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J Symes

Publications and source records attributed to J Symes.

At least 19 recordsLinked to original sources
PubMed1998

Photoperiod-induced phase-shifts of the endogenous clock controlling reproduction in the rainbow trout: a circannual phase-response curve.

Different groups of winter-spawning female rainbow trout that had been maintained under seasonally changing daylength and temperature were exposed to 2 months of continuous light at different times of the year. The same photoperiod produced advances in the time of spawning of up to 232 days and delays of up to 80 days, depending upon the timing of exposure in relation to the phase of the reproductive cycle. The proportion of fish spawning in each group varied from 18% to 100%, again dependent on the timing of exposure to continuous light. The photoperiod-induced changes in spawning time can be interpreted as phase-dependent phase-shifts of an endogenous circannual clock controlling maturation. It is proposed that long days, occurring earlier or later than they would under a natural photoperiod, were perceived as indications that the clock was running slow or fast, thus initiating corrective forward adjustments (advance phase-shifts) or backward adjustments (delay phase-shifts), respectively. Collectively, these responses can be described in the form of a circannual phase-response curve.

Animals↗
PubMed1997

Temperature during cardiopulmonary bypass for coronary artery operations does not influence postoperative cognitive function: a prospective, randomized trial.

OBJECTIVE: The objective was to examine the effect of temperature (28 degrees vs 36 degrees C) during cardiopulmonary bypass on postoperative cognitive functions in a prospective, double-blind, and randomized manner. METHODS: Sixty-two patients scheduled for coronary operations were randomized to warm or cold cardiopulmonary bypass. Preoperative and postoperative (7 days) neuropsychologic evaluations were performed by an observer unaware of cardiopulmonary bypass temperature. RESULTS: Fifty-four patients completed the study (cold bypass, n = 24; warm bypass, n = 30). Significant (p < 0.01) postoperative deterioration for tests of psychomotor coordination and verbal memory was noted in both warm and cold groups, but no differences were observed between groups. CONCLUSION: Temperature during cardiopulmonary bypass for coronary operations does not influence postoperative cognitive function.

Adult↗
PubMed1997

Vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) in normal and atherosclerotic human arteries.

Vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) is an endothelial-cell-specific mitogen; as such, its role in angiogenesis has been studied extensively. VEGF/VPF may also serve as a local, endogenous regulator of large-vessel endothelial cell integrity. Surprisingly, however, VEGF/VPF expression in normal and/or atherosclerotic vessels has not been previously characterized. Accordingly, we studied normal human arteries and veins as well as atherosclerotic and restenotic human coronary arteries for evidence of VEGF/VPF expression. VEGF/VPF was detected immunohistochemically in sections of normal human aorta, mammary artery, and saphenous vein. Moreover, VEGF/ VPF expression was identified in 32 (97%) of 33 pathological coronary arterial specimens; the extent of VEGF/VPF staining was graded as moderate to strong in 21 of the 32 (66%) positive specimens. VEGF/VPF double immunostaining and in situ hybridization demonstrated that smooth muscle cells constitute the principal cellular source of VEGF/VPF. VEGF/VPF immunostaining among primary atherosclerotic lesions localized predominantly to the extracellular matrix. In restenotic specimens, VEGF/VPF immunostaining was more prominently cellular, particularly among proliferating smooth muscle cells. Although VEGF/VPF expression was observed in areas of macrophage infiltration, double immunostaining failed to localize VEGF/VPF to macrophages in these foci; instead, double immunostaining clearly identified CD45RO-positive cells as responsible for VEGF/VPF expression in such areas. No correlation could be demonstrated between VEGF/VPF immunostaining and extent of vasa vasorum. These findings thus establish that postnatal VEGF/VPF expression is a feature of normal human arteries and veins and is often extensively expressed in arteries narrowed by atherosclerotic plaque. VEGF/VPF expression in the wall and/or plaque of medium to large vessels suggests a role for VEGF/VPF other than promoting angiogenesis. This role may involve maintenance and repair of luminal endothelium.

Aorta, Thoracic↗
PubMed1997

Breast cancer audit--the Isle of Wight experience.

The United Kingdom has the unwelcome distinction of having the highest incidence of breast cancer in the world (World Health Organisation Statistics Annual 1985). Publication of the Forrest Report in 1986 (Forrest, 1986) stimulated the introduction of the Breast Screening Programme in 1988.

Breast Neoplasms↗
PubMed1997

Practice charters: a survey in south and west Devon.

A postal survey was conducted in 1995 in South and West Devon to explore the perceived value of practice charters; 79 (77%) of the practices surveyed had a charter and 24 (23%) did not. Three-quarters of responding practices with a charter felt that its effects were neither positive nor negative. Fears about charters raising patients' expectations and increasing the number of complaints appear to have been unfounded, but at least 14 of the practices were still not intending to produce their own charter.

