Biomedical subjects

A Baron

Publications and source records attributed to A Baron.

At least 19 recordsLinked to original sources

PubMed1992

Autoanti-phosphatidylinositide antibodies specifically inhibit noradrenaline effects on Ca2+ and Cl- channels in rat portal vein myocytes.

High levels of circulating autoantibodies (auto-Ab) directed against phosphatidylinositides have been identified in the sera of patients with malignant tumors. These polyclonal autoantibodies had higher avidity and specificity for phosphatidylinositol (PtdIns) than for the other phosphatidylinositides. Effects of the auto-Ab were studied in smooth muscle myocytes in the PtdIns-involving transduction mechanism triggered by activation of alpha 1-adrenoceptors. Noradrenaline activated a Ca(2+)-dependent Cl- current through the Ca(2+)-releasing action of inositol 1,4,5-trisphosphate (InsP3) and enhanced the Ca2+ channel current through a diacylglycerol and protein kinase C-dependent mechanism. External applications of auto-Ab (0.03-0.3 mg/ml) were without effect on noradrenaline-induced responses whereas intracellular applications (0.0004-0.012 mg/ml) inhibited both Cl- current activation and Ca2+ channel current stimulation. Intracellular applications of IgG from healthy donors had no effect on noradrenaline-induced responses. When anti-PtdIns Ab were preincubated with PtdIns the inhibition of the noradrenaline-induced responses on Ca2+ and Cl- channels was not observed. Autoanti-PtdIns Ab inhibited also the acetylcholine-activated Cl- current, confirming that the acetylcholine response was mediated through the phosphatidylinositol breakdown. In contrast, the autoanti-PtdIns Ab were ineffective against the transduction pathway after beta-adrenoceptor activation. Therefore, these results suggest that the biological effect of autoanti-PtdIns Ab results from a specific binding to membrane PtdIns or PtdIns metabolites and thereby prevented InsP3 and diacylglycerol production. These autoanti-PtdIns Ab appear to be a new specific tool to identify the role of phosphatidylinositides in intracellular transduction processes.

Acetylcholine↗

PubMed1992

Phenotypic changes accompanying positive selection of CD4+CD8+ thymocytes.

We know little about the way mature CD4 (helper) and CD8 (killer) T cells develop from thymic CD4+CD8+ precursors. Here we show that small but not large CD4+CD8+ cells with high levels of the alpha beta T cell receptor (TcRhigh) result from positive selection. Neither CD4+CD8+ cells with low TcR levels nor large CD4+CD8+ thymocytes with high TcR levels differentiate in vitro. However, small CD4+CD8+ cells with high TcR levels develop in vitro into mature cells by gradually decreasing the surface levels of one or the other co-receptor and acquiring the potential to respond with proliferation to ligation of the TcR. Small CD4+CD8+ cells with high levels of a major histocompatibility complex (MHC) class I-restricted transgenic TcR develop in vitro exclusively into CD4-CD8+ cells while small CD4+CD8+ TcRhigh cells with heterogeneous TcR from various mice yield both CD4 and CD8 T cells. While these experiments are consistent with an instructive model of CD4/CD8 lineage commitment they do not rule out other mechanisms which require multiple TcR-MHC ligand interactions in the generation of mature alpha beta T cells.

Animals↗

PubMed1992

T cell receptor (TCR) beta chain homodimers on the surface of immature but not mature alpha, gamma, delta chain deficient T cell lines.

Transfected T cell receptor (TCR) beta chain genes are expressed as homodimers on the surface of immature (Sci/ET27F) but not on mature (58 alpha-beta-) T cell lines which lack TCR alpha, gamma and delta chains. The homodimer on Sci/ET27F cells is tightly bound to CD3 delta and CD3 epsilon while the association with CD3 gamma and CD3 zeta proteins is rather weak. Crosslinking of the TCR beta homodimers resulted in a strong and rapid calcium flux. In 58 alpha-beta- T cells the beta TCR chain could be easily visualized intracellularly but was not transported to the cell surface. The Scid cell lines considerably facilitate the molecular analysis of early differentiation events in the thymus which are likely to be regulated by the beta TCR homodimer.

Animals↗

PubMed1992

Fetal gender differences in preterm birth: findings in a North American cohort.

