Joe E. Springer focuses on Internal medicine, Endocrinology, Spinal cord injury, Cell biology and Spinal cord. His Biochemistry research extends to Internal medicine, which is thematically connected. His study on Endocrinology is mostly dedicated to connecting different topics, such as Nerve growth factor.
In his study, which falls under the umbrella issue of Spinal cord injury, 4-Hydroxynonenal, Amino acid and Ischemia is strongly linked to Lesion. The study incorporates disciplines such as Caspase 3 and Apoptosis in addition to Cell biology. His Spinal cord study combines topics in areas such as Programmed cell death and Pathology.
His primary scientific interests are in Neuroscience, Internal medicine, Endocrinology, Spinal cord and Spinal cord injury. His Neuroscience research incorporates themes from Amyotrophic lateral sclerosis, Signal transduction and Nerve growth factor. His Endocrinology research focuses on subjects like Glutamate receptor, which are linked to Glutamic acid.
His Spinal cord course of study focuses on Pathology and Microglia. His studies in Spinal cord injury integrate themes in fields like Caspase 3, Anesthesia, Neuroprotection, Pharmacology and Mitochondrion. His studies deal with areas such as Lipid peroxidation, Oxidative stress, Reactive oxygen species and Abscess as well as Anesthesia.
His primary areas of investigation include Mitochondrion, Cell biology, Neuroscience, Pediatrics and Endoplasmic reticulum. His Mitochondrion research incorporates themes from Inflammation, Central nervous system, Tumor necrosis factor alpha and Crosstalk. The Central nervous system study combines topics in areas such as Adenosine triphosphate, Function and Mitochondrial permeability transition pore.
His work on Mitochondrial protein is typically connected to Mouse cortex as part of general Cell biology study, connecting several disciplines of science. His study deals with a combination of Neuroscience and mir-223. He focuses mostly in the field of Pediatrics, narrowing it down to matters related to Incidence and, in some cases, Anesthesia and Abscess.
The scientist’s investigation covers issues in Mitochondrion, Neuroscience, Cell biology, mir-223 and Traumatic brain injury. His Mitochondrion research incorporates elements of Central nervous system, NIM811, Mitochondrial permeability transition pore and Adenosine triphosphate. His work on Mitochondrial protein as part of general Cell biology research is frequently linked to Mouse cortex, thereby connecting diverse disciplines of science.
His study of mir-223 brings together topics like Dicer, Gene silencing, Argonaute and Neurodegeneration. Traumatic brain injury is intertwined with Crosstalk, Bioinformatics, Oxidative damage and Cellular activity in his research.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Acute Inflammatory Response in Spinal Cord Following Impact Injury
Sonia L. Carlson;Mark E. Parrish;Joe E. Springer;Ketah Doty.
Experimental Neurology (1998)
Activation of the caspase-3 apoptotic cascade in traumatic spinal cord injury.
Joe E. Springer;Robert D. Azbill;Pamela E. Knapp.
Nature Medicine (1999)
Neuroprotection and acute spinal cord injury: a reappraisal.
Edward D. Hall;Joe E. Springer.
Prolonged survival and decreased abnormal movements in transgenic model of Huntington disease, with administration of the transglutaminase inhibitor cystamine.
Marcela V. Karpuj;Mark W. Becher;Joe E. Springer;Dorothee Chabas.
Nature Medicine (2002)
Mitochondrial permeability transition in CNS trauma: cause or effect of neuronal cell death?
P.G. Sullivan;A.G. Rabchevsky;P.C. Waldmeier;J.E. Springer.
Journal of Neuroscience Research (2005)
Impaired mitochondrial function, oxidative stress and altered antioxidant enzyme activities following traumatic spinal cord injury
Robert D Azbill;Xiaojun Mu;Annadora J Bruce-Keller;Mark P Mattson.
Brain Research (1997)
Demonstration of the retrograde transport of nerve growth factor receptor in the peripheral and central nervous system
EM Johnson;M Taniuchi;HB Clark;JE Springer.
The Journal of Neuroscience (1987)
ALS-Linked Cu/Zn–SOD Mutation Increases Vulnerability of Motor Neurons to Excitotoxicity by a Mechanism Involving Increased Oxidative Stress and Perturbed Calcium Homeostasis
Inna I. Kruman;Ward A. Pedersen;Joe E. Springer;Mark P. Mattson.
Experimental Neurology (1999)
Expression of GDNF mRNA in rat and human nervous tissue.
J E Springer;X Mu;L W Bergmann;J Q Trojanowski.
Experimental Neurology (1994)
Calcineurin-mediated BAD dephosphorylation activates the caspase-3 apoptotic cascade in traumatic spinal cord injury.
Joe E. Springer;Robert D. Azbill;Stephanie A. Nottingham;Sarah E. Kennedy.
The Journal of Neuroscience (2000)
If you think any of the details on this page are incorrect, let us know.
We appreciate your kind effort to assist us to improve this page, it would be helpful providing us with as much detail as possible in the text box below: