Interpretation of BSE statistics.
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Biomedical subjects
Publications and source records attributed to D Matthews.
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The first diagnosis of bovine spongiform encephalopathy (BSE) in the United Kingdom in 1986 was to stimulate the most intensive epidemiological study of any animal disease of all time in that country. It led also to the initiation of a broad-based research programme with an international flavour. This principally involved scientists and veterinarians in Europe (especially the United Kingdom) and the United States of America, especially those with experience of slow infections in general and experimental scrapie in particular. This final chapter highlights some of the significant discoveries made in the study of BSE and related diseases of this group but also emphasises the deficits in knowledge which need to be corrected before such diseases as scrapie in sheep and goats can be brought under control. The benefits resultant upon effective disease control will be manifest as improvement in animal production, welfare and, importantly, the removal of trading barriers currently in place to protect countries in which diseases such as BSE and scrapie do not exist. Of key importance is the development of a simple, cheap and effective diagnostic test for use in the live animal before the onset of clinical signs. This will be difficult since the nature of the causal agents is uncertain and none provokes either a detectable immune response or inflammatory reaction in the host. The earlier chapters, written by acknowledged specialists from around the world, deal with the specific diseases in detail and all present some of the most recent knowledge available. Here the authors emphasise the important role that major national and international agencies have in effecting the highest level of control possible in the absence of key information. International collaboration with countries in which these diseases exist, and as well as those where they are absent, is of paramount importance. It is essential that the BSE epidemic which has severely affected the cattle industry of the United Kingdom is not allowed to happen in developing countries. Whereas the former has implemented stringent control measures based on scientific knowledge and is well on the way to eradicating the disease, the latter could have much greater difficulty in establishing control. The answer is clear. BSE must be prevented from occurring elsewhere. To do that, knowledge of BSE and other members of the group should be widely dispersed and it is the purpose of this issue to do just that.
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OBJECTIVE: The aim was to study the relationship between growth hormone (GH) and insulin-like growth factor-I (IGF-I) in critically ill patients. DESIGN: Case-control study of critically ill patients admitted to the intensive care unit was carried out. PATIENTS: Six critically ill patients (51-78 years) who required ventilation and parenteral nutrition and six age, weight, height, and sex-matched healthy adults were studied. MEASUREMENTS: The patients and controls were studied for two 24-hour periods; the patients before and after starting parenteral feeding, and the controls during a 36-hour fast and when taking meals equivalent in calories and protein to the patients' parenteral feed. Serum GH was measured at 20-minute intervals and analysed by a pulse detection algorithm (Pulsar) and Fourier transformation. IGF-I was measured at 0, 12, and 24 hours. RESULTS: Patients had low serum IGF-I levels compared with controls, whether fasted or fed, despite having mean GH levels similar to fasted controls. For fasted patients vs fasted controls the mean (+/- 1 SD) GH levels were 4.5 +/- 2.0 vs 4.0 +/- 2.4 mU/l respectively, and IGF-I levels at the end of the fast were 0.17 +/- 0.11 vs 0.78 +/- 0.29 U/ml (P = 0.003). Patients showed elevated baseline GH levels compared with controls when fasted and during parenteral feeding (patients vs controls fasted 3.1 +/- 1.9 vs 0.8 +/- 0.5 mU/l, P = 0.01; patients vs controls fed 4.2 +/- 4.5 vs 0.5 +/- 0.04 mU/l, P = 0.028). Fourier transformation confirmed oscillatory GH levels in the controls, fasted or fed, but this activity was attenuated in the patients. Parenteral feeding had no effect on the GH profiles or IGF-I levels of patients, but controls showed greater mean GH levels during their fast than when fed. CONCLUSIONS: We have demonstrated that critically ill patients have low IGF-I levels associated with augmented baseline GH levels which show reduced oscillatory activity. The results would be compatible with the hypothesis that there is an adaptive change in critically ill patients away from the indirect effects of GH (stimulation of IGF-I production and anabolism) and toward the direct effects (lipolysis and insulin antagonism) which increase the availability of energy substrates. The pattern of GH levels seen in our patients may be important in this adaptation.
Two years after the introduction of a slaughter policy for BSE, the author summarizes the development of the epidemic and introduction of Government controls. In conclusion, the risk to humans is discussed.
Dorsal and palmar subluxation of the distal ulna can be difficult to both diagnose and treat. Patients often present long after their initial injuries with posttraumatic arthritic changes in the distal radioulnar joint. Hemiresection interposition arthroplasty is a salvage procedure that is reliable for both pain relief and restoration of motion.
Sheep producers throughout the United States have begun using accelerated lambing programs to enlarge their net income by increasing the number of lambs produced per ewe per year. These new intensive systems have produced some unique problems and concerns. This article attempts to educate the veterinarian as to the justification for these programs. Areas in which veterinary intervention can greatly influence the success or failure of these new accelerated lambing systems are identified. Selection of ewe type, ultrasound pregnancy diagnosis, ram evaluation, specific flock health concerns, and critical ewe nutrition are discussed.
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We add five cases of 20p deletion to the 10 cases already published. Four had craniofacial, vertebral, ocular, and cardiovascular features of Alagille syndrome, which adds weight to the assignment of this disorder to the short arm of chromosome 20. Included in our series is the first report of familial transmission of a 20p deletion.
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The liver and beta cells function in a negative feedback loop, which appears to have a predominant role in regulating both the basal plasma glucose and insulin concentrations. The degree of basal hyperglycemia in diabetes probably provides a bioassay of both the effect of a reduction in insulin secretory capacity and the degree of insulin resistance. A mathematic model of the interaction of insulin deficiency and insulin resistance has been constructed, based on the known response characteristics of the beta cells to glucose, and of plasma glucose and insulin control of hepatic and peripherpal glucose flux. The degree to which beta cell deficiency increases basal plasma glucose reflects the hyperbolic shape of the normal insulin secretory response to different glucose concentrations. The height of basal plasma insulin is a function of the degree of insulin resistance. From the basal plasma insulin and glucose concentrations, the model provides an estimate of the degree to which both beta cell deficiency and insulin resistance contribute to diabetes. The predictions arising from the model are in accord with experimental data in man and in animals. In normal-weight diabetics who do not have increased insulin resistance, the model predicts that more than 85% of beta cell function has to be lost for the basal plasma glucose to rise to 6 mmol/liter, but a further 5%--10% loss increases the basal plasma glucose to over 10 mmol/liter. In a third of a consecutive series of 65 newly presenting, uncomplicated diabetics, both normal weight and obese, the analysis from the model suggested that insulin resistance, rather than beta cell deficit, was the predominant feature.
1. Infusion of sufficient renin to raise the blood pressure of normal rats to hypertensive levels resulted in increased renin in the arterial wall. 2. Arterial wall renin and renal venous renin were normal in younger spontaneously hypertensive rats, but in older spontaneously hypertensive rats arterial wall renin was significantly increased and renal venous renin was significantly decreased. 3. Arterial wall renin in rats with either acute or chronic two-kidney Goldblatt renal hypertension was significantly increased, whereas circulatory renin was elevated in the former, but depressed in the latter. 4. Arterial wall renin may play a role in the maintenance of acute and chronic renal hypertension and also perhaps of spontaneous hypertension of long duration in older rats.
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