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Description
Five immunocompetent C57BL/6-cBrd/cBrd/Cr (albino C57BL/6) mice were injected with GL261-luc2 cells, a cell line sharing characteristics of human glioblastoma multiforme (GBM). The mice were imaged using magnetic resonance (MR) at five separate time points to characterize growth and development of the tumor. After 25 days, the final tumor volumes of the mice varied from 12 mm3 to 62 mm3, even though mice were inoculated from the same tumor cell line under carefully controlled conditions. We generated hypotheses to explore large variances in final tumor size and tested them with our simple reaction-diffusion model in both a 3-dimensional (3D) finite difference method and a 2-dimensional (2D) level set method. The parameters obtained from a best-fit procedure, designed to yield simulated tumors as close as possible to the observed ones, vary by an order of magnitude between the three mice analyzed in detail. These differences may reflect morphological and biological variability in tumor growth, as well as errors in the mathematical model, perhaps from an oversimplification of the tumor dynamics or nonidentifiability of parameters. Our results generate parameters that match other experimental in vitro and in vivo measurements. Additionally, we calculate wave speed, which matches with other rat and human measurements.
ContributorsRutter, Erica (Author) / Stepien, Tracy (Author) / Anderies, Barrett (Author) / Plasencia, Jonathan (Author) / Woolf, Eric C. (Author) / Scheck, Adrienne C. (Author) / Turner, Gregory H. (Author) / Liu, Qingwei (Author) / Frakes, David (Author) / Kodibagkar, Vikram (Author) / Kuang, Yang (Author) / Preul, Mark C. (Author) / Kostelich, Eric (Author) / College of Liberal Arts and Sciences (Contributor)
Created2017-05-31
Description
Mathematical epidemiology, one of the oldest and richest areas in mathematical biology, has significantly enhanced our understanding of how pathogens emerge, evolve, and spread. Classical epidemiological models, the standard for predicting and managing the spread of infectious disease, assume that contacts between susceptible and infectious individuals depend on their relative frequency in the population. The behavioral factors that underpin contact rates are not generally addressed. There is, however, an emerging a class of models that addresses the feedbacks between infectious disease dynamics and the behavioral decisions driving host contact. Referred to as “economic epidemiology” or “epidemiological economics,” the approach explores the determinants of decisions about the number and type of contacts made by individuals, using insights and methods from economics. We show how the approach has the potential both to improve predictions of the course of infectious disease, and to support development of novel approaches to infectious disease management.
ContributorsPerrings, Charles (Author) / Castillo-Chavez, Carlos (Author) / Chowell-Puente, Gerardo (Author) / Daszak, Peter (Author) / Fenichel, Eli P. (Author) / Finnoff, David (Author) / Horan, Richard D. (Author) / Kilpatrick, A. Marm (Author) / Kinzig, Ann (Author) / Kuminoff, Nicolai (Author) / Levin, Simon (Author) / Morin, Benjamin (Author) / Smith, Katherine F. (Author) / Springborn, Michael (Author) / Simon M. Levin Mathematical, Computational and Modeling Sciences Center (Contributor) / College of Liberal Arts and Sciences (Contributor) / School of Life Sciences (Contributor) / School of Human Evolution and Social Change (Contributor) / W.P. Carey School of Business (Contributor) / Economics (Contributor) / Julie Ann Wrigley Global Institute of Sustainability (Contributor)
Created2015-12-01
Description
Preserving a system’s viability in the presence of diversity erosion is critical if the goal is to sustainably support biodiversity. Reduction in population heterogeneity, whether inter- or intraspecies, may increase population fragility, either decreasing its ability to adapt effectively to environmental changes or facilitating the survival and success of ordinarily rare phenotypes. The latter may result in over-representation of individuals who may participate in resource utilization patterns that can lead to over-exploitation, exhaustion, and, ultimately, collapse of both the resource and the population that depends on it. Here, we aim to identify regimes that can signal whether a consumer–resource system is capable of supporting viable degrees of heterogeneity. The framework used here is an expansion of a previously introduced consumer–resource type system of a population of individuals classified by their resource consumption. Application of the Reduction Theorem to the system enables us to evaluate the health of the system through tracking both the mean value of the parameter of resource (over)consumption, and the population variance, as both change over time. The article concludes with a discussion that highlights applicability of the proposed system to investigation of systems that are affected by particularly devastating overly adapted populations, namely cancerous cells. Potential intervention approaches for system management are discussed in the context of cancer therapies.
