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Biomedical subjects

A Evans

Publications and source records attributed to A Evans.

At least 271 records · Page 15Linked to original sources
PubMed1995

Morphometry in temporal lobe epilepsy.

We demonstrate a method for quantitating changes in volume and morphology of the temporal lobe in epilepsy. The temporal lobes of 10 neurologically normal subjects and six subjects with well defined left-sided mesial temporal epilepsy were studied. From high resolution T1-weighted magnetic resonance images, the grey and white matter were manually segmented over a predetermined extent. The volumes of the grey and white matter were determined. Using the segmented images, the grey matter/CSF surface and the white matter/grey matter surface were reconstructed, allowing estimates of the surface area and calculation of indices of curvature for the two surfaces. The index of curvature was calculated for each vertex of a polygonal mesh that was fitted to the surfaces. An index of grey matter thickness (grey matter volume/white matter surface area) was also calculated. There was a significant bilateral decrease in the total volume (p < .01), grey matter volume (p < .001) and grey matter thickness index (p < .05) in epileptic subjects. In addition, there was a bilateral decrease in white matter surface area (p < .05) and a small left-sided decrease in white matter volume (p < .05) in epileptic subjects. The average distributions of indices of curvature for both surfaces differed significantly (p < .05) between normal and epileptic subjects. In the grey matter/CSF surface of normal subjects, a large peak corresponding to surface concavity was present. The amplitude of this peak was significantly lower in epileptic subjects (p < .05 for the right hemisphere; p < .001) for the left hemisphere).

Adult↗
PubMed1995

Angiotensin I converting enzyme gene polymorphism and coronary heart disease.

Genetic variations in the renin-angiotensin and kallikrein-kinin systems could prove to be significant pathophysiological mechanisms affecting coronary heart disease (CHD), particularly given the powerful vasoactivity of products such as angiotensin II and bradykinin. Indeed, studies show that angiotensin converting enzyme (ACE) gene polymorphism is associated with an increased risk of myocardial infarction and death, even in otherwise low-risk subjects. Genetic differences do not appear to be a risk factor for atherosclerosis or hypertension, however. Because ACE polymorphism modulates local production of angiotensin II, a powerful coronary vasoconstrictor, it may influence left ventricular mass in general as well as in coexisting disease states such as hypertension and cardiomyopathy. However, further study is needed to clarify the implications of ACE polymorphism in patients with left ventricular hypertrophy. Interactions between ACE and angiotensin II type-1 receptors may have clinical implications for preventing and managing CHD. Screening for genetic risk, as evidenced by certain variants in receptor coding sequence, may prove worthwhile if detrimental effects can be countered by drugs such as ACE inhibitors and angiotensin II receptor blockers. Given the important roles of angiotensin II and bradykinin as modulators of cellular growth and of vasoactivity, deleterious and beneficial effect at different stages of the atherosclerotic process and during acute events leading to myocardial infarction or sudden death can be suspected.

Aging↗
PubMed1995

Medical treatment of myocardial infarction in France and Northern Ireland. Results from the ECTIM study. Enquête cas-Témoins de l'Infarctus du Myocarde.

As part of the ECTIM Study, the medical treatment given to male patients (25-64 years) 3 to 9 months after myocardial infarction (MI) were analysed in France and Northern Ireland. On univariate analysis, hypolipidaemic drugs, angiotensin-converting enzyme inhibitors and antiarrhythmic drugs were found to be prescribed more frequently in France, while beta-blockers were more common in Northern Ireland. No differences were found for diuretics, calcium channel blockers, antithrombotic and anti-anginal drugs, although the Northern Irish patients were mainly on antiplatelet drugs and nitrates, while the French patients received nitrates and non-nitrates, as well as oral anticoagulants and antiplatelet drugs in similar amounts. These differences remained after adjustment for personal history of diabetes, hyperlipidaemia, hypertension, and previous myocardial infarction, but the beta-blocker prescription was no longer significant. When the French centres were analysed, patients from Strasbourg were more frequently on oral anticoagulants and diuretics and less frequently on antiplatelet drugs, while patients from Toulouse had fewer anti-anginal drugs. Hence, although the current guidelines for secondary prevention of myocardial infarction are generally well applied in France and Northern Ireland, significant differences exist regarding the choice of the active drug.

Adult↗
PubMed1995

Failure of "effective" treatment for heart failure to improve normal customary activity.