A higher incidence of preterm birth (PTB) and premature rupture of membranes (PROM) has been observed among women delivering male newborns compared with female newborns in different populations. Some authors have speculated that this higher incidence of PTB may be related to the relatively greater weight at lower gestational age of male newborns compared with female newborns. Others have suggested that the greater incidence of PTB and PROM is caused by an increased vulnerability to infection in women carrying males. To understand possible pathogenic factors leading to PTB further, we examined the association between PTB and infant gender in a cohort of North American women. In addition, incidences of PROM, chorioamnionitis, and postpartum endometritis were analyzed for women delivering males versus females. Overall, males were more likely than females to deliver at 33 to 36 weeks' gestation (OR = 1.21; 95% CI: 1.02-1.42). This increase in PTB among males was not accompanied by an increased number of males with low birthweight; rather, males were less likely than females to weigh between 2000 and 2499 gm (OR = 0.71; 95% CI: 0.60-0.84). The difference in PTB by gender could not be explained by an increased occurrence of PROM, chorioamnionitis, endometritis, or other infection-linked processes. Our findings suggest that shorter gestation in males in this population may be related to their relatively increased size and birthweight. Male gender-associated factors that predispose to infection-mediated preterm birth may play greater roles in populations at higher risk for reproductive tract infection during pregnancy.

Adolescent↗

PubMed1992

Hypertension during chronic exposure to cold: comparison between Sprague-Dawley and Long-Evans strains.

It is now well established that chronic exposure of rats to cold (5-6 degrees C) induces an elevation of systolic, diastolic, and mean blood pressures and cardiac hypertrophy within 3 weeks. Since rats of the Long-Evans (LE) strain are known to be resistant to the induction of deoxycorticosterone salt induced hypertension, their cardiovascular responses to chronic exposure to cold were compared with those of rats of the Sprague-Dawley (SD) strain. The results of these studies revealed clear differences between the LE and SD strains of rats. Thus, rats of the SD strain had a significant elevation in their blood pressure; a significantly increased urinary output of norepinephrine and epinephrine; a significantly greater dipsogenic responsiveness to acute administration of angiotensin II, and significant increases in weights of the heart, kidneys, adrenals, and brown adipose tissue compared with their warm-adapted controls. All of these changes are characteristic of rats acclimated to cold. In contrast, rats of the LE strain appear to be less responsive to cold in that blood pressure failed to rise as sharply and to attain as high a level. Furthermore, urinary outputs of norepinephrine and epinephrine were significantly lower in cold-treated rats of the LE strain compared with cold-treated rats of the SD strain, but dipsogenic responsiveness to angiotensin II was unchanged. Although increases in the weight of the previously mentioned organs were also observed in cold-treated rats of the LE strain compared with their warm-adapted controls, weights of the heart and interscapular brown adipose tissue of both groups were significantly less than those of counterparts of the SD strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1992

Gene expression of GLUT4 in skeletal muscle from insulin-resistant patients with obesity, IGT, GDM, and NIDDM.

In obesity, impaired glucose tolerance (IGT), non-insulin-dependent diabetes mellitus (NIDDM), and gestational diabetes mellitus (GDM), defects in glucose transport system activity, contribute to insulin resistance in target tissues. In adipocytes from obese and NIDDM patients, we found that pretranslational suppression of the insulin-responsive GLUT4 glucose transporter isoform is a major cause of cellular insulin resistance; however, whether this process is operative in skeletal muscle is not clear. To address this issue, we performed percutaneous biopsies of the vastus lateralis in lean and obese control subjects and in obese patients with IGT and NIDDM and open biopsies of the rectus abdominis at cesarian section in lean and obese gravidas and gravidas with GDM. GLUT4 was measured in total postnuclear membrane fractions from both muscles by immunoblot analyses. The maximally insulin-stimulated rate of in vivo glucose disposal, assessed with euglycemic glucose clamps, decreased 26% in obesity and 74% in NIDDM, reflecting diminished glucose uptake by muscle. However, in vastus lateralis, relative amounts of GLUT4 per milligram membrane protein were similar (NS) among lean (1.0 +/- 0.2) and obese (1.5 +/- 0.3) subjects and patients with IGT (1.4 +/- 0.2) and NIDDM (1.2 +/- 0.2). GLUT4 content was also unchanged when levels were normalized per wet weight, per total protein, and per DNA as an index of cell number. Levels of GLUT4 mRNA were similarly not affected by obesity, IGT, or NIDDM whether normalized per RNA or for the amount of an unrelated constitutive mRNA species. Because muscle fibers (types I and II) exhibit different capacities for insulin-mediated glucose uptake, we tested whether a change in fiber composition could cause insulin resistance without altering overall levels of GLUT4. However, we found that quantities of fiber-specific isoenzymes (phopholamban and types I and II Ca(2+)-ATPase) were similar in all subject groups. In rectus abdominis, GLUT4 content was similar in the lean, obese, and GDM gravidas whether normalized per milligram membrane protein (relative levels were 1.0 +/- 0.2, 1.3 +/- 0.1, and 1.0 +/- 0.2, respectively) or per wet weight, total protein, and DNA. We conclude that in human disease states characterized by insulin resistance, i.e., obesity, IGT, NIDDM, and GDM, GLUT4 gene expression is normal in vastus lateralis or rectus abdominis. To the extent that these muscles are representative of total muscle mass, insulin resistance in skeletal muscle may involve impaired GLUT4 function or translocation and not transporter depletion as observed in adipose tissue.

