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2.
Hosp Pediatr ; 2021 Dec 01.
Article in English | MEDLINE | ID: mdl-34808670

ABSTRACT

BACKGROUND: The coronavirus disease 2019 pandemic has required modifications to family-centered rounds (FCR), although the specific changes and the effects on patients, families, and providers are not well known. In this study, we explore physician perspectives on changes made to FCR during the initial wave of the coronavirus disease 2019 pandemic and recommendations for the future. METHODS: Semistructured individual interviews were conducted with 20 pediatric attending and resident physicians who cared for hospitalized patients between March and May 2020 on pediatric hospital medicine and subspecialty services that typically perform FCR. Transcripts were reviewed by using principles of framework analysis to iteratively develop a codebook. Review of coded segments, with attention to code co-occurrences, was used to clarify themes in the data relating to the research objective and the conceptual framework. RESULTS: The rounding format changed for all providers and varied on the basis of clinical service and phase of the pandemic. Themes highlighted specific areas of change: (1) the process of FCR, (2) reaching consensus with families, (3) collaboration with members of the medical team, and (4) resident education, modeling, and supervision. Participants offered recommendations, including standardization of rounds, intentional involvement of nursing staff, and inclusion of families through virtual or small-group bedside rounds. CONCLUSIONS: The pandemic led to a variety of modifications to FCR, and these changes had varied effects on communication and education. These findings provide insight into the state of FCR during the pandemic and may frame future recommendations for the development of shared guidelines for circumstances requiring limited bedside rounding.

3.
Med Sci Educ ; 31(2): 313-314, 2021 Apr.
Article in English | MEDLINE | ID: mdl-33643686

ABSTRACT

As COVID-19 necessitated student removal from clinical environments, a virtual curriculum involving existing and novel clerkship elements was developed that utilized near peers for both teaching and feedback. Shelf scores, engagement, and satisfaction demonstrated success of these new curricular elements, many of which will be incorporated for future students.

4.
Article in English | MEDLINE | ID: mdl-31167805

ABSTRACT

Heterozygous deleterious variants in PHIP have been associated with behavioral problems, intellectual disability/developmental delay, obesity/overweight, and dysmorphic features (BIDOD syndrome). We report an additional 10 individuals with pleckstrin homology domain-interacting protein (PHIP)-predicted deleterious variants (four frameshift, three missense, two nonsense, and one splice site; six of which are confirmed de novo). The mutation spectrum is diverse, and there is no clustering of mutations across the protein. The clinical phenotype of these individuals is consistent with previous reports and includes behavioral problems, intellectual disability, developmental delay, hypotonia, and dysmorphic features. The additional individuals we report have a lower frequency of obesity than previous reports and a higher frequency of gastrointestinal problems, social deficits, and behavioral challenges. Characterizing additional individuals with diverse mutations longitudinally will provide better natural history data to assist with medical management and educational and behavioral support.


Subject(s)
Intracellular Signaling Peptides and Proteins/genetics , Intracellular Signaling Peptides and Proteins/metabolism , Abnormalities, Multiple/genetics , Adolescent , Child , Child, Preschool , Developmental Disabilities/genetics , Exome/genetics , Female , Frameshift Mutation/genetics , Heterozygote , Humans , Imidazoles , Infant , Intellectual Disability/genetics , Male , Muscle Hypotonia/genetics , Mutation/genetics , Phenotype , Transcription Factors/genetics , Exome Sequencing/methods
5.
J Am Acad Child Adolesc Psychiatry ; 57(3): 166-174, 2018 03.
Article in English | MEDLINE | ID: mdl-29496125

ABSTRACT

OBJECTIVE: Working memory (WM) deficits are consistently reported in schizophrenia and are related to poor functional outcomes. Functional magnetic resonance imaging studies of adult-onset schizophrenia have reported decreased functional activations and connectivity in the WM network, but no prior functional magnetic resonance imaging study has examined WM in childhood-onset schizophrenia (COS). The aim of this study was to examine the neural correlates of WM in COS. METHOD: Adult patients with COS (n = 32, 21.3 ± 1.1 years), nonpsychotic siblings of patients with COS (n = 30, 19.4 ± 0.8 years), and healthy controls (n = 39, 20.0 ± 0.7 years) completed 1- and 2-back WM tasks during 3-T functional magnetic resonance imaging. Functional activation and connectivity analyses were conducted. A separate group of 23 younger patients with COS (17.9 ± 7.4 years) could not perform the tasks after twice completing a standard training and are not included in this report. RESULTS: Patients with COS who were included scored significantly lower than controls on all tasks (p < .001). Patients with COS showed significantly lower activations in the dorsolateral prefrontal cortices, posterior parietal cortices, cerebellum, and caudate and decreased frontoparietal and corticostriatal functional connectivity compared with controls (p < .05, corrected). Siblings had functional activations and connectivity intermediate between those of patients and controls in a similar set of regions (p < .05, corrected). In patients, functional connectivity strength in the left frontoparietal network correlated positively with accuracy scores during the 1-back task (p = .0023, corrected). CONCLUSION: Decreased functional activation and connectivity in the WM network in COS supports pathophysiologic continuity with adult-onset schizophrenia. The low participation rate and accuracy of the patients highlights the disease severity of COS. Hypo-activations and hypo-connectivity were shared by siblings of patients with COS, suggesting COS as a potential endophenotype. CLINICAL TRIAL REGISTRATION INFORMATION: Evaluating Genetic Risk Factors for Childhood-Onset Schizophrenia; http://ClinicalTrials.gov;NCT00001198.


