Cited by 108Spinal Cord Injury ResearchTraumatic Brain Injury and Neurovascular DisturbancesSpinal Hematomas and Complications

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Biomarkers in Spinal Cord Injury: Prognostic Insights and Future Potentials

Open access

Abstract

Spinal Cord Injury (SCI) is a major challenge in Neurotrauma research. Complex pathophysiological processes take place immediately after the injury and later on as the chronic injury develops. Moreover, SCI is usually accompanied by traumatic injuries because the most common modality of injury is road traffic accidents and falls. Patients develop significant permanent neurological deficits that depend on the extent and the location of the injury itself and in time they develop further neurological and body changes that may risk their mere survival. In our review, we explored the recent updates with regards to SCI biomarkers. We observed two methods that may lead to the appearance of biomarkers for SCI. First, during the first few weeks following the injury the Blood Spinal Cord Barrier (BSCB) disruption that releases several neurologic structure components from the injured tissue. These components find their way to Cerebrospinal Fluid (CSF) and the systemic circulation. Also, as the injury develops several components of the pathological process are expressed or released such as in neuroinflammation, apoptosis, reactive oxygen species, and excitotoxicity sequences. Therefore, there is a growing interest in examining any correlations between these components and the degrees or the outcomes of the injury. Additionally, some of the candidate biomarkers are theorized to track the progressive changes of SCI which offers an insight on the patients' prognoses, potential-treatments-outcomes assessment, and monitoring the progression of the complications of chronic SCI such as Pressure Ulcers and urinary dysfunction. An extensive literature review was performed covering literature, published in English, until February 2018 using the Medline/PubMed database. Experimental and human studies were included and titles, PMID, publication year, authors, biomarkers studies, the method of validation, relationship to SCI pathophysiology, and concluded correlation were reported. Potential SCI biomarkers need further validation using clinical studies. The selection of the appropriate biomarker group should be made based on the stage of the injuries, the accompanying trauma and with regards to any surgical, or medical interference that might have been done. Additionally, we suggest testing multiple biomarkers related to the several pathological changes coinciding to offer a more precise prediction of the outcome.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3389/fneur.2019.00027

