FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2087357068> ?p ?o ?g. }

• W2087357068 endingPage "2584" @default.
• W2087357068 startingPage "2577" @default.
• W2087357068 abstract "Study Design. The authors investigated the association of L5 proximal nerve root injury with spinal cord neuronal apoptosis (histologic) and whether exogenous erythropoietin therapy might reduce apoptosis/or pain (behavioral). Objectives. The first objective was to determine whether nerve root crush induces specific programmed cell death of spinal neurons in the dorsal and ventral horn and whether this is correlated with pain behaviors. The second objective was to determine if exogenous erythropoietin might reduce apoptosis and/or pain. Summary of Background Data. Whether spinal neuronal apoptosis is correlated with pain behaviors following nerve root injury remains unknown. It has been hypothesized that neuroprotective factors may alleviate pain behaviors by protecting neurons from death. Erythropoietin is a hematopoietic growth factor that recently has been demonstrated as a potent neuroprotective factor against ischemic damage in the brain. The effects of erythropoietin on pain and spinal cord neurons have not been examined. Methods. Sprague-Dawley rats received a L5 proximal nerve root crush injury or sham operation and were separated into two treatment groups for subcutaneous injection: 1) vehicle; 2) recombinant human erythropoietin, 2680 U/kg. The rats were sacrificed, and spinal cords were removed for apoptotic and immunohistochemical analysis at 0, 1, and 3 days after surgery. To determine whether recombinant human erythropoietin prevented mechanical allodynia in animals with nerve root crushes (n = 12/group), both treatment groups were tested for pain behaviors using the von Frey test at −1, −2, −3, 1, 3, 7, 11, and 14 days after surgery. Results. After nerve root injury, apoptotic neurons increased by 80% in the ipsilateral spinal cord and moderately in contralateral spinal cord in vehicle-treated animals compared to uninjured controls. Recombinant human erythropoietin reduced (P < 0.05) neuronal apoptosis in both superficial dorsal and ventral horns of the spinal cord. This corresponded with identification of erythropoietin and its receptors on spinal neurons and reductions in TNF–α colocalization in ventral horn neurons. Mechanical allodynia developed in the corresponding ipsilateral hind paw within 1 day and was sustaineduntil day 14. Recombinant human erythropoietin-treated animals demonstrated faster recovery from mechanical allodynia compared with vehicle-treated controls (P < 0.05). Conclusions. Our findings indicated that L5 proximal nerve root crush increased neuronal apoptosis in the superficial dorsal and ventral horn that correlated with mechanical allodynia. Exogenous recombinant human erythropoietin facilitated receptor-mediated neuroprotection of spinal cord neurons and faster recovery from mechanical allodynia. Erythropoietin may be a potential therapeutic factor for patients with low back pain by providing pain relief and neuroprotection." @default.
• W2087357068 created "2016-06-24" @default.
• W2087357068 creator A5034496276 @default.
• W2087357068 creator A5047440491 @default.
• W2087357068 creator A5047518428 @default.
• W2087357068 creator A5060835501 @default.
• W2087357068 date "2003-12-01" @default.
• W2087357068 modified "2023-10-03" @default.
• W2087357068 title "ISSLS Prize Winner: Erythropoietin Inhibits Spinal Neuronal Apoptosis and Pain Following Nerve Root Crush" @default.
• W2087357068 cites W1504583940 @default.
• W2087357068 cites W152617135 @default.
• W2087357068 cites W1567615855 @default.
• W2087357068 cites W1973178224 @default.
• W2087357068 cites W1976256963 @default.
• W2087357068 cites W1976869427 @default.
• W2087357068 cites W1978726693 @default.
• W2087357068 cites W1997031088 @default.
• W2087357068 cites W1997966386 @default.
• W2087357068 cites W2019152169 @default.
• W2087357068 cites W2032053313 @default.
• W2087357068 cites W2034987918 @default.
• W2087357068 cites W2041098348 @default.
• W2087357068 cites W2044561802 @default.
• W2087357068 cites W2068596895 @default.
• W2087357068 cites W2072650744 @default.
• W2087357068 cites W2078467799 @default.
• W2087357068 cites W2079162394 @default.
• W2087357068 cites W2081881569 @default.
• W2087357068 cites W2091013562 @default.
• W2087357068 cites W2093836826 @default.
• W2087357068 cites W2118234034 @default.
• W2087357068 cites W2125806058 @default.
• W2087357068 cites W2142463112 @default.
• W2087357068 cites W2162264368 @default.
• W2087357068 cites W2168323957 @default.
• W2087357068 cites W2318612759 @default.
• W2087357068 cites W377849966 @default.
• W2087357068 doi "https://doi.org/10.1097/01.brs.0000096674.12519.12" @default.
• W2087357068 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14652474" @default.
• W2087357068 hasPublicationYear "2003" @default.
• W2087357068 type Work @default.
• W2087357068 sameAs 2087357068 @default.
• W2087357068 citedByCount "70" @default.
• W2087357068 countsByYear W20873570682012 @default.
• W2087357068 countsByYear W20873570682013 @default.
• W2087357068 countsByYear W20873570682014 @default.
• W2087357068 countsByYear W20873570682015 @default.
• W2087357068 countsByYear W20873570682016 @default.
• W2087357068 countsByYear W20873570682017 @default.
• W2087357068 countsByYear W20873570682019 @default.
• W2087357068 countsByYear W20873570682020 @default.
• W2087357068 countsByYear W20873570682021 @default.
• W2087357068 countsByYear W20873570682022 @default.
• W2087357068 crossrefType "journal-article" @default.
• W2087357068 hasAuthorship W2087357068A5034496276 @default.
• W2087357068 hasAuthorship W2087357068A5047440491 @default.
• W2087357068 hasAuthorship W2087357068A5047518428 @default.
• W2087357068 hasAuthorship W2087357068A5060835501 @default.
• W2087357068 hasConcept C118552586 @default.
• W2087357068 hasConcept C126322002 @default.
• W2087357068 hasConcept C141071460 @default.
• W2087357068 hasConcept C15490471 @default.
• W2087357068 hasConcept C170493617 @default.
• W2087357068 hasConcept C178409289 @default.
• W2087357068 hasConcept C190283241 @default.
• W2087357068 hasConcept C25498285 @default.
• W2087357068 hasConcept C2775991916 @default.
• W2087357068 hasConcept C2777883359 @default.
• W2087357068 hasConcept C2778334475 @default.
• W2087357068 hasConcept C2778423431 @default.
• W2087357068 hasConcept C2778534260 @default.
• W2087357068 hasConcept C2779245659 @default.
• W2087357068 hasConcept C2780775167 @default.
• W2087357068 hasConcept C2780999072 @default.
• W2087357068 hasConcept C42219234 @default.
• W2087357068 hasConcept C55493867 @default.
• W2087357068 hasConcept C71924100 @default.
• W2087357068 hasConcept C86803240 @default.
• W2087357068 hasConceptScore W2087357068C118552586 @default.
• W2087357068 hasConceptScore W2087357068C126322002 @default.
• W2087357068 hasConceptScore W2087357068C141071460 @default.
• W2087357068 hasConceptScore W2087357068C15490471 @default.
• W2087357068 hasConceptScore W2087357068C170493617 @default.
• W2087357068 hasConceptScore W2087357068C178409289 @default.
• W2087357068 hasConceptScore W2087357068C190283241 @default.
• W2087357068 hasConceptScore W2087357068C25498285 @default.
• W2087357068 hasConceptScore W2087357068C2775991916 @default.
• W2087357068 hasConceptScore W2087357068C2777883359 @default.
• W2087357068 hasConceptScore W2087357068C2778334475 @default.
• W2087357068 hasConceptScore W2087357068C2778423431 @default.
• W2087357068 hasConceptScore W2087357068C2778534260 @default.
• W2087357068 hasConceptScore W2087357068C2779245659 @default.
• W2087357068 hasConceptScore W2087357068C2780775167 @default.
• W2087357068 hasConceptScore W2087357068C2780999072 @default.
• W2087357068 hasConceptScore W2087357068C42219234 @default.
• W2087357068 hasConceptScore W2087357068C55493867 @default.
• W2087357068 hasConceptScore W2087357068C71924100 @default.
• W2087357068 hasConceptScore W2087357068C86803240 @default.

• next