ContributorsKareva, Irina (Author) / Morin, Benjamin (Author) / Castillo-Chavez, Carlos (Author) / Simon M. Levin Mathematical, Computational and Modeling Sciences Center (Contributor) / College of Liberal Arts and Sciences (Contributor) / School of Human Evolution and Social Change (Contributor) / Julie Ann Wrigley Global Institute of Sustainability (Contributor)
Created2015-02-01
Description
Background
In the weeks following the first imported case of Ebola in the U. S. on September 29, 2014, coverage of the very limited outbreak dominated the news media, in a manner quite disproportionate to the actual threat to national public health; by the end of October, 2014, there were only four laboratory confirmed cases of Ebola in the entire nation. Public interest in these events was high, as reflected in the millions of Ebola-related Internet searches and tweets performed in the month following the first confirmed case. Use of trending Internet searches and tweets has been proposed in the past for real-time prediction of outbreaks (a field referred to as “digital epidemiology”), but accounting for the biases of public panic has been problematic. In the case of the limited U. S. Ebola outbreak, we know that the Ebola-related searches and tweets originating the U. S. during the outbreak were due only to public interest or panic, providing an unprecedented means to determine how these dynamics affect such data, and how news media may be driving these trends.
Methodology
We examine daily Ebola-related Internet search and Twitter data in the U. S. during the six week period ending Oct 31, 2014. TV news coverage data were obtained from the daily number of Ebola-related news videos appearing on two major news networks. We fit the parameters of a mathematical contagion model to the data to determine if the news coverage was a significant factor in the temporal patterns in Ebola-related Internet and Twitter data.
Conclusions
We find significant evidence of contagion, with each Ebola-related news video inspiring tens of thousands of Ebola-related tweets and Internet searches. Between 65% to 76% of the variance in all samples is described by the news media contagion model.
In the weeks following the first imported case of Ebola in the U. S. on September 29, 2014, coverage of the very limited outbreak dominated the news media, in a manner quite disproportionate to the actual threat to national public health; by the end of October, 2014, there were only four laboratory confirmed cases of Ebola in the entire nation. Public interest in these events was high, as reflected in the millions of Ebola-related Internet searches and tweets performed in the month following the first confirmed case. Use of trending Internet searches and tweets has been proposed in the past for real-time prediction of outbreaks (a field referred to as “digital epidemiology”), but accounting for the biases of public panic has been problematic. In the case of the limited U. S. Ebola outbreak, we know that the Ebola-related searches and tweets originating the U. S. during the outbreak were due only to public interest or panic, providing an unprecedented means to determine how these dynamics affect such data, and how news media may be driving these trends.
Methodology
We examine daily Ebola-related Internet search and Twitter data in the U. S. during the six week period ending Oct 31, 2014. TV news coverage data were obtained from the daily number of Ebola-related news videos appearing on two major news networks. We fit the parameters of a mathematical contagion model to the data to determine if the news coverage was a significant factor in the temporal patterns in Ebola-related Internet and Twitter data.
Conclusions
We find significant evidence of contagion, with each Ebola-related news video inspiring tens of thousands of Ebola-related tweets and Internet searches. Between 65% to 76% of the variance in all samples is described by the news media contagion model.
ContributorsTowers, Sherry (Author) / Afzal, Shehzad (Author) / Bernal, Gilbert (Author) / Bliss, Nadya (Author) / Brown, Shala (Author) / Espinoza, Baltazar (Author) / Jackson, Jasmine (Author) / Judson-Garcia, Julia (Author) / Khan, Maryam (Author) / Lin, Michael (Author) / Mamada, Robert (Author) / Moreno, Victor (Author) / Nazari, Fereshteh (Author) / Okuneye, Kamaldeen (Author) / Ross, Mary (Author) / Rodriguez, Claudia (Author) / Medlock, Jan (Author) / Ebert, David (Author) / Castillo-Chavez, Carlos (Author) / Simon M. Levin Mathematical, Computational and Modeling Sciences Center (Contributor) / College of Liberal Arts and Sciences (Contributor) / School of Human Evolution and Social Change (Contributor) / Mary Lou Fulton Teachers College (Contributor) / Educational Leadership and Innovation (Contributor) / School of Mathematical and Statistical Sciences (Contributor) / Global Security Initiative (Contributor)
Created2015-06-11
Description
Background
Seroepidemiological studies before and after the epidemic wave of H1N1-2009 are useful for estimating population attack rates with a potential to validate early estimates of the reproduction number, R, in modeling studies.
