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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 22 of 22. This is the beginning of the thread.
Posted by zeugma on July 4, 2004, at 11:37:01
I am suffering from a bout of (intensified) vegetative depression, which does not come completely as a surprise to me, as I tend to fall apart completely when not working (I teach and it's summer break). I was depressed when working, but it was mitigated by the need to function and interact with others. Now i feel completely adrift and lethargic. I am going to give my AD one last chance, by raising the nortriptyline dose from 75 to 100 mg tonight.
I also take Provigil, 100 mg, and it has absolutely no energizing effect whatsoever. But I don't think I'll have given it a fair trial until I've gotten to 200 mg. If nothing else, 100 mg nortriptyline should counteract the Provigil insomnia (ironic that a drug that is not energizing should make it harder for me to sleep). From my experience, nortriptyline is the reverse of a drug like remeron (it gets more sedating as the dosage is increased). I also have Lexapro samples but don't think much about Lex as a treatment for vegetative depression. What gives me a little hope is that I have read studies suggesting that there is a window within the window for nortrip plasma levels (about 80-120 ng/mL, within the larger window of 50-150 ng/ml) at which nortrip becomes its most effective. I hope this pulls me out of this depression.
Posted by Sad Panda on July 5, 2004, at 10:29:46
In reply to vegetative depression, nortriptyline dosage, posted by zeugma on July 4, 2004, at 11:37:01
> I am suffering from a bout of (intensified) vegetative depression, which does not come completely as a surprise to me, as I tend to fall apart completely when not working (I teach and it's summer break). I was depressed when working, but it was mitigated by the need to function and interact with others. Now i feel completely adrift and lethargic. I am going to give my AD one last chance, by raising the nortriptyline dose from 75 to 100 mg tonight.
>
> I also take Provigil, 100 mg, and it has absolutely no energizing effect whatsoever. But I don't think I'll have given it a fair trial until I've gotten to 200 mg. If nothing else, 100 mg nortriptyline should counteract the Provigil insomnia (ironic that a drug that is not energizing should make it harder for me to sleep). From my experience, nortriptyline is the reverse of a drug like remeron (it gets more sedating as the dosage is increased). I also have Lexapro samples but don't think much about Lex as a treatment for vegetative depression. What gives me a little hope is that I have read studies suggesting that there is a window within the window for nortrip plasma levels (about 80-120 ng/mL, within the larger window of 50-150 ng/ml) at which nortrip becomes its most effective. I hope this pulls me out of this depression.
>
>Hiya Zeugma,
It's been a while since you visited. Have you tried adding an SSRI to your Nortrip? Forgive me if you've answered this before as my memory
is not what it use to be :) I think you were thinking about clomipramine, but decided not to last time you were here?Cheers,
Panda.
Posted by zeugma on July 5, 2004, at 12:42:37
In reply to Re: vegetative depression, nortriptyline dosage » zeugma, posted by Sad Panda on July 5, 2004, at 10:29:46
Hiya Zeugma,
It's been a while since you visited. Have you tried adding an SSRI to your Nortrip? Forgive me if you've answered this before as my memory
is not what it use to be :) I think you were thinking about clomipramine, but decided not to last time you were here?Cheers,
Panda.Hi Panda,
yes I was thinking about clomipramine, but my pdoc gave me the Lex samples instead. I suppose nortriptyline + Lexapro would simulate clomipramine. I almost took a Lex pill last night, as I was so depressed, but decided to stick to my original plan to take an extra 25 mg nortriptyline capsule instead. Provigil is causing insomnia, nausea, sexual dysfunction: I have no desire to compound these with an SSRI. And I suspect the Lexapro would make me fatigued as well. Since provigil isn't helping with fatigue at all, but causing these side effects, I may drop it and see if the higher dose of nortrip has an 'alerting' effect like Strattera, good for my ADD, without worsening the fatigue.
The basic problem I'm having now is that I feel like I have so many different disorders that treating one means worsening another. Nortriptyline doesn't worsen any of them, and helps a good several, so I've stuck with it. Clonazepam helps with social phobia but seems to lower my mood so I keep the dose as low as possible. Provigil, besides its other s/e and inefficacy at helping fatigue, may be lowering my mood. It does have a 'slowing' effect on my thought process which is good for my ADD, but I have a feeling that it is this very effect which is worsening my mood... other stimulants I have taken in the past had this very same effect. So now I'm considering using the higher dose of nortrip as a surrogate for the Strattera that was effective for my ADD, and finding some way of adapting or reconciling myself to a chronically low level of energy.
z
Posted by King Vultan on July 6, 2004, at 8:06:48
In reply to vegetative depression, nortriptyline dosage, posted by zeugma on July 4, 2004, at 11:37:01
I found desipramine and Vivactil (protriptyline) to both be much more energizing and activating than nortriptyline. Of the two, desipramine has fewer side effects and is much cheaper. However, Vivactil does have some unique stimulatory properties. Too bad it's so anticholinergic.
