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Mapping employment dynamics in public agencies with payroll data: A methodological framework with an application to Chile
(Public Library of Science (PLoS), 2024-12-31)
HERRERA MARÍN, MAURICIO RENÉ
;
Daniel Brieba
;
Floris Vermeulen
<jats:p>This study introduces a novel, replicable methodology for analyzing employment dynamics within public sector agencies, focusing on turnover and staff longevity. The methodology is designed to be generalizable and applicable to diverse national contexts where detailed administrative data is available. Using payroll data from over 325,000 Chilean civil servants (2006—2020), we apply mixed-effects Cox survival models and linear mixed models to examine patterns of employment stability across state agencies. By incorporating Propensity Score Matching, we further enhance the causal interpretation of turnover changes, especially in post-election years. Finally, we introduce two key metrics—Service Frailty and Relative Turnover Difference—to quantify long-term stability and short-term, post-electoral disruptions. Our findings highlight substantial differences in turnover patterns between regular and post-election years, as well as significant inter-agency heterogeneity in turnover and employee longevity, largely driven by latent agency characteristics. While major covariates like contract type and staff rank account for some variation, much of the disparity stems from agency-specific factors. This framework offers precise, cross-nationally comparable benchmarks for understanding public sector employment dynamics. Additionally, the methodology contributes to the literature by providing transparent and scalable tools for analyzing workforce stability across different contexts.</jats:p>
1
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Understanding the phenotypic variability in Niemann-Pick disease type C (NPC): a need for precision medicine
(2023)
Macarena Las Heras
;
Benjamín Szenfeld
;
Rami A. Ballout
;
Emanuele Buratti
;
Silvana Zanlungo
<jats:title>Abstract</jats:title><jats:p>Niemann-Pick type C (NPC) disease is a lysosomal storage disease (LSD) characterized by the buildup of endo-lysosomal cholesterol and glycosphingolipids due to loss of function mutations in the <jats:italic>NPC1</jats:italic> and <jats:italic>NPC2</jats:italic> genes. NPC patients can present with a broad phenotypic spectrum, with differences at the age of onset, rate of progression, severity, organs involved, effects on the central nervous system, and even response to pharmacological treatments. This article reviews the phenotypic variation of NPC and discusses its possible causes, such as the remaining function of the defective protein, modifier genes, sex, environmental cues, and splicing factors, among others. We propose that these factors should be considered when designing or repurposing treatments for this disease. Despite its seeming complexity, this proposition is not far-fetched, considering the expanding interest in precision medicine and easier access to multi-omics technologies.</jats:p>
Scopus© Citations 7 2
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Identification of genetic modifiers of murine hepatic β-glucocerebrosidase activity
(2021)
Anyelo Durán
;
Boris Rebolledo-Jaramillo
;
Valeria Olguin
;
Marcelo Rojas-Herrera
;
Macarena Las Heras
Scopus© Citations 6 2
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A Mouse Systems Genetics Approach Reveals Common and Uncommon Genetic Modifiers of Hepatic Lysosomal Enzyme Activities and Glycosphingolipids
(2023)
Anyelo Durán
;
David A. Priestman
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Macarena Las Las Heras
;
Boris Rebolledo-Jaramillo
;
Valeria Olguín
<jats:p>Identification of genetic modulators of lysosomal enzyme activities and glycosphingolipids (GSLs) may facilitate the development of therapeutics for diseases in which they participate, including Lysosomal Storage Disorders (LSDs). To this end, we used a systems genetics approach: we measured 11 hepatic lysosomal enzymes and many of their natural substrates (GSLs), followed by modifier gene mapping by GWAS and transcriptomics associations in a panel of inbred strains. Unexpectedly, most GSLs showed no association between their levels and the enzyme activity that catabolizes them. Genomic mapping identified 30 shared predicted modifier genes between the enzymes and GSLs, which are clustered in three pathways and are associated with other diseases. Surprisingly, they are regulated by ten common transcription factors, and their majority by miRNA-340p. In conclusion, we have identified novel regulators of GSL metabolism, which may serve as therapeutic targets for LSDs and may suggest the involvement of GSL metabolism in other pathologies.</jats:p>
