Re: Marijuana

2001-06-22 Thread Steve Leibel

In article [EMAIL PROTECTED],
 [EMAIL PROTECTED] (Eamon) wrote:

 (c) Reduced motor co-ordination, e.g. when driving a car
 

Numerous studies have shown that marijuana actually improves driving 
ability.  It makes people more attentive and less aggressive.  You could 
look it up.


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Re: Marijuana

2001-06-22 Thread Rich Ulrich

On Fri, 22 Jun 2001 18:45:52 GMT, Steve Leibel [EMAIL PROTECTED]
wrote:

 In article [EMAIL PROTECTED],
  [EMAIL PROTECTED] (Eamon) wrote:
 
  (c) Reduced motor co-ordination, e.g. when driving a car
  
 
 Numerous studies have shown that marijuana actually improves driving 
 ability.  It makes people more attentive and less aggressive.  You could 
 look it up.

An intoxicant does *that*?  

I think I recall in the literature, that people getting 
stoned, on whatever, occasionally  *think*  that 
their reaction time or sense of humor or other 
performance is getting better.   

Improving your driving by getting mildly stoned 
(omitting the episodes of hallucinating)
seems unlikely enough, to me, 
that  *I*  think the burden of proof is the stranger named Steve.

-- 
Rich Ulrich, [EMAIL PROTECTED]
http://www.pitt.edu/~wpilib/index.html


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Re: Normality in Factor Analysis

2001-06-22 Thread Robert Ehrlich

Calculation of eigenvalues and eigenvalues requires no assumption.
However evaluation of the results IMHO implicitly assumes at least a
unimodal distribution and reasonably homogeneous variance for the same
reasons as ANOVA or regression.  So think of th consequencesof calculating
means and variances of a strongly bimodal distribution where no sample
ocurrs near the mean and all samples are tens of standard devatiations
from the mean.

 Hi,

 I have a question regarding factor analysis: Is normality an important
 precondition for using factor analysis?

 If no, are there any books that justify this.



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Re: Marijuana

2001-06-22 Thread Steve Leibel

In article [EMAIL PROTECTED],
 Rich Ulrich [EMAIL PROTECTED] wrote:

 On Fri, 22 Jun 2001 18:45:52 GMT, Steve Leibel [EMAIL PROTECTED]
 wrote:
 
  In article [EMAIL PROTECTED],
   [EMAIL PROTECTED] (Eamon) wrote:
  
   (c) Reduced motor co-ordination, e.g. when driving a car
   
  
  Numerous studies have shown that marijuana actually improves driving 
  ability.  It makes people more attentive and less aggressive.  You could 
  look it up.
 
 An intoxicant does *that*?  
 
 I think I recall in the literature, that people getting 
 stoned, on whatever, occasionally  *think*  that 
 their reaction time or sense of humor or other 
 performance is getting better.   
 
 Improving your driving by getting mildly stoned 
 (omitting the episodes of hallucinating)
 seems unlikely enough, to me, 
 that  *I*  think the burden of proof is the stranger named Steve.



Hallucinating?  On pot?  What are YOU smokin'?  Pot doesn't cause 
hallucinations -- although a lot of anti-drug hysteria certainly does.

A cursory web search turned up these links among many others to support 
my statement.  Naturally this subject is controversial and there are 
lots of conflicting studies.  The consensus is that at worst pot causes 
minor driving impairment similar to many prescription medications.  At 
least one study showed that pot users had FEWER fatal crashes than non 
users!  

And stranger named Steve?  I've been on this newsgroup since 1995.  
Not as famous as James Harris, maybe, but certainly no stranger.

This is a small sample of what came up when I entered marijuana 
driving into Google.  Read and learn.

http://www.norml.org/canorml/myths/myth1.shtml 

http://www.reconsider.org/issues/marijuana/driving.htm

http://www.cannabisnews.com/news/thread1016.shtml

http://www.marijuana-hemp.com/cin/facts/drivehi.shtml  When the data 
were analyzed, cannabis consumers actually showed a lower likelihood of 
being involved in a fatal crash than that of a drug-free control group, 
though the difference was not judged to be statistically significant.

http://www.hoboes.com/pub/Prohibition/Drug%20Information/Marijuana/Drivin
g/Driving

http://www.taima.org/en/driving.htm  It was of some interest that 
cannabis tended to show a negative effect on relative risk when other 
drug groups showed an increase.

http://www.norml.org.nz/norml/Marijuana/Driving.htm#abc981014

Steve L


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probability that Xi = X1...Xn

2001-06-22 Thread Fabio Ulisse Pardi

Can anybody give me a hint about this problem?

Let the random variables X1,...,Xn be independent and let M be the index

of the maximum among them (i.e. M=i implies Xi = X1,...,Xn).
We want to find nice formulas that calculate the distribution of M from
the distributions of X1...Xn, that we suppose belonging to the same
class
of distributions:
for instance if we assume that all of X1...Xn are normally distributed,
with parameters (m1,v1),...,(mn,vn), we would like to obtain a formula
of the kind
   Pr[M=i] = Fi(m1,...,mn,v1,...,vn)
for every i=1..n.

