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Article ; Online: Are Parent Discharge Readiness Scores Effective for Patients With Congenital Heart Disease After Cardiac Surgery?

Kim, Michael E / Kasparian, Nadine A / Zang, Huaiyu / Pater, Colleen / Chlebowski, Meghan M / Marcuccio, Elisa / Florez, Amy / Morales, David L S / Madsen, Nicolas / Moore, Ryan A

The Journal of pediatrics

2023 Volume 257, Page(s) 113361

Abstract: Objective: To assess discharge readiness and clinical engagement post-discharge in families of children undergoing congenital heart surgery.: Study design: This prospective cross-sectional study was performed at a major tertiary pediatric cardiac ... ...

Abstract	Objective: To assess discharge readiness and clinical engagement post-discharge in families of children undergoing congenital heart surgery. Study design: This prospective cross-sectional study was performed at a major tertiary pediatric cardiac referral center. Eligible parents and caregivers completed a discharge readiness tool, the Readiness for Hospital Discharge Scale for Parents of Hospitalized Children, via online survey on the day of discharge. Clinical engagement data included subsequent phone calls, clinic visits, emergency department visits, and hospital readmissions. Readiness for Hospital Discharge Scale for Parents of Hospitalized Children scores were measured as follows: very high (9-10), high (8-8.9), moderate (7-7.9), and low (<7). Descriptive statistics were used to describe demographic data. Results: In total, 128 families enrolled between April and December 2021. Parent discharge readiness scores ranged from "high" to "very high." Families with lower socioeconomic status and younger patients (especially single-ventricle infants or "interstage") had a greater proportion of clinic visits, emergency department visits, and hospital readmissions within 30-days postdischarge compared with other groups. Conclusions: Discharge readiness scores were not associated with clinical engagement. We identified vulnerable populations as evidenced by a greater frequency of clinical engagement in the immediate postoperative period, particularly younger patients and first-time surgeries. Although these visits may be appropriate, novel programs could enhance education and emotional support to prevent delay in seeking care or creating excessive stress and anxiety after discharge.
MeSH term(s)	Infant ; Humans ; Child ; Patient Discharge ; Aftercare ; Prospective Studies ; Cross-Sectional Studies ; Parents/psychology ; Heart Defects, Congenital/surgery ; Cardiac Surgical Procedures
Language	English
Publishing date	2023-02-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3102-1
ISSN	1097-6833 ; 0022-3476
ISSN (online)	1097-6833
ISSN	0022-3476
DOI	10.1016/j.jpeds.2023.02.008
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Article ; Online: Predictors for Screen Time Exposure among Children between 3 and 5 Years Old in Southern Brazil.

Frata, Bruna / Souza, Janaina M / Montemezzo, Dayane / Henning, Elisa / Menegol, Natalia A / Okubo, Rodrigo / Sonza, Anelise / Sanada, Luciana S

Journal of tropical pediatrics

2021 Volume 67, Issue 5

Abstract: Background: The use of technology is an increasingly common practice among preschoolers. Little is known about the relationship between screen time exposure (STE) and aspects related to family and the environment.: Aim: The aim is to characterize STE ...

Abstract	Background: The use of technology is an increasingly common practice among preschoolers. Little is known about the relationship between screen time exposure (STE) and aspects related to family and the environment. Aim: The aim is to characterize STE in Brazilian children aged between 3 and 5 years. Furthermore, the objective of this study is to associate the STE of children and of their parents with sociodemographic variables. Methods: Children aged between 3 and 5 years from southern Brazil and their parents participated in this study. To investigate STE, the researchers developed a specific questionnaire. To compare STE between age groups, the Kruskal-Wallis test was performed, followed by Dunn's post hoc test. Spearman's correlation and linear regression were used to correlate the variables. Results: Children (n = 237) spend an average of 3.7 ± 0.8 h/day in front of screens. The STE of children had a moderately positive correlation with the STE of their parents (r = 0.4; p-value < 0.001). Only the variables of the children's and parents' STE had a significant and positive association. The model is significant (F = 6164, p-value < 0.001) and the residuals of the model met the necessary assumptions, with normal distribution, constant variance and without the presence of outliers. Conclusion: Children in southern Brazil remain in front of screens four times longer than the recommended amount of time. It was also found that the STE of parents directly influences that of their children.
MeSH term(s)	Brazil/epidemiology ; Child ; Child, Preschool ; Humans ; Screen Time ; Surveys and Questionnaires
Language	English
Publishing date	2021-11-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	800065-7
ISSN	1465-3664 ; 0449-3281 ; 0142-6338
ISSN (online)	1465-3664
ISSN	0449-3281 ; 0142-6338
DOI	10.1093/tropej/fmab092
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Article ; Online: Sustained effects of rapidly acting antidepressants require BDNF-dependent MeCP2 phosphorylation.

