scholarly journals Computational Simulation of Tumor Surgical Resection Coupled with the Immune System Response to Neoplastic Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-5
Author(s):  
J. Jesús Naveja ◽  
Flavio F. Contreras-Torres ◽  
Andrés Rodríguez-Galván ◽  
Erick Martínez-Lorán

Numerous mathematical and computational models have arisen to study and predict the effects of diverse therapies against cancer (e.g., chemotherapy, immunotherapy, and even therapies under research with oncolytic viruses) but, unfortunately, few efforts have been directed towards development of tumor resection models, the first therapy against cancer. The model hereby presented was stated upon fundamental assumptions to produce a predictor of the clinical outcomes of patients undergoing a tumor resection. It uses ordinary differential equations validated for predicting the immune system response and the tumor growth in oncologic patients. This model could be further extended to a personalized prognosis predictor and tools for improving therapeutic strategies.

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii124-ii124
Author(s):  
Jan Remsik ◽  
Xinran Tong ◽  
Ugur Sener ◽  
Danille Isakov ◽  
Yudan Chi ◽  
...  

Abstract For decades, the central nervous system was considered to be an immune privileged organ with limited access to systemic immunity. However, the leptomeninges, the cerebrospinal fluid (CSF)-filled anatomical structure that protects the brain and spinal cord, represent a relatively immune-rich environment. Despite the presence of immune cells, complications in the CSF, such as infectious meningitis and a neurological development of cancer known as leptomeningeal metastasis, are difficult to treat and are frequently fatal. We show that immune cells entering the CSF are held in an ‘idle’ state that limits their cytotoxic arsenal and antigen presentation machinery. To understand this underappreciated neuroanatomic niche, we used unique mouse models and rare patient samples to characterize its cellular composition and critical signaling events in health and disease at a single-cell resolution. Revealing the mediators of CSF immune response will allow us to re-evaluate current therapeutic protocols and employ rational combinations with immunotherapies, therefore turning the patient’s own immune system into an active weapon against pathogens and cancer.


2020 ◽  
Vol 2020 (1) ◽  
Author(s):  
Behzad Ghanbari

Abstract Humans are always exposed to the threat of infectious diseases. It has been proven that there is a direct link between the strength or weakness of the immune system and the spread of infectious diseases such as tuberculosis, hepatitis, AIDS, and Covid-19 as soon as the immune system has no the power to fight infections and infectious diseases. Moreover, it has been proven that mathematical modeling is a great tool to accurately describe complex biological phenomena. In the recent literature, we can easily find that these effective tools provide important contributions to our understanding and analysis of such problems such as tumor growth. This is indeed one of the main reasons for the need to study computational models of how the immune system interacts with other factors involved. To this end, in this paper, we present some new approximate solutions to a computational formulation that models the interaction between tumor growth and the immune system with several fractional and fractal operators. The operators used in this model are the Liouville–Caputo, Caputo–Fabrizio, and Atangana–Baleanu–Caputo in both fractional and fractal-fractional senses. The existence and uniqueness of the solution in each of these cases is also verified. To complete our analysis, we include numerous numerical simulations to show the behavior of tumors. These diagrams help us explain mathematical results and better describe related biological concepts. In many cases the approximate results obtained have a chaotic structure, which justifies the complexity of unpredictable and uncontrollable behavior of cancerous tumors. As a result, the newly implemented operators certainly open new research windows in further computational models arising in the modeling of different diseases. It is confirmed that similar problems in the field can be also be modeled by the approaches employed in this paper.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Radu Albulescu ◽  
Elena Codrici ◽  
Ionela Daniela Popescu ◽  
Simona Mihai ◽  
Laura Georgiana Necula ◽  
...  

Inflammation represents the immune system response to external or internal aggressors such as injury or infection in certain tissues. The body’s response to cancer has many parallels with inflammation and repair; the inflammatory cells and cytokines present in tumours are more likely to contribute to tumour growth, progression, and immunosuppression, rather than in building an effective antitumour defence. Using new proteomic technology, we have investigated serum profile of pro- (IL-1β, IL-6, IL-8, IL-12, GM-CSF, and TNF-α) and anti-inflammatory cytokines (IL-4, IL-10), along with angiogenic factors (VEGF, bFGF) in order to assess tumoural aggressiveness. Our results indicate significant dysregulation in serum levels of cytokines and angiogenic factors, with over threefold upregulation of IL-6, IL-1β, TNF-α, and IL-10 and up to twofold upregulation of VEGF, FGF-2, IL-8, IL-2, and GM-CSF. These molecules are involved in tumour progression and aggressiveness, and are also involved in a generation of disease associated pain.


2019 ◽  
Author(s):  
soumya banerjee

How different is the immune system in a human from that of a mouse? Do pathogens replicate at the same rate in different species? Answers to these questions have impact on human health since multi-host pathogens that jump from animals to humans affect millions worldwide.It is not known how rates of immune response and viral dynamics vary from species to species and how they depend on species body size. Metabolic scalingtheory predicts that intracellular processes will be slower in larger animals since cellular metabolic rates are slower. We test how rates of pathogenesis and immune system response rates depend on species body size.


2006 ◽  
Vol 244 (2) ◽  
pp. 77-79 ◽  
Author(s):  
V. Baldazzi ◽  
F. Castiglione ◽  
M. Bernaschi

2014 ◽  
Vol 2014 ◽  
pp. 1-15
Author(s):  
Mohamed Abdo Abd Al-Hady ◽  
Amr Ahmed Badr ◽  
Mostafa Abd Al-Azim Mostafa

The immune system has a cognitive ability to differentiate between healthy and unhealthy cells. The immune system response (ISR) is stimulated by a disorder in the temporary fuzzy state that is oscillating between the healthy and unhealthy states. However, modeling the immune system is an enormous challenge; the paper introduces an extensive summary of how the immune system response functions, as an overview of a complex topic, to present the immune system as a cognitive intelligent agent. The homogeneity and perfection of the natural immune system have been always standing out as the sought-after model we attempted to imitate while building our proposed model of cognitive architecture. The paper divides the ISR into four logical phases: setting a computational architectural diagram for each phase, proceeding from functional perspectives (input, process, and output), and their consequences. The proposed architecture components are defined by matching biological operations with computational functions and hence with the framework of the paper. On the other hand, the architecture focuses on the interoperability of main theoretical immunological perspectives (classic, cognitive, and danger theory), as related to computer science terminologies. The paper presents a descriptive model of immune system, to figure out the nature of response, deemed to be intrinsic for building a hybrid computational model based on a cognitive intelligent agent perspective and inspired by the natural biology. To that end, this paper highlights the ISR phases as applied to a case study on hepatitis C virus, meanwhile illustrating our proposed architecture perspective.


2021 ◽  
Author(s):  
Maicom Peters Xavier ◽  
Lara T. Pompei ◽  
Ana Carolina G. de O. Vieira ◽  
Matheus A. M. de Paula ◽  
Carla R. B. Bonin ◽  
...  

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