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Target Concepts:
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Query: UNIPROT:Q9UIJ5 (
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58,342
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The brains from 18 cats were examined for the presence of the fibrils and modified
PrP
protein which are molecular diagnostic markers for scrapie-like diseases. Thirteen cats were referred with clinical neurological signs potentially indicative of feline spongiform encephalopathy (FSE). Of these, five had histopathological changes of FSE, five had other lesions of the central nervous system, and in three the brain was normal. The remaining five cats had no clinical neurological signs and were selected as controls. Fibrils and modified
PrP
protein were found in the brains of the five cats with FSE and in one of the cats with neurological signs but no histopathological changes in the central nervous system. Fibrils were present in the absence of modified
PrP
in the brains of two cats, one with neurological signs and a histologically confirmed meningioma, and one with no neurological signs and a histologically normal brain.
Vet
Rec
1992 Oct 03
PMID:Feline spongiform encephalopathy: fibril and PrP studies. 127 83
One hundred and sixty-seven sheep of 32 breeds and crossbreeds affected by natural scrapie throughout Britain were tested for the presence of restriction fragment length polymorphisms of the
PrP
gene observed when their DNA was digested with EcoRI or HindIII. These polymorphisms have already been associated with different susceptibilities to experimental scrapie (controlled by alleles of the Sip gene) in a flock of Cheviot sheep. In two studies 86 to 92 per cent of the sheep were found to carry the
PrP
gene EcoRI fragment e1 which is associated with high susceptibility (or the sA allele of Sip) to experimental scrapie. The
PrP
gene HindIII genotypes of the natural scrapie sheep were not apparently associated with differences in susceptibility to scrapie. There was no link between the polymorphisms and the age or breed of the affected sheep.
Vet
Rec
1992 May 02
PMID:Natural scrapie in British sheep: breeds, ages and PrP gene polymorphisms. 135 94
A 19-month-old greater kudu (Tragelaphus strepsiceros), whose dam had died 15 months earlier with spongiform encephalopathy, required euthanasia after developing severe ataxia and depression with an apparently sudden onset. No macroscopic abnormalities were detected on post mortem examination but a scrapie-like spongiform encephalomyelopathy was apparent on histopathological examination of brain and segments of spinal cord. Negative stain electron microscopy of proteinase K-treated detergent extracts of tissue from the brain stem revealed the presence of scrapie associated fibrils, and a 25 to 28 kDa band comparable with that identified as abnormal
PrP
(prion protein) from the brains of domestic cattle with spongiform encephalopathy was detected using rabbit antiserum raised against mouse
PrP
. The animal was born nine months after the statutory ban on the inclusion of ruminant-derived protein in ruminant feeds and, as no other possible sources of the disease were apparent, it appears likely that the infection was acquired from the dam.
Vet
Rec
1992 Apr 25
PMID:Scrapie-like encephalopathy in a greater kudu (Tragelaphus strepsiceros) which had not been fed ruminant-derived protein. 160 83
The usefulness of detecting the scrapie-associated fibrillar protein (
PrP
) in the lymphoreticular organs of sheep as a diagnostic tool was investigated. The
PrP
was detected by means of a rabbit-anti-sheep
PrP
polyclonal antibody by Western blot analysis.
PrP
was detected in samples from the central nervous system (CNS) of five of six sheep showing clinical signs of natural scrapie infection, in spleen samples from four of the six sheep and in lymph node samples taken from three of the sheep.
PrP
was detected in the spleen and lymph node samples, but not in the CNS samples from one of the six sheep that was clinically and histopathologically abnormal. This animal appeared to be in the early clinical stage of the disease. A total of 47 clinically normal sheep were examined for the presence of
PrP
. It was detected in spleen samples from three of the 47 sheep and in lymph node samples from three of the 39 sheep tested. Similarly,
PrP
was detected in a sample of lymph node obtained surgically from one of three experimentally infected sheep 14 months after inoculation. The
PrP
-positive sheep and one of the remaining
PrP
-negative sheep showed clinical signs of scrapie six and five months later respectively. One sheep euthanased 18 months after experimental infection was positive for
PrP
in the CNS, spleen and lymph node, but five other sheep which were killed or died two, eight, 16, 18 and 21 months after infection were negative or doubtful for the detection of
PrP
.
Vet
Rec
1991 Mar 23
PMID:Pre-clinical and clinical diagnosis of scrapie by detection of PrP protein in tissues of sheep. 167 26
Bovine spongiform encephalopathy (BSE) is one of a family of scrapie-like diseases which affect various mammals. Polymorphisms and mutations of the
PrP
gene have been associated with the incidence of experimental and natural scrapie in other animals and this study of the bovine
PrP
gene was undertaken to discover whether there was a similar association with
PrP
genotype in cattle with BSE. There are two known polymorphisms of the coding region of the bovine
PrP
gene, a silent HindII restriction site polymorphism and a difference in the number of an octapeptide repeated sequence (either five or six copies). An analysis of 370 cattle in Scotland revealed no difference between the frequencies of these
PrP
genotypes in healthy cattle and cattle with BSE.
Vet
Rec
1994 Oct 22
PMID:Frequencies of PrP gene variants in healthy cattle and cattle with BSE in Scotland. 785 30
Cheviot sheep from the Neuropathogenesis Unit flock were examined for
PrP
in brain sections using immunocytochemistry in order to aid scrapie diagnosis. Brains were collected from sheep which had been naturally or experimentally infected with scrapie and fixed in periodate-lysine-paraformaldehyde or in formalin. Immunolabelling was achieved using a monoclonal antibody (FH11) raised to the N-terminus of recombinant
PrP
protein. Several pre-treatments were studied in an effort to enhance
PrP
immunolabelling such as trypsin, formic acid and hydrated autoclaving. Trypsin was successful in highlighting
PrP
staining in formalin-fixed tissue.
