Proactive suppression is an implicit process that cannot be summoned on demand.

We examined whether proactive suppression can be applied on demand. A prompt cue indicated the to-be-ignored distractor color for each trial. Participants needed to use this cue to know which of two target shapes to respond to. To assess proactive suppression of the cued distractor color, we presented a probe letter recall task on a minority (25%) of the trials. A letter appeared inside each of the six shapes of the search array and participants recalled as many letters as they could. When the to-be-ignored color was fixed in Experiment 1, probe recall accuracy was lower for probe letters inside to-be-ignored-color distractors than target-color distractors, known as the probe suppression effect. However, when the prompted to-be-ignored color varied from trial to trial, the probe suppression effect disappeared, regardless of whether the prompt was a colored circle (Experiment 2) or a colored word (Experiment 3). Experiment 4 tested the search and destroy hypothesis by shortening the search display duration from 200 to 50 ms. No capture effect by the to-be-ignored color was evident, suggesting that participants did not first search for the to-be-ignored color, prior to suppressing it. We conclude that when rejection of a distractor color is required on demand, one cannot accomplish such suppression proactively but instead must deal with the distractor reactively, incurring a large cost in performance. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

On preventing capture: Does greater salience cause greater suppression?

It has been proposed that salient objects have high potential to disrupt target performance, and so people learn to proactively suppress them, thereby preventing these salient distractors from capturing attention in the future. Consistent with this hypothesis, Gaspar et al. (Proceedings of the National Academy of Sciences, 113(13), 3693-3698, 2016) reported that the PD (believed to index suppression) was larger for high-salient color distractors than for low-salient color distractors. The present study looked for converging evidence that salience triggers suppression using established behavior measures of suppression. Following Gaspar et al., our participants searched for a yellow target circle among nine background circles, which sometimes included one circle with a unique color. The distractor was either high or low in salience with respect to the background circles. The question was whether the high-salient color would be proactively suppressed more strongly than the low-salient color. This was assessed using the capture-probe paradigm. On 33% of trials, probe letters appeared inside colored circles and participants were to report those letters. If high-salient colors are more strongly suppressed, then probe recall accuracy should be lower at locations with the high-salient color than those with the low-salient color. Experiment 1 found no such effect. A similar finding was observed in Experiment 2 after addressing possible floor effects. These findings suggest that proactive suppression is not caused by salience. We propose that the PD reflects not only proactive suppression but also reactive suppression.

Do salient abrupt onsets trigger suppression?

Many studies have indicated that abrupt onsets can capture our attention involuntarily. The present study examined whether task-irrelevant onsets trigger strong suppression of their features, to reduce the ability of the onsets to capture attention. We used a capture-probe paradigm with salient abrupt onsets as precues. Participants performed a search task (70% of the trials) with occasional probe tasks mixed in (30% of the trials). In Experiment 1, two irrelevant-color distractors appeared simultaneously with the target, one of which was always precued by the abrupt onset. The question was whether an abrupt onset cue would promote suppression of the correlated color, thereby impeding recall of probe letters at a location with that color. This did not happen. The same result was obtained in Experiment 2, despite removing the target shape from the probe display to minimize floor effects and despite presenting only one distractor color per trial to further strengthen the onset-color association. In Experiment 3, one of the two irrelevant-color distractors abruptly onsetted 50 ms before the other search elements. Despite efforts to promote suppression of the cued distractor color, probe recall accuracy was again similar for the cued and non-cued distractor colors. We conclude that distractor features are suppressed but that making them especially salient does not noticeably enhance this suppression. The suppression mechanism is therefore geared towards helping observers discriminate between target features and distractor features, not towards beating down the most threatening object.

The role of visual working memory capacity in attention capture among video game players.

It is well established that attention can be captured by salient distractors. Some studies have found that action video game players were less susceptible to attention capture by irrelevant distractors than non-players. Other studies have also found that individuals with greater visual working memory capacity are less susceptible to capture by irrelevant distractors than individuals with lower visual working memory capacity. The present study examined whether action video game players were less susceptible to be captured by salient distractors and, if so, whether that relationship was due to greater visual working memory capacity. Participants completed a questionnaire reporting their video game playing experience, followed by a color change detection task assessing their visual working memory capacity. They then performed an attention capture task, where they determined the orientation of a bar within a shape singleton while attempting to ignore a color singleton distractor that appeared in 50% of the trials. Results showed that action video game players did not produce less capture effect than non-action video game players. However, high visual working memory capacity individuals produced less capture effect than low visual working memory capacity individuals regardless of their video game experience. These results suggest that the ability to resist capture by irrelevant distractors may be better explained by individual differences in visual working memory capacity than by action video game experience.

