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Heart rates of healthy cows and cows suspected of having bovine spongiform encephalopathy were measured by auscultation and by a portable cardiac monitor. Bradycardia was demonstrated in suspect cases which were confirmed histopathologically. Disturbances in cardiac rhythm were also evident in some cases. Healthy cows deprived of food exhibited bradycardia. The administration of pharmacological doses of atropine indicated that bradycardia in BSE was mediated by increased vagal influence, suggesting that the cardioinhibitory reflexes in the caudal brainstem were functionally altered by the disease.
Vet Rec 1997 Oct 04
PMID:Abnormalities of heart rate and rhythm in bovine spongiform encephalopathy. 935 Nov 81

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

The efficacy of the procedures in use at the two rendering plants in the Netherlands was assessed on a laboratory-scale using procedures that simulated the pressure cooking part of the rendering process. A pool of bovine spongiform encephalopathy (BSE)-infected brainstem from the United Kingdom and a pool of scrapie-infected brainstem from Dutch sheep were used to spike the rendering materials. The mixtures were subjected to various time-temperature combinations of hyperbaric heat treatment related to the conditions used in Dutch rendering plants in the early 1990s, and to the combination of 20 minutes at 133 degrees C required by the EU Directive on rendering of 1996. The efficacy of the procedures in inactivating BSE or scrapie infectivity was measured by titrating the materials before and after heat treatment in inbred mice, by combined intracerebral and intraperitoneal inoculations at limiting dilutions. Two independent series of experiments were carried out. The design of the study allowed for minimum inactivations of up to 2.2 log (2.0 in the second series) to be measured in the diluted infective material and 3.1 log in the undiluted material. After 20 minutes at 133 degrees C there was a reduction of BSE infectivity of about 2.2 log in the first series (with some residual infectivity detected), and in the second series more than 2.0 log (with no residual infectivity detected). With undiluted brain material there was an inactivation of about 3.0 log (with some residual infectivity detected). With the same procedure, scrapie infectivity was reduced by more than 1.7 log in the first series and by more than 2.2 log in the second series. With undiluted brain material there was an inactivation of more than 3.1 log. In each case no residual scrapie infectivity was detected. The BSE agent consistently appeared to be more resistant to heat inactivation procedures than the scrapie agent, particularly at lower temperatures and shorter times.
Vet Rec 1998 May 02
PMID:Studies on the efficacy of hyperbaric rendering procedures in inactivating bovine spongiform encephalopathy (BSE) and scrapie agents. 961 12

The study was designed to determine the effect on bovine spongiform encephalopathy (BSE) and scrapie agents of the solvent extraction processes used in the past by British renderers. The raw material was mouse spleen infected with either the 22A strain of scrapie agent or the 301V strain of BSE agent. Samples were exposed to hexane, heptane, petroleum spirit or perchlorethylene at the relevant temperatures for the appropriate times. Control samples were exposed to the same range of temperatures for the same range of times in saline. Other samples were exposed to the hot solvents, followed by treatment with dry heat at 100 degrees C for 30 minutes and steam at 100 degrees C for 30 minutes. Further samples were exposed only to the dry heat and steam cycles. No single complete process was significantly more effective than any of the others, and they all produced only slight inactivation, less than one log on average for both strains of agent. The average degree of inactivation produced by exposure to hot saline was generally comparable to that produced by exposure to the hot solvents. This was also true for the samples exposed only to dry heat and steam compared with those exposed to hot solvent before treatment with dry heat and steam, and suggests that the slight inactivation was caused by the heat rather than by the solvents. It is concluded that the solvent extraction processes used by renderers in Britain had little capacity to inactivate BSE and scrapie agents.
Vet Rec 1998 Jul 04
PMID:Solvent extraction as an adjunct to rendering: the effect on BSE and scrapie agents of hot solvents followed by dry heat and steam. 969 25

