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PubMed1984

The effects of retroactive and proactive interference on learning and memory in old and young rats.

The effects of interference on learning and memory in old and young rats were compared using a visual discrimination task. In Experiment I, discrimination training was followed by one of three interference treatments and finally by retesting on the discrimination task. There were no age differences in original learning but old rats were significantly impaired in remembering the visual discrimination when a high-interference treatment involving similar stimuli was introduced between original learning and retesting. In Experiment II, old rats were impaired on discrimination learning when the high-interference treatment was administered before discrimination training. Analysis of response patterns showed that the exaggerated susceptibility of old rats to interference effects resulted in a general behavioral inflexibility similar to that observed in young adult rats with damage to the hippocampal region.

Aging↗
PubMed2003

Exploring semantic memory by investigating buildup and release of proactive interference in healthy older adults and individuals with dementia of the Alzheimer type.

There is debate regarding the integrity of semantic memory in dementia of the Alzheimer type (DAT). One view argues that DAT is associated with a breakdown in semantic memory; the other argues that DAT is associated with predominantly preserved semantic memory and a breakdown in retrieval. The classic release from proactive interference (RPI) paradigm was used to shed light on this debate. Individuals with early-stage DAT (n = 36) and healthy older adult controls (n = 45) participated in an RPI paradigm. Each trial was a Brown-Peterson task in which participants read three-word lists, counted (for 0, 3, 6, or 9 s), and recalled the words. Both groups showed significant proactive interference (PI), but the size of the PI was significantly smaller in the DAT group. The group difference in PI may be due to the faster forgetting rate in the DAT group. Both groups showed significant RPI and there was no group difference in size when RPI was considered in terms of PI levels. Both groups showed PI and RPI in prior list intrusions. The DAT group's significant buildup and release of PI based on semantic categories suggest predominantly preserved semantic memory activity, at least, in early-stage DAT individuals.

Aged↗
PubMed1979

Decay and interference processes in short-term retention of normal and brain-damaged patients.

The present study examined decay and interference mechanisms in short-term verbal retention in brain damaged patients with and without clinical memory impairment. Petersons' distractor technique was modified for this purpose. Results indicated that decay and impaired consolidation of memory traces was greater in organic amnesics, accounting for a greater degree of forgetting than proactive interference. Absence of an interference function is discussed in terms of the modified technique utilizing repeated trials to recall and more rigorously eliminating covert rehearsal, in addition to employing a more representative sample of organic amnesics than in provious studies.

Adult↗
PubMed1988

Cued recall and release from proactive interference in Alzheimer's disease.

Two tasks were administered to 13 mildly to moderately impaired subjects who met clinical research criteria for AD, and 17 controls matched for age and education. In the first task, subjects were administered a cued recall test (Buschke, 1984). AD subjects were found to be variably impaired in their ability to perform the initial stimulus-processing procedure, which involved matching cues with referents. The subsequent cued recall test did not typically facilitate performance. In the second task, subjects were administered a release from proactive interference (PI) paradigm consisting of semantically related and unrelated word lists. AD subjects did not develop the expected proactive interference effect for the semantically related words or show a resulting "release from PI" on related word list recall compared to normal controls. Results are discussed in terms of the role of semantic processing in episodic memory tasks.

Aged↗
PubMed1988

Long-term proactive interference and novelty enhancement effect in monkey list memory.

Serial-probe-recognition (SPR) performance by 2 monkeys deteriorated over several months of training. Three hundred and twenty different items were presented without repetition within a session (trial unique) but were repeated between sessions. The cause of the deterioration was identified as proactive interference (PI) due to repetitive use of items from day to day. Introduction of novel stimuli across days improved performance from 63% to 82% correct (Experiment 1). Tests with only probe items and no list items (Experiment 2) revealed that the monkeys were using a familiar/novel response strategy in combination with a relational strategy (relating the probe item to the list items) to further improve their SPR performance. Intermixing familiar baseline trials and novel transfer trials within a session (Experiment 3) encouraged the subjects to use a relational strategy, and it improved performance on baseline trials as well as on transfer trials. Possible qualitative similarity between the relational strategy and the familiar/novel response strategy is discussed along with theoretical implications of these findings for experiments which have used small number of repeating stimuli within a session.

