The study of epidemic disease has always been a topic where biological issues mix with social ones.
The aim of this presentation was to modelize in Python language the propagation of Ebola Hemoragic Fever in a modern city thus using SIR model based on Ordinary Differential Equations system and also to produce an amazing Cellular Automaton.
RFC's impact on project using Kolmogorov model and PythonJean-Luc Caut
The aim of this Powerpoint is to use a Kolmogorov model in order to describe the impact of Request For Change (RFC) on Project Life Cycle.
The hidden goal is to ingnite a spark of interest in Project Managers to go further than just learning the basic knowledge provided by PMI with its PMBoK:
This presentation is a case study including a diagnostic of the Digital Marketing current implementation at Dupont de Neumours Personal Protections Europe. It also includes Opportunities and technical solutions to implement and monitor a Web 2.0 strategy in the future.
Leveraging Machine Learning or IA in order to detect Credit Card Fraud and suspicious transations. The aim of this presentation is to help you to improve your knowledge in Machnie Learning and to start development of multiple families of algorithms in Python.
RFC's impact on project using Kolmogorov model and PythonJean-Luc Caut
The aim of this Powerpoint is to use a Kolmogorov model in order to describe the impact of Request For Change (RFC) on Project Life Cycle.
The hidden goal is to ingnite a spark of interest in Project Managers to go further than just learning the basic knowledge provided by PMI with its PMBoK:
This presentation is a case study including a diagnostic of the Digital Marketing current implementation at Dupont de Neumours Personal Protections Europe. It also includes Opportunities and technical solutions to implement and monitor a Web 2.0 strategy in the future.
Leveraging Machine Learning or IA in order to detect Credit Card Fraud and suspicious transations. The aim of this presentation is to help you to improve your knowledge in Machnie Learning and to start development of multiple families of algorithms in Python.
Modelling malaria transmission dynamics in irrigated areas of Tana River Coun...ILRI
Poster by Joseph Muriuki, Philip Kitala, Gerald Muchemi and Bernard Bett presented at the fifth South African Centre for Epidemiological Modelling and Analysis (SACEMA) annual clinic on the meaningful modelling of epidemiological data, Muizenberg, Cape Town, South Africa, 2-13 June 2014.
Algoritma dan pemrograman - Disusun oleh Fitri Ratna DewiFitri Ratna Dewi
Materi yang terdapat dalam salindia ini berdasarkan beberapa referensi buku dan situs web. Semoga bisa bermanfaat bagi yang mau belajar algoritma dan pemrograman ataupun sebagai bahan ajar untuk dibahas lebih lanjut. Keep learning and don't forget to share.
Modelling malaria transmission dynamics in irrigated areas of Tana River Coun...ILRI
Poster by Joseph Muriuki, Philip Kitala, Gerald Muchemi and Bernard Bett presented at the fifth South African Centre for Epidemiological Modelling and Analysis (SACEMA) annual clinic on the meaningful modelling of epidemiological data, Muizenberg, Cape Town, South Africa, 2-13 June 2014.
Algoritma dan pemrograman - Disusun oleh Fitri Ratna DewiFitri Ratna Dewi
Materi yang terdapat dalam salindia ini berdasarkan beberapa referensi buku dan situs web. Semoga bisa bermanfaat bagi yang mau belajar algoritma dan pemrograman ataupun sebagai bahan ajar untuk dibahas lebih lanjut. Keep learning and don't forget to share.
A COMPUTER VIRUS PROPAGATION MODEL USING DELAY DIFFERENTIAL EQUATIONS WITH PR...IJCNCJournal
The SIR model is used extensively in the field of epidemiology, in particular, for the analysis of communal
diseases. One problem with SIR and other existing models is that they are tailored to random or Erdos type networks since they do not consider the varying probabilities of infection or immunity per node. In this paper, we present the application and the simulation results of the pSEIRS model that takes into account the probabilities, and is thus suitable for more realistic scale free networks. In the pSEIRS model, the death rate and the excess death rate are constant for infective nodes. Latent and immune periods are assumed to be constant and the infection rate is assumed to be proportional to I (t) N(t) , where N (t) is the size of the total population and I(t) is the size of the infected population. A node recovers from an infection
temporarily with a probability p and dies from the infection with probability (1-p).
