Publications by authors named "Lilianna Suarez"

6 Publications

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Weight-Related Behaviors of Children with Obesity during the COVID-19 Pandemic.

Child Obes 2021 Apr 26. Epub 2021 Apr 26.

Department of Population Health Sciences, Duke University School of Medicine, Durham, NC, USA.

During the coronavirus disease 2019 (COVID-19) pandemic, children and families have had to adapt their daily lives. The purpose of this study was to describe changes in the weight-related behaviors of children with obesity after the onset of the COVID-19 pandemic. Semistructured interviews ( = 51) were conducted from April to June 2020 with parents of children with obesity. Families were participants in a randomized trial testing a clinic-community pediatric obesity treatment model. During interviews, families described their experience during the COVID-19 pandemic, with a particular emphasis on children's diet, physical activity, sleep, and screen time behaviors. Rapid qualitative analysis methods were used to identify themes around changes in children's weight-related behaviors. The mean child age was 9.7 (±2.8) years and the majority of children were Black (46%) or Hispanic (39%) and from low-income families (62%). Most parent participants were mothers (88%). There were differences in the perceived physical activity level of children, with some parents attributing increases in activity or maintenance of activity level to increased outdoor time, whereas others reported a decline due to lack of outdoor time, school, and structured activities. Key dietary changes included increased snacking and more meals prepared and consumed at home. There was a shift in sleep schedules with children going to bed and waking up later and an increase in leisure-based screen time. Parents played a role in promoting activity and managing children's screen time. The COVID-19 pandemic has created unique lifestyle challenges and opportunities for lifestyle modification. Clinical Trials ID: NCT03339440.
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http://dx.doi.org/10.1089/chi.2021.0038DOI Listing
April 2021

SARS-CoV-2 Infections Among Children in the Biospecimens from Respiratory Virus-Exposed Kids (BRAVE Kids) Study.

Clin Infect Dis 2020 Nov 3. Epub 2020 Nov 3.

Department of Medicine, Division of Infectious Diseases, Duke University School of Medicine, Durham, NC.

Background: Children with SARS-CoV-2 infection typically have mild symptoms that do not require medical attention, leaving a gap in our understanding of the spectrum of illnesses that the virus causes in children.

Methods: We conducted a prospective cohort study of children and adolescents (<21 years of age) with a SARS-CoV-2-infected close contact. We collected nasopharyngeal or nasal swabs at enrollment and tested for SARS-CoV-2 using a real-time PCR assay.

Results: Of 382 children, 293 (77%) were SARS-CoV-2-infected. SARS-CoV-2-infected children were more likely to be Hispanic (p<0.0001), less likely to have asthma (p=0.005), and more likely to have an infected sibling contact (p=0.001) than uninfected children. Children ages 6-13 years were frequently asymptomatic (39%) and had respiratory symptoms less often than younger children (29% vs. 48%; p=0.01) or adolescents (29% vs. 60%; p<0.0001). Compared to children ages 6-13 years, adolescents more frequently reported influenza-like (61% vs. 39%; p<0.0001), gastrointestinal (27% vs. 9%; p=0.002), and sensory symptoms (42% vs. 9%; p<0.0001), and had more prolonged illnesses [median (IQR) duration: 7 (4, 12) vs. 4 (3, 8) days; p=0.01]. Despite the age-related variability in symptoms, we found no differences in nasopharyngeal viral load by age or between symptomatic and asymptomatic children.

Conclusions: Hispanic ethnicity and an infected sibling close contact are associated with increased SARS-CoV-2 infection risk among children, while asthma is associated with decreased risk. Age-related differences in the clinical manifestations of SARS-CoV-2 infection must be considered when evaluating children for COVID-19 and in developing screening strategies for schools and childcare settings.
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http://dx.doi.org/10.1093/cid/ciaa1693DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7665428PMC
November 2020

Reactive microglia and IL1β/IL-1R1-signaling mediate neuroprotection in excitotoxin-damaged mouse retina.

J Neuroinflammation 2019 Jun 6;16(1):118. Epub 2019 Jun 6.

Department of Neuroscience, College of Medicine, The Ohio State University, 3020 Graves Hall, 333 W. 10th Ave, Columbus, OH, 43210-1239, USA.

Background: Microglia and inflammation have context-specific impacts upon neuronal survival in different models of central nervous system (CNS) disease. Herein, we investigate how inflammatory mediators, including microglia, interleukin 1 beta (IL1β), and signaling through interleukin 1 receptor type 1 (IL-1R1), influence the survival of retinal neurons in response to excitotoxic damage.

Methods: Excitotoxic retinal damage was induced via intraocular injections of NMDA. Microglial phenotype and neuronal survival were assessed by immunohistochemistry. Single-cell RNA sequencing was performed to obtain transcriptomic profiles. Microglia were ablated by using clodronate liposome or PLX5622. Retinas were treated with IL1β prior to NMDA damage and cell death was assessed in wild type, IL-1R1 null mice, and mice expressing IL-1R1 only in astrocytes.

Results: NMDA-induced damage included neuronal cell death, microglial reactivity, upregulation of pro-inflammatory cytokines, and genes associated with IL1β-signaling in different types of retinal neurons and glia. Expression of the IL1β receptor, IL-1R1, was evident in astrocytes, endothelial cells, some Müller glia, and OFF bipolar cells. Ablation of microglia with clodronate liposomes or Csf1r antagonist (PLX5622) resulted in elevated cell death and diminished neuronal survival in excitotoxin-damaged retinas. Exogenous IL1β stimulated the proliferation and reactivity of microglia in the absence of damage, reduced numbers of dying cells in damaged retinas, and increased neuronal survival following an insult. IL1β failed to provide neuroprotection in the IL-1R1-null retina, but IL1β-mediated neuroprotection was rescued when expression of IL-1R1 was restored in astrocytes.

