Effects of upstream shear forces on priming of platelets for downstream adhesion and activation
[Display omitted] Platelets in flowing blood are sometimes exposed to elevated shear forces caused by anastomotic stenosis at the blood vessel-vascular implant interface. The objective of this study was to determine how effective upstream shear forces are in priming platelets for downstream adhesion...
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| creator | Rahman, Shekh M. Eichinger, Colin D. Hlady, Vladimir |
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Platelets in flowing blood are sometimes exposed to elevated shear forces caused by anastomotic stenosis at the blood vessel-vascular implant interface. The objective of this study was to determine how effective upstream shear forces are in priming platelets for downstream adhesion and activation. Flow chambers with upstream stenotic regions (shear rates of 400–1000 s−1) were manufactured by relief molding of polydimethylsiloxane. Downstream from the stenotic regions, microcontact printing was used to covalently immobilize three different proteins (fibrinogen, collagen, or von Willebrand factor) to serve as platelet capture agents. Anticoagulated whole blood was perfused through the flow chambers and platelet adhesion to the downstream capture region was quantified. It was found that transient exposure of platelets to increased shear forces resulted in higher platelet adhesion on all three proteins. The duration of the platelet exposure to elevated shear forces was varied by changing the length of the stenotic regions. The results indicated that, in addition to the magnitude of shear forces, the duration of exposure to these forces was also an important factor in priming platelets. The effect of upstream shear forces on platelet activation was assessed by quantifying P-selectin, integrin αIIbβ3, lysosomal glycoprotein, and phosphatidylserine exposure using flow cytometry. The results suggested that increased shear forces were capable of increasing the priming of platelets for downstream activation. This study implicates the anastomotic region(s) of vascular implants as a locus of platelet pre-activation that may lead to thrombus formation downstream.
A synthetic small-diameter vascular graft can often become stenotic due to intimal fibrous hyperplasia, either generally along the inside of the graft or at the anastomotic regions, leading to an increased shear force on flowing platelets. Our lab is studying how the upstream platelet preactivation (aka “priming”) in flowing blood affects their downstream adhesion and activation. This manuscript describes a study in which priming of platelets is achieved by upstream stenotic narrowing in a microfluidic flow chamber. Such experimental design was intended to mimic a vascular implant with stenotic upstream anastomosis and downstream exposed platelet protein agonists. Understanding how the pre-activated platelets respond to imperfect vascular implant surfaces downstream is an important factor in |
| doi_str_mv | 10.1016/j.actbio.2018.04.002 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5985216</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1742706118301922</els_id><sourcerecordid>2087378462</sourcerecordid><originalsourceid>FETCH-LOGICAL-c544t-53e2ddc964b9b662cf2eb2fdf49618536a1ea6b9f4d8003e3bbf5bcf4236aa953</originalsourceid><addsrcrecordid>eNp9kUuPFCEUhYnROOPoPzCmEjduqgQKKNiYmMn4SCZxo2vC4zJNpxpaqOqJ_1463Y6PhSuKnO9c7qmD0EuCB4KJeLsdjFtszAPFRA6YDRjTR-iSyEn2ExfycfueGO0nLMgFelbrFuNREiqfoguqBGdKjZdI34QAbqldDt26r0sBs-vqBkzpQi4OmpC6fYm7mO6OzH42C8zQDE3ufL5PZ4_xG6ixwSb5rm0WD2Zp1-foSTBzhRfn8wp9-3Dz9fpTf_vl4-fr97e944wtPR-Beu-UYFZZIagLFCwNPjAliOSjMASMsCowL1sMGK0N3LrAaJOM4uMVeneau1_tDryDtBQz6-PmpvzQ2UT9t5LiRt_lg-ZKckpEG_DmPKDk7yvURe9idTDPJkFeq6aY8pEIJVRDX_-DbvNaUovXKDmNk2SCNoqdKFdyrQXCwzIE62ODeqtPDepjgxoz3Rpstld_Bnkw_arsd1Jov_MQoejqIiQHPpbWpPY5_v-Fn14DsQI</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2087378462</pqid></control><display><type>article</type><title>Effects of upstream shear forces on priming of platelets for downstream adhesion and activation</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Rahman, Shekh M. ; Eichinger, Colin D. ; Hlady, Vladimir</creator><creatorcontrib>Rahman, Shekh M. ; Eichinger, Colin D. ; Hlady, Vladimir</creatorcontrib><description>[Display omitted]