The SIR Model and the 2014 Ebola Virus Disease Outbreak in Guinea, Liberia an...CSCJournals
This research presents a mathematical model aimed at understanding the spread of the 2014 Ebola Virus Disease (EVD) using the standard SIR model. In modelling infectious disease dynamics, it is necessary to investigate whether the disease spread could attain an epidemic level or it could be wiped out. Data from the 2014 Ebola Virus Disease outbreak is used and Guinea where the outbreak started is considered in this study. A three dimensional non-linear differential equation is formulated and solved numerically using the Runge-Kutta 4th order method in the Vensim Personal Learning Edition Software. It is shown from the study that, with public health interventions, the effective reproductive number can be reduced making it possible for the outbreak to die out. It is also shown mathematically that the epidemic can only die out when there are no new infected individuals in the population.
Simulation rules are almost the same to what I coded using Python bu.pdfsnewfashion
Simulation rules are almost the same to what I coded using Python but with one interesting
addition a partial immunity (see details below). The main difference between the Python version
and R-version of the code would be the use of vectorization. You should use as little as possible
of loops. In fact, there should be just one loop for the days-count. If anyone tries to create the
exact copy of my Python code but in R, the grade will be quite low. Below are rules that should
help you building a simulation model:
1. We assume that there are N_population citizens in a population. N_population is an input
parameter. During development and testing you can have it small, but your code should be able
to handle a reasonably large value for population size.
2. Every citizen has a health state healthy, sick, dead (or you can code it as 0, 1, 2). When we
start, all citizens are alive and healthy
3. To start the pandemic, you randomly mark a small number of citizens as sick there can be a
parameter for the number of initially infected citizens. You can start with 1 or 2 initial sick cases.
4. One iteration is one day. During the day, every citizen can meet a random number (say
between 0 and 20 inclusive) of randomly selected citizens. You dont really need to control all
citizens as we are interested in meetings of sick people only. We dont care how many healthy
people meet each other.
5. Every sick citizen can stay sick and infectious for 10 days, hence you should have some
counter for each sick citizen. After 10 days a sick citizen becomes healthy and stops spreading
the virus
6. Obviously, dead citizens cannot become sick, they dont meet anyone and, as a result, cannot
infect anyone.
7. During the day every sick citizen has a probability to die (mortality rate) from the disease with
probability 0.5% (quite low probability).
8. If a sick citizen does not die, then they can meet other people as per the rule 4 above, and if
they meet a healthy person, that person might become sick too and start infecting other people
starting from the next day (that is an infection day is day 0 of their sickness). The probability for
a citizen of becoming sick (infection rate) after a contact is 30% (this is quite high).
9. (New rule!) After surviving the infection and getting healthy, the person becomes immune.
This is a partial immunity. It does not make the person invincible but reduces the chance of
infection in future meetings with sick people. Take the immunity coefficient as 0.1. That is, a
probability of being infected for immune person is ten times lower than for the person without an
immunity. The infection rate for the immune person is the original infection rate multiplied by
the immunity coefficient, e.g. (0.3*0.1).
For the test, you can set immunity coefficient equal 1, which means no benefits of immunity and
the result should be the same as in Python example I presented.
10. You should run this simulation for a number of days (iterations) and store each da.
Modeling the Effect of Variation of Recruitment Rate on the Transmission Dyna...IOSR Journals
In this Paper, the effect of the variation of recruitment rate on the transmission dynamics of
tuberculosis was studied by modifying an existing model. While the recruitment rate into the susceptible class of
the existing model is constant, in our modified model we used a varying recruitment rate. The models were
analyzed analytically and numerically and these results were compared. The Disease Free Equilibrium (DFE)
state of the existing model was found to be
,0,0,0
, the DFE of the modified model was found to be
( ,0,0,0) * S where * S is arbitrary. While all the eigenvalue of the existing model are negative, one of the
eigenvalues of the modified model is zero. The basic reproduction number o R of both models are established to
be the same. The numerical experiments show a gradual decline in the infected and exposed populations as the
recruitment rates increase in both models but the decline is more in the modified model than in the existing
model. This implies that eradication will be achieved faster using the model with a varying recruitment rate.
Modeling and Simulation of Spread and Effect of Malaria EpidemicWaqas Tariq
The purpose of this paper is to consider malaria infection (A) and the control of malaria (B) as the two sets of soldiers engage in a war. The principal objectives are to see if it is possible with time to reduce and eradicate malaria in our environment taking reasonable precaution. The methodology approach is to model a mathematical equation using battling method approach to find the time(t) that control malaria in our environment will conquer the malaria infection i.e. when A(t)=0. The number of provided facilities (n) for the protection of malaria is also considered and varied. The result shows that as the number of malaria control increases the control time is decreasing.
