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structure. in data , and. structure. in models. …uncertainty and complexity. What do I mean by structure?. The key idea is conditional independence : x and z are conditionally independent given y if p(x,z|y) = p(x|y)p(z|y) - PowerPoint PPT Presentation
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What do I mean by structure?The key idea is conditional independence:
x and z are conditionally independent given y if p(x,z|y) = p(x|y)p(z|y)
… implying, for example, that p(x|y,z) = p(x|y)
CI turns out to be a remarkably powerful and pervasive idea in probability and statistics
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How to represent this structure?• The idea of graphical modelling: we
draw graphs in which nodes represent variables, connected by lines and arrows representing relationships
• We separate logical (the graph) and quantitative (the assumed distributions) aspects of the model
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Markov chains
Graphical models
Contingencytables
Spatial statistics
Sufficiency
Regression
Covariance selection
Statisticalphysics
Genetics
AI
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Graphical modelling [1]
• Assuming structure to do probability calculations
• Inferring structure to make substantive conclusions
• Structure in model building
• Inference about latent variables
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Basic DAG
)|()( )(pa vVv
v xxpxp
in general:
for example:
a b
c
d
p(a,b,c,d)=p(a)p(b)p(c|a,b)p(d|c)
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DNA forensics example(thanks to Julia Mortera)
• A blood stain is found at a crime scene
• A body is found somewhere else!
• There is a suspect
• DNA profiles on all three - crime scene sample is a ‘mixed trace’: is it a mix of the victim and the suspect?
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DNA forensics in Hugin
• Disaggregate problem in terms of paternal and maternal genes of both victim and suspect.
• Assume Hardy-Weinberg equilibrium
• We have profiles on 8 STR markers - treated as independent (linkage equilibrium)
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DNA forensics
The data:
2 of 8 markers show more than 2 alleles at crime scene mixture of 2 or more people
Marker Victim Suspect Crime sceneD3S1358 18 18 16 16 16 18VWA 17 17 17 18 17 18TH01 6 7 6 7 6 7TPOX 8 8 8 11 8 11D5S818 12 13 12 12 12 13D13S317 8 8 8 11 8 11FGA 22 26 24 25 22 24 25 26D7S820 8 10 8 11 8 10 11
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Allele probability8 .18510 .13511 .234x .233y .214
DNA forensics
Population gene frequencies for D7S820 (used as ‘prior’ on ‘founder’ nodes):
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DNA forensics
Results (suspect+victim vs. unknown+victim):
Marker Victim Suspect Crime scene Likelihoodratio (sv/uv)
D3S1358 18 18 16 16 16 18 11.35VWA 17 17 17 18 17 18 15.43TH01 6 7 6 7 6 7 5.48TPOX 8 8 8 11 8 11 3.00D5S818 12 13 12 12 12 13 14.79D13S317 8 8 8 11 8 11 24.45FGA 22 26 24 25 22 24 25 26 76.92D7S820 8 10 8 11 8 10 11 4.90overall 3.93108
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How does it work?
(1) Manipulate DAG to corresponding (undirected) conditional independence graph(draw an (undirected) edge between
variables and if they are not conditionally independent given all other variables)
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2
a cliqueanother cliquea separator
For any 2 cliques C and D, CD is a subset of every node between them in the junction tree
(3) Construct junction tree
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How does it work?
(4) any joint distribution with a triangulated graph can be factorised:
until
sss
ccc
x
xxp
)(
)()(
cliques
separators
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How does it work?
