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Full-Text Articles in Nervous System
A Cytochemical Evaluation Of Blood-Brain Barrier Sodium, Potassium- And Calcium-Adenosine Triphosphatase Polarity, Panya Steve Manoonkitiwongsa
A Cytochemical Evaluation Of Blood-Brain Barrier Sodium, Potassium- And Calcium-Adenosine Triphosphatase Polarity, Panya Steve Manoonkitiwongsa
Loma Linda University Electronic Theses, Dissertations & Projects
The blood-brain barrier (BBB) is formed by cerebral vascular endothelial cells. Brain ion and fluid homeotasis essential for proper neural functioning is due to the BBB. Sodium-potassium and calcium-activated adenosine triphosphatase (Na+, K+-ATPase and Ca2+-ATPase) serve as one of the main mechanisms controlling brain Na+, K+, and Ca2+ concentrations. The present accepted concept is that both of these enzymes are localized to the abluminal plasma membrane of endothelial cells although there have been contrary results from some studies. Because of these discrepancies, further work was needed. Various cytochemical procedures …
Myelin-Associated Glycoprotein Interacts With Neurons Via A Sialic Acid Binding Site At Arg118 And A Distinct Neurite Inhibition Site, Song Tang, Ying Jing Shen, Maria Elena Debellard, Gitali Mukhopadhyay, James L. Salzer, Paul R. Crocker, Marie T. Filbin
Myelin-Associated Glycoprotein Interacts With Neurons Via A Sialic Acid Binding Site At Arg118 And A Distinct Neurite Inhibition Site, Song Tang, Ying Jing Shen, Maria Elena Debellard, Gitali Mukhopadhyay, James L. Salzer, Paul R. Crocker, Marie T. Filbin
Publications and Research
Inhibitory components in myelin are largely responsible for the lack of regeneration in the mammalian CNS. Myelin-associated glycoprotein (MAG), a sialic acid binding protein and a component of myelin, is a potent inhibitor of neurite outgrowth from a variety of neurons both in vitro and in vivo. Here, we show that MAG’s sialic acid binding site is distinct from its neurite inhibitory activity. Alone, sialic acid–dependent binding of MAG to neurons is insufficient to effect inhibition of axonal growth. Thus, while soluble MAG-Fc (MAG extracellular domain fused to Fc), a truncated form of MAG-Fc missing Ig-domains 4 and 5, MAG(d1-3)-Fc, …
Reference Serum Chemistry And Hematological Values For Spinal Cord Injured Patients, Michael S. Laymon, Antone L. Davis Ii
Reference Serum Chemistry And Hematological Values For Spinal Cord Injured Patients, Michael S. Laymon, Antone L. Davis Ii
Loma Linda University Electronic Theses, Dissertations & Projects
Serum chemistry and hematological values from 220 traumatic spinal cord injured patients (157 male and 63 female between the ages of 15-47, with greater than six months from injury) were compiled via chart review. Traumatic spinal cord injured patient’s reference ranges were determined and compared with the general population reference ranges. Reference ranges within the spinal cord population were compared by age, gender, level of injury and chronicity of injury. The reference ranges determined for all groups within this spinal cord population fall within the reference ranges of the general population. This supports recent research which suggests that a decrease …
Analysis Of Mutant Platelet-Derived Growth Factor Receptors Expressed In Pc12 Cells Identifies Signals Governing Sodium Channel Induction During Neuronal Differentiation., Gary R. Fanger, Richard R. Vaillancourt, Lynn E. Heasley, Jean-Pierre P. Montmayeur, Gary L. Johnson, Robert A. Maue
Analysis Of Mutant Platelet-Derived Growth Factor Receptors Expressed In Pc12 Cells Identifies Signals Governing Sodium Channel Induction During Neuronal Differentiation., Gary R. Fanger, Richard R. Vaillancourt, Lynn E. Heasley, Jean-Pierre P. Montmayeur, Gary L. Johnson, Robert A. Maue
Dartmouth Scholarship
The mechanisms governing neuronal differentiation, including the signals underlying the induction of voltage-dependent sodium (Na+) channel expression by neurotrophic factors, which occurs independent of Ras activity, are not well understood. Therefore, Na+ channel induction was analyzed in sublines of PC12 cells stably expressing platelet-derived growth factor (PDGF) beta receptors with mutations that eliminate activation of specific signalling molecules. Mutations eliminating activation of phosphatidylinositol 3-kinase (PI3K), phospholipase C gamma (PLC gamma), the GTPase-activating protein (GAP), and Syp phosphatase failed to diminish the induction of type II Na+ channel alpha-subunit mRNA and functional Na+ channel expression by PDGF, as determined by RNase …