- Location
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
1742-2094
- Extent
-
Online-Ressource
- Language
-
Englisch
- Notes
-
online resource.
- Bibliographic citation
-
CCL3 contributes to secondary damage after spinal cord injury ; volume:17 ; number:1 ; day:27 ; month:11 ; year:2020 ; pages:1-16 ; date:12.2020
Journal of neuroinflammation ; 17, Heft 1 (27.11.2020), 1-16, 12.2020
- Creator
-
Pelisch, Nicolas
Rosas Almanza, Jose
Stehlik, Kyle E.
Aperi, Brandy V.
Kroner, Antje
- Contributor
-
SpringerLink (Online service)
- DOI
-
10.1186/s12974-020-02037-3
- URN
-
urn:nbn:de:101:1-2021010718544528721834
- Rights
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
15.08.2025, 7:27 AM CEST
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Pelisch, Nicolas
- Rosas Almanza, Jose
- Stehlik, Kyle E.
- Aperi, Brandy V.
- Kroner, Antje
- SpringerLink (Online service)
Other Objects (12)
Correction to: CCL3 contributes to secondary damage after spinal cord injury
Etanercept prevents histopathological damage after spinal cord injury in rats
The NAMPT inhibitor FK866 reverts the damage in spinal cord injury
Inhibition of EGFR/MAPK signaling reduces microglial inflammatory response and the associated secondary damage in rats after spinal cord injury
Enhanced neural recovery and reduction of secondary damage in spinal cord injury through modulation of oxidative stress and neural response
Tumor necrosis factor superfamily member APRIL contributes to fibrotic scar formation after spinal cord injury
Ischemic damage may play an important role in spinal cord injury during dancing
Upregulation of casein kinase 1ε in dorsal root ganglia and spinal cord after mouse spinal nerve injury contributes to neuropathic pain
The voltage-gated proton channel Hv1 contributes to neuronal injury and motor deficits in a mouse model of spinal cord injury
Tauroursodeoxycholic acid alleviates secondary injury in spinal cord injury mice by reducing oxidative stress, apoptosis, and inflammatory response
Neuromodulation with transcranial direct current stimulation contributes to motor function recovery via microglia in spinal cord injury
Cervicothoracic spinal cord and pontomedullary injury secondary to high-voltage electrocution: a case report
Correction to: CCL3 contributes to secondary damage after spinal cord injury
Etanercept prevents histopathological damage after spinal cord injury in rats
The NAMPT inhibitor FK866 reverts the damage in spinal cord injury
Inhibition of EGFR/MAPK signaling reduces microglial inflammatory response and the associated secondary damage in rats after spinal cord injury
Enhanced neural recovery and reduction of secondary damage in spinal cord injury through modulation of oxidative stress and neural response
Tumor necrosis factor superfamily member APRIL contributes to fibrotic scar formation after spinal cord injury
Ischemic damage may play an important role in spinal cord injury during dancing
Upregulation of casein kinase 1ε in dorsal root ganglia and spinal cord after mouse spinal nerve injury contributes to neuropathic pain
The voltage-gated proton channel Hv1 contributes to neuronal injury and motor deficits in a mouse model of spinal cord injury
Tauroursodeoxycholic acid alleviates secondary injury in spinal cord injury mice by reducing oxidative stress, apoptosis, and inflammatory response
Neuromodulation with transcranial direct current stimulation contributes to motor function recovery via microglia in spinal cord injury
Cervicothoracic spinal cord and pontomedullary injury secondary to high-voltage electrocution: a case report
Correction to: CCL3 contributes to secondary damage after spinal cord injury
Etanercept prevents histopathological damage after spinal cord injury in rats
The NAMPT inhibitor FK866 reverts the damage in spinal cord injury
Inhibition of EGFR/MAPK signaling reduces microglial inflammatory response and the associated secondary damage in rats after spinal cord injury
Enhanced neural recovery and reduction of secondary damage in spinal cord injury through modulation of oxidative stress and neural response
Tumor necrosis factor superfamily member APRIL contributes to fibrotic scar formation after spinal cord injury
Ischemic damage may play an important role in spinal cord injury during dancing
Upregulation of casein kinase 1ε in dorsal root ganglia and spinal cord after mouse spinal nerve injury contributes to neuropathic pain
The voltage-gated proton channel Hv1 contributes to neuronal injury and motor deficits in a mouse model of spinal cord injury
Tauroursodeoxycholic acid alleviates secondary injury in spinal cord injury mice by reducing oxidative stress, apoptosis, and inflammatory response
Neuromodulation with transcranial direct current stimulation contributes to motor function recovery via microglia in spinal cord injury