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Biomedical subjects

P Reed

Publications and source records attributed to P Reed.

At least 73 records · Page 4Linked to original sources
PubMed1989

Marking effects in instrumental performance on DRH schedules.

Three experiments investigated the effect of presenting a brief stimulus after a response sequence on the rate of lever-pressing by rats on differential reinforcement of high rate (DRH) schedules. In Experiment 1 enhanced responding was produced by a visual stimulus presented during a 500-msec delay of reinforcement compared to a condition in which no stimulus was presented. In Experiment 2 rats responded on a multiple DRH DRH schedule in which the DRH contingency was reinforced on a 50% schedule in each component. Equivalent levels of responding occurred in the components when reinforcement was signalled in one component and when the signal was presented following the non-reinforced schedules in the other components. A further group of rats received the stimulus presented after non-reinforced schedules in one component but not at all in the other component; responding was enhanced in the former component relative to the latter component. In Experiment 3 brief stimuli presented after the completion of DRH components on a second-order VR (DRH) schedule elevated response rates irrespective of whether the signal was presented paired or unpaired with reinforcement. The present data support the view that a brief signal may serve to mark a response sequence in memory and facilitate instrumental performance.

Animals↗
PubMed1989

Atrial septal defect and constrictive pericarditis. An unusual combination.

We describe a case of atrial septal defect associated with constrictive pericarditis. This combination is extremely rare and clinically misleading, since it may simulate other more common conditions. A variety of techniques, such as computerized tomography, echocardiography and cardiac catheterization were necessary for establishing the right diagnosis. Although there are suggestions of a possible association of atrial septal defect with pericardial disease, it is difficult to prove that this combination is other than coincidence.

Aged↗
PubMed1988

Effects of isoproterenol on Cl transport in rat submandibular salivary-gland acini.

In the absence of the beta-adrenoceptor agonist, isoproterenol, acini accumulated 36Cl in a time-dependent manner until a steady-state content of 7.4 +/- 0.2 nmol/mg protein was attained after 5 min of incubation. In the presence of 10 microM isoproterenol the tracer content increased significantly in the first few minutes (40 per cent after 2 min, 33 per cent after 5 min) but then decreased and was essentially the same as in the absence of agonist after 15 min. This effect was inhibited by 1 mM furosemide but was still observed when the cells were incubated in K-free medium. Exposure of tracer-preloaded cells with steady-state isotope content to 10 microM isoproterenol likewise caused a transient but significant increase in tracer content (32 per cent after 6 min); exposure to 1 microM acetylcholine caused a significant and sustained decrease in tracer content (30 per cent), which was not prevented by pre-incubating the cells for 5 min with isoproterenol. Similar transient increases in tracer content of preloaded cells were observed upon exposure to 10 microM concentrations of forskolin or dibutyryl cAMP. Stimulation of beta-receptors does not therefore cause a net Cl efflux in salivary acini and does not prevent the net efflux induced by stimulation of cholinergic receptors. As this efflux may be via a conductance pathway or channels in the apical membrane, these channels do not seem to be regulated by a beta-receptor-coupled, cAMP-mediated pathway in salivary cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effect of alpha-receptor stimulation on Cl transport by rat submandibular acini.

Dispersed salivary acini isolated from the rat submandibular gland by enzymatic digestion were used to study the effects of alpha-receptor stimulation on transmembrane transport of 36Cl. In the absence of secretagogue, the tracer accumulated in the cells in a time-dependent manner until a steady-state content of 6.8 +/- 0.1 nmol/mg protein was attained after 3-5 min of incubation. Epinephrine (1 mumol/L) alone did not modify 36Cl accumulation but in the presence of the beta-receptor blocker propranolol (1 mumol/L) caused a significant (21%) reduction in the isotope content of the cells to 5.2 +/- 0.1 nmol/mg protein. In acini pre-loaded with 36Cl for 12 min, 1 mumol/L epinephrine caused a rapid but transient net efflux of tracer, but the isotope content subsequently increased to pre-stimulation levels. In the presence of propranolol, however, the efflux of 36Cl induced by epinephrine was larger and more sustained and was partially inhibited by the K-channel blocker quinidine (1 mmol/L) and significantly by the absence of Ca2+ in the incubation medium. The alpha-agonist phenylephrine (10 mumol/L) also significantly reduced the steady-state 36Cl content of tracer-pre-loaded cells. By contrast, exposure of the acini to epinephrine in the presence of the alpha-receptor blocker phentolamine, or the beta-agonist isoproterenol, increased the tracer content of the cells, whether the drugs were added at time zero or to tracer-pre-loaded cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effects of magnitude of food reinforcement on free-operant response rates.

