Biomedical subjects
Publications and source records attributed to M Kidd.
The use of computer systems to produce prescriptions offers many benefits at a reasonable cost. This article summarises the benefits and costs and the steps recommended for general practitioners who wish to start using a computer to generate their prescriptions.
Recent advances in computer hardware, software and telecommunications, and particularly in the development of the electronic medical record, mean that family practitioners around the world now have access to a multiplicity of tools which offer the potential for significant time savings and improved quality of health care provision. Areas such as practice management medication management and prescription generation, clinical record keeping, decision support, medical research and continuing medical education can all be aided through the use of information technology in a family practice setting. Yet family medicine, or general practice, has largely been slow to take up the challenge of implementing information technology in most parts of the Asia-Pacific region. This contrasts sharply with many other areas of medicine which have been very active in embracing this technology. This paper examines the potential advantages and the difficulties of computerisation for general practitioners and their patients in the Asia-Pacific region. It is hoped that the lessons already learned in some countries in this region can be adapted and applied elsewhere.
This paper aims to assist candidates in their preparation for the RACGP Fellowship examination. Particular emphasis is placed on what to do before the event and the techniques to use on the day. Explanations about the rating schedules for the various segments are also given.
At the request of the largest children's hospital in Moscow, McKenzie and colleagues made recommendations for improving the service. Restrictions on visiting and fears of contracting illness from non-disposable needles have discouraged the local population from using the hospital. Consequently the hospital is underused and overstaffed. Serious shortages of drugs and surgical supplies compromise care. Fundamental changes are needed in nursing and postgraduate education. The authors encouraged their Russian colleagues to address the health care needs of their local population and to develop family centred care, and they offered training in London.
Explore the source record for details and available documents.
We describe the preparation and characterisation of an immunoaffinity column of immobilised monoclonal antibody 1G10/2/3 which was raised against a synthetic peptide representing residues 8-17 of the A4 amyloid protein (or beta-protein) of Alzheimer's disease (AD). In previous work we have shown that this antibody reacts in formalin-fixed, paraffin-embedded tissue sections with plaque cores, plaque periphery and cerebrovascular amyloid of AD. We have used the column in the immunoaffinity isolation from extracts prepared from AD brain tissue of a protein with an apparent molecular weight of 31,000; this protein is reactive with 1G10/2/3 in Western blots. The same protein is also present, but at lower level, in normal control brain tissue. Possible relationships of this protein to the predicted structures for full-length A4-precursors are discussed. However, in view of the preliminary nature of the observations and potential problems relating to proteolysis occurring post-mortem or during the extraction process, firm conclusions cannot be drawn about any role for this molecule in the normal functioning of A4-precursors or in the conversion of A4-precursor to the deposits of A4 seen in AD brain. Nevertheless, we conclude that we are seeing a stable but truncated form of A4-precursor and it will be of interest to see if further studies can clarify the possible relevance of the protein to normal or pathological processes in human brain tissue.
The charts of 83 patients with iridocorneal endothelial (ICE) syndrome were retrospectively reviewed. Forty-two eyes of 42 patients had had filtering surgery, 37 of whom had had a trabeculectomy to reduce uncontrolled intraocular pressure. Twenty-four of these trabeculectomy patients required a second surgery, and 8 required a third surgery. The results are presented using a survival analysis. The success rates at one year of follow-up for the first, second, and third trabeculectomies were 64%, 79%, and 63%, respectively. Patients subclassified as having Chandler's syndrome, essential iris atrophy, and Cogan-Reese syndrome responded with approximately the same success rates within the first two years following their first surgery. The success rates for repeated surgeries are comparable with those of initial surgery in patients with primary open angle glaucoma. On the basis of this study, further surgery is recommended despite initial failure in this group of difficult patients.
The existence of inhibitors of plasminogen activator has been shown to play an important role in regulation of fibrinolysis and postoperative thrombosis. Platelets and endothelium are sources of plasminogen activator inhibitor (PAI). This study determines the contribution of platelet-released PAI to perioperative fibrinolytic shutdown. PAI levels were measured in 25 patients having aortic surgery. In nine patients the platelet-released PAI contribution was determined by in vitro activation of platelets with phorbol-myristate-acetate (PMA). Mean preoperative PAI levels (3.78 +/- 1.19 U/ml) were similar to controls (3.01 +/- 1.04 U/ml) (p greater than 0.05). Plasma PAI showed an operative increase to a maximum at 8 hours postoperatively and returning to preoperative values by the second postoperative day. In the nine patients who were subjected to studies with in vitro activation, the preoperative PAI level (4.0 +/- 0.9 U/ml) was elevated to 5.1 +/- 0.7 U/ml (p = 0.001) with PMA induction. Maximum stimulated release of platelet granule contents (platelet releasate) could account for an increase of only 1.0 U/ml compared with a postoperative increase of 2.3 U/ml. Postoperative mean peak plasma PAI (6.3 +/- 0.4 U/ml) could not be further elevated by induced release (6.3 +/- 0.4 U/ml) (p = 0.003). A statistically significant increase in PAI occurred in aortic surgery patients postoperatively. The platelet releasable pool of PAI contributed to the increase and was functionally exhausted postoperatively. Postoperative increases of PAI were twice that induced by platelet in vitro stimulation alone. The perioperative increase in PAI was partly due to platelet release.