1
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Genome Sequencing Variations in the Octodon degus, an Unconventional Natural Model of Aging and Alzheimer's Disease
(2022)
Michael J. Hurley
;
Claudio Urra
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B. Maximiliano Garduno
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Agostino Bruno
;
Allison Kimbell
<jats:p>The degu (<jats:italic>Octodon degus</jats:italic>) is a diurnal long-lived rodent that can spontaneously develop molecular and behavioral changes that mirror those seen in human aging. With age some degu, but not all individuals, develop cognitive decline and brain pathology like that observed in Alzheimer's disease including neuroinflammation, hyperphosphorylated tau and amyloid plaques, together with other co-morbidities associated with aging such as macular degeneration, cataracts, alterations in circadian rhythm, diabetes and atherosclerosis. Here we report the whole-genome sequencing and analysis of the degu genome, which revealed unique features and molecular adaptations consistent with aging and Alzheimer's disease. We identified single nucleotide polymorphisms in genes associated with Alzheimer's disease including a novel apolipoprotein E (<jats:italic>Apoe</jats:italic>) gene variant that correlated with an increase in amyloid plaques in brain and modified the <jats:italic>in silico</jats:italic> predicted degu APOE protein structure and functionality. The reported genome of an unconventional long-lived animal model of aging and Alzheimer's disease offers the opportunity for understanding molecular pathways involved in aging and should help advance biomedical research into treatments for Alzheimer's disease.</jats:p>
3Scopus© Citations 12
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Genetic Background Matters: Population-Based Studies in Model Organisms for Translational Research
(2022)
Valeria Olguín
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Anyelo Durán
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Macarena Las Heras
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Juan Carlos Rubilar
;
Francisco A. Cubillos
<jats:p>We are all similar but a bit different. These differences are partially due to variations in our genomes and are related to the heterogeneity of symptoms and responses to treatments that patients exhibit. Most animal studies are performed in one single strain with one manipulation. However, due to the lack of variability, therapies are not always reproducible when treatments are translated to humans. Panels of already sequenced organisms are valuable tools for mimicking human phenotypic heterogeneities and gene mapping. This review summarizes the current knowledge of mouse, fly, and yeast panels with insightful applications for translational research.</jats:p>
46Scopus© Citations 8
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Deletions in Genes Participating in Innate Immune Response Modify the Clinical Course of Andes Orthohantavirus Infection
(2019)
Grazielle Esteves Ribeiro
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Luis Edgardo Leon
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Ruth Perez
;
Analia Cuiza
;
Pablo Agustin Vial
<jats:p>Andes orthohantavirus (ANDV) is an important human pathogen causing hantavirus cardiopulmonary syndrome (HCPS) with a fatality rate of 30% in Chile. Around 60% of all cases have a severe clinical course, while the others have a mild clinical course. The main goal of this study was to understand if the genetic variation of patients is associated with the clinical course they develop after ANDV infection. For this, the frequency of copy number variants (CNVs, i.e., deletions and duplications) was studied in 195 patients, 88 with mild and 107 with severe HCPS. CNVs were called from intensity data of the Affymetrix Genome-Wide SNP Array 6.0. The analysis of the data was performed with PennCNV, ParseCNV and R softwares; Results: a deletion of 19, 416 bp in the q31.3 region of chromosome 1 is found more frequently in severe patients (p < 0.05). This region contains Complement Factor H Related (CFHR1) and CFHR3 genes, regulators of the complement cascade. A second deletion of 1.81 kb located in the p13 region of chr20 was significantly more frequent in mild patients (p < 0.05). This region contains the SIRPB1 gene, which participates in the innate immune response, more specifically in neutrophil trans-epithelial migration. Both deletions are associated with the clinical course of HCPS, the first being a risk factor and the second being protective. The participation of genes contained in both deletions in ANDV infection pathophysiology deserves further investigation.</jats:p>
Scopus© Citations 8 2

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