(5) ‘pass messages’ along junction tree: manipulate the terms of the expression
until
from which marginal probabilities can be read off
sss
ccc
x
xxp
)(
)()(
)()( ccc xpx )()( sss xpx
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Limitations
• of message passing:– all variables discrete, or– CG distributions (both continuous and
discrete variables, but discrete precede continuous, determining a multivariate normal distribution for them)
• of Hugin:– complexity seems forbidding for truly realistic
medical expert systems
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Graphical modelling [2]
• Assuming structure to do probability calculations
• Inferring structure to make substantive conclusions
• Structure in model building
• Inference about latent variables
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Conditional independence graphdraw an (undirected) edge between
variables and if they are not conditionally independent given all other variables
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Infant mortality example
Data on infant mortality from 2 clinics, by level of ante-natal care (Bishop, Biometrics,
1969):
Ante Survived Died % diedless 373 20 5.1more 316 6 1.9
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Infant mortality example
Same data broken down also by clinic:
Clinic Ante Survived Died % diedA less 176 3 1.7
more 293 4 1.3B less 197 17 7.9
more 23 2 8.0
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Analysis of deviance
• Resid Resid• Df Deviance Df Dev P(>|Chi|)• NULL 7 1066.43 • Clinic 1 80.06 6 986.36 3.625e-19• Ante 1 7.06 5 979.30 0.01• Survival 1 767.82 4 211.48 5.355e-169• Clinic:Ante 1 193.65 3 17.83 5.068e-44• Clinic:Survival 1 17.75 2 0.08 2.524e-05• Ante:Survival 1 0.04 1 0.04 0.84• Clinic:Ante:Survival 1 0.04 0 1.007e-12 0.84
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Infant mortality example
ante
clinic
survival
survival and clinic are dependent
and ante and clinic are dependent
but survival and ante are CI given clinic
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Prognostic factors for coronary heart disease
strenuous physical work?
family history of CHD?
strenuous mental work?
blood pressure > 140?
smoking?
ratio of and lipoproteins >3?
Analysis of a 26 contingency table(Edwards & Havranek, Biometrika, 1985)
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How does it work?
Hypothesis testing approaches:
Tests on deviances, possibly penalised (AIC/BIC, etc.), MDL, cross-validation...
Problem is how to search model space when dimension is large
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How does it work?
Bayesian approaches:
Typically place prior on all graphs, and conjugate prior on parameters (hyper-Markov laws, Dawid & Lauritzen), then use MCMC (see later) to update both graphs and parameters to simulate posterior distribution
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For example, Giudici & Green (Biometrika, 2000) use junction tree representation for fast local updates to graph
7 6 5
2 3 41
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2
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Graphical modelling [3]
• Assuming structure to do probability calculations
• Inferring structure to make substantive conclusions
• Structure in model building
• Inference about latent variables
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Modelling with undirected graphsDirected acyclic graphs are a natural
representation of the way we usually specify a statistical model - directionally:
• disease symptom• past future• parameters data …..
However, sometimes (e.g. spatial models) there is no natural direction
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Scottish lip cancer data
The rates of lip cancer in 56 counties in Scotland have been analysed by Clayton and Kaldor (1987) and Breslow and Clayton (1993)
(the analysis here is based on the example in the WinBugs manual)
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Scottish lip cancer data (2)The data include
• a covariate measuring the percentage of the population engaged in agriculture, fishing, or forestry, and• the "position'' of each county expressed as a list of adjacent counties.
• the observed and expected cases (expected numbers based on the population and its age and sex distribution in the county),
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Scottish lip cancer data (3)
County Obs Exp x SMR Adjacent
cases cases (% in counties
agric.)
1 9 1.4 16 652.2 5,9,11,19
2 39 8.7 16 450.3 7,10
... ... ... ... ... ...
