RESUMO
School closures during the COVID-19 pandemic have been reported to influence adolescents' behavioral health and may have altered their exposure to injury risk. We aimed to determine how in-person school attendance of individual adolescents in the United States during the pandemic was correlated with a range of risky health behaviors. We used self-reported data from adolescents 14-18 years old enrolled in grades 9-12 who participated in the 2020 Adolescent Behaviors and Experiences Survey. The exposure of interest was in-person vs remote school attendance in the previous 30 days. Risk behavior outcomes included not wearing a seatbelt when riding in a car; riding with someone who was drinking and driving; suffering intimate partner violence (IPV); forced sexual encounters; suicidal ideation; suicidal planning; electronic bullying; gun carrying; and physical fighting. Based on a multivariable analysis of 5202 students (65% attending school in-person) adjusted for age, sex, race, ethnicity, sexual orientation, parental unemployment, food insecurity, and homelessness, we found that in-person school attendance was associated with increased odds of every risk behavior except suicidal ideation and electronic bullying, with adjusted odds ratios ranging from 1.40 (95% confidence interval [CI]: 1.04, 1.88) for not wearing a seatbelt to 3.43 for IPV (95% CI: 1.97, 5.97). Our analyses demonstrate that in-person school attendance during the COVID-19 pandemic was associated with higher rates of risk behavior among adolescents. Further research is needed explore if this relationship is causal, and how these risks could be mitigated, as most adolescents have now returned to in-person schooling.
Assuntos
Comportamento do Adolescente , COVID-19 , Humanos , Masculino , Estados Unidos/epidemiologia , Adolescente , Feminino , Pandemias , COVID-19/epidemiologia , Comportamento Sexual , Assunção de Riscos , Ideação Suicida , Instituições AcadêmicasRESUMO
We reported that maternal PFBS, an emerging pollutant, exposure is positively associated with preeclampsia which can result from aberrant trophoblasts invasion and subsequent placental ischemia. In this study, we investigated the effects of PFBS on trophoblasts proliferation/invasion and signaling pathways. We exposed a human trophoblast line, HTR8/SVneo, to PFBS. Cell viability, proliferation, and cell cycle were evaluated by the MTS assay, Ki-67 staining, and flow cytometry, respectively. We assessed cell migration and invasion with live-cell imaging-based migration assay and matrigel invasion assay, respectively. Signaling pathways were examined by Western blot, RNA-seq, and qPCR. PFBS exposure interrupted cell proliferation and invasion in a dose-dependent manner. PFBS (100 µM) did not cause cell death but instead significant cell proliferation without cell cycle disruption. PFBS (10 and 100 µM) decreased cell migration and invasion, while PFBS (0.1 µM) significantly increased cell invasion but not migration. Further, RNA-seq analysis identified dysregulated HIF-1α target genes that are relevant to cell proliferation/invasion and preeclampsia, while Western Blot data showed the activation of HIF-1α, but not Notch, ERK1/2, (PI3K)AKT, and P38 pathways. PBFS exposure altered trophoblast cell proliferation/invasion which might be mediated by preeclampsia-related genes, suggesting a possible association between prenatal PFBS exposure and adverse placentation.
