Origins and characteristics of pathogenic variants of feline leukaemia virus.
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Biomedical subjects
Publications and source records attributed to M Rigby.
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Recent physiologic studies have indirectly suggested that interstitial pulmonary edema may develop at maximal exercise in normal humans at sea level. Therefore, we compared chest radiographs taken before and immediately after incremental exercise to maximum in 5 healthy young subjects. We looked for evidence of redistribution of pulmonary blood flow, pulmonary venous distension, loss of sharp definition of pulmonary vascular markings, hilar blurring, Kerley's A, B, or C lines, peribronchial or perivascular cuffing, widening of fissures, pleural effusion, and diffuse opacity. We also quantitated radiographic density in 6 areas of the film in each subject. There was no radiographic change to suggest an increase in lung water in any lung zone in any of the subjects. Given the documented sensitivity of chest radiography in this respect, we conclude that any increase in extravascular lung water during exercise must be trivial.
The discovery of the first example of retroviral transduction of an immunological effector molecule has led us to reconsider the possible importance of cell surface receptors of the immune system in leukaemia development. Antigen receptors on lymphoid cells not only bind external ligands but are crucial in the control of cellular proliferation. The concept of autocrine stimulation in oncogenesis is already well established and we see no reason to exclude the possibility of analogous mechanism operating through antigen receptors. At present, we are investigating the oncogenic function of the retrovirus (FeLV-T17) carrying a T-cell receptor gene (v-tcr). In addressing the general concept of oncogenesis by ligand/receptor interactions in the immune system we face the problem of the diversity and, for T-cell antigen receptors, the complex nature of receptor-ligand interaction. Nevertheless, the implications of the model encourage us to continue to search for new experimental tools and approaches to the question.
Seven patients with double-outlet right ventricle and subpulmonary ventricular septal defect (the Taussig-Bing anomaly) underwent anatomical repair at the arterial level with transfer of the coronary arteries. At the time of operation, patient ages ranged from 6 weeks to 33 months (mean 14.1 months) and weight ranged from 3.7 to 11.5 kg (mean 7.0 kg). Four patients had prior pulmonary artery banding: Two of these four also had coarctation repairs, and one had a Blalock-Hanlon septectomy. Three different patterns of coronary artery distribution were encountered. Five patients had side-to-side great arteries, and two had more or less anteroposterior great arterial relationships. There was one operative death (14.3%: 70% confidence limits 1.9 - 40.7%) resulting from muscular subvalvular right ventricular outflow tract obstruction (RVOTO). There have been no late deaths in the six survivors followed 6 to 31 months postoperatively (mean 14.8 months). One patient required closure of a residual ventricular septal defect (VSD) and infundibular resection for RVOTO 4 months postoperatively. All other survivors are functionally NYHA Class I. Five of the six survivors have undergone postoperative catheterization (mean interval 5.8 months). There was no aortic insufficiency and good ventricular function in all patients. In addition to the patient with the residual VSD, two other asymptomatic patients had mild or moderate RVOTO. Compared with alternative surgical procedures for this anomaly, anatomic correction has the advantages of acceptable operative mortality, use of the left ventricle as the systemic ventricle, no need for extracardiac conduits, and applicability to patients with all variations of coronary artery and great artery anatomy.
Seven postmortem hearts from children who underwent anatomical correction for complete transposition (6 cases) and double outlet right ventricle (1 case) were examined in order to gain a better understanding of the pathological morphology in relation to the surgical procedure. Associated malformations were ventricular septal defect in all, patient arterial duct in 4 and aortic coarctation in 3. In all hearts the coronary arteries arose from the facing aortic sinuses and were relocated into the facing sinuses of the pulmonary trunk with minimal displacement. The orifices of the coronary arteries were reduced in caliber in one case. The sinus node artery arising from a lateral atrial artery was transected in one case. The Lecompte maneuver was performed in 4 cases and tension on the pulmonary trunk was observed in 2 cases. Potential right ventricular outflow tract obstruction was evident in all (including one in which it had been resected during surgery). The substrates of obstruction were anomalous parietal insertion of the outlet septum (2 cases), anomalous muscular trabeculation (1 case), rightward displacement of the outlet septum (1 case), parietal insertion of the outlet septum (1 case) and restrictive muscular infundibulum (1 case--DORV). In addition, all the complete transposition cases had hypertrophy of the parietal right ventricular wall. This study highlighted the anatomical features which could lead to poor results in the anatomical correction procedure. Some of the potential problems could be avoided by minor modifications to the technique.
