Role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia
Abstract Chronic hypoxic pulmonary hypertension (HPH) is associated with large pulmonary artery (PA) stiffening, which is correlated with collagen accumulation. However, the mechanisms by which collagen contributes to PA stiffening remain largely unexplored. Moreover, HPH may alter mechanical proper...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Wang, Zhijie [verfasserIn] Chesler, Naomi C. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2011 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Biomechanics and modeling in mechanobiology - Berlin : Springer, 2002, 11(2011), 1-2 vom: 03. Mai, Seite 279-289 |
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| Übergeordnetes Werk: |
volume:11 ; year:2011 ; number:1-2 ; day:03 ; month:05 ; pages:279-289 |
| Links: |
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| DOI / URN: |
10.1007/s10237-011-0309-z |
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SPR009217444 |
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| 520 | |a Abstract Chronic hypoxic pulmonary hypertension (HPH) is associated with large pulmonary artery (PA) stiffening, which is correlated with collagen accumulation. However, the mechanisms by which collagen contributes to PA stiffening remain largely unexplored. Moreover, HPH may alter mechanical properties other than stiffness, such as pulse damping capacity, which also affects ventricular workload but is rarely quantified. We hypothesized that collagen content and cross-linking differentially regulate the stiffness and damping capacity of large PAs during HPH progression. The hypothesis was tested with transgenic mice that synthesize collagen type I resistant to collagenase degradation ($ Col1a1^{R/R} $). These mice and littermate controls ($ Col1a1^{+/+} $) were exposed to hypoxia for 10 days; some were treated with β-aminopropionitrile (BAPN), which prevents new cross-link formation. Isolated PA dynamic mechanical tests were performed, and collagen content and cross-linking were measured. In $ Col1a1^{+/+} $ mice, HPH increased both collagen content and cross-linking, and BAPN treatment prevented these increases. Similar trends were observed in $ Col1a1^{R/R} $ mice except that collagen content further increased with BAPN treatment. Mechanical tests showed that in $ Col1a1^{+/+} $ mice, HPH increased PA stiffness and damping capacity, and these increases were impeded by BAPN treatment. In $ Col1a1^{R/R} $ mice, HPH led to a smaller but significant increase in PA stiffness and a decrease in damping capacity. These mechanical changes were not affected by BAPN treatment. Vessel-specific correlations for each strain showed that the stiffness and damping capacity were correlated with the total content rather than cross-linking of collagen. Our results suggest that collagen total content is critical to extralobar PA stiffening during HPH. | ||
| 650 | 4 | |a Hypoxic pulmonary hypertension |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Pulmonary artery biomechanics |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Viscoelasticity |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Damping capacity |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Chesler, Naomi C. |e verfasserin |4 aut | |
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10.1007/s10237-011-0309-z doi (DE-627)SPR009217444 (SPR)s10237-011-0309-z-e DE-627 ger DE-627 rakwb eng 570 540 ASE 42.12 bkl 44.09 bkl 76.12 bkl Wang, Zhijie verfasserin aut Role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Chronic hypoxic pulmonary hypertension (HPH) is associated with large pulmonary artery (PA) stiffening, which is correlated with collagen accumulation. However, the mechanisms by which collagen contributes to PA stiffening remain largely unexplored. Moreover, HPH may alter mechanical properties other than stiffness, such as pulse damping capacity, which also affects ventricular workload but is rarely quantified. We hypothesized that collagen content and cross-linking differentially regulate the stiffness and damping capacity of large PAs during HPH progression. The hypothesis was tested with transgenic mice that synthesize collagen type I resistant to collagenase degradation ($ Col1a1^{R/R} $). These mice and littermate controls ($ Col1a1^{+/+} $) were exposed to hypoxia for 10 days; some were treated with β-aminopropionitrile (BAPN), which prevents new cross-link formation. Isolated PA dynamic mechanical tests were performed, and collagen content and cross-linking were measured. In $ Col1a1^{+/+} $ mice, HPH increased both collagen content and cross-linking, and BAPN