The saving enhanced memory effect can be observed when only a subset of items are saved.

Saving one list of words, such as on a computer or by writing them down, can improve a person's ability to learn and remember a second list of words that are not saved. This phenomenon, known as the saving enhanced memory effect, is typically observed by comparing the recall of nonsaved items when other items are saved versus when they are not saved. In past research, the effect has been shown to occur when participants save an entire list before learning a new list. In the current research, we examined whether the effect can be observed when participants save a subset of items within a single list. The results of two experiments confirmed that partial saving can lead to a saving enhanced memory effect, with the effect observed regardless of whether participants saved items by clicking a button on the computer or writing them out by hand. The effect was observed on an item-specific cued-recall test (Experiment 1) as well as a free recall test that did not control the order of output (Experiment 2). However, the effect size did vary as a function of how participants attempted to recall the items on the final test. Specifically, participants who initiated their output by recalling nonsaved items exhibited a significantly larger saving enhanced memory effect than those who initiated their output by reproducing saved items. Together, these findings expand our understanding of the saving enhanced memory effect and shine new light on the impacts of cognitive offloading on human memory.

Femoral Nailing in a Porcine Model Causes Bone Marrow Emboli in the Lungs and Systemic Emboli in the Heart and Brain.

Background: Shaft fractures of the femur are commonly treated with intramedullary nailing, which can release bone marrow emboli into the bloodstream. Emboli can travel to the lungs, impairing gas exchange and causing inflammation. Occasionally, emboli traverse from the pulmonary to the systemic circulation, hindering perfusion and resulting in injuries such as heart and brain infarctions, known as fat embolism syndrome. We studied the extent of systemic bone marrow embolization in a pig model. Methods: Twelve anesthetized pigs underwent bilateral intramedullary nailing of the femur, while 3 animals served as sham controls. Monitoring included transesophageal echocardiography (TEE), pulse oximetry, electrocardiography, arterial blood pressure measurement, and blood gas and troponin-I analysis. After surgery, animals were monitored for 240 minutes before euthanasia. Post mortem, the heart, lungs, and brain were biopsied. Results: Bone marrow emboli were found in the heart and lungs of all 12 of the pigs that underwent intramedullary nailing and in the brains of 11 of them. No emboli were found in the sham group. The pigs subjected to intramedullary nailing exhibited significant hypoxia (PaO2/FiO2 ratio, 410 mm Hg [95% confidence interval (CI), 310 to 510) compared with the sham group (594 mm Hg [95% CI, 528 to 660]). The nailing group exhibited ST-segment alterations consistent with myocardial ischemia and a significant increase in the troponin-I level compared with the sham group (1,580 ng/L [95% CI, 0 to 3,456] versus 241 ng/L [95% CI, 0 to 625] at the 240-minute time point; p = 0.005). TEE detected emboli in the right ventricular outflow tract, but not systemically, in the nailing group. Conclusions: Bilateral intramedullary nailing caused bone marrow emboli in the lungs and systemic emboli in the heart and brain in this pig model. The observed clinical manifestations were consistent with coronary and pulmonary emboli. TEE detected pulmonary but not systemic embolization. Clinical Relevance: Femoral intramedullary nailing in humans is likely to result in embolization as described in our pig model. Focused monitoring is necessary for detection of fat embolism syndrome. Absence of visual emboli in the left ventricle on TEE does not exclude the occurrence of systemic bone marrow emboli.

Real-time feedback on chest compression efficacy by hands-free carotid Doppler in a porcine model.