Kim, Ji-Woon / Autry, Anita E / Na, Elisa S / Adachi, Megumi / Björkholm, Carl / Kavalali, Ege T / Monteggia, Lisa M

Nature neuroscience

2021 Volume 24, Issue 8, Page(s) 1100–1109

Abstract: The rapidly acting antidepressants ketamine and scopolamine exert behavioral effects that can last from several days to more than a week in some patients. The molecular mechanisms underlying the maintenance of these antidepressant effects are unknown. ... ...

Abstract	The rapidly acting antidepressants ketamine and scopolamine exert behavioral effects that can last from several days to more than a week in some patients. The molecular mechanisms underlying the maintenance of these antidepressant effects are unknown. Here we show that methyl-CpG-binding protein 2 (MeCP2) phosphorylation at Ser421 (pMeCP2) is essential for the sustained, but not the rapid, antidepressant effects of ketamine and scopolamine in mice. Our results reveal that pMeCP2 is downstream of BDNF, a critical factor in ketamine and scopolamine antidepressant action. In addition, we show that pMeCP2 is required for the long-term regulation of synaptic strength after ketamine or scopolamine administration. These results demonstrate that pMeCP2 and associated synaptic plasticity are essential determinants of sustained antidepressant effects.
MeSH term(s)	Animals ; Antidepressive Agents/pharmacology ; Brain/drug effects ; Brain/metabolism ; Brain-Derived Neurotrophic Factor/metabolism ; Ketamine/pharmacology ; Methyl-CpG-Binding Protein 2/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neuronal Plasticity/drug effects ; Neuronal Plasticity/physiology ; Phosphorylation ; Scopolamine/pharmacology
Chemical Substances	Antidepressive Agents ; Bdnf protein, mouse ; Brain-Derived Neurotrophic Factor ; Mecp2 protein, mouse ; Methyl-CpG-Binding Protein 2 ; Ketamine (690G0D6V8H) ; Scopolamine (DL48G20X8X)
Language	English
Publishing date	2021-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1420596-8
ISSN	1546-1726 ; 1097-6256
ISSN (online)	1546-1726
ISSN	1097-6256
DOI	10.1038/s41593-021-00868-8
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Zs.A 4891: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Primate-specific ZNF808 is essential for pancreatic development in humans.

Nature genetics

2023 Volume 55, Issue 12, Page(s) 2075–2081

Abstract: Identifying genes linked to extreme phenotypes in humans has the potential to highlight biological processes not shared with all other mammals. Here, we report the identification of homozygous loss-of-function variants in the primate-specific gene ZNF808 ...

Abstract	Identifying genes linked to extreme phenotypes in humans has the potential to highlight biological processes not shared with all other mammals. Here, we report the identification of homozygous loss-of-function variants in the primate-specific gene ZNF808 as a cause of pancreatic agenesis. ZNF808 is a member of the KRAB zinc finger protein family, a large and rapidly evolving group of epigenetic silencers which target transposable elements. We show that loss of ZNF808 in vitro results in aberrant activation of regulatory potential contained in the primate-specific transposable elements it represses during early pancreas development. This leads to inappropriate specification of cell fate with induction of genes associated with liver identity. Our results highlight the essential role of ZNF808 in pancreatic development in humans and the contribution of primate-specific regions of the human genome to congenital developmental disease.
MeSH term(s)	Animals ; Humans ; Cell Differentiation ; DNA Transposable Elements ; Genome, Human ; Primates/abnormalities ; Primates/genetics ; DNA-Binding Proteins/genetics ; Congenital Abnormalities/genetics ; Pancreas/abnormalities
Chemical Substances	DNA Transposable Elements ; ZNF808 protein, human ; DNA-Binding Proteins
Language	English
Publishing date	2023-11-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-023-01565-x
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Zs.A 3613: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 46: Show issues

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Article ; Online: Decreased sensitivity to the anorectic effects of leptin in mice that lack a Pomc-specific neural enhancer.