Adult↗

PubMed1992

Smokers with IDDM experience excess morbidity. The Colorado IDDM Registry.

OBJECTIVE--To determine whether there is an association between smoking and the self-reported morbidity of people with IDDM and to evaluate the nature of a possible interaction between smoking and IDDM in increasing the risk of morbidity among smokers with IDDM. RESEARCH DESIGN AND METHODS--Subjects were non-Hispanic whites aged 18-28 yr who participated in the Colorado IDDM Registry Follow-up Survey (case subjects, n = 24) or the 1985 NHIS (control subjects, n = 5876). Assessments of self-reported morbidity included any hospitalization in the past year; bed days, sick days, and limited-activity days in the past 2 wk; and ratings of poor health. The criteria outlined by Saracci were used to determine whether smoking was associated with greater morbidity among IDDM case compared to control subjects (smoking by IDDM interaction). RESULTS--Age- and sex-adjusted ORs, estimated from logistic regression, showed that people with IDDM reported excess morbidity compared with control subjects, regardless of smoking status. Smokers with IDDM reported morbidity 3-10 times as often as nonsmoking control subjects and were 2-3 times more likely to report morbidity than nonsmokers with IDDM. The smoking by IDDM interaction was more than multiplicative for all morbidity measures. Fifty to 75% of excess morbidity in young smokers with IDDM over simple additive effects was related to the interaction between smoking and IDDM. CONCLUSIONS--There was excess reported morbidity among people with IDDM who smoked, greater than that expected from the combined effects of smoking and IDDM. Smoking cessation in young people with IDDM may alleviate some of this excess, but more study is needed to determine whether smoking serves as an indicator of poor IDDM care practices or has a physiological impact that compounds the morbidity experienced by people with IDDM.

Adult↗

PubMed1991

Production and specificity of monoclonal antibodies against calmodulin from Dictyostelium discoideum.

Monoclonal antibodies were raised against calmodulin purified from Dictyostelium discoideum. To increase its antigenicity, the calmodulin was conjugated to keyhole limpet hemocyanin; mice were immunized with the conjugate. Hybridomas producing antibodies against calmodulin were identified by screening culture supernatants with calmodulin coupled to bovine serum albumin. The specificity of antibodies from hybridoma culture supernatants was tested by Western blot of Dictyostelium cell lysates. For the purpose, methods were developed that permitted sensitive detection of calmodulin bound to membranes. The key elements of the blotting protocol were used of PVDF membrane, transfer conducted in phosphate buffer, and glutaraldehyde fixation after transfer. These methods permitted detection of as little as 0.1 ng of calmodulin spotted directly onto the membrane, or 10 ng transferred from an SDS polyacrylamide gel. Ten calmodulin-specific antibodies were identified; most of these reacted preferentially with the calcium-containing form of Dictyostelium calmodulin. Several of the monoclonal antibodies cross-reacted with calmodulin from bovine brain.

Animals↗

PubMed1991

Pharmacological block of Ca(2+)-activated Cl- current in rat vascular smooth muscle cells in short-term primary culture.