Methodology/Principal Findings
Since the final epidemic size, the proportion of individuals in a population who become infected during an epidemic, is not the result of a binomial sampling process because infection events are not independent of each other, we propose the use of an asymptotic distribution of the final size to compute approximate 95% confidence intervals of the observed final size. This allows the comparison of the observed final sizes against predictions based on the modeling study (R = 1.15, 1.40 and 1.90), which also yields simple formulae for determining sample sizes for future seroepidemiological studies. We examine a total of eleven published seroepidemiological studies of H1N1-2009 that took place after observing the peak incidence in a number of countries. Observed seropositive proportions in six studies appear to be smaller than that predicted from R = 1.40; four of the six studies sampled serum less than one month after the reported peak incidence. The comparison of the observed final sizes against R = 1.15 and 1.90 reveals that all eleven studies appear not to be significantly deviating from the prediction with R = 1.15, but final sizes in nine studies indicate overestimation if the value R = 1.90 is used.
Conclusions
Sample sizes of published seroepidemiological studies were too small to assess the validity of model predictions except when R = 1.90 was used. We recommend the use of the proposed approach in determining the sample size of post-epidemic seroepidemiological studies, calculating the 95% confidence interval of observed final size, and conducting relevant hypothesis testing instead of the use of methods that rely on a binomial proportion.
Seroepidemiological studies before and after the epidemic wave of H1N1-2009 are useful for estimating population attack rates with a potential to validate early estimates of the reproduction number, R, in modeling studies.
Methodology/Principal Findings
Since the final epidemic size, the proportion of individuals in a population who become infected during an epidemic, is not the result of a binomial sampling process because infection events are not independent of each other, we propose the use of an asymptotic distribution of the final size to compute approximate 95% confidence intervals of the observed final size. This allows the comparison of the observed final sizes against predictions based on the modeling study (R = 1.15, 1.40 and 1.90), which also yields simple formulae for determining sample sizes for future seroepidemiological studies. We examine a total of eleven published seroepidemiological studies of H1N1-2009 that took place after observing the peak incidence in a number of countries. Observed seropositive proportions in six studies appear to be smaller than that predicted from R = 1.40; four of the six studies sampled serum less than one month after the reported peak incidence. The comparison of the observed final sizes against R = 1.15 and 1.90 reveals that all eleven studies appear not to be significantly deviating from the prediction with R = 1.15, but final sizes in nine studies indicate overestimation if the value R = 1.90 is used.
Conclusions
Sample sizes of published seroepidemiological studies were too small to assess the validity of model predictions except when R = 1.90 was used. We recommend the use of the proposed approach in determining the sample size of post-epidemic seroepidemiological studies, calculating the 95% confidence interval of observed final size, and conducting relevant hypothesis testing instead of the use of methods that rely on a binomial proportion.
ContributorsNishiura, Hiroshi (Author) / Chowell-Puente, Gerardo (Author) / Castillo-Chavez, Carlos (Author) / Simon M. Levin Mathematical, Computational and Modeling Sciences Center (Contributor) / College of Liberal Arts and Sciences (Contributor) / School of Human Evolution and Social Change (Contributor)
Created2011-03-24
Description
Background
Several past studies have found that media reports of suicides and homicides appear to subsequently increase the incidence of similar events in the community, apparently due to the coverage planting the seeds of ideation in at-risk individuals to commit similar acts.
Methods
Here we explore whether or not contagion is evident in more high-profile incidents, such as school shootings and mass killings (incidents with four or more people killed). We fit a contagion model to recent data sets related to such incidents in the US, with terms that take into account the fact that a school shooting or mass murder may temporarily increase the probability of a similar event in the immediate future, by assuming an exponential decay in contagiousness after an event.