OBJECTIVES: To examine the effects of drug treatment on laboratory exercise tests in relation to measures of daily activity in patients with chronic heart failure. SETTING: University teaching hospital. SUBJECTS: 18 patients with mild to moderate chronic heart failure (New York Heart Association functional class II-III) and 10 age matched healthy controls. METHODS: Assessments were made before and after 12 weeks of vasodilator drug treatment. Exercise capacity was measured during two different types of treadmill exercise, one using a ramp protocol and the other a fixed work load. Corridor walk tests at three self selected speeds were also undertaken and measures of customary activity assessed from pedometer scores. RESULTS: Exercise times were significantly increased from baseline (P < 0.01) with both treadmill protocols after 12 weeks of drug treatment, with a positive correlation between the duration of treadmill exercise for both protocols (r = 0.69, P < 0.01). Corridor walk tests of 100 m at a self selected slow speed also improved (P < 0.02) but these did not correlate with the changes in treadmill exercise time. The pedometer scores of the patients with heart failure were greatly reduced compared with those of the controls (258 (45) x 10(2) v 619 (67) x 10(2) steps/week, P < 0.001) and after 12 weeks of treatment were unchanged (261 (42) x 10(2) steps/week). CONCLUSIONS: These data confirm the need to use different exercise protocols when assessing the benefits of drug treatment in patients with chronic heart failure. Treatments that seem effective with conventional laboratory based exercise tests may not improve daily activities. This may reflect a failure of apparently successful treatment and should be considered when interpreting clinical trials.

Activities of Daily Living↗
PubMed1995

Validation of British Thoracic Society guidelines for the diagnosis of the sleep apnoea/hypopnoea syndrome: can polysomnography be avoided?

BACKGROUND: The British Thoracic Society report on the diagnosis and treatment of the sleep apnoea/hypopnoea syndrome (SAHS) suggests that, if the pulse oximetry baseline oxygen saturation is above 90%, then 15 4% oxygen desaturation/hour in bed will diagnose SAHS requiring treatment. The diagnostic outcome of applying these guidelines has been studied. METHODS: One hundred patients referred to a district general hospital sleep clinic were recruited. After initial clinical assessment, overnight pulse oximetry measurements were performed, followed by full polysomnography at the regional laboratory. RESULTS: Sixty nine patients underwent both pulse oximetry and polysomnography. All 10 patients with more than 15 4% desaturations/hour on pulse oximetry had SAHS confirmed on polysomnography (specificity = 100%). Twenty two patients with SAHS were misdiagnosed using pulse oximetry alone (sensitivity = 31%). These patients had low apnoea scores but high hypopnoea scores. CONCLUSIONS: The BTS pulse oximetry criteria are highly specific when positive (specificity = 100%), but may miss patients with the SAHS who have hypopnoeic episodes which cause arousal but not significant oxygen desaturation (sensitivity = 31%). It should be emphasised that pulse oximetry alone does not always give sufficient information to discriminate between those patients with or without SAHS. Patients with "negative" pulse oximetry and symptoms of SAHS should undergo polysomnography or multi-channel recording.

False Negative Reactions↗
PubMed1995

Differential expression and effect of 1,25-dihydroxyvitamin D3 on myosin in arterial tree of rats.

The hypothesis that 1,25-dihydroxyvitamin D3 [1,25(OH)2D3, also known as calcitriol] modulates myosin expression in vascular smooth muscle was tested. Wistar-Kyoto or spontaneously hypertensive rats given intraperitoneal injections of 25 ng 1,25(OH)2D3/100 g body weight for varying periods of time showed a greater than twofold increase in aortic mRNA encoding the myosin regulatory light chain relative to 18S rRNA (P < 0.05). 1,25(OH)2D3 administration to Wistar rats caused a significant increase in the aortic content of total myosin regulatory light chain and total myosin heavy chain. The increase in myosin light chain was the result of a specific increase in expression of its smooth muscle isoform [control = 65.2 +/- 3.4% vs. 1,25(OH)2D3 = 78.7 +/- 3.6%, P = 0.020]. 1,25(OH)2D3 had no effect on total myosin light chain or heavy chain in the superior mesenteric artery. The hormone did, however, increase the proportion of the smooth muscle isoform of the light chain in this vessel [control = 81.4 +/- 2.6% vs. 1,25(OH)2D3 = 88.8 +/- 2.1%, P = 0.048]. In branch II and III mesenteric resistance arteries, 1,25(OH)2D3 significantly increased the active stress response to 10 mumol/l norepinephrine but was without effect on total myosin light chain or heavy chain content or on the relative expression of the myosin light chain isoforms [control = 94.0 +/- 1.4% vs. 1,25(OH)2D3 = 95.8 +/- 1.1%, P = 0.33].(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Functional PET scanning in the preoperative assessment of cerebral arteriovenous malformations.