Aim: Current guidelines for cardiopulmonary resuscitation (CPR) recommend a one-size-fits-all approach in relation to the positioning of chest compressions. We recently developed RescueDoppler, a hands-free Doppler ultrasound device for continuous monitoring of carotid blood flow velocity during CPR. The aim of the present study is to investigate whether RescueDoppler via real-time hemodynamic feedback, could identify both optimal and suboptimal compression positions. Methods: In this model of animal cardiac arrest, we induced ventricular fibrillation in five domestic pigs. Manual chest compressions were performed for ten seconds at three different positions on the sternum in random order and repeated six times. We analysed Time Average Velocity (TAV) with chest compression position as a fixed effect and animal, position, and sequential time within animals as random effects. Furthermore, we compared TAV to invasive blood pressure from the contralateral carotid artery. Results: We were able to detect changes in TAV when altering positions. The positions with the highest (range 19 to 48 cm/s) and lowest (6-25 cm/s) TAV were identified in all animals, with corresponding peak pressure 50-81 mmHg, and 46-64 mmHg, respectively. Blood flow velocity was, on average, highest at the middle position (TAV 33 cm/s), but with significant variability between animals (SD 2.8) and positions within the same animal (SD 9.3). Conclusion: RescueDoppler detected TAV changes during CPR with alternating chest compression positions, identifying the position yielding maximal TAV. Future clinical studies should investigate if RescueDoppler can be used as a real-time hemodynamical feedback device to guide compression position.

Corrigendum: Iatrogenic air embolism: pathoanatomy, thromboinflammation, endotheliopathy, and therapies.

[This corrects the article DOI: 10.3389/fimmu.2023.1230049.].

Iatrogenic air embolism: pathoanatomy, thromboinflammation, endotheliopathy, and therapies.

Iatrogenic vascular air embolism is a relatively infrequent event but is associated with significant morbidity and mortality. These emboli can arise in many clinical settings such as neurosurgery, cardiac surgery, and liver transplantation, but more recently, endoscopy, hemodialysis, thoracentesis, tissue biopsy, angiography, and central and peripheral venous access and removal have overtaken surgery and trauma as significant causes of vascular air embolism. The true incidence may be greater since many of these air emboli are asymptomatic and frequently go undiagnosed or unreported. Due to the rarity of vascular air embolism and because of the many manifestations, diagnoses can be difficult and require immediate therapeutic intervention. An iatrogenic air embolism can result in both venous and arterial emboli whose anatomic locations dictate the clinical course. Most clinically significant iatrogenic air emboli are caused by arterial obstruction of small vessels because the pulmonary gas exchange filters the more frequent, smaller volume bubbles that gain access to the venous circulation. However, there is a subset of patients with venous air emboli caused by larger volumes of air who present with more protean manifestations. There have been significant gains in the understanding of the interactions of fluid dynamics, hemostasis, and inflammation caused by air emboli due to in vitro and in vivo studies on flow dynamics of bubbles in small vessels. Intensive research regarding the thromboinflammatory changes at the level of the endothelium has been described recently. The obstruction of vessels by air emboli causes immediate pathoanatomic and immunologic and thromboinflammatory responses at the level of the endothelium. In this review, we describe those immunologic and thromboinflammatory responses at the level of the endothelium as well as evaluate traditional and novel forms of therapy for this rare and often unrecognized clinical condition.

Are you sure? Examining the potential benefits of truth-checking as a learning activity.

Learners may be uncertain about whether encountered information is true. Uncertainty may encourage people to critically assess information's accuracy, serving as a kind of desirable difficulty that benefits learning. Uncertainty may also have negative effects, however, leading people to mistrust true information or to later misremember false information as true. In three experiments, participants read history statements. In one condition, all statements were true, and the participants knew it. In the other two conditions, some statements were true, and others were false. Participants were either told the statements' accuracy or they guessed the statements' accuracy prior to feedback, a manipulation we refer to as truth-checking. All participants were then tested on recalling the true information and on recognising true versus false statements. We observed a significant benefit of truth-checking in one of the three experiments, suggesting that truth-checking may have some potential to enhance learning, perhaps by inducing people to encode to-be-learned information more deeply than they would otherwise. Even so, the benefit may come at a cost-truth-checking took significantly longer than study alone, and it led to a greater likelihood of thinking false information was true, suggesting costs of truth-checking may tend to outweigh benefits.