Todd
Posted by SLS on July 6, 2004, at 9:26:55
In reply to Re: vegetative depression, nortriptyline dosage » zeugma, posted by King Vultan on July 6, 2004, at 8:06:48
> However, Vivactil does have some unique stimulatory properties. Too bad it's so anticholinergic.
You're not kidding. It's the worst I've ever taken.
- Scott
Posted by zeugma on July 6, 2004, at 11:00:39
In reply to Re: vegetative depression, nortriptyline dosage » zeugma, posted by King Vultan on July 6, 2004, at 8:06:48
> I found desipramine and Vivactil (protriptyline) to both be much more energizing and activating than nortriptyline. Of the two, desipramine has fewer side effects and is much cheaper. However, Vivactil does have some unique stimulatory properties. Too bad it's so anticholinergic.
I'm not worried about anticholinergic effects (I think I'm hyper-cholinergic), but I have a terrible time getting to sleep, and after a week or two after a dose increase, nortriptyline's antihistaminic fog dissipates and I feel relatively 'energized' by the drug (while its sleep-promoting effects remain intact).
I'm wary of stimulants at this point (Strattera was 'stimulating' at first) because I am very prone to a feeling of 'overstimulation' (even watching television can overstimulate me) and I feel also like I have reached a limit with how well I am going to get with medications. Stimulants can also cause depression and that concerns me (Provigil seemed to depress me).
>
> Toddz
Posted by SLS on July 6, 2004, at 12:22:44
In reply to Re: vegetative depression, nortriptyline dosage » King Vultan, posted by zeugma on July 6, 2004, at 11:00:39
> I'm not worried about anticholinergic effects (I think I'm hyper-cholinergic),
Do you dream too much?
- Scott
Posted by zeugma on July 6, 2004, at 12:27:02
In reply to Re: vegetative depression, nortriptyline dosage, posted by SLS on July 6, 2004, at 12:22:44
>
> > I'm not worried about anticholinergic effects (I think I'm hyper-cholinergic),
>
>
> Do you dream too much?
YES!! i go into REM immediately after falling asleep, and usually wake up (when not on TCA) with a sensation of having dreamed myself into exhaustion. does this happen to you?>
>
> - Scott
>
Posted by SLS on July 6, 2004, at 15:06:30
In reply to Re: vegetative depression, nortriptyline dosage » SLS, posted by zeugma on July 6, 2004, at 12:27:02
> >
> > > I'm not worried about anticholinergic effects (I think I'm hyper-cholinergic),
> >
> >
> > Do you dream too much?
>
>
> YES!! i go into REM immediately after falling asleep, and usually wake up (when not on TCA) with a sensation of having dreamed myself into exhaustion. does this happen to you?
Not really, but it is consistent with your hypothesis that your system is in a hypercholinergic state. How did you come to this conclusion?I would say that I hit REM sometime between 1/2 to 1 hour after falling asleep. This is consistent with endogenous depression. In healthy individuals, REM latency is closer to 90 minutes.
- Scott
Posted by zeugma on July 6, 2004, at 15:43:57
In reply to Re: vegetative depression, nortriptyline dosage » zeugma, posted by SLS on July 6, 2004, at 15:06:30
> > >
> > > > I'm not worried about anticholinergic effects (I think I'm hyper-cholinergic),
> > >
> > >
> > > Do you dream too much?
> >
> >
> > YES!! i go into REM immediately after falling asleep, and usually wake up (when not on TCA) with a sensation of having dreamed myself into exhaustion. does this happen to you?
>
>
> Not really, but it is consistent with your hypothesis that your system is in a hypercholinergic state. How did you come to this conclusion?
>
> I would say that I hit REM sometime between 1/2 to 1 hour after falling asleep. This is consistent with endogenous depression. In healthy individuals, REM latency is closer to 90 minutes.