We have evaluated positron emission tomography (PET) scanning during sensory stimulation or during the performance of auditory, visually based or expressive language tasks (activation PET scanning) to determine its reliability in establishing the relationships of cerebral arteriovenous malformations (AVMs) to the ambient cortex in 10 patients. Five patients with a central AVM underwent activation PET scanning combined with three-dimensional MRI during vibrotactile stimulation of the contralateral hand, and 5 patients with AVMs in or around speech areas were similarly scanned during a language task. Vibrotactile stimulation identified the post-central gyrus, establishing the relationship of the AVM to the central region. The results of language activation were specific to the modality (visual, auditory, articulate) on which the task was based. Sensory PET activation scanning is reliable in identifying the pre- and post-central gyri and useful in assessing AVMs in and around the central region. A greater understanding of results in normal controls for specific visual, auditory, and expressive language tasks is necessary before language activation PET scanning can be confidently applied to clinical cases.

Brain↗
PubMed1995

The floppy infant: a new manifestation of nonaccidental injury.

A 9-week-old infant who sustained a nonaccidental cervical spine fracture with spinal cord injury is reported. Such an injury has not been previously reported in such a young child. The clinical features raised initial difficulties in diagnosis, and management was hampered by the lack of recorded experience of such an injury in such a young infant. Conservative management was employed and the infant has made a partial recovery. The distinctive features of spinal injury in young children are discussed.

Battered Child Syndrome↗
PubMed1995

Alcohol intake modulates the effect of a polymorphism of the cholesteryl ester transfer protein gene on plasma high density lipoprotein and the risk of myocardial infarction.

A polymorphism of the CETP gene (CETP/TaqIB) with two alleles B1 (60%) and B2 (40%) has been investigated in relation to lipid variables and the risk of myocardial infarction in a large case-control study (ECTIM) of men aged 25-64. No association was observed between the polymorphism and LDL or VLDL related lipid variables. Conversely, B2 carriers had reduced levels of plasma CETP (P < 0.0001) and increased levels of HDL cholesterol (P < 0.0001) and of other HDL related lipid variables. The effects of the polymorphism on plasma CETP and HDL cholesterol were independent, suggesting the presence of at least two functional variants linked to B2. A search for these variants on the coding sequence of the CETP gene failed to identify them. The effect of B2 on plasma HDL cholesterol was absent in subjects drinking < 25 grams/d of alcohol but increased commensurably, with higher values of alcohol consumption (interaction: P < 0.0001). A similar interaction was not observed for plasma CETP. The odds-ratio for myocardial infarction of B2 homozygotes decreased from 1.0 in nondrinkers to 0.34 in those drinking 75 grams/d or more. These results provide the first demonstration of a gene-environment interaction affecting HDL cholesterol levels and coronary heart disease risk.

Adult↗
PubMed1995

Functional neuroanatomy of CCK4-induced anxiety in normal healthy volunteers.

OBJECTIVE: The authors tested the prediction of temporal cortex activation during experimentally induced anxiety by using positron emission tomography and the [15O]H2O bolus-subtraction method to determine regional cerebral blood flow (CBF) changes in normal volunteers challenged with a bolus injection of cholecystokinin tetrapeptide (CCK4). METHOD: Eight right-handed healthy subjects (five male, three female; mean age, 26.4 years) underwent four 60-second [15O]H2O scans separated by 15-minute intervals; each scan followed an intravenous bolus injection of either saline (placebo) or CCK4 (50 micrograms). Each subject received CCK4 once, as the first or second bolus, in a random-order, placebo-controlled, double-blind fashion. Two of the three placebo conditions were nominally identical, and the remaining placebo was used to control for anticipatory anxiety. Magnetic resonance imaging scans were obtained for subsequent anatomical correlation of blood flow changes. RESULTS: CCK4, but not placebo, elicited a marked anxiogenic response, reflected by robust increases in subjective anxiety ratings and heart rate. CCK4-induced anxiety was associated with 1) robust and bilateral increases in extracerebral blood flow in the vicinity of the superficial temporal artery territory and 2) CBF increases in the anterior cingulate gyrus, the claustrum-insular-amygdala region, and the cerebellar vermis. CONCLUSIONS: Some of the temporopolar cortex CBF activation peaks previously reported in humans in association with drug- and non-drug-induced anxiety, as well as the increase in regional CBF in the claustrum-insular-amygdala region, may be of vascular and/or muscular origin.