Hands-free continuous carotid Doppler ultrasound for detection of the pulse during cardiac arrest in a porcine model.

Background/Purpose: Pulse palpation is an unreliable method for diagnosing cardiac arrest. To address this limitation, continuous hemodynamic monitoring may be a viable solution. Therefore, we developed a novel, hands-free Doppler system, RescueDoppler, to detect the pulse continuously in the carotid artery. Methods: In twelve pigs, we evaluated RescueDopplers potential to measure blood flow velocity in three situations where pulse palpation of the carotid artery was insufficient: (1) systolic blood pressure below 60 mmHg, (2) ventricular fibrillation (VF) and (3) pulseless electrical activity (PEA). (1) Low blood pressure was induced using a Fogarty balloon catheter to occlude the inferior vena cava. (2) An implantable cardioverter-defibrillator induced VF. (3) Myocardial infarction after microembolization of the left coronary artery caused True-PEA. Invasive blood pressure was measured in the contralateral carotid artery. Time-averaged blood flow velocity (TAV) in the carotid artery was related to mean arterial pressure (MAP) in a linear mixed model. Results: RescueDoppler identified pulsatile blood flow in 41/41 events with systolic blood pressure below 60 mmHg, with lowest blood pressure of 19 mmHg. In addition the absence of spontaneous circulation was identified in 21/21 VF events and true PEA in 2/2 events. The intraclass correlation coefficient within animals for TAV and MAP was 0.94 (95% CI. 0.85-0.98). Conclusions: In a porcine model, RescueDoppler reliably identified pulsative blood flow with blood pressures below 60 mmHg. During VF and PEA, circulatory arrest was rapidly and accurately demonstrated. RescueDoppler could potentially replace unreliable pulse palpation during cardiac arrest and cardiopulmonary resuscitation.

Examining the effect size and duration of retrieval-induced facilitation.

Under certain conditions, the retrieval of some information can increase the recall of other information, a phenomenon known as retrieval-induced facilitation. Chan (Journal of Memory and Language 61:153-170, 2009) proposed two moderating factors to account for why retrieval causes facilitation in some situations and forgetting in others: (1) integration at the time of encoding and (2) the delay between retrieval practice and final test. Chan found a 9-11% facilitation effect when the materials were well integrated and the final test occurred after a 24-h delay. Two sets of experiments sought to replicate and extend Chan's study by examining retrieval-induced facilitation not only following a 24-h delay but after longer delays (i.e., 1 or 2 weeks). A meta-analysis including these replications and the original experiments was also conducted. The results provide additional evidence of retrieval-induced facilitation, with no evidence that the effect varies as a function of the final delay. However, the size of the effect was found to be somewhat smaller than previously observed.

Acute exercise on memory: application of the retrieval-induced forgetting paradigm.

Accumulating research has shown that acute exercise can enhance memory function. Although counterintuitive, acute exercise may also facilitate aspects of forgetting. Specifically, retrieving a subset of items from memory can facilitate the retention of retrieved items (retrieval practice) and inhibit the subsequent retrieval of non-retrieved items from the same category (retrieval-induced forgetting; RIF). Given that acute exercise has been shown to enhance cognition-related inhibition, acute exercise may facilitate RIF, which was evaluated in three experiments. In Experiment 1, a sample of 180 young adults completed either a control (N = 60), moderate-intensity acute exercise (N = 57), or vigorous-intensity acute exercise session (N = 63). Both acute exercise sessions lasted 20 min and occurred prior to the study list. Participants then completed a standard RIF protocol, with the final test occurring via a recognition task. Acute exercise, regardless of intensity, had no effect on RIF. Experiment 2 (N = 225) was similar to Experiment 1 but used a cued recall final test, and also showed no effects of acute exercise on RIF. In Experiment 3 (N = 158), two cued recall tests were implemented, with acute exercise occurring between the two tests. Acute exercise, but not a control scenario, preserved the RIF effect across the cued recall assessments. These findings suggest that acute exercise prior to study may not influence RIF, but when positioned between two recall assessments, acute exercise may preserve the RIF effect over time.

