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update renv
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nhejazi committed Sep 20, 2024
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20 changes: 10 additions & 10 deletions 04-roadmap.Rmd
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Expand Up @@ -94,7 +94,7 @@ variance $\sigma^2$. More generally, a parametric model may be defined as
\end{equation*}
which describes a constrained statistical model consisting of all distributions
$P_{\theta}$ that are indexed by some finite, $d$-dimensional parameter
$\theta$.
$\theta$.

The assumption that $P_0$ has a specific, parametric form is made quite
commonly. Unfortunately, this is even the case when such assumptions are not
Expand Down Expand Up @@ -142,7 +142,7 @@ scientific conventions, accepted hypotheses, and operational assumptions.
rp: This is vague. What's an example of scientific conventions, example of
accepted hypotheses, and example of operational assumptions that would be
incorporated in M?
-->
-->
It is then the data scientist's responsibility to translate the domain knowledge
into statistical knowledge about $P_0$, and then to define the statistical model
$\M$ so that it respects what is known about $P_0$ and makes no further
Expand Down Expand Up @@ -437,11 +437,11 @@ ggdag(tidy_dag) +
While DAGs like the above provide a convenient means by which to express the
causal relations between variables, these same causal relations can be
equivalently represented by an SCM:
\begin{align*}
$$\begin{align*}
W &= f_W(U_W) \\
A &= f_A(W, U_A) \\
Y &= f_Y(W, A, U_Y),
\end{align*}
\end{align*}$$
where the $f$'s are unspecified deterministic functions that generate the
corresponding random variables as a function of the variable's "parents" (i.e.,
upstream nodes with arrows into the given random variable) in the DAG, and the
Expand Down Expand Up @@ -474,17 +474,17 @@ of the outcome distribution in the population under two distinct interventions:
These interventions may be thought of as operations that imply changes
to the structural equations in the system under study. For the case $A = 1$, we
have
\begin{align*}
$$\begin{align*}
W &= f_W(U_W) \\
A &= 1 \\
Y(1) &= f_Y(W, 1, U_Y) \ ,
\end{align*}
\end{align*}$$
while, for the case $A=0$,
\begin{align*}
$$\begin{align*}
W &= f_W(U_W) \\
A &= 0 \\
Y(0) &= f_Y(W, 0, U_Y) \ .
\end{align*}
\end{align*}$$

In these equations, $A$ is no longer a function of $W$ because the intervention
on the system set $A$ deterministically
Expand Down Expand Up @@ -569,12 +569,12 @@ all four are necessary when working within the potential outcomes framework
Under these assumptions, the ATE may be re-written as a function of $P_0$, the
distribution of the observed data:

\begin{align}
$$\begin{align}
\psi_{\text{ATE}} &= \E_0[Y(1) - Y(0)] \\ \nonumber
&= \E_0 [\E_0[Y \mid A = 1, W] -
\E_0[Y \mid A = 0, W]] \ .
(\#eq:estimand)
\end{align}
\end{align}$$
In words, the ATE is the mean difference in the predicted outcome values for
each subject, under the contrast of treatment conditions ($A = 0$ versus $A =
1$), in the population (when averaged over all observations). Thus, a parameter
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3 changes: 3 additions & 0 deletions dependencies.R
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@@ -0,0 +1,3 @@
library(sysfonts)
library(rmarkdown)
library(bookdown)
32 changes: 23 additions & 9 deletions renv.lock
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Expand Up @@ -448,14 +448,15 @@
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Expand All @@ -466,7 +467,7 @@
"xfun",
"yaml"
],
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"Hash": "896a79478a50c78fb035a37148638f4e"
},
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Expand Down Expand Up @@ -3519,6 +3520,19 @@
"Repository": "CRAN",
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