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Every day a plethora of people-such as curators, boards, collection managers, donors, marketing staff, educators and even visitors-decide whose objects are collected, and which stories are featured on the website, showcased in an exhibit, or included in school programs- and, by extension, those that are not. Some, like Museums Victoria, have engaged in processes of repatriation and apology.2 As teachers we need to recognise and acknowledge that the study of History as a discipline has traditionally placed value on written archival records or academic writings, thus devaluing and excluding the oral and performance methods of preserving history used by First Nations people.3 Last year I returned to high-school History teaching with first-hand experience of the application of history in museums as well as aspirations to more closely work at the intersection of the two worlds. [...]the Paul Revere House does not house any archives. [...]his 1768 portrait hangs in the Museum of Fine Arts Boston alongside artist John Singleton Copley's many other works.

Infants with Congenital Heart Disease (CHD) are at risk for developmental delays, though the mechanisms of brain injury that impair development are unknown. Potential causes could include cerebral hypoxia and cerebrovascular instability. We hypothesized that we would detect significantly reduced cerebral oxygen saturation and greater cerebrovascular instability in CHD infants compared to the healthy controls. We performed a secondary analysis on a sample of 43 term infants (28 CHD, 15 healthy controls) that assessed prospectively in temporal cross-section before or at 12 days of age. CHD infants were assessed prior to open-heart surgery. Cerebral oxygen saturation levels were estimated using Near-Infrared Spectroscopy, and cerebrovascular stability was assessed with the response of cerebral oxygen saturation after a postural change (supine to sitting). Cerebral oxygen saturation was 9 points lower in CHD than control infants in both postures (β = -9.3; 95%CI = -17.68, -1.00; p = 0.028), even after controlling for differences in peripheral oxygen saturation. Cerebrovascular stability was significantly impaired in CHD compared to healthy infants (β = -2.4; 95%CI = -4.12, -.61; p = 0.008), and in CHD infants with single ventricle compared with biventricular defects (β = -1.5; 95%CI = -2.95, -0.05; p = 0.04). CHD infants had cerebral hypoxia and decreased cerebral oxygen saturation values following a postural change, suggesting cerebrovascular instability. Future longitudinal studies should assess the associations of cerebral hypoxia and cerebrovascular instability with long-term neurodevelopmental outcomes in CHD infants.

Understanding the vulnerability of marine calcifiers to ocean acidification is a critical issue, especially in the Southern Ocean (SO), which is likely to be the one of the first, and most severely affected regions. Since the industrial revolution, ~30% of anthropogenic CO 2 has been absorbed by the global oceans. Average surface seawater pH levels have already decreased by 0.1 and are projected to decline by ~0.3 by the year 2100. This process, known as ocean acidification (OA), is shallowing the saturation horizon, which is the depth below which calcium carbonate (CaCO 3 ) dissolves, likely increasing the vulnerability of many resident marine calcifiers to dissolution. The negative impact of OA may be seen first in species depositing more soluble CaCO 3 mineral phases such as aragonite and high-Mg calcite (HMC). Ocean warming could further exacerbate the effects of OA in these particular species. Here we combine a review and a quantitative meta-analysis to provide an overview of the current state of knowledge about skeletal mineralogy of major taxonomic groups of SO marine calcifiers and to make projections about how OA might affect a broad range of SO taxa. We consider a species' geographic range, skeletal mineralogy, biological traits, and potential strategies to overcome OA. The meta-analysis of studies investigating the effects of the OA on a range of biological responses such as shell state, development and growth rate illustrates that the response variation is largely dependent on mineralogical composition. Species-specific responses due to mineralogical composition indicate that taxa with calcitic, aragonitic, and HMC skeletons, could be at greater risk to expected future carbonate chemistry alterations, and low-Mg calcite (LMC) species could be mostly resilient to these changes. Environmental and biological control on the calcification process and/or Mg content in calcite, biological traits, and physiological processes are also expected to influence species-specific responses.