On preventing attention capture: Is singleton suppression actually singleton suppression?

It is commonly assumed that salient singletons generate an "attend-to-me signal" which causes suppression to develop over time, eventually preventing capture. Despite this assumption and the name "singleton suppression," a causal link between salience and suppression has not yet been clearly established. We point out the plausibility of a simple alternative mechanism: distractors might be suppressed because they are distractors rather than targets, even when non-salient. To look for evidence of salience-based suppression, we had participants search for a target shape among distractors, which sometimes included irrelevant-colored distractors. The critical manipulation was whether the irrelevant-colored distractor was salient (a color singleton) or non-salient (three non-target colored shapes; a triplet). On 30% of trials, probe letters were presented briefly inside each shape and participants were to report those letters. Probe recall below baseline indicates suppression. Experiment 1 showed that suppression was not triggered any more strongly by salient distractors (singletons) than by non-salient distractors (triplets). Experiment 2 showed that strong suppression effects developed rapidly even in the absence of salient singletons. These findings raise the thus far neglected question of whether salience plays any role in suppression.

Bacterial Infections After Burn Injuries: Impact of Multidrug Resistance.

Patients who are admitted to the hospital after sustaining a large burn injury are at high risk for developing hospital-associated infections. If patients survive the initial 72 hours after a burn injury, infections are the most common cause of death. Ventilator-associated pneumonia is the most important infection in this patient population. The risk of infections caused by multidrug-resistant bacterial pathogens increases with hospital length of stay in burn patients. In the first days of the postburn hospitalization, more susceptible, Gram-positive organisms predominate, whereas later more resistant Gram-negative organisms are found. These findings impact the choice of empiric antibiotics in critically ill burn patients. A proactive infection control approach is essential in burn units. Furthermore, a multidisciplinary approach to burn patients with a team that includes an infectious disease specialist and a pharmacist in addition to the burn surgeon is highly recommended.

Increasing Rates of Fluoroquinolone Resistance in Escherichia coli Isolated From the Blood and Urine of Patients with Hematologic Malignancies and Stem Cell Transplant Recipients.

Fluoroquinolone (FQ) antibiotics have been shown to reduce mortality and the number of febrile episodes when used as prophylaxis during neutropenia. Prior studies suggest that prophylaxis may result in increasing rates of FQ resistance. Fluoroquinolone non-susceptibility trends in Escherichia coli isolated from blood and urine cultures were evaluated over a 16-year period during which prophylaxis was initiated in patients with hematologic malignancies and stem cell transplants. Non-susceptibility rates increased after the introduction of prophylaxis, with yearly non-susceptibility rates rising from 30%-33% to 40%-88% in blood isolates. The high rates of non-susceptibility now observed raise concerns about the continued efficacy of FQ prophylaxis. This concern exists particularly in those patients undergoing stem cell transplants where the total FQ non-susceptibility rates over the study period were 82.3%. Further evaluation of the effect of FQ prophylaxis on antibiotic resistance and its efficacy in the setting of increased rates of resistance is warranted.

Systemic hypertension: the roles of salt, vascular Na+/K+ ATPase and the endogenous glycosides, ouabain and marinobufagenin.

Essential hypertension has been shown to be significantly associated with an increased risk for cardiovascular disease and is not well controlled in many patients. In a large portion of people with essential hypertension, sodium intake has been shown to play a significant role in the production of their hypertension. The mechanism through which increased sodium intake manifests hypertension is unresolved and likely multifactorial. Endogenous cardiac glycosides such as endogenous ouabain (EO) and marinobufagenin have been proposed to play a role in salt-sensitive essential hypertension through their inhibition of Na/K ATPase (NKA). The normal function of the NKA pump is to extrude Na from the intracellular environment and import K. Blocking the NKA disrupts its normal maintenance function. EO is proposed to produce alteration in smooth muscle cell contractility by inhibiting the α2-isoform of NKA, altering Na in a microdomain of the cell. In this region of the plasma membrane the α2-isoform of the NKA colocalizes with another transmembrane protein, the Na/Ca exchanger (NCX). The normal function of NCX is to extrude Ca and import Na. Inhibition of NKA produces an increase in Na within the microdomain, which in turn alters the function of the NCX so that less Ca is extruded, leading to increased intracellular Ca and increased vascular contraction. EO has been shown to be synthesized and secreted by the adrenal cortex in response to chronically elevated sodium intake. The levels of EO have been shown to be significantly elevated in 40% of all untreated hypertensive patients. Marinobufagenin, another cardiac glycoside, has also been implicated as a possible cause of essential hypertension through its preferential inhibition of the α1-isoform of NKA. Antagonism of the endogenous inhibitors of NKA is currently a target of clinical research for the development of innovative antihypertensive treatments.