treatment prevented these increases. Similar trends were observed in $ Col1a1^{R/R} $ mice except that collagen content further increased with BAPN treatment. Mechanical tests showed that in $ Col1a1^{+/+} $ mice, HPH increased PA stiffness and damping capacity, and these increases were impeded by BAPN treatment. In $ Col1a1^{R/R} $ mice, HPH led to a smaller but significant increase in PA stiffness and a decrease in damping capacity. These mechanical changes were not affected by BAPN treatment. Vessel-specific correlations for each strain showed that the stiffness and damping capacity were correlated with the total content rather than cross-linking of collagen. Our results suggest that collagen total content is critical to extralobar PA stiffening during HPH. Hypoxic pulmonary hypertension (dpeaa)DE-He213 Pulmonary artery biomechanics (dpeaa)DE-He213 Viscoelasticity (dpeaa)DE-He213 Damping capacity (dpeaa)DE-He213 Chesler, Naomi C. verfasserin aut Enthalten in Biomechanics and modeling in mechanobiology Berlin : Springer, 2002 11(2011), 1-2 vom: 03. Mai, Seite 279-289 (DE-627)339869836 (DE-600)2064972-1 1617-7940 nnns volume:11 year:2011 number:1-2 day:03 month:05 pages:279-289 https://dx.doi.org/10.1007/s10237-011-0309-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.12 ASE 44.09 ASE 76.12 ASE AR 11 2011 1-2 03 05 279-289 |
| spelling |
10.1007/s10237-011-0309-z doi (DE-627)SPR009217444 (SPR)s10237-011-0309-z-e DE-627 ger DE-627 rakwb eng 570 540 ASE 42.12 bkl 44.09 bkl 76.12 bkl Wang, Zhijie verfasserin aut Role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Chronic hypoxic pulmonary hypertension (HPH) is associated with large pulmonary artery (PA) stiffening, which is correlated with collagen accumulation. However, the mechanisms by which collagen contributes to PA stiffening remain largely unexplored. Moreover, HPH may alter mechanical properties other than stiffness, such as pulse damping capacity, which also affects ventricular workload but is rarely quantified. We hypothesized that collagen content and cross-linking differentially regulate the stiffness and damping capacity of large PAs during HPH progression. The hypothesis was tested with transgenic mice that synthesize collagen type I resistant to collagenase degradation ($ Col1a1^{R/R} $). These mice and littermate controls ($ Col1a1^{+/+} $) were exposed to hypoxia for 10 days; some were treated with β-aminopropionitrile (BAPN), which prevents new cross-link formation. Isolated PA dynamic mechanical tests were performed, and collagen content and cross-linking were measured. In $ Col1a1^{+/+} $ mice, HPH increased both collagen content and cross-linking, and BAPN treatment prevented these increases. Similar trends were observed in $ Col1a1^{R/R} $ mice except that collagen content further increased with BAPN treatment. Mechanical tests showed that in $ Col1a1^{+/+} $ mice, HPH increased PA stiffness and damping capacity, and these increases were impeded by BAPN treatment. In $ Col1a1^{R/R} $ mice, HPH led to a smaller but significant increase in PA stiffness and a decrease in damping capacity. These mechanical changes were not affected by BAPN treatment. Vessel-specific correlations for each strain showed that the stiffness and damping capacity were correlated with the total content rather than cross-linking of collagen. Our results suggest that collagen total content is critical to extralobar PA stiffening during HPH. Hypoxic pulmonary hypertension (dpeaa)DE-He213 Pulmonary artery biomechanics (dpeaa)DE-He213 Viscoelasticity (dpeaa)DE-He213 Damping capacity (dpeaa)DE-He213 Chesler, Naomi C. verfasserin aut Enthalten in Biomechanics and modeling in mechanobiology Berlin : Springer, 2002 11(2011), 1-2 vom: 03. Mai, Seite 279-289 (DE-627)339869836 (DE-600)2064972-1 1617-7940 nnns volume:11 year:2011 number:1-2 day:03 month:05 pages:279-289 https://dx.doi.org/10.1007/s10237-011-0309-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.12 ASE 44.09 ASE 76.12 ASE AR 11 2011 1-2 03 05 279-289 |
