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Biomedical subjects

E A Lloyd

Publications and source records attributed to E A Lloyd.

At least 19 recordsLinked to original sources
PubMed2000

Peptides isolated from cell walls of Medicago truncatula nodules and uninfected root.

The hydroxyproline-rich root nodules of legumes provide a microaerobic niche for symbiotic nitrogen-fixing Rhizobacteria. The contributions of the cell wall and associated structural proteins, particularly the hydroxyproline-rich glycoproteins (HRGPs), are therefore of interest. Our approach involved identification of the protein components by direct chemical analysis of the insoluble wall. Chymotryptic peptide mapping showed a "P3-type" extensin containing the highly arabinosylated Ser-Hyp4-Ser-Hyp-Ser-Hyp4-Tyr3-Lys motif as a major component. Cell wall amino acid analyses and quantitative hydroxyproline arabinoside profiles, predominantly of tri- and tetraarabinosides, confirmed this extensin as the major structural protein in the cell walls of both root nodules and uninfected roots. On the other hand, judging from the Pro, Glu and non-glycosylated Hyp content, the nodule-specific proline-rich glycoproteins, such as the early nodulins (ENOD-PRPs), are present in much lesser amounts. Although we isolated no PRP peptides from nodule cell walls, a single PRP peptide from root cell walls confirmed the presence of a PRP in roots and represented the first direct evidence for a crosslinked PRP in muro. Compared with root cell walls (approximately 7% protein dry weight) nodule cell walls contained significantly more protein (approximately 13% dry weight) with an overall amino acid and peptide composition indicating the presence of structural protein unrelated to the HRGPs.

Amino Acid Sequence↗
PubMed1999

Individuality and adaptation across levels of selection: how shall we name and generalize the unit of Darwinism?

Two major clarifications have greatly abetted the understanding and fruitful expansion of the theory of natural selection in recent years: the acknowledgment that interactors, not replicators, constitute the causal unit of selection; and the recognition that interactors are Darwinian individuals, and that such individuals exist with potency at several levels of organization (genes, organisms, demes, and species in particular), thus engendering a rich hierarchical theory of selection in contrast with Darwin's own emphasis on the organismic level. But a piece of the argument has been missing, and individuals at levels distinct from organisms have been denied potency (although granted existence within the undeniable logic of the theory), because they do not achieve individuality with the same devices used by organisms and therefore seem weak by comparison. We show here that different features define Darwinian individuality across scales of size and time. In particular, species-individuals may develop few emergent features as direct adaptations. The interactor approach works with emergent fitnesses, not with emergent features; and species, as a consequence of their different mechanism for achieving individuality (reproductive exclusivity among subparts, that is, among organisms), express many effects from other levels. Organisms, by contrast, suppress upwardly cascading effects, because the organismic style of individuality (by functional integration of subparts) does not permit much competition or differential reproduction of parts from within. Species do not suppress the operation of lower levels; such effects therefore become available as exaptations conferring emergent fitness-a primary source of the different strength that species achieve as effective Darwinian individuals in evolution.

Animals↗
PubMed1993

Species selection on variability.

Most analyses of species selection require emergent, as opposed to aggregate, characters at the species level. This "emergent character" approach tends to focus on the search for adaptations at the species level. Such an approach seems to banish the most potent evolutionary property of populations--variability itself--from arguments about species selection (for variation is an aggregate character). We wish, instead, to extend the legitimate domain of species selection to aggregate characters. This extension of selection theory to the species level will concentrate, instead, on the relation between fitness and the species character, whether aggregate or emergent. Examination of the role of genetic variability in the long-term evolution of clades illustrates the cogency of broadening the definition of species selection to include aggregate characters. We reinterpret, in this light, a classic case presented in support of species selection. As originally presented, the species selection explanation of volutid neogastropod evolution was vulnerable to a counterinterpretation at the organism level. Once this case is recast within a definition of species selection that reflects the essential structure and broad applicability of hierarchical selection models, the organism-level reinterpretation of variability loses its force. We conclude that species selection on variability is a major force of macroevolution.

Journal Article↗
PubMed1988

Beta-blockade by sotalol in early myocardial infarction decreases ventricular arrhythmias without increasing left ventricular volume.