Platelets in flowing blood are sometimes exposed to elevated shear forces caused by anastomotic stenosis at the blood vessel-vascular implant interface. The objective of this study was to determine how effective upstream shear forces are in priming platelets for downstream adhesion and activation. Flow chambers with upstream stenotic regions (shear rates of 400–1000 s−1) were manufactured by relief molding of polydimethylsiloxane. Downstream from the stenotic regions, microcontact printing was used to covalently immobilize three different proteins (fibrinogen, collagen, or von Willebrand factor) to serve as platelet capture agents. Anticoagulated whole blood was perfused through the flow chambers and platelet adhesion to the downstream capture region was quantified. It was found that transient exposure of platelets to increased shear forces resulted in higher platelet adhesion on all three proteins. The duration of the platelet exposure to elevated shear forces was varied by changing the length of the stenotic regions. The results indicated that, in addition to the magnitude of shear forces, the duration of exposure to these forces was also an important factor in priming platelets. The effect of upstream shear forces on platelet activation was assessed by quantifying P-selectin, integrin αIIbβ3, lysosomal glycoprotein, and phosphatidylserine exposure using flow cytometry. The results suggested that increased shear forces were capable of increasing the priming of platelets for downstream activation. This study implicates the anastomotic region(s) of vascular implants as a locus of platelet pre-activation that may lead to thrombus formation downstream.
A synthetic small-diameter vascular graft can often become stenotic due to intimal fibrous hyperplasia, either generally along the inside of the graft or at the anastomotic regions, leading to an increased shear force on flowing platelets. Our lab is studying how the upstream platelet preactivation (aka “priming”) in flowing blood affects their downstream adhesion and activation. This manuscript describes a study in which priming of platelets is achieved by upstream stenotic narrowing in a microfluidic flow chamber. Such experimental design was intended to mimic a vascular implant with stenotic upstream anastomosis and downstream exposed platelet protein agonists. Understanding how the pre-activated platelets respond to imperfect vascular implant surfaces downstream is an important factor in designing better vascular implants.</description><identifier>ISSN: 1742-7061</identifier><identifier>EISSN: 1878-7568</identifier><identifier>DOI: 10.1016/j.actbio.2018.04.002</identifier><identifier>PMID: 29654993</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Activation ; Activation analysis ; Adhesion ; Anastomosis ; Anastomotic stenosis ; Blood Coagulation ; Blood platelets ; Blood Platelets - cytology ; Blood Platelets - metabolism ; Blood vessels ; Collagen ; Design of experiments ; Downstream ; Downstream effects ; Experimental design ; Exposure ; Fibrinogen ; Flow chambers ; Flow cytometry ; Flow Cytometry - instrumentation ; Flow Cytometry - methods ; Glycoproteins ; Humans ; Hyperplasia ; Implants ; Microcontact printing ; Microfluidics ; P-selectin ; Phosphatidylserine ; Platelet adhesion and activation ; Platelet Adhesiveness ; Platelets ; Polydimethylsiloxane ; Priming ; Proteins ; Shear ; Shear Strength ; Shear stress ; Stenosis ; Thrombosis ; Upstream ; Vascular implants ; Von Willebrand factor</subject><ispartof>Acta biomaterialia, 2018-06, Vol.73, p.228-235</ispartof><rights>2018 Acta Materialia Inc.</rights><rights>Copyright © 2018 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.</rights><rights>Copyright Elsevier BV Jun 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c544t-53e2ddc964b9b662cf2eb2fdf49618536a1ea6b9f4d8003e3bbf5bcf4236aa953</citedby><cites>FETCH-LOGICAL-c544t-53e2ddc964b9b662cf2eb2fdf49618536a1ea6b9f4d8003e3bbf5bcf4236aa953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1742706118301922$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29654993$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rahman, Shekh M.</creatorcontrib><creatorcontrib>Eichinger, Colin D.</creatorcontrib><creatorcontrib>Hlady, Vladimir</creatorcontrib><title>Effects of upstream shear forces on priming of platelets for downstream adhesion and activation</title><title>Acta biomaterialia</title><addtitle>Acta Biomater</addtitle><description>[Display omitted]