Conclusions: We conclude that reactive microglia provide protection to retinal neurons, since the absence of microglia is detrimental to survival. We propose that, at least in part, the survival-influencing effects of microglia may be mediated by IL1β, IL-1R1, and interactions of microglia and other macroglia.
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http://dx.doi.org/10.1186/s12974-019-1505-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6555727PMC
June 2019

Retinoic Acid-Signaling Regulates the Proliferative and Neurogenic Capacity of Müller Glia-Derived Progenitor Cells in the Avian Retina.

Stem Cells 2018 03 27;36(3):392-405. Epub 2017 Nov 27.

Department of Neuroscience, College of Medicine, The Ohio State University, Columbus, Ohio, USA.

In the retina, Müller glia have the potential to become progenitor cells with the ability to proliferate and regenerate neurons. However, the ability of Müller glia-derived progenitor cells (MGPCs) to proliferate and produce neurons is limited in higher vertebrates. Using the chick model system, we investigate how retinoic acid (RA)-signaling influences the proliferation and the formation of MGPCs. We observed an upregulation of cellular RA binding proteins (CRABP) in the Müller glia of damaged retinas where the formation of MGPCs is known to occur. Activation of RA-signaling was stimulated, whereas inhibition suppressed the proliferation of MGPCs in damaged retinas and in fibroblast growth factor 2-treated undamaged retinas. Furthermore, inhibition of RA-degradation stimulated the proliferation of MGPCs. Levels of Pax6, Klf4, and cFos were upregulated in MGPCs by RA agonists and downregulated in MGPCs by RA antagonists. Activation of RA-signaling following MGPC proliferation increased the percentage of progeny that differentiated as neurons. Similarly, the combination of RA and insulin-like growth factor 1 (IGF1) significantly increased neurogenesis from retinal progenitors in the circumferential marginal zone (CMZ). In summary, RA-signaling stimulates the formation of proliferating MGPCs and enhances the neurogenic potential of MGPCs and stem cells in the CMZ. Stem Cells 2018;36:392-405.
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http://dx.doi.org/10.1002/stem.2742DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5823757PMC
March 2018

Jak/Stat signaling regulates the proliferation and neurogenic potential of Müller glia-derived progenitor cells in the avian retina.

Sci Rep 2016 10 19;6:35703. Epub 2016 Oct 19.

Department of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Ave, Columbus, OH 43210, USA.

Müller glia are capable of de-differentiating and proliferating to become Müller glia-derived progenitor cells (MGPCs) with the ability to regenerate retinal neurons. One of the cell-signaling pathways that drives the reprogramming of Müller glia into MGPCs in the zebrafish retina is the Jak/Stat-pathway. However, nothing is known about the influence of Jak/Stat-signaling during the formation of MGPCs in the retinas of warm-blooded vertebrates. Accordingly, we examined whether Jak/Stat-signaling influences the formation of MGPCs and differentiation of progeny in the avian retina. We found that Jak/Stat-signaling is activated in Müller glia in response to NMDA-induced retinal damage or by CNTF or FGF2 in the absence of retinal damage. Inhibition of gp130, Jak2, or Stat3 suppressed the formation of proliferating MGPCs in NMDA-damaged and FGF2-treated retinas. Additionally, CNTF combined with FGF2 enhanced the formation of proliferating MGPCs in the absence of retinal damage. In contrast to the zebrafish model, where activation of gp130/Jak/Stat is sufficient to drive neural regeneration from MGPCs, signaling through gp130 inhibits the neurogenic potential of MGPCs and promotes glial differentiation. We conclude that gp130/Jak/Stat-signaling plays an important role in the network of pathways that drives the formation of proliferating MGPCs; however, this pathway inhibits the neural differentiation of the progeny.
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http://dx.doi.org/10.1038/srep35703DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5069623PMC
October 2016

Comparative analysis of glucagonergic cells, glia, and the circumferential marginal zone in the reptilian retina.

J Comp Neurol 2016 Jan 25;524(1):74-89. Epub 2015 Jun 25.

Department of Neuroscience, College of Medicine, The Ohio State University, Columbus, Ohio, 43210.

Retinal progenitors in the circumferential marginal zone (CMZ) and Müller glia-derived progenitors have been well described for the eyes of fish, amphibians, and birds. However, there is no information regarding a CMZ and the nature of retinal glia in species phylogenetically bridging amphibians and birds. The purpose of this study was to examine the retinal glia and investigate whether a CMZ is present in the eyes of reptilian species. We used immunohistochemical analyses to study retinal glia, neurons that could influence CMZ progenitors, the retinal margin, and the nonpigmented epithelium of ciliary body of garter snakes, queen snakes, anole lizards, snapping turtles, and painted turtles. We compare our observations on reptile eyes to the CMZ and glia of fish, amphibians, and birds. In all species, Sox9, Pax6, and the glucocorticoid receptor are expressed by Müller glia and cells at the retinal margin. However, proliferating cells were found only in the CMZ of turtles and not in the eyes of anoles and snakes. Similar to eyes of chickens, the retinal margin in turtles contains accumulations of GLP1/glucagonergic neurites. We find that filamentous proteins, vimentin and GFAP, are expressed by Müller glia, but have different patterns of subcellular localization in the different species of reptiles. We provide evidence that the reptile retina may contain nonastrocytic inner retinal glial cells, similar to those described in the avian retina. We conclude that the retinal glia, glucagonergic neurons, and CMZ of turtles appear to be most similar to those of fish, amphibians, and birds.
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http://dx.doi.org/10.1002/cne.23823DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4659723PMC
January 2016