The Cape Darnley region in East Antarctica has been an area of scientific interest for a variety of disciplines over the last three decades. The recent acquisition of several high-resolution bathymetry datasets enabled the compilation of a detailed regional bathymetry grid. We present a high-resolution bathymetric compilation of the Cape Darnley region in East Antarctica, including areas of the Mac.Robertson Land shelf, slope and adjacent deep sea. A variety of data, single-beam and multibeam swath bathymetry and digitized depths from nautical charts were sourced from numerous institutions. The 100 m-resolution gridded bathymetric dataset improves previous bathymetric representations of the region and enables visualization of the seafloor morphology in unprecedented detail. The bathymetry grid has been constructed using a layered hierarchy approach based on the source of each dataset. This data compilation forms important baseline information for a range of scientific applications and end users including oceanographers, glacial modellers, biologists and geologists. The compilation will aid numerical modelling of ocean circulation, reconstruction of palaeo-ice streams and refinement of ice-sheet models.

We tested the potential for Gazefinder eye-tracking to support early autism identification, including feasible use with infants, and preliminary concurrent validity of trial-level gaze data against clinical assessment scores. We embedded the ~ 2-min ‘Scene 1S4’ protocol within a comprehensive clinical assessment for 54 consecutively-referred, clinically-indicated infants (prematurity-corrected age 9–14 months). Alongside % tracking rate as a broad indicator of feasible assessment/data capture, we report infant gaze data to pre-specified regions of interest (ROI) across four trial types and associations with scores on established clinical/behavioural tools. Most infants tolerated Gazefinder eye-tracking well, returning high overall % tracking rate. As a group, infants directed more gaze towards social vs. non-social (or more vs. less socially-salient) ROIs within trials. Behavioural autism features were correlated with increased gaze towards non-social/geometry (vs. social/people) scenes. No associations were found for gaze directed to ROIs within other stimulus types. Notably, there were no associations between developmental/cognitive ability or adaptive behaviour with gaze towards any ROI. Gazefinder assessment seems highly feasible with clinically-indicated infants, and the people vs. geometry stimuli show concurrent predictive validity for behavioural autism features. Aggregating data across the ~ 2-min autism identification protocol might plausibly offer greater utility than stimulus-level analysis alone.

Infants with congenital heart disease (CHD) may have impaired cerebral autoregulation (CA) associated with cerebral fractional tissue oxygen extraction (FTOE). We conducted a pilot study in nine CHD neonates to validate a noninvasive CA measure, cerebrovascular stability index (CSI), by eliciting responses to postural tilts. We compared CSI to an invasive measure of CA and to FTOE collected during tilts (FTOE Spot ). FTOE Spot correlated with CSI, as did the change in FTOE during tilts, but CSI’s correlation with impaired CA did not reach significance. Larger trials are indicated to validate CSI, allowing for noninvasive CA measurements and measurements in outpatient settings.

ObjectiveTo describe outcomes of acute coronavirus disease 2019 in paediatric and young adult patients with underlying cardiac disease and evaluate the association between cardiac risk factors and hospitalisation.Study designWe conducted a retrospective single-institution review of patients with known cardiac disease and positive severe acute respiratory syndrome coronavirus 2 RT-PCR from 1 March, 2020 to 30 November, 2020. Extracardiac comorbidities and cardiac risk factors were compared between those admitted for coronavirus disease 2019 illness and the rest of the cohort using univariate analysis.ResultsForty-two patients with a mean age of 7.7 ± 6.7 years were identified. Six were 18 years of age or more with the oldest being 22 years of age. Seventy-six percent were Hispanic. The most common cardiac diagnoses were repaired cyanotic (n = 7, 16.6%) and palliated single ventricle (n = 7, 16.6%) congenital heart disease. Fourteen patients (33.3%) had underlying syndromes or chromosomal anomalies, nine (21%) had chronic pulmonary disease and eight (19%) were immunosuppressed. Nineteen patients (47.6%) reported no symptoms. Sixteen (38.1%) reported only mild symptoms. Six patients (14.3%) were admitted to the hospital for acute coronavirus disease 2019 illness. Noncardiac comorbidities were associated with an increased risk of hospitalisation (p = 0.02), particularly chronic pulmonary disease (p = 0.01) and baseline supplemental oxygen requirement (p = 0.007). None of the single ventricle patients who tested positive required admission.ConclusionsHospitalisations for coronavirus disease 2019 were rare among children and young adults with underlying cardiac disease. Extracardiac comorbidities like pulmonary disease were associated with increased risk of hospitalisation while cardiac risk factors were not.

