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C Pope

Publications and source records attributed to C Pope.

At least 55 records · Page 3Linked to original sources

Reaching the parts other methods cannot reach: an introduction to qualitative methods in health and health services research.

Qualitative research methods have a long history in the social sciences and deserve to be an essential component in health and health services research. Qualitative and quantitative approaches to research tend to be portrayed as antithetical; the aim of this series of papers is to show the value of a range of qualitative techniques and how they can complement quantitative research.

Health Services Research↗

Possible involvement of a neurotrophic factor during the early stages of organophosphate-induced delayed neurotoxicity.

Little is known regarding early biochemical events in organophosphate-induced delayed neurotoxicity (OPIDN) except for the essential inhibition of neurotoxic esterase (NTE). We hypothesized that a trophic factor may be produced in situ shortly after exposure to the OP which participates in the progression of OPIDN. To bioassay for such a growth-modulating factor(s), we treated chickens with the neuropathic agents diisopropylfluorophosphate (DFP) or cyclic phenyl saligenin phosphate (PSP), with or without phenylmethylsulfonyl fluoride (PMSF, a chemical which markedly modifies OPIDN). Soluble extracts of cervical spinal cord (a region of the nervous system which degenerates with OPIDN) were collected 24 h later and these were incubated with human neuroblastoma SY5Y cells in culture. The cells were allowed to grow for another 6 days and observed for changes in morphology and growth. After 3 days in culture, tissue extracts from OP-treated chickens caused SY5Y cells to begin to elongate and extend processes (neurites), similar to cells treated with nerve growth factor (1 microgram/ml). Extracts from chickens not receiving OP had no or minimal effects on cell morphology. In addition, extracts from chickens in which OPIDN was prevented by pretreatment with PMSF did not cause the marked extension of cell processes exhibited after exposure of SY5Y cells to extracts from chickens given regimens known to cause OPIDN. In parallel-treated animals. DFP and PSP caused clinical dysfunction characteristic of OPIDN, PMSF posttreatment markedly amplified the clinical deficits and PMSF pretreatment prevented OPIDN. In vivo DFP treatment also caused a marked reduction in the activity of the growth-related enzyme ornithine decarboxylase (ODC) in spinal cord but DFP was without effect on ODC activity in vitro (up to 1 mM final concentration). Characterization of this growth-modulating factor(s) may aid in the elucidation of pathological mechanisms of OPIDN.

Animals↗

Mental health status as a predictor of morbidity and mortality: a 15-year follow-up of members of a health maintenance organization.

OBJECTIVES: This study sought to relate preexisting depression, worries, affect balance, and mental health symptoms to subsequent risk of morbidity and mortality. METHODS: A random sample of members of a health maintenance organization were interviewed at home in a 1970/71 survey. Baseline psychological measures from that survey were then related to 15-year mortality and first incidence of cancer, heart disease, hypertension, stroke, functional gastrointestinal disease, and hyperimmune diseases. RESULTS: Baseline depression and the Langner Mental Health Index predicted incidence of functional gastrointestinal and hyperimmune diseases. The relationship of the Langner index to hyperimmune diseases was particularly strong; mortality, cancer, heart disease, hypertension, and stroke incidence were not related to that index. Except for affect balance, which was worst in the elderly, indications of psychological dysfunction were strongest in the young. CONCLUSIONS: Psychological indices detected increased risk for functional gastrointestinal and hyperimmune diseases but were not related to mortality risk. Further research is needed to disaggregate relationships of the specific conditions that were included in the hyperimmune group. Functional gastrointestinal disease might be preventable with early attention to depressed persons and to those scoring high on the Langner index.

Adolescent↗

Opening the black box: an encounter in the corridors of health services research.

Health services research has become more prominent as a result of the NHS reforms. Both providers and purchasers want to know exactly where the money is spent and how it could be used more effectively. How best to obtain information about health services is the subject of some debate within and between disciplines engaged in such research. Because of their training doctors are often sceptical of anything other than formal clinical trials and research which produces statistical data. Some sociologists argue that another way to find out what is actually happening in the NHS is to observe people at work and talk to them. This article debates these differing views of research methods. For effective research both quantitative and qualitative approaches need to be used.

