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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 9 of 9. This is the beginning of the thread.
Posted by dj on January 28, 2000, at 16:34:58
Suicidal tendencies treatable, Ottawa scientists say: Discovery raises concerns genetic marker will be used to stigmatize people who have it
Brad Evenson
National PostDr. David Bakish, and Dr. Pavel Hrdina of the Royal Ottawa Hospital led the study that found a gene mutation that more than doubles the risk of suicidal behaviour. The discovery could lead to a "suicide test."
OTTAWA - Confirming a 2,000-year-old belief that self-destructiveness runs in families, scientists from the Royal Ottawa Hospital have found that a gene mutation leads to suicide.The discovery may lead to a "suicide test" that would identify patients at risk and could also open a philosophical debate on how this dark fragment of personality will be used in an age when medical records are kept electronically and are difficult to keep confidential.
The researchers found a mutation in the gene encoding for the serotonin 5-HT2A receptor, a protein that transmits brain signals, which more than doubles the risk of suicidal behaviour in those who carry it.
"Individuals who carry the [mutation] are at higher risk when a situation that triggers their suicidal tendencies will occur," says neurobiologist Dr. Pavel Hrdina, who co-authored the landmark study.
The study looked at patients suffering from major depression, so its results do not apply to healthy people who may attempt suicide as a one-time "cry for help" or to gain attention. However, the researchers say it is possible the 5-HT2A receptor mutation may also be linked to the elevated risk of suicide among schizophrenics.
People have believed since Biblical times that mental illness and suicide are inherited.
When Margaux Hemingway committed suicide in 1996, it gained attention not only because she was the world's highest-paid model and the granddaughter of Ernest Hemingway, but because it marked four generations of suicide in the famous American family.
"Alcoholism and suicide seem to be something we Hemingways have inherited," she once said.
A diagnostic test for this trait would identify people in need of medical help, including gene therapy. Suicide is now the world's ninth leading cause of death and growing fast. Each year in Canada, there are 30,000 suicide attempts; on average, 4,000 succeed.
"Suicidal ideation is a treatable condition," says co-author Dr. David Bakish.
"This could help save lives."
However, this mutation could also prove to be a "Scarlet Letter" whose presence makes it impossible to buy life insurance, fly an airplane, or even hold a position of trust in society. The risk of unwanted exposure may be considerable.
"There are huge issues of privacy and discrimination here, and they just get ratcheted up because you're talking about psychiatric illness," says Dr. Kay Redfield Jamison, a professor of psychiatry at Johns Hopkins University in Baltimore, Maryland.
The discovery will be published on Feb. 7 in the American Journal of Medical Genetics. Along with Drs. Hrdina and Bakish, the researchers included molecular geneticist Dr. Lisheng Du, and Drs. Yvon Lapierre and Arun Ravindran.
In the study, the Ottawa researchers looked at blood samples from 120 patients with major depressive disorders, of whom 78 were suicidal and 42 were non-suicidal. They compared these with samples from 131 men and women with no mental illness.
An analysis of the DNA showed 41% of the suicidal patients had the 5-HT2A receptor mutation, compared with 24% of the non-suicidal patients and 18% of the healthy subjects.
"In biological terms, that's a tremendous difference," said Dr. Hrdina. He stressed the results would have to be replicated before they gain scientific acceptance.
Located on the long arm of chromosome 13, the mutation can be detected from a droplet of blood in almost any laboratory with advanced gene identification equipment.
The principal function of the 5-HT2A receptor is to transmit signals from serotonin, a brain chemical that puts the brakes on impulsive thoughts that may develop in the cerebral cortex. Over 50% of suicide attempts take place with less than five minutes of premeditation, so impulse is known to be a strong contributor.
It's believed the 5-HT2A receptor gene mutation may weaken the brain's ability to control the impulse to commit suicide. There may also be more mutations to genes controlling serotonin levels that may increase the risk of suicide.
However, the presence of this mutation does not mean suicide is inevitable.
In her new book on suicide, Night Falls Fast, Dr. Jamison points out: "It simply makes it more likely that given enough cumulative stress or a devastating, acute one, suicide may be an option more readily summoned."
She continues: "A genetic vulnerability for heart disease, cancer, or asthma, for example ... does not ensure that illness will occur."