PrP
staining was regularly observed in the dorsal vagus nucleus of the medulla oblongata and in the thalamus. Differences in the distribution and intensity of
PrP
immunostaining were apparent between the scrapie sources ME7 and SSBP/I.
Vet
Rec
1996 Nov 23
PMID:Immunolocalisation of the prion protein (PrP) in the brains of sheep with scrapie. 895 91
The incidence of natural scrapie in sheep is associated with polymorphisms of the
PrP
gene, particularly those at codons 136, 154 and 171. In many breeds, the
PrP
allele encoding valine at codon 136 confers an extremely high risk of scrapie, but in Suffolk sheep this allele is vanishingly rare. In this study of a single closed flock of Suffolk sheep in Scotland, scrapie occurred primarily in animals which were homozygous for glutamine at codon 171, a genotype which was significantly less frequent in healthy flockmates. However, the apparent linkage between glutamine at codon 171 and scrapie was not completely recessive because two of 64 scrapie cases were heterozygous glutamine/arginine. These results suggest that breeding for increased resistance to scrapie in Suffolks by the selection of animals according to their
PrP
genotype is a feasible option.
Vet
Rec
1997 Jan 18
PMID:Association between natural scrapie and PrP genotype in a flock of Suffolk sheep in Scotland. 902 5
Natural scrapie in sheep is associated with polymorphisms of the
PrP
gene, particularly at amino acid codons 136, 154 and 171. This paper reports the results of nine scrapie case-control studies in Bleu du Maine, Herdwick, Merino x Shetland, Poll Dorset, Scottish Halfbred, Shetland, Soay, Suffolk and Swaledale sheep from British flocks affected by scrapie. In some outbreaks, scrapie was found to occur only in animals with at least one
PrP
allele encoding valine at codon 136 (V136), usually a relatively rare allele in healthy controls. In other outbreaks, the V136,
PrP
allele was either not found or was not an absolute prerequisite for scrapie to develop. Although scrapie had a strong tendency to affect sheep with
PrP
genotypes homozygous for glutamine at codon 171 (QQ171), these genotypes (QQ171 but varying at other codon positions) were relatively common in healthy controls. The reliable prediction of scrapie susceptibility in previously uninvestigated sheep flocks will therefore require information at least about
PrP
genotypes at codons 136 and 171.
Vet
Rec
1997 Aug 09
PMID:Natural scrapie and PrP genotype: case-control studies in British sheep. 928 41
Further preliminary observations are reported of an experiment to examine the spread of infectivity and the occurrence of pathological changes in cattle exposed orally to infection with bovine spongiform encephalopathy. Calves were dosed at four months of age and clinically monitored groups were killed sequentially from two to 40 months after inoculation. Tissues were collected for bioassay, for histopathological examinations and for the detection of
PrP
. Previous reported observations have included the presence of infectivity in the distal ileum of cattle killed after six to 18 months, the earliest onset of clinical signs in an exposed animal after 35 months, and diagnostic histopathological changes in the brain, in association with clinical disease, after 36, 38 and 40 months. In spite of the relative inefficiency of the bioassay of scrapie-like agents across a species barrier the new observations confirm that the onset of clinical signs and pathological changes in the central nervous system (CNS) occur at approximately the same time. The earliest pathological change, the presence of abnormal
PrP
32 months after inoculation, coincided with the earliest detected infectivity in the CNS and occurred shortly before there was evidence of typical spongiform changes in the brain 36 months after inoculation. Infectivity has now been demonstrated in the peripheral nervous system, in the cervical and thoracic dorsal root ganglia 32 to 40 months after inoculation and in the trigeminal ganglion 36 and 38 months after inoculation. At the time of writing evidence of infectivity in other tissues is confined to the distal ileum, not only after six to 18 months but also after 38 and 40 months, but these findings may be supplemented by the results of further mouse assays. Nevertheless, they are in general agreement with current knowledge of the pathogenesis of scrapie.
Vet
Rec
1998 Jan 31
PMID:Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update. 950 84
A randomised sample of 2,809 apparently healthy sheep, 55 per cent of them less than 15 months of age, which were slaughtered for human consumption at abattoirs in Great Britain in 1997/98, was taken to establish the prevalence of scrapie infection. The medulla oblongata of each sheep was examined histopathologically at the level of the obex, and fresh brain tissue was examined for scrapie-associated fibrils (SAF) to establish whether there was evidence of scrapie. In addition, histological sections of the medulla from 500 of the sheep were immunostained with an antiserum to
PrP
, and the same technique was also applied to any animal found positive or inconclusive by the histological or SAF examinations. Any sheep which was positive by any of these diagnostic methods was also examined by Western immunoblotting, for the detection of the disease-specific protein
PrP
(Sc). A total of 2,798 sheep (99.6 per cent) were negative by all the methods applied. Ten animals were SAF-positive but negative by all the other methods, and in one animal there was immunohistochemical staining which could not be interpreted unequivocally as disease-specific. A mathematical model was used to estimate the prevalence of scrapie infection in the national slaughtered sheep population which would be consistent with these results. By this model, the absence of unequivocally substantiated cases of scrapie in the sample was consistent with a prevalence of infection in the slaughter population of up to 11 per cent.
Vet
Rec
2000 Apr 01
PMID:Scrapie surveillance in Great Britain: results of an abattoir survey, 1997/98. 1088 3
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