Publications
214 results found
Chambers JC, Obeid O, McGregor A, et al., 1998, Physiological elevation in homocysteine after a protein meal is associated with impaired vascular endothelial function and san be prevented by the anti-oxidant, vitamin-C., CIRCULATION, Vol: 98, Pages: 848-848, ISSN: 0009-7322
Hermansen F, Ashburner J, Spinks TJ, et al., 1998, Generation of myocardial factor images directly from the dynamic oxygen-15-water scan without use of an oxygen-15 carbon monoxide blood-pool scan, JOURNAL OF NUCLEAR MEDICINE, Vol: 39, Pages: 1696-1702, ISSN: 0161-5505
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- Citations: 70
Hermansen F, Rosen SD, Fath-Ordoubadi F, et al., 1998, Measurement of myocardial blood flow with oxygen-15 labelled water: comparison of different administration protocols, EUROPEAN JOURNAL OF NUCLEAR MEDICINE, Vol: 25, Pages: 751-759, ISSN: 0340-6997
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- Citations: 93
Kooner JS, Baliga RR, Wilding J, et al., 1998, Abdominal obesity, impaired nonesterified fatty acid suppression, and insulin-mediated glucose disposal are early metabolic abnormalities in families with premature myocardial infarction, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 18, Pages: 1021-1026, ISSN: 1079-5642
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- Citations: 53
Michie CA, Chambers J, Abramsky L, et al., 1998, Folate deficiency, neural tube defects, and cardiac disease in UK Indians and Pakistanis, LANCET, Vol: 351, Pages: 1105-1105, ISSN: 0140-6736
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- Citations: 14
Baliga RR, Rosen SD, Camici PG, et al., 1998, Regional myocardial blood flow redistribution as a cause of postprandial angina pectoris, CIRCULATION, Vol: 97, Pages: 1144-1149, ISSN: 0009-7322
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- Citations: 24
Forouhi NG, Mullick S, McKeigue PM, et al., 1998, Sex differences in postprandial lipids are explained by abdominal fat but not insulin resistance or percent body fat, CIRCULATION, Vol: 97, Pages: 819-819, ISSN: 0009-7322
Chambers JC, McGregor A, Jean-Marie J, et al., 1998, Acute hyperhomocysteinaemia and endothelial dysfunction, LANCET, Vol: 351, Pages: 36-37, ISSN: 0140-6736
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- Citations: 188
Kooner JS, 1997, Coronary heart disease in UK Indian Asians: The potential for reducing mortality, HEART, Vol: 78, Pages: 530-532, ISSN: 1355-6037
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- Citations: 15
Kooner JS, May CN, Peart S, et al., 1997, Separation of peripheral and central cardiovascular actions of angiotensin II, AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, Vol: 273, Pages: H2620-H2626, ISSN: 0363-6135
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- Citations: 9
Kooner JS, Chambers JC, McGregor A, et al., 1997, Endothelial dysfunction in patients with Behcet's syndrome., CIRCULATION, Vol: 96, Pages: 514-514, ISSN: 0009-7322
Chambers JC, McGregor A, JeanMarie J, et al., 1997, Racial differences in endothelial function may contribute to higher coronary heart disease mortality in UK Indian Asians compared to European whites, CIRCULATION, Vol: 96, Pages: 3306-3306, ISSN: 0009-7322
Baliga R, Rampling MW, Kooner JS, 1997, High fat meal induces changes in blood rheology in patients with coronary artery disease, CIRCULATION, Vol: 96, Pages: 2206-2206, ISSN: 0009-7322
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- Citations: 1
Narang R, Ridout D, Nonis C, et al., 1997, Serum calcium, phosphorus and albumin levels in relation to the angiographic severity of coronary artery disease, INTERNATIONAL JOURNAL OF CARDIOLOGY, Vol: 60, Pages: 73-79, ISSN: 0167-5273
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- Citations: 66
Baliga RR, Burden L, Sidhu MK, et al., 1997, Effects of components of meals (carbohydrate, fat, protein) in causing postprandial exertional angina pectoris., Am J Cardiol, Vol: 79, Pages: 1397-1400, ISSN: 0002-9149
We have shown that unlike fat, protein, xylose, or water, the carbohydrate component of the meal accelerates myocardial ischemia, reduces exercise capacity, and is associated with a more rapid increase in the determinants of myocardial oxygen consumption than exercise in the fasting state. Our results suggest a role for a larger increase in sympathetic nervous activity and/or release of vasoactive gastrointestinal peptides after carbohydrate, but not fat or protein, meals in postprandial angina.