Anthropology, Cultural↗

Developmental changes in carbachol-stimulated inositolphosphate release in pigmented rat retina.

Carbachol-stimulated release of inositolphosphates (IP) was studied in the whole retina from Long-Evans rats of different ages (day 5, 10, 15, 20, adult) following in vitro incorporation of [3H]myo-inositol. Unlike the albino rat retina, the pigmented retina was highly light-sensitive, making it necessary to dark adapt the animals and perform retinal dissections under low illumination to prevent light-induced IP release. Retinae from postnatal day 10 rats showed the highest amount of carbachol-stimulated IP released. This response to carbachol decreased with age until postnatal day 20 when it reached adult levels. The pigmented rat retina showed a sharp fall in the degree of carbachol (1 mM)-stimulated IP released at the time of eye-opening (450% above basal in retinae from 10 day old animals, as compared to 230% above basal in 15 day old retinae). Basal release of IP was not altered in the retina during development. Muscarinic cholinergic receptor density was, however, found to increase 5 fold with age, reaching adult levels by PND 20. Retinal weight and protein per retina also increased (four fold) from day 5 to adult; however, the in vitro incorporation of [3H]myo-inositol into phosphoinositides (calculated as per mg protein) did not change during development. Thus, in animals prior to eye opening, a much higher proportion of phosphoinositides appears to be hydrolyzed upon muscarinic receptor stimulation. During retinal development a change in sensitivity to the agonist-sensitive pool(s) of phosphoinositides may occur and/or there may be alterations in the efficacy of receptor coupling to the second messenger system resulting in the disassociation observed between the drastic increase in receptor number and the apparent decrease in receptor-stimulated release of IP.

Aging↗

Murine susceptibility to organophosphorus-induced delayed neuropathy (OPIDN).

This study reports that CD-1 strain mice are neuropathologically and biochemically responsive to acute doses of tri-ortho-cresyl phosphate (TOCP). Young (25-30 g) male and female animals were exposed (po) to a single dose of TOCP (580-3480 mg/kg) and sampled for neurotoxic esterase (NTE) activity at 24 and 44 hr postexposure and for neuropathic damage 14 days later. Biochemically, high intragroup variability existed at the lower doses, and at higher levels of TOCP exposure (i.e., greater than or equal to 1160 mg/kg), mean brain NTE inhibition never exceeded 68%. Hen and mouse brain NTE activity, assayed in vitro for sensitivity to inhibition by tolyl saligenin phosphate (TSP), the active neurotoxic metabolite of TOCP, showed similar IC50 values. Histologically, highly variable spinal cord damage was recorded throughout treatment groups and mean damage scores followed a dose-response pattern with no apparent correlation to threshold (i.e., greater than or equal to 65%) inhibition of brain NTE activity. Topographically, axonal degeneration in the mouse spinal cord predominated in the lateral and ventral columns of the upper cervical cord. Unlike the rat, which displays degeneration in the upper cervical cord's dorsal columns (i.e., gracilis fasciculus) in response to TOCP intoxication, treated mice showed minimal damage to this tract. To examine this discrepancy further, ultrastructural morphometric analysis of axon diameters in the cervical cord was performed in control mice and rats. These results indicated that in both species, the largest diameter (greater than or equal to 4 microns) axons are housed in the ventral columns of the cervical spinal cord, suggesting that axon length and diameter may not be the only criteria underlying fiber tract vulnerability in OPIDN.

Animals↗

Adolescents as victims: an overview of the special impact of sexual abuse.

Although under-reported, sexual abuse is an increasingly critical problem facing adolescents and their care providers. All care providers must consider the possibility of abuse in their clinical practice. This paper will address the significance of the problem and offer suggestions for immediate nursing intervention.