Mathematical Modeling Of Syphilis Disease A Case Study With Reference To Anan...IJERA Editor
In this paper we have analyzed the Mathematical modeling of Syphilis disease, Syphilis is a highly contagious disease spread primarily by sexual activity, including oral and anal sex. Occasionally, the disease can be passed to another person through prolonged kissing or close bodily contact. Although this disease is spread from sores, the vast majority of those sores go unrecognized. The infected person is often unaware of the disease and unknowingly passes it on to his or her sexual partner. Pregnant women with the disease can spread it to their baby. This disease, called congenital syphilis, can cause abnormalities or even death to the child. Syphilis cannot be spread by toilet seats, door knobs, swimming pools, hot tubs, bath tubs, shared clothing, or eating utensils.
Engineering Research Publication
Best International Journals, High Impact Journals,
International Journal of Engineering & Technical Research
ISSN : 2321-0869 (O) 2454-4698 (P)
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IJETR, IJMCTR,
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Monthly Journal,
Good quality Journals,
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Free Journals, Open access Journals,
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Science Journals,
The local and global stability of the disease free equilibrium in a co infect...iosrjce
IOSR Journal of Mathematics(IOSR-JM) is a double blind peer reviewed International Journal that provides rapid publication (within a month) of articles in all areas of mathemetics and its applications. The journal welcomes publications of high quality papers on theoretical developments and practical applications in mathematics. Original research papers, state-of-the-art reviews, and high quality technical notes are invited for publications.
Ebola hemorrhagic fever is a disease caused by one of five different Ebola viruses. Four of the strains can cause severe illness in humans and animals. Humans can be infected by other humans if they come in contact with body fluids from an infected person or contaminated objects from infected persons. Humans can also be exposed to the virus, for example, by butchering infected animals. Deadly human Ebola outbreaks have been confirmed in the following countries: Democratic Republic of the Congo (DRC), Gabon, South Sudan, Ivory Coast, Uganda, and Republic of the Congo (ROC), Guinea and Liberia. In this sense, it is of vital importance to analysis the history data and predicts its propagation. More specifically, a model based k-means algorithm to determine the optimal locations of virus delivery is constructed and tested Using Mab-lab programming. By experiment, we find that our model can work well and lead to a relatively accurate prediction, which can help the government forecast the epidemic spread more efficiently
Sensitivity Analysis of the Dynamical Spread of Ebola Virus DiseaseAI Publications
The deterministic epidemiological model of (S, E, Iu, Id, R) were studied to gain insight into the dynamical spread of Ebola virus disease. Local and global stability of the model are explored for disease-free and endemic equilibria. Sensitivity analysis is performed on basic reproduction number to check the importance of each parameter on the transmission of Ebola disease. Positivity solution is analyzed for mathematical and epidemiological posedness of the model. Numerical simulation was analyzed by MAPLE 18 software using embedded Runge-Kutta method of order (4) which shows the parameter that has high impact in the spread of the disease spread of Ebola virus disease.
International Journal of Engineering Research and Applications (IJERA) is an open access online peer reviewed international journal that publishes research and review articles in the fields of Computer Science, Neural Networks, Electrical Engineering, Software Engineering, Information Technology, Mechanical Engineering, Chemical Engineering, Plastic Engineering, Food Technology, Textile Engineering, Nano Technology & science, Power Electronics, Electronics & Communication Engineering, Computational mathematics, Image processing, Civil Engineering, Structural Engineering, Environmental Engineering, VLSI Testing & Low Power VLSI Design etc.
Similar to Modelisation of Ebola Hemoragic Fever propagation in a modern city (20)
Seminar of U.V. Spectroscopy by SAMIR PANDASAMIR PANDA
Spectroscopy is a branch of science dealing the study of interaction of electromagnetic radiation with matter.
Ultraviolet-visible spectroscopy refers to absorption spectroscopy or reflect spectroscopy in the UV-VIS spectral region.
Ultraviolet-visible spectroscopy is an analytical method that can measure the amount of light received by the analyte.