Platelets in flowing blood are sometimes exposed to elevated shear forces caused by anastomotic stenosis at the blood vessel-vascular implant interface. The objective of this study was to determine how effective upstream shear forces are in priming platelets for downstream adhesion and activation. Flow chambers with upstream stenotic regions (shear rates of 400–1000 s−1) were manufactured by relief molding of polydimethylsiloxane. Downstream from the stenotic regions, microcontact printing was used to covalently immobilize three different proteins (fibrinogen, collagen, or von Willebrand factor) to serve as platelet capture agents. Anticoagulated whole blood was perfused through the flow chambers and platelet adhesion to the downstream capture region was quantified. It was found that transient exposure of platelets to increased shear forces resulted in higher platelet adhesion on all three proteins. The duration of the platelet exposure to elevated shear forces was varied by changing the length of the stenotic regions. The results indicated that, in addition to the magnitude of shear forces, the duration of exposure to these forces was also an important factor in priming platelets. The effect of upstream shear forces on platelet activation was assessed by quantifying P-selectin, integrin αIIbβ3, lysosomal glycoprotein, and phosphatidylserine exposure using flow cytometry. The results suggested that increased shear forces were capable of increasing the priming of platelets for downstream activation. This study implicates the anastomotic region(s) of vascular implants as a locus of platelet pre-activation that may lead to thrombus formation downstream.
A synthetic small-diameter vascular graft can often become stenotic due to intimal fibrous hyperplasia, either generally along the inside of the graft or at the anastomotic regions, leading to an increased shear force on flowing platelets. Our lab is studying how the upstream platelet preactivation (aka “priming”) in flowing blood affects their downstream adhesion and activation. This manuscript describes a study in which priming of platelets is achieved by upstream stenotic narrowing in a microfluidic flow chamber. Such experimental design was intended to mimic a vascular implant with stenotic upstream anastomosis and downstream exposed platelet protein agonists. Understanding how the pre-activated platelets respond to imperfect vascular implant surfaces downstream is an important factor in designing better vascular implants.</description><subject>Activation</subject><subject>Activation analysis</subject><subject>Adhesion</subject><subject>Anastomosis</subject><subject>Anastomotic stenosis</subject><subject>Blood Coagulation</subject><subject>Blood platelets</subject><subject>Blood Platelets - cytology</subject><subject>Blood Platelets - metabolism</subject><subject>Blood vessels</subject><subject>Collagen</subject><subject>Design of experiments</subject><subject>Downstream</subject><subject>Downstream effects</subject><subject>Experimental design</subject><subject>Exposure</subject><subject>Fibrinogen</subject><subject>Flow chambers</subject><subject>Flow cytometry</subject><subject>Flow Cytometry - instrumentation</subject><subject>Flow Cytometry - methods</subject><subject>Glycoproteins</subject><subject>Humans</subject><subject>Hyperplasia</subject><subject>Implants</subject><subject>Microcontact printing</subject><subject>Microfluidics</subject><subject>P-selectin</subject><subject>Phosphatidylserine</subject><subject>Platelet adhesion and activation</subject><subject>Platelet Adhesiveness</subject><subject>Platelets</subject><subject>Polydimethylsiloxane</subject><subject>Priming</subject><subject>Proteins</subject><subject>Shear</subject><subject>Shear Strength</subject><subject>Shear stress</subject><subject>Stenosis</subject><subject>Thrombosis</subject><subject>Upstream</subject><subject>Vascular implants</subject><subject>Von