Adolescent↗

The neurotoxicity of subchronic acetylcholinesterase (AChE) inhibition in rat hippocampus.

The neurotoxic effects of long-term, low-level exposure to the commercially available insecticide, Fenthion, were examined in the present study. Young (2 month) adult, male Long-Evans rats were dermally exposed to Fenthion (25 mg/kg, 3X week) and sampled after 2 and 10 months exposure to assess neurotoxic damage in the hippocampus using morphological and biochemical endpoints. Histopathology, consisting of gliosis, swollen and necrotic neurons, and cell dropout, occurred in the dentate gyrus (DG), CA4 (hilus), and CA3 sectors as early as 2 months postexposure. Acetylcholinesterase (AChE) staining of brain tissues taken at this time was severely reduced in the septal nuclei, the DG molecular layer, the CA4, and the hippocampus proper. After 10 months exposure to Fenthion, cellular necrosis and gliosis intensified in the CA4 and CA3 regions and occasionally involved the CA2. Radiometric assays of AChE activity in the hippocampus indicated a 65 and 85% depression after 2 and 10 months exposure, respectively. Quinuclidinyl benzilate binding for the hippocampal muscarinic receptor was reduced by 6 and 15%, after 2 and 10 months exposure, respectively. A separate group of older (12 month) rats was exposed to the same dosing regimen of Fenthion and examined for neuropathological damage after 2 and 10 months exposure. Aged animals exposed for only 2 months expressed severe hippocampal degeneration in a pattern similar to that seen in the young adult after 10 months exposure (viz., DG, CA4, CA3). Aged animals exposed for 10 months showed more extensive histopathology of the CA4-2 and occasionally CA1. These observations indicate that in both young adult and aged animals, subchronic, low-level exposure to anticholinesterase compounds can result in serious neurotoxic consequences to the mammalian hippocampus.

Acetylcholinesterase↗

Calcium and phosphorus solubility in neonatal intravenous feeding solutions.

The limited solubility of calcium and phosphorus in standard parenteral nutrition formulations has restricted the ability to provide sufficient minerals to preterm infants to prevent substrate deficient metabolic bone disease. We determined the solubility limits of calcium and phosphorus in a total of 160 formulations under carefully controlled conditions. By increasing the concentrations of dextrose, amino acids, and by using Addiphos instead of 8.7% dipotassium hydrogen phosphate as the phosphorus source, higher concentrations of both calcium and phosphorus were held in solution. This should permit the delivery of increased concentrations of these minerals at rates which approximate fetal accretion.

Amino Acids↗

Acid-base state of the preterm infant and the formulation of intravenous feeding solutions.

An acidic intravenous source of phosphorus (Addiphos) was compared with dipotassium hydrogen phosphate in 25 preterm infants to study acid-base state. Eight infants were given either Addiphos or dipotassium hydrogen phosphate alternately for 48 hour periods and similar amounts of calcium and phosphorus were delivered. There were no significant differences in calcium and phosphorus intake, calcium and phosphate plasma concentrations, or acid-base state between study periods on the two solutions. Seventeen infants were given the two solutions alternately for 72 hour periods; Addiphos was used to increase the amounts of calcium and phosphorus being delivered. Calcium and phosphorus intake was decreased on dipotassium hydrogen phosphate, but Addiphos significantly increased calcium and phosphorus intake and plasma calcium and phosphate concentrations. It also lowered the pH of the urine and raised the titratable acidity. Acid-base state, however, was not significantly different. It is therefore possible to increase intake of calcium and phosphorus in preterm infants without causing a significant metabolic acidosis.

Acid-Base Equilibrium↗

The neurotoxicity of parathion-induced acetylcholinesterase inhibition in neonatal rats.