The clinical findings in 50 cows with suspected and subsequently confirmed bovine spongiform encephalopathy (BSE) (group A) were compared with the clinical signs in 22 cows with suspected BSE, but with no histological evidence of the disease (group B). The chi-square test for association was used to compare the frequencies with which diagnostic signs or combinations of signs, were positive in the cows of groups A and B. When the frequency of a sign differed significantly, its sensitivity, specificity, efficiency and positive and negative predictive values were calculated. With respect to changes in behaviour the cows in group A more frequently showed increased excitability, nervous ear and eye movements, increased salivation and increased licking of the muzzle than the cows of group B. With respect to changes in sensitivity the cows in group A were more frequently hypersensitive to touch, noise and light than the cows of group B. With respect to changes in locomotion the cows in group A were more frequently ataxic than the cows in group B.
Vet Rec 1998 Jul 25
PMID:Diagnostic reliability of clinical signs in cows with suspected bovine spongiform encephalopathy. 972 75

This study assessed the performance of a system for making decisions about the diagnosis of bovine spongiform encephalopathy (BSE). The system consisted of four pattern-matching models. The sensitivity, specificity, likelihood ratios and accuracy of each model were determined by using clinical descriptions of 100 suspect BSE cases which had been submitted for brain histopathology by veterinary officers of the Ministry of Agriculture, Fisheries and Food, 50 of which were true positive cases (confirmed by histopathology) and 50 false positive cases (not confirmed by histopathology). The clinical description of each case consisted of 14 clinical signs, each of which was defined as either present or absent. The system compared the case descriptions with the profiles of possible differential diagnoses, each profile consisting of the frequency of occurrence of the same 14 clinical signs. The pattern-matching models used the sums of the sign frequencies to rank the differential diagnoses. Models 1 and 2 derived information only from the presence of signs; models 3 and 4 derived information from the presence and absence of signs. Models 2 and 4 excluded diagnoses which did not have in their profile a sign which was observed, and diagnoses which had a sign in their profile which should always be present according to the profile description but which was not observed. The best performances by the models were: sensitivity 96 per cent (model 1 and model 2), specificity 72 per cent (model 4), accuracy 72 per cent (model 4), likelihood ratio of a positive test 2.00 (model 4), likelihood ratio of a negative test 0.21 (model 4).
Vet Rec 1999 May 29
PMID:Pattern-matching models for the differential diagnosis of bovine spongiform encephalopathy. 1039 Aug

Fifteen cows with bovine spongiform encephalopathy (BSE) and 90 healthy cows were given xylazine intramuscularly at a dosage of 0.15 mg/kg bodyweight. The onset of sedation and of drooling was recorded, and the heart and respiratory rates and the systolic and diastolic blood pressure were measured every five minutes for 40 minutes. All the healthy cows but only five of the 15 cows with BSE became sedated, and the period between the administration of xylazine and the onset of sedation was twice as long in the cows with BSE than in the healthy cows (15.0 [7.5] and 7.6 [2.6] minutes). Throughout the observation period, the blood pressure of the cows with BSE was significantly higher than that of the healthy cows, and the blood pressure of the healthy cows, but not of the cows with BSE, decreased significantly towards the end of the observation period.
Vet Rec 1999 Jun 26
PMID:Decreased sedation by xylazine and high blood pressure in cows with BSE. 1042 14

The objective of this study was to model the expected numbers of cattle incubating bovine spongiform encephalopathy (BSE) and the numbers of clinical cases of BSE in the Swiss cattle population between 1984 and 2005. The results were compared with the observed number of clinical BSE cases and with the results of a culling and testing scheme on herdmates of cattle with BSE. The age distribution of the Swiss cattle population, the age-at-death distribution of the first 235 BSE cases and exposure information were used to calculate the expected number of infected cattle in each birth cohort and the resulting numbers of clinical cases and survivors incubating the disease for each year. The model which did not assume any under-reporting of cases fitted the observed epidemic curve of clinical cases reasonably well, and predicted that the Swiss BSE epidemic would come to an end between 2003 and 2005. The age of survivors incubating BSE is increasing. The higher than expected incidence of subclinical cases observed in animals from the culling scheme is most probably the result of the heterogeneous distribution of infected animals and affected herds in the population. The results of the model need to be taken into account when designing surveillance and testing schemes for BSE.
Vet Rec 1999 Aug 07
PMID:Modelling the expected numbers of preclinical and clinical cases of bovine spongiform encephalopathy in Switzerland. 1046 72