The problem is that the integral that calculates Pr[M=i] is quite
complicated, and I haven't figured out how to express its value as a
simple function of the parameters.





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Re: Marijuana

2001-06-22 Thread David C. Ullrich

On Thu, 21 Jun 2001 21:14:44 -0700, Chas F Brown
[EMAIL PROTECTED] wrote:



David C. Ullrich wrote:
 
 On Fri, 15 Jun 2001 15:23:03 +0100, Paul Jones
 [EMAIL PROTECTED] wrote:
 
 David C. Ullrich wrote:
 
  But analyzing it this way simply makes no sense. Those
  trials you're talking about are _far_ from independent;
  each trial is associated with a particular person, and
  there will be a very strong correlation between various
  trials for the same person at different hours.
 
 Okay then, how should it be analysed?
 
 I've explained at least twice why I do not believe it
 is _possible_ to draw the sort of inference you want
 to draw from the data you've given us. You must
 be reading _some_ of those posts or you wouldn't
 keep replying.
 

Well, although I've agreed with most of your complaints about trying to
derive any information from the scanty data shown, there is *something*
we can notice about the data set which has some relevance.

Let's say we look at a sampling of 100 people who have both had heart
attacks within the last year and have smoked an aspirin an average of
once a week during that year.

Now, without knowing what the average percentage of people who smoke
aspirin each year, and the average percentage of people who have heart
attacks each year without smoking aspirin, these numbers alone would be
pretty useless.

But if 95% of the people in the data set had their 1 heart attack inside
of 1 minute after smoking an aspirin, you'd have some reason to further
examine the hypothesis that, for some segment of the population, smoking
an aspirin could trigger a heart attack. (Of course it could also be
that impending heart attacks bring on the desire to smoke aspirin, or
some other hypothesis that correlates the two phenomena).

One the other hand, one would expect if there were no immediate
correlation between smoking aspirin and heart attacks, the average time
between smoking aspirin and heart attack would be more like 1/2 week.
This would then indicate that it was not particularly worthwhile to
investigate an immediate link between asprinin smoking and heart
attacks.

That seems to be the type of correlation that was reported here - some
distribution of MJ smoking, and its *temporal* correlation with heart
attacks.

Now, that says exactly nothing about whether MJ use increases or
decreases the liklihood of having a heart attack in general (it could in
fact in general *decrease* heart attacks, even in our data set);

That's exactly right. When I say that there's nothing we can conlude
from the data given I didn't mean there's _nothing_ we can conclude,
rather nothing we can conclude _concerning_ the question of
whether smoking increases the risk of a heart attack.

I don't see how we can even quite conclude that the risk of a heart
attack is higher among users immediately after smoking, for various
reasons: I doubt that most users' use is uniformly distributed
during the 24 hours of the day, I have no idea whether heart
attacks are uniformly distributed throuought the day, so it could
well be that the times people tend to smoke are the same as the
times they tend to have heart attacks. Or they tend to smoke
before meals (I knew some people like that years ago in college)
and tend to have heart attacks after meals. Or they tend to
smoke when they start to feel little chest pains, as someone
suggested.

Then even if it _is_ true that a smoker is more likely to
have a heart attack immediately after smoking a joint, that
does _NOT_ show that smoking increases the risk! Could be
as you say that it actually decreases the risk, but regardless
the time immediately after smoking is the riskiest time.

So it seems clear to me that there is _nothing_ we can conclude
about whether smoking increases the risk of a heart attack -
it also seems clear that that is _the_ question of interest
here.

Not that I'm claiming that it _is_ the case that smoking
decreases the risk of heart attack although the hour
immediately afterwards is the riskiest time. I have no
reason to think that's so. Also no reason to think it's
not so: People who assume such a thing is ridiculous 
think so because they've classified the world into
Good things and Bad things - actual things in the world
are not that simple:

(i) Aspirin is a Good thing. Good for pain and fever relief,
and actually an aspirin a day helps prevent heart attack
or stroke, I forget which. The reason I forget which is
it's irrelevant to me: For me aspirin is a Very Bad thing,
because of other medical problems.

(ii) Alcohol is a Bad thing. Except for that bit about
how a glass of red wine a day is good for you, in terms
os risk of heart attack or stroke, again I forget which.
Alas, it doesn't follow that a quart of whiskey a day
is good for you.

Given that there _are_ plenty of legitimate medical
uses for marijuana and given that the interaction between
the body and chemicals is simply _not_ a matter of some
chemicals Good and some Bad, the idea that 

Re: calculation of an effect size with medians

2001-06-22 Thread Konrad Halupka

Marc wrote:
 
 As a part of a report
 I have to perform a meta-analysis of
 some clinical trials.
 These trials report the median effect in the
 treatment group and the median effect in the control group
 (days of hospitalization). P-values from Mann-Whitney U-Tests
 are reported and the numbers of patients in treatment
 and control.
 My Question: How can I calculate an effect size
 (eg median difference between treatment and
 control)and confidence intervals with that data?

You'd need raw data to calculate the effect size for Mann-Whitney test.

Regards,
Konrad


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