Despite an extensive literature on the brain substrates of response inhibition, it still remains to be determined which is the best functional comparison to tease apart neural activity underlying this cognitive process. Here we aimed to shed light on this issue be recording event-related potentials while participants performed a modified stop-signal task that allowed us to compare the following conditions: successful versus unsuccessful response inhibitions, successful response inhibitions versus successful response executions, and easy versus difficult response inhibitions. Electrophysiological activity related to response inhibition was best isolated by comparing easy and difficult inhibitions. This activity was observed at fronto-central scalp electrodes between 260 and 300 milliseconds after stop-stimulus presentation. Notably, the stop-signal reaction time (an estimate of the time required to inhibit the motor response) fell within this window interval.

This study aimed to identify which ERP are specifically related to response inhibition. Electrophysiological activity was recorded from 30 subjects, and was submitted to a temporospatial principal component analysis to detect and quantify the main components associated with response inhibition. A modified go/nogo composed of three types of stimuli (frequentGo, infrequentGo, and infrequentNogo) was used to dissociate activity related to response inhibition from that related to novelty processing. InfrequentGo and infrequentNogo trials differed in the type of response (execution vs. inhibition), but not in their frequency of appearance. Neither the anterior nor the posterior N2 displayed larger amplitudes for infrequentNogo than infrequentGo trials. By contrast, both the anterior and the posterior P3 showed larger amplitudes for infrequentNogo than for infrequentGo trials. Present results suggest that P3 plays a key role in motor response inhibition. These findings substantiate and extend the current evidence and previous findings from our group.

There is extensive evidence that glucocorticoid hormones enhance memory consolidation, helping to ensure that emotionally significant events are well remembered. Prior findings suggest that the anteroventral region of bed nuclei of the stria terminalis (avBST) regulates glucocorticoid release, suggesting the potential for avBST activity to influence memory consolidation following an emotionally arousing learning event. To investigate this issue, male Sprague-Dawley rats underwent inhibitory avoidance training and repeated measurement of stress hormones, immediately followed by optogenetic manipulations of either the avBST or its projections to downstream regions, and 48 h later were tested for retention. The results indicate that avBST inhibition augmented posttraining pituitary-adrenal output and enhanced the memory for inhibitory avoidance training. Pretreatment with a glucocorticoid synthesis inhibitor blocked the memory enhancement as well as the potentiated corticosterone response, indicating the dependence of the memory enhancement on glucocorticoid release during the immediate posttraining period. In contrast, posttraining avBST stimulation decreased retention yet had no effect on stress hormonal output. Subsequent experiments revealed that inhibition of avBST input to the paraventricular hypothalamus enhanced stress hormonal output and subsequent retention, whereas stimulation did not affect either. Conversely, stimulation-but not inhibition-of avBST input to the ventrolateral periaqueductal gray impaired consolidation, whereas neither manipulation affected glucocorticoid secretion. These findings indicate that divergent pathways from the avBST are responsible for the mnemonic effects of avBST inhibition versus stimulation and do so via glucocorticoid-dependent and -independent mechanisms, respectively.

Hydra has a tubular bilayered epithelial body column with a dome-shaped head on one end and a foot on the other. Hydra lacks a permanent mouth: its head epithelium is sealed. Upon neuronal activation, a mouth opens at the apex of the head which can exceed the body column diameter in seconds, allowing Hydra to ingest prey larger than itself. While the kinematics of mouth opening are well characterized, the underlying mechanism is unknown. We show that Hydra mouth opening is generated by independent local contractions that require tissue-level coordination. We model the head epithelium as an active viscoelastic nonlinear spring network. The model reproduces the size, timescale and symmetry of mouth opening. It shows that radial contractions, travelling inwards from the outer boundary of the head, pull the mouth open. Nonlinear elasticity makes mouth opening larger and faster, contrary to expectations. The model correctly predicts changes in mouth shape in response to external forces. By generating innervated : nerve-free chimera in experiments and simulations, we show that nearest-neighbour mechanical signalling suffices to coordinate mouth opening. Hydra mouth opening shows that in the absence of long-range chemical or neuronal signals, short-range mechanical coupling is sufficient to produce long-range order in tissue deformations.

There is extensive evidence that glucocorticoid hormones enhance memory consolidation, helping to ensure that emotionally significant events are well remembered. Prior findings suggest that the anteroventral region of bed nuclei of the stria terminalis (avBST) regulates glucocorticoid release, suggesting the potential for avBST activity to influence memory consolidation following an emotionally arousing learning event. To investigate this issue, male Sprague-Dawley rats underwent inhibitory avoidance training and repeated measurement of stress hormones, immediately followed by optogenetic manipulations of either the avBST or its projections to downstream regions, and 48 h later were tested for retention. The results indicate that avBST inhibition augmented posttraining pituitary-adrenal output and enhanced the memory for inhibitory avoidance training. Pretreatment with a glucocorticoid synthesis inhibitor blocked the memory enhancement as well as the potentiated corticosterone response, indicating the dependence of the memory enhancement on glucocorticoid release during the immediate posttraining period. In contrast, posttraining avBST stimulation decreased retention yet had no effect on stress hormonal output. Subsequent experiments revealed that inhibition of avBST input to the paraventricular hypothalamus enhanced stress hormonal output and subsequent retention, whereas stimulation did not affect either. Conversely, stimulation-but not inhibition-of avBST input to the ventrolateral periaqueductal gray impaired consolidation, whereas neither manipulation affected glucocorticoid secretion. These findings indicate that divergent pathways from the avBST are responsible for the mnemonic effects of avBST inhibition versus stimulation and do so via glucocorticoid-dependent and -independent mechanisms, respectively.

The multifaceted long-term impairments resulting from critical illness and COVID-19 require interdisciplinary management approaches in the recovery phase of illness. Operational insights into the structure and process of recovery clinics (RCs) from heterogeneous health systems are needed. This study describes the structure and process characteristics of existing and newly implemented ICU-RCs and COVID-RCs in a subset of large health systems in the United States.

Design

Cross-sectional survey.

Setting

Thirty-nine RCs, representing a combined 156 hospitals within 29 health systems participated.

Patients

None.

Interventions

None.

Measurement and main results

RC demographics, referral criteria, and operating characteristics were collected, including measures used to assess physical, psychologic, and cognitive recoveries. Thirty-nine RC surveys were completed (94% response rate). ICU-RC teams included physicians, pharmacists, social workers, physical therapists, and advanced practice providers. Funding sources for ICU-RCs included clinical billing (n = 20, 77%), volunteer staff support (n = 15, 58%), institutional staff/space support (n = 13, 46%), and grant or foundation funding (n = 3, 12%). Forty-six percent of RCs report patient visit durations of 1 hour or longer. ICU-RC teams reported use of validated scales to assess psychologic recovery (93%), physical recovery (89%), and cognitive recovery (86%) more often in standard visits compared with COVID-RC teams (psychologic, 54%; physical, 69%; and cognitive, 46%).

Conclusions

Operating structures of RCs vary, though almost all describe modest capacity and reliance on volunteerism and discretionary institutional support. ICU- and COVID-RCs in the United States employ varied funding sources and endorse different assessment measures during visits to guide care coordination. Common features include integration of ICU clinicians, interdisciplinary approach, and focus on severe critical illness. The heterogeneity in RC structures and processes contributes to future research on the optimal structure and process to achieve the best postintensive care syndrome and postacute sequelae of COVID outcomes.

Objective

To determine the impact of policy changes for pulse oximetry oxygen saturation (SpO₂) alarm limits on neonatal mortality and morbidity among infants born very preterm.

Study design

This was a retrospective cohort study of infants born very preterm in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network. Infants were classified based on treatment at a hospital with an SpO₂ alarm policy change and study epoch (before vs after policy change). We used a generalized linear mixed model to determine the effect of hospital group and epoch on the primary outcomes of mortality and severe retinopathy of prematurity (ROP) and secondary outcomes of necrotizing enterocolitis, bronchopulmonary dysplasia, and any ROP.

Results

There were 3809 infants in 10 hospitals with an SpO₂ alarm policy change and 3685 infants in 9 hospitals without a policy change. The nature of most policy changes was to narrow the SpO₂ alarm settings. Mortality was lower in hospitals without a policy change (aOR 0.63; 95% CI 0.50-0.80) but did not differ between epochs in policy change hospitals. The odds of bronchopulmonary dysplasia were greater for hospitals with a policy change (aOR 1.65; 95% CI 1.36-2.00) but did not differ for hospitals without a policy change. Severe ROP and necrotizing enterocolitis did not differ between epochs for either group. The adjusted odds of any ROP were lower in recent years in both hospital groups.

Conclusions

Changing SpO₂ alarm policies was not associated with reduced mortality or increased severe ROP among infants born very preterm.