Covert video surveillance of children. Role of police.
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Biomedical subjects
Publications and source records attributed to J Fox.
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OBJECTIVE: To determine the effect of transdermal oestrogen replacement therapy on the haemostatic balance of menopausal women. DESIGN: Open, parallel group, prospective study. SETTING: Three hospital-based menopause clinics. SUBJECTS: Fifty-two postmenopausal women receiving transdermal hormone replacement therapy (Estrapak 50) for 6 months. Comparison group of 48 untreated postmenopausal women studied in parallel. MAIN OUTCOME MEASURES: Changes in platelet number, plasma concentrations of coagulation factors and their natural inhibitors, fibrinolytic activity, and rheological parameters. RESULTS: Estrapak 50 had no significant thrombophilic effect on any of the outcome measures. CONCLUSION: The haemostatic balance and thus the risk of thrombosis would not appear to be upset by this dose of transdermal oestrogen.
The problems of developing sound and safe expert systems are discussed, with particular reference to medicine. The concepts, notations, methods, results and technologies which have emerged from the study of mathematical logic as a computational paradigm offer many benefits for improving the quality of expert systems. Logic programming offers a better discipline for design, specification and implementation than ad hoc development methodologies. When logic programming is combined with software engineering methods, such as a software development life-cycle, the probability of routinely developing large-scale yet efficient and sound applications will be increased. However, although soundness is a necessary property of any technology it is not sufficient for assuring safety. Established methods for improved software safety are discussed, and a number of approaches to improving the safety of medical expert systems is identified. The possibility of introducing an appropriately extended life-cycle, and the potential benefits of a formal theory of safety are discussed.
Symbolic decision procedures offer a flexible alternative to classical quantitative procedures for decision making, particularly when precise parameters (such as probabilities) are hard to estimate. One such procedure, based on a logic of argumentation, is described. Specifications of inference methods for such functions as proposing and refining decision options, deducing and inheriting arguments for and against options, and selecting among alternatives are presented. These exploit declarative models for patient data, domain and task knowledge. A simple method for translating the specifications into executable Prolog is described. A practical and efficient toolset for using the procedure in a wide range of clinical environments is being developed within the DILEMMA project of the European Commission's Advanced Informatics in Medicine research programme.
In May-June 1992 cases of infection with verocytotoxin-producing (VT+) Escherichia coli O157 in South Yorkshire could have been associated with prior consumption of beef from a local abattoir. During investigation of the abattoir, bovine rectal swabs and samples of meat and surface swabs from beef carcasses were examined for E. coli O157, isolates of which were tested for toxigenicity, plasmid content and phage type. E. coli O157 was isolated from 84 (4%) of 2103 bovine rectal swabs; of these 84, 78 (93%) were VT+, the most common phage types being 2 and 8, the types implicated in the cluster of human cases. Positive cattle were from diverse sources within England. E. coli O157 was isolated from 7 (30%) of 23 carcasses of rectal swab-positive cattle and from 2 (8%) of 25 carcasses of rectal swab-negative cattle. The study has shown that cattle may be a reservoir of VT+ E. coli O157, and that contamination of carcasses during slaughter and processing may be how beef and beef products become contaminated and thereby transmit the organism to man.
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It is now established that all of the components necessary for the local formation of angiotensin II (ANG II) coexist in the kidney and can alter local ANG II production rate. However, data on ANG II concentrations in different compartments within the kidney are limited. Recently, proximal tubule fluid ANG II concentrations in the nanomolar range were reported. Using an ANG II radioimmunoassay procedure with enhanced sensitivity, we performed experiments to explore proximal tubular fluid ANG II levels further and to determine the source of the ANG II. Total free-flow proximal tubular fluid samples (n = 11) had an average ANG II concentration of 13 +/- 2 nM. These concentrations were similar (10 +/- 2 nM) in samples collected into pipettes containing the inhibitors enalaprilat and EDTA (n = 17). Fluid collected from blocked proximal tubules that were perfused with artificial tubular fluid showed similar ANG II concentrations both in the presence (22 +/- 3 nM) and absence (22 +/- 4 nM) of the angiotensin-converting-enzyme inhibitor, enalaprilat, in the perfusate. Plasma ANG II concentrations were much lower and averaged 155 +/- 26 pM. Isotonic saline expansion lowered plasma ANG II levels to 30 +/- 5 pM (P < 0.01) but did not significantly decrease intraluminal ANG II (8 +/- 1 nM). These data provide further evidence that intratubular ANG II concentrations are in the nanomolar range and are regulated independently of the plasma ANG II levels. The data obtained from perfused tubules indicate that the proximal tubule adds substantial amounts of ANG II or a precursor into the tubular lumen.
Educational programmes for nurses and the allied professions have increasingly been located within the marketplace through the introduction of educational contracts. But the use of clinical placements and related costs are not addressed within such contractual arrangements. Dawn Forman and Jane Fox assess the advantages and disadvantages.