Conclusions
We find significant evidence that mass killings involving firearms are incented by similar events in the immediate past. On average, this temporary increase in probability lasts 13 days, and each incident incites at least 0.30 new incidents (p = 0.0015). We also find significant evidence of contagion in school shootings, for which an incident is contagious for an average of 13 days, and incites an average of at least 0.22 new incidents (p = 0.0001). All p-values are assessed based on a likelihood ratio test comparing the likelihood of a contagion model to that of a null model with no contagion. On average, mass killings involving firearms occur approximately every two weeks in the US, while school shootings occur on average monthly. We find that state prevalence of firearm ownership is significantly associated with the state incidence of mass killings with firearms, school shootings, and mass shootings.
Several past studies have found that media reports of suicides and homicides appear to subsequently increase the incidence of similar events in the community, apparently due to the coverage planting the seeds of ideation in at-risk individuals to commit similar acts.
Methods
Here we explore whether or not contagion is evident in more high-profile incidents, such as school shootings and mass killings (incidents with four or more people killed). We fit a contagion model to recent data sets related to such incidents in the US, with terms that take into account the fact that a school shooting or mass murder may temporarily increase the probability of a similar event in the immediate future, by assuming an exponential decay in contagiousness after an event.
Conclusions
We find significant evidence that mass killings involving firearms are incented by similar events in the immediate past. On average, this temporary increase in probability lasts 13 days, and each incident incites at least 0.30 new incidents (p = 0.0015). We also find significant evidence of contagion in school shootings, for which an incident is contagious for an average of 13 days, and incites an average of at least 0.22 new incidents (p = 0.0001). All p-values are assessed based on a likelihood ratio test comparing the likelihood of a contagion model to that of a null model with no contagion. On average, mass killings involving firearms occur approximately every two weeks in the US, while school shootings occur on average monthly. We find that state prevalence of firearm ownership is significantly associated with the state incidence of mass killings with firearms, school shootings, and mass shootings.
ContributorsTowers, Sherry (Author) / Gomez-Lievano, Andres (Author) / Khan, Maryam (Author) / Mubayi, Anuj (Author) / Castillo-Chavez, Carlos (Author) / Simon M. Levin Mathematical, Computational and Modeling Sciences Center (Contributor) / College of Liberal Arts and Sciences (Contributor) / School of Human Evolution and Social Change (Contributor)
Created2015-07-02
Description
Background
The transmission dynamics of Tuberculosis (TB) involve complex epidemiological and socio-economical interactions between individuals living in highly distinct regional conditions. The level of exogenous reinfection and first time infection rates within high-incidence settings may influence the impact of control programs on TB prevalence. The impact that effective population size and the distribution of individuals’ residence times in different patches have on TB transmission and control are studied using selected scenarios where risk is defined by the estimated or perceive first time infection and/or exogenous re-infection rates.
Methods
This study aims at enhancing the understanding of TB dynamics, within simplified, two patch, risk-defined environments, in the presence of short term mobility and variations in reinfection and infection rates via a mathematical model. The modeling framework captures the role of individuals’ ‘daily’ dynamics within and between places of residency, work or business via the average proportion of time spent in residence and as visitors to TB-risk environments (patches). As a result, the effective population size of Patch i (home of i-residents) at time t must account for visitors and residents of Patch i, at time t.
Results
The study identifies critical social behaviors mechanisms that can facilitate or eliminate TB infection in vulnerable populations. The results suggest that short-term mobility between heterogeneous patches contributes to significant overall increases in TB prevalence when risk is considered only in terms of direct new infection transmission, compared to the effect of exogenous reinfection. Although, the role of exogenous reinfection increases the risk that come from large movement of individuals, due to catastrophes or conflict, to TB-free areas.
Conclusions
The study highlights that allowing infected individuals to move from high to low TB prevalence areas (for example via the sharing of treatment and isolation facilities) may lead to a reduction in the total TB prevalence in the overall population. The higher the population size heterogeneity between distinct risk patches, the larger the benefit (low overall prevalence) under the same “traveling” patterns. Policies need to account for population specific factors (such as risks that are inherent with high levels of migration, local and regional mobility patterns, and first time infection rates) in order to be long lasting, effective and results in low number of drug resistant cases.
The transmission dynamics of Tuberculosis (TB) involve complex epidemiological and socio-economical interactions between individuals living in highly distinct regional conditions. The level of exogenous reinfection and first time infection rates within high-incidence settings may influence the impact of control programs on TB prevalence. The impact that effective population size and the distribution of individuals’ residence times in different patches have on TB transmission and control are studied using selected scenarios where risk is defined by the estimated or perceive first time infection and/or exogenous re-infection rates.
