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Biomedical subjects

A G Turner

Publications and source records attributed to A G Turner.

At least 19 recordsLinked to original sources
PubMed2001

Incidence of Helicobacter pylori in patients with interstitial cystitis.

OBJECTIVE: Chronic gastritis has compelling similarities to interstitial cystitis (IC). It is characterised by chronic pain in a tubular organ. Histologically, epithelial damage, inflammatory response in the lamina propria and epithelial ulcerations are seen. An infective cause was rarely considered until the emergence of Helicobacter pylori over the past 15 years. We have had experience of patients with bladder pain and irritability reporting improvement with antihistamines. It has also been reported that IC symptoms improved dramatically after treatment for H. pylori infection. Previous studies have determined the incidence of H. pylori antibodies in women with IC but we examined bladder material histologically and performed the Campylobacter-like organism (CLO) test on the biopsy specimens. MATERIALS AND METHODS: A prospective controlled study was performed. Patients with urinary symptoms fulfilling the National Institute of Diabetes and Digestive and Kidney Diseases criteria for IC underwent GA cystoscopy at which the macroscopic appearance of the bladder was noted and biopsies were taken. The biopsy material underwent histological examination and CLO test. Control patients who were undergoing cystoscopy for reasons other than investigation of IC also had biopsy taken and the CLO test was performed on these specimens. RESULTS: Five of 15 patients with symptoms and signs of IC had a positive CLO test. Three of 15 patients of the control group had a positive CLO test. With the 2-sided chi(2) test there was no statistical difference between the 2 groups. CONCLUSION: Our small prospective control study does not support the hypothesis that H. pylori is an important component in the pathogenesis of interstitial cystitis.

Cystitis, Interstitial↗
PubMed2000

Paratesticular liposarcoma with smooth muscle differentiation mimicking angiomyolipoma.

AIMS: To discuss the differential diagnosis of a case of well-differentiated liposarcoma which had areas resembling angiomyolipoma-a feature which, to our knowledge, has not been reported previously. METHODS AND RESULTS: A tumour in the paratesticular region had apparently been present for 40 years, but had grown recently. A fat component containing lipoblasts was admixed with areas resembling angiomyolipoma, i.e. desmin positive, but HMB45-negative smooth muscle proliferation with atypia and thick-walled blood vessels devoid of elastin. CONCLUSION: The diagnosis of liposarcoma, rather than angiomyolipoma with adipose atypia, in this case is based on the fact that smooth muscle differentiation is documented in liposarcoma, lack of HMB45 staining and recent clonality studies which suggest that the fat in angiomyolipoma is not neoplastic.

Angiomyolipoma↗
PubMed1999

Human obesity is associated with a chronic elevation in brain 5-hydroxytryptamine turnover.

The afferent signals that evoke changes in energy intake with regard to body weight regulation are presumed to arise partly from body stores, with the most likely candidate being adipose tissue depots. However, clinical investigation of the neuronal circuitry involved in the central nervous system's processing of such satiety signals remains largely unexplored. Using percutaneously placed catheters in either the right or left internal jugular veins, we were able to quantify the release of central nervous system monoamine and indoleamine neurotransmitters in 64 weight-stable male subjects with varying degrees of adiposity. Veno-arterial plasma concentration differences and internal jugular blood or plasma flow were used, according to the Fick Principle, to quantify the amount of neurotransmitter stemming from the brain. By combining this technique with a noradrenaline and adrenaline isotope dilution method for examining neuronal transmitter release, we were able to examine the association between central nervous system neurotransmitters and efferent sympathetic nervous outflow and adrenomedullary function in human obesity. We found that brain 5-hydroxytryptamine (serotonin) turnover is chronically elevated in proportion to adiposity and is increased postprandially to a similar degree in lean and obese individuals. There was no difference in the degree of sympathetic nervous activity or rate of adrenaline secretion in the subjects examined. It therefore seems that in human obesity, in the face of a chronic elevation in peripheral satiety signals, brain serotonergic processes are switched on accordingly, but the subsequent physiological response involving a reduction in food intake, increased thermogenesis and sympathetic activity is in some way impeded.

Adult↗
PubMed1998

Sympathetic activity in patients with panic disorder at rest, under laboratory mental stress, and during panic attacks.