The biochemical and morphological effects of postnatal acetylcholinesterase (AChE) inhibition were examined in rat pups dosed with parathion, at time points critical to hippocampal neurogenesis and synaptogenesis (i.e., day 5-20). In treated pups, sacrificed on day 21, hippocampal histopathology, as assessed by light and electron microscopy, consisted of cellular disruption and necrosis in the dentate gyrus (DG), and CA4 regions. Synaptic disruption in the DG molecular layer was suggested by histochemical preparation using both the Timm's and AChE stains. In parathion-treated pups, sampled at day 12, hippocampal AChE was depressed 73% and [3H] quinuclidinyl benzilate (QNB) binding was depressed by 36%. The above results indicate that morphological and biochemical consequences are associated with persistent AChE depression in neonatal rats.

Acetylcholinesterase↗

Comparison of platelet scintigraphy, impedance plethysmography gray scale and color flow duplex ultrasound and venography for the diagnosis of venous thrombosis.

The several techniques available for the diagnosis of venous thrombosis have not been directly compared in the same patient population. Thus color and gray scale duplex ultrasound (U), impedance plethysmography (IPG), 3-4 hr platelet imaging (PS) were compared to venography (V), in 104 consecutive patients (in hospital and out). PS and V were read by two, and IPG and U by one, blinded reader. Comparisons were made for the calf (CA), popliteal (Pop) and femoral (Fem) vessels. Reproducibility of V and PS was 84 and 87%. (table; see text) We conclude that PS, while having a very high specificity, has an unacceptably low sensitivity. However, while both impedance plethysmography and color flow ultrasound have excellent and similar diagnostic accuracy in the femoral, these techniques have either a low sensitivity or low technical success rate in the calf or popliteal veins.

Blood Platelets↗

The neurotoxicity of parathion-induced acetylcholinesterase inhibition in neonatal rats.

The biochemical and morphological effects of postnatal acetylcholinesterase (AChE) inhibition were examined in rat pups dosed with paration, at time points critical to hippocampal neurogenesis and synaptogenesis (i.e., day 5-20). In treated pups, sacrificed on day 21, hippocampal histopathology, as assessed by light and electron microscopy, consisted of cellular disruption and necrosis in the dentate gyrus (DG), and CA4 regions. Synaptic disruption in the DG molecular layer was suggested by histochemical preparation using both the Timm's and AChE stains. In parathion-treated pups, sampled at day 12, hippocampal AChE was depressed 73% and [3H] quinuclidiny benzilate (QNB) binding was depressed by 36%. The above results indicate that morphological and biochemical consequences are associated with persistent AChE depression in neonatal rats.

Acetylcholinesterase↗

Safety and efficacy of esmolol for unstable angina pectoris.

Esmolol is a rapidly metabolized cardioselective beta-adrenergic blocker that provides steady state beta-adrenergic blockade when administered by continuous intravenous infusion. To determine the efficacy of esmolol in the management of unstable angina, 23 patients with known coronary artery disease, who averaged 3.7 +/- 2.7 daily episodes of chest pain at rest, were randomized to receive either a continuous infusion of esmolol (n = 12) or oral propranolol (n = 11), as an adjunct to concomitant antianginal therapy. Patients with systolic blood pressure less than 110 mm Hg, heart rate less than 60 beats/min or known contraindications to beta blockade were excluded. Esmolol was titrated in a step-wise fashion from 2 to 24 mg/min at 5-minute intervals up to a 30% reduction in heart rate and systolic blood pressure double-product. The propranolol dose was increased every 6 hours by 50 to 100% to achieve a similar reduction in heart rate and blood pressure. When compared with their 24-hour baseline periods, both groups achieved a significant reduction in episodes of chest pain, from 4.6 +/- 3.3 to 1.4 +/- 1.5 in the esmolol group (p less than 0.02) and 2.6 +/- 1.4 to 1.0 +/- 1.5 in the propranolol group (p less than 0.02) during the subsequent study period. The cardiac event rate and incidence of drug side effects were similar between the 2 groups; however, side effects seen with esmolol did not require treatment after drug discontinuation. Thus, maximally tolerated beta blockade is an effective therapy for unstable angina.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