56 0 1.8 10 0.0 18,24,30,33,45,55
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Model for lip cancer data(1) Graph
observed counts
random spatial effects
covariate
regressioncoefficient
relative risks
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Model for lip cancer data
• Data:• Link function:
• Random spatial effects:
• Priors:
)(Poisson~ iiO
iiii bxE 10/loglog 10
ji
jin
n bbbbp~
22/1 )4/)(exp()|,...,(
),(~ dr Uniform~, 10
(2) Distributions
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WinBugs for lip cancer data• Bugs and WinBugs are systems for
estimating the posterior distribution in a Bayesian model by simulation, using MCMC
• Data analytic techniques can be used to summarise (marginal) posteriors for parameters of interest
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Bugs code for lip cancer data
model{b[1:regions] ~ car.normal(adj[], weights[], num[], tau)b.mean <- mean(b[])for (i in 1 : regions) { O[i] ~ dpois(mu[i]) log(mu[i]) <- log(E[i]) + alpha0 + alpha1 * x[i] / 10 + b[i] SMRhat[i] <- 100 * mu[i] / E[i] }alpha1 ~ dnorm(0.0, 1.0E-5)alpha0 ~ dflat()tau ~ dgamma(r, d) sigma <- 1 / sqrt(tau)} skip
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Bugs code for lip cancer data
model{b[1:regions] ~ car.normal(adj[], weights[], num[], tau)b.mean <- mean(b[])for (i in 1 : regions) { O[i] ~ dpois(mu[i]) log(mu[i]) <- log(E[i]) + alpha0 + alpha1 * x[i] / 10 + b[i] SMRhat[i] <- 100 * mu[i] / E[i] }alpha1 ~ dnorm(0.0, 1.0E-5)alpha0 ~ dflat()tau ~ dgamma(r, d) sigma <- 1 / sqrt(tau)}
)(Poisson~ iiO
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Bugs code for lip cancer data
model{b[1:regions] ~ car.normal(adj[], weights[], num[], tau)b.mean <- mean(b[])for (i in 1 : regions) { O[i] ~ dpois(mu[i]) log(mu[i]) <- log(E[i]) + alpha0 + alpha1 * x[i] / 10 + b[i] SMRhat[i] <- 100 * mu[i] / E[i] }alpha1 ~ dnorm(0.0, 1.0E-5)alpha0 ~ dflat()tau ~ dgamma(r, d) sigma <- 1 / sqrt(tau)}
iiii bxE 10/loglog 10
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Bugs code for lip cancer data
model{b[1:regions] ~ car.normal(adj[], weights[], num[], tau)b.mean <- mean(b[])for (i in 1 : regions) { O[i] ~ dpois(mu[i]) log(mu[i]) <- log(E[i]) + alpha0 + alpha1 * x[i] / 10 + b[i] SMRhat[i] <- 100 * mu[i] / E[i] }alpha1 ~ dnorm(0.0, 1.0E-5)alpha0 ~ dflat()tau ~ dgamma(r, d) sigma <- 1 / sqrt(tau)}
ji
jin
n bbbbp~
22/1 )4/)(exp()|,...,(
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Bugs code for lip cancer data
model{b[1:regions] ~ car.normal(adj[], weights[], num[], tau)b.mean <- mean(b[])for (i in 1 : regions) { O[i] ~ dpois(mu[i]) log(mu[i]) <- log(E[i]) + alpha0 + alpha1 * x[i] / 10 + b[i] SMRhat[i] <- 100 * mu[i] / E[i] }alpha1 ~ dnorm(0.0, 1.0E-5)alpha0 ~ dflat()tau ~ dgamma(r, d) sigma <- 1 / sqrt(tau)}
),(~ dr
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WinBugs for lip cancer data
Dynamic traces for some parameters:alpha1
iteration1695016900168501680016750167001665016600
-0.25
0.0
0.25
0.5
0.75
tau
iteration1695016900168501680016750167001665016600
0.0
2.0
4.0
6.0
mu[1]
iteration1695016900168501680016750167001665016600
0.0
5.0
10.0
15.0
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WinBugs for lip cancer data
Posterior densities for some parameters:
alpha1 sample: 7000
-0.5 0.0 0.5 1.0
0.0
1.0
2.0
3.0
4.0
mu[1] sample: 7000
0.0 5.0 10.0 15.0
0.0
0.1
0.2
0.3
tau sample: 7000
0.0 2.0 4.0
0.0
0.2
0.4
0.6
0.8
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How does it work?