Na, Elisa S / Lam, Daniel D / Yokosawa, Eva / Adams, Jessica M / Olson, David P / Low, Malcolm J

PloS one

2020 Volume 15, Issue 12, Page(s) e0244793

Abstract: Enhancer redundancy has been postulated to provide a buffer for gene expression against genetic and environmental perturbations. While work in Drosophila has identified functionally overlapping enhancers, work in mammalian models has been limited. ... ...

Abstract	Enhancer redundancy has been postulated to provide a buffer for gene expression against genetic and environmental perturbations. While work in Drosophila has identified functionally overlapping enhancers, work in mammalian models has been limited. Recently, we have identified two partially redundant enhancers, nPE1 and nPE2, that drive proopiomelanocortin gene expression in the hypothalamus. Here we demonstrate that deletion of nPE1 produces mild obesity while knockout of nPE2 has no discernible metabolic phenotypes. Additionally, we show that acute leptin administration has significant effects on nPE1 knockout mice, with food intake and body weight change significantly impacted by peripheral leptin treatment. nPE1 knockout mice became less responsive to leptin treatment over time as percent body weight change increased over 2 week exposure to peripheral leptin. Both Pomc and Agrp mRNA were not differentially affected by chronic leptin treatment however we did see a decrease in Pomc and Agrp mRNA in both nPE1 and nPE2 knockout calorie restricted mice as compared to calorie restricted PBS-treated WT mice. Collectively, these data suggest dynamic regulation of Pomc by nPE1 such that mice with nPE1 knockout become less responsive to the anorectic effects of leptin treatment over time. Our results also support our earlier findings in which nPE2 may only be critical in adult mice that lack nPE1, indicating that these neural enhancers work synergistically to influence metabolism.
MeSH term(s)	Animals ; Appetite Depressants/pharmacology ; Body Weight/drug effects ; Eating/drug effects ; Enhancer Elements, Genetic ; Hypothalamus/drug effects ; Hypothalamus/metabolism ; Leptin/pharmacology ; Male ; Mice ; Mice, Knockout ; Neurons/drug effects ; Neurons/metabolism ; Pro-Opiomelanocortin/genetics
Chemical Substances	Appetite Depressants ; Leptin ; Pro-Opiomelanocortin (66796-54-1)
Language	English
Publishing date	2020-12-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0244793
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Article ; Online: Human Retrotransposons and the Global Shutdown of Homeostatic Innate Immunity by Oncolytic Parvovirus H-1PV in Pancreatic Cancer.

Neulinger-Muñoz, Matthias / Schaack, Dominik / Grekova, Svetlana P / Bauer, Andrea S / Giese, Thomas / Salg, Gabriel A / Espinet, Elisa / Leuchs, Barbara / Heller, Anette / Nüesch, Jürg P F / Schenk, Miriam / Volkmar, Michael / Giese, Nathalia A

Viruses

2021 Volume 13, Issue 6

Abstract: ... human endogenous retroviruses (HERVs), were evaluated using qRT-PCR, ELISA, Western blot, and RNA-Seq techniques ...

