type": "PropertyValue", 
        "value": [
          "ef7ef8d964e7bbb820093d891e62b85a4561875237abd53f5594e90314a067a3"
        ]
      }, 
      {
        "name": "dimensions_id", 
        "type": "PropertyValue", 
        "value": [
          "pub.1050275112"
        ]
      }
    ], 
    "publisher": {
      "location": "Tokyo", 
      "name": "Springer Japan", 
      "type": "Organisation"
    }, 
    "sameAs": [
      "https://doi.org/10.1007/978-4-431-66925-8_28", 
      "https://app.dimensions.ai/details/publication/pub.1050275112"
    ], 
    "sdDataset": "chapters", 
    "sdDatePublished": "2019-04-15T18:59", 
    "sdLicense": "https://scigraph.springernature.com/explorer/license/", 
    "sdPublisher": {
      "name": "Springer Nature - SN SciGraph project", 
      "type": "Organization"
    }, 
    "sdSource": "s3://com-uberresearch-data-dimensions-target-20181106-alternative/cleanup/v134/2549eaecd7973599484d7c17b260dba0a4ecb94b/merge/v9/a6c9fde33151104705d4d7ff012ea9563521a3ce/jats-lookup/v90/0000000001_0000000264/records_8684_00000086.jsonl", 
    "type": "Chapter", 
    "url": "http://link.springer.com/10.1007/978-4-431-66925-8_28"
  }
]
 

Download the RDF metadata as:  json-ld nt turtle xml License info

HOW TO GET THIS DATA PROGRAMMATICALLY:

JSON-LD is a popular format for linked data which is fully compatible with JSON.

curl -H 'Accept: application/ld+json' 'https://scigraph.springernature.com/pub.10.1007/978-4-431-66925-8_28'

N-Triples is a line-based linked data format ideal for batch operations.

curl -H 'Accept: application/n-triples' 'https://scigraph.springernature.com/pub.10.1007/978-4-431-66925-8_28'

Turtle is a human-readable linked data format.

curl -H 'Accept: text/turtle' 'https://scigraph.springernature.com/pub.10.1007/978-4-431-66925-8_28'

RDF/XML is a standard XML format for linked data.

curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/pub.10.1007/978-4-431-66925-8_28'


 

This table displays all metadata directly associated to this object as RDF triples.

