Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain
Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural acti...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Yang, Xiangyu [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
|---|
| Schlagwörter: |
|---|
| Umfang: |
11 |
|---|
| Übergeordnetes Werk: |
Enthalten in: Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes - March, Brayden ELSEVIER, 2023, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:125 ; year:2017 ; pages:284-294 ; extent:11 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.neuropharm.2017.06.031 |
|---|
| Katalog-ID: |
ELV025679627 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV025679627 | ||
| 003 | DE-627 | ||
| 005 | 20230625145159.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180603s2017 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.neuropharm.2017.06.031 |2 doi | |
| 028 | 5 | 2 | |a GBVA2017022000015.pica |
| 035 | |a (DE-627)ELV025679627 | ||
| 035 | |a (ELSEVIER)S0028-3908(17)30304-0 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | |a 610 | |
| 082 | 0 | 4 | |a 610 |q DE-600 |
| 082 | 0 | 4 | |a 610 |q VZ |
| 084 | |a 44.88 |2 bkl | ||
| 100 | 1 | |a Yang, Xiangyu |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain |
| 264 | 1 | |c 2017transfer abstract | |
| 300 | |a 11 | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). | ||
| 520 | |a Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). | ||
| 650 | 7 | |a Central sensitization |2 Elsevier | |
| 650 | 7 | |a LIM-Kinase |2 Elsevier | |
| 650 | 7 | |a Chronic pain |2 Elsevier | |
| 700 | 1 | |a He, Guiqin |4 oth | |
| 700 | 1 | |a Zhang, Xiaoyun |4 oth | |
| 700 | 1 | |a Chen, Lu |4 oth | |
| 700 | 1 | |a Kong, Yue |4 oth | |
| 700 | 1 | |a Xie, Wei |4 oth | |
| 700 | 1 | |a Jia, Zhengping |4 oth | |
| 700 | 1 | |a Liu, Wen-Tao |4 oth | |
| 700 | 1 | |a Zhou, Zikai |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a March, Brayden ELSEVIER |t Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes |d 2023 |g Amsterdam [u.a.] |w (DE-627)ELV009446303 |
| 773 | 1 | 8 | |g volume:125 |g year:2017 |g pages:284-294 |g extent:11 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.neuropharm.2017.06.031 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 912 | |a SSG-OLC-PHA | ||
| 936 | b | k | |a 44.88 |j Urologie |j Nephrologie |q VZ |
| 951 | |a AR | ||
| 952 | |d 125 |j 2017 |h 284-294 |g 11 | ||
| 953 | |2 045F |a 610 | ||
| author_variant |
x y xy |
|---|---|
| matchkey_str |
yangxiangyuheguiqinzhangxiaoyunchenlukon:2017----:rninihbtoolmsinfcnlatnaecnrlestztoadeae |
| hierarchy_sort_str |
2017transfer abstract |
| bklnumber |
44.88 |
| publishDate |
2017 |
| allfields |
10.1016/j.neuropharm.2017.06.031 doi GBVA2017022000015.pica (DE-627)ELV025679627 (ELSEVIER)S0028-3908(17)30304-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.88 bkl Yang, Xiangyu verfasserin aut Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). Central sensitization Elsevier LIM-Kinase Elsevier Chronic pain Elsevier He, Guiqin oth Zhang, Xiaoyun oth Chen, Lu oth Kong, Yue oth Xie, Wei oth Jia, Zhengping oth Liu, Wen-Tao oth Zhou, Zikai oth Enthalten in Elsevier Science March, Brayden ELSEVIER Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes 2023 Amsterdam [u.a.] (DE-627)ELV009446303 volume:125 year:2017 pages:284-294 extent:11 https://doi.org/10.1016/j.neuropharm.2017.06.031 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.88 Urologie Nephrologie VZ AR 125 2017 284-294 11 045F 610 |
| spelling |
10.1016/j.neuropharm.2017.06.031 doi GBVA2017022000015.pica (DE-627)ELV025679627 (ELSEVIER)S0028-3908(17)30304-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.88 bkl Yang, Xiangyu verfasserin aut Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). Central sensitization Elsevier LIM-Kinase Elsevier Chronic pain Elsevier He, Guiqin oth Zhang, Xiaoyun oth Chen, Lu oth Kong, Yue oth Xie, Wei oth Jia, Zhengping oth Liu, Wen-Tao oth Zhou, Zikai oth Enthalten in Elsevier Science March, Brayden ELSEVIER Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes 2023 Amsterdam [u.a.] (DE-627)ELV009446303 volume:125 year:2017 pages:284-294 extent:11 https://doi.org/10.1016/j.neuropharm.2017.06.031 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.88 Urologie Nephrologie VZ AR 125 2017 284-294 11 045F 610 |
| allfields_unstemmed |
10.1016/j.neuropharm.2017.06.031 doi GBVA2017022000015.pica (DE-627)ELV025679627 (ELSEVIER)S0028-3908(17)30304-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.88 bkl Yang, Xiangyu verfasserin aut Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). Central sensitization Elsevier LIM-Kinase Elsevier Chronic pain Elsevier He, Guiqin oth Zhang, Xiaoyun oth Chen, Lu oth Kong, Yue oth Xie, Wei oth Jia, Zhengping oth Liu, Wen-Tao oth Zhou, Zikai oth Enthalten in Elsevier Science March, Brayden ELSEVIER Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes 2023 Amsterdam [u.a.] (DE-627)ELV009446303 volume:125 year:2017 pages:284-294 extent:11 https://doi.org/10.1016/j.neuropharm.2017.06.031 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.88 Urologie Nephrologie VZ AR 125 2017 284-294 11 045F 610 |
| allfieldsGer |
10.1016/j.neuropharm.2017.06.031 doi GBVA2017022000015.pica (DE-627)ELV025679627 (ELSEVIER)S0028-3908(17)30304-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.88 bkl Yang, Xiangyu verfasserin aut Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). Central sensitization Elsevier LIM-Kinase Elsevier Chronic pain Elsevier He, Guiqin oth Zhang, Xiaoyun oth Chen, Lu oth Kong, Yue oth Xie, Wei oth Jia, Zhengping oth Liu, Wen-Tao oth Zhou, Zikai oth Enthalten in Elsevier Science March, Brayden ELSEVIER Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes 2023 Amsterdam [u.a.] (DE-627)ELV009446303 volume:125 year:2017 pages:284-294 extent:11 https://doi.org/10.1016/j.neuropharm.2017.06.031 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.88 Urologie Nephrologie VZ AR 125 2017 284-294 11 045F 610 |