Assuntos
Proliferação de Células , Fluorocarbonos/efeitos adversos , Regulação da Expressão Gênica/efeitos dos fármacos , Placenta/patologia , Pré-Eclâmpsia/patologia , Ácidos Sulfônicos/efeitos adversos , Trofoblastos/patologia , Apoptose , Ciclo Celular , Movimento Celular , Células Cultivadas , Feminino , Perfilação da Expressão Gênica , Humanos , Proteínas Quinases Ativadas por Mitógeno/genética , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Fosfatidilinositol 3-Quinases/genética , Fosfatidilinositol 3-Quinases/metabolismo , Placenta/efeitos dos fármacos , Placenta/metabolismo , Pré-Eclâmpsia/induzido quimicamente , Pré-Eclâmpsia/genética , Pré-Eclâmpsia/metabolismo , Gravidez , Proteínas Proto-Oncogênicas c-akt/genética , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais , Trofoblastos/efeitos dos fármacos , Trofoblastos/metabolismoRESUMO
Angiogenesis is a regulated process involving the proliferation, migration, and remodeling of different cell types particularly mature endothelial and their progenitor cells, nominated as endothelial progenitor cells (EPCs). Tie2/Tek is a tyrosine kinase receptor expressed by endothelial cells that induces signal transduction pathways involved in endothelial biology. To address the potential importance of the various tyrosine residues of Tie2 in EPC development, we generated a series of Tie2 tyrosine mutated (Y1106F, Y1100F, and Y1111F) EPCs and then assess the biological features of these cells. Clonogenic, tubulogenic, proliferative, migratory, and functional properties of these cells were analyzed. Next, GFP-positive EPCs containing Tie2 tyrosine mutations were systemically transplanted into sublethaly irradiated mice to analyze the potency of these cells for marrow reconstitution. We found that mutation in the Tie2 tyrosine 1106 residue directed EPCs toward a mature endothelial phenotype, which was associated with augmented tubulogenic and migratory properties, and increased phosphorylation of the active site (tyrosine 992) as well as increased vascular perfusion in the in vivo Matrigel plug assay. Moreover, transplantation of 1106 Tie2 mutant EPCs failed to reconstitute the bone marrow after myeloablation, whereas transplantation of EPCs with the 1100 or 1111 Tie2 tyrosine mutation resulted in bone marrow engraftment, leading to improved survival of recipient mice. Our findings demonstrate that the tyrosine 1106 residue in Tie2 plays a key role to maintain the stemness features of EPCs.
Assuntos
Diferenciação Celular/fisiologia , Células Progenitoras Endoteliais/citologia , Células Progenitoras Endoteliais/metabolismo , Neovascularização Fisiológica/fisiologia , Receptor TIE-2/metabolismo , Animais , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Fenótipo , FosforilaçãoRESUMO
Sugar-sweetened beverage (SSB) consumption remains a major target for interventions to treat severe obesity in children. Understanding how total energy consumption is divided among different types of beverages remains unclear. This study retrospectively examined how the consumption of beverage calories (kcal) from 100% fruit juice and SSBs, and body mass index, assessed as a percent of the 95th sex- and age-specific percentile (%of 95BMI), changed during the treatment of children with obesity aged 2-18 years. Treatment was provided by an integrative multi-disciplinary team, comprising a physician, a dietician/ nutritionist and a behavioralist employing motivational interviewing and a small change approach to promote improved sustainable health habits and induce a net negative energy balance. The sample included 155 patients, with 341 visits. The median age was 11 years, 60% were girls, and there was a median follow-up of 3.1 months. At baseline, the median %of 95BMI was 135 and the median kcal/day intake was 436 from juice and 263 from SSB. For each additional 100 kcal consumed/day from SSB and juice, the %of 95BMI increased by 1.4 percentage points. In the follow-up, each additional month was associated with 7 fewer kcal/day from SSB and juice combined, with a 0.5 percentage point increase in %of 95BMI. Children in this treatment program consumed fewer calories from SSB over time, although the %of 95BMI did not decrease. SSBs other than soda accounted for the majority of beverage kcal intake, therefore potentially providing a targeted direction for interventions.
Assuntos
Obesidade Infantil , Feminino , Humanos , Criança , Masculino , Obesidade Infantil/terapia , Estudos Retrospectivos , Bebidas , Bebidas Gaseificadas , Ingestão de Energia , Sacarose AlimentarRESUMO
The current study aimed to determine the community-based COVID-19 prevalence and compare the symptom-based and test-based prevalence rates in the Omicron peak (February 20 to March 20, 2022) to assess community involvement and provide effective healthcare. This cross-sectional and population-based study examined the prevalence of COVID-19 from February 20 to March 20, 2022, in the city of Khomein in Markazi Province (located in central Iran) through random cluster sampling. The period prevalence of recurrent Omicron symptoms was 37.69%. Factors such as residence in urban areas (OR = 1.25, 95% CI: 0.95-1.66), number of COVID-19 vaccine doses (OR = 0.80, 95% CI: 0.67-0.95), the interval of last vaccination dose (OR = 1.04, 95% CI: 0.97-1.11) and a history of COVID-19 (OR =1.20, 95% CI: 1.04-1.39) were among the most important risk factors for Omicron. Ongoing efforts to vaccinate high-risk populations as well as stronger actions to diminish the Omicron consequences are fundamental obligations of the health system.