Although early beta-blockade in acute myocardial infarction (AMI) may have potential benefits owing to an anti-arrhythmic effect and limitation of infarct size, the haemodynamic effects are not well characterised. Accordingly, we studied the effects of intravenous beta-blockade by sotalol in AMI, commencing a mean of 6 hours after the onset of chest pain, with particular reference to systemic haemodynamic changes and left ventricular (LV) volumes. Thirty patients were randomised to a control group or to sotalol therapy starting with 40 mg and increasing to 120 mg, followed by the maximal dose tolerated every 6 hours for 72 hours. Sotalol reduced heart rate and mean blood pressure without elevating pulmonary wedge pressure or increasing enzymatic infarct size. Sotalol also decreased the incidence of ventricular tachycardia (P less than 0.001). An important new finding was that there was no increase in the LV volume measured by radionuclide techniques. Therefore intravenous sotalol safely achieved its beneficial effects without causing LV dilatation.

Adult↗
PubMed1985

Tiapamil--a new calcium antagonist.

Calcium antagonists are an important new modality in cardiovascular therapy. Tiapamil, a congener of verapamil, is undergoing clinical and laboratory evaluation. We have undertaken experimental studies on the anti-arrhythmic properties of tiapamil, and on the intravenous use of this agent in patients with acute myocardial infarction. Reasons are given for suggesting that tiapamil warrants further clinical evaluation, after which it may join the more established calcium antagonists as a valuable therapeutic agent.

Acute Disease↗
PubMed1985

Tiapamil, a new calcium antagonist: hemodynamic effects in patients with acute myocardial infarction.

The afterload reduction and myocardial oxygen sparing that results after administration of calcium antagonists suggests a possible role for these drugs in intervention after onset of acute myocardial infarction, but their use in this setting is limited by the possibility that left ventricular failure will develop. Tiapamil is a new verapamil congener. The hemodynamic effects of this drug (1 mg/kg followed by 25 micrograms/kg/min over 36 hr) were studied in 30 patients randomly assigned in a double-blind manner to a tiapamil or control group within 12 hr of the onset of acute myocardial infarction as diagnosed by Swan-Ganz catheterization and gated blood pool scans. Tiapamil reduced heart rate from 83 +/- 20 beats/min (mean +/- SD) before to 74 +/- 19 beats/min after drug (over an average 36 hr), arterial pressure from 128 +/- 22/87 +/- 14 to 118 +/- 16/74 +/- 11 mm Hg, rate-pressure product from 10,695 +/- 3492 to 8800 +/- 2550 units, and systemic vascular resistance from 1732 +/- 351 to 1400 +/- 350 dynes X sec X cm-5. Tiapamil also increased stroke volume index from 34.7 +/- 12.1 to 41.6 +/- 12.0 ml/m2, left ventricular ejection fraction from 50.1 +/- 14.8% to 56.4 +/- 17.4% (at 24 hr), left ventricular end-diastolic volume index from 71.3 +/- 23.1 to 80.5 +/- 23.7 ml/m2, and peak diastolic filling rate (an index of diastolic relaxation) from 2.1 +/- 0.9 to 2.6 +/- 0.8 end-diastolic volumes/sec (p less than .05 for all changes). Cardiac index, wedge pressure, left ventricular end-systolic volume, and PR interval remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1984

Hemodynamic effects of sublingual nifedipine in acute myocardial infarction.

Twenty-six patients with acute myocardial infarction (mean delay time 6 hours after onset of symptoms) were randomized to control or nifedipine treatment (10 mg sublingually, followed by 10 mg every 6 hours for a total of 24 hours). Nifedipine reduced arterial blood pressure from 127/78 to 115/70 mm Hg at 30 minutes (p less than 0.001) and continued to reduce the blood pressure significantly for 12 to 18 hours. Nifedipine also reduced systemic vascular resistance and the rate-pressure product. Cardiac output increased from 4.9 liters/min before nifedipine to 5.4 liters/min at 60 minutes (p less than 0.05 vs controls). In patients with high initial pulmonary wedge pressures, sublingual nifedipine decreased the wedge pressure (p less than 0.001) more effectively than did 80 mg of furosemide given intravenously. Thus, nifedipine may be useful in patients with early myocardial infarction and left ventricular failure.

Adrenergic beta-Antagonists↗
PubMed1984

The efficacy of quinidine and disopyramide in the maintenance of sinus rhythm after electroconversion from atrial fibrillation. A double-blind study comparing quinidine, disopyramide and placebo.