Multi-source connectivity as the driver of solar wind variability in the heli...Sérgio Sacani
The ambient solar wind that flls the heliosphere originates from multiple
sources in the solar corona and is highly structured. It is often described
as high-speed, relatively homogeneous, plasma streams from coronal
holes and slow-speed, highly variable, streams whose source regions are
under debate. A key goal of ESA/NASA’s Solar Orbiter mission is to identify
solar wind sources and understand what drives the complexity seen in the
heliosphere. By combining magnetic feld modelling and spectroscopic
techniques with high-resolution observations and measurements, we show
that the solar wind variability detected in situ by Solar Orbiter in March
2022 is driven by spatio-temporal changes in the magnetic connectivity to
multiple sources in the solar atmosphere. The magnetic feld footpoints
connected to the spacecraft moved from the boundaries of a coronal hole
to one active region (12961) and then across to another region (12957). This
is refected in the in situ measurements, which show the transition from fast
to highly Alfvénic then to slow solar wind that is disrupted by the arrival of
a coronal mass ejection. Our results describe solar wind variability at 0.5 au
but are applicable to near-Earth observatories.
Deep Behavioral Phenotyping in Systems Neuroscience for Functional Atlasing a...Ana Luísa Pinho
Functional Magnetic Resonance Imaging (fMRI) provides means to characterize brain activations in response to behavior. However, cognitive neuroscience has been limited to group-level effects referring to the performance of specific tasks. To obtain the functional profile of elementary cognitive mechanisms, the combination of brain responses to many tasks is required. Yet, to date, both structural atlases and parcellation-based activations do not fully account for cognitive function and still present several limitations. Further, they do not adapt overall to individual characteristics. In this talk, I will give an account of deep-behavioral phenotyping strategies, namely data-driven methods in large task-fMRI datasets, to optimize functional brain-data collection and improve inference of effects-of-interest related to mental processes. Key to this approach is the employment of fast multi-functional paradigms rich on features that can be well parametrized and, consequently, facilitate the creation of psycho-physiological constructs to be modelled with imaging data. Particular emphasis will be given to music stimuli when studying high-order cognitive mechanisms, due to their ecological nature and quality to enable complex behavior compounded by discrete entities. I will also discuss how deep-behavioral phenotyping and individualized models applied to neuroimaging data can better account for the subject-specific organization of domain-general cognitive systems in the human brain. Finally, the accumulation of functional brain signatures brings the possibility to clarify relationships among tasks and create a univocal link between brain systems and mental functions through: (1) the development of ontologies proposing an organization of cognitive processes; and (2) brain-network taxonomies describing functional specialization. To this end, tools to improve commensurability in cognitive science are necessary, such as public repositories, ontology-based platforms and automated meta-analysis tools. I will thus discuss some brain-atlasing resources currently under development, and their applicability in cognitive as well as clinical neuroscience.
This pdf is about the Schizophrenia.
For more details visit on YouTube; @SELF-EXPLANATORY;
https://www.youtube.com/channel/UCAiarMZDNhe1A3Rnpr_WkzA/videos
Thanks...!
Introduction:
RNA interference (RNAi) or Post-Transcriptional Gene Silencing (PTGS) is an important biological process for modulating eukaryotic gene expression.
It is highly conserved process of posttranscriptional gene silencing by which double stranded RNA (dsRNA) causes sequence-specific degradation of mRNA sequences.
dsRNA-induced gene silencing (RNAi) is reported in a wide range of eukaryotes ranging from worms, insects, mammals and plants.
This process mediates resistance to both endogenous parasitic and exogenous pathogenic nucleic acids, and regulates the expression of protein-coding genes.
What are small ncRNAs?
micro RNA (miRNA)
short interfering RNA (siRNA)
Properties of small non-coding RNA:
Involved in silencing mRNA transcripts.
Called “small” because they are usually only about 21-24 nucleotides long.
Synthesized by first cutting up longer precursor sequences (like the 61nt one that Lee discovered).
Silence an mRNA by base pairing with some sequence on the mRNA.
Discovery of siRNA?
The first small RNA:
In 1993 Rosalind Lee (Victor Ambros lab) was studying a non- coding gene in C. elegans, lin-4, that was involved in silencing of another gene, lin-14, at the appropriate time in the
development of the worm C. elegans.
Two small transcripts of lin-4 (22nt and 61nt) were found to be complementary to a sequence in the 3' UTR of lin-14.