The objectives of this study were first to describe the pattern of the epidemic of bovine spongiform encephalopathy (BSE) in Great Britain in terms of the temporal change in the proportion of all cattle holdings that had experienced at least one confirmed case of BSE to June 30, 1997, and secondly to identify risk factors that influenced the date of onset of a holding's first confirmed BSE case. The analyses were based on the population of British cattle at risk, derived from agricultural census data collected between 1986 and 1996, and the BSE case data collected up to June 30, 1997. The unit of interest was the cattle holding and included all those recorded at least once on annual agricultural censuses conducted between June 30, 1986, and June 30, 1996. The outcome of interest was the date on which clinical signs were recorded in a holding's first confirmed case of BSE, termed the BSE onset date. Univariate and multivariate survival analysis techniques were used to describe the temporal pattern of the epidemic. The BSE epidemic in Great Britain started in November 1986, with the majority of affected holdings having their BSE onset date after February 1992. After adjusting for the effect of the size and type of holding, holdings in the south of England (specifically those in the Eastern, South east and South west regions) had 2.22 to 2.43 (95 per cent confidence interval [CI] 2.07 to 2.58) times as great a monthly hazard of having a BSE index case as holdings in Scotland. After adjusting for the effect of region and type of holding, holdings with more than 53 adult cattle had 5.91 (95 per cent CI 5.62 to 6.21) times as great a monthly hazard of having a BSE index case as holdings with seven to 21 adult cattle. Dairy holdings had 3.06 (95 per cent CI 2.96 to 3.16) times as great a monthly hazard of having a BSE index case as beef suckler holdings. These analyses show that there were different rates of onset in different regions and in holdings of different sizes and types, that the epidemic was propagated most strongly in the south of the country, and that the growth of the epidemic followed essentially the same pattern in each region of the country, with modest temporal lags between them. The control measures imposed in 1988 and 1990 brought the expansion of the epidemic under control, although the rate of progress was slowed by those regions where the effectiveness of the control methods took some time to take full effect.
Vet Rec 2000 Sep 16
PMID:Temporal aspects of the epidemic of bovine spongiform encephalopathy in Great Britain: holding-associated risk factors for the disease. 1105 20

As part of a nutritional study lasting from six weeks before calving to 22 weeks of lactation, blood samples collected from 47 dairy cows maintained under well-defined conditions were analysed for a variety of metabolites and hormones. At various times after the completion of the study, six of the animals developed clinical signs of bovine spongiform encephalopathy (BSE), although when they were sampled it was not known that they were incubating the disease. The data were used to make comparisons between the animals that developed BSE and those that did not develop the disease and which had been maintained under the same conditions. The greatest differences between the animals incubating BSE and the control animals were observed at times of nutritional stress, at the start of lactation and when the intake of concentrate feeds was reduced at week 13 of lactation. In the animals that subsequently developed BSE, feed intakes were lower in early lactation; plasma beta-hydroxbutyrate concentrations were significantly higher (P<0.001) at weeks 3 and 5 of lactation; adjusted milk yields were lower until week 6 of lactation and milk fat concentrations were consistently lower. There was no effect on plasma glucose concentrations, although insulin concentrations were significantly lower in week 1 of lactation (2-27 v 2.50 microiu/ml) (P<0.05). The concentrations of plasma proteins and urea were unaffected by BSE incubation, apart from protein concentrations being significantly higher one week before calving, and the concentration of urea being significantly lower five weeks before calving. The plasma concentrations of somatotrophin, prolactin, oestradiol and progesterone were similar in the two groups of animals throughout the study. The differences observed indicate that the energy metabolism of dairy cows incubating BSE may be subtly altered before the onset of clinical signs of the disease.
Vet Rec 2000 Oct 07
PMID:Aspects of the metabolism of dairy cows during the incubation of bovine spongiform encephalopathy. 1107 85


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