A monoclonal antibody to a synthetic peptide consisting of residues 8-17 of the amyloid beta protein of Alzheimer disease was used in immunohistochemical studies to reveal binding sites for this peptide in vesicular elements in the islets of Langerhans of the pancreas and the zona reticularis of the adrenal gland. These binding sites may represent a specific membrane receptor. These results, together with similarities in structural features between the precursors for epidermal growth factor and beta protein, suggest that the beta-protein precursor may be processed to release an active peptide ligand rather than acting as a membrane receptor. In Alzheimer disease, abnormal processing of this active peptide precursor may result in the deposition of beta-protein amyloid fibrils in the brain.
The amyloid plaques found in neurodegenerative diseases show considerable morphologic diversity. Two amyloidogenic proteins have been isolated from the brains of humans and animals with neurodegenerative diseases--beta-protein from Alzheimer's disease (AD) and Down's syndrome, and prion protein (PrP) from scrapie and Creutzfeldt-Jakob disease (CJD). Using monoclonal antibodies to a synthetic peptide corresponding to a portion of beta-protein and rabbit antiserum to hamster scrapie PrP 27-30, we examined in situ amyloid plaques on sections from cases of neurodegenerative diseases, including cases with a spectrum of plaque types. Anti-beta-peptide stained cerebrovascular and plaque core amyloid in all AD cases as well as cerebrovascular amyloid and senile plaque core amyloid in five elderly CJD cases. Anti-PrP stained plaques in CJD, kuru, and Gerstmann-Sträussler syndrome cases but not cerebrovascular amyloid or plaques in AD. Dual localization experiments showed that in cases with a mixture of plaque types, the antibodies identified different populations of plaques that showed anatomic heterogeneity. Colocalization of the two proteins was not observed in any plaque type. The data suggest that in neurodegenerative diseases two major plaque types exist, which have different etiologic origins. Our results emphasize the need for classification of CNS amyloids based not on their morphology but on the macromolecular components comprising these pathologic polymers.
A monoclonal antibody raised to a synthetic peptide consisting of residues 8 to 17 of the amyloid beta protein of Alzheimer's disease was employed for immunogold electron microscopic studies on amyloid fibrils of cerebrovascular walls and neuritic plaques in this disease. Electron microscopy revealed a specific gold labeling of the amyloid fibrils in these structures. This provides ultrastructural evidence that beta protein is intimately associated with the amyloid fibril. With previous chemical evidence, this observation supports the concentration that it is an intrinsic component of the fibril.
Four monoclonal antibodies (1D2/1/2, 1G10/2/3, 3B6/1/1, 4D12/2/6) were raised against a synthetic peptide consisting of residues 8-17 of a protein reported to be common to senile plaque cores, cerebrovascular amyloid and neurofibrillary tangles in Alzheimer's disease. In an immunoperoxidase study of Alzheimer brain tissue, these antibodies stained plaque and vascular amyloid but not tangles, suggesting that the polypeptide chain in the region of residues 8-17 is exposed in the former two but, if present, inaccessible in the latter. In addition, staining of granular material in the plaque periphery was observed. These antibodies will be useful tools for future work on the origin of this protein.
Frontal and temporal cortical tissue from the brains of elderly cases of Down's syndrome was used to make preparations of neuronal cell bodies containing senile plaque cores. Polarisation microscopy revealed normal "classical" plaque cores, and also a high proportion of unusual "amorphous" plaque cores which we have not seen in Alzheimer's disease. These two forms were easily distinguished by electron microscopy. This suggests that late Down's syndrome may not be an exact model for Alzheimer's disease.
Explore the source record for details and available documents.
A new method has been developed for the isolation of intact senile (neuritic) plaque cores from post-mortem brains of patients with Alzheimer's disease. The plaque cores were found to be insoluble in various protein denaturants. The amino acid composition of the plaque core protein does not resemble that of any known form of amyloid.
One hundred and thirteen patients with insulin dependent diabetes mellitus for at least 15 years were typed for 22 HLA antigens of the A and B series. Fifty-six patients had severe bilateral proliferative retinopathy and 57 had no retinopathy. There was no statistical difference in frequency of HLA antigens between the 2 groups of diabetic patients. There was a significantly higher frequency of HLA B15 and a significant lower frequency of HLA B14, B17 in the combined diabetic groups than in a control population of 200 normal blood donors.
Explore the source record for details and available documents.
Explore the source record for details and available documents.