In Experiment 1 rats were trained to press a lever on a variable-ratio schedule of food presentation and were then exposed to progressively increasing magnitudes of food reinforcement. Response running rates (rates exclusive of the postreinforcement pause) were found to increase as a function of increasing reinforcement magnitudes. The effect of reinforcement magnitude on response rates inclusive of the postreinforcement pause, however, was less pronounced. Increases in the magnitude of reinforcement were also found to increase the length of the postreinforcement pause. Rats in Experiment 2 were trained to respond on a chained differential-reinforcement-of-low-rate variable-ratio schedule, and were exposed to increasing magnitudes of reinforcement as in Experiment 1. Response running rates increased in the variable-ratio component but decreased in the other component of the schedule. The results are discussed with reference to incentive accounts of reinforcement and the action of reinforcement on the response units generated by the operative contingencies.

Journal Article↗
PubMed1987

An examination of functional linkage between K efflux and 36Cl efflux in rat submandibular salivary gland acini in vitro.

Suspensions of dispersed acini isolated by enzymatic (collagenase) digestion were used to investigate possible interactions between transmembrane K and Cl movements. The isotopic tracer 36Cl monitored uptake and efflux of Cl under conditions where K efflux was either stimulated or inhibited. Uptake (accumulation) of 36Cl in the absence of experimental manipulation was time-dependent, resulting in a steady-state isotope content of 8.9 +/- 0.2 nmol/mg protein after 3-5 min of incubation. This content was reduced 28 per cent by the K-ionophore, valinomycin (10 microM), which also caused a net efflux of 36Cl (28 per cent) from tracer-preloaded acini. Valinomycin also released 38 per cent of the cellular K content and caused efflux of 86Rb from acini preloaded with this tracer. The efflux of 36Cl induced by 1 microM acetylcholine (23 per cent) was blocked by the K-channel blocker, quinidine (1 mM), and incompletely by apamin (1 mM). Efflux of 36Cl was also blocked by the chloride-channel blocker, 3,5-dichlorophenyl-2-amine-carboxylic acid. Thus, induction of K release (efflux) in these acini is balanced by a parallel efflux of Cl, and blockade of K release inhibits acetylcholine-induced 36Cl efflux, which suggests a functional linkage between these two events. According to current opinion, these ion movements occur, respectively, in the basolateral (K) and apical (Cl) cell membranes, so any linkage implies that the apical Cl conductance can be regulated, at least in part, by changes in membrane potential which are secondary to secretagogue-induced changes in K conductance.(ABSTRACT TRUNCATED AT 250 WORDS)

Aniline Compounds↗
PubMed1987

Does the measurement of serum fructosamine accurately reflect levels of glycated albumin in insulin-dependent diabetes?

We have measured serum glycated albumin (GSA) by affinity chromatography and immunoturbidimetry, and serum fructosamine using a Cobas FARA analyser in blood samples from 37 type I diabetics and 21 healthy controls. Random blood glucose and glycated haemoglobin levels were also measured. Glycated haemoglobin (HbA1) correlated with glycated albumin and fructosamine in the diabetic group. A less clear relationship was found between glycated albumin and fructosamine. HbA1, GSA and fructosamine correlated poorly with random blood glucose levels. These data indicate that serum fructosamine levels do not accurately reflect those of glycated albumin, as has recently been suggested, in type I insulin-dependent diabetics where glycaemic control fluctuates more than in type II diabetics. It is postulated that the two methods reflect varying glycaemic levels to a different degree, thereby accounting for the disparity.

Adolescent↗
PubMed1984

The urinary excretion of heparan sulfate by juvenile- and adult-onset diabetic patients.

The daily urinary excretions of total polymeric glycosaminoglycans and of polymeric heparan sulfate have been measured in the urine of juvenile-onset and adult-onset diabetics of both sexes and in those of normal controls. The results indicate that diabetic patients excrete more polymeric heparan sulfate than their controls, either in an absolute amount or as a percentage of the total glycosaminoglycans excreted. These results suggest that in the course of diabetes there is an increased degradation of heparan sulfate to large oligosaccharide fragments. These are excreted before being completely degraded to monosaccharides and inorganic sulfate.

Adolescent↗
PubMed1984

Synthesis and sulfation of glycosaminoglycans in fibroblasts from a patient with Lowe's syndrome.

