How we measure 'reads'
A 'read' is counted each time someone views a publication summary (such as the title, abstract, and list of authors), clicks on a figure, or views or downloads the full-text. Learn more
Citations since 2017
3 Research Items
I am a computer scientist interested in data science, big data, computational economics, evolutionary computation, machine learning and complex systems.
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....
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...
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...
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...
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...
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...
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...
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...
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...
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...
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...
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...
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...
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...
Is cancer cell motility in the early stages of cancer much lower than in the advanced stage of cancer? What is the reason?
Is there correspondence between the dose level in radiotherapy and the cancer cells killed?
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%.
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?
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.
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?
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.
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.