| allfieldsSound |
10.1016/j.neuropharm.2017.06.031 doi GBVA2017022000015.pica (DE-627)ELV025679627 (ELSEVIER)S0028-3908(17)30304-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.88 bkl Yang, Xiangyu verfasserin aut Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). Central sensitization Elsevier LIM-Kinase Elsevier Chronic pain Elsevier He, Guiqin oth Zhang, Xiaoyun oth Chen, Lu oth Kong, Yue oth Xie, Wei oth Jia, Zhengping oth Liu, Wen-Tao oth Zhou, Zikai oth Enthalten in Elsevier Science March, Brayden ELSEVIER Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes 2023 Amsterdam [u.a.] (DE-627)ELV009446303 volume:125 year:2017 pages:284-294 extent:11 https://doi.org/10.1016/j.neuropharm.2017.06.031 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.88 Urologie Nephrologie VZ AR 125 2017 284-294 11 045F 610 |
| language |
English |
| source |
Enthalten in Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes Amsterdam [u.a.] volume:125 year:2017 pages:284-294 extent:11 |
| sourceStr |
Enthalten in Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes Amsterdam [u.a.] volume:125 year:2017 pages:284-294 extent:11 |
| format_phy_str_mv |
Article |
| bklname |
Urologie Nephrologie |
| institution |
findex.gbv.de |
| topic_facet |
Central sensitization LIM-Kinase Chronic pain |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes |
| authorswithroles_txt_mv |
Yang, Xiangyu @@aut@@ He, Guiqin @@oth@@ Zhang, Xiaoyun @@oth@@ Chen, Lu @@oth@@ Kong, Yue @@oth@@ Xie, Wei @@oth@@ Jia, Zhengping @@oth@@ Liu, Wen-Tao @@oth@@ Zhou, Zikai @@oth@@ |
| publishDateDaySort_date |
2017-01-01T00:00:00Z |
| hierarchy_top_id |
ELV009446303 |
| dewey-sort |
3610 |
| id |
ELV025679627 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV025679627</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625145159.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.neuropharm.2017.06.031</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2017022000015.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV025679627</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0028-3908(17)30304-0</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.88</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Yang, Xiangyu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">11</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP).</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP).</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Central sensitization</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">LIM-Kinase</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Chronic pain</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">He, Guiqin</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Xiaoyun</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Lu</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kong, Yue</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xie, Wei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Jia, Zhengping</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liu, Wen-Tao</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhou, Zikai</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">March, Brayden ELSEVIER</subfield><subfield code="t">Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes</subfield><subfield code="d">2023</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV009446303</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:125</subfield><subfield code="g">year:2017</subfield><subfield code="g">pages:284-294</subfield><subfield code="g">extent:11</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.neuropharm.2017.06.031</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.88</subfield><subfield code="j">Urologie</subfield><subfield code="j">Nephrologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">125</subfield><subfield code="j">2017</subfield><subfield code="h">284-294</subfield><subfield code="g">11</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| author |
Yang, Xiangyu |
| spellingShingle |
Yang, Xiangyu ddc 610 bkl 44.88 Elsevier Central sensitization Elsevier LIM-Kinase Elsevier Chronic pain Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain |
| authorStr |
Yang, Xiangyu |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV009446303 |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 610 DE-600 610 VZ 44.88 bkl Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain Central sensitization Elsevier LIM-Kinase Elsevier Chronic pain Elsevier |
| topic |
ddc 610 bkl 44.88 Elsevier Central sensitization Elsevier LIM-Kinase Elsevier Chronic pain |
| topic_unstemmed |
ddc 610 bkl 44.88 Elsevier Central sensitization Elsevier LIM-Kinase Elsevier Chronic pain |
| topic_browse |
ddc 610 bkl 44.88 Elsevier Central sensitization Elsevier LIM-Kinase Elsevier Chronic pain |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
g h gh x z xz l c lc y k yk w x wx z j zj w t l wtl z z zz |
| hierarchy_parent_title |
Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes |
| hierarchy_parent_id |
ELV009446303 |
| dewey-tens |
610 - Medicine & health |
| hierarchy_top_title |
Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV009446303 |
| title |
Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain |
| ctrlnum |
(DE-627)ELV025679627 (ELSEVIER)S0028-3908(17)30304-0 |
| title_full |
Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain |
| author_sort |
Yang, Xiangyu |
| journal |
Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes |
| journalStr |
Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology |
| recordtype |
marc |
| publishDateSort |
2017 |
| contenttype_str_mv |
zzz |
| container_start_page |
284 |
| author_browse |
Yang, Xiangyu |
| container_volume |
125 |
| physical |
11 |
| class |
610 610 DE-600 610 VZ 44.88 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Yang, Xiangyu |
| doi_str_mv |
10.1016/j.neuropharm.2017.06.031 |
| dewey-full |
610 |
| title_sort |
transient inhibition of limks significantly attenuated central sensitization and delayed the development of chronic pain |
| title_auth |
Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain |
| abstract |
Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). |
| abstractGer |
Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). |
| abstract_unstemmed |
Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP). |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA |
| title_short |
Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain |
| url |
https://doi.org/10.1016/j.neuropharm.2017.06.031 |
| remote_bool |
true |
| author2 |
He, Guiqin Zhang, Xiaoyun Chen, Lu Kong, Yue Xie, Wei Jia, Zhengping Liu, Wen-Tao Zhou, Zikai |
| author2Str |
He, Guiqin Zhang, Xiaoyun Chen, Lu Kong, Yue Xie, Wei Jia, Zhengping Liu, Wen-Tao Zhou, Zikai |
| ppnlink |
ELV009446303 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth oth oth oth oth |
| doi_str |
10.1016/j.neuropharm.2017.06.031 |
| up_date |
2024-07-06T18:11:38.805Z |
| _version_ |
1803854281501048832 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV025679627</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625145159.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.neuropharm.2017.06.031</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2017022000015.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV025679627</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0028-3908(17)30304-0</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.88</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Yang, Xiangyu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Transient inhibition of LIMKs significantly attenuated central sensitization and delayed the development of chronic pain</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">11</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP).</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Central sensitization represents a key mechanism mediating chronic pain, a major clinical problem lacking effective treatment options. LIM-domain kinases (LIMKs) selectively regulate several substrates, e.g. cofilin and cAMP response element-binding protein (CREB), that profoundly affect neural activities, such as synaptogenesis and gene expression, thus critical in the consolidation of long-term synaptic potentiation and memory in the brain. In this study, we demonstrate that LIMK deficiency significantly impaired the development of multiple forms of chronic pain. Mechanistic studies focusing on spared nerve injury (SNI) model reveal a pivotal role of LIMKs in the up-regulation of spontaneous excitatory synaptic transmission and synaptogenesis after pain induction. Depending on the pain induction methods, LIMKs can be transiently activated with distinct time courses. Accordingly, pharmacological inhibition of LIMKs targeting this critical period remarkably attenuated central sensitization in the spinal cord and alleviated pain behaviors. We propose selectively targeting LIMKs during their activation phase as a potential therapeutic strategy for clinical management of chronic pain, especially for chronic pain with predictable onset and development time courses, such as chronic post-surgical pain (PSP).</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Central sensitization</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">LIM-Kinase</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Chronic pain</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">He, Guiqin</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Xiaoyun</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Lu</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kong, Yue</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xie, Wei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Jia, Zhengping</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liu, Wen-Tao</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhou, Zikai</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">March, Brayden ELSEVIER</subfield><subfield code="t">Phallus Preservation for Locally Advanced Proximal Primary Urethral Carcinoma: Technique and Outcomes</subfield><subfield code="d">2023</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV009446303</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:125</subfield><subfield code="g">year:2017</subfield><subfield code="g">pages:284-294</subfield><subfield code="g">extent:11</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.neuropharm.2017.06.031</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.88</subfield><subfield code="j">Urologie</subfield><subfield code="j">Nephrologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">125</subfield><subfield code="j">2017</subfield><subfield code="h">284-294</subfield><subfield code="g">11</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| score |
7.4006386 |