Because lin-4 encoded no protein, she deduced that it must be these transcripts that are causing the silencing by RNA-RNA interactions.
Types of RNAi ( non coding RNA)
MiRNA
Length (23-25 nt)
Trans acting
Binds with target MRNA in mismatch
Translation inhibition
Si RNA
Length 21 nt.
Cis acting
Bind with target Mrna in perfect complementary sequence
Piwi-RNA
Length ; 25 to 36 nt.
Expressed in Germ Cells
Regulates trnasposomes activity
MECHANISM OF RNAI:
First the double-stranded RNA teams up with a protein complex named Dicer, which cuts the long RNA into short pieces.
Then another protein complex called RISC (RNA-induced silencing complex) discards one of the two RNA strands.
The RISC-docked, single-stranded RNA then pairs with the homologous mRNA and destroys it.
THE RISC COMPLEX:
RISC is large(>500kD) RNA multi- protein Binding complex which triggers MRNA degradation in response to MRNA
Unwinding of double stranded Si RNA by ATP independent Helicase
Active component of RISC is Ago proteins( ENDONUCLEASE) which cleave target MRNA.
DICER: endonuclease (RNase Family III)
Argonaute: Central Component of the RNA-Induced Silencing Complex (RISC)
One strand of the dsRNA produced by Dicer is retained in the RISC complex in association with Argonaute
ARGONAUTE PROTEIN :
1.PAZ(PIWI/Argonaute/ Zwille)- Recognition of target MRNA
2.PIWI (p-element induced wimpy Testis)- breaks Phosphodiester bond of mRNA.)RNAse H activity.
MiRNA:
The Double-stranded RNAs are naturally produced in eukaryotic cells during development, and they have a key role in regulating gene expression .
THE IMPORTANCE OF MARTIAN ATMOSPHERE SAMPLE RETURN.Sérgio Sacani
The return of a sample of near-surface atmosphere from Mars would facilitate answers to several first-order science questions surrounding the formation and evolution of the planet. One of the important aspects of terrestrial planet formation in general is the role that primary atmospheres played in influencing the chemistry and structure of the planets and their antecedents. Studies of the martian atmosphere can be used to investigate the role of a primary atmosphere in its history. Atmosphere samples would also inform our understanding of the near-surface chemistry of the planet, and ultimately the prospects for life. High-precision isotopic analyses of constituent gases are needed to address these questions, requiring that the analyses are made on returned samples rather than in situ.
Earliest Galaxies in the JADES Origins Field: Luminosity Function and Cosmic ...Sérgio Sacani
We characterize the earliest galaxy population in the JADES Origins Field (JOF), the deepest
imaging field observed with JWST. We make use of the ancillary Hubble optical images (5 filters
spanning 0.4−0.9µm) and novel JWST images with 14 filters spanning 0.8−5µm, including 7 mediumband filters, and reaching total exposure times of up to 46 hours per filter. We combine all our data
at > 2.3µm to construct an ultradeep image, reaching as deep as ≈ 31.4 AB mag in the stack and
30.3-31.0 AB mag (5σ, r = 0.1” circular aperture) in individual filters. We measure photometric
redshifts and use robust selection criteria to identify a sample of eight galaxy candidates at redshifts
z = 11.5 − 15. These objects show compact half-light radii of R1/2 ∼ 50 − 200pc, stellar masses of
M⋆ ∼ 107−108M⊙, and star-formation rates of SFR ∼ 0.1−1 M⊙ yr−1
. Our search finds no candidates
at 15 < z < 20, placing upper limits at these redshifts. We develop a forward modeling approach to
infer the properties of the evolving luminosity function without binning in redshift or luminosity that
marginalizes over the photometric redshift uncertainty of our candidate galaxies and incorporates the
impact of non-detections. We find a z = 12 luminosity function in good agreement with prior results,
and that the luminosity function normalization and UV luminosity density decline by a factor of ∼ 2.5
from z = 12 to z = 14. We discuss the possible implications of our results in the context of theoretical
models for evolution of the dark matter halo mass function.
Cancer cell metabolism: special Reference to Lactate PathwayAADYARAJPANDEY1
Normal Cell Metabolism:
Cellular respiration describes the series of steps that cells use to break down sugar and other chemicals to get the energy we need to function.
Energy is stored in the bonds of glucose and when glucose is broken down, much of that energy is released.
Cell utilize energy in the form of ATP.