In order to compare the relative efficacy of quinidine, disopyramide and a placebo in the maintenance of sinus rhythm after cardioversion from atrial fibrillation and in order to examine the incidence of side-effects, 82 patients with continuous atrial fibrillation (duration more than 1 month but less than 3 years) were randomized in a double-blind fashion to receive quinidine, disopyramide or placebo. Six months after cardioversion there was no significant difference between any of the three groups as regards the number of patients remaining in sinus rhythm. The greater distortion of the atrial architecture which occurs in patients with rheumatic mitral valve disease may explain the failure of these anti-arrhythmic agents to prolong the duration of sinus rhythm in this study, in which patients with valvular heart disease comprised 76% of the total group.

Adolescent↗
PubMed1984

Arrhythmias in patients with drug toxicity, electrolyte, and endocrine disturbances.

The common rhythm disturbances related to electrolyte imbalance are due predominantly to abnormalities of potassium. An understanding of the mechanism underlying these abnormalities is facilitated by a brief review of normal electrical activity during impulse propagation in cardiac tissue. Also discussed are the actions of all cardioactive and antiarrhythmic drugs on membrane permeability to ions. Lastly, the nonspecific arrhythmias associated with endocrine disturbances are outlined.

Anti-Arrhythmia Agents↗
PubMed1983

Amiodarone in the treatment of patients with refractory symptomatic ventricular and supraventricular arrhythmias. A long-term follow-up study.

Fifty-two patients with refractory symptomatic supraventricular and ventricular arrhythmias were treated with amiodarone (Cordarone-X; Reckitt & Colman) and followed up for a mean period of 36,4 months (range 3-54 months). Amiodarone was effective in controlling supraventricular arrhythmias in 18 of 22 patients (82%) and ventricular arrhythmias in 18 of 30 (60%), giving an overall success rate of 72%. The incidence of sudden death in the patients with ventricular arrhythmias was significantly higher (P less than 0,01) in patients whose symptoms were not controlled by amiodarone than in those in whom control was achieved. Although side-effects occurred in 50 of the 52 patients they seldom necessitated withdrawal of the drug. This is the first report in which a substantial number of patients have been closely followed up for a mean period exceeding 22 months. The results described here demonstrate that the potent antiarrhythmic properties of amiodarone, previously observed for shorter periods of time, are maintained for up to 4 1/2 years, and that there is neither an increased incidence nor progression of side-effects in patients exposed to the drug for these longer periods of time.

Adolescent↗
PubMed1983

Syncope and ventricular tachycardia in patients with ventricular preexcitation.

Four patients with ventricular preexcitation whose syncope initially was attributed to an arrhythmia utilizing the accessory pathway are presented. At electrophysiologic study, the electrophysiologic characteristics of the accessory pathways were considered unlikely to support a tachycardia of a rate sufficient to result in syncope. Programmed stimulation of the right ventricle, however, reproducibly induced ventricular tachycardia to which the syncope was subsequently attributed in 3 patients. The importance of identifying ventricular tachycardia as the cause of syncope in these patients is emphasized.

Adult↗
PubMed1983

Calcium antagonists and the acutely ischemic heart: experimental effects on ventricular fibrillation and enzyme release.

To investigate and to compare the protective action of verapamil, nifedipine and diltiazem on the acutely infarcting myocardium, we studied effects on cellular damage and mechanical function in the isolated working rat heart preparation subjected to left main coronary artery ligation. First, the fall in the ventricular fibrillation threshold (VFT) was diminished by all three agents, but non-specific effects of these agents were operating at least in part. All three compounds afforded substantial dose-dependent reduction of lactate dehydrogenase release, which was taken as an index of cellular damage, and preserved ATP stores in the infarcting myocardium. The range of effective concentrations was small and close to doses which produced atrioventricular conduction disturbances (verapamil, diltiazem) or LV pump failure (nifedipine). It is argued that these concentrations may be therapeutically relevant, whereas the concentration of a beta-adrenoceptor antagonist agent required comparably to inhibit enzyme release was supra-therapeutic (metoprolol 10(-4) M). There are substantial differences between such animal models and the situation in acute myocardial infarction in man, where preliminary data show benefits both for beta-adrenergic blockade by sotalol and for calcium antagonism by nifedipine.

Adrenergic beta-Antagonists↗
PubMed1983

Clinical electrophysiology of ventricular tachycardia.

Programmed ventricular stimulation, electrophysiologic effects of various antiarrhythmic drugs, and the results of serial electrophysiologic testing in patients with ventricular arrhythmias are discussed. The use of discriminant analysis to predict the efficacy of antiarrhythmic drugs is also briefly analyzed.

Anti-Arrhythmia Agents↗