Animals↗
PubMed1989

Buildup and release from proactive interference in a rhesus monkey.

The potential of the buildup and release from proactive interference (PI) technique in the study of animal categorization was demonstrated with a rhesus monkey. A serial probe recognition task was used with a list of 4 consecutive slide pictures (upper screen) followed by a single probe picture (lower screen). The monkey moved a lever to indicate whether or not the probe was contained in the list. PI built over 40 consecutive trials tested with either flowers or primate faces. PI was released on category change and then built during 40 trials with the second category. The first 2 serial positions showed somewhat greater PI buildup and release, supporting conclusions from human studies that the effects occur primarily in secondary memory. A second experiment provided 2 replications of the main effect and showed through color border changes and elimination of color differences that color was not a critical feature.

Animals↗
PubMed2006

[Platelet function after a high dose bolus of tirofiban immediately after coronary angioplasty].

In the TARGET trial, the lower incidence of cardiac events at one month with abciximab compared with tirofiban was attributed to a lack of efficacy in the first hour because of suboptimal dosage. The object of this study was to confirm that high dose tirofibal is associated with over 90% platelet inhibition during the first hour and to analyse the effect of this new dosage on platelet activation. Thirty-three patients treated with clopidogrel and aspirin for an acute coronary syndrome without ST elevation were given before angioplasty a bolus of 25 microg/Kg of tirofiban injected in 3 minutes, followed by an infusion of 0.15 microg/kg/min. Blood samples were taken before the treatment (TO) and at the 45th minute (T1) to measure platelet aggregation induced by ADP, the expression of P-selection, the quantification of circulating monocyte-platelet aggregates and the phospholyration of VASP protein. The results showed that all patients had over 90% (100%) inhibition of platelet aggregation at T1. The expression of P-selection was significantly reduced (T0: 0.195 +/- 0.057 MFI; T1: 0.186 +/- 0.055 MFI, p = 0.03). There was no significant difference in the number of monocyte-platelet aggregates or in the phosphorylation of VASP. In conclusion, a bolus of 25 microg/Kg/3 min of tirofiban provides over 90% inhibition of platelet aggregation in the first hour. The initial platelet proactivator effect at this dosage was shown to have disappeared with an inhibition of platelet activation.

Acute Disease↗
PubMed1979

Dextran-induced lowering of parameters of the kallikrein-kinin system in rat plasma.

Pretreatment of rats with tranexamic acid inhibited the rapid lowering of the plasma levels of acetone/kaolin-activated prekallikrein proactivator and prekallikrein caused by intravenous injection of dextran, but did not inhibit the reduction in the level of plasminogen, and potentiated the lowering of high molecular weight kininogen. By acetone/kaolin activation of normal rat plasma a mixture of surface-bound factor XIIa and unbound XIIf was obtained, and a BAEe-esterase (MW about 47,000) possessing weak kininogenase activity was present in addition to kallikrein. In activated plasma from dextran-treated rats the cleavage of XIIa was strongly reduced, and the second esterase was almost absent. It is suggested that dextran induces the loss of a plasma factor which is important for the cleavage of factor XIIa in the adopted procedure. This factor was not high molecular weight kininogen, and the lowering of plasminogen was too small to account for the reduction in PKA-activity.

Animals↗
PubMed1989

Heparin inhibition of endotoxin-dependent Limulus amebocyte lysate coagulation.