The first step of respiration is called glycolysis. In a series of steps, glycolysis breaks glucose into two smaller molecules - a chemical called pyruvate. A small amount of ATP is formed during this process.
Most healthy cells continue the breakdown in a second process, called the Kreb's cycle. The Kreb's cycle allows cells to “burn” the pyruvates made in glycolysis to get more ATP.
The last step in the breakdown of glucose is called oxidative phosphorylation (Ox-Phos).
It takes place in specialized cell structures called mitochondria. This process produces a large amount of ATP. Importantly, cells need oxygen to complete oxidative phosphorylation.
If a cell completes only glycolysis, only 2 molecules of ATP are made per glucose. However, if the cell completes the entire respiration process (glycolysis - Kreb's - oxidative phosphorylation), about 36 molecules of ATP are created, giving it much more energy to use.
IN CANCER CELL:
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
introduction to WARBERG PHENOMENA:
WARBURG EFFECT Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside.
Otto Heinrich Warburg (; 8 October 1883 – 1 August 1970) In 1931 was awarded the Nobel Prize in Physiology for his "discovery of the nature and mode of action of the respiratory enzyme.
WARNBURG EFFECT : cancer cells under aerobic (well-oxygenated) conditions to metabolize glucose to lactate (aerobic glycolysis) is known as the Warburg effect. Warburg made the observation that tumor slices consume glucose and secrete lactate at a higher rate than normal tissues.
Professional air quality monitoring systems provide immediate, on-site data for analysis, compliance, and decision-making.
Monitor common gases, weather parameters, particulates.
4. The study of epidemic disease has always been a topic where biological issues mix with social ones.
When we talk about epidemic disease, we will be thinking of contagious diseases caused by biological pathogens, things like influenza, measles, and today Ebola or Marburg fever diseases, which spread from person to person.
Epidemics can pass explosively through a population. In extreme cases, a single disease outbreak can have a significant effect on a whole civilization, as with the epidemics started by the arrival of Europeans in the Americas, or the outbreak of bubonic plague that killed 20% of the population of Europe over a seven-year period in the 1300s.
The patterns by which epidemics spread through groups of people is determined not just by the properties of the pathogen carrying it, including its contagiousness, the length of its infectious period, and its severity, but also by network structures within the population it is affecting.
5. But more generally, the opportunities for a disease to spread are given by a contact network: there is a node for each person, and an edge if two people come into contact with each other in a way that makes it possible for the disease to spread from one to the other.
The transmission from one person to another is a sufficiently complex and unobservable process at the person-to-person level that it is most useful to model it as random.
That is, we will generally assume that when two people are directly linked in the contact network, and one of them has the disease, there is a given probability that he or she will pass it to the other.
This use of randomness allows us to abstract away questions about the mechanics of how one person catches a disease from another for which we have no useful simple models.
7. The simplest model of contagion, which we refer to as a branching process is working as follows.
(First wave.) Suppose that a person carrying a new disease enters a population, and transmits it to each person he meets independently with a probability of p. Further, suppose that he meets k people while he is contagious; let’s call these k people the first wave of the epidemic.
Based on the random transmission of the disease from the initial person, some of the people in the first wave may get infected with the disease, while others may not.
(Second wave.) Now, each person in the first wave goes out into the population and meets k different people, resulting in a second wave of k · k = k2 people. Each infected person in the first wave passes the disease independently to each of the k second-wave people they meet, again independently with probability p.
(Subsequent waves.) Further waves are formed in the same way, by having each person in the current wave meet k new people, passing the disease to each independently with probability p.
8. Thus the contact network for this epidemic can be drawn as in figure below
(with k = 3 land only the first three waves shown). We refer to such a network as a tree.
This tree is a representation of the Ebola spreading process where each person contaminated will also contaminate from 1 to 4 other persons.
9. Basic Reproductive Number and a Dichotomy for Branching Processes
So there are only two possibilities for a disease in the branching process model:
If the disease ever reaches a wave where it fails to infect anyone, then it has died out: since people in future waves can only catch the disease from others higher up in the tree, no one in any future wave will be infected either.
Or it continues to infect people in every wave, proceeding infinitely through the contact network.
It turns out that there is a simple condition to tell these two possibilities apart, based on a quantity called the basic reproductive number of the disease.
The basic reproductive number, denoted R0 , is the expected number of new cases of the disease caused by a single individual. Since in our model everyone meets k new people and infects each with probability p, the basic reproductive number here is given by R0 = pk.
