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Angel Monteagudo

Angel Monteagudo

PhD in Computer Science

About

15
Publications
1,934
Reads
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240
Citations
Citations since 2017
3 Research Items
192 Citations
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201720182019202020212022202301020304050
201720182019202020212022202301020304050
Introduction
I am a computer scientist interested in data science, big data, computational economics, evolutionary computation, machine learning and complex systems.
Additional affiliations
March 2016 - present
University of A Coruña
Position
  • Research Assistant

Publications

Publications (15)
Article
Full-text available
The COVID-19 pandemic led to restrictions on activities and mobility in many parts of the world. After the main peak of the crisis, restrictions were gradually removed, returning to a new normal situation. This process has impacted urban mobility. The limited information on the new normal situation shows changes that can be permanent or reversible....
Article
Full-text available
Background The canonical code, although prevailing in complex genomes, is not universal. It was shown the canonical genetic code superior robustness compared to random codes, but it is not clearly determined how it evolved towards its current form.The error minimization theory considers the minimization of point mutation adverse effect as the main...
Chapter
We have used cellular automata to model tumor growth behavior in multicellular systems. We modeled the behavior at a cellular level, based on the presence of the main cancer hallmarks in each cell in the avascular phase. The abstract model of cancer hallmarks and the cellular automata tool allow the analysis of the emergent behavior of the multicel...
Article
Full-text available
Cancer can be viewed as an emergent behavior in terms of complex system theory and artificial life, Cellular Automata (CA) being the tool most used for studying and characterizing the emergent behavior. Different approaches with CA models were used to model cancer growth. The use of the abstract model of acquired cancer hallmarks permits the direct...
Conference Paper
We used evolutionary computing for optimizing cancer treatments taking into account the presence and effects of cancer stem cells. We used a cellular automaton to model tumor growth at cellular level, based on the presence of the main cancer hallmarks in the cells. The cellular automaton allows the study of the emergent behavior of the multicellula...
Article
The authors used computational biology as an approach for analysing the emergent dynamics of tumour growth at cellular level. They applied cellular automata for modelling the behaviour of cells when the main cancer cell hallmarks are present. Their model is oriented to mimic the development of multicellular spheroids of tumour cells. In their model...
Article
We used a cellular automaton model for cancer growth simulation at cellular level, based on the presence of different cancer hallmarks acquired by the cells. The presence of the hallmarks in each of the cells determines cell mitotic and apoptotic behaviors. Depending on the presence of the different hallmarks and some associated parameters of the h...
Conference Paper
We used a cellular automaton model for cancer growth simulation at cellular level, based on the presence of different cancer hallmarks acquired by the cells. The rules of the cellular automaton determine cell mitotic and apoptotic behaviors, which are based on the acquisition of the hallmarks in the cells by means of mutations. The simulation tool...
Conference Paper
We studied the relative importance of the different cancer hallmarks in tumor growth in a multicellular system. Tumor growth was modeled with a cellular automaton which determines cell mitotic and apoptotic behaviors. These behaviors depend on the cancer hallmarks acquired in each cell as consequence of mutations. Additionally, these hallmarks are...
Conference Paper
We used cellular automata for simulating tumor growth in a multicellular system. Cells have a genome associated with different cancer hallmarks, indicating if those are activated as consequence of mutations. The presence of the cancer hallmarks defines cell states and cell mitotic behaviors. These hallmarks are associated with a series of parameter...
Article
Full-text available
As the canonical code is not universal, different theories about its origin and organization have appeared. The optimization or level of adaptation of the canonical genetic code was measured taking into account the harmful consequences resulting from point mutations leading to the replacement of one amino acid for another. There are two basic theor...
Article
We used simulated evolution to study the adaptability level of the canonical genetic code. An adapted genetic algorithm (GA) searches for optimal hypothetical codes. Adaptability is measured as the average variation of the hydrophobicity that the encoded amino acids undergo when errors or mutations are present in the codons of the hypothetical code...
Article
We have studied the canonical genetic code optimality by means of simulated evolution. A genetic algorithm is used to search for better adapted hypothetical codes and as a method to guess the difficulty in finding such alternative codes. Such analysis is performed within the coevolution theory of the genetic code organization. We have studied the p...
Conference Paper
In this work we use simulated evolution to corroborate the adaptability of the natural genetic code. An adapted genetic algorithm searches for optimal hypothetical codes. The adaptability is measured as the average variation of the hydrophobicity that experiment the encoded amino acids when errors or mutations are presented in the codons of the hy...

Questions

Questions (17)
Question
I'm looking for an equation:
prob(death) = ...
Question
Is cancer cell motility in the early stages of cancer much lower than in the advanced stage of cancer? What is the reason?
Question
clinical trials or something else?
Question
It can be in 2d or 3d models (multicellular spheroids).
Question
Is there correspondence between the dose level in radiotherapy and the cancer cells killed?
For example:
at a dose of 80 Gy the percentage of cancer cells killed is x% 
at a dose of 90 Gy the percentage of cancer cells killed is x%.
...
Question
For instance, in FOLFOX4 the recommended dose:
Oxaliplatin 85 mg/m² IV infusion 2 h. Is this high or low dose?
Leucovorin 200 mg/m² IV infusion over 120 minutes. Is this high or low dose?
Fluorouracil 400 mg/m² IV bolus 2 min. Is this high or low dose?
Why is better Fluorouracil 400 mg/m² over 2minutes than Fluorouracil 200mg/m² over 4minutes?
Question
Cancer stem cells (CSCs) are cancer cells that possess characteristics associated with normal stem cells, specifically the ability to give rise to all cell types found in a particular cancer sample.
But I would like to know more about their motility.
Question
For instance, in FOLFOX the frequency is every 2 weeks (the treatment is repeated every 2 weeks).
Question
The Hayflick limit is the number of times a normal human cell population will divide until cell division stops. Hayflick concluded that a cell could complete mitosis only forty to sixty times before undergoing apoptosis and subsequent death. Dou you know any type of cell with a maximum number of divisions around 30-35?
Question
Do you know any study about possible behaviour transitions with in-vitro experiments (specially in multicellular spheroids) when a drug, with different concentrations, is applied? That is, I am not asking about the efficacy of a drug, but the possible effects with different drug concentrations.

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Cited By

Projects

Projects (5)
Project
To simulate different kinds of tumor treatment
Project
Understanding the evolution of the genetic code is key to elucidate the origin of life.
Project
Therapies targeting cancer stem cells. Current therapeutic strategies against cancer have severe limitations that frequently lead to treatment failure. Cancer stem cells (CSC) have several properties which allow them to survive cancer therapy. These surviving CSC then repopulate the tumor, causing relapse.