Evaluation of serum phosphorylated neurofilament subunit NF-H as a prognostic biomarker in dogs with thoracolumbar intervertebral disc herniation.
OBJECTIVE
To investigate whether pNF-H is a prognostic biomarker of spinal cord injury (SCI) in paraplegic dogs with thoracolumbar intervertebral disc herniation (IVDH).
METHODS
Prospective, case-control clinical study
METHODS
Dogs (n = 60) with SCI from IVDH and 6 healthy dogs.
METHODS
Serum from 60 thoracolumbar IVDH dogs (Grade 4: 22 dogs; Grade 5: 38 dogs) collected 1-3 days after injury, and 6 control dogs, was analyzed using enzyme-linked immunosorbent assay (ELISA) against a phosphorylated form of the high-molecular-weight neurofilament subunit NF-H (pNF-H). Serum pNF-H levels were compared between different IVDH grades and their prognostic value was investigated.
RESULTS
pNF-H levels were significantly greater in Grade 5 than Grade 4 dogs. There were significant differences in pNF-H levels between dogs that regained voluntarily ambulation and those that did not. All 8 dogs that had high pNF-H levels 1-3 days after injury did not regain the ability to walk after surgery.
CONCLUSIONS
Serum pNF-H levels might be a biomarker for predicting prognosis of canine SCI.
Phosphorylated neurofilament subunit NF–H as a biomarker for evaluating the severity of spinal cord injury patients, a pilot study.
METHODS
A pilot cross-sectional study of patients with acute cervical spinal cord injury (SCI).
OBJECTIVE
The precise evaluation of the severity of SCI is important for developing novel therapies. Although several biomarkers in cerebrospinal fluid have been tested, few analyses of blood samples have been reported. A novel biomarker for axonal injury, phosphorylated form of the high-molecular-weight neurofilament subunit NF-H (pNF-H), has been reported to be elevated in blood from rodent SCI model. The aim of this study is to investigate whether pNF-H values in blood can serve as a biomarker to evaluate the severity of patients with SCI.
METHODS
Tokyo Metropolitan Bokutoh Hospital and National Rehabilitation Center, Japan.
METHODS
This study enrolled 14 patients with acute cervical SCI. Sequential plasma samples were obtained from 6 h to 21 days after injury. Patients were classified according to American Spinal Injury Association impairment scale (AIS) at the end of the follow-up (average, 229.1 days). Plasma pNF-H values were compared between different AIS grades.
RESULTS
In patients with complete SCI, pNF-H became detectable at 12 h after injury and remained elevated at 21 days after injury. There was a statistically significant difference between AIS A (complete paralysis) patients and AIS C (incomplete paralysis) patients.
CONCLUSIONS
Plasma pNF-H was elevated in accordance with the severity of SCI and reflected a greater magnitude of axonal damage. Therefore, pNF-H is a potential biomarker to independently distinguish AIS A patients (complete SCI) from AIS C-E patients (incomplete SCI). However, further studies are required to evaluate its utility in predicting prognosis of patients in the incomplete category.
Hyperphosphorylated neurofilament NF–H as a biomarker of the efficacy of minocycline therapy for spinal cord injury.
METHODS
An in vivo study in a rat model of acute spinal cord contusion.
OBJECTIVE
To assess the efficacy of novel therapies for acute spinal cord injury (SCI), methods to evaluate accurately the effects of these therapies should be developed. Although neurological examination is commonly used for this purpose, unstable clinical conditions and the spontaneous recovery of neurological function in the acute and subacute phases after injury make this measurement unreliable. Recent studies have reported that the phosphorylated form of the high-molecular-weight neurofilament subunit NF-H (pNF-H), a new biomarker for axonal degeneration, can be measured in serum samples in experimental SCI animals. Therefore, we aimed to investigate the use of plasma pNF-H as an indicator of the efficacy of minocycline, a neuroprotective drug, for treating SCI.