Abstract	Although the oncolytic parvovirus H-1PV has entered clinical trials, predicting therapeutic success remains challenging. We investigated whether the antiviral state in tumor cells determines the parvoviral oncolytic efficacy. The interferon/interferon-stimulated genes (IFN/ISG)-circuit and its major configurator, human endogenous retroviruses (HERVs), were evaluated using qRT-PCR, ELISA, Western blot, and RNA-Seq techniques. In pancreatic cancer cell lines, H-1PV caused a late global shutdown of innate immunity, whereby the concomitant inhibition of HERVs and IFN/ISGs was co-regulatory rather than causative. The growth-inhibitory IC50 doses correlated with the power of suppression but not with absolute ISG levels. Moreover, H-1PV was not sensitive to exogenous IFN despite upregulated antiviral ISGs. Such resistance questioned the biological necessity of the oncotropic ISG-shutdown, which instead might represent a surrogate marker for personalized oncolytic efficacy. The disabled antiviral homeostasis may modify the activity of other viruses, as demonstrated by the reemergence of endogenous AluY-retrotransposons. This way of suppression may compromise the interferogenicity of drugs having gemcitabine-like mechanisms of action. This shortcoming in immunogenic cell death induction is however amendable by immune cells which release IFN in response to H-1PV.
MeSH term(s)	Cell Death/immunology ; Cell Line, Tumor ; Cytokines ; H-1 parvovirus/immunology ; H-1 parvovirus/pathogenicity ; Homeostasis/immunology ; Humans ; Immunity, Innate ; Interferons/immunology ; Leukocytes, Mononuclear/virology ; Oncolytic Viruses/genetics ; Oncolytic Viruses/immunology ; Oncolytic Viruses/pathogenicity ; Pancreatic Neoplasms/virology ; Parvoviridae Infections/complications ; Parvoviridae Infections/virology
Chemical Substances	Cytokines ; Interferons (9008-11-1)
Language	English
Publishing date	2021-05-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v13061019
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Article ; Online: Decreased sensitivity to the anorectic effects of leptin in mice that lack a Pomc-specific neural enhancer.

Elisa S Na / Daniel D Lam / Eva Yokosawa / Jessica M Adams / David P Olson / Malcolm J Low

PLoS ONE, Vol 15, Iss 12, p e

2020 Volume 0244793

Abstract	Enhancer redundancy has been postulated to provide a buffer for gene expression against genetic and environmental perturbations. While work in Drosophila has identified functionally overlapping enhancers, work in mammalian models has been limited. Recently, we have identified two partially redundant enhancers, nPE1 and nPE2, that drive proopiomelanocortin gene expression in the hypothalamus. Here we demonstrate that deletion of nPE1 produces mild obesity while knockout of nPE2 has no discernible metabolic phenotypes. Additionally, we show that acute leptin administration has significant effects on nPE1 knockout mice, with food intake and body weight change significantly impacted by peripheral leptin treatment. nPE1 knockout mice became less responsive to leptin treatment over time as percent body weight change increased over 2 week exposure to peripheral leptin. Both Pomc and Agrp mRNA were not differentially affected by chronic leptin treatment however we did see a decrease in Pomc and Agrp mRNA in both nPE1 and nPE2 knockout calorie restricted mice as compared to calorie restricted PBS-treated WT mice. Collectively, these data suggest dynamic regulation of Pomc by nPE1 such that mice with nPE1 knockout become less responsive to the anorectic effects of leptin treatment over time. Our results also support our earlier findings in which nPE2 may only be critical in adult mice that lack nPE1, indicating that these neural enhancers work synergistically to influence metabolism.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: [No title information]

Mitra, Anish R / Fergusson, Nicholas A / Lloyd-Smith, Elisa / Wormsbecker, Andrew / Foster, Denise / Karpov, Andrei / Crowe, Sarah / Haljan, Greg / Chittock, Dean R / Kanji, Hussein D / Sekhon, Mypinder S / Griesdale, Donald E G

CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne

2020 Volume 192, Issue 47, Page(s) E1550–E1558

Title translation	Caractéristiques de départ et issues chez des patients atteints de COVID-19 hospitalisés dans des unités de soins intensifs à Vancouver (Canada) : série de cas.
MeSH term(s)	Aged ; COVID-19/diagnosis ; COVID-19/epidemiology ; COVID-19/mortality ; COVID-19/therapy ; COVID-19 Testing ; Canada/epidemiology ; Critical Care ; Female ; Hospitalization ; Humans ; Male ; Middle Aged ; Severity of Illness Index ; Treatment Outcome
Language	French
Publishing date	2020-09-19
Publishing country	Canada
Document type	Journal Article ; Multicenter Study
ZDB-ID	215506-0
ISSN	1488-2329 ; 0008-4409 ; 0820-3946
ISSN (online)	1488-2329
ISSN	0008-4409 ; 0820-3946
DOI	10.1503/cmaj.200794-f
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Ua VI Zs.136: Show issues

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Article ; Online: Perinatal exposure to high fat diet alters expression of MeCP2 in the hypothalamus.