BACKGROUND: The sympathetic nervous system has long been believed to be involved in the pathogenesis of panic disorder, but studies to date, most using peripheral venous catecholamine measurements, have yielded conflicting and equivocal results. We tested sympathetic nervous function in patients with panic disorder by using more sensitive methods. METHODS: Sympathetic nervous and adrenal medullary function was measured by using direct nerve recording (clinical microneurography) and whole-body and cardiac catecholamine kinetics in 13 patients with panic disorder as defined by the DSM-IV, and 14 healthy control subjects. Measurements were made at rest, during laboratory stress (forced mental arithmetic), and, for 4 patients, during panic attacks occurring spontaneously in the laboratory setting. RESULTS: Muscle sympathetic activity, arterial plasma concentration of norepinephrine, and the total and cardiac norepinephrine spillover rates to plasma were similar in patients and control subjects at rest, as was whole-body epinephrine secretion. Epinephrine spillover from the heart was elevated in patients with panic disorder (P=.01). Responses to laboratory mental stress were almost identical in patient and control groups. During panic attacks, there were marked increases in epinephrine secretion and large increases in the sympathetic activity in muscle in 2 patients but smaller changes in the total norepinephrine spillover to plasma. CONCLUSIONS: Whole-body and regional sympathetic nervous activity are not elevated at rest in patients with panic disorder. Epinephrine is released from the heart at rest in patients with panic disorder, possibly due to loading of cardiac neuronal stores by uptake from plasma during surges of epinephrine secretion in panic attacks. Contrary to popular belief, the sympathetic nervous system is not globally activated during panic attacks.

Adrenal Medulla↗
PubMed1998

Internal jugular venous spillover of noradrenaline and metabolites and their association with sympathetic nervous activity.

It is recognized that the brain plays a pivotal role in the maintenance of blood pressure and the control of myocardial function. By combining direct sampling of internal jugular venous blood with a noradrenaline isotope dilution method, for examining neuronal transmitter release, and microneurographic nerve recording, we were able to quantify the release of central nervous system noradrenaline and its metabolites and investigate their association with efferent sympathetic nervous outflow in healthy subjects and patients with pure autonomic failure. To further investigate the relationship between brain noradrenaline, sympathetic nervous activity and blood pressure regulation we examined brain catecholamine turnover, based on the internal jugular venous overflow of noradrenaline and its principal central nervous system metabolites, in response to a variety of pharmacological challenges. A substantial increase was seen in brain noradrenaline turnover following trimethaphan, presumably resulting from a compensatory response in sympathoexcitatory forebrain noradrenergic neurones in the face of interruption of sympathetic neural traffic and reduction in arterial blood pressure. In contrast, reduction in central nervous system noradrenaline turnover accompanied the blood pressure fall produced by intravenous clonidine administration, thus representing the blood pressure lowering action of the drug. Following vasodilatation elicited by intravenous adrenaline infusion, brain noradrenaline turnover increased in parallel with elevation in muscle sympathetic nervous activity. While it is difficult to assess the source of the noradrenaline and metabolites determined in our studies, available evidence implicates noradrenergic cell groups of the posterolateral hypothalamus, amygdala, the A5 region and the locus coeruleus as being involved in the regulation of sympathetic outflow and autonomic cardiovascular control.

Adolescent↗
PubMed1997

Cerebral noradrenaline spillover and its relation to muscle sympathetic nervous activity in healthy human subjects.