Ca(2+)-activated Cl- currents were studied in isolated cells from rat portal vein smooth muscle in short-term primary culture using the whole-cell patch-clamp technique. Cl- currents can be activated separately by Ca2+ release from intracellular stores (in response to external applications of caffeine or noradrenaline) and by Ca2+ influx through voltage-dependent Ca2+ channels. The effects of several Cl- channel blockers and of spironolactone (a substance known to reduce internal Ca2+ loading) on both Cl- and Ca2+ currents were examined. Diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), anthracene-9-carboxylic acid (9-AC) and diphenylamine-2,2'-dicarboxylic acid (DPC) inhibited the Ca(2+)-activated Cl- current (IC50 values between 16.5 and 306 microM) with no effects on the inward Ca2+ current and on internal Ca2+ loading (testing by measuring the Ca(2+)-activated K+ current). These results indicate that the inhibition of Cl- current by these compounds is due to a direct interaction with the Cl- channel. In contrast, spironolactone inhibited both K+ and Cl- currents (IC50 = 7.6 microM) by reducing the amount of Ca2+ located in the internal stores, whereas the Cl- current activated by Ca2+ current through T-type Ca2+ channels was unchanged. This preparation and the protocols developed in this study appears to be appropriate for analysis of substances interfering with Cl- channels or intracellular Ca2+ stores.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1991

Ca2+ channel activation and membrane depolarization mediated by Cl- channels in response to noradrenaline in vascular myocytes.

1. The effects of noradrenaline (NA) were studied on vascular smooth muscle cells isolated from rat portal vein. 2. Two types of single-Ca2+ channel currents with conductances of 17 pS and 8 pS were obtained in cell-attached configuration. Bath application of NA increased the open probability of both channels during depolarizing pulses without a change of background membrane conductance. However, NA did not open Ca2+ channels when the membrane patch potential was held at -50 mV, which is about the resting potential in physiological conditions. 3. In the whole-cell configuration, studies of voltage-dependent Ca2+ channel currents showed that the peak conductance curve was not shifted to more negative potentials by NA. 4. Measurements of internal Ca(2+)-concentration ([Ca2+]i) with Indo-1 indicated that NA increased [Ca2+]i at a holding potential of -50 mV and evoked a Ca(2+)-activated Cl- current. These effects were blocked when heparin was included in the pipette solution. 5. A Cl- channel blocker without effect on Ca2+ channels (anthracene-9-carboxylic acid) inhibited the contractions of portal vein strips induced by NA in a manner similar to that produced by a Ca2+ channel inhibitor (isradipine). The NA-induced contraction was completely suppressed in the presence of ryanodine which depletes intracellular Ca2+ stores. 6. The present study suggests that activation of Cl- channels by Ca2+ release produces a membrane depolarization which is a prerequisite for enhanced opening of voltage-dependent Ca2+ channels in response to NA in venous smooth muscle.

Animals↗

PubMed1991

Large conductance calcium-activated non-selective cation channel in smooth muscle cells isolated from rat portal vein.

1. Membrane currents of isolated smooth muscle cells from rat portal vein were studied using the whole-cell patch-clamp technique. 2. In addition to the Ca(2+)-dependent Cl- current, single-channel activities were recorded in response to external applications of 10 mM-caffeine, in the absence of EGTA in the pipette solution. The conductance of this novel type of channel was around 200 pS for membrane potentials ranging from -100 to +60 mV. 3. The single-channel activities were also induced by external application of noradrenaline (10(-5)M) or acetylcholine (10(-5)M), by Ca2+ entry through voltage-dependent Ca2+ channels, and by intracellular application of ryanodine (10(-5)M). The caffeine-activated single-channel currents disappeared when 10 mM-EGTA was added to the pipette solution or after replacement of external Ca2+ with Ba2+. These results show that these channels are Ca2+ dependent. 4. Alterations of the Cl- equilibrium potential did not produce any change in the reversal potential of the caffeine-activated single-channel current indicating that it was not carried by Cl- ions. The value of the reversal potential was about +10 mV, irrespective of the CsCl-, KCl- or NaCl-containing solutions used to fill the pipette. This observation indicates that the channel was equally permeable to these monovalent cations. 5. Caffeine activated single-channel currents when cells were bathed in 90 mM-Ba2+ plus 1 mM-Ca(2+)- or 91 mM-Ca(2+)-containing solutions, showing that divalent cations permeate the channels. The permeability for Ca2+ over Na+ was high as the ratio PCa/PNa was estimated to be 21. 6. Single-channel activities induced by caffeine were not modified by Ca2+ channel blockers such as dihydropyridines and phenylalkylamines. 7. It is concluded that portal vein smooth muscle cells possess Ca(2+)-activated nonspecific channels which are highly permeable to Ca2+ ions.