Adult↗
PubMed1995

The Countess of Aberdeen's health promotion caravans.

Lady Aberdeen took up the leadership of the Women's National Health Association of Ireland on its foundation in 1907. The Association's main objective was to combat tuberculosis, which was a considerable health problem in Ireland at the beginning of the century. Exhibitions on tuberculosis prevention were organised and a horse-drawn caravan equipped with health education material was dispatched to the more remote parts of the island in 1908. It carried the Crusade to the north-west of Ireland until the caravan was unfortunately burnt in Co. Donegal in March 1909. Although there are ample reasons for suspecting that the fire might have been malicious, all the evidence points to an accidental cause. A local photographer took photographs of the caravan on fire. Its replacement, Phoenix, went on the road shortly afterwards, followed two years later by Blue Bird.

Health Education↗
PubMed1995

Genetic variation at the angiotensinogen locus in relation to high blood pressure and myocardial infarction: the ECTIM Study.

OBJECTIVES: To study the association between polymorphisms of the angiotensinogen (AGT) gene and blood pressure in population-based samples, and to determine whether genetic variation at the AGT locus is involved in the susceptibility to myocardial infarction. METHODS: The study population comprised 630 cases who survived a myocardial infarction, recruited from the World Health Organization Monitoring Cardiovascular Diseases registers in Belfast, Lille, Strasbourg and Toulouse, and 741 controls drawn from the corresponding populations. The AGT polymorphisms investigated were T174M and M235T. High blood pressure was defined as diastolic blood pressure > 100 mmHg or the use of antihypertensive medication, or both. RESULTS: In the controls the mean +/- SEM frequency of the M174 allele was 0.116 +/- 0.008, and that of the T235 allele was 0.401 +/- 0.013. In the whole population blood pressure levels and prevalence of high blood pressure did not vary according to T174M and M235T genotypes. However, obesity appeared as a crucial factor influencing the relationship between high blood pressure and T174M. In subjects with body mass index < 26 kg/m2 there was a 2.4-fold increase of the prevalence of high blood pressure in carriers of the M174 allele compared with in homozygotes for the T174 allele, whereas no association was detected in subjects with body mass index > 26 kg/m2. The association between high blood pressure and M235T was not significant in either group. The T174M and M235T genotype distributions did not differ between survivors of myocardial infarction and controls. CONCLUSIONS: These data suggest that the AGT gene could be involved in the predisposition to high blood pressure in non-overweight, but not in overweight men, possibly reflecting genetically different types of hypertension. No significant impact of the AGT locus in the risk of non-fatal myocardial infarction was detected.

Adult↗
PubMed1995

Oxygen saturation and hemodynamic response in critically ill, mechanically ventilated adults during intrahospital transport.

BACKGROUND: Despite the frequency of intrahospital transport of critically ill patients, little research has been done on this topic and the findings are contradictory. OBJECTIVES: To describe arterial oxygen saturation by pulse oximetry, heart rate, heart rhythm, and systolic blood pressure and equipment problems in critically ill, mechanically ventilated adults during intrahospital transport. METHODS: The sample consisted of 36 critically ill, mechanically ventilated adults who required transport out of the intensive care unit for diagnostic testing or procedures within the hospital. Arterial oxygen saturation, heart rate, heart rhythm, and systolic blood pressure were measured at baseline, at least every 5 minutes during transport to and from the test site and at the test site, and every 5 minutes for 15 minutes after return to the unit. Descriptive statistics were used to analyze the data. RESULTS: Nineteen patients (53%) had clinically important changes in arterial oxygen saturation, heart rate, and/or systolic blood pressure. New cardiac arrhythmias developed in two patients. The clinically important changes occurred most frequently at the test/procedure site. Equipment problems such as monitor power failure and ventilator disconnection occurred during transport of 4 patients (11%). Total time out of ICU averaged 62 +/- 30 (range = 26 to 166) minutes. CONCLUSIONS: Transport outside the intensive care unit places the critically ill patient at additional risk. Although transport is often unavoidable, its risks versus benefits should be carefully and collaboratively evaluated for every patient prior to making the decision for transport.

Adult↗
PubMed1995

The 4G/5G genetic polymorphism in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene is associated with differences in plasma PAI-1 activity but not with risk of myocardial infarction in the ECTIM study. Etude CasTemoins de I'nfarctus du Mycocarde.