METHODS
This study was carried out at Saitama, Japan.
METHODS
Spinal cord injured rats received either minocycline or saline intraperitoneally. The plasma pNF-H levels and functional hind limb score were determined after the injury.
RESULTS
Minocycline treatment reduced plasma pNF-H levels at 3 and 4 days post-injury (dpi). Rats with lower plasma pNF-H levels at 3 dpi had higher hind limb motor score at 28 dpi.
CONCLUSIONS
pNF-H levels may serve as a biomarker for evaluating the efficacy of therapies for SCI.
Hyperphosphorylated neurofilament NF–H as a predictor of mortality after brain injury in children.
OBJECTIVE
The aim of the study was to determine whether serum levels of hyperphosphorylated neurofilament NF-H correlate with severity of brain injury in children.
METHODS
Forty-nine patients with traumatic brain injury (TBI) were enrolled into the prospective study. Venous blood samples were taken after admission and every 24 h for a maximum of 6 consecutive days. Serum NF-H concentrations were quantified by enzyme-linked immunosorbent assay. The outcome was evaluated 6 months after TBI using Glasgow Outcome Scale (GOS) in all patients.
RESULTS
The quantitative level of pNF-H remained significantly higher in patients with poor outcome (GOS = 1) in comparison with the other patients for the 2nd-4th day (p = 0.027; p = 0.019; p = 0.01). Levels of pNF-H were significantly higher in patients with diffuse axonal injury on initial CT scan (p = 0.004). Normal levels pNF-H in the paediatric population are unknown. Objective ROC analysis was identification of optimal cut-offs of proteins for prediction of GOS = 1.
CONCLUSIONS
Although further, prospective study is warranted, these findings suggest that levels of hyperphosphorylated neurofilament NF-H correlate with mortality and may be useful as predictors of outcome in children with TBI.
Neurofilament (NEFH, Neurofilament H, Neurofilament Heavy Polypeptide 200kD, Neurofilament Triplet H Protein, NF-H, NF200, NF-H) (AP) |
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| MBS6124402-01mL | MyBiosource | 0.1(mL | 935 EUR |
Neurofilament (NEFH, Neurofilament H, Neurofilament Heavy Polypeptide 200kD, Neurofilament Triplet H Protein, NF-H, NF200, NF-H) (AP) |
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| MBS6124402-5x01mL | MyBiosource | 5x0.1mL | 4050 EUR |
Neurofilament (NEFH, Neurofilament H, Neurofilament Heavy Polypeptide 200kD, Neurofilament Triplet H Protein, NF-H, NF200, NF-H) (PE) |
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| MBS6124407-01mL | MyBiosource | 0.1(mL | 935 EUR |
Neurofilament (NEFH, Neurofilament H, Neurofilament Heavy Polypeptide 200kD, Neurofilament Triplet H Protein, NF-H, NF200, NF-H) (PE) |
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| MBS6124407-5x01mL | MyBiosource | 5x0.1mL | 4050 EUR |
Neurofilament NF-H, phosphylated (Neurofilament H, Neurofilament Heavy Polypeptide, NF-H, Neurofilament Triplet H Protein, 200kD Neurofilament Protein, NEFH, NFH) |
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| MBS6003485-01mL | MyBiosource | 0.1(mL | 645 EUR |
Neurofilament NF-H, phosphylated (Neurofilament H, Neurofilament Heavy Polypeptide, NF-H, Neurofilament Triplet H Protein, 200kD Neurofilament Protein, NEFH, NFH) |
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| MBS6003485-5x01mL | MyBiosource | 5x0.1mL | 2750 EUR |
Neurofilament (NEFH, Neurofilament H, Neurofilament Heavy Polypeptide 200kD, Neurofilament Triplet H Protein, NF-H, NF200, NF-H) (APC) |
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| MBS6124403-01mL | MyBiosource | 0.1(mL | 935 EUR |
Neurofilament (NEFH, Neurofilament H, Neurofilament Heavy Polypeptide 200kD, Neurofilament Triplet H Protein, NF-H, NF200, NF-H) (APC) |