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 2 references

Research works printed but not linked: 98

  1. 2016, (SCI) Facts and figures at a glance, J Spinal Cord Med., 39, 493, 10.1080/10790268.2016.1210925 · DOI
  2. Taylor, 2017, Presentation of neurogenic shock within the emergency department, Emerg Med J., 34, 157, 10.1136/emermed-2016-205780 · DOI
  3. Rowland, 2008, Current status of acute spinal cord injury pathophysiology and emerging therapies: promise on the horizon, Neurosurg Focus, 25, E2, 10.3171/FOC.2008.25.11.E2 · DOI
  4. Stein, 2015, Management of acute spinal cord injury, Contin Lifelong Learn Neurol., 21, 159, 10.1212/01.CON.0000461091.09736.0c · DOI
  5. Witiw, 2015, Acute spinal cord injury, J Spinal Disord Tech., 28, 202, 10.1097/BSD.0000000000000287 · DOI
  6. 2008, Early acute management in adults with spinal cord injury: a clinical practice guideline for health-care professionals, J Spinal Cord Med., 31, 403, 10.1080/10790268.2008.11760744 · DOI
  7. Eckert, 2017, Trauma: spinal cord injury, Surg Clin North Am., 97, 1031, 10.1016/j.suc.2017.06.008 · DOI
  8. Sekhon, 2001, Epidemiology, demographics, and pathophysiology of acute spinal cord injury, Spine, 26, S2, 10.1097/00007632-200112151-00002 · DOI
  9. Anwar, 2016, Inflammogenesis of secondary spinal cord injury, Front Cell Neurosci., 10, 98, 10.3389/fncel.2016.00098 · DOI
  10. Jia, 2012, Oxidative stress in spinal cord injury and antioxidant-based intervention, Spinal Cord, 50, 264, 10.1038/sc.2011.111 · DOI
  11. Hulme, 2017, The developing landscape of diagnostic and prognostic biomarkers for spinal cord injury in cerebrospinal fluid and blood, Spinal Cord, 55, 114, 10.1038/sc.2016.174 · DOI
  12. Badhiwala, 2018, A review of clinical trials in spinal cord injury including biomarkers, J Neurotraumaneu, 2018, 5935, 10.1089/neu.2018.5935 · DOI
  13. Kwon, 2011, Inflammatory and structural biomarkers in acute traumatic spinal cord injury, Clin Chem Lab Med., 49, 425, 10.1515/CCLM.2011.068 · DOI
  14. Wu, 2016, Parallel metabolomic profiling of cerebrospinal fluid and serum for identifying biomarkers of injury severity after acute human spinal cord injury, Sci Rep., 6, 38718, 10.1038/srep38718 · DOI
  15. Sengupta, 2014, CSF proteomics of secondary phase spinal cord injury in human subjects: perturbed molecular pathways post injury, PLoS ONE, 9, e110885, 10.1371/journal.pone.0110885 · DOI
  16. Courtine, 2007, Can experiments in nonhuman primates expedite the translation of treatments for spinal cord injury in humans?, Nat Med., 13, 561, 10.1038/nm1595 · DOI
  17. Furlan, 2011, Assessment of disability in patients with acute traumatic spinal cord injury: a systematic review of the literature, J Neurotra., 28, 1413, 10.1089/neu.2009.1148 · DOI
  18. Papurica, 2016, Advances in biomarkers in critical Ill polytrauma patients, Clin Lab., 62, 977, 10.7754/Clin.Lab.2015.151103 · DOI
  19. Pouw, 2014, Structural biomarkers in the cerebrospinal fluid within 24 h after a traumatic spinal cord injury: a descriptive analysis of 16 subjects, Spinal Cord, 52, 428, 10.1038/sc.2014.26 · DOI
  20. Guéz, 2003, Nervous tissue damage markers in cerebrospinal fluid after cervical spine injuries and whiplash trauma, J Neurotr., 20, 853, 10.1089/089771503322385782 · DOI
  21. Kuhle, 2015, Serum neurofilament light chain is a biomarker of human spinal cord injury severity and outcome, J Neurol Neurosurg Psychiatry, 86, 273, 10.1136/jnnp-2013-307454 · DOI
  22. Hayakawa, 2012, Phosphorylated neurofilament subunit NF-H as a biomarker for evaluating the severity of spinal cord injury patients, a pilot study, Spinal Cord, 50, 493, 10.1038/sc.2011.184 · DOI