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10.1007/s10237-011-0309-z doi (DE-627)SPR009217444 (SPR)s10237-011-0309-z-e DE-627 ger DE-627 rakwb eng 570 540 ASE 42.12 bkl 44.09 bkl 76.12 bkl Wang, Zhijie verfasserin aut Role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Chronic hypoxic pulmonary hypertension (HPH) is associated with large pulmonary artery (PA) stiffening, which is correlated with collagen accumulation. However, the mechanisms by which collagen contributes to PA stiffening remain largely unexplored. Moreover, HPH may alter mechanical properties other than stiffness, such as pulse damping capacity, which also affects ventricular workload but is rarely quantified. We hypothesized that collagen content and cross-linking differentially regulate the stiffness and damping capacity of large PAs during HPH progression. The hypothesis was tested with transgenic mice that synthesize collagen type I resistant to collagenase degradation ($ Col1a1^{R/R} $). These mice and littermate controls ($ Col1a1^{+/+} $) were exposed to hypoxia for 10 days; some were treated with β-aminopropionitrile (BAPN), which prevents new cross-link formation. Isolated PA dynamic mechanical tests were performed, and collagen content and cross-linking were measured. In $ Col1a1^{+/+} $ mice, HPH increased both collagen content and cross-linking, and BAPN treatment prevented these increases. Similar trends were observed in $ Col1a1^{R/R} $ mice except that collagen content further increased with BAPN treatment. Mechanical tests showed that in $ Col1a1^{+/+} $ mice, HPH increased PA stiffness and damping capacity, and these increases were impeded by BAPN treatment. In $ Col1a1^{R/R} $ mice, HPH led to a smaller but significant increase in PA stiffness and a decrease in damping capacity. These mechanical changes were not affected by BAPN treatment. Vessel-specific correlations for each strain showed that the stiffness and damping capacity were correlated with the total content rather than cross-linking of collagen. Our results suggest that collagen total content is critical to extralobar PA stiffening during HPH. Hypoxic pulmonary hypertension (dpeaa)DE-He213 Pulmonary artery biomechanics (dpeaa)DE-He213 Viscoelasticity (dpeaa)DE-He213 Damping capacity (dpeaa)DE-He213 Chesler, Naomi C. verfasserin aut Enthalten in Biomechanics and modeling in mechanobiology Berlin : Springer, 2002 11(2011), 1-2 vom: 03. Mai, Seite 279-289 (DE-627)339869836 (DE-600)2064972-1 1617-7940 nnns volume:11 year:2011 number:1-2 day:03 month:05 pages:279-289 https://dx.doi.org/10.1007/s10237-011-0309-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.12 ASE 44.09 ASE 76.12 ASE AR 11 2011 1-2 03 05 279-289 |
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10.1007/s10237-011-0309-z doi (DE-627)SPR009217444 (SPR)s10237-011-0309-z-e DE-627 ger DE-627 rakwb eng 570 540 ASE 42.12 bkl 44.09 bkl 76.12 bkl Wang, Zhijie verfasserin aut Role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Chronic hypoxic pulmonary hypertension (HPH) is associated with large pulmonary artery (PA) stiffening, which is correlated with collagen accumulation. However, the mechanisms by which collagen contributes to PA stiffening remain largely unexplored. Moreover, HPH may alter mechanical properties other than stiffness, such as pulse damping capacity, which also affects ventricular workload but is rarely quantified. We hypothesized that collagen content and cross-linking differentially regulate the stiffness and damping capacity of large PAs during HPH progression. The hypothesis was tested with transgenic mice that synthesize collagen type I resistant to collagenase degradation ($ Col1a1^{R/R} $). These mice and littermate controls ($ Col1a1^{+/+} $) were exposed to hypoxia for 10 days; some were treated with β-aminopropionitrile (BAPN), which prevents new cross-link formation. Isolated PA dynamic mechanical tests were performed, and collagen content and cross-linking were measured. In $ Col1a1^{+/+} $ mice, HPH increased both collagen content and cross-linking, and BAPN treatment prevented these increases. Similar trends were observed in $ Col1a1^{R/R} $ mice except that collagen content further increased with BAPN treatment. Mechanical tests showed that in $ Col1a1^{+/+} $ mice, HPH increased PA stiffness and damping capacity, and these increases were impeded by BAPN treatment. In $ Col1a1^{R/R} $ mice, HPH led to a smaller but significant increase in PA stiffness and a decrease in damping capacity. These mechanical changes were not affected by BAPN treatment. Vessel-specific correlations for each strain showed that the stiffness and damping capacity were correlated with the total content rather than cross-linking of collagen. Our results suggest that collagen total content is critical to extralobar PA stiffening during HPH. Hypoxic pulmonary hypertension (dpeaa)DE-He213 Pulmonary artery biomechanics (dpeaa)DE-He213 Viscoelasticity (dpeaa)DE-He213 Damping capacity (dpeaa)DE-He213 Chesler, Naomi C. verfasserin aut Enthalten in Biomechanics and modeling in mechanobiology Berlin : Springer, 2002 11(2011), 1-2 vom: 03. Mai, Seite 279-289 (DE-627)339869836 (DE-600)2064972-1 1617-7940 nnns volume:11 year:2011 number:1-2 day:03 month:05 pages:279-289 https://dx.doi.org/10.1007/s10237-011-0309-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.12 ASE 44.09 ASE 76.12 ASE AR 11 2011 1-2 03 05 279-289 |