England↗
PubMed1996

Arterial gene transfer for therapeutic angiogenesis in patients with peripheral artery disease.

The age-adjusted prevalence of peripheral arterial disease (PAD) in the U.S. population has been estimated to approach 12%. The clinical consequences of occlusive peripheral arterial disease (PAD) include pain on walking (claudication), pain at rest, and loss of tissue integrity in the distal limbs; the latter may ultimately lead to amputation of a portion of the lower extremity. Surgical bypass techniques and percutaneous catheter-based interventions may be used to successfully revascularize the limbs of certain patients with PAD. In many patients, however, the anatomic extent and distribution of arterial occlusion is too severe to permit relief of pain and/or healing of ischemic ulcers. No effective medical therapy is available for the treatment of such patients. The purpose of this clinical protocol is to document the safety of therapeutic angiogenesis achieved in this case by percutaneous catheter-based delivery of the gene encoding vascular endothelial growth factor (VEGF) in patients with PAD; and, as secondary objectives, investigate the bioactivity of this strategy to relieve rest pain and heal ischemic ulcers of the lower extremities. The rationale for this human protocol is based upon preclinical studies performed in a rabbit model of hindlimb ischemia. These studies are described in detail below and in the manuscripts enclosed in the Appendix to this proposal. In brief, a single intra-arterial bolus of VEGF recombinant human protein, delivered percutaneously to the ischemic limb via an intravascular catheter, resulted in angiographic, hemodynamic, physiologic, and histologic evidence of augmented collateral artery development. Subsequently, similar results were achieved using an angioplasty catheter with a hydrogel-coated balloon to deliver 400 micrograms of a plasmid containing the cDNA for VEGF to the internal iliac artery in the same animal model. Accordingly, we propose to administer arterial gene (VEGF) therapy to patients with rest pain and/or ischemic leg ulcers considered not to be candidates for conventional revascularization techniques. The dose of plasmid to be administered will be progressively escalated beginning with 500 micrograms for the first four patients, 1000 micrograms for the following six patients, 2000 micrograms for the third group of six patients, and 400 micrograms for the fourth group of six patients.

Arteries↗
PubMed1996

Gene transfer of naked DNA encoding for three isoforms of vascular endothelial growth factor stimulates collateral development in vivo.

Vascular endothelial growth factor (VEGF) is a naturally secreted endothelial cell-specific mitogen. We investigated the hypothesis that naked DNA encoding for VEGF could be used in a strategy of arterial gene therapy to stimulate collateral artery development. Plasmid DNA encoding each of the three principal human VEGF isoforms (phVEGF121, phVEGF165, or phVEGF189) was applied to the hydrogel polymer coating of an angioplasty balloon and delivered percutaneously to one iliac artery of rabbits with operatively induced hindlimb ischemia. Compared with control animals transfected with LacZ, site-specific transfection of phVEGF resulted in augmented collateral vessel development documented by serial angiography, and improvement in calf blood pressure ratio (ischemic to normal limb), resting and maximum blood flow, and capillary to myocyte ratio. Similar results were obtained with phVEGF121, phVEGF165, and phVEGF189, which suggests that these isoforms are biologically equivalent with respect to in vivo angiogenesis. The fact that viral or other adjunctive vectors were not required further suggests that secreted gene products may have potential therapeutic utility even when the number of successfully transfected cells remains low. Arterial gene transfer of naked DNA encoding for a secreted angiogenic cytokine, thus, represents a potential alternative to recombinant protein administration for stimulating collateral vessel development.

Animals↗
PubMed1987

Brief periods of myocardial ischemia followed by reperfusion: a model in the dog of sudden cardiac death in humans.

Most experimental interest has focused on the electrophysiologic mechanisms which may underlie sudden death. The purpose of the present study was to develop a model in the dog where ischemia would produce not just ventricular fibrillation but also histologic abnormalities similar to those previously reported in sudden death in humans. First, the collateral blood flow to a portion of the ventricle was surgically abolished and then the arterial blood supply to this region was interrupted for 15 minutes after which nutrient flow was restored for 30 minutes. If the animal survived, this cycle was repeated up to seven times. Thirty-six animals were studied: 15 controls (Group A) survived an average of 1.75 +/- 0.8 cycles (mean +/- SD); 11 others (Group B) received a loading dose of sodium verapamil and survived 3.7 +/- 1.8 cycles while 10 (Group C) received a continuous infusion as well as the loading dose of sodium verapamil and survived 4.4 +/- 2.6 cycles--the difference between each group being significant (p less than 0.05). Four animals in Group C survived all 7 cycles; out of the other 32, 27 fibrillated just after reperfusion and the rest during ischemia. Histological examination revealed small foci of contraction band necrosis widely interspersed amongst large areas of morphologically normal tissue. The beneficial effect of verapamil and the histologic findings suggest cellular calcium overload may be important in the genesis of the fatal arrhythmias produced by reperfusion.