We have investigated the interrelationships of plasma PAI-1 activity, the PAI-1 4G/5G polymorphism and risk of myocardial infarction (MI) in the ECTIM study, a case-control study of MI based in Belfast, Lille, Strasbourg and Toulouse. Mean PAI-1 levels in cases were similar across all centres but in controls, levels in the French centres were significantly higher. Only in Belfast were PAIl1 levels higher in cases (11.7 AU/ml) than controls (10.5 AU/ml). The PAI-1 4G allele frequency was similar in cases and controls (0.55 and 0.54). In all groups, 4G homozygotes had the highest mean plasma PAI-1 level (4G4G vs 5G5G; cases overall: 14.2 vs 12.1AU/ml; controls overall: 15.0 vs 12.6AU/ml), with the heterozygotes generally intermediate. The data from Belfast are consistent with the literature implicating PAI-1 level as an MI risk factor. In ECTIM, the PAI-1 4G/5G polymorphism is not a genetic risk factor for MI but is associated with PAI-1 activity. Thus homozygosity for the 4G allele may predispose to elevated PAI-1 and impaired fibrinolysis, perhaps requiring interaction with other genetic or environmental factors to influence MI risk.

Adult↗
PubMed1995

Lipoprotein lipase gene polymorphisms: associations with myocardial infarction and lipoprotein levels, the ECTIM study. Etude Cas Témoin sur l'Infarctus du Myocarde.

Several lipoprotein lipase (LPL) gene polymorphisms have been found associated with fasting lipid levels, but their impact on coronary heart disease (CHD) is less clearly established. We investigated associations of LPL polymorphisms (HindIII, PvuII, Ser447-->Ter) and the newly described mutation Asn291-->Ser with the risk of myocardial infarction (MI), severity of atherosclerosis, and fasting plasma lipoprotein concentrations in the ECTIM study (614 patients and 733 controls). The Ter447 allele had a lowering effect on triglycerides (P < 0.01), VLDL-cholesterol (P < 0.05), apoC-III (P < 0.001), LpE:B (P < 0.01), and LpCIII:B (P < 0.05), and a raising effect on apoA-I levels (P < 0.05). The H- allele of the HindIII polymorphism was associated with lower apoC-III (P < 0.01) and higher HDL-cholesterol (P < 0.05) levels. The PvuII and Asn291-->Ser polymorphisms did not exhibit any significant association with the biochemical traits examined. The HindIII genotype distributions differed between cases and controls, the odds ratios for MI associated with H+H+ and H+H- genotypes being 2.05 (P < 0.01) and 1.74 (P < 0.05) by reference to H-H-. The lack of association between Ser447-->Ter and MI suggested that this mutation was unlikely to be the cause of the association found with HindIII. In some cases, the severity of atherosclerosis assessed by coronarography increased with the presence of P+ allele (coronary scores: 1.41, 1.57, and 1.64 in P-P-, P-P+, and P+P+ individuals respectively, P < 0.05). A similar trend on the coronary score was observed with the presence of the Asn291-->Ser mutation (1.58 vs. 1.90, P = 0.06). Our results suggest that the LPL gene is involved in the determination of lipoprotein profiles, the predisposition to CHD, and the severity of atherosclerosis.

Adult↗
PubMed1994

Synergistic effects of angiotensin-converting enzyme and angiotensin-II type 1 receptor gene polymorphisms on risk of myocardial infarction.

We reported from our previous multicentre case-control study that the deletion (D) polymorphism of the gene encoding angiotensin-converting enzyme (ACE) was associated with increased risk of myocardial infarction. The main function of ACE is to convert angiotensin I into angiotensin II, which exerts its known cellular actions through the angiotensin II AT1 receptor subtype (AGT1R). We have now investigated the role of a common polymorphism of the AT1 receptor gene (an A-->C transversion at position 1166 of AGT1R) and looked for an interaction between ACE and AGT1R gene polymorphisms on the risk of myocardial infarction. We analysed DNA from 613 patients with myocardial infarction and 723 age-matched population controls. We found a significant interaction between ACE and AGT1R gene polymorphisms; the odds ratio for myocardial infarction associated with the ACE DD genotype was 1.05 (95% CI 0.75-1.49) for subjects without the AGT1R C allele, 1.52 (1.06-2.18) in AC heterozygotes, and 3.95 (1.26-12.4) in CC homozygotes (test for trend, p < 0.02). Among patients defined as low risk by traditional risk factors (serum apolipoprotein B < 1.25 g/L, body-mass index < 26 kg/m2) the interaction was even stronger (odds ratios 1.64 [0.68-3.92], 7.03 [2.61-19.0], and 13.3 [p = 0.05], respectively). These findings, if confirmed, could have clinical implications for the prevention and treatment of coronary heart disease.

Adult↗