Fernando Sempertegui

Dr. Fernando Sempertegui


Research Focus & Metrics

Academic Career Length

16Years (2011-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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3 November 2011 in Environmental Health
Verified
Journal Article
Open access
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AHAaron M Harris
Aaron M Harris
FSFernando Sempertegui
Fernando Sempertegui
BEBERTHA ESTRELLA
BERTHA ESTRELLA
XNXimena Narváez
Ximena Narváez
JEJuan Egas
Juan Egas
JGJeffrey K Griffiths
Jeffrey K Griffiths
Background: Ambient air pollution and malnutrition, particularly anemia, are risk factors for pneumonia, a leading cause of death in children under five. We simultaneously assessed these risk factors in Quito, Ecuador. Methods: In 2005, we studied two socioeconomically similar neighborhoods in Quito: Lucha de los Pobres (LP) and Jaime Roldos (JR). LP had relatively high levels of air pollution (annual median PM2.5 = 20.4 μg/m3; NO2 = 29.5 μg/m3) compared to JR (annual median PM2.5 = 15.3 μg/m3; NO2 = 16.6 μg/m3). We enrolled 408 children from LP (more polluted) and 413 children from JR (less polluted). All subjects were aged 18-42 months. We obtained medical histories of prior physician visits and hospitalizations during the previous year, anthropometric nutrition data, hemoglobin levels, and hemoglobin oxygen saturation via oximetry. Results: In anemic children, higher pollution exposure was significantly associated with pneumonia hospitalization (OR = 6.82, 95%CI = 1.45-32.00; P = 0.015). In non-anemic children, no difference in hospitalizations by pollution exposure status was detected (OR = 1.04, NS). Children exposed to higher levels of air pollution had more pneumonia hospitalizations (OR = 3.68, 1.09-12.44; P = 0.036), total respiratory illness (OR = 2.93, 95% CI 1.92-4.47; P < 0.001), stunting (OR = 1.88, 1.36-2.60; P < 0.001) and anemia (OR = 1.45, 1.09-1.93; P = 0.013) compared to children exposed to lower levels of air pollution. Also, children exposed to higher levels of air pollution had significantly lower oxygen saturation (92.2% ± 2.6% vs. 95.8% ± 2.2%; P < 0.0001), consistent with air pollution related dyshemoglobinemia. Conclusions: Ambient air pollution is associated with rates of hospitalization for pneumonia and with physician's consultations for acute respiratory infections. Anemia may interact with air pollution to increase pneumonia hospitalizations. If confirmed in larger studies, improving nutrition-related anemia, as well as decreasing the levels of air pollution in Quito, may reduce pneumonia incidence.

TFTania Alarcon Falconi
Tania Alarcon Falconi
BEBERTHA ESTRELLA
BERTHA ESTRELLA
FSFernando Sempertegui
Fernando Sempertegui
ENElena N. Naumova
Elena N. Naumova
Time series analysis in epidemiological studies is typically conducted on aggregated counts, although data tend to be collected at finer temporal resolutions. The decision to aggregate data is rarely discussed in epidemiological literature although it has been shown to impact model results. We present a critical thinking process for making decisions about data aggregation in time series analysis of seasonal infections. We systematically build a harmonic regression model to characterize peak timing and amplitude of three respiratory and enteric infections that have different seasonal patterns and incidence. We show that irregularities introduced when aggregating data must be controlled during modeling to prevent erroneous results. Aggregation irregularities had a minimal impact on the estimates of trend, amplitude, and peak timing for daily and weekly data regardless of the disease. However, estimates of peak timing of the more common infections changed by as much as 2.5 months when controlling for monthly data irregularities. Building a systematic model that controls for data irregularities is essential to accurately characterize temporal patterns of infections. With the urgent need to characterize temporal patterns of novel infections, such as COVID-19, this tutorial is timely and highly valuable for experts in many disciplines.

29 January 2021 in Vaccines
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Journal Article
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JPJorge Pérez-Galaza
Jorge Pérez-Galaza
CPCésar Prócel
César Prócel
CHCristina Cañadas Herrera
Cristina Cañadas Herrera
DVDiana Fernanda Aguirre Villacis
Diana Fernanda Aguirre Villacis
RPRonny Pibaque
Ronny Pibaque
Lucy BaldeónLucy Baldeón
Lucy Baldeón
In December 2019, a novel coronavirus known as SARS-CoV-2 was first detected in Wuhan, China, causing outbreaks of the coronavirus disease COVID-19 that has now spread globally. For this reason, The World Health Organization (WHO) declared COVID-19 a public health emergency in March 2020. People living with pre-existing conditions such as obesity, cardiovascular diseases, type 2 diabetes (T2D), and chronic kidney and lung diseases, are prone to develop severe forms of disease with fatal outcomes. Metabolic diseases such as obesity and T2D alter the balance of innate and adaptive responses. Both diseases share common features characterized by augmented adiposity associated with a chronic systemic low-grade inflammation, senescence, immunoglobulin glycation, and abnormalities in the number and function of adaptive immune cells. In obese and T2D patients infected by SARS-CoV-2, where immune cells are already hampered, this response appears to be stronger. In this review, we describe the abnormalities of the immune system, and summarize clinical findings of COVID-19 patients with pre-existing conditions such as obesity and T2D as this group is at greater risk of suffering severe and fatal clinical outcomes.