Animals↗
PubMed1980

Differentiation between reperfusion and occlusion myocardial necrosis with technetium-99m pyrophospate scans.

Although infarct-avid scanning is used to diagnose myocardial infarction, no distinction is made between two very different mechanisms of myocardial cell death. These are occlusion necrosis and reperfusion necrosis. The former is the major form of cell injury after a sustained occlusion of a coronary artery; the latter occurs immediately after reperfusion of ischemic myocardium. The present study examines whether the technetium pyrophosphate scan becomes positive more rapidly with one form of injury rather than the other. Myocardial damage was produced in dogs by either sustained coronary occlusion (Group I, 6 dogs) or reperfusion (Group II, 18 dogs). Infarct-avid myocardial scans obtained with technetium-99m pyrophosphate were positive in only one of six animals in Group I when isotope was injected 4.5 hours after sustained coronary occlusion. In contrast, 12 or 13 animals (Group IIa) with reperfusion necrosis had a positive scan when isotope was injected 3.5 hours after reperfusion. When isotope was injected only 30 minutes after the onset of reperfusion (Group IIb), only two of five scans were clearly positive. The results indicate that if the interval between myocardial injury and a positive scan is known, inference can be made concerning the predominant type of injury.

Animals↗
PubMed1980

Ventricular aneurysm: false or True? An important distinction.

A case of ventricular false aneurysm withe the typical clinical, radiological, electrocardiographic, and angiographic features of this entity is presented. The distinction between false ventricular aneurysm and true aneurysm is discussed. This distinction is important because of the propensity of false aneurysms to rupture. An early diastolic murmur was present prior to, but not after, resection of the aneurysmal sac. A theory as to the origin of this murmur is offered.

Cardiac Catheterization↗
PubMed1980

Causes of perioperative myocardial infarction: their identification and prevention.

Despite major technical advances in coronary bypass surgery and myocardial preservation, perioperative infarction remains a serious problem. The authors review the pathogenesis of the two different types of myocardial injury, occlusion necrosis and reperfusion necrosis. These two entities can be distinguished clinically by radioisotope scanning. Experimental studies have demonstrated that reperfusion necrosis can be prevented pharmacologically. Since the majority of perioperative infarcts are probably due to reperfusion, the importance of distinguishing between these two entities is evident.

Animals↗
PubMed1979

Fallibility of the epicardial electrocardiogram in quantitation of myocardial necrosis.

Estimation of infarct size utilising the epicardial electrocardiogram has been the subject of considerable controversy. The present study re-examines this technique in a dog model. It demonstrates that epicardial Q waves and S-T elevation are qualitative markers of local necrosis with different degrees of reliability; neither, however, is quantitatively related in a simple linear fashion to extent of necrosis. Conclusions from previous studies have been influenced both by different mathematical analyses of data and the inclusions of nonhomogenous sites in linear regression models.

Animals↗
PubMed1978

Significance of epicardial Q waves as an acute marker of myocardial necrosis in dogs.

This study examines the significance of epicardial Q waves as a marker of myocardial cell necrosis. Ischaemia was produced in dogs by two methods: coronary artery occlusion sustained for 24 h (Group 1) and occlusion for 1 h followed by reperfusion (Group 2). Q waves did not appear until after 3 h of sustained occlusion, but were present within 40 min of reperfusion. In both groups, Q waves were not transient but persisted for at least 24 h. CPK levels were determined at 24 h in specimens from each lead site. In Group 1, Q sites had 66.6 +/- 5.9% (mean +/- SEM) less CPK than R wave sites (P less than 0.005). In Group 2, Q sites had only 28.2 +/- 4.5% less CPK than R sites. These results suggest that the extent of necrosis was greater at Q sites with sustained occlusion than with reperfusion. A similar relationship existed for the levels of ATP and CP determined at Q and R sites at 24 h. Histological examination by light and electron microscopy confirmed that in both groups, Q sites corresponded to areas of necrosis, while R sites indicated normal myocardium. However, the type of necrosis depended on the pathogenesis. Our results demonstrated that epicardial Q waves were a reliable marker of cell death, but that the morphological picture and extent of cell death depended on the mechanism and manner of injury. These conclusions were tested in a final series (Group 3) in which propranolol was given before and with release of the occlusion (0.5 mg.kg-1 at each time). In 47 sites at risk, in five dogs only two Q waves appeared. In each of these two, cell death was confirmed by evidence of CPK depletion and morphological alteration. In the remaining sites, no CPK depletion occurred. Histological examination revealed only infrequent small islands of subendocardial necrosis. The results confirm the validity of the epicardial electrocardiographic findings and illustrate the role of propranolol in preventing reperfusion necrosis.

Animals↗