The outcome of the disease in a branching process model is determined by whether the basic reproductive number is smaller or larger than 1.
If R0 < 1, then with probability 1, the disease dies out after a finite
number of waves.
If R0 > 1, then with probability greater than 0 the disease
persists by infecting at least one person in each wave.
10. Here below a real Ebola propagation with k = 10 in Gabon in 2001.
Ebola: Human transmission of the disease
13. The SIR epidemic model can be applied to any network model structure.
To do this, we preserve the basic ingredients of the branching process model at the level of individual nodes, but make the contact structure much more general. An individual node in the branching process model goes through three potential stages during the course of the epidemic:
Susceptible: Before the node has caught the disease, it is susceptible to infection from
its neighbors.
Infectious: Once the node has caught the disease, it is infectious and has some probability of infecting each of its susceptible neighbors.
Recovered: After a particular node has experienced the full infectious period, this node is removed from consideration, since it no longer poses a threat of future infection.
14. This model was for the first time proposed by O. Kermack and Anderson Gray McKendrick as a special case of what we now call Kermack-McKendrick theory, and followed work McKendrick had done with the Ronald Ross.
The dynamics of the SIR model are given by the system of Ordinary Differential Equations:
Where b is the rate at which an infected person infects a susceptible, and g is the recovery rate of infected people.
Where:
- S(t) : Number of persons susceptible to be infected by the pathogen agent
- I(t) : Number of infectious persons
- R(t) : Number of persons that recovered
풅푺 풅풕 =− 휷푺푰
풅푰 풅풕 =휷푺푰 − 휸푰
풅푹 풅풕 =휸푰
15. This system is non-linear, and does not admit a generic analytic solution. Nevertheless, significant results can be derived analytically.
Firstly note that from:
it follows that:
expressing in mathematical terms the constancy of population N. Note that the above relationship implies that one need only study the equation for two of the three variables.
Secondly, we note that the dynamics of the infectious class depends on the following ratio:
풅푺 풅풕 + 풅푰 풅풕 + 풅푹 풅풕 =ퟎ
푺풕+ 푰풕+푹(풕) = N = constant
푹ퟎ= 휷 휸 N
16. The SIR model developed in Python is set with the following data for simulating Ebola outbreak in a total population of 1.000 people.
Assuming that the population is quarantined and no additional population is added during the period.
For Ebola:
휸 = 1/10 (Recovery rate)
N = S + I + R = 1.000 (Total population )
I(0) = 1 (Initial infected population )
휷 = 0.3 (Infection rate)
푹ퟎ = 3 ( 1< 푹ퟎ <4 )
17. . Resolution of SIR Ordinary Differential Equation system with python:
18. . Resolution of SIR Ordinary Differential Equation system with python:
20. Cellular Automaton is more appropriate when it comes to visualize the propagation of a disease on a map.
Cellular automata (CA) consist of dicrete agents or particules, which occupy some or all sites of a regular lattice.
These particules have a discrete or continuous internal state variables and a set of rules describing the evolution of their state and position.
The change of state of particule depends on the current state of the particule and those of neighboring particles.
Concerning my Ebola CA developped in Python, 푹ퟎ ∈ {1;4} meaning that each contaminated cell is going to contaminate between 1 to 4 cells during its contagious state. In my model I am using a probabilistic method when deciding which particules are going to be contaminated thus using Normal law and a Monte-Carlo method.
More each contaminated cell will have a probability of 70% to die thus allowing only 30% of recovery rate as per current Ebola disease in west Africa.
21. Cellular Automaton principles
The CA starts with a single infected cell (in red). The first step will test all its eigth neighbors in order to check if they are susceptible (in blue) to be infected.
Assuming that all the eight neighbors are susceptible we launch a random process in order to contaminate between 1 to 4 of these eight susceptible cells.
After that we are starting a new random process implementing a normal law N(0,1) in order to change the internal state of the Infected cell thus killing it with a 70% death rate probability.
In order to take into account that contaminated cells are not statics nor quarantined the CA is simulating some movements and contaminates randomly some cells elsewhere in the city.
22. Presentation of the Cellular Automaton
The CA is representing a city composed by 7.000 cells or houses. Some of them are free (in white), orange cells are representing streets, green cells are for parks, dark blue cell is for susceptible to be infected, red is the infected, and cyan is for recovered .