>
>
> - Scott
>
>
II began getting hypnagogic/hypnopompic hallucinations (dreamlike states mixed with features of waking consciousness) at the age of 23. At times I have the 'dream within a dream' (false awakening) experience and when I actually wake up, less than 5 minutes have gone by on the clock. As far as I know, the images formed during stage 1 sleep do not have this quality at all; it aapears to be confined to REM states.These hallucinations/premature REM events are blocked to varying extents by nortriptyline, buspirone, and Strattera, but not by clonazepam, and of these four medications, only clonazepam is not a strong REM inhibitor.
When I took Strattera at the same time as clonazepam, and then fell asleep, I did not experience these states, consistent with Strattera's rapid absorption and powerful REM-suppressing effect (for more on this see http://www.sro.org/pdf/863.pdf, which used Strattera's cousin, nisoxetine). When I fell asleep after taking Provigil, I experienced extremely vivid dreams and did not feel rested at all.
Posted by SLS on July 6, 2004, at 16:05:58
In reply to Re: vegetative depression, nortriptyline dosage » SLS, posted by zeugma on July 6, 2004, at 15:43:57
Hi Zeugma.
> II began getting hypnagogic/hypnopompic hallucinations (dreamlike states mixed with features of waking consciousness) at the age of 23. At times I have the 'dream within a dream' (false awakening) experience and when I actually wake up, less than 5 minutes have gone by on the clock. As far as I know, the images formed during stage 1 sleep do not have this quality at all; it aapears to be confined to REM states.
> These hallucinations/premature REM events are blocked to varying extents by nortriptyline, buspirone, and Strattera, but not by clonazepam, and of these four medications, only clonazepam is not a strong REM inhibitor.
> When I took Strattera at the same time as clonazepam, and then fell asleep, I did not experience these states, consistent with Strattera's rapid absorption and powerful REM-suppressing effect (for more on this see http://www.sro.org/pdf/863.pdf, which used Strattera's cousin, nisoxetine). When I fell asleep after taking Provigil, I experienced extremely vivid dreams and did not feel rested at all.
Have you developed any tolerance to the REM inhibiting effects of these drugs?When I first took tricyclics and MAOIs, they had a profound effect in reducing or completely abolishing dreaming and presumably REM sleep in me. Upon discontinuation of these drugs, I would experience an intense REM rebound where I would experience the type of waking dreams you described. These things don't happen to me anymore. I wish they did.
- Scott
Posted by zeugma on July 6, 2004, at 16:40:38
In reply to Re: vegetative depression, nortriptyline dosage, posted by SLS on July 6, 2004, at 16:05:58
> Hi Zeugma.
>
> > II began getting hypnagogic/hypnopompic hallucinations (dreamlike states mixed with features of waking consciousness) at the age of 23. At times I have the 'dream within a dream' (false awakening) experience and when I actually wake up, less than 5 minutes have gone by on the clock. As far as I know, the images formed during stage 1 sleep do not have this quality at all; it aapears to be confined to REM states.
>
> > These hallucinations/premature REM events are blocked to varying extents by nortriptyline, buspirone, and Strattera, but not by clonazepam, and of these four medications, only clonazepam is not a strong REM inhibitor.
>
> > When I took Strattera at the same time as clonazepam, and then fell asleep, I did not experience these states, consistent with Strattera's rapid absorption and powerful REM-suppressing effect (for more on this see http://www.sro.org/pdf/863.pdf, which used Strattera's cousin, nisoxetine). When I fell asleep after taking Provigil, I experienced extremely vivid dreams and did not feel rested at all.
>
>
> Have you developed any tolerance to the REM inhibiting effects of these drugs?
>
> When I first took tricyclics and MAOIs, they had a profound effect in reducing or completely abolishing dreaming and presumably REM sleep in me. Upon discontinuation of these drugs, I would experience an intense REM rebound where I would experience the type of waking dreams you described. These things don't happen to me anymore. I wish they did.
>
>
> - Scott
Hi Scott,I haven't developed tolerance to the REM suppressing effects yet. I've only been on nortriptyline for about two years now (I was on it for a year and a half in my early 20's also- maybe that played a role in triggering the REM events at 23? though I had discontinued at 22). Did you find that mood improvement correlated with REM suppression?