Dr. Hrdina said significantly more males in the study had the mutation than females. While it's premature to say what this result means, four times as many males die of suicide as females -- although women attempt to kill themselves in numbers roughly equal to men.
A genetic variability might also explain why suicide rates vary strongly between populations with different ethnic origins. For example, the annual suicide rate in Finland (for males) is 43 per 100,000 people, one of the highest rates in the world.
But the rate for neighbouring Norway is only 21 per 100,000, less than half.
"It may be interesting to look into the distribution of the [mutation] in these countries," said Dr. Hrdina.
-----------------More articles at:
http://www.nationalpost.com/
Posted by Adam on January 28, 2000, at 18:54:36
In reply to "Suicide linked to defective gene", posted by dj on January 28, 2000, at 16:34:58
I think this is wonderful. This is exactly the kind of information we need. It's a no-brainer, as far as I'm concerned, given my family history, so I have fully expected information of this sort to come out eventually. The author is right: In biomedical science, correlations of this magnitude really are enormous, so it would suprise me if it were a spurious result. And it also is no suprise that, like many heritable predispositions, it is clearly not the only factor, and that exogenous forces may play a role too.
I've said it before: I have had problems with suicidal ideation and OCD much of my life. The 5-HT2A receptor is implicated in both. While on Serzone (nefazodone), a 5-HT2A antagonist, my condition worsened so badly so quickly I felt like I was losing my mind. I have wondered about that coincidence so much. What happened to me?
Wouldn't it be wonderful if there were a test some day that maybe said, at the very least, "keep this man off of nefazodone. Give him (drugX) instead. It works for people with this mutation."
I think once the paper gets published I may try to find out if I have the mutation (or one similar) myself. All I need is the reference and Genebank. I sequence stuff all the time. I'll just draw a little blood, make some cDNA or extract and digest some genomic DNA, whichever is most appropriate, order the oligos (with my own money), do the reaction, and stick it on a gel I'm already running. I really would be interested to find out. It would cost my employer less than the rubber bands that get stolen every day.
I worry that future diagnostics based on such information could be used unethically too, but as far as I can see, we're already faced with that issue, since numerous, incontrovertable correlations between mutations and disease already exist, including neurological diseases. The genie is already out of the bottle.
Such discoveries WILL come, more and more, at a faster and faster pace, as the human genome is completely sequenced and the differentials are exposed. Mark my words, the information revolution that gives us Dr. Bob and the WWW has facilitated the next big revolution, one far more radical, IMO: the genomic revolution. It won't be that long before there are complete databases on just about everything that makes you tick. That knowledge will give a certain subset of the population an enormous amount of power over you, for good or ill. Please, please, please: Go to the polls. Go to debates. Vote for candidates and laws that uphold medical ethics which will protect us all from depredation and denial.
> Suicidal tendencies treatable, Ottawa scientists say: Discovery raises concerns genetic marker will be used to stigmatize people who have it
>
> Brad Evenson
> National Post
>
> Dr. David Bakish, and Dr. Pavel Hrdina of the Royal Ottawa Hospital led the study that found a gene mutation that more than doubles the risk of suicidal behaviour. The discovery could lead to a "suicide test."
>
>
> OTTAWA - Confirming a 2,000-year-old belief that self-destructiveness runs in families, scientists from the Royal Ottawa Hospital have found that a gene mutation leads to suicide.
>
> The discovery may lead to a "suicide test" that would identify patients at risk and could also open a philosophical debate on how this dark fragment of personality will be used in an age when medical records are kept electronically and are difficult to keep confidential.
>
> The researchers found a mutation in the gene encoding for the serotonin 5-HT2A receptor, a protein that transmits brain signals, which more than doubles the risk of suicidal behaviour in those who carry it.
>
> "Individuals who carry the [mutation] are at higher risk when a situation that triggers their suicidal tendencies will occur," says neurobiologist Dr. Pavel Hrdina, who co-authored the landmark study.
>
> The study looked at patients suffering from major depression, so its results do not apply to healthy people who may attempt suicide as a one-time "cry for help" or to gain attention. However, the researchers say it is possible the 5-HT2A receptor mutation may also be linked to the elevated risk of suicide among schizophrenics.
>
> People have believed since Biblical times that mental illness and suicide are inherited.