Remembering what to do when the time comes: The effects of offloading in a complex prospective memory task.

Two experiments examined the effects of cognitive offloading on a complex prospective memory task. Participants underwent a simulated telehealth examination in which they learned about dry eye disease and its treatment. They were asked to email the experimenter at 7:00 p.m., 2 days later, at which point they attempted to recall the medical information about dry eye. Participants in the offload condition were instructed to set a reminder; participants in the internal condition were not. At 7:15 p.m., all participants received an email requesting them to complete the free-recall test, allowing for an assessment of memory performance even when participants failed to email the experimenter. Participants in the offload condition significantly outperformed participants in the internal condition, both in terms of emailing the experimenter on time and in terms of completing the second phase of the experiment at all. No differences were observed regarding performance on the memory test. Results related to rehearsals, metacognitive judgments, and conscientiousness are also reported. Overall, the study provides new insight into how reminders can affect performance on a complex prospective memory task and how reminders may have the potential to be used in medical contexts to optimize patient outcomes. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Does taking multiple photos lead to a photo-taking-impairment effect?

The photo-taking-impairment effect is observed when photographed information is less likely to be remembered than nonphotographed information. Three experiments examined whether this effect persists when multiple photos are taken. Experiment 1 used a within-subjects laboratory-based design in which participants viewed images of paintings and were instructed to photograph them once, five times, or not at all. Participants' memory was measured using a visual detail test, and the photo-taking-impairment effect was observed when participants took multiple photos. Experiment 2 examined the photo-taking-impairment effect using a between-subjects design. Participants either photographed all of the paintings they saw once, five times, or not at all, before being tested on their memory for the paintings. The photo-taking-impairment effect was observed in both photo-taking conditions relative to the no photo baseline. Experiment 3 replicated this pattern of results even when participants who took multiple photos were instructed to take five unique photos. These findings indicate that the photo-taking-impairment effect is robust, occurring even when multiple photos are taken, and after nonselective photo-taking.

Application of the C3 inhibitor compstatin in a human whole blood model designed for complement research - 20 years of experience and future perspectives.

The complex molecular and cellular biological systems that maintain host homeostasis undergo continuous crosstalk. Complement, a component of innate immunity, is one such system. Initially regarded as a system to protect the host from infection, complement has more recently been shown to have numerous other functions, including involvement in embryonic development, tissue modeling, and repair. Furthermore, the complement system plays a major role in the pathophysiology of many diseases. Through interactions with other plasma cascades, including hemostasis, complement activation leads to the broad host-protective response known as thromboinflammation. Most complement research has been limited to reductionistic models of purified components and cells and their interactions in vitro. However, to study the pathophysiology of complement-driven diseases, including the interaction between the complement system and other inflammatory systems, holistic models demonstrating only minimal interference with complement activity are needed. Here we describe two such models; whole blood anticoagulated with either the thrombin inhibitor lepirudin or the fibrin polymerization peptide blocker GPRP, both of which retain complement activity and preserve the ability of complement to be mutually reactive with other inflammatory systems. For instance, to examine the relative roles of C3 and C5 in complement activation, it is possible to compare the effects of the C3 inhibitor compstatin effects to those of inhibitors of C5 and C5aR1. We also discuss how complement is activated by both pathogen-associated molecular patterns, inducing infectious inflammation caused by organisms such as Gram-negative and Gram-positive bacteria, and by sterile damage-associated molecular patterns, including cholesterol crystals and artificial materials used in clinical medicine. When C3 is inhibited, it is important to determine the mechanism by which inflammation is attenuated, i.e., whether the attenuation derives directly from C3 activation products or via downstream activation of C5, since the mechanism involved may determine the appropriate choice of inhibitor under various conditions. With some exceptions, most inflammatory responses are dependent on C5 and C5aR1; one exception is venous air embolism, in which air bubbles enter the blood circulation and trigger a mainly C3-dependent thromboembolism, with the formation of an active C3 convertase, without a corresponding C5 activation. Under such conditions, an inhibitor of C3 is needed to attenuate the inflammation. Our holistic blood models will be useful for further studies of the inhibition of any complement target, not just C3 or C5. The focus here will be on targeting the critical complement component, activation product, or receptor that is important for the pathophysiology in a variety of disease conditions.