Baliga RR, Burden L, Sidhu MK, et al., 1997, Effects of components of meals (carbohydrate, fat, protein) in causing postprandial exertional angina pectoris, AMERICAN JOURNAL OF CARDIOLOGY, Vol: 79, Pages: 1397-&, ISSN: 0002-9149
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- Citations: 23
Kooner JS, 1996, Ethnic differences in cardiovascular disease: Focus on Asians, Cardiovascular Forum, Publisher: MARK ALLEN PUBLISHING LTD, Pages: 544-544, ISSN: 0007-1064
Paternostro G, Camici PG, Lammerstma AA, et al., 1996, Cardiac and skeletal muscle insulin resistance in patients with coronary heart disease - A study with positron emission tomography, JOURNAL OF CLINICAL INVESTIGATION, Vol: 98, Pages: 2094-2099, ISSN: 0021-9738
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- Citations: 134
Baliga RR, Burden L, Kooner JS, 1996, Octreotide prevents post-prandial angina pectoris and improves exercise capacity after food ingestion., CIRCULATION, Vol: 94, Pages: 4268-4268, ISSN: 0009-7322
Baliga R, Lammertsma A, Rhodes C, et al., 1996, Positron emission tomography localises insulin resistance to skeletal muscle in premature coronary heart disease., HEART, Vol: 75, Pages: 48-48, ISSN: 1355-6037
KOONER JS, BALIGA RR, WILDING J, et al., 1995, METABOLIC PHENOTYPES FOR GENETIC-ANALYSIS IN CORONARY HEART-DISEASE, CIRCULATION, Vol: 92, Pages: 76-76, ISSN: 0009-7322
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- Citations: 1
BALIGA R, LAMMERTSMA A, RHODES C, et al., 1995, POSITRON EMISSION TOMOGRAPHY LOCALIZES INSULIN-RESISTANCE TO SKELETAL-MUSCLE IN PREMATURE CORONARY HEART-DISEASE, CIRCULATION, Vol: 92, Pages: 77-77, ISSN: 0009-7322
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- Citations: 3
KOONER JS, MAY CN, PEART S, et al., 1994, DISPARATE VASCULAR AND PRESSOR-RESPONSES TO ANGIOTENSIN-II AFTER SYMPATHETIC BLOCKADE IN CONSCIOUS RABBITS - SEPARATION OF PERIPHERAL AND CENTRAL ACTIONS OF ANGIOTENSIN-II, CIRCULATION, Vol: 90, Pages: 456-456, ISSN: 0009-7322
BALIGA RR, ROSEN SD, CAMICI PG, et al., 1994, REGIONAL MYOCARDIAL BLOOD-FLOW IN RESPONSE TO FOOD INGESTION IN POSTPRANDIAL ANGINA, CIRCULATION, Vol: 90, Pages: 448-448, ISSN: 0009-7322
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- Citations: 1
KOONER JS, BALIGA RR, BIRCH R, et al., 1994, ANGIOTENSIN-II INDUCES DIFFERENTIAL CHANGES IN THE INNERVATED AND DENERVATED LIMBS OF PATIENTS WITH UNILATERAL BRACHIAL-PLEXUS INJURY, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Pages: A479-A479, ISSN: 0735-1097
KOONER JS, BALIGA RR, PEART WS, et al., 1994, HYPOTENSION INDUCED BY CAPTOPRIL IN PATIENTS WITH PRIMARY AUTONOMIC FAILURE OCCURS INDEPENDENTLY OF PLASMA-RENIN LEVELS AND SYMPATHETIC NERVOUS ACTIVITY, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Pages: A376-A376, ISSN: 0735-1097
Kooner JS, Peart WS, Mathias CJ, 1991, The sympathetic nervous system in hypertension due to unilateral renal artery stenosis in man., Clin Auton Res, Vol: 1, Pages: 195-204, ISSN: 0959-9851
The contribution of neurogenic mechanisms in maintaining hypertension was investigated in 13 patients with unilateral renal artery stenosis (twelve with normal, one with grossly elevated plasma renin levels) by determining the haemodynamic and hormonal responses to the centrally acting sympatholytic agent, clonidine. The same patients were studied after captopril to determine the dependency of their blood pressure on the direct peripheral effects of angiotensin-II. Sixteen patients with essential hypertension (normal plasma renin) were additionally studied after clonidine. After clonidine, blood pressure fell markedly in patients with renal artery stenosis (17 +/- 3%) and essential hypertension (18 +/- 2%). In both groups, clonidine lowered cardiac output by a reduction in stroke volume and heart rate; forearm vascular resistance was unchanged but digital skin vascular resistance fell. Plasma noradrenaline levels were normal in both groups and fell after clonidine; plasma renin activity and aldosterone levels were unchanged. After captopril, blood pressure fell minimally (5 +/- 3%) in renal artery stenosis patients; cardiac output fell and forearm and digital skin vascular resistance were unchanged. Plasma renin activity rose, plasma aldosterone fell and plasma noradrenaline was unchanged after captopril. In the patient with grossly elevated renin levels, blood pressure fell minimally (6%) after clonidine, but unlike others fell profoundly (37%) after captopril. We conclude that, in the majority of our renal artery stenosis patients, despite the elevated blood pressure, sympathetic nervous activity was not reduced. Central neurogenic mechanisms appear to play an important role in maintaining raised blood pressure. In the same patients the peripheral effects of angiotensin-II did not maintain vascular tone or hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
KOONER JS, BIRCH R, FRANKEL HL, et al., 1991, HEMODYNAMIC AND NEUROHORMONAL EFFECTS OF CLONIDINE IN PATIENTS WITH PREGANGLIONIC AND POSTGANGLIONIC SYMPATHETIC LESIONS - EVIDENCE FOR A CENTRAL SYMPATHOLYTIC ACTION, CIRCULATION, Vol: 84, Pages: 75-83, ISSN: 0009-7322
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- Citations: 45
KOONER JS, FEW JD, LEE CY, et al., 1991, INVESTIGATION OF THE SALIVARY 18-HYDROXYCORTICOSTERONE - ALDOSTERONE RATIO IN MAN USING A DIRECT ASSAY, JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY, Vol: 38, Pages: 377-382, ISSN: 0960-0760
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- Citations: 4
KOONER JS, PEART WS, BANNISTER R, et al., 1990, HYPOTENSION AFTER CAPTOPRIL OCCURS INDEPENDENTLY OF PLASMA-RENIN ACTIVITY AND SYMPATHETIC NERVOUS ACTIVITY IN PATIENTS WITH PRIMARY AUTONOMIC FAILURE, BRITISH HEART JOURNAL, Vol: 64, Pages: 55-55, ISSN: 0007-0769
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