• The simplest MCMC method is the Gibbs sampler:
• in each sweep, ‘visit’ each variable in turn, and replace its current value by a random draw from its full conditional distribution - i.e. its conditional distribution given all other variables including the data
skip
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Full conditionals in a DAG
Basic DAG factorisation
Bayes’ theorem gives full conditionals
involving only parents, children and spouses.
Often this is a standard distribution, by conjugacy.
)|()( )(pa vVv
v xxpxp
)|()|()|( )(pa)(pa:
)(pa wwvw
wvvvv xxpxxpxxp
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Beyond the Gibbs sampler
Where the full conditional is not a standard distribution, other MCMC updates can be used: the Metropolis-Hastings methods use the full conditionals algebraically
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Limitations of MCMC
• You can’t beat errors
• Autocorrelation limits efficiency
• Possibly-undiagnosed failure to converge
N/1
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Graphical modelling [4]
• Assuming structure to do probability calculations
• Inferring structure to make substantive conclusions
• Structure in model building
• Inference about latent variables
59
Latent variable problems
variable unknown variable known
edges known
value set knownvalue set unknown
edges unknown
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relativerisk
parameters
Hidden Markov models
• Richardson & Green (2000) used a hidden Markov random field model for disease mapping
)(Poisson~ izi Eyi
observedincidence
expectedincidencehidden
MRF
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Latent variable problems
variable unknown variable known
edges known
value set knownvalue set unknown
edges unknown
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Ion channelmodel DAG
levels &variances
modelindicator
transitionrates
hiddenstate
data
binarysignal
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levels &variances
modelindicator
transitionrates
hiddenstate
data
binarysignal
O1 O2
C1 C2 C3
** *
******
**
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‘Alarm’ network
Learning a Bayesian network,for an ICUventilatormanagement system,from 10000 cases on 37 variables(Spirtes & Meek, 1995)
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Latent variable problems
variable unknown variable known
edges known
value set knownvalue set unknown
edges unknown
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Wisconsin students college plans
10,318 high school seniors (Sewell & Shah, 1968, and many authors since)
5 categorical variables:
sex (2)socioeconomic status (4)IQ (4)parental encouragement (2)college plans (2)
sessex
peiq
cp
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sessex
peiq
cp
5 categorical variables:
sex (2)socioeconomic status (4)IQ (4)parental encouragement (2)college plans (2)
(Vastly) most probable graphaccording to an exact Bayesian analysis by Heckerman (1999)
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CSS book (Complex Stochastic Systems)
• Graphical models and Causality: S Lauritzen• Hidden Markov models: H Künsch• Monte Carlo and Genetics: E Thompson• MCMC: P Green• F den Hollander and G Reinert
ed: O Barndorff-Nielsen, D Cox and
C Klüppelberg, Chapman and Hall (2001)
75
HSSS book (Highly Structured Stochastic Systems)
• Graphical models and causality– T Richardson/P Spirtes, S Lauritzen,
P Dawid, R Dahlhaus/M Eichler
• Spatial statistics– S Richardson, A Penttinen,
H Rue/M Hurn/O Husby
• MCMC– G Roberts, P Green, C Berzuini/W Gilks
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HSSS book (ctd)
• Biological applications– N Becker, S Heath, R Griffiths
• Beyond parametrics– N Hjort, A O’Hagan
... with 30 discussants
editors: N Hjort, S Richardson & P Green
OUP (2002?), to appear
77
Further reading
• J Whittaker, Graphical models in applied multivariate statistics, Wiley, 1990
• D Edwards, Introduction to graphical modelling, Springer, 1995
• D Cox and N Wermuth, Multivariate dependencies, Chapman and Hall, 1996
• S Lauritzen, Graphical models, Oxford, 1996• M Jordan (ed), Learning in graphical models,
MIT press, 1999