Venous Air Embolism Activates Complement C3 Without Corresponding C5 Activation and Trigger Thromboinflammation in Pigs.

Introduction: Air embolism may complicate invasive medical procedures. Bubbles trigger complement C3-mediated cytokine release, coagulation, and platelet activation in vitro in human whole blood. Since these findings have not been verified in vivo, we aimed to examine the effects of air embolism in pigs on thromboinflammation. Methods: Forty-five landrace pigs, average 17 kg (range 8.5-30), underwent intravenous air infusion for 300 or 360 minutes (n=29) or served as sham (n=14). Fourteen pigs were excluded due to e.g. infections or persistent foramen ovale. Blood was analyzed for white blood cells (WBC), complement activation (C3a and terminal C5b-9 complement complex [TCC]), cytokines, and hemostatic parameters including thrombin-antithrombin (TAT) using immunoassays and rotational thromboelastometry (ROTEM). Lung tissue was analyzed for complement and cytokines using qPCR and immunoassays. Results are presented as medians with interquartile range. Results: In 24 pigs receiving air infusion, WBC increased from 17×109/L (10-24) to 28 (16-42) (p<0.001). C3a increased from 21 ng/mL (15-46) to 67 (39-84) (p<0.001), whereas TCC increased only modestly (p=0.02). TAT increased from 35 µg/mL (28-42) to 51 (38-89) (p=0.002). ROTEM changed during first 120 minutes: Clotting time decreased from 613 seconds (531-677) to 538 (399-620) (p=0.006), clot formation time decreased from 161 seconds (122-195) to 124 (83-162) (p=0.02) and α-angle increased from 62 degrees (57-68) to 68 (62-74) (p=0.02). In lungs from pigs receiving air compared to sham animals, C3a was 34 ng/mL (14-50) versus 4.1 (2.4-5.7) (p<0.001), whereas TCC was 0.3 CAU/mL (0.2-0.3) versus 0.2 (0.1-0.2) (p=0.02). Lung cytokines in pigs receiving air compared to sham animals were: IL-1ß 302 pg/mL (190-437) versus 107 (66-120), IL-6 644 pg/mL (358-1094) versus 25 (23-30), IL-8 203 pg/mL (81-377) versus 21 (20-35), and TNF 113 pg/mL (96-147) versus 16 (13-22) (all p<0.001). Cytokine mRNA in lung tissue from pigs receiving air compared to sham animals increased 12-fold for IL-1ß, 121-fold for IL-6, and 17-fold for IL-8 (all p<0.001). Conclusion: Venous air embolism in pigs activated C3 without a corresponding C5 activation and triggered thromboinflammation, consistent with a C3-dependent mechanism. C3-inhibition might represent a therapeutic approach to attenuate this response.

Pretesting can be beneficial even when using the internet to answer questions.

Research on the pretesting effect has shown that attempting to retrieve or generate information, even when unsuccessful, can potentiate the subsequent learning and remembering of that information. In the current research, we tested the hypothesis that when information can be accessed online, people may be less likely to retrieve or generate information on their own, thus making them less likely to benefit from the pretesting effect. The results of two experiments failed to provide support for this hypothesis. Participants remembered pretested information better than non-pretested information regardless of whether they were required to attempt to retrieve answers from memory or search for the answers using Google. The results suggest that the benefits of pretesting can be observed even when people rely on the internet to answer the questions they encounter.

Relearning can eliminate the effect of retrieval-induced forgetting.