Methods
This study aims at enhancing the understanding of TB dynamics, within simplified, two patch, risk-defined environments, in the presence of short term mobility and variations in reinfection and infection rates via a mathematical model. The modeling framework captures the role of individuals’ ‘daily’ dynamics within and between places of residency, work or business via the average proportion of time spent in residence and as visitors to TB-risk environments (patches). As a result, the effective population size of Patch i (home of i-residents) at time t must account for visitors and residents of Patch i, at time t.
Results
The study identifies critical social behaviors mechanisms that can facilitate or eliminate TB infection in vulnerable populations. The results suggest that short-term mobility between heterogeneous patches contributes to significant overall increases in TB prevalence when risk is considered only in terms of direct new infection transmission, compared to the effect of exogenous reinfection. Although, the role of exogenous reinfection increases the risk that come from large movement of individuals, due to catastrophes or conflict, to TB-free areas.
Conclusions
The study highlights that allowing infected individuals to move from high to low TB prevalence areas (for example via the sharing of treatment and isolation facilities) may lead to a reduction in the total TB prevalence in the overall population. The higher the population size heterogeneity between distinct risk patches, the larger the benefit (low overall prevalence) under the same “traveling” patterns. Policies need to account for population specific factors (such as risks that are inherent with high levels of migration, local and regional mobility patterns, and first time infection rates) in order to be long lasting, effective and results in low number of drug resistant cases.
ContributorsMoreno Martinez, Victor (Author) / Espinoza Cortes, Baltazar (Author) / Barley, Kamal (Author) / Paredes Gutierrez, Marlio (Author) / Bichara, Derdei (Author) / Mubayi, Anuj (Author) / Castillo-Chavez, Carlos (Author) / Simon M. Levin Mathematical, Computational and Modeling Sciences Center (Contributor) / College of Liberal Arts and Sciences (Contributor) / School of Human Evolution and Social Change (Contributor)
Created2017-01-11
Description
Glioblastoma multiforme (GBM) is a malignant, aggressive and infiltrative cancer of the central nervous system with a median survival of 14.6 months with standard care. Diagnosis of GBM is made using medical imaging such as magnetic resonance imaging (MRI) or computed tomography (CT). Treatment is informed by medical images and includes chemotherapy, radiation therapy, and surgical removal if the tumor is surgically accessible. Treatment seldom results in a significant increase in longevity, partly due to the lack of precise information regarding tumor size and location. This lack of information arises from the physical limitations of MR and CT imaging coupled with the diffusive nature of glioblastoma tumors. GBM tumor cells can migrate far beyond the visible boundaries of the tumor and will result in a recurring tumor if not killed or removed. Since medical images are the only readily available information about the tumor, we aim to improve mathematical models of tumor growth to better estimate the missing information. Particularly, we investigate the effect of random variation in tumor cell behavior (anisotropy) using stochastic parameterizations of an established proliferation-diffusion model of tumor growth. To evaluate the performance of our mathematical model, we use MR images from an animal model consisting of Murine GL261 tumors implanted in immunocompetent mice, which provides consistency in tumor initiation and location, immune response, genetic variation, and treatment. Compared to non-stochastic simulations, stochastic simulations showed improved volume accuracy when proliferation variability was high, but diffusion variability was found to only marginally affect tumor volume estimates. Neither proliferation nor diffusion variability significantly affected the spatial distribution accuracy of the simulations. While certain cases of stochastic parameterizations improved volume accuracy, they failed to significantly improve simulation accuracy overall. Both the non-stochastic and stochastic simulations failed to achieve over 75% spatial distribution accuracy, suggesting that the underlying structure of the model fails to capture one or more biological processes that affect tumor growth. Two biological features that are candidates for further investigation are angiogenesis and anisotropy resulting from differences between white and gray matter. Time-dependent proliferation and diffusion terms could be introduced to model angiogenesis, and diffusion weighed imaging (DTI) could be used to differentiate between white and gray matter, which might allow for improved estimates brain anisotropy.