| allfieldsSound |
10.1007/s10237-011-0309-z doi (DE-627)SPR009217444 (SPR)s10237-011-0309-z-e DE-627 ger DE-627 rakwb eng 570 540 ASE 42.12 bkl 44.09 bkl 76.12 bkl Wang, Zhijie verfasserin aut Role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Chronic hypoxic pulmonary hypertension (HPH) is associated with large pulmonary artery (PA) stiffening, which is correlated with collagen accumulation. However, the mechanisms by which collagen contributes to PA stiffening remain largely unexplored. Moreover, HPH may alter mechanical properties other than stiffness, such as pulse damping capacity, which also affects ventricular workload but is rarely quantified. We hypothesized that collagen content and cross-linking differentially regulate the stiffness and damping capacity of large PAs during HPH progression. The hypothesis was tested with transgenic mice that synthesize collagen type I resistant to collagenase degradation ($ Col1a1^{R/R} $). These mice and littermate controls ($ Col1a1^{+/+} $) were exposed to hypoxia for 10 days; some were treated with β-aminopropionitrile (BAPN), which prevents new cross-link formation. Isolated PA dynamic mechanical tests were performed, and collagen content and cross-linking were measured. In $ Col1a1^{+/+} $ mice, HPH increased both collagen content and cross-linking, and BAPN treatment prevented these increases. Similar trends were observed in $ Col1a1^{R/R} $ mice except that collagen content further increased with BAPN treatment. Mechanical tests showed that in $ Col1a1^{+/+} $ mice, HPH increased PA stiffness and damping capacity, and these increases were impeded by BAPN treatment. In $ Col1a1^{R/R} $ mice, HPH led to a smaller but significant increase in PA stiffness and a decrease in damping capacity. These mechanical changes were not affected by BAPN treatment. Vessel-specific correlations for each strain showed that the stiffness and damping capacity were correlated with the total content rather than cross-linking of collagen. Our results suggest that collagen total content is critical to extralobar PA stiffening during HPH. Hypoxic pulmonary hypertension (dpeaa)DE-He213 Pulmonary artery biomechanics (dpeaa)DE-He213 Viscoelasticity (dpeaa)DE-He213 Damping capacity (dpeaa)DE-He213 Chesler, Naomi C. verfasserin aut Enthalten in Biomechanics and modeling in mechanobiology Berlin : Springer, 2002 11(2011), 1-2 vom: 03. Mai, Seite 279-289 (DE-627)339869836 (DE-600)2064972-1 1617-7940 nnns volume:11 year:2011 number:1-2 day:03 month:05 pages:279-289 https://dx.doi.org/10.1007/s10237-011-0309-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.12 ASE 44.09 ASE 76.12 ASE AR 11 2011 1-2 03 05 279-289 |
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English |
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Enthalten in Biomechanics and modeling in mechanobiology 11(2011), 1-2 vom: 03. Mai, Seite 279-289 volume:11 year:2011 number:1-2 day:03 month:05 pages:279-289 |
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Enthalten in Biomechanics and modeling in mechanobiology 11(2011), 1-2 vom: 03. Mai, Seite 279-289 volume:11 year:2011 number:1-2 day:03 month:05 pages:279-289 |
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Hypoxic pulmonary hypertension Pulmonary artery biomechanics Viscoelasticity Damping capacity |
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Biomechanics and modeling in mechanobiology |
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Wang, Zhijie @@aut@@ Chesler, Naomi C. @@aut@@ |
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2011-05-03T00:00:00Z |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR009217444</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519190850.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201005s2011 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s10237-011-0309-z</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR009217444</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s10237-011-0309-z-e</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="4"><subfield code="a">570</subfield><subfield code="a">540</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">42.12</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.09</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">76.12</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Wang, Zhijie</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2011</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Chronic hypoxic pulmonary hypertension (HPH) is associated with large pulmonary artery (PA) stiffening, which is correlated with collagen accumulation. However, the mechanisms by which collagen contributes to PA stiffening remain largely unexplored. Moreover, HPH may alter mechanical properties other than stiffness, such as pulse damping capacity, which also affects ventricular workload but is rarely quantified. We hypothesized that collagen content and cross-linking differentially regulate the stiffness and damping capacity of large PAs during HPH progression. The hypothesis was tested with transgenic mice that synthesize collagen type I resistant to collagenase degradation ($ Col1a1^{R/R} $). These mice and littermate controls ($ Col1a1^{+/+} $) were exposed to hypoxia for 10 days; some were treated with β-aminopropionitrile (BAPN), which prevents new cross-link formation. Isolated PA dynamic mechanical tests were performed, and collagen content and cross-linking were measured. In $ Col1a1^{+/+} $ mice, HPH increased both collagen content and cross-linking, and BAPN treatment prevented these increases. Similar trends were observed in $ Col1a1^{R/R} $ mice except that collagen content further increased with BAPN treatment. Mechanical tests showed that in $ Col1a1^{+/+} $ mice, HPH increased PA stiffness and damping capacity, and these increases were impeded by BAPN treatment. In $ Col1a1^{R/R} $ mice, HPH led to a smaller but significant increase in PA stiffness and a decrease in damping capacity. These mechanical changes were not affected by BAPN treatment. Vessel-specific correlations for each strain showed that the stiffness and damping capacity were correlated with the total content rather than cross-linking of collagen. 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Wang, Zhijie |
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Wang, Zhijie ddc 570 bkl 42.12 bkl 44.09 bkl 76.12 misc Hypoxic pulmonary hypertension misc Pulmonary artery biomechanics misc Viscoelasticity misc Damping capacity Role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia |
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570 540 ASE 42.12 bkl 44.09 bkl 76.12 bkl Role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia Hypoxic pulmonary hypertension (dpeaa)DE-He213 Pulmonary artery biomechanics (dpeaa)DE-He213 Viscoelasticity (dpeaa)DE-He213 Damping capacity (dpeaa)DE-He213 |
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ddc 570 bkl 42.12 bkl 44.09 bkl 76.12 misc Hypoxic pulmonary hypertension misc Pulmonary artery biomechanics misc Viscoelasticity misc Damping capacity |
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ddc 570 bkl 42.12 bkl 44.09 bkl 76.12 misc Hypoxic pulmonary hypertension misc Pulmonary artery biomechanics misc Viscoelasticity misc Damping capacity |
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Role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia |
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Role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia |
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role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia |
| title_auth |
Role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia |
| abstract |
Abstract Chronic hypoxic pulmonary hypertension (HPH) is associated with large pulmonary artery (PA) stiffening, which is correlated with collagen accumulation. However, the mechanisms by which collagen contributes to PA stiffening remain largely unexplored. Moreover, HPH may alter mechanical properties other than stiffness, such as pulse damping capacity, which also affects ventricular workload but is rarely quantified. We hypothesized that collagen content and cross-linking differentially regulate the stiffness and damping capacity of large PAs during HPH progression. The hypothesis was tested with transgenic mice that synthesize collagen type I resistant to collagenase degradation ($ Col1a1^{R/R} $). These mice and littermate controls ($ Col1a1^{+/+} $) were exposed to hypoxia for 10 days; some were treated with β-aminopropionitrile (BAPN), which prevents new cross-link formation. Isolated PA dynamic mechanical tests were performed, and collagen content and cross-linking were measured. In $ Col1a1^{+/+} $ mice, HPH increased both collagen content and cross-linking, and BAPN treatment prevented these increases. Similar trends were observed in $ Col1a1^{R/R} $ mice except that collagen content further increased with BAPN treatment. Mechanical tests showed that in $ Col1a1^{+/+} $ mice, HPH increased PA stiffness and damping capacity, and these increases were impeded by BAPN treatment. In $ Col1a1^{R/R} $ mice, HPH led to a smaller but significant increase in PA stiffness and a decrease in damping capacity. These mechanical changes were not affected by BAPN treatment. Vessel-specific correlations for each strain showed that the stiffness and damping capacity were correlated with the total content rather than cross-linking of collagen. Our results suggest that collagen total content is critical to extralobar PA stiffening during HPH. |