Frayre, Jessica / Frayre, Priscila / Wong, Ida / Mithani, Anusha / Bishop, Stephanie / Mani, Chelsy / Ponce-Rubio, Karen / Virk, Ruvaid / Morris, Michael J / Na, Elisa S

Behavioural brain research

2021 Volume 415, Page(s) 113518

Abstract: Obesity is a complex disease that is the result of a number of different factors including genetic, environmental, and endocrine abnormalities. Given that monogenic forms of obesity are rare, it is important to identify other mechanisms that contribute ... ...

Abstract	Obesity is a complex disease that is the result of a number of different factors including genetic, environmental, and endocrine abnormalities. Given that monogenic forms of obesity are rare, it is important to identify other mechanisms that contribute to its etiology. Methyl-Cp-G binding protein 2 (MeCP2) is a neuroepigenetic factor that binds to methylated regions of DNA to influence transcription. Past studies demonstrate that disruption in MeCP2 function produces obesity in mice. Using a diet-induced obesity mouse model, we show that perinatal exposure to high fat diet significantly decreases MeCP2 protein expression in the hypothalamus of female mice, effects not seen when high fat diet is given to mice during adulthood. Moreover, these effects are seen specifically in a subregion of the hypothalamus known as the arcuate nucleus with females having decreased MeCP2 expression in rostral areas and males having decreased MeCP2 expression in intermediate regions of the arcuate nucleus. Interestingly, mice gain more weight when exposed to high fat diet during adulthood relative to mice exposed to high fat diet perinatally, suggesting that perhaps high fat diet exposure during adulthood may be affecting mechanisms independent of MeCP2 function. Collectively, our data demonstrate that there are developmentally sensitive periods in which MeCP2 expression is influenced by high fat diet exposure and this occurs in a sexually dimorphic manner.
MeSH term(s)	Age Factors ; Animals ; Animals, Newborn ; Diet, High-Fat ; Disease Models, Animal ; Female ; Hypothalamus/metabolism ; Male ; Methyl-CpG-Binding Protein 2/metabolism ; Mice ; Obesity/metabolism ; Sex Characteristics
Chemical Substances	Mecp2 protein, mouse ; Methyl-CpG-Binding Protein 2
Language	English
Publishing date	2021-08-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2021.113518
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Zs.A 1599: Show issues

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Article ; Online: Impact of DNMT1 and DNMT3a forebrain knockout on depressive- and anxiety like behavior in mice.

Morris, Michael J / Na, Elisa S / Autry, Anita E / Monteggia, Lisa M

Neurobiology of learning and memory

2016 Volume 135, Page(s) 139–145

Abstract: DNA methylation has been shown to impact certain forms of synaptic and behavioral plasticity that have been implicated in the development in psychiatric disorders. DNA methylation is catalyzed by DNA methyltransferase (DNMT) enzymes that continue to be ... ...

Abstract	DNA methylation has been shown to impact certain forms of synaptic and behavioral plasticity that have been implicated in the development in psychiatric disorders. DNA methylation is catalyzed by DNA methyltransferase (DNMT) enzymes that continue to be expressed in postmitotic neurons in the forebrain. Using a conditional forebrain knockout of DNMT1 or DNMT3a we assessed the role of these DNMTs in anxiety and depressive-like behavior in mice using an array of behavioral testing paradigms. Forebrain deletion of DNMT1 had anxiolytic and antidepressant-like properties as assessed by elevated plus maze, novelty suppressed feeding, forced swim, and social interaction tests. DNMT3a knockout mice, by contrast, did not exhibit significant behavioral alterations in these tests. Given the putative role of altered DNA methylation patterns in the development of schizophrenia, we also assessed DNMT1 and DNMT3a knockout mice in a prepulse inhibition task and found an enhanced prepulse inhibition of startle in DNMT1 knockouts relative to wild type mice, with no change evident in DNMT3a knockout mice. Our data suggest that DNMT1 and DNMT3a are distinctly involved in affective behavior and that DNMT1 may ultimately represent a potential target for treatment of certain affective behavioral disorders.
Language	English
Publishing date	2016-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	1223366-3
ISSN	1095-9564 ; 1074-7427
ISSN (online)	1095-9564
ISSN	1074-7427
DOI	10.1016/j.nlm.2016.08.012
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