Animals↗

PubMed1991

Reduction in the elevated blood pressure of Dahl salt-sensitive rats treated chronically with L-5-hydroxytryptophan.

Rats of the Dahl salt-sensitive (DS) and Dahl salt-resistant (DR) strains were placed on a 4% NaCl diet and blood pressures were monitored. Chronic subcutaneous infusion L-5-hydroxytryptophan (L-5-HTP, 12.6 mg/day) by osmotic minipumps significantly decreased the elevated systolic blood pressure of DS rats on a 4% NaCl diet. Blood pressures of DR rats were unaffected by treatment with L-5-HTP. Cardiac hypertrophy was associated with Dahl salt-induced hypertension. However, treatment with L-5-HTP failed to reduce the weight of the heart significantly. These results suggest that chronic administration of L-5-HTP was effective in reducing the elevated blood pressure in the DS model. The specific mechanisms by which L-5-HTP reduces the elevated blood pressure in DS rats is not clear and remains for further study.

5-Hydroxytryptophan↗

PubMed1991

Effect of chronic dietary treatment with L-tryptophan on the development of cold-induced hypertension in rats.

This study was designed to assess the effect of chronic dietary administration (2.5 and 5.0% by weight) of the neutral amino acid, L-tryptophan, on the development of hypertension during chronic exposure to cold. In addition, a warm-adapted and cold-treated control group receiving unsupplemented food were used. Chronic administration of the lower dose of L-tryptophan (850 mg/day) prevented the elevation of blood pressure attenuated cardiac hypertrophy, and had no effect on body weight during exposure to cold. The higher dose of L-tryptophan (1,690 mg/day) attenuated the rate of blood pressure increase, did not affect cardiac hypertrophy, attenuated the gain in body weight, and increased the urinary output of epinephrine. Thus, this dose may be associated with some toxicity. Both doses of tryptophan failed to prevent certain other responses characteristically occurring during exposure to cold: i.e. increased weight of the kidneys, adrenal glands and brown adipose tissue; increased food and water consumption; increased dipsogenic responsiveness to angiotensin II, and increased plasma aldosterone concentration. The results indicate that chronic dietary administration of L-tryptophan (850 mg/day) can prevent the development of cold-induced hypertension, as it can in all other models of hypertension tested thus far in rats.

Aldosterone↗

PubMed1991

Effect of chronic treatment with clonidine and spironolactone on cold-induced elevation of blood pressure.

The present study was designed to determine whether antihypertensive agents known to affect the renin-angiotensin-aldosterone (RAA) system might affect the elevation of blood pressure induced by chronic exposure to cold. Spironolactone, a mineralocorticoid receptor blocker, was added to the food and administered to rats chronically exposed to cold. In addition, clonidine, and alpha 2-adrenergic agonist and inhibitor of renin secretion, was administered to another group of cold-exposed rats by daily intraperitoneal injection. A warm-adapted and a cold-treated control group were also used. Chronic administration of spironolactone prevented the development of hypertension but failed to prevent other adaptive physiological changes characteristically occurring during exposure to cold and seen in the cold-treated control rats. Thus, increased weight of the heart, kidneys, adrenals and brown adipose tissue, increased dipsogenic responsiveness to angiotensin II, increased urinary outputs of norepinephrine and epinephrine, and increased food and water consumption were observed in all rats, treated and untreated, during exposure to cold. Similarly, daily injection of clonidine attenuated the elevation of blood pressure but also failed to prevent the other adaptive physiological changes characteristic of cold. These results are consistent with the hypothesis that the RAA system plays a role in the development of the cold-induced elevation of blood pressure.

Aldosterone↗

PubMed1991

Calcium-activated cation channel in rat portal vein myocytes.