| abstractGer |
Abstract Chronic hypoxic pulmonary hypertension (HPH) is associated with large pulmonary artery (PA) stiffening, which is correlated with collagen accumulation. However, the mechanisms by which collagen contributes to PA stiffening remain largely unexplored. Moreover, HPH may alter mechanical properties other than stiffness, such as pulse damping capacity, which also affects ventricular workload but is rarely quantified. We hypothesized that collagen content and cross-linking differentially regulate the stiffness and damping capacity of large PAs during HPH progression. The hypothesis was tested with transgenic mice that synthesize collagen type I resistant to collagenase degradation ($ Col1a1^{R/R} $). These mice and littermate controls ($ Col1a1^{+/+} $) were exposed to hypoxia for 10 days; some were treated with β-aminopropionitrile (BAPN), which prevents new cross-link formation. Isolated PA dynamic mechanical tests were performed, and collagen content and cross-linking were measured. In $ Col1a1^{+/+} $ mice, HPH increased both collagen content and cross-linking, and BAPN treatment prevented these increases. Similar trends were observed in $ Col1a1^{R/R} $ mice except that collagen content further increased with BAPN treatment. Mechanical tests showed that in $ Col1a1^{+/+} $ mice, HPH increased PA stiffness and damping capacity, and these increases were impeded by BAPN treatment. In $ Col1a1^{R/R} $ mice, HPH led to a smaller but significant increase in PA stiffness and a decrease in damping capacity. These mechanical changes were not affected by BAPN treatment. Vessel-specific correlations for each strain showed that the stiffness and damping capacity were correlated with the total content rather than cross-linking of collagen. Our results suggest that collagen total content is critical to extralobar PA stiffening during HPH. |
| abstract_unstemmed |
Abstract Chronic hypoxic pulmonary hypertension (HPH) is associated with large pulmonary artery (PA) stiffening, which is correlated with collagen accumulation. However, the mechanisms by which collagen contributes to PA stiffening remain largely unexplored. Moreover, HPH may alter mechanical properties other than stiffness, such as pulse damping capacity, which also affects ventricular workload but is rarely quantified. We hypothesized that collagen content and cross-linking differentially regulate the stiffness and damping capacity of large PAs during HPH progression. The hypothesis was tested with transgenic mice that synthesize collagen type I resistant to collagenase degradation ($ Col1a1^{R/R} $). These mice and littermate controls ($ Col1a1^{+/+} $) were exposed to hypoxia for 10 days; some were treated with β-aminopropionitrile (BAPN), which prevents new cross-link formation. Isolated PA dynamic mechanical tests were performed, and collagen content and cross-linking were measured. In $ Col1a1^{+/+} $ mice, HPH increased both collagen content and cross-linking, and BAPN treatment prevented these increases. Similar trends were observed in $ Col1a1^{R/R} $ mice except that collagen content further increased with BAPN treatment. Mechanical tests showed that in $ Col1a1^{+/+} $ mice, HPH increased PA stiffness and damping capacity, and these increases were impeded by BAPN treatment. In $ Col1a1^{R/R} $ mice, HPH led to a smaller but significant increase in PA stiffness and a decrease in damping capacity. These mechanical changes were not affected by BAPN treatment. Vessel-specific correlations for each strain showed that the stiffness and damping capacity were correlated with the total content rather than cross-linking of collagen. Our results suggest that collagen total content is critical to extralobar PA stiffening during HPH. |
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| container_issue |
1-2 |
| title_short |
Role of collagen content and cross-linking in large pulmonary arterial stiffening after chronic hypoxia |
| url |
https://dx.doi.org/10.1007/s10237-011-0309-z |
| remote_bool |
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| author2 |
Chesler, Naomi C. |
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| doi_str |
10.1007/s10237-011-0309-z |
| up_date |
2024-07-04T01:09:32.574Z |
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|
| score |
7.399596 |