Studies using internal jugular vein blood sampling in human subjects have demonstrated the release of noradrenaline from the brain and have provided a link between central nervous system noradrenergic neuronal activity and renal, cardiac and total body sympathetic activity. The aim of this study was to further categorise the dependence of regional sympathetic nervous function on central nervous system noradrenergic neuronal processes by combining measures of internal jugular venous noradrenaline spillover, as an indicator of brain noradrenaline release, and cerebral blood flow scans with measures of the overall integrated neuronal firing rate for the body as a whole, the spillover of noradrenaline into the coronary sinus and with measurements of resting muscle sympathetic nerve activity. Positive veno-arterial plasma noradrenaline gradients were found across the brain, with the plasma concentration being 17 +/- 3% (p < 0.01) greater in the internal jugular vein. Linear regression analysis revealed a significant relationship between the degree of muscle sympathetic nerve activity and the spillover of noradrenaline from subcortical brain regions (y = 0.1 x + 16.0; r = 0.81, p < 0.02). The rate of spillover of noradrenaline for the body as a whole also bore a significant association with the rate of subcortical noradrenaline spillover (y = 0.01x + 2.33; r = 0.71, p < 0.05). Cortical noradrenaline spillover was not related to any of the sympathetic nervous system parameters measured in this study. The demonstration of a direct relationship between the rate of peroneal nerve firing and the spillover of noradrenaline from subcortical brain regions provides further support for the concept of central nervous system noradrenergic cell groups behaving in a sympathoexcitatory role.

Adult↗
PubMed1997

Multiple striate keratotomy: a treatment for corneal erosions caused by epithelial basement membrane disease.

OBJECTIVE: To study the efficacy of multiple striate keratotomy for the treatment of persistent corneal erosions suspected to be caused by primary corneal epithelial basement membrane disease. DESIGN: A retrospective study. ANIMALS: 16 dogs, three cats and one Australian dingo. PROCEDURE: A technique called multiple striate keratotomy was used to treat twenty animals suffering from persistent corneal erosions. RESULTS: All persistent corneal erosions healed with only one treatment. Most cases healed within 2 weeks. One case developed a second erosion in the same eye but in a different position to the original erosion. CONCLUSIONS: Multiple striate keratotomy is a safe, effective and well tolerated technique for the treatment of persistent corneal erosions thought to be caused by corneal epithelial basement membrane disease.

Animals↗
PubMed1996

Oxygen consumption in the heart, hepatomesenteric bed, and brain in young and elderly human subjects, and accompanying sympathetic nervous activity.

Although the reduction in whole-body energy expenditure with aging has been well documented, there is little information about the changes that individual organs undergo. We therefore measured oxygen consumption in the heart, hepatomesenteric bed, and brain in elderly subjects and young controls, using central venous catheter techniques and the application of Fick's principle. We also measured whole-body, cardiac, and hepatomesenteric sympathetic nervous activity using isotope dilution methodology. Cardiac, hepatomesenteric, and cerebral oxygen consumption was similar in both groups. Whole-body and hepatomesenteric sympathetic nervous activity was also similar in the study groups, whereas cardiac norepinephrine (NE) spillover was significantly higher in the elderly. In contrast to the young, cardiac sympathetic nervous activity as assessed from NE spillover was not related to either cardiac oxygen consumption or cardiac work in the elderly. The data suggest that although oxygen consumption in the heart, hepatomesenteric bed, and brain are not different between young and elderly individuals, the relationship between sympathetic nervous activity and oxygen consumption in individual organs may alter with aging.

Adult↗
PubMed1996

A not quite as quick but much cleaner alternative to the Expanded Programme on Immunization (EPI) Cluster Survey design.

BACKGROUND: Although the Expanded Programme on Immunization (EPI) cluster survey methodology has been successfully used for assessing levels of immunization programme coverage in developing country settings, certain features of the methodology, as it is usually carried out, make it less-than-optimal choice for large, national surveys and/or surveys with multiple measurement objectives. What is needed is a 'middle ground' between rigorous cluster sampling methods, which are seen as unfeasible for routine use in many developing country settings, and the EPI cluster survey approach. METHODS: This article suggests some fairly straightforward modifications to the basic EPI cluster survey design that put it on a solid probability footing and render it easily adaptable to differing and/or multiple measurement objectives, without incurring prohibitive costs or adding appreciably to the complexity of survey operations. The proposed modifications concern primarily the manner in which households are chosen at the second stage of sample selection. CONCLUSIONS: Because the modified sampling strategy maintains the scientific rigor of conventional cluster sampling methods while retaining many of the desirable features of the EPI survey methodology, the methodology is likely to be a preferred 'middle ground' survey design, relevant for many applications, particularly surveys designed to monitor multiple health indicators over time. The fieldwork burden in the modified design is only marginally higher than in EPI cluster surveys, and considerably lower than in conventional cluster surveys.