Addition of commercial heparin to preparations of the coagulation system obtained by hypotonic lysis of Limulus amebocytes, prior to the addition of endotoxin from gram-negative bacteria, inhibited gelation. Activation of the cell-lysate proclotting enzyme, utilizing a diluted lysate preparation and synthetic substrates, was inhibited to a comparable extent with either anticoagulantly active or inactive heparin. Other glycosaminoglycans, including heparan sulfate, dermatan sulfate, chondroitin 4-sulfate, and chondroitin 6-sulfate, did not inhibit the generation of clotting enzyme activity. Experiments conducted with preparations of proactivator(s) and proclotting enzyme, obtained by fractionation of lysate with heparin-Sepharose, revealed that inhibition of endotoxin-dependent activation of amebocyte lysate by heparin is mediated by precipitation of the proactivator(s) and can be prevented by increasing the salt concentration.

Animals↗
PubMed2006

Proactive interference and item similarity in working memory.

Proactive interference (PI) may influence the predictive utility of working memory span tasks. Participants in one experiment (N=70) completed Ravens Advanced Progressive Matrices (RAPM) and multiple versions of operation span and probed recall, modified for the type of memoranda (digits or words). Changing memoranda within- or across-trials released PI, but not doing so permitted PI buildup. Scores from PI-build trials, but not PI-release trials, correlated with RAPM and accounted for as much variance in RAPM as unmodified tasks. These results are consistent with controlled attention and inhibition accounts of working memory, and they elucidate a fundamental component of working memory span tasks.

Adult↗
PubMed2000

Working memory, inhibitory control, and reading disability.

The relationships among working memory, inhibitory control, and reading skills were studied in 966 individuals, 6-49 years old. In addition to a standardized measure of word recognition, they received a working memory (listening span) task in the standard, blocked format (three sets containing two-, three-, or four-item trials) or in a mixed format (three sets each containing two-, three-, and four-item trials) to determine whether scores derived from the standard format are influenced by proactive interference. Intrusion errors were investigated in order to determine whether deficits in working memory were associated with the access, deletion, or restraint functions of inhibitory control. The results indicated that deficits in working memory were characteristic of individuals with reading disabilities at all ages. These deficits may be associated with the access and restraint functions of inhibition. Working memory skills increased until the age of 19. The blocked format showed a gradual decline in adulthood whereas the mixed format did not. The different patterns suggest that the decline in working memory skills associated with aging may result from growing inefficiencies in inhibitory control, and not diminished capacity.

Adolescent↗
PubMed1996

Calpain activation in plasma membrane bleb formation during tert-butyl hydroperoxide-induced rat hepatocyte injury.

BACKGROUND & AIMS: The mechanism of plasma membrane blebbing (dissociation of the lipid bilayer from the membrane cytoskeleton) in hepatocyte injury is not known. The aim of this study was to investigate the role of calpain, a calcium-dependent cytosolic protease, in bleb formation induced by oxidative stress. METHODS: Hepatocytes from Wistar rats were injured with tertbutyl hydroperoxide in the presence or absence of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) or a specific calpain inhibitor, calpeptin (Z-Leu-nLeu-H). Bleb formation was examined by phase-contrast and transmission electron microscopies. Intracellular calcium concentration was measured using Fura-2. Western blot analyses were performed for cytoskeletal proteins (talin, alpha-actinin, and vinculin) and the intermediate (activated) and proactivated forms of calpain mu. RESULTS: tert-Butyl hydroperoxide induced a sustained increase in intracellular calciu, bleb formation, and, ultimately, hepatocyte death. Talin and alpha-actinin were degraded in a time-dependent manner, although no apparent changes of actin filament were observed. Before the cytoskeletal protein degradation, the intermediate form of calpain mu appeared as its proactivated form decreased. In addition, calpeptin or EGTA inhibited not only calpain mu activation but also cytoskeletal protein degradation and bleb formation. CONCLUSIONS: In tert-butyl hydroperoxide-treated hepatocytes, the activation of calpain promotes membrane blebbing via degradation of cytoskeletal proteins.

Animals↗
PubMed1999

Identification of determinants of pesticide exposure among Kenyan agricultural workers using empirical modelling.