  23. Shaw, 2005, Hyperphosphorylated neurofilament NF-H is a serum biomarker of axonal injury, Biochem Biophys Res Commun., 336, 1268, 10.1016/j.bbrc.2005.08.252 · DOI
  24. Ahadi, 2015, Diagnostic value of serum levels of GFAP, pNF-H, and NSE compared with clinical findings in severity assessment of human traumatic spinal cord injury, Spine, 40, E823, 10.1097/BRS.0000000000000654 · DOI
  25. Kwon, 2010, Cerebrospinal fluid inflammatory cytokines and biomarkers of injury severity in acute human spinal cord injury, J Neurotr., 27, 669, 10.1089/neu.2009.1080 · DOI
  26. Kwon, 2017, Cerebrospinal fluid biomarkers to stratify injury severity and predict outcome in human traumatic spinal cord injury, J Neurotr., 34, 567, 10.1089/neu.2016.4435 · DOI
  27. Loy, 2005, Serum biomarkers for experimental acute spinal cord injury: rapid elevation of neuron-specific enolase and S-100beta, Neurosurgery, 56, 391, 10.1227/01.NEU.0000207967.91316.8D · DOI
  28. Cao, 2008, Elevation of neuron-specific enolase and S-100β protein level in experimental acute spinal cord injury, J Clin Neurosci., 15, 541, 10.1016/j.jocn.2007.05.014 · DOI
  29. Zhang, 2000, Cytoskeletal disruption following contusion injury to the rat spinal cord, J Neuropathol Exp Neurol., 59, 287, 10.1093/jnen/59.4.287 · DOI
  30. Hesp, 2015, Chronic oligodendrogenesis and remyelination after spinal cord injury in mice and rats, J Neurosci., 35, 1274, 10.1523/JNEUROSCI.2568-14.2015 · DOI · Paper page
  31. Zhang, 2011, Neurological, functional, and biomechanical characteristics after high-velocity behind armor blunt trauma of the spine, J Trauma, 71, 1680, 10.1097/TA.0b013e318231bce7 · DOI
  32. Moghaddam, 2017, Exploratory study to suggest the possibility of MMP-8 and MMP-9 serum levels as early markers for remission after traumatic spinal cord injury, Spinal Cord, 55, 8, 10.1038/sc.2016.104 · DOI
  33. Light, 2012, Multiplex array proteomics detects increased MMP-8 in CSF after spinal cord injury, J Neuroinflam., 9, 122, 10.1186/1742-2094-9-122 · DOI
  34. Nagano, 2011, Matrix metalloprotease-9 activity in the cerebrospinal fluid and spinal injury severity in dogs with intervertebral disc herniation, Res Vet Sci., 91, 482, 10.1016/j.rvsc.2010.09.009 · DOI
  35. Buss, 2008, TGF-β1 and TGF-β2 expression after traumatic human spinal cord injury, Spinal Cord, 46, 364, 10.1038/sj.sc.3102148 · DOI
  36. Ferbert, 2017, Tracking spinal cord injury: differences in cytokine expression of IGF-1, TGF- B1, and sCD95l can be measured in blood samples and correspond to neurological remission in a 12-week follow-up, J Neurotr., 34, 607, 10.1089/neu.2015.4294 · DOI
  37. Moghaddam, 2016, Elevated serum insulin-like growth factor 1 levels in patients with neurological remission after traumatic spinal cord injury, PLoS ONE, 11, e0159764, 10.1371/journal.pone.0159764 · DOI
  38. Biglari, 2013, Increase in soluble CD95L during subacute phases after human spinal cord injury: a potential therapeutic target, Spinal Cord, 51, 183, 10.1038/sc.2012.139 · DOI
  39. Biglari, 2015, Serum sCD95L concentration in patients with spinal cord injury, J Int Med Res., 43, 250, 10.1177/0300060514559794 · DOI
  40. Biglari, 2015, A pilot study on temporal changes in IL-1β and TNF-α serum levels after spinal cord injury: The serum level of TNF-α in acute SCI patients as a possible marker for neurological remission, Spinal Cord, 53, 510, 10.1038/sc.2015.28 · DOI
  41. Davies, 2007, Clinical correlates of elevated serum concentrations of cytokines and autoantibodies in patients with spinal cord injury, Arch Phys Med Rehabil., 88, 1384, 10.1016/j.apmr.2007.08.004 · DOI
