Gonzalo Mena

Dr. Gonzalo Mena


Research Focus & Metrics

Academic Career Length

11Years (2016-Present)

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

Representative Publications

View All Publications
28 May 2021 in Science
Verified
Journal Article
Open access
PDF file
GMGonzalo Mena
Gonzalo Mena
PMPamela P. Martinez
Pamela P. Martinez
AMAyesha S. Mahmud
Ayesha S. Mahmud
PMPablo Marquet
Pablo Marquet
CBCaroline O. Buckee
Caroline O. Buckee
MSMauricio Santillana
Mauricio Santillana
Urban socioeconomics and mortality: Santiago, Chile, is a highly segregated city with distinct zones of affluence and deprivation. This setting offers a window on how social factors propel the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic in an economically vulnerable society with high levels of income inequality. Mena et al. analyzed incidence and mortality attributed to SARS-CoV-2 to understand spatial variations in disease burden. Infection fatality rates were higher in lower-income municipalities because of comorbidities and lack of access to health care. Disparities between municipalities in the quality of their health care delivery system became apparent in testing delays and capacity. These indicators explain a large part of the variation in COVID-19 underreporting and deaths and show that these inequalities disproportionately affected younger people. Science , abg5298, this issue p. eabg5298

13 November 2017 in PLOS Computational Biology
Verified
Journal Article
Open access
PDF file
GMGonzalo Mena
Gonzalo Mena
LGLauren E. Grosberg
Lauren E. Grosberg
SMSasidhar Madugula
Sasidhar Madugula
PHPaweł Hottowy
Paweł Hottowy
ALAlan Litke
Alan Litke
LPLiam Paninski
Liam Paninski
Simultaneous electrical stimulation and recording using multi-electrode arrays can provide a valuable technique for studying circuit connectivity and engineering neural interfaces. However, interpreting these measurements is challenging because the spike sorting process (identifying and segregating action potentials arising from different neurons) is greatly complicated by electrical stimulation artifacts across the array, which can exhibit complex and nonlinear waveforms, and overlap temporarily with evoked spikes. Here we develop a scalable algorithm based on a structured Gaussian Process model to estimate the artifact and identify evoked spikes. The effectiveness of our methods is demonstrated in both real and simulated 512-electrode recordings in the peripheral primate retina with single-electrode and several types of multi-electrode stimulation. We establish small error rates in the identification of evoked spikes, with a computational complexity that is compatible with real-time data analysis. This technology may be helpful in the design of future high-resolution sensory prostheses based on tailored stimulation (e.g., retinal prostheses), and for closed-loop neural stimulation at a much larger scale than currently possible. Simultaneous electrical stimulation and recording using multi-electrode arrays can provide a valuable technique for studying circuit connectivity and engineering neural interfaces. However, interpreting these recordings is challenging because the spike sorting process (identifying and segregating action potentials arising from different neurons) is largely stymied by electrical stimulation artifacts across the array, which are typically larger than the signals of interest. We develop a novel computational framework to estimate and subtract away this contaminating artifact, enabling the large-scale analysis of responses of possibly hundreds of cells to tailored stimulation. Importantly, we suggest that this technology may also be helpful for the development of future high-resolution neural prosthetic devices (e.g., retinal prostheses).

19 August 2022 in BMJ Open
Verified
Journal Article
Open access
PDF file
GMGonzalo Mena
Gonzalo Mena
JAJose Manuel Aburto
Jose Manuel Aburto
Objectives To quantify the impact of the COVID-19 pandemic on life expectancy in Chile categorised by rural and urban areas, and to correlate life expectancy changes with socioeconomic factors at the municipal level. Design Retrospective cross-sectional demographic analysis using aggregated national all-cause death data stratified by year, sex and municipality during the period 2010–2020. Setting and population Chilean population by age, sex and municipality from 2002 to 2020. Main outcome measures Stratified mortality rates using a Bayesian methodology. These were based on vital and demographic statistics from the national institute of statistics and department of vital statistics of ministry of health. With this, we assessed the unequal impact of the pandemic in 2020 on life expectancy across Chilean municipalities for males and females and analysed previous mortality trends since 2010. Results Life expectancy declined for both males and females in 2020 compared with 2019. Urban areas were the most affected, with males losing 1.89 years and females 1.33 years. The strength of the decline in life expectancy correlated positively with indicators of social deprivation and poverty. Also, inequality in life expectancy between municipalities increased, largely due to excess mortality among the working-age population in socially disadvantaged municipalities. Conclusions Not only do people in poorer areas live shorter lives, they also have been substantially more affected by the COVID-19 pandemic, leading to increased population health inequalities. Quantifying the impact of the COVID-19 pandemic on life expectancy provides a more comprehensive picture of the toll.