The influence of factors such as type of pesticides used, use of personal protective devices and hygienic behaviour on acetylcholinesterase inhibition and activity levels in red blood cells of agricultural workers was studied in four areas in Kenya. Empirical modelling techniques were used to identify and quantify factors affecting acetylcholinesterase inhibition and activity. Use of personal protective devices was almost non-existent in areas 3 and 4 where mainly subsistence farmers were studied. Differences in hygienic behaviour between areas were relative small. WHO Class I pesticides were mostly found in area 1 (mainly large farms growing flowers) which also had highest amounts of pesticide use and highest frequency of pesticide spraying. Despite widespread use of protective devices in this area significant inhibition occurred. It became unclear whether acetylcholinesterase inhibition occurred as a result of protective clothing soaked with pesticides, thereby increasing dermal exposure, or because of other (unmeasured) factors. Inhibition, however, could have been much worse without protective devices. In area 1, most workers wore boots, which were found to be protective only when combined with an overall; wearing boots alone led to increased inhibition. Access to a washing facility or bathing facility had a positive effect on acetylcholinesterase levels. However, washing of hands and bathing immediately after spraying seemed reactive behaviour rather than proactive behaviour. Spraying was found to lead to more profound acetylcholinesterase inhibition than mixing. Workers who sprayed WHO Class III pesticides had less acetylcholinesterase inhibition than workers spraying more toxic pesticides.

Acetylcholinesterase↗
PubMed1998

Postoperative pain care.

In addition to decreasing patient suffering, adequate perioperative pain control is necessary for healing and recovery. Perioperative pain care is a proactive plan based on assessments and individualized interventions to inhibit nociception while controlling other symptoms and applying analgesic principles to promote rehabilitation with continuous evaluation.

Analgesics↗
PubMed1972

The fibrinolytic pathway of human plasma. Isolation and characterization of the plasminogen proactivator.

The conversion of the plasminogen proactivator to plasminogen activator by activated Hageman factor or its fragments has been recognized as an essential step in the conversion of plasminogen to plasmin. The plasminogen proactivator has been completely separated from prekallikrein and pre-PTA, two other proenzyme substrates of activated Hageman factor or its fragments. Plasminogen proactivator, free of any contaminating proteins as assessed by disc gel electrophoresis or isoelectric focusing, revealed a single band with an isoelectric point of 8.9 corresponding in position to the Hageman factor activatable material eluted from replicate unstained gels. After conversion of plasminogen proactivator by Hageman factor fragments to the plasminogen activator, the active site of the plasminogen activator is not inhibited by C1INH and is thus readily distinguished from that of kallikrein or PTA. The plasminogen activator is susceptible to inactivation by DFP while the plasminogen proactivator is not, as has been the case for esterases having a serine in the active site. Its interaction with plasminogen is inhibited by epsilon-aminocaproic acid.

Aminocaproates↗
PubMed1982

The initial phase of the dextran-induced anaphylactoid reaction in the rat: a comparison of inhibitors of the blood pressure fall.

The histamine H2-receptor antagonist cimetidine (25-100 mg/kg) caused a partial inhibition of the pronounced blood pressure fall induced by dextran (Macrodex, 40-100 mg/kg) in the rat. The inhibition by cimetidine could not be distinguished from the inhibition achieved by the serotonin D-receptor antagonist bromolysergic acid diethylamide (BOL, 1-4 mg/kg). Doses of cimetidine and BOL that gave submaximum inhibitory effects separately, showed approximately additive effects when combined. The combined effect of these drugs never exceeded the maximum effects of the drugs separately, whereas injection of tranexamic acid (AMCHA, 100-300 mg/kg) together with cimetidine or BOL, increased the total inhibition. Previous works showed that dextran injected intravenously into rats reduced the level of plasminogen (PG) and plasminogen proactivator (pro-PGA) in plasma (Briseid et al. 1979; Berstad 1980a; Berstad & Briseid 1982). High doses of AMCHA (200 mg/kg) did not inhibit these effects, but significantly increased the lowering caused by dextran of the capacity of high molecular weight kininogen (HMWK) to function as a cofactor in the activation of factor XII. BOL (1-4 mg/kg, Berstad 1981) and cimetidine (50-100 mg/kg) also reduced the cofactor capacity of HMWK in the doses that were required to provide a manifest inhibition of the dextran-induced blood pressure fall. It is suggested that the early phase of the state of shock induced by dextran in the rat can be counteracted at different sites, correlated with histamine and serotonin receptors on the one hand, and with an effect antagonized by AMCHA, on the other. The lowest effective doses of cimetidine and BOL were rather high, suggesting a less specific mechanism for their effects than inhibition at selective receptor sites.