Humans↗
PubMed1996

Cerebral metabolism and its relationship with sympathetic nervous activity in essential hypertension: evaluation of the Dickinson hypothesis.

OBJECTIVE: To examine Dickinson's hypothesis in mild essential hypertension, in which neurogenic mechanisms are believed to be particularly relevant, by combining measures of cerebral oxygen consumption with the concurrent assessment of sympathetic nervous activity. DESIGN AND METHODS: Twenty-five untreated essential hypertensive subjects and 28 healthy age-matched volunteers underwent direct blood sampling using percutaneously inserted catheters advanced into the internal jugular vein, with cerebral blood flow scans to differentiate between cortical and subcortical venous drainage of the brain. Venoarterial blood gas measurements and internal jugular vein blood flows were used to calculate cerebral respiratory quotients and cerebral oxygen utilization. The total body rate of noradrenaline spillover into plasma was measured to assess relationships between cerebral oxidative metabolism and sympathetic nervous activity. RESULTS: Compared with controls, the hypertensive subjects exhibited reductions in internal jugular vein blood flow (482 +/- 29 versus 410 +/- 15 ml/min), cerebral oxygen consumption (27 +/- 2 versus 23 +/- 1 ml/min) and cerebral oxygen supply (93 +/- 6 versus 78 +/- 3 ml/min). The cerebral respiratory quotients were identical (1.00 +/- 0.04 in normotensives and 0.98 +/- 0.03 in hypertensives). Technetium blood flow scans revealed that the reductions in internal jugular blood flow and cerebral oxygen consumption in the hypertensive patients were confined to cortical brain regions. Cortical blood flow was quantitatively linked to the matching respiratory quotient and oxygen consumption, neither of which bore any relation to the level of sympathetic nervous activity. The spillover of noradrenaline into the plasma for the body as a whole did not differ between the two groups. CONCLUSIONS: In accord with Dickinson's hypothesis, we have established a reduction in internal jugular vein blood flow and cerebral oxygen utilization in hypertension. These reductions were confined to cortical brain regions. However, cerebral respiratory quotients in our hypertensive study group were no different from those in our controls, suggesting that glucose remained as the major cerebral metabolic substrate in hypertension. We were not able to establish a link between cerebral metabolism and blood pressure or sympathetic nervous activity in mildly hypertensive patients.

Adult↗
PubMed1995

Fallibility of plasma noradrenaline measurements in studying postprandial sympathetic nervous responses.

The use of the plasma noradrenaline (NA) concentration as an index of sympathetic nervous system (SNS) activity in the postprandial state is associated with several problems: (i) It does not take into account the contribution of alterations in clearance to the plasma NA level, (ii) when antecubital venous blood is sampled, it reflects regional forearm rather than whole body SNS activity and (iii) no insight is gained into the regional pattern of SNS activation. These potential confounders were addressed in this study performed in 17 healthy young men. The validity of plasma NA measurements in assessing postprandial changes in sympathetic nervous activation was evaluated in relation to that of whole body and regional plasma NA spillover, derived using isotope dilution methodology. Plasma clearance of NA is significantly altered following a meal, with a transient elevation in the early postprandial phase which may lead to an underestimation of SNS activation when assessed from arterial plasma NA levels. Forearm plasma NA spillover increases postprandially, such that despite significant postprandial elevations in arterial plasma NA, the plasma arterial contribution to antecubital venous plasma NA levels is maintained at less than 40%, the rest being derived locally from the forearm. This makes venous plasma samples unsuitable for the assessment of SNS activation in organs and vascular sites distant from the sampling site. The kidneys and skeletal muscle are the major regional sites of postprandial sympathetic nervous activation, while cardiac plasma NE spillover is unaltered postprandially. This regional pattern of SNS activation postprandially must be taken into account when relating increments in plasma NA levels to specific physiological events.

Adolescent↗
PubMed1995

Regional origins of 3-methoxy-4-hydroxyphenylglycol in plasma: effects of chronic sympathetic nervous activation and denervation, and acute reflex sympathetic stimulation.