The effects on the composition of rat submandibular saliva, of superimposing low frequency sympathetic nerve stimulation on parasympathetic nerve stimulation have been investigated. During continuous parasympathetic stimulation, additional sympathetic stimulation resulted in a frequency-dependent rise of both protein and K+ concentrations. The threshold of frequency of stimulation for the protein response was 0.1 Hz and for the K+ response 0.4 Hz. The protein secretion is presumed to be acinar in origin whilst the K+ is believed to be secreted mainly by ducts other than the main excretory duct.
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Fluid was introduced into the pleural space in upright anesthetized, ventilated and/or spontaneously breathing dogs, and its distribution was studied radiographically and confirmed on frozen slices. Various lobes were collapsed to determine the resulting effect on fluid distribution and thereby gain an understanding of so-called "atypical" effusions in a clinical setting. It was found that fluid collects in the dependent portion of the thorax and its distribution is affected by deformation of the chest wall and lung. Airway obstruction causes lobar collapse, which creates negative local pressures secondary to distortion of the lung and chest wall. The effusion moves to the area of distortion to diminish these presures. To the extent that these mechanisms operate in man, it appears that pleural effusions remain subpulmonary until atelecasis of the adjacent lung or distortion of the chest wall causes fluid redistribution.
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1. The effector and catalytic proteins of glucocerebrosidase associated in the presence of acidic phospholipid to give active enzyme. 2. At optimum concentrations of acidic phospholipid (about 0.15 mM), the association reached equilibrium instantaneously. 3. From the experimental data, a tentative model of the association was deduced. This involved a two-step complex formation. When the effector concentration was limiting, a simple binary complex was formed between one molecule each of effector and catalytic proteins; the reaction proceeded rapidly to completion. When the effector was in excess, a ternary complex was formed by the addition of another molecule of effector; this reaction did not go to completion and was characterised by a finite equilibrium constant. 4. The experimental data were curve fitted to an equation derived from the model
We evaluated 54 patients with pulmonary atresia and ventricular septal defect who were referred during the first year of life between 1972 and 1992. Particular emphasis was given to the nature of the pulmonary blood supply and its influence on outcome. Ductal supply of confluent pulmonary arteries was present in 30 patients (55.6%, group I), whereas 24 patients (44.4%, group II) had a pulmonary blood supply that was entirely (31.4%) or predominantly (13.0%) dependent on systemic collateral arteries. Over the 20 years there was no significant difference in actuarial survival between the two groups. Corrective surgery was performed in 8 of 30 patients in group I (26.7%)-significantly more than in group II (4 of 24, 16.7%). Arborization abnormalities of the pulmonary arteries (stenosis of unbranched and intrapulmonary arteries) were almost exclusively present in patients with systemic collateral arteries (p < 0.03), accounting for the lower probability of undergoing corrective surgery in group II patients. During the first decade of this study (1973-1983) corrective surgery was attempted in 9.6% of patients, with 42% mortality; and during the second decade (1983-1993) surgery was performed in 39.1% of patients, with 26% mortality, a significantly lower figure. Improving surgical results, complete preoperative demarcation of the pulmonary blood supply, and a more aggressive approach with early unifocalization of the pulmonary blood supply may invalidate comparison with retrospective data on the advisability of attempting to correct this anomaly. The present paper provides data against which treatment of infants with pulmonary atresia and ventricular septal defect presenting during the next decade can be compared.
A 3-week-old baby presented with recurrent supraventricular tachycardias unresponsive to medical treatment. Several DC shocks were required to terminate tachycardia. An abbreviated electrophysiological study was undertaken to determine the cause of the tachycardia. Rapid ventricular burst pacing successfully terminated repeated attacks of tachycardia until successful therapy with amiodarone was established. This patient demonstrates the value of pacemaker treatment of a resistant atrioventricular tachycardia in a neonate.
A case of mitral stenosis following mitral valve replacement in a patient with endocardial fibroelastosis is reported. A 14-year-old boy presented with cardiac failure. He had been diagnosed as having endocardial fibroelastosis at the age of 7 months and had undergone resection of endocardial fibrous tissue in the left ventricle at that time. Five years later his mitral valve was resected owing to mitral stenosis, with Bjork-Shiley valve replacement. Cross-sectional echocardiography on this admission showed restrictive left ventricular inflow due to a thickened immobile prosthetic valve with severely dyskinetic left ventricle (ejection fraction 8%). The electrocardiogram showed atrioventricular reentry tachycardia. Despite direct current cardioversion and continual amiodarone infusion he suffered a cardiac arrest and died 12 days after admission. Postmortem examination showed left ventricular endocardial fibroelastosis with severe inflow obstruction due to the formation of a complete fibrous ring of pannus/fibrosis around the prosthetic margin on the ventricular aspect of the left ventricle. This complication has not previously been described in children after mitral valve replacement.
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