Anaphylaxis↗
PubMed2006

Cognitive inflexibility after prefrontal serotonin depletion is behaviorally and neurochemically specific.

We have previously demonstrated that prefrontal serotonin depletion impairs orbitofrontal cortex (OFC)-mediated serial discrimination reversal (SDR) learning but not lateral prefrontal cortex (PFC)-mediated attentional set shifting. To address the neurochemical specificity of this reversal deficit, Experiment 1 compared the effects of selective serotonin and selective dopamine depletions of the OFC on performance of the SDR task. Whereas serotonin depletions markedly impaired performance, OFC dopamine depletions were without effect. The behavioral specificity of this reversal impairment was investigated in Experiment 2 by examining the effect of OFC serotonin depletion on performance of a modified SDR task designed to distinguish between 3 possible causes of the impairment. The results showed that the reversal deficit induced by prefrontal serotonin depletion was not due to a failure to approach a previously unrewarded stimulus (enhanced learned avoidance) or reduced proactive interference. Instead, it was due specifically to a failure to inhibit responding to the previously rewarded stimulus. The neurochemical and behavioral specificity of this particular form of cognitive inflexibility is of particular relevance to our understanding of the aetiology and treatment of inflexible behavior apparent in many neuropsychiatric and neurodegenerative disorders involving the PFC.

5,7-Dihydroxytryptamine↗
PubMed1998

Inhibition of hepatocytic autophagy by adenosine, aminoimidazole-4-carboxamide riboside, and N6-mercaptopurine riboside. Evidence for involvement of amp-activated protein kinase.

To examine the role of AMP-activated protein kinase (AMPK; EC 2.7.1. 109) in the regulation of autophagy, rat hepatocytes were incubated with the AMPK proactivators, adenosine, 5-amino-4-imidazole carboxamide riboside (AICAR), or N6-mercaptopurine riboside. Autophagic activity was inhibited by all three nucleosides, AICAR and N6-mercaptopurine riboside being more potent (IC50 = 0.3 mM) than adenosine (IC50 = 1 mM). 2'-Deoxycoformycin, an adenosine deaminase (EC 3.5.4.4) inhibitor, increased the potency of adenosine 5-fold, suggesting that the effectiveness of adenosine as an autophagy inhibitor was curtailed by its intracellular deamination. 5-Iodotubercidin, an adenosine kinase (EC 2.7.1.20) inhibitor, abolished the effects of all three nucleosides, indicating that they needed to be phosphorylated to inhibit autophagy. A 5-iodotubercidin-suppressible phosphorylation of AICAR to 5-aminoimidazole-4-carboxamide riboside monophosphate was confirmed by chromatographic analysis. AICAR, up to 0.4 mM, had no significant effect on intracellular ATP concentrations. Because activated AMPK phosphorylates and inactivates 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase (EC 1.1.1.88), the rate-limiting enzyme in cholesterol synthesis, the strong inhibition of hepatocytic cholesterol synthesis by all three nucleosides confirmed their ability to activate AMPK under the conditions used. Lovastatin and simvastatin, inhibitors of HMG-CoA reductase, strongly suppressed cholesterol synthesis while having no effect on autophagic activity, suggesting that AMPK inhibits autophagy independently of its effects on HMG-CoA reductase and cholesterol metabolism.

AMP-Activated Protein Kinases↗