Willebrand factor</subject><issn>1742-7061</issn><issn>1878-7568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUuPFCEUhYnROOPoPzCmEjduqgQKKNiYmMn4SCZxo2vC4zJNpxpaqOqJ_1463Y6PhSuKnO9c7qmD0EuCB4KJeLsdjFtszAPFRA6YDRjTR-iSyEn2ExfycfueGO0nLMgFelbrFuNREiqfoguqBGdKjZdI34QAbqldDt26r0sBs-vqBkzpQi4OmpC6fYm7mO6OzH42C8zQDE3ufL5PZ4_xG6ixwSb5rm0WD2Zp1-foSTBzhRfn8wp9-3Dz9fpTf_vl4-fr97e944wtPR-Beu-UYFZZIagLFCwNPjAliOSjMASMsCowL1sMGK0N3LrAaJOM4uMVeneau1_tDryDtBQz6-PmpvzQ2UT9t5LiRt_lg-ZKckpEG_DmPKDk7yvURe9idTDPJkFeq6aY8pEIJVRDX_-DbvNaUovXKDmNk2SCNoqdKFdyrQXCwzIE62ODeqtPDepjgxoz3Rpstld_Bnkw_arsd1Jov_MQoejqIiQHPpbWpPY5_v-Fn14DsQI</recordid><startdate>20180601</startdate><enddate>20180601</enddate><creator>Rahman, Shekh M.</creator><creator>Eichinger, Colin D.</creator><creator>Hlady, Vladimir</creator><general>Elsevier Ltd</general><general>Elsevier BV</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>7QF</scope><scope>7QO</scope><scope>7QQ</scope><scope>7SC</scope><scope>7SE</scope><scope>7SP</scope><scope>7SR</scope><scope>7T7</scope><scope>7TA</scope><scope>7TB</scope><scope>7U5</scope><scope>8BQ</scope><scope>8FD</scope><scope>C1K</scope><scope>F28</scope><scope>FR3</scope><scope>H8D</scope><scope>H8G</scope><scope>JG9</scope><scope>JQ2</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180601</creationdate><title>Effects of upstream shear forces on priming of platelets for downstream adhesion and activation</title><author>Rahman, Shekh M. ; Eichinger, Colin D. ; Hlady, Vladimir</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c544t-53e2ddc964b9b662cf2eb2fdf49618536a1ea6b9f4d8003e3bbf5bcf4236aa953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Activation</topic><topic>Activation analysis</topic><topic>Adhesion</topic><topic>Anastomosis</topic><topic>Anastomotic stenosis</topic><topic>Blood Coagulation</topic><topic>Blood platelets</topic><topic>Blood Platelets - cytology</topic><topic>Blood Platelets - metabolism</topic><topic>Blood vessels</topic><topic>Collagen</topic><topic>Design of experiments</topic><topic>Downstream</topic><topic>Downstream effects</topic><topic>Experimental design</topic><topic>Exposure</topic><topic>Fibrinogen</topic><topic>Flow chambers</topic><topic>Flow cytometry</topic><topic>Flow Cytometry - instrumentation</topic><topic>Flow Cytometry - methods</topic><topic>Glycoproteins</topic><topic>Humans</topic><topic>Hyperplasia</topic><topic>Implants</topic><topic>Microcontact printing</topic><topic>Microfluidics</topic><topic>P-selectin</topic><topic>Phosphatidylserine</topic><topic>Platelet adhesion and activation</topic><topic>Platelet Adhesiveness</topic><topic>Platelets</topic><topic>Polydimethylsiloxane</topic><topic>Priming</topic><topic>Proteins</topic><topic>Shear</topic><topic>Shear Strength</topic><topic>Shear stress</topic><topic>Stenosis</topic><topic>Thrombosis</topic><topic>Upstream</topic><topic>Vascular implants</topic><topic>Von Willebrand factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rahman, Shekh M.</creatorcontrib><creatorcontrib>Eichinger, Colin D.</creatorcontrib><creatorcontrib>Hlady, Vladimir</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Aluminium Industry Abstracts</collection><collection>Biotechnology Research Abstracts</collection><collection>Ceramic Abstracts</collection><collection>Computer and Information Systems Abstracts</collection><collection>Corrosion Abstracts</collection><collection>Electronics & Communications Abstracts</collection><collection>Engineered Materials Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Materials Business File</collection><collection>Mechanical & Transportation Engineering Abstracts</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>METADEX</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ANTE: Abstracts in New Technology & Engineering</collection><collection>Engineering Research Database</collection><collection>Aerospace Database</collection><collection>Copper Technical Reference Library</collection><collection>Materials Research Database</collection><collection>ProQuest Computer Science Collection</collection><collection>Civil Engineering Abstracts</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>Computer and Information Systems Abstracts Academic</collection><collection>Computer and Information Systems Abstracts Professional</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Acta biomaterialia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rahman, Shekh M.