The retrieval of a subset of items can cause the forgetting of other, non-retrieved items, a phenomenon known as retrieval-induced forgetting. Initial work suggested that giving people the opportunity to restudy non-retrieved items following retrieval practice is sufficient to eliminate the effect of retrieval-induced forgetting, but more recent work has suggested otherwise. If retrieval-induced forgetting is not eliminated by restudy, then such a finding would have important implications for understanding the theoretical nature of retrieval-induced forgetting. It would suggest, for example, that retrieval-induced forgetting reflects more than the temporary reduction in the accessibility of non-retrieved items in memory. The two experiments reported here sought to clarify this issue, with the results suggesting that retrieval-induced forgetting can be eliminated by restudy. Indeed, retrieval-induced forgetting was eliminated by restudy even when the forgetting effect was produced by three rounds of retrieval practice instead of one round of retrieval practice. These findings are consistent with the idea that retrieval-induced forgetting, at least under the conditions of the current experiments, reflects a temporary reduction in the accessibility of non-retrieved items in memory.

Intraosseous fluid resuscitation causes systemic fat emboli in a porcine hemorrhagic shock model.

BACKGROUND: Intraosseous cannulation can be life-saving when intravenous access cannot be readily achieved. However, it has been shown that the procedure may cause fat emboli to the lungs and brain. Fat embolization may cause serious respiratory failure and fat embolism syndrome. We investigated whether intraosseous fluid resuscitation in pigs in hemorrhagic shock caused pulmonary or systemic embolization to the heart, brain, or kidneys and if this was enhanced by open chest conditions. METHODS: We induced hemorrhagic shock in anesthetized pigs followed by fluid-resuscitation through bilaterally placed tibial (hind leg) intraosseous cannulas. The fluid-resuscitation was limited to intraosseous or i.v. fluid therapy, and did not involve cardiopulmonary resuscitation or other interventions. A subgroup underwent median sternotomy with pericardiectomy and pleurotomy before hemorrhagic shock was induced. We used invasive hemodynamic and respiratory monitoring including Swan Ganz pulmonary artery catheter and transesophageal echocardiography and obtained biopsies from the lungs, heart, brain, and left kidney postmortem. RESULTS: All pigs exposed to intraosseous infusion had pulmonary fat emboli in postmortem biopsies. Additionally, seven of twenty-one pigs had coronary fat emboli. None of the pigs with open chest had fat emboli in postmortem lung, heart, or kidney biopsies. During intraosseous fluid-resuscitation, three pigs developed significant ST-elevations on ECG; all of these animals had coronary fat emboli on postmortem biopsies. CONCLUSIONS: Systemic fat embolism occurred in the form of coronary fat emboli in a third of the animals who underwent intraosseous fluid resuscitation. Open chest conditions did not increase the incidence of systemic fat embolization.

Air Bubbles Activate Complement and Trigger Hemostasis and C3-Dependent Cytokine Release Ex Vivo in Human Whole Blood.