I wonder if anyone has investigated poopout in terms of tolerance to REM suppression. From what I've been able to dredge up, it's the initial period of sleep (REM latency) that is crucial for maintainance of response:
: Biol Psychiatry. 1997 Oct 1;42(7):560-7. Related Articles, Links
Maintenance nortriptyline effects on electroencephalographic sleep in elderly patients with recurrent major depression: double-blind, placebo- and plasma-level-controlled evaluation.Reynolds CF 3rd, Buysse DJ, Brunner DP, Begley AE, Dew MA, Hoch CC, Hall M, Houck PR, Mazumdar S, Perel JM, Kupfer DJ.
Mental Health Clinical Research Center for the Study of Late-Life Mood Disorders, University of Pittsburgh Medical Center, Pennsylvania, USA.
Our aim was to contrast the effects of maintenance nortriptyline and placebo on electroencephalographic sleep measures in elderly recurrent depressives who survived 1-year without recurrence of depression. Patients on nortriptyline took longer to fall asleep and did not maintain sleep better than patients on placebo; however, maintenance nortriptyline was associated with more delta-wave production and higher delta-wave density in the first non-REM (NREM) period relative to the second. Nortriptyline levels were positively but weakly related to all-night delta-wave production during maintenance (accounting for 6.6% of the variance in delta-wave counts). Total phasic REM activity increased 100% under chronic nortriptyline relative to placebo, with a robust increase in the rate of REM activity generation across the night. Effective long-term pharmacotherapy of recurrent major depression is associated with enhancement in the rate of delta-wave production in the first NREM period (i.e., delta sleep ratio) and of REM activity throughout the night.
Many of the same people have been working on a theory of depression (or a certain type of depression: there are clearly many types of depression) as linked to abnormal REM/NREM patterns. I had thought this work had been abandoned years ago, with the advent of SSRI's and the total domination of research funded by companies promoting them, but here it is:: Psychiatry Res. 2000 Apr 10;98(2):71-91. Related Articles, Links
Towards a neurobiology of dysfunctional arousal in depression: the relationship between beta EEG power and regional cerebral glucose metabolism during NREM sleep.Nofzinger EA, Price JC, Meltzer CC, Buysse DJ, Villemagne VL, Miewald JM, Sembrat RC, Steppe DA, Kupfer DJ.
Department of Psychiatry, Western Psychiatric Institute and Clinic, 3811 O'Hara Street, Pittsburgh, PA 15213-2593, USA. nofzingerea@msx.upmc.edu
This study sought to clarify the neurobiological basis of variations in one aspect of central nervous system 'arousal' in depression by characterizing the functional neuroanatomic correlates of beta electroencephalographic (EEG) power density during non-rapid eye movement (NREM) sleep. First, nine healthy (n=9) subjects underwent concurrent EEG sleep studies and [18F]2-fluoro-2-deoxy-D-glucose ([18F]FDG) positron emission tomography (PET) scans during their first NREM period of sleep in order to generate hypotheses about specific brain structures that show a relationship between increased beta power and increased relative glucose metabolism. Second, brain structures identified in the healthy subjects were then used as a priori regions of interest in similar analyses from identical studies in 12 depressed subjects. Statistical parametric mapping was used to identify the relationship between beta power and relative regional cerebral glucose metabolism (rCMRglu) during NREM sleep. Regions that demonstrated significant correlations between beta power and relative cerebral glucose metabolism in both the healthy and depressed subjects included the ventromedial prefrontal cortex and the right lateral inferior occipital cortex. During a baseline night of sleep, depressed patients demonstrated a trend toward greater beta power in relation to a separate age- and gender-matched healthy control group. In both healthy and depressed subjects, beta power negatively correlated with subjective sleep quality. Finally, in the depressed group, there was a trend for beta power to correlate with an indirect measure of absolute whole brain metabolism during NREM sleep. This study demonstrates a similar relationship between electrophysiological arousal and glucose metabolism in the ventromedial prefrontal cortex in depressed and healthy subjects. Given the increased electrophysiological arousal in some depressed patients and the known anatomical relations between the ventromedial prefrontal cortex and brain activating structures, this study raises the possibility that the ventromedial prefrontal cortex plays a significant role in mediating one aspect of dysfunctional arousal found in more severely aroused depressed patients.
PMID: 10762734 [PubMed - indexed for MEDLINE]
-z
Posted by SLS on July 6, 2004, at 18:58:43
In reply to Re: vegetative depression, nortriptyline dosage » SLS, posted by zeugma on July 6, 2004, at 16:40:38
Hi Zeugma.
I'm afraid that I am having trouble making the connections between these abstracts. How do you interpret them?