  42. Xu, 2015, Tumor necrosis factor-alpha is a potential diagnostic biomarker for chronic neuropathic pain after spinal cord injury, Neurosci Lett., 595, 30, 10.1016/j.neulet.2015.04.004 · DOI
  43. Al-Chalabi, 2003, Neurofilaments and neurological disease, BioEssays, 25, 346, 10.1002/bies.10251 · DOI
  44. Yokobori, 2015, Acute diagnostic biomarkers for spinal cord injury: review of the literature and preliminary research report, World Neurosurg., 83, 867, 10.1016/j.wneu.2013.03.012 · DOI
  45. Diaz-Arrastia, 2014, Acute biomarkers of traumatic brain injury: relationship between plasma levels of ubiquitin C-terminal hydrolase-L1 and glial fibrillary acidic protein, J Neurotr., 31, 19, 10.1089/neu.2013.3040 · DOI
  46. Haque, 2016, Neuron specific enolase: a promising therapeutic target in acute spinal cord injury, Metab Brain Dis., 31, 487, 10.1007/s11011-016-9801-6 · DOI
  47. Li, 2014, Temporal-spatial expression of ENOLASE after acute spinal cord injury in adult rats, Neurosci Res., 79, 76, 10.1016/j.neures.2013.12.001 · DOI
  48. Garner, 1988, Selective localization of messenger RNA for cytoskeletal protein MAP2 in dendrites, Nature, 336, 674, 10.1038/336674a0 · DOI
  49. Husted, 2006, Structural insight into the role of myelin basic protein in multiple sclerosis, Proc Natl Acad Sci USA., 103, 4339, 10.1073/pnas.0601002103 · DOI
  50. Zhang, 2010, Matrix Metalloproteinases and Neurotrauma: Evolving Roles in Injury and Reparative Processes
  51. de Castro, 2000, Metalloproteinase increases in the injured rat spinal cord, Neuroreport, 11, 3551, 10.1097/00001756-200011090-00029 · DOI
  52. Lifshitz, 2013, TGF-β, 1647, 10.1016/B978-0-12-385095-9.00225-6 · DOI
  53. Schachtrup, 2010, Fibrinogen triggers astrocyte scar formation by promoting the availability of active TGF- after vascular damage, J Neurosci., 30, 5843, 10.1523/JNEUROSCI.0137-10.2010 · DOI
  54. Krieglstein, 2011, More than being protective: functional roles for TGF-β/activin signaling pathways at central synapses, Trends Neurosci., 34, 421, 10.1016/j.tins.2011.06.002 · DOI · Paper page
  55. Bartholdi, 1997, Expression of pro-inflammatory cytokine and chemokine mRNA upon experimental spinal cord injury in mouse: an in situ hybridization study, Eur J Neurosci., 9, 1422, 10.1111/j.1460-9568.1997.tb01497.x · DOI
  56. Harrington, 2005, Shedding of tumor necrosis factor type 1 receptor after experimental spinal cord injury, J Neurotr., 22, 919, 10.1089/neu.2005.22.919 · DOI
  57. Neefkes-Zonneveld, 2015, Effect of long-term physical activity and acute exercise on markers of systemic inflammation in persons with chronic spinal cord injury: A systematic review, Arch Phys Med Rehabil., 96, 30, 10.1016/j.apmr.2014.07.006 · DOI
  58. Gleeson, 2011, The anti-inflammatory effects of exercise: mechanisms and implications for the prevention and treatment of disease, Nat Rev Immunol., 11, 607, 10.1038/nri3041 · DOI · Paper page
  59. Beavers, 2010, Effect of exercise training on chronic inflammation, Clin Chim Acta, 411, 785, 10.1016/j.cca.2010.02.069 · DOI
  60. Hollis, 2009, IGF-I gene delivery promotes corticospinal neuronal survival but not regeneration after adult CNS injury, Exp Neurol., 215, 53, 10.1016/j.expneurol.2008.09.014 · DOI
  61. Wang, 1997, Increase of interleukin-lβ mRNA and protein in the spinal cord following experimental traumatic injury in the rat, Brain Res., 759, 190, 10.1016/S0006-8993(97)00254-0 · DOI
  62. Springer, 1999, Activation of the caspase-3 apoptotic cascade in traumatic spinal cord injury, Nat Med., 5, 943, 10.1038/11387 · DOI · Paper page
