A comparison of manual and semi‐automated methods in the assessment of axonal injury

Gentleman,; McKenzie, David R.; Royston,; McIntosh, James R.; Graham,

doi:10.1046/j.1365-2990.1999.00159.x

Cited by 14 publications

(15 citation statements)

References 21 publications

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“…4F). Cases H4, H7, and H8 had APP loads ranging from 0% to 0.5% in the posterior regions, corresponding to mild axonal damage or a rating of 1 on our previously established manual grading scheme (Gentleman et al, 1995(Gentleman et al, , 1999. Cases H1, H2, H3, and H5 had APP loads greater than 1% in at least one of the posterior regions examined.…”

Section: Resultsmentioning

confidence: 97%

“…In our previous study of the corpus callosum, the analysis of APP load was performed using a SeeScan image analyzer (Gentleman et al, 1999). Load measurements were defined by measuring the area occupied by APP immunostaining and dividing by the area of the sample field.…”

Section: Quantitative Analysismentioning

confidence: 99%

“…APP load (area covered by APP immunoreactive profiles as a percentage of the total area of interest) has been used as a tool to evaluate the amount of axonal injury present after blunt head injury (Gentleman et al, 1999). Compared with other semiquantitative methods, it was found to be sensitive, reproducible, and more accurate.…”

Section: Introduction T He Pathology Of Human Traumatic Brain Injurymentioning

confidence: 99%

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Axonal Injury Is Accentuated in the Caudal Corpus Callosum of Head-Injured Patients

Leclercq¹,

McKenzie²,

Graham

et al. 2001

Journal of Neurotrauma

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Amyloid precursor protein (APP) accumulation is a sensitive marker for the axonal damage that is commonly seen in the brain as the result of head injury. This form of damage is particularly associated with midline structures such as the corpus callosum, although it is not clear whether some areas are more susceptible than others. The aim of this study was to determine if there was a differential distribution of axonal injury throughout the corpus callosum after head injury in an unselected group of cases. Coronal tissue sections from eight cases were taken at different levels through the corpus callosum, including the genu, body, and splenium. The sections were immunostained with an antibody to APP, and the amount of axonal damage at the different levels was quantified using computer image analysis to build up a rostro-caudal profile for each case. The profiles revealed a significantly higher APP load in caudal parts of the corpus callosum. This supports previous nonquantitative reports in the literature and has important implications in terms of choosing where tissue should be sampled to maximize the chance of detecting axonal injury post mortem.

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Section: Resultsmentioning

confidence: 97%

Section: Quantitative Analysismentioning

confidence: 99%

Section: Introduction T He Pathology Of Human Traumatic Brain Injurymentioning

confidence: 99%

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Axonal Injury Is Accentuated in the Caudal Corpus Callosum of Head-Injured Patients

Leclercq¹,

McKenzie²,

Graham

et al. 2001

Journal of Neurotrauma

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“…Bioinformatics tools, Blast 2 sequences, Clustal W (Thompson et al, 1994), MEGA 3, Bioconductor in R (Gentleman et al, 1999), were used for sequence analysis.…”

Section: Methodsmentioning

confidence: 99%

SEQUENCE DIVERSITY AND PHYLOGENETIC ANALYSIS IN PAKISTANI SPOTTED DEER (Axis axis)

Abbas¹,

Nadeem²,

Babar³

et al. 2016

PAKJAS

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Spotted deer or "Chital" are one of the most common wild herbivore found in forests. The main objective of the study was to assess the genetic variations in mitochondrial cytochrome-b gene, mitochondrial cytochrome-c gene and mitochondrial d-loop region in Pakistani spotted deer. DNA was extracted from fecal samples of unrelated animals of spotted deer from different localities. PCR primers were designed by Primer software and amplification of gene was done by Polymerase Chain Reaction. The PCR products were sequenced. Variations in nucleotide were identified by alignment. Blast 2 sequences, Clustal W, MEGA 3, Bioconductor in "R" were used for analysis. Multidimensional scaling plot of mitochondrial cytochrome-b, c and dloop region, Pair Wise Evolutionary Distance and Phylogenetic Tree was constructed. Variable sites in Cytochrome-b, Cytochrome-c and d-loop region were identified in spotted deer. Allele frequency of all variations was calculated and low mutant allele frequency was observed. High homozygosity was observed in all spotted deer and differences were very low. This is the first report on molecular genetics of spotted deer from Pakistan. The finding of this research is prerequisite for future research.

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“…16 Briefly, tissue sections were digitized using a Nikon LS-2000 slide scanner. Regions of focal axonal damage were selected by density thresholding in Adobe Photoshop 4.0 and the areas were calculated and summated using the public domain NIH image program (developed at the U.S. National Institutes of Health and available on the Internet at http://rsb.info.nih.gov/nihimage/) (Figure 1; A to C).…”

Section: Quantitation Of Axonal Injury and Image Analysismentioning

confidence: 99%

Axonal Injury in Cerebral Malaria

Medana¹,

Day²,

Hien³

et al. 2002

The American Journal of Pathology

155

130

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Impairment of consciousness and other signs of cerebral dysfunction are common complications of severe Plasmodium falciparum malaria. Although the majority of patients make a complete recovery a significant minority, particularly children, have sequelae. The pathological process by which P. falciparum malaria induces severe but usually reversible neurological complications has not been elucidated. Impairment of transport within nerve fibers could induce neurological dysfunction and may have the potential either to resolve or to progress to irreversible damage. ␤-amyloid precursor protein (␤-APP) immunocytochemistry, quantified using digital image analysis, was used to detect defects in axonal transport in brain sections from 54 Vietnamese cases with P. falciparum malaria. The frequency and extent of ␤-APP staining were more severe in patients with cerebral malaria than in those with no clinical cerebral involvement. ␤-APP staining was often associated with hemorrhages and areas of demyelination, suggesting that multiple processes may be involved in neuronal injury. The age of focal axonal damage, as determined by the extent of the associated microglial response, varied considerably within tissue sections from individual patients. These findings suggest that axons are vulnerable to a broad range of cerebral insults that occur during P. falciparum malaria infection. Disruption in axonal transport may represent a final common pathway leading to neurological dysfunction in cerebral malaria. Cerebral malaria (CM) is a diffuse, potentially reversible, encephalopathy, caused by infection with the protozoan parasite Plasmodium falciparum. CM presents clinically with convulsions and coma, and carries 15 to 20% mortality. The malaria parasite invades and develops within erythrocytes that sequester in the cerebral microvasculature and other vital organs by adhesion to specific endothelial receptors. 1,2 The pathophysiological consequences of severe malaria infection have not been satisfactorily resolved. In particular it is not known how parasitized red blood cells, which remain within the vascular space, influence parenchymal brain function to induce coma and death. Histopathological studies reveal a variety of neurological abnormalities including chromatolysis, neuronophagia, and decreased glial cell numbers. [2][3][4][5]

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A comparison of manual and semi‐automated methods in the assessment of axonal injury

Cited by 14 publications

References 21 publications

Axonal Injury Is Accentuated in the Caudal Corpus Callosum of Head-Injured Patients

Axonal Injury Is Accentuated in the Caudal Corpus Callosum of Head-Injured Patients

SEQUENCE DIVERSITY AND PHYLOGENETIC ANALYSIS IN PAKISTANI SPOTTED DEER (Axis axis)

Axonal Injury in Cerebral Malaria

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