>
> When Margaux Hemingway committed suicide in 1996, it gained attention not only because she was the world's highest-paid model and the granddaughter of Ernest Hemingway, but because it marked four generations of suicide in the famous American family.
>
> "Alcoholism and suicide seem to be something we Hemingways have inherited," she once said.
>
> A diagnostic test for this trait would identify people in need of medical help, including gene therapy. Suicide is now the world's ninth leading cause of death and growing fast. Each year in Canada, there are 30,000 suicide attempts; on average, 4,000 succeed.
>
> "Suicidal ideation is a treatable condition," says co-author Dr. David Bakish.
>
> "This could help save lives."
>
> However, this mutation could also prove to be a "Scarlet Letter" whose presence makes it impossible to buy life insurance, fly an airplane, or even hold a position of trust in society. The risk of unwanted exposure may be considerable.
>
> "There are huge issues of privacy and discrimination here, and they just get ratcheted up because you're talking about psychiatric illness," says Dr. Kay Redfield Jamison, a professor of psychiatry at Johns Hopkins University in Baltimore, Maryland.
>
> The discovery will be published on Feb. 7 in the American Journal of Medical Genetics. Along with Drs. Hrdina and Bakish, the researchers included molecular geneticist Dr. Lisheng Du, and Drs. Yvon Lapierre and Arun Ravindran.
>
> In the study, the Ottawa researchers looked at blood samples from 120 patients with major depressive disorders, of whom 78 were suicidal and 42 were non-suicidal. They compared these with samples from 131 men and women with no mental illness.
>
> An analysis of the DNA showed 41% of the suicidal patients had the 5-HT2A receptor mutation, compared with 24% of the non-suicidal patients and 18% of the healthy subjects.
>
> "In biological terms, that's a tremendous difference," said Dr. Hrdina. He stressed the results would have to be replicated before they gain scientific acceptance.
>
> Located on the long arm of chromosome 13, the mutation can be detected from a droplet of blood in almost any laboratory with advanced gene identification equipment.
>
> The principal function of the 5-HT2A receptor is to transmit signals from serotonin, a brain chemical that puts the brakes on impulsive thoughts that may develop in the cerebral cortex. Over 50% of suicide attempts take place with less than five minutes of premeditation, so impulse is known to be a strong contributor.
>
> It's believed the 5-HT2A receptor gene mutation may weaken the brain's ability to control the impulse to commit suicide. There may also be more mutations to genes controlling serotonin levels that may increase the risk of suicide.
>
> However, the presence of this mutation does not mean suicide is inevitable.
>
> In her new book on suicide, Night Falls Fast, Dr. Jamison points out: "It simply makes it more likely that given enough cumulative stress or a devastating, acute one, suicide may be an option more readily summoned."
>
> She continues: "A genetic vulnerability for heart disease, cancer, or asthma, for example ... does not ensure that illness will occur."
>
> Dr. Hrdina said significantly more males in the study had the mutation than females. While it's premature to say what this result means, four times as many males die of suicide as females -- although women attempt to kill themselves in numbers roughly equal to men.
>
> A genetic variability might also explain why suicide rates vary strongly between populations with different ethnic origins. For example, the annual suicide rate in Finland (for males) is 43 per 100,000 people, one of the highest rates in the world.
>
> But the rate for neighbouring Norway is only 21 per 100,000, less than half.
>
> "It may be interesting to look into the distribution of the [mutation] in these countries," said Dr. Hrdina.
>
>
> -----------------
>
> More articles at:
> http://www.nationalpost.com/
Posted by Scott L. Schofield on January 29, 2000, at 21:57:00
In reply to Re: "Suicide linked to defective gene", posted by Adam on January 28, 2000, at 18:54:36
> > The researchers found a mutation in the gene encoding for the serotonin 5-HT2A receptor, a protein that transmits brain signals, which more than doubles the risk of suicidal behaviour in those who carry it.
> I think this is wonderful. This is exactly the kind of information we need.
This *is* wonderful. It looks as though things are beginning to come together... PLEASE!