  63. Emery, 1998, Apoptosis after traumatic human spinal cord injury, J Neurosurg., 89, 911, 10.3171/jns.1998.89.6.0911 · DOI
  64. Peter, 2015, The role of CD95 and CD95 ligand in cancer, Cell Death Differ., 22, 549, 10.1038/cdd.2015.3 · DOI
  65. Janssen, 2003, CD95 ligand - death factor and costimulatory molecule?, Cell Death Differ., 10, 1215, 10.1038/sj.cdd.4401305 · DOI
  66. Zurita, 2001, Presence and significance of CD-95 (Fas/APO1) expression after spinal cord injury, J Neurosurg., 94, 257, 10.3171/spi.2001.94.2.0257 · DOI
  67. Yoshino, 2004, The role of Fas-mediated apoptosis after traumatic spinal cord injury, Spine, 29, 1394, 10.1097/01.BRS.0000129894.34550.48 · DOI
  68. Hu, 2010, Glial scar and neuroregeneration: histological, functional, and magnetic resonance imaging analysis in chronic spinal cord injury, J Neurosurg Spine, 13, 169, 10.3171/2010.3.SPINE09190 · DOI
  69. Demjen, 2004, Neutralization of CD95 ligand promotes regeneration and functional recovery after spinal cord injury, Nat Med., 10, 389, 10.1038/nm1007 · DOI
  70. Awad, 2015, Potential role of growth factors in the management of spinal cord injury, World Neurosurg., 83, 120, 10.1016/j.wneu.2013.01.042 · DOI
  71. Whalley, 2006, Changes in response to spinal cord injury with development: Vascularization, hemorrhage and apoptosis, Neuroscience, 137, 821, 10.1016/j.neuroscience.2005.07.064 · DOI
  72. McTigue, 1998, Selective chemokine mRNA accumulation in the rat spinal cord after contusion injury, J Neurosci Res, 53, 368, 10.1002/(SICI)1097-4547(19980801)53:3<368::AID-JNR11>3.0.C.O.;2-1 · DOI
  73. Zhang, 2015, Inhibition of monocyte chemoattractant peptide-1 decreases secondary spinal cord injury, Mol Med Rep., 11, 4262, 10.3892/mmr.2015.3330 · DOI
  74. Perrin, 2005, Involvement of monocyte chemoattractant protein-1, macrophage inflammatory protein-1 and interleukin-1 in Wallerian degeneration, Brain, 128, 854, 10.1093/brain/awh407 · DOI
  75. Ousman, 2001, MIP-1alpha, MCP-1, GM-CSF, and TNF-alpha control the immune cell response that mediates rapid phagocytosis of myelin from the adult mouse spinal cord, J Neurosci., 21, 4649, 10.1523/JNEUROSCI.21-13-04649.2001 · DOI
  76. He, 2003, Proteomics in biomarker discovery and drug development, J Cell Biochem., 89, 868, 10.1002/jcb.10576 · DOI
  77. Parker, 2014, Mass spectrometry based biomarker discovery, verification, and validation - Quality assurance and control of protein biomarker assays, Mol Oncol., 8, 840, 10.1016/j.molonc.2014.03.006 · DOI
  78. Moghieb, 2016, Differential neuroproteomic and systems biology analysis of spinal cord injury, Mol Cell Proteom., 15, 2379, 10.1074/mcp.M116.058115 · DOI
  79. Didangelos, 2016, High-throughput proteomics reveal alarmins as amplifiers of tissue pathology and inflammation after spinal cord injury, Sci Rep., 6, 21607, 10.1038/srep21607 · DOI
  80. Lala, 2014, Impact of pressure ulcers on individuals living with a spinal cord injury, Arch Phys Med Rehabil., 95, 2312, 10.1016/j.apmr.2014.08.003 · DOI
  81. Niazi, 1997, Recurrence of initial pressure ulcer in persons with spinal cord injuries, Adv Wound Care, 10, 38
  82. Chan, 2013, The average cost of pressure ulcer management in a community dwelling spinal cord injury population, Int Wound J., 10, 431, 10.1111/j.1742-481X.2012.01002.x · DOI
  83. Salzberg, 1996, A new pressure ulcer risk assessment scale for individuals with spinal cord injury, Am J Phys Med Rehabil., 75, 96, 10.1097/00002060-199603000-00004 · DOI
  84. Velnar, 2009, The wound healing process: an overview of the cellular and molecular mechanisms, J Int Med Res., 37, 1528, 10.1177/147323000903700531 · DOI