Subject(s)
Brain/physiopathology , Memory, Short-Term/physiology , Neural Pathways/physiopathology , Schizophrenia, Childhood/complications , Adult , Brain Mapping/methods , Endophenotypes , Female , Humans , Image Processing, Computer-Assisted , Magnetic Resonance Imaging , Male , Schizophrenia, Childhood/genetics , Schizophrenic Psychology , Siblings , Young Adult
6.
Schizophr Res ; 197: 71-77, 2018 07.
Article in English | MEDLINE | ID: mdl-29146021

ABSTRACT

OBJECTIVE: This study investigated symptom dimensions and subgroups in the National Institute of Mental Health (NIMH) childhood-onset schizophrenia (COS) cohort and their similarities to adult-onset schizophrenia (AOS) literature. METHOD: Scores from the Scales for the Assessment of Positive and Negative Symptoms (SAPS & SANS) from 125 COS patients were assessed for fit with previously established symptom dimensions from AOS literature using confirmatory factor analysis (CFA). K-means cluster analysis of each individual's scores on the best fitting set of dimensions was used to form patient clusters, which were then compared using demographic and clinical data. RESULTS: CFA showed the SAPS & SANS data was well suited to a 2-dimension solution, including positive and negative dimensions, out of five well established models. Cluster analysis identified three patient groups characterized by different dimension scores: (1) low scores on both dimensions, (2) high negative, low positive scores, and (3) high scores on both dimensions. These groups had different Full scale IQ, Children's Global Assessment Scale (CGAS) scores, ages of onset, and prevalence of some co-morbid behavior disorders (all p<3.57E-03). CONCLUSION: Our analysis found distinct symptom-based subgroups within the NIMH COS cohort using an established AOS symptom structure. These findings confirm the heterogeneity of COS and were generally consistent with AOS literature.


Subject(s)
Schizophrenia/classification , Schizophrenia/physiopathology , Adolescent , Age of Onset , Child , Cluster Analysis , Factor Analysis, Statistical , Female , Humans , Longitudinal Studies , Male
7.
Neurochem Res ; 42(9): 2646-2657, 2017 Sep.
Article in English | MEDLINE | ID: mdl-28285415

ABSTRACT

Glutamate carboxypeptidase II (GCPII) inactivates the peptide neurotransmitter N-acetylaspartylglutamate (NAAG) following synaptic release. Inhibitors of GCPII increase extracellular NAAG levels and are efficacious in animal models of clinical disorders via NAAG activation of a group II metabotropic glutamate receptor. mGluR2 and mGluR3 knock-out (ko) mice were used to test the hypothesis that mGluR3 mediates the activity of GCPII inhibitors ZJ43 and 2-PMPA in animal models of memory and memory loss. Short- (1.5 h) and long- (24 h) term novel object recognition tests were used to assess memory. Treatment with ZJ43 or 2-PMPA prior to acquisition trials increased long-term memory in mGluR2, but not mGluR3, ko mice. Nine month-old triple transgenic Alzheimer's disease model mice exhibited impaired short-term novel object recognition memory that was rescued by treatment with a NAAG peptidase inhibitor. NAAG peptidase inhibitors and the group II mGluR agonist, LY354740, reversed the short-term memory deficit induced by acute ethanol administration in wild type mice. 2-PMPA also moderated the effect of ethanol on short-term memory in mGluR2 ko mice but failed to do so in mGluR3 ko mice. LY354740 and ZJ43 blocked ethanol-induced motor activation. Both GCPII inhibitors and LY354740 also significantly moderated the loss of motor coordination induced by 2.1 g/kg ethanol treatment. These data support the conclusion that inhibitors of glutamate carboxypeptidase II are efficacious in object recognition models of normal memory and memory deficits via an mGluR3 mediated process, actions that could have widespread clinical applications.


Subject(s)
Alcoholic Intoxication/metabolism , Alzheimer Disease/metabolism , Glutamate Carboxypeptidase II/metabolism , Memory/physiology , Receptors, Metabotropic Glutamate/deficiency , Urea/analogs & derivatives , Alcoholic Intoxication/genetics , Alzheimer Disease/genetics , Animals , Disease Models, Animal , Ethanol/administration & dosage , Excitatory Amino Acid Antagonists/pharmacology , Glutamate Carboxypeptidase II/antagonists & inhibitors , Glutamate Carboxypeptidase II/genetics , Male , Memory/drug effects , Memory Disorders/genetics , Memory Disorders/metabolism , Mice , Mice, 129 Strain , Mice, Knockout , Mice, Transgenic , Motor Activity/drug effects , Motor Activity/physiology , Receptors, Metabotropic Glutamate/antagonists & inhibitors , Urea/pharmacology
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