In organ repair following injury, macrophages accumulate and granulation tissue, comprised of fibroblasts and endothelial cells, develops in the injured area. Basic fibroblast growth factor (bFGF), a potent stimulator of fibroblast and endothelial cell growth, has been linked to the fibroproliferative process. Macrophages are thought to play a central role in the fibroproliferative response, and prior studies indicate that they produce bFGF. Whereas it is plausible that macrophages produce bFGF in a fibroproliferative process, currently no data exists that directly identifies the macrophage as a source of bFGF in a fibroproliferative disorder. We used the model of acute intraalveolar granulation tissue formation following lung injury to determine if the macrophage was a cellular source of bFGF in a naturally occurring fibroproliferative process. To examine this hypothesis, patients with severe acute lung injury underwent bronchoalveolar lavage during the phase of lung repair. Polymerase chain reaction and Northern analysis of macrophage RNA revealed the presence of two species of bFGF messenger RNA (4.4 kb and 1.9 kb). Metabolic labeling studies of recovered macrophages revealed a newly synthesized 18-kd protein with antigenic similarity to bFGF. Immunohistochemical evaluation of lung tissue from patients who died following acute lung injury, showed numerous bFGF immunoreactive macrophages present within airspaces containing fibroblastic and vascular tissue proliferation. This investigation has identified the alveolar macrophage as a cellular source of bFGF in the fibroproliferative disorder of intraalveolar fibrosis following acute lung injury.
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This paper is based on, and summarises, papers read at the second annual international conference of Nurse Education Tomorrow held at the University of Durham (UK) September 1991. To this end this paper will offer: Some Accreditation of Prior Learning (APL) definition and process as reflected in the literature available. A distinction will be made between APL and Accreditation of Prior Experiential Learning (APEL) although the procedures and processes for assessing them will be shown to be the same. A brief outline of corporate strategy, as it applies to APL, will be given to form the basis for logical demonstration of how Derbyshire Institute of Health and Community Studies has employed such a corporate strategy. Insights developed and gained from APL research currently being undertaken through the college of nursing and midwifery will be used to inform the development and nature of corporate strategy. A flowchart of the operationalisation of the corporate strategy is offered as an integrative summary of how all the APL ideas have had a positive cumulative effect. The paper finishes by highlighting the possible strengths and limitations of APL corporate strategy.
Pregnancy is accompanied by an increased cardiac and neural sensitivity to some local anesthetic agents such as bupivacaine. The current study was initiated to investigate the relationship between increased progesterone concentrations and the electrophysiologic effects of bupivacaine, and lidocaine in isolated Purkinje fiber (PF)-ventricular muscle (VM) preparations. Twenty-four oophorectomized female white rabbits were killed after receiving 30 mg.kg-1.day-1 of progesterone intramuscularly or peanut oil alone for 4 days. PF and VM action potentials were recorded using standard electrophysiologic procedures. Plasma progesterone concentrations were 5 +/- 2.9 ng/ml in control animals compared to 59.8 +/- 11.0 ng/ml in progesterone-treated animals (P less than 0.05). Bupivacaine (3.5-17.4 microM) depressed the maximal rate of depolarization (Vmax) of PF to a significantly greater extent in tissues from progesterone-treated animals as compared to control animals. For example, at 3.5 microM bupivacaine decreased PF Vmax 52% in progesterone-treated tissues compared to 32% in controls (P less than 0.05); the Vmax of VM was also depressed to a greater extent in tissues from progesterone-treated animals (P less than 0.001). Lidocaine did not demonstrate an enhanced depressant effect in tissues from progesterone-treated animals. These results indicate that progesterone selectively increases the cardiac membrane depressant effects of bupivacaine but not lidocaine. This may contribute to the enhanced toxicity of bupivacaine in pregnant animals.