4 August 2023 in Science Advances
Verified
Journal Article
Open access
SLSoren L. Larsen
Soren L. Larsen
ISIkgyu Shin
Ikgyu Shin
JJJefrin Joseph
Jefrin Joseph
HWHaylee West
Haylee West
RARafael Anorga
Rafael Anorga
PMPamela P. Martinez
Pamela P. Martinez
SARS-CoV-2 vaccines have been distributed at unprecedented speed. Still, little is known about temporal vaccination trends, their association with socioeconomic inequality, and their consequences for disease control. Using data from 161 countries/territories and 58 states, we examined vaccination rates across high and low socioeconomic status (SES), showing that disparities in coverage exist at national and subnational levels. We also identified two distinct vaccination trends: a rapid initial rollout, quickly reaching a plateau, or sigmoidal and slow to begin. Informed by these patterns, we implemented an SES-stratified mechanistic model, finding profound differences in mortality and incidence across these two vaccination types. Timing of initial rollout affects disease outcomes more substantially than final coverage or degree of SES disparity. Unexpectedly, timing is not associated with wealth inequality or GDP per capita. While socioeconomic disparity should be addressed, accelerating initial rollout for all over focusing on increasing coverage is an accessible intervention that could minimize the burden of disease across socioeconomic groups.

15 January 2021 in medRxiv
Verified
Preprint
Open access
PDF file
GMGonzalo Mena
Gonzalo Mena
PMPamela P. Martinez
Pamela P. Martinez
AMAyesha S. Mahmud
Ayesha S. Mahmud
PMPablo A. Marquet
Pablo A. Marquet
CBCaroline O. Buckee
Caroline O. Buckee
MSMauricio Santillana
Mauricio Santillana
The current coronavirus disease 2019 (COVID-19) pandemic has impacted dense urban populations particularly hard. Here, we provide an in-depth characterization of disease incidence and mortality patterns, and their dependence on demographic and socioeconomic strata in Santiago, a highly segregated city and the capital of Chile. We find that among all age groups, there is a strong association between socioeconomic status and both mortality –measured either by direct COVID-19 attributed deaths or excess deaths– and public health capacity. Specifically, we show that behavioral factors like human mobility, as well as health system factors such as testing volumes, testing delays, and test positivity rates are associated with disease outcomes. These robust patterns suggest multiple possibly interacting pathways that can explain the observed disease burden and mortality differentials: (i) in lower socioeconomic status municipalities, human mobility was not reduced as much as in more affluent municipalities; (ii) testing volumes in these locations were insufficient early in the pandemic and public health interventions were applied too late to be effective; (iii) test positivity and testing delays were much higher in less affluent municipalities, indicating an impaired capacity of the health-care system to contain the spread of the epidemic; and (iv) infection fatality rates appear much higher in the lower end of the socioeconomic spectrum. Together, these findings highlight the exacerbated consequences of health-care inequalities in a large city of the developing world, and provide practical methodological approaches useful for characterizing COVID-19 burden and mortality in other segregated urban centers.

10 June 2024 in bioRxiv
Verified
Preprint
Open access
PDF file
AAAnamika Agrawal
Anamika Agrawal
VRVictoria M. Rachleff
Victoria M. Rachleff
KTKyle J. Travaglini
Kyle J. Travaglini
SMShubhabrata Mukherjee
Shubhabrata Mukherjee
PCPaul Crane
Paul Crane
MGMariano I. Gabitto
Mariano I. Gabitto
Throughout an organism’s life, a multitude of complex and interdependent biological systems transition through biophysical processes that serve as indicators of the underlying biological states. Inferring these latent, unobserved states is a goal of modern biology and neuroscience. However, in many experimental setups, we can at best obtain discrete snapshots of the system at different times and for different individuals. This challenge is particularly relevant in the study of Alzheimer’s Disease (AD) progression, where we observe the aggregation of pathology in brain donors, but the underlying disease state is unknown. This paper proposes a biophysically motivated Bayesian framework (B-BIND: Biophysical Bayesian Inference for Neurode-generative Dynamics), where the disease state is modeled and continuously inferred from observed quantifications of multiple AD pathological proteins. Inspired by biophysical models, we describe pathological burden as an exponential process. The progression of AD is modeled by assigning a latent score, termed pseudotime, to each pathological state, creating a pseudotemporal order of donors based on their pathological burden. We study the theoretical properties of the model using linearization to reveal convergence and identifiability properties. We provide Markov chain Monte Carlo estimation algorithms, illustrating the effectiveness of our approach with multiple simulation studies across various data conditions. Applying this methodology to data from the Seattle Alzheimer’s Disease Brain Cell Atlas, we infer the pseudotime ordering of donors. Finally, we analyze the information within each pathological feature to refine the model, focusing on the most informative pathologies. This framework lays the groundwork for continuous pseudotime modeling in the analysis of neurodegenerative diseases.