  85. Cruse, 2002, Cellular and molecular alterations in spinal cord injury patients with pressure ulcers: a preliminary report, Exp Mol Pathol., 72, 124, 10.1006/exmp.2002.2420 · DOI
  86. Gurcay, 2009, Evaluation of blood and serum markers in spinal cord injured patients with pressure sores, Saudi Med J., 30, 413
  87. Krishnan, 2016, Early detection of pressure ulcer development following traumatic spinal cord injury using inflammatory mediators, Arch Phys Med Rehabil., 97, 1656, 10.1016/j.apmr.2016.01.003 · DOI
  88. DeJong, 2013, Rehospitalization in the first year of traumatic spinal cord injury after discharge from medical rehabilitation, Arch Phys Med Rehabil., 94, S87, 10.1016/j.apmr.2012.10.037 · DOI
  89. Ku, 2006, The management of neurogenic bladder and quality of life in spinal cord injury, BJU Int., 98, 739, 10.1111/j.1464-410X.2006.06395.x · DOI
  90. Simpson, 2012, Wolfe and the spinal cord injury. the health and life priorities of individuals with spinal cord injury: a systematic review, J Neurotr., 29, 1548, 10.1089/neu.2011.2226 · DOI
  91. Sahai, 2011, Neurogenic detrusor overactivity in patients with spinal cord injury: evaluation and management, Curr Urol Rep., 12, 404, 10.1007/s11934-011-0221-1 · DOI
  92. Ahmed, 2006, Management of detrusor–external sphincter dyssynergia, Nat Clin Pract Urol., 3, 368, 10.1038/ncpuro0521 · DOI
  93. Cruz, 2015, Biomarkers of spinal cord injury and ensuing bladder dysfunction, Adv Drug Deliv Rev., 153, 10.1016/j.addr.2014.11.007 · DOI
  94. Mehnert, 2012, Treatment of neurogenic stress urinary incontinence using an adjustable continence device: 4-year followup, J Urol., 188, 2274, 10.1016/j.juro.2012.07.131 · DOI
  95. Giannantoni, 2008, Botulinum A toxin intravesical injection in patients with painful bladder syndrome: 1-year followup, J Urol., 179, 1031, 10.1016/j.juro.2007.10.032 · DOI
  96. Kuo, 2010, Can urinary nerve growth factor be a biomarker for overactive bladder?, Rev Urol., 12, e69, 10.3909/riu0432 · DOI
  97. Giannantoni, 2006, Botulinum-a toxin injections into the detrusor muscle decrease nerve growth factor bladder tissue levels in patients with neurogenic detrusor overactivity, J Urol., 175, 2341, 10.1016/S0022-5347(06)00258-8 · DOI
  98. Krebs, 2017, Nerve growth factor does not seem to be a biomarker for neurogenic lower urinary tract dysfunction after spinal cord injury, Neurourol Urodyn., 36, 659, 10.1002/nau.22987 · DOI

Cited by

Sorted by citations

Metadata

Authors
Albayar, A. A., Roche, A., Swiatkowski, P., Antar, S., Ouda, N., Emara, E., Smith, D. H., Ozturk, A. K., & Awad, B. I.
Affiliations
  • University of Pennsylvania (US)
  • Mansoura University (EG)
Corresponding author
Albayar, Ahmed A.
Venue
Frontiers in Neurology
Published
2019-01-29
Volume
10
Pages
27-27
ISSN
1664-2295 (ISSN-L)
OpenAlex
W2913249489
Cited by
108
References
2
Citations by year
2026: 13 · 2025: 15 · 2024: 16 · 2023: 12 · 2022: 14 · 2021: 22 · 2020: 12 · 2019: 4
FWCI
1.94
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Neurology (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Greater South Information System
Topics
  • Health Sciences › Medicine › Clinical Neurology › Spinal Cord Injury Research
  • Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Surgery › Spinal Hematomas and Complications
Keywords
spinal cord injury, biomarkers, prognostic factors, cerebrospinal fluid biomarkers, neuroinflammation, apoptosis, reactive oxygen species, excitotoxicity, chronic spinal cord injury, pressure ulcers, urinary dysfunction, neurological outcome prediction

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review