ContributorsAnderies, Barrett James (Author) / Kostelich, Eric (Thesis director) / Kuang, Yang (Committee member) / Stepien, Tracy (Committee member) / Harrington Bioengineering Program (Contributor) / School of Mathematical and Statistical Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2016-05
Description
Transorbital surgery has gained recent notoriety due to its incorporation into endoscopic skull base surgery. The body of published literature on the field is cadaveric and observation. The pre-clinical studies are focused on the use of the endoscope only. Furthermore the methodology utilised in the published literature is inconsistent and does not embody the optimal principles of scientific experimentation. This body of work evaluates a minimally invasive novel surgical corridor - the transorbital approach - its validity in neurosurgical practice, as well as both qualitatively and quantitatively assessing available technological advances in a robust experimental fashion. While the endoscope is an established means of visualisation used in clinical transorbital surgery, the microscope has never been assessed with respect to the transorbital approach. This question is investigated here and the anatomical and surgical benefits and limitations of microscopic visualisation demonstrated. The comparative studies provide increased knowledge on specifics pertinent to neurosurgeons and other skull base specialists when planning pre-operatively, such as pathology location, involved anatomical structures, instrument maneuvrability and the advantages and disadvantages of the distinct visualisation technologies. This is all with the intention of selecting the most suitable surgical approach and technology, specific to the patient, pathology and anatomy, so as to perform the best surgical procedure. The research findings illustrated in this body of work are diverse, reproducible and applicable. The transorbital surgical corridor has substantive potential for access to the anterior cranial fossa and specific surgical target structures. The neuroquantitative metrics investigated confirm the utility and benefits specific to the respective visualisation technologies i.e. the endoscope and microscope. The most appropriate setting wherein the approach should be used is also discussed. The transorbital corridor has impressive potential, can utilise all available technological advances, promotes multi-disciplinary co-operation and learning amongst clinicians and ultimately, is a means of improving operative patient care.
ContributorsHoulihan, Lena Mary (Author) / Preul, Mark C. (Thesis advisor) / Vernon, Brent (Thesis advisor) / O' Sullivan, Michael G.J. (Committee member) / Lawton, Michael T. (Committee member) / Santarelli, Griffin (Committee member) / Smith, Brian (Committee member) / Arizona State University (Publisher)
Created2021
Description
A description of numerical and analytical work pertaining to models that describe the growth and progression of glioblastoma multiforme (GBM), an aggressive form of primary brain cancer. Two reaction-diffusion models are used: the Fisher-Kolmogorov-Petrovsky-Piskunov equation and a 2-population model that divides the tumor into actively proliferating and quiescent (or necrotic) cells. The numerical portion of this work (chapter 2) focuses on simulating GBM expansion in patients undergoing treatment for recurrence of tumor following initial surgery. The models are simulated on 3-dimensional brain geometries derived from magnetic resonance imaging (MRI) scans provided by the Barrow Neurological Institute. The study consists of 17 clinical time intervals across 10 patients that have been followed in detail, each of whom shows significant progression of tumor over a period of 1 to 3 months on sequential follow up scans. A Taguchi sampling design is implemented to estimate the variability of the predicted tumors to using 144 different choices of model parameters. In 9 cases, model parameters can be identified such that the simulated tumor contains at least 40 percent of the volume of the observed tumor. In the analytical portion of the paper (chapters 3 and 4), a positively invariant region for our 2-population model is identified. Then, a rigorous derivation of the critical patch size associated with the model is performed. The critical patch (KISS) size is the minimum habitat size needed for a population to survive in a region. Habitats larger than the critical patch size allow a population to persist, while smaller habitats lead to extinction. The critical patch size of the 2-population model is consistent with that of the Fisher-Kolmogorov-Petrovsky-Piskunov equation, one of the first reaction-diffusion models proposed for GBM. The critical patch size may indicate that GBM tumors have a minimum size depending on the location in the brain. A theoretical relationship between the size of a GBM tumor at steady-state and its maximum cell density is also derived, which has potential applications for patient-specific parameter estimation based on magnetic resonance imaging data.
ContributorsHarris, Duane C. (Author) / Kuang, Yang (Thesis advisor) / Kostelich, Eric J. (Thesis advisor) / Preul, Mark C. (Committee member) / Crook, Sharon (Committee member) / Gardner, Carl (Committee member) / Arizona State University (Publisher)
Created2023