Venous air embolism, which may complicate medical and surgical procedures, activates complement and triggers thromboinflammation. In lepirudin-anticoagulated human whole blood, we examined the effect of air bubbles on complement and its role in thromboinflammation. Whole blood from 16 donors was incubated with air bubbles without or with inhibitors of C3, C5, C5aR1, or CD14. Complement activation, hemostasis, and cytokine release were measured using ELISA and quantitative PCR. Compared with no air, incubating blood with air bubbles increased, on average, C3a 6.5-fold, C3bc 6-fold, C3bBbP 3.7-fold, C5a 4.6-fold, terminal complement complex sC5b9 3.6-fold, prothrombin fragments 1+2 (PTF1+2) 25-fold, tissue factor mRNA (TF-mRNA) 26-fold, microparticle tissue factor 6.1-fold, ß-thromboglobulin 26-fold (all p < 0.05), and 25 cytokines 11-fold (range, 1.5-78-fold; all p < 0.0001). C3 inhibition attenuated complement and reduced PTF1+2 2-fold, TF-mRNA 5.4-fold, microparticle tissue factor 2-fold, and the 25 cytokines 2.7-fold (range, 1.4-4.9-fold; all p < 0.05). C5 inhibition reduced PTF1+2 2-fold and TF-mRNA 12-fold (all p < 0.05). C5 or CD14 inhibition alone reduced three cytokines, including IL-1ß (p = 0.02 and p = 0.03). Combined C3 and CD14 inhibition reduced all cytokines 3.9-fold (range, 1.3-9.5-fold; p < 0.003) and was most pronounced for IL-1ß (3.2- versus 6.4-fold), IL-6 (2.5- versus 9.3-fold), IL-8 (4.9- versus 8.6-fold), and IFN-γ (5- versus 9.5-fold). Antifoam activated complement and was avoided. PTF1+2 was generated in whole blood but not in plasma. In summary, air bubbles activated complement and triggered a C3-driven thromboinflammation. C3 inhibition reduced all mediators, whereas C5 inhibition reduced only TF-mRNA. Combined C5 and CD14 inhibition reduced IL-1ß release. These data have implications for future mechanistic studies and possible pharmacological interventions in patients with air embolism.

A little can go a long way: giving learners some context can enhance the benefits of pretesting.

Tests given to learners before they study new information can enhance the learning of that information. When responding to these pretests, learners typically generate answers that are incorrect but that are nevertheless helpful for improving the learning of the correct answers. The present research examined how providing learners with context prior to pretesting can enhance the benefits of pretesting. Across two experiments, participants were given a pretest for half of the to-be-learned information and then asked to read a passage about a fictional topic, an alien civilisation known as Yoffas (Experiment 1 and Experiment 2), or a unique fruit called the Anona (Experiment 2). Participants who read a short paragraph contextualising the to-be-learned information exhibited a significantly larger pretesting effect than participants who did not, with this interaction being observed regardless of whether memory was tested after a 5-min delay or 1-week delay, and regardless of whether contextualisation was manipulated between-subjects or within-subjects. These results suggest that what learners know prior to a pretest can have an impact on the extent to which learners benefit from that pretest.

Saved information is remembered less well than deleted information, if the saving process is perceived as reliable.

Prior research has shown that people are more likely to remember information that is deleted from a computer than information that is saved on a computer, presumably because saving serves as a form of cognitive offloading. Given recent concerns about the robustness and replicability of this "Google Effect," we conducted two experiments seeking to replicate and extend the phenomenon by identifying a potential boundary condition for when it is observed. In Experiment 1, we replicated the Google Effect, but only when participants experienced a practice phase demonstrating the reliability of the saving process. No evidence of a Google Effect was observed when participants experienced a practice phase demonstrating the saving process to be unreliable. In Experiment 2, we replicated the results of Experiment 1 in the reliable condition, while demonstrating the effect to be robust across 10 different topics of trivia statements. Taken together, these results suggest that the Google Effect is a replicable phenomenon, but that the perceived reliability of the saving process is critical for determining whether it is observed.

Effects of acute aerobic and resistance exercise on episodic memory function.

Accumulating research provides suggestive evidence that acute aerobic exercise may, potentially, enhance episodic memory function post-exercise. Limited research has evaluated whether acute resistance exercise may also enhance episodic memory post-exercise. Furthermore, whether these two exercise modalities have a differential effect on post-exercise episodic memory is relatively unknown. To address these research questions, three experimental studies were conducted (N = 104) among young adults (18-25 years). The experiments implemented acute bouts of aerobic or resistance exercise for 15 min. Episodic memory was comprehensively evaluated post-exercise with a list-learning paradigm and a computerised assessment of what-where-when aspects of episodic memory. Various manipulations (e.g., between vs. within-group) of the study design were implemented across the experiments. Across these three experiments, we failed to find consistent evidence of either type of acute exercise affecting episodic memory performance post-exercise.