The plasma level and urinary excretion of 3-methoxy-4-hydroxyphenylglycol (MHPG), the principal metabolite of noradrenaline in the brain, are often used as indicators of central nervous system noradrenergic activity. Using percutaneously placed catheters, we studied the regional inputs into the plasma MHPG pool in 62 healthy volunteers. Veno-arterial plasma concentration differences and regional organ blood flows were used to quantify the relative amounts of MHPG contributed by various sites into plasma. Positive veno-arterial concentration gradients were found across the forearm, cardiac and jugular vessels in the healthy subjects. By far the majority of MHPG in plasma was derived from skeletal muscle, 5.3 +/- 1.8 nmol/min, with only minimal contribution (0.9 +/- 0.2 nmol/min) from the brain. Thus, to obtain an accurate indication of central nervous system noradrenergic activity the confounding influences of regional MHPG production must be excluded. 34 patients with chronic congestive heart failure, 6 patients with pure autonomic failure and 9 recent heart transplant recipients were used to investigate the possible effects of chronic sympathetic nervous system overactivity and sympathetic underactivity and denervation on peripheral MHPG production and plasma MHPG concentration. To examine the utility of plasma MHPG determinations as an indicator of acute alterations in sympathetic nervous activity we examined the influence of a variety of laboratory stressors on the arterial level and cardiac production of MHPG. The resting arterial plasma MHPG concentration mirrored sympathetic function in the patients with cardiac failure (sympathetic activation) and pure autonomic failure (sympathetic denervation), with mean MHPG plasma concentrations being 180 and 40% of those in healthy subjects. Cardiac MHPG production was increased in heart failure patients, and near zero with the cardiac sympathetic denervation accompanying transplantation and pure autonomic failure. In contrast, acute reflex stimulation of sympathetic nervous activity was not associated with parallel changes in the arterial level or cardiac production of MHPG. Measurements of peripheral plasma MHPG levels provide an index of prevailing sympathetic nervous function in clinical models of sympathetic overactivity and denervation, but are insensitive to acute sympathetic nervous system responses.

Adrenergic Uptake Inhibitors↗
PubMed1995

Increased central nervous system monoamine neurotransmitter turnover and its association with sympathetic nervous activity in treated heart failure patients.

BACKGROUND: Congestive heart failure is a debilitating disease characterized by impaired cardiac function with accompanying activation of a variety of neural and hormonal counter-regulatory systems. Abnormal activity of the sympathetic nervous system and renin-angiotensin-aldosterone axis and a predisposition to the generation of fatal ventricular arrhythmias are often associated with the development of the disease. Although the underlying cause of sudden death in these patients remains to be unequivocally elucidated, abnormally increased cardiac sympathetic nervous activity may be involved. METHODS AND RESULTS: Twenty-two patients with severe congestive heart failure (New York Heart Association functional class III or IV with left ventricular ejection fraction of 18 +/- 1%) and 29 healthy male volunteers participated in this study. By combining direct sampling of internal jugular venous blood via a percutaneously placed catheter with a norepinephrine and epinephrine isotope dilution method for examining neuronal transmitter release, we were able to quantify the release of central nervous system monoamine and indoleamine neurotransmitters and investigate their association with the increased efferent sympathetic outflow that is variably present in treated patients with this condition. Mean cardiac norepinephrine spillover was 145% higher in treated heart failure patients than in healthy subjects (P < .05), with norepinephrine release from the heart in 6 of 22 patients being more than the highest control value. Raised internal jugular venous spillover of epinephrine (26 +/- 12 versus 2 +/- 4 pmol/min, P < .05) and of norepinephrine and its metabolites (2740 +/- 480 versus 875 +/- 338 pmol/min, P < .05), indicative of increased central nervous system turnover of both catecholamines, occurred in cardiac failure and was quantitatively linked to the degree of activation of the cardiac sympathetic nervous outflow, as was the jugular overflow of the principal serotonin metabolite, 5-hydroxyindoleacetic acid. CONCLUSIONS: An association between the degree of activation of central monoaminergic neurons and the level of sympathetic nervous tone in the heart was identified in treated patients with heart failure. Epinephrine neurons in the brain may contribute to the sympathoexcitation that is seen in this condition, with the activation of sympathoexcitatory noradrenergic neurons, most likely those of the forebrain, playing an accessory role.

Angiotensin-Converting Enzyme Inhibitors↗