70 TRIPLES      22 PREDICATES      27 URIs      20 LITERALS      8 BLANK NODES

Subject Predicate Object
1 sg:pub.10.1007/978-4-431-66925-8_28 schema:about anzsrc-for:09
2 anzsrc-for:0903
3 schema:author N8fee807232db4c7aa8f71cec4190dbdd
4 schema:datePublished 1992
5 schema:datePublishedReg 1992-01-01
6 schema:description The activation of body defence mechanisms during extracorporeal circulation often causes local and systemic adverse effects on the body. The former is exemplified as thrombus formation at the blood-material interfaces, and the latter as peripheral circulation failure associated with microemboli and granulocyte aggregation, resulting in symptoms such as systemic hypertension and peripheral hypotension. Understanding the biological responses at the blood-material interface of extracorporeal devices, such as a hemodialysis, plasmapheresis and artificial oxygenator, is very important for upgrading the biocompatibility of a device under development. The body defence mechanisms associated with thrombus formation and immunological alterations include many biological systems, including the coagulation, complement and cellular systems. As schematically shown in Fig. 1, the multiple activations of these biological systems occur as blood comes in contact with a foreign surface. The characteristic feature of body defence mechanisms leading to thrombus formation is that, although they are independently activated at blood-material surfaces, there exists a positive feed-back mechanism in which an activated form also activates other biological systems. For instance, the activated form (Factor XIIa) of the coagulation system can activate the third component of the complement system, and the activated complement factor (C5a) is a potent aggregation activator of granulocytes. Besides participation in thrombus formation, immunological alterations are involved in humoral and cellular activation. Therefore, the understanding of molecular events at a blood-material interface is of particular importance for the logical surface design of blood-contacting material, particularly that used in extracorporeal devices.
7 schema:editor N941621a823be44f8ae385cbca6b65e7b
8 schema:genre chapter
9 schema:inLanguage en
10 schema:isAccessibleForFree false
11 schema:isPartOf Nf192235c85d54444a533137b5980dd4d
12 schema:name Biological Responses at Artificial Surfaces and Recent Progress in Extracorporeal Circulation
13 schema:pagination 169-176
14 schema:productId N3afc27a24dc04255a26d2f9b0ddf9baf
15 Ndec9de5e953440448c2056ee119afe95
16 Nf8a6ba975b924e2c981c08869ad690cb
17 schema:publisher Nea4a6ae68f7845f095503b86c16b86ee
18 schema:sameAs https://app.dimensions.ai/details/publication/pub.1050275112
19 https://doi.org/10.1007/978-4-431-66925-8_28
20 schema:sdDatePublished 2019-04-15T18:59
21 schema:sdLicense https://scigraph.springernature.com/explorer/license/
22 schema:sdPublisher Na6264e0d49f448adadf1cb306464fed4
23 schema:url http://link.springer.com/10.1007/978-4-431-66925-8_28
24 sgo:license sg:explorer/license/
25 sgo:sdDataset chapters
26 rdf:type schema:Chapter
27 N3afc27a24dc04255a26d2f9b0ddf9baf schema:name readcube_id
28 schema:value ef7ef8d964e7bbb820093d891e62b85a4561875237abd53f5594e90314a067a3
29 rdf:type schema:PropertyValue
30 N60d063659c3e441d956ee53b5df65e96 rdf:first N9dd61a0ac89c47c8b2d1443c0f833b4a
31 rdf:rest rdf:nil
32 N6bcba6cfe3b544d4bf9722fa6ab61d29 schema:familyName Takada
33 schema:givenName A.
34 rdf:type schema:Person
35 N8fee807232db4c7aa8f71cec4190dbdd rdf:first sg:person.016364747632.42
36 rdf:rest rdf:nil
37 N941621a823be44f8ae385cbca6b65e7b rdf:first N6bcba6cfe3b544d4bf9722fa6ab61d29
38 rdf:rest N60d063659c3e441d956ee53b5df65e96
39 N9dd61a0ac89c47c8b2d1443c0f833b4a schema:familyName Budzynski
40 schema:givenName A. Z.
41 rdf:type schema:Person
42 Na6264e0d49f448adadf1cb306464fed4 schema:name Springer Nature - SN SciGraph project
43 rdf:type schema:Organization
44 Ndec9de5e953440448c2056ee119afe95 schema:name doi
45 schema:value 10.1007/978-4-431-66925-8_28
46 rdf:type schema:PropertyValue
47 Nea4a6ae68f7845f095503b86c16b86ee schema:location Tokyo
48 schema:name Springer Japan
49 rdf:type schema:Organisation
50 Nf192235c85d54444a533137b5980dd4d schema:isbn 978-4-431-66925-8
51 978-4-431-70096-8
52 schema:name Hemostasis and Circulation
53 rdf:type schema:Book
54 Nf8a6ba975b924e2c981c08869ad690cb schema:name dimensions_id
55 schema:value pub.1050275112
56 rdf:type schema:PropertyValue
57 anzsrc-for:09 schema:inDefinedTermSet anzsrc-for:
58 schema:name Engineering
59 rdf:type schema:DefinedTerm
60 anzsrc-for:0903 schema:inDefinedTermSet anzsrc-for:
61 schema:name Biomedical Engineering
62 rdf:type schema:DefinedTerm
63 sg:person.016364747632.42 schema:affiliation https://www.grid.ac/institutes/grid.410796.d
64 schema:familyName Matsuda
65 schema:givenName Takehisa
66 schema:sameAs https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.016364747632.42
67 rdf:type schema:Person
68 https://www.grid.ac/institutes/grid.410796.d schema:alternateName National Cerebral and Cardiovascular Center
69 schema:name Dept. of Bioengineering, National Cardiovascular Center Research Institute, 5–7–1 Fujishirodai, Suita, Osaka, Japan
70 rdf:type schema:Organization
 




Preview window. Press ESC to close (or click here)


...