> I have had problems with suicidal ideation and OCD much of my life. The 5-HT2A receptor is implicated in both. While on Serzone (nefazodone), a 5-HT2A antagonist, my condition worsened so badly so quickly I felt like I was losing my mind. I have wondered about that coincidence so much. What happened to me?> Wouldn't it be wonderful if there were a test some day that maybe said, at the very least, "keep this man off of nefazodone. Give him (drugX) instead. It works for people with this mutation."
> I think once the paper gets published I may try to find out if I have the mutation (or one similar) myself.
That would certainly be worth a blurb in some medical journal.
> I worry that future diagnostics based on such information could be used unethically too, but as far as I can see, we're already faced with that issue, since numerous, incontrovertable correlations between mutations and disease already exist, including neurological diseases. The genie is already out of the bottle.> Such discoveries WILL come, more and more, at a faster and faster pace, as the human genome is completely sequenced and the differentials are exposed. Mark my words, the information revolution that gives us Dr. Bob and the WWW has facilitated the next big revolution, one far more radical, IMO: the genomic revolution. It won't be that long before there are complete databases on just about everything that makes you tick. That knowledge will give a certain subset of the population an enormous amount of power over you, for good or ill. Please, please, please: Go to the polls. Go to debates. Vote for candidates and laws that uphold medical ethics which will protect us all from depredation and denial.
GENOMIC REVOLUTION - Your words are marked and they do scare me.
Thanks Adam.
Very much.
- Scott
Posted by Ant-Rock on January 30, 2000, at 13:36:12
In reply to Re: "Suicide linked to defective gene", posted by Scott L. Schofield on January 29, 2000, at 21:57:00
Hi Adam,
My name is Anthony, and I was hoping you could help me out with some info. You mentioned having some negative effects while on Serzone.
A few years back I had a very bad adverse reaction to the drug Amoxapine, which I was taking for depression. My nervous system went into some kind of shock, with my legs feeling like rubber and a severe worsening of my depression. I had tried many different meds in the past and never had a bad experience before with AD's.
Anyway,
Three years later while taking a small dose of Risperdal, also for depression, I had another severe and lasting reaction much like the Amoxapine one.
I guess I was wondering if you could tell me whether these two meds are in any way related or if their mechanism of action are similar. You seem to have a grasp of the way these meds can "cause" positive or negative reactions.
Thanks again Adam, or anyone else reading this with any feedback they can provide.Anthony
Posted by Scott L. Schofield on January 30, 2000, at 15:46:26
In reply to Re: "Suicide linked " "Question for Adam...", posted by Ant-Rock on January 30, 2000, at 13:36:12
> Hi Adam,
> My name is Anthony, and I was hoping you could help me out with some info. You mentioned having some negative effects while on Serzone.
> A few years back I had a very bad adverse reaction to the drug Amoxapine, which I was taking for depression. My nervous system went into some kind of shock, with my legs feeling like rubber and a severe worsening of my depression. I had tried many different meds in the past and never had a bad experience before with AD's.
> Anyway,
> Three years later while taking a small dose of Risperdal, also for depression, I had another severe and lasting reaction much like the Amoxapine one.
> I guess I was wondering if you could tell me whether these two meds are in any way related or if their mechanism of action are similar. You seem to have a grasp of the way these meds can "cause" positive or negative reactions.
> Thanks again Adam, or anyone else reading this with any feedback they can provide.
>
> Anthony
Dopamine.These two drugs have in common the ability to block (antagonize) dopamine receptors. Amoxapine (Ascendin) is derived from loxapine, an antipsychotic tranquilizer that probably works because of its ability to block DA receptors. I too experienced a worsening of my depression while taking amoxapine.
This is one tricyclic that should never have made it to market. Even the pilot-studies that were done in the beginning of the approval process yielded several cases of EPS (extrapyramidal symptoms). These phenomena include abnormal or uncontrolled movements (dyskinesia), feeling like you want to crawl out of your skin (akathisia), tremor, muscle rigidity, and more. EPS are common side-effects seen with the DA-blocking antipsychotics, and are usually deemed to be an acceptable trade-off for the benefits these drugs can bring. However, such liabilities for an antidepressant like amoxapine would be hard to justify.
My negative reaction to amoxapine over fifteen years ago was one of the facts that I felt corroborated a theory I had developed by that time regarding the major role that dopamine function may play in my case.