Because it is common to manipulate PaCO2 during neurosurgery, it is essential to characterize the relationship between cerebral blood flow (CBF) and changes in PaCO2. The purpose of this study was to investigate the effects of propofol-N2O anesthesia on the CBF response to changes in PaCO2 in healthy subjects. In seven patients, anesthesia was induced with propofol 2.0-2.5 mg/kg and then maintained with a propofol infusion of 12 mg.kg-1.h-1 for 10 min and then 9 mg.kg-1.h-1 for 10 min and then was reduced to 3-6 mg.kg-1.h-1 for the remainder of the study. The subjects' lungs were ventilated with N2O in O2 (FIO2 0.3) to the end-tidal CO2 present before anesthesia, and then CBF was measured using intravenous 133Xe and ten scintillation counters, five over each cerebral hemisphere. ETCO2 then was increased to 50 mmHg and CBF measurement repeated; ETCO2 then was reduced to 30 mmHg and CBF measurement repeated. Concurrent with each CBF measurement, arterial blood was sampled for PaCO2 and hemoglobin measurement. CBF at normocapnia (PaCO2 42 +/- 2 mmHg) was 33 +/- 7 ml.100 g-1.min-1, which increased to 58 +/- 10 ml.100 g-1.min-1 and decreased to 19 +/- 4 ml.100 g-1.min-1 on increasing PaCO2 (53 +/- 4 mmHg) and decreasing PaCO2 (31 +/- 2 mmHg), respectively. Both the PaCO2 and CBF values were statistically different from those measured at any other time (CBF P less than 0.002, PaCO2 P less than 0.001). The slope of CBF versus PaCO2 was 1.56 ml.100 g-1.min-1.mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
The changes in plasma calcium, phosphate, and parathyroid hormone (PTH) levels that accompany 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] administration to experimental animals represent major obstacles to determining the precise role that 1,25(OH)2D3 plays in cell function in vivo. These difficulties arise because calcium, phosphate, and PTH have major cellular effects independent of 1,25(OH)2D3. To circumvent this obstacle, we have developed an animal model in which plasma 1,25(OH)2D3 levels were raised from 20 +/- 3 to 96 +/- 19, 240 +/- 49, and 459 +/- 66 pg/ml in vitamin D-deficient rats without influencing plasma ionized calcium, total calcium, phosphate, or NH2-terminal immunoreactive PTH (irPTH) levels. The elevated 1,25(OH)2D3 levels were achieved by constant subcutaneous infusion of 1,25(OH)2D3 using osmotic minipumps. Progressive reduction in the calcium and phosphorus content of the diet as the 1,25(OH)2D3 infusion rate was increased prevented concomitant changes in plasma calcium, phosphate, and irPTH levels. This experimental model, in conjunction with our previously developed normocalcemic rat model of vitamin D deficiency, provides a powerful experimental tool for the investigation of 1,25(OH)2D3 effects in vivo in the absence of concomitant changes in other parameters of calcium homeostasis.
This study determined whether acute decreases in plasma ionized calcium (Ca2+) levels regulate plasma 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] levels independent of changes in parathyroid hormone (PTH) secretion and plasma phosphate levels. Chronically catheterized rats were subjected to a hypocalcemic clamp (mean decrement of Ca2+ levels 0.38 +/- 0.04 mM), a rat PTH-(1-34) infusion, and a PTH vehicle infusion for 2 h. Plasma NH2-terminal immunoreactive PTH levels were elevated 3.2- and 8.7-fold during hypocalcemia and PTH infusion, respectively. Plasma phosphate decreased by 23 +/- 4 and 42 +/- 3% during hypocalcemia and PTH infusion, respectively. In response to hypocalcemia, plasma 1,25(OH)2D3 levels increased promptly, were significantly elevated by 15 min (56 +/- 23% increase), and continued to increase until the end of the experiment at 5 h (350 +/- 30% increase). In contrast, no changes in plasma 1,25(OH)2D3 levels occurred during the PTH infusion, but levels were elevated by 5 h, i.e., 3 h after the end of the infusion (360 +/- 20% increase). No significant changes in 25(OH)D3 or 24,25(OH)2D3 levels occurred in any protocol. Thus hypocalcemia rapidly elevates 1,25(OH)2D3 levels in rats, but the increase is not caused by elevated PTH secretion, hypophosphatemia, or elevated 25(OH)D3 levels. Furthermore, the increase in 1,25(OH)2D3 levels by hypophosphatemia does not occur rapidly. These studies show that there is a calcium-dependent mechanism that is independent of changes in PTH secretion and that results in the rapid elevation of plasma 1,25(OH)2D3 levels to counteract hypocalcemia.
This study was designed to improve and validate methods for the accurate and consistent quantitation of angiotensin (ANG) I and II levels in rat kidney and to determine the effects on renal ANG I and II of changes in dietary sodium intake and ANG-converting enzyme (ACE) inhibition. Kidneys from pentobarbital-anesthetized rats were rapidly removed and homogenized in methanol before extraction and purification of ANG peptides by solid-phase extraction and high-performance liquid chromatography (HPLC). Recoveries of 125I-ANG I and II were greater than 80%. Reversed-phase HPLC of the partially purified methanol extract showed that greater than 75% of the ANG I- and greater than 82% of the ANG II-like immunoreactivity coeluted with ANG I and II, respectively. Dietary sodium deprivation (0.003 meq/g) and excess (1.34 meq/g) for 7 days significantly (P less than 0.01) increased and decreased renal ANG I (296 +/- 30 and 82.6 +/- 15.8 vs. 161 +/- 18 fmol/g) and ANG II (216 +/- 16 and 45.6 +/- 11.8 vs. 98 +/- 16 fmol/g) contents, respectively. Plasma ANG I and II levels showed similar changes. ACE activity was significantly upregulated by sodium deprivation in both kidney (44% increase) and plasma (30% increase). In rats fed normal chow, infusion of enalaprilat for 1 h abolished plasma ACE activity but decreased renal ACE activity by only 58%. ACE inhibition increased renal and plasma ANG I levels 2.8- and 12-fold, respectively, and decreased renal and plasma ANG II levels 75-78%.(ABSTRACT TRUNCATED AT 250 WORDS)