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2.
PLoS One ; 14(11): e0221389, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-31693667

RESUMEN

BACKGROUND: Respiratory disease and, specifically, pneumonia, is the major cause of mortality and morbidity in young children. Diagnosis of both pneumonia and asthma in primary care rests principally on clinical signs, history taking, and bronchodilator responsiveness. This study aimed to describe clinical practices in diverse global primary care settings concerning differential diagnosis of respiratory disease in young children, especially between pneumonia and asthma. METHODS: Health professionals in Greece, Kyrgyzstan, Vietnam, and Uganda were observed during consultations with children aged 2-59 months, presenting with cough and/or difficult breathing. Data were analyzed descriptively and included consultation duration, practices, diagnoses and availability/use of medications and equipment. The study is part of the European Horizon 2020 FRESH AIR project. RESULTS: In total, 771 consultations by 127 health professionals at 74 facilities in the four countries were observed. Consultations were shorter in Vietnam and Uganda (3 to 4 minutes) compared to Greece and Kyrgyzstan (15 to 20 minutes). History taking was most comprehensive in Greece. Clinical examination was more comprehensive in Vietnam and Kyrgyzstan and less in Uganda. Viral upper respiratory tract infections were the most common diagnoses (41.7% to 67%). Pneumonia was diagnosed frequently in Uganda (16.3% of children), and rarely in other countries (0.8% to 2.9%). Asthma diagnosis was rare (0% to 2.8%). Antibiotics were prescribed frequently in all countries (32% to 69%). Short acting ß-agonist trials were seldom available and used during consultations in Kyrgyzstan (0%) and Uganda (1.8%), and often in Greece (38.9%) and Vietnam (12.6%). CONCLUSIONS: Duration and comprehensiveness of clinical consultations observed in this study seemed insufficient to guide respiratory diagnosis in young children. Appropriate treatment options may further not be available in certain studied settings. Actions aiming at educating and raising professional awareness, along with developing easy-to-use tools to support diagnosis and a general strengthening of health systems are important goals.


Asunto(s)
Enfermedades Respiratorias/diagnóstico , Asma/diagnóstico , Preescolar , Países Desarrollados , Países en Desarrollo , Diagnóstico Diferencial , Femenino , Grecia , Humanos , Lactante , Kirguistán , Masculino , Neumonía/diagnóstico , Pobreza , Atención Primaria de Salud , Derivación y Consulta , Enfermedades Respiratorias/terapia , Factores Socioeconómicos , Uganda , Vietnam
3.
Artículo en Inglés | MEDLINE | ID: mdl-29732438

RESUMEN

Chronic insufficient sleep is a major societal problem and is associated with increased risk of metabolic disease. Hypothalamic inflammation contributes to hyperphagia and weight gain in diet-induced obesity, but insufficient sleep-induced neuroinflammation has yet to be examined in relation to metabolic function. We therefore fragmented sleep of adult male C57BL/6J mice for 18 h daily for 9 days to determine whether sleep disruption elicits inflammatory responses in brain regions that regulate energy balance and whether this relates to glycemic control. To additionally test the hypothesis that exposure to multiple inflammatory factors exacerbates metabolic outcomes, responses were compared in mice exposed to sleep fragmentation (SF), high-fat diet (HFD), both SF and HFD, or control conditions. Three or 9 days of high-fat feeding reduced glucose tolerance but SF alone did not. Transient loss of body mass in SF mice may have affected outcomes. Comparisons of pro-inflammatory cytokine concentrations among central and peripheral metabolic tissues indicate that patterns of liver interleukin-1ß concentrations best reflects observed changes in glucose tolerance. However, we demonstrate that SF rapidly and potently increases Iba1 immunoreactivity (-ir), a marker of microglia. After 9 days of manipulations, Iba1-ir remains elevated only in mice exposed to both SF and HFD, indicating a novel interaction between sleep and diet on microglial activation that warrants further investigation.

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