Coronary artery dilation in non-hospitalised children with asymptomatic or mild COVID-19.

INTRODUCTION: Infection with Sars-CoV-2 is known to cause cardiac injury and coronary artery changes in moderate to severe acute COVID-19 and post-acute multisystem inflammatory syndrome in children (MIS-C). However, little is known about the potential for cardiac involvement, in particular coronary artery dilation, in asymptomatic or mild cases of COVID-19. METHODS: A retrospective review of children ≤ 18 years of age with a history of asymptomatic or mild COVID-19 disease who underwent echocardiography after Sars-CoV-2 infection is conducted. Patients were excluded if they had been hospitalised for COVID-19/MIS-C or had a history of cardiac disease that could affect coronary artery dimension. Coronary artery dilation was defined as the Boston Z-score greater than 2.0. RESULTS: One hundred and fifty-seven patients met inclusion criteria with a mean age of 9.4 years (+/- 5.4 years). Eighty-four (54%) patients were identified as having COVID-19 through positive antibody testing. All patients underwent electrocardiogram and echocardiogram as part of their cardiology evaluation. One hundred and thirty-five (86%) patients had a normal evaluation or only a minor variant on electrocardiogram, while 22 patients had abnormalities on echocardiogram, 4 of which demonstrated coronary artery dilation based on the Boston Z-score. CONCLUSIONS: Much of the literature for post-infectious screening and follow-up focuses on patients with a history of moderate to severe COVID-19 disease, emphasising the need for surveillance for the potential development of myocarditis. In this study, 4 out of 157 (2.5%) children with a history of asymptomatic or mild COVID-19 disease without MIS-C were found to have some degree of coronary artery dilation. The significance of this finding currently remains unknown.

High trait anxiety blocks olfactory plasticity induced by aversive learning.

Aversive learning normally induces alterations in sensory function as the brain's sensory systems are tuned to optimize detection and discrimination of threat-predictive stimuli. Anxiety disorders can disrupt behavioral discrimination between threat-predictive and neutral stimuli, resulting in overgeneralization of negative affective responses to non-threatening situations. We thus hypothesized that anxiety could disrupt learning-induced improvement in sensory discrimination. We tested perceptual discrimination between similar odorants before and after discriminative aversive conditioning. Participants exhibiting normal levels of trait anxiety developed a larger skin conductance response (SCR) to the shock-predictive odorant and substantial improvement in their perceptual discrimination between the two odors. Repeated exposure to the odors without shock partially extinguished the SCRs but the perceptual effect persisted. By contrast, participants with high levels of trait anxiety developed comparably sized SCRs to both odors and displayed no perceptual improvement. Learning-induced perceptual plasticity can thus be impaired in people with high levels of trait anxiety.

Connecting older grandmothers raising grandchildren with community resources improves family resiliency, social support, and caregiver self-efficacy.

Custodial grandparenting can be especially challenging for older grandmothers facing age specific issues. Kinship navigator programs are social service delivery programs intended to inform grandparents and other relatives raising children about available resources and services, provide information specific to their individual needs, and help families navigate service systems. Our study utilizes self-report data from one kinship navigator federal demonstration project, which used a randomized control trial, to examine demographic characteristics for grandmothers under and over 55 years of age, whether grandmother caregivers (≥55 years) improve family resilience, social support, and caregiver self-efficacy, and which interventions improved outcomes for grandmothers (≥55 years). Each participant was randomly assigned to one of four groups: Usual Care (traditional child welfare services), Standard Care (family support and case management), Peer-to-Peer Care Only, and Full Kin Tech Care (peer navigators with computer access and interdisciplinary team). Thirty-nine percent of grandmothers (55-75 years) were mostly living in poverty, predominantly Caucasian, with 36% identifying as African American/Black, with at least one to two children at home. Repeated-measures ANOVAs for each subscale showed statistically significant within- and between-group differences for Family Functioning, Social Supports, Concrete Supports, Child Development, and Nurturing and Attachment, with the exception of Usual Care, which showed a decline in protective factors consistently across subscales. Future research with kinship families could qualitatively examine the experiences for older women in navigator programs and replication of kinship navigator programs could build capacity in data collection and maintenance systems to gain better perspective about how systems of care impact families.

Fear learning enhances neural responses to threat-predictive sensory stimuli.

The central nervous system rapidly learns that particular stimuli predict imminent danger. This learning is thought to involve associations between neutral and harmful stimuli in cortical and limbic brain regions, though associative neuroplasticity in sensory structures is increasingly appreciated. We observed the synaptic output of olfactory sensory neurons (OSNs) in individual mice before and after they learned that a particular odor indicated an impending foot shock. OSNs are the first cells in the olfactory system, physically contacting the odor molecules in the nose and projecting their axons to the brain's olfactory bulb. OSN output evoked by the shock-predictive odor was selectively facilitated after fear conditioning. These results indicate that affective information about a stimulus can be encoded in its very earliest representation in the nervous system.

Odor-specific, olfactory marker protein-mediated sparsening of primary olfactory input to the brain after odor exposure.

Long-term plasticity in sensory systems is usually conceptualized as changing the interpretation of the brain of sensory information, not an alteration of how the sensor itself responds to external stimuli. However, here we demonstrate that, in the adult mouse olfactory system, a 1-week-long exposure to an artificially odorized environment narrows the range of odorants that can induce neurotransmitter release from olfactory sensory neurons (OSNs) and reduces the total transmitter release from responsive neurons. In animals heterozygous for the olfactory marker protein (OMP), this adaptive plasticity was strongest in the populations of OSNs that originally responded to the exposure odorant (an ester) and also observed in the responses to a similar odorant (another ester) but had no effect on the responses to odorants dissimilar to the exposure odorant (a ketone and an aldehyde). In contrast, in OMP knock-out mice, odorant exposure reduced the number and amplitude of OSN responses evoked by all four types of odorants equally. The effect of this plasticity is to preferentially sparsen the primary neural representations of common olfactory stimuli, which has the computational benefit of increasing the number of distinct sensory patterns that could be represented in the circuit and might thus underlie the improvements in olfactory discrimination often observed after odorant exposure (Mandairon et al., 2006a). The absence of odorant specificity in this adaptive plasticity in OMP knock-out mice suggests a potential role for this protein in adaptively reshaping OSN responses to function in different environments.

Functional rehabilitation of cadmium-induced neurotoxicity despite persistent peripheral pathophysiology in the olfactory system.

Intranasal exposure to the heavy metal cadmium has been linked to olfactory dysfunction and neurotoxicity. Here, we combine optical imaging of in vivo neurophysiology, genetically defined anatomical tract tracing, mass spectrometry, and behavioral psychophysical methods to evaluate the persistent harmful effects of acute intranasal exposure to cadmium in a mouse model and to investigate the functional consequences of sensory rehabilitation training. We find that an acute intranasal instillation of cadmium chloride leads to an accumulation of cadmium in the brain's olfactory bulb that persists for at least 4 weeks. This is accompanied by persistent severe pathophysiology of the olfactory nerve, a gradual reduction in axonal projections from the olfactory epithelium, and complete impairment on an olfactory detection task. Remarkably, 2 weeks of odorant-guided operant conditioning training proved sufficient to restore olfactory detection performance to control levels in cadmium-exposed mice. Optical imaging from rehabilitated mice showed that this training did not cause any detectable restoration of olfactory nerve function, suggesting that the recovery of function was mediated by central neuroplasticity in which the brain learned to interpret the degraded sensory input. These data demonstrate that sensory learning can mask even severe damage from neurotoxicants and suggest that explicit sensory training may be useful in rehabilitation of olfactory dysfunction.