Perhaps such a bad reaction to amoxapine is an indicator that pro-dopaminergic drugs like MAO-inhibitors, amineptine, pergolide, low-dose amisulipiride, or psychostimulants may be worthwhile looking in to.
- Scott
P.S.
There are probably people out there for whom amoxapine may be the only drug that works for them. I'm sure they can think of plenty of reasons for why it was a good idea to approve it.
Posted by Adam on January 30, 2000, at 15:48:28
In reply to Re: "Suicide linked " "Question for Adam...", posted by Ant-Rock on January 30, 2000, at 13:36:12
Scott, Ant,
As for my rather horrific experiences at the beginning of 1999, all I can say is that I got off Wellbutrin, which I wasn't satisfied with as an antidepressant (though I had no adverse reactions to it) and started on Serzone. I stayed on Serzone for eight weeks (about four weeks longer than I wanted to, but I did what my doctor told me to do) and it took about that long to go from severely depressed but functioning to a state that I can confidently say was the worst thing I have ever experienced in my life. I was certainly unhappy enough before to think about suicide at least five or six times a day, but on Serzone I made the transition from ideation to attempt, and felt the pain was so unbearable that I was compelled to do so. It all may have been a result of getting off Wellbutrin, which I could have underestimated. I have no way of knowing for sure. My doctors just shrug when I bring it up.
As for my curiosity about my own genetic makeup, I've thought about the experiment since then, and there are a lot of potential problems that could make it not really worth doing. Also, if my 5-HT2A receptor were defective, then how can I explain my reaction to Serzone mechanistically, or the fact that I did not have such an adverse reaction to Remeron, which is also a 5-HT2 antagonist (though it does a number of other things too, just like Serzone).
Lastly, I would only do it if I thought it was such a trivial experiment (i.e. conditions were near perfect) that the costs in time and money would be negligible. I would be using some of the facilities of my employer for decidedly irrelevant purposes to their interests, would be doing so without permission, and hence any discovery I made would be worth nothing to anyone scientifically, and would only be a rather selfish way to satisfy my own curiosity.
Hence, it's probably a really bad idea, and I just got carried away.
> Hi Adam,
> My name is Anthony, and I was hoping you could help me out with some info. You mentioned having some negative effects while on Serzone.
> A few years back I had a very bad adverse reaction to the drug Amoxapine, which I was taking for depression. My nervous system went into some kind of shock, with my legs feeling like rubber and a severe worsening of my depression. I had tried many different meds in the past and never had a bad experience before with AD's.
> Anyway,
> Three years later while taking a small dose of Risperdal, also for depression, I had another severe and lasting reaction much like the Amoxapine one.
> I guess I was wondering if you could tell me whether these two meds are in any way related or if their mechanism of action are similar. You seem to have a grasp of the way these meds can "cause" positive or negative reactions.
> Thanks again Adam, or anyone else reading this with any feedback they can provide.
>
> Anthony
Posted by Ant-Rock on January 30, 2000, at 16:35:09
In reply to Re: Suicide linked - Question for Adam - Amoxapine, posted by Scott L. Schofield on January 30, 2000, at 15:46:26
> > Hi Adam,
> > My name is Anthony, and I was hoping you could help me out with some info. You mentioned having some negative effects while on Serzone.
> > A few years back I had a very bad adverse reaction to the drug Amoxapine, which I was taking for depression. My nervous system went into some kind of shock, with my legs feeling like rubber and a severe worsening of my depression. I had tried many different meds in the past and never had a bad experience before with AD's.
> > Anyway,
> > Three years later while taking a small dose of Risperdal, also for depression, I had another severe and lasting reaction much like the Amoxapine one.
> > I guess I was wondering if you could tell me whether these two meds are in any way related or if their mechanism of action are similar. You seem to have a grasp of the way these meds can "cause" positive or negative reactions.
> > Thanks again Adam, or anyone else reading this with any feedback they can provide.
> >
> > Anthony
>
>
> Dopamine.
>
> These two drugs have in common the ability to block (antagonize) dopamine receptors. Amoxapine (Ascendin) is derived from loxapine, an antipsychotic tranquilizer that probably works because of its ability to block DA receptors. I too experienced a worsening of my depression while taking amoxapine.