RESUMO
Cell-cell fusion or syncytialization is fundamental to the reproduction, development, and homeostasis of multicellular organisms. In addition to various cell type-specific fusogenic proteins, cell surface externalization of phosphatidylserine (PS), a universal eat-me signal in apoptotic cells, has been observed in different cell fusion events. Nevertheless, the molecular underpinnings of PS externalization and cellular mechanisms of PS-facilitated cell-cell fusion are unclear. Here, we report that TMEM16F, a Ca2+-activated phospholipid scramblase (CaPLSase), plays an essential role in placental trophoblast fusion by translocating PS to cell surface independent of apoptosis. The placentas from the TMEM16F knockout mice exhibit deficiency in trophoblast syncytialization and placental development, which lead to perinatal lethality. We thus identified a new biological function of TMEM16F CaPLSase in trophoblast fusion and placental development. Our findings provide insight into understanding cell-cell fusion mechanism of other cell types and on mitigating pregnancy complications such as miscarriage, intrauterine growth restriction, and preeclampsia.
Assuntos
Anoctaminas , Proteínas de Transferência de Fosfolipídeos , Animais , Anoctaminas/genética , Anoctaminas/metabolismo , Feminino , Camundongos , Fosfatidilserinas/metabolismo , Proteínas de Transferência de Fosfolipídeos/genética , Proteínas de Transferência de Fosfolipídeos/metabolismo , Placenta/metabolismo , Placentação , Gravidez , Trofoblastos/metabolismoRESUMO
KEY POINTS: "Dyspnoea" during exercise is a common complaint in seemingly otherwise healthy athletes, which may be associated with fatigue and underperformance.Because dyspnoea is an general term and may be caused by numerous factors, ranging from poor aerobic fitness to serious, potentially fatal respiratory and nonrespiratory pathologies, it is important for clinicians to obtain an appropriate case history and ask relevant exercise-specific questions to fully characterise the nature of the complaint so that a targeted diagnostic plan can be developed.Exercise-induced bronchoconstriction and exercise-induced laryngeal obstruction are two common causes of dyspnoea in athletes, and both are regularly misdiagnosed and mismanaged due to poor adherence to available practice parameters.Aside from airway dysfunction, iron deficiency and anaemia, infectious disease, and musculoskeletal conditions are common problems in athletes which ultimately may lead to complaints of dyspnoea. EDUCATIONAL AIMS: To inform readers of the common causes of dyspnoea encountered in athletes.To highlight that airway diseases, such as asthma and exercise-induced bronchoconstriction, are commonly misdiagnosed and mismanaged.To introduce readers to common nonairway causes of dyspnoea in athletes, including clinical features and general principles of diagnosis, and management.To emphasise the importance of a detailed case history and proper adherence to established protocols in evaluating and managing the dyspnoeic athlete.To provide readers with a general framework of appropriate questions that are useful for developing a targeted diagnostic plan for evaluating dyspnoeic athletes. Dyspnoea during exercise is a common chief complaint in athletes and active individuals. It is not uncommon for dyspnoeic athletes to be diagnosed with asthma, "exercise-induced asthma" or exercise-induced bronchoconstriction based on their symptoms, but this strategy regularly leads to misdiagnosis and improper patient management. Dyspnoea during exercise can ultimately be caused by numerous respiratory and nonrespiratory conditions, ranging from nonpathological to potentially fatal in severity. As, such it is important for healthcare providers to be familiar with the many factors that can cause dyspnoea during exercise in seemingly otherwise-healthy individuals and have a general understanding of the clinical approach to this patient population. This article reviews common conditions that ultimately cause athletes to report dyspnoea and associated symptoms, and provides insight for developing an efficient diagnostic plan.