</au><au>Eichinger, Colin D.</au><au>Hlady, Vladimir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of upstream shear forces on priming of platelets for downstream adhesion and activation</atitle><jtitle>Acta biomaterialia</jtitle><addtitle>Acta Biomater</addtitle><date>2018-06-01</date><risdate>2018</risdate><volume>73</volume><spage>228</spage><epage>235</epage><pages>228-235</pages><issn>1742-7061</issn><eissn>1878-7568</eissn><abstract>[Display omitted]
Platelets in flowing blood are sometimes exposed to elevated shear forces caused by anastomotic stenosis at the blood vessel-vascular implant interface. The objective of this study was to determine how effective upstream shear forces are in priming platelets for downstream adhesion and activation. Flow chambers with upstream stenotic regions (shear rates of 400–1000 s−1) were manufactured by relief molding of polydimethylsiloxane. Downstream from the stenotic regions, microcontact printing was used to covalently immobilize three different proteins (fibrinogen, collagen, or von Willebrand factor) to serve as platelet capture agents. Anticoagulated whole blood was perfused through the flow chambers and platelet adhesion to the downstream capture region was quantified. It was found that transient exposure of platelets to increased shear forces resulted in higher platelet adhesion on all three proteins. The duration of the platelet exposure to elevated shear forces was varied by changing the length of the stenotic regions. The results indicated that, in addition to the magnitude of shear forces, the duration of exposure to these forces was also an important factor in priming platelets. The effect of upstream shear forces on platelet activation was assessed by quantifying P-selectin, integrin αIIbβ3, lysosomal glycoprotein, and phosphatidylserine exposure using flow cytometry. The results suggested that increased shear forces were capable of increasing the priming of platelets for downstream activation. This study implicates the anastomotic region(s) of vascular implants as a locus of platelet pre-activation that may lead to thrombus formation downstream.
A synthetic small-diameter vascular graft can often become stenotic due to intimal fibrous hyperplasia, either generally along the inside of the graft or at the anastomotic regions, leading to an increased shear force on flowing platelets. Our lab is studying how the upstream platelet preactivation (aka “priming”) in flowing blood affects their downstream adhesion and activation. This manuscript describes a study in which priming of platelets is achieved by upstream stenotic narrowing in a microfluidic flow chamber. Such experimental design was intended to mimic a vascular implant with stenotic upstream anastomosis and downstream exposed platelet protein agonists. Understanding how the pre-activated platelets respond to imperfect vascular implant surfaces downstream is an important factor in designing better vascular implants.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>29654993</pmid><doi>10.1016/j.actbio.2018.04.002</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Acta biomaterialia, 2018-06, Vol.73, p.228-235 |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Activation Activation analysis Adhesion Anastomosis Anastomotic stenosis Blood Coagulation Blood platelets Blood Platelets - cytology Blood Platelets - metabolism Blood vessels Collagen Design of experiments Downstream Downstream effects Experimental design Exposure Fibrinogen Flow chambers Flow cytometry Flow Cytometry - instrumentation Flow Cytometry - methods Glycoproteins Humans Hyperplasia Implants Microcontact printing Microfluidics P-selectin Phosphatidylserine Platelet adhesion and activation Platelet Adhesiveness Platelets Polydimethylsiloxane Priming Proteins Shear Shear Strength Shear stress Stenosis Thrombosis Upstream Vascular implants Von Willebrand factor |
| title | Effects of upstream shear forces on priming of platelets for downstream adhesion and activation |
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