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| MBS6124403-5x01mL | MyBiosource | 5x0.1mL | 4050 EUR |
Neurofilament (NEFH, Neurofilament H, Neurofilament Heavy Polypeptide 200kD, Neurofilament Triplet H Protein, NF-H, NF200, NF-H) (Biotin) |
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| MBS6124404-01mL | MyBiosource | 0.1(mL | 935 EUR |
Neurofilament (NEFH, Neurofilament H, Neurofilament Heavy Polypeptide 200kD, Neurofilament Triplet H Protein, NF-H, NF200, NF-H) (Biotin) |
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| MBS6124404-5x01mL | MyBiosource | 5x0.1mL | 4050 EUR |
Neurofilament (NEFH, Neurofilament H, Neurofilament Heavy Polypeptide 200kD, Neurofilament Triplet H Protein, NF-H, NF200, NF-H) (FITC) |
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| MBS6124405-01mL | MyBiosource | 0.1(mL | 935 EUR |
Neurofilament (NEFH, Neurofilament H, Neurofilament Heavy Polypeptide 200kD, Neurofilament Triplet H Protein, NF-H, NF200, NF-H) (FITC) |
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| MBS6124405-5x01mL | MyBiosource | 5x0.1mL | 4050 EUR |
Neurofilament (NEFH, Neurofilament H, Neurofilament Heavy Polypeptide 200kD, Neurofilament Triplet H Protein, NF-H, NF200, NF-H) (HRP) |
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| MBS6124406-01mL | MyBiosource | 0.1(mL | 935 EUR |
Neurofilament (NEFH, Neurofilament H, Neurofilament Heavy Polypeptide 200kD, Neurofilament Triplet H Protein, NF-H, NF200, NF-H) (HRP) |
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| MBS6124406-5x01mL | MyBiosource | 5x0.1mL | 4050 EUR |
Neurofilament NF-H |
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| CH22104 | Neuromics | 50 ul | 490.8 EUR |
Neurofilament NF-H |
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| CH23015 | Neuromics | 200 ul | 553.2 EUR |
Neurofilament NF-H |
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| PC-189 | Kamiya Biomedical Company | Polyclonal | Ask for price |
Neurofilament NF-H |
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| MO22103 | Neuromics | 100 ul | 412.8 EUR |
Neurofilament NF-H |
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| MO22120 | Neuromics | 100 ul | 490.8 EUR |
Neurofilament NF-H |
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| MO22187 | Neuromics | 100 ug | 490.8 EUR |
Neurofilament NF-H |
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| GT22109 | Neuromics | each | 272.7 EUR |
Neurofilament NF-H |
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| MBS555055-01mL | MyBiosource | 0.1mL | 345 EUR |
How the projection domains of NF-L and alpha-internexin determine the conformations of NF-M and NF–H in neurofilaments.
Making use of a numerical self-consistent field method and polymer brush concepts, we model the solvated corona of neurofilaments (NF) composed of projection domains (unstructured tails) of constituent proteins. Projections are modeled with amino acid resolution. We focus on the importance of the two shortest ones (alpha-internexin and NF-L) in regulating the conformations of the two longer ones (NF-M and NF-H) in an isolated NF.
We take the wild-type NF with no alpha-internexin as the reference, for which the phosphorylation-induced translocation of M- and H-tails has been examined previously. We demonstrate that a subbrush of L-tails creates an electrostatic potential profile with an approximately parabolic shape. An experimentally relevant (2:1) ratio of L- to alpha-projections reduces the charge density of the L subbrush and shifts the translocation transition of the H-tails to slightly higher degrees of phosphorylation. Replacing all L-tails by alpha-projections destroys the substructure of the NF corona and this alters the NF response to the phosphorylation of long tails.