Complex congenital heart disease (CHD) is associated with neurodevelopmental impairment, the mechanism of which is unknown. Cerebral cortical dysmaturation in CHD is linked to white matter abnormalities, including developmental vulnerability of the subplate, in relation to oxygen delivery and metabolism deficits. In this study, we report associations between subcortical morphology and white matter metabolism in neonates with CHD using quantitative magnetic resonance imaging (MRI) and spectroscopy (MRS). Multi-modal brain imaging was performed in three groups of neonates close to term-equivalent age: (1) term CHD (n = 56); (2) preterm CHD (n = 37) and (3) preterm control group (n = 22). Thalamic volume and cerebellar transverse diameter were obtained in relation to cerebral metrics and white matter metabolism. Short echo single-voxel MRS of parietal and frontal white matter was used to quantitate metabolites related to brain maturation (n-acetyl aspartate [NAA], choline, myo-inositol), neurotransmitter (glutamate), and energy metabolism (glutamine, citrate, creatine and lactate). Multi-variate regression was performed to delineate associations between subcortical morphological measurements and white matter metabolism controlling for age and white matter injury. Reduced thalamic volume, most pronounced in the preterm control group, was associated with increased citrate levels in all three group in the parietal white matter. In contrast, reduced cerebellar volume, most pronounced in the preterm CHD group, was associated with reduced glutamine in parietal grey matter in both CHD groups. Single ventricle anatomy, aortic arch obstruction, and cyanotic lesion were predictive of the relationship between reduced subcortical morphometry and reduced GLX (particularly glutamine) in both CHD cohorts (frontal white matter and parietal grey matter). Subcortical morphological associations with brain metabolism were also distinct within each of the three groups, suggesting these relationships in the CHD groups were not directly related to prematurity or white matter injury alone. Taken together, these findings suggest that subplate vulnerability in CHD is likely relevant to understanding the mechanism of both cortical and subcortical dysmaturation in CHD infants. Future work is needed to link this potential pattern of encephalopathy of CHD (including the constellation of grey matter, white matter and brain metabolism deficits) to not only abnormal fetal substrate delivery and oxygen conformance, but also regional deficits in cerebral energy metabolism.

Objective: Term congenital heart disease (CHD) neonates display abnormalities of brain structure and maturation, which are possibly related to underlying patient factors and perioperative insults. Our primary goal was to delineate associations between clinical factors and postnatal brain microstructure in term CHD neonates using diffusion tensor imaging (DTI) magnetic resonance (MR) acquisition combined with complementary data-driven connectome and seed-based tractography quantitative analysis. Our secondary goal was to delineate associations between mild dysplastic structural abnormalities and connectome and seed-base tractography as our primary goal. Methods: Neonates undergoing cardiac surgery for CHD were prospectively recruited from two large centers. Both pre- and postoperative magnetic resonance (MR) brain scans were obtained. DTI in 42 directions was segmented to 90 regions using neonatal brain template and three weighted methods. Seed- based tractography was performed in parallel. Clinical data :18 patient-specific and 9 preoperative variables associated with preoperative scan and 6 intraoperative and 12 postoperative variables associated with postoperative scan. A composite Brain Dysplasia Score (BDS) was created including cerebellar, olfactory bulbs, and hippocampus abnormalities. The outcomes included (1) connectome metrics: cost and global/nodal efficiency (2) seed-based tractography: fractional anisotropy. Statistics: multiple regression with false discovery rate correction (FDR). Results: A total of 133 term neonates with complex CHD were prospectively enrolled and 110 had analyzable DTI. Multiple patient-specific factors including d-transposition of the great arteries physiology and severity of impairment of fetal cerebral substrate delivery were predictive of preoperative reduced cost (p<0.0073), reduced global/nodal efficiency (p <0.03). Multiple postoperative factors (extracorporeal membrane oxygenation [ECMO], seizures, cardiopulmonary resuscitation) were predictive of postoperative reduced cost, reduced global/nodal efficiency (p < 0.05). All three subcortical structures of the BDS (including olfactory bulb/sulcus, cerebellum, and hippocampus) predicted distinct patterns of altered nodal efficiency (p<0.05). Conclusion: Patient-specific and postoperative clinical factors were most predictive of diffuse postnatal microstructural dysmaturation in term CHD neonates. In contrast, subcortical components of a structurally based- brain dysplasia score, predicted more regional based postnatal microstructural differences. Collectively, these findings suggest that brain DTI connectome may facilitate deciphering the mechanistic relative contribution of clinical and genetic risk factors related to poor neurodevelopmental outcomes in CHD.