Glycosaminoglycans of cultured normal skin fibroblasts and fibroblasts of a patient with Lowe's syndrome were labelled for 72 h with either [14C]-glucosamine or with 35SO4. For each culture, the incorporation was measured in total glycosaminoglycans per culture and in the glycosaminoglycans isolated from the intracellular, pericellular and extracellular pools. The synthesis of the sulfated glycosaminoglycans in the three pools and the total 35SO4 incorporation in the glycosaminoglycans of the two types of cultures were strictly comparable. However, Lowe's intracellular glycosaminoglycans were less sulfated than the corresponding normal ones. Undersulfated glycosaminoglycans were present in the pericellular pool of Lowe's cells, while hypersulfated ones were present in their extracellular pool. Degradation of the different pools with chondroitinases indicated that hyposulfated chondroitin 4- and 6-sulfates are present on the cell surface of Lowe's cells, where an increased amount of normally sulfated heparan sulfate may be demonstrated. This abnormal distribution of pericellular glycosaminoglycans in Lowe's cells has been described already. However, the demonstration that the total incorporation of 35SO4 is normal in Lowe's cells does not support the possibility that this abnormal distribution is the consequence of excessive hydrolysis of the phosphosulfate bond of adenosine 3'-phosphate 5'-phosphosulfate.

Carbon Radioisotopes↗
PubMed1980

An innovative approach to methadone detoxification.

An atmosphere can be created in which the user's anxiety during methadone or heroin detoxification is reduced via the facilitation of adaptive, druglike experiences provided through behavioral and psychological means. The switch to a nondrug life-style is promoted by the continued satisfaction of underlying needs which, through appropriate dosage, can lead to a higher probability of self-reliance abd abstinence. The addictive dependency on the nondrug, need-gratifying therapy is resolved through clinically monitored and graded frustrations.

Fantasy↗
PubMed1979

Prostacyclin: a solution to some problems of extracorporeal circulation. Experiments in greyhounds.

In cardiopulmonary-bypass experiments in greyhounds the effects of adding prostacyclin, prostacyclin plus heparin, and heparin alone to the extracorporeal circulation were compared. With heparin alone platelet count and function were reduced, the pressure differential across the arterial filters rose, platelet deposits were found on the arterial filters, and plasma-fibrinogen levels fell. Plasma from these dogs was toxic to fetal-mouse hearts in culture. With prostacyclin alone, fibrinogen levels fell, but the platelets were preserved. With a combination of prostacyclin and heparin, platelet count and function were maintained, there was no consumption of fibrinogen, and there was little deposition on the arterial filters.

Animals↗
PubMed1978

An antiserum to 5,6-dihydro prostacyclin (PGI1) which also binds prostacyclin.

An antiserum was raised in rabbits using 5,6-dihydro prostacyclin, a stable analogue of prostacyclin, as the hapten, conjugated to bovine serum albumin. When added to platelet rich plasma the antiserum neutralised the inhibitory activity of prostacyclin, prostaglandin E1 and D2. The amount of antiserum required to neutralise completely a dose of prostacyclin giving 90-95% inhibition of ADP induced aggregation was 10-30 times less than that required for the other two prostaglandins. Small amounts of antiserum prevented the inhibitory activity of prostacyclin generated from endothelial cells in platelet rich plasma.

Animals↗
PubMed1975

X-autosome translocation with a 47,XXXY qs,t(9p-;Xq+) karyotype.

A male with a karyotype 47,XXXY qs,t(9p-;Xq+) was ascertained utilizing ASG-banding. The karyotype was repeated because the original diagnosis of Klinefelter syndrome (47,XXY) was inconsistent with many of the stigmata present. It is suggested that many karyotypes completed prior to the advent of banding techniques will be repeated in an attempt to provide more accurate diagnosis, describe more aberrations, and possibly establish new syndromes.

Child↗
PubMed1975

Antibiotic inhibitors of mitochondrial ATP synthesis.

Fourteen antibiotics have been found to inhibit oxidative phosphorylation and uncoupler-stimulated adenosinetriphosphatase in mitochondria. Four different types of binding sites for these inhibitors have been found. The first (1) binds aurovertin to purified MF1 ATPase in the stoichiometric ratio of two aurovertin molecules per molecule of ATPase. Site II is the locus for efrapeptin (A23871) and may be a catalytic site on purified ATPase. The remaining two sites have been demonstrated only in mitochondria or submitochondrial particles when the APTase is bound to other membrane components. Oligomycin, venturiciden, venturicidin X and ossamycin probably all bind at site III. Leucinostatin (A20668) binds at site IV. At low concentrations, this antibiotic acts like oligomycin; at higher concentrations it uncouples oxidative phosphorylation. Venturicidin appears to prevent leucinostation from binding at site IV for it allows uncoupling to occur at very low concentrations of the latter antibiotic. Venturicidin aglycone, which is a more effective inhibitor than its parent compound, does not exert this effect. It is concluded that sites III and IV are in juxtaposition and that when venturicidin binds at site III its sugar moiety projects into the area of site IV to prevent leucinostation from binding at its inhibitory site.

Adenosine Triphosphatases↗