A rapid transient rise in the free cytosolic Ca2+ concentration is one of the earliest events in smooth muscle cell activation and is involved in the opening of several classes of Ca2(+)-sensitive ion channels such as K+ channels and Cl- channels. In portal vein smooth muscle cells, in addition to the Ca(2+)-dependent Cl-current, single-channel activities were recorded in response to external application of 10 mM caffeine, in the absence of EGTA in the pipette solution. The conductance of this novel type of channel was around 200 pS for membrane potentials ranging between -100 to +60 mV. The single-channel activities were also induced by external application of noradrenaline (10(-5) M) or acetylcholine (10(-5) M), by Ca2+ entry through voltage-dependent Ca(2+)-channels, and by intracellular application of ryanodine (10(-5) M). The caffeine-activated single-channel currents disappeared when 10 mM EGTA were added to the pipette solution or after replacement of external Ca2+ with Ba2+. These results show that these channels are Ca(2+)-dependent. Alteration of the Cl- equilibrium potential did not produce any change in the reversal potential of the caffeine-activated single-channel current, indicating that it was not carried by Cl- ions. The value of the reversal potential was about + 10 mV, irrespective of the CsCl-, KCl- or NaCl-containing solutions used to fill the pipette. Caffeine activated single-channel currents when cells were bathed in 90 mM Ba2+ plus 1 mM Ca(2+)- or 91 mM Ca(2+)-containing solutions, showing that divalent cations permeate the channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1990

Ligand specificities of recombinant retinoic acid receptors RAR alpha and RAR beta.

Binding of retinoic acid (RA) to specific RA receptors alpha and beta (RAR alpha and RAR beta) was studied. Receptors were obtained in two ways: (1) full-length receptors were produced by transient expression of the respective human cDNAs in COS 1 cells; and (2) the ligand-binding domains of RAR alpha and RAR beta were produced in Escherichia coli. RA binding to the wild-type and truncated forms of the receptor was identical for both RAR alpha and RAR beta, indicating that the ligand-binding domains have retained the binding characteristics of the intact receptors. Furthermore, RA bound with the same affinity to both RAR alpha and RAR beta. Only retinoid analogues with an acidic end-group were able to actively bind to both receptors. On measuring the binding of various retinoids, we have found that the properties of the ligand-binding sites of RAR alpha and RAR beta were rather similar. Two retinoid analogues were capable of binding preferentially to either RAR alpha or RAR beta, suggesting that it may be possible to synthesize specific ligands for RAR alpha and RAR beta.

Animals↗

PubMed1990

The murine genes Hox-5.1 and Hox-4.1 belong to the same HOX complex on chromosome 2.

Two different loci of Antennapedia-related homeobox-containing genes have been shown to map to mouse chromosome 2: the HOX-5 complex and the Hox-4.1 gene. These independently derived loci are likely to be parts of a single gene complex, although their close linkage has not yet been demonstrated. Since cosmid walks to extend the HOX-5 cluster and to potentially link the two loci were unsuccessful, we have used large restriction fragments separated by pulsed-field gel electrophoresis to demonstrate the linkage between probes from the HOX-5 region and sequences near Hox-4.1. To further define the distance between the two linked loci, we screened a NotI jumping library with sequences near the Hox-5.1 gene to obtain a marker within the region predicted to contain Hox-4.1. The jumping endpoint lies within genomic clones from a lambda phage walk extending from the 5' end of Hox-4.1, and thus provides clear evidence of linkage between the two Hox loci. Our results demonstrate that Hox-4.1 lies approximately 35 kb downstream of the Hox-5.1 gene and that the two loci do indeed thus constitute parts of the same HOX complex.

Animals↗

PubMed1990

Age-related effects of reinforced practice on recognition memory: consistent versus varied stimulus-response relations.

Healthy older (64-74 years) and younger (19-26 years) men received extended exposure to tasks requiring visual recognition memory (memory scanning). The older men's speeds increased substantially when fast responding was differentially reinforced by time limits placed on the recognition response. Gains were matched by the younger men, however, so that age differences were not reduced. These improvements by the older men occurred under conditions of varied stimulus-response relations (as well as consistent relations), a procedure that has been regarded as especially taxing of the cognitive resources of older adults. Although the study did not provide evidence that age differences in recognition memory were reduced by reinforced practice, the equivalent practice effects and the transfer of these effects from visual to auditory stimuli indicated that the older men's learning abilities were the equal of those of the young adult controls.

Adult↗