>
> This is one tricyclic that should never have made it to market. Even the pilot-studies that were done in the beginning of the approval process yielded several cases of EPS (extrapyramidal symptoms). These phenomena include abnormal or uncontrolled movements (dyskinesia), feeling like you want to crawl out of your skin (akathisia), tremor, muscle rigidity, and more. EPS are common side-effects seen with the DA-blocking antipsychotics, and are usually deemed to be an acceptable trade-off for the benefits these drugs can bring. However, such liabilities for an antidepressant like amoxapine would be hard to justify.
>
> My negative reaction to amoxapine over fifteen years ago was one of the facts that I felt corroborated a theory I had developed by that time regarding the major role that dopamine function may play in my case.
>
> Perhaps such a bad reaction to amoxapine is an indicator that pro-dopaminergic drugs like MAO-inhibitors, amineptine, pergolide, low-dose amisulipiride, or psychostimulants may be worthwhile looking in to.
>
> - Scott
>Thank you very much Scott for responding to my post. I can't tell you how good it feels to know that my reactions to these two meds wasn't all in my head. When I first began having the reaction to Amox., the Dr. I was seeing actually wanted me to INCREASE the dosage. It was like he didn't want to even try to understand what was happening to me. My body was shaking, I had overwhelming feelings of intense grief, and this lasted all of 10 days without relief, crying nonstop and wondering what the hell was happening to me.
What started out as trying to get help for a low grade chronic depression/fatigue, turned into a nightmare. Unfortunately Scott, these two reactions have left me in a much worse state than I ever possibly could have imagined. Since 1997 I've been dealing with ongoing anhedonia,fatigue,total loss of sex drive, and inability to even really care about resuming a "normal" life.
I've tried Parnate twice, and it did help to a degree, underwent Transcranial Magnetic Stimulation at Beth-Isreal, which also helped temporarily. I even tried Amineptine. Right now I am on Reboxetine, increased to 8 mgs three days ago and am cautiously optimistic. In my second week at 4mg I had one afternoon where I had so much energy it was like a blast from my past, but this effect didn't continue. I may augment Selegline with the Reboxetine if the 8mgs doesn't do the trick after a fair trial.
I haven't yet tried a psychostimulant or amisulpride. Hopefully someday this muscle weakness and fatigue will remit, and for a while I had given up trying to find out what damage these adverse reactions could have done because the Dr.'s I've seen couln't give me an explanation.
I thank you once again Scott, but am amazed that two psychiatrists & a neuroligist couldn't explain to me that these two drugs target the same substance.Anthony
Posted by Scott L. Schofield on January 31, 2000, at 11:35:50
In reply to Scott, Ant, posted by Adam on January 30, 2000, at 15:48:28
> As for my curiosity about my own genetic makeup, I've thought about the experiment since then, and there are a lot of potential problems that could make it not really worth doing. Also, if my 5-HT2A receptor were defective, then how can I explain my reaction to Serzone mechanistically, or the fact that I did not have such an adverse reaction to Remeron, which is also a 5-HT2 antagonist (though it does a number of other things too, just like Serzone).
It seems that the serotonin synapse is quite complex. There are different types of receptors all over the place. I really haven't focused on the details of these sites, but there are a few things that come to mind. I noticed that you specified the 5-HT2a as the receptor transcribed from the "defective" gene. Are there more than one type of 5-HT2 receptor? If there are, perhaps differences in the drugs' binding selectivities could account for the apparent inconsistency of observations. Pharmacokinetics may also be a determinant in your differential reactions to Serzone versus Remeron.
Would these two drugs produce a different ratio of receptor activity due to their behaviors at other serotonin sites, for instance, 5-HT3? Perhaps the ability of Remeron to antagonize presynaptic alpha-1 noradrenergic receptors and the resultant increase in NE activity provides an offset to, or shunt of, the suspect serotonergic pathways. Histamine?
All of these questions would be immensely fascinating, if the answers weren't so critical to our lives.
Does anyone care to summarize the features of the serotonin synapse?
- Scott
Posted by Noa on January 31, 2000, at 11:56:12
In reply to Re: Scott, Ant, posted by Scott L. Schofield on January 31, 2000, at 11:35:50
>
> Does anyone care to summarize the features of the serotonin synapse?
>
>
Too bad this board isn't formatted for drawings to go with the words!
This is the end of the thread.
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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
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