15 January 2016 in Diabetology & Metabolic Syndrome
Verified
Journal Article
Open access
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Lucy BaldeónLucy Baldeón
Lucy Baldeón
KWKarin Weigelt
Karin Weigelt
HWHarm de Wit
Harm de Wit
BOBehiye Ozcan
Behiye Ozcan
AOAdri van Oudenaren
Adri van Oudenaren
PLPieter Leenen
Pieter Leenen
Recently, we reported signs of inflammation (raised IL-8, reduced miR-146a) and signs of vascular repair (raised HGF) in the serum of Ecuadorian patients with type 2 diabetes (T2D). In contrast, we found that the circulating monocytes lacked up-regulation of classical inflammatory genes (IL-1B, IL-6, and TNF) and there was even significant down-regulation of PTGS2. Notably, genes and a microRNA involved in adhesion, cell differentiation and morphology (CD9, DHRS3, PTPN7 and miR-34c-5p) were up-regulated in the T2D monocytes, suggesting a role of the anti-inflammatory cells in adhesion, vascular repair and invasion. To determine the gene expression of the vascular repair factor HGF in the circulating monocytes of patients with T2D and to investigate the relationship between HGF and the expression of the other previously tested monocyte genes and the contribution to the raised serum level of HGF. In addition, we tested the level of 6 microRNAs, which were previously found abnormal in the circulating monocytes, in the serum of the patients. A gene and microRNA expression study in monocytes and serum of 64 Ecuadorian patients with T2D (37–85 years) and 44 non-diabetic controls (32–87 years). The gene expression of HGF was significantly raised in the monocytes of the patients with T2D and associated with the expression of genes involved in adhesion, cell differentiation and morphology. HGF gene expression did not correlate with the serum level of HGF. The monocyte expression of pro-inflammatory cytokine genes was also not associated with the serum levels of these cytokines. The level of miR-574-3p was significantly decreased in the serum of the patients with T2D, and correlated in expression with the decreased well-established inflammation-regulating miR-146a. The level of the microRNAs in serum did not correlate with their expression level in monocytes. In circulating monocytes of Ecuadorian T2D patients, the microRNA and gene expression of important inflammatory/chemotactic/motility/vascular repair factors differs from the expression in serum. While monocytes show a gene expression profile compatible with an anti-inflammatory state, serum shows a molecular profile compatible with an inflammatory state. Both compartments show molecular signs of vascular repair support, i.e. up-regulated HGF levels.

1 April 2020 in The American Journal of Tropical Medicine and Hygiene
Verified
Journal Article
Closed access
LSLora L. Sabin
Lora L. Sabin
BEBERTHA ESTRELLA
BERTHA ESTRELLA
FSFernando Sempertegui
Fernando Sempertegui
NFNorman Farquhar
Norman Farquhar
AMAldina Mesic
Aldina Mesic
DHDavidson H Hamer
Davidson H Hamer
Pneumonia remains a leading cause of morbidity and mortality in young children. The total cost of pneumonia-related hospitalization, including household-level cost, is poorly understood. To better understand this burden in an urban setting in South America, we incorporated a cost study into a trial assessing zinc supplements in treatment of severe pneumonia among children aged 2-59 months at a public hospital in Quito, Ecuador, which provides such treatment at no charge. Data were collected from children's caregivers at hospitalization and discharge on out-of-pocket payments for medical and nonmedical items, and on employment and lost work time. Analyses encompassed three categories: direct medical costs, direct nonmedical costs, and indirect costs, which covered foregone wages (from caregivers' self-reported lost earnings) and opportunity cost of caregivers' lost time (based on the unskilled labor wage in Ecuador). Caregivers of 153 children completed all questionnaires. Overall, 57% of children were aged less than 12 months, and 46% were female. Just over 50% of mothers and fathers had completed middle school. Most reported direct costs, which averaged $33. Most also reported indirect costs, the mean of which was $74. Fifty-seven reported lost earnings (mean = $79); 29 reported lost time (estimated mean cost = $37). Stratified analyses revealed similar costs for children < 12 months and ≥ 12 months, with variations for specific items. Costs for hospital-based treatment of severe pneumonia in young children represent a major burden for households in low- to middle-income settings, even when such treatment is intended to be provided at no cost.