- Scott
Posted by zeugma on July 6, 2004, at 20:02:18
In reply to Re: vegetative depression, nortriptyline dosage » zeugma, posted by SLS on July 6, 2004, at 18:58:43
> Hi Zeugma.
>
> I'm afraid that I am having trouble making the connections between these abstracts. How do you interpret them?
>
>
> - ScottHi Scott
brainwave states range from beta to delta:http://brain.web-us.com/brainwavesfunction.htm
beta states are the most aroused, and characteristic of waking (in its most engaged states- this article uses the example of someone in active debate). delta waves are characteristic of dreamless sleep (proper to NREM). If beta waves are generated during NREM then rather than being restorative this is going to be sleep that operates at the same energy level as waking. Normalization of this state would result in increased delta ratio for NREM.z
Posted by Sad Panda on July 6, 2004, at 21:33:59
In reply to Re: vegetative depression, nortriptyline dosage » SLS, posted by zeugma on July 6, 2004, at 20:02:18
Hiya's Scott & ~Z~
I just got back from my pdoc with a script for Nortriptyline, I am going to try & replace my Remeron with it. I'm looking for any wisdom from both of you. :)
First question is how essential is getting a ECG beforehand?
Cheers,
Panda.
Posted by SLS on July 6, 2004, at 21:47:49
In reply to Re: vegetative depression, nortriptyline dosage » SLS, posted by zeugma on July 6, 2004, at 20:02:18
> > Hi Zeugma.
> >
> > I'm afraid that I am having trouble making the connections between these abstracts. How do you interpret them?
> >
> >
> > - Scott
>
> Hi Scott
>
> brainwave states range from beta to delta:http://brain.web-us.com/brainwavesfunction.htm
That's a nice little review. I guess I was wondering if there was any data linking tolerance to the REM suppressing effects of ADs to loss of efficacy. Drugs worked best for me when they suppressed REM. 120mg of Parnate doesn't do it anymore, if you can believe it.
- Scott
Posted by SLS on July 6, 2004, at 21:56:10
In reply to Nortriptyline Experiences, posted by Sad Panda on July 6, 2004, at 21:33:59
> Hiya's Scott & ~Z~
>
> I just got back from my pdoc with a script for Nortriptyline, I am going to try & replace my Remeron with it. I'm looking for any wisdom from both of you. :)
>
> First question is how essential is getting a ECG beforehand?
Hi Panda.I've never had a doctor ask me to have an ECG done before starting a tricyclic (1982-present). I've never had a discussion about it either, so I really don't know the extent to which it is considered necessary or desirable. I guess if there are any predisposing factors for developing cardiac conduction problems, it makes sense to get a before and after.
What's your target dosage?
Good luck!
- Scott
Posted by zeugma on July 6, 2004, at 22:16:06
In reply to Re: Nortriptyline Experiences » Sad Panda, posted by SLS on July 6, 2004, at 21:56:10
Hi Scott and Panda,
I've never had an ECG performed or had a dr. ask me about it either. The only problem I have experienced in connection with nortrip is lowered bp, so I was advised to eat salty foods and keep myself well hydrated, which solved the problem. I get my bp monitored every month.
Scott:
I suspect strongly that AD efficacy is connected to REM suppression,and/or changes in NREM, though I don't have anything on hand to suggest that loss of efficacy is due to tolerance to REM suppression. What little evidence I've seen connected to poopout (not related to REM) suggests that it develops more frequently with MAOI's than TCA's.
I haven't come across anything in the narcolepsy literature that suggests that TCA's lose efficacy in the suppression of cataplexy (which is the intrusion of REM atonia into waking). Narcolepsy is a lifelong condition, and TCA efficacy is directly connected to suppression of REM, so there must be some anecdotal evidence somewhere that is relevant to your concern.
Poopout as a phenomenon only seems to have become the focus of attention lately, and primarily in connection with SSRI's.
Have you spoken to your doctor about the tolerance to REM suppression effects? Maybe he or she could shed some insight on the matter.
z
Posted by zeugma on July 6, 2004, at 22:44:11
In reply to Re: vegetative depression, nortriptyline dosage » zeugma, posted by SLS on July 6, 2004, at 21:47:49
> > > Hi Zeugma.
> > >
> > > I'm afraid that I am having trouble making the connections between these abstracts. How do you interpret them?
> > >
> > >
> > > - Scott
> >
> > Hi Scott
> >
> > brainwave states range from beta to delta:http://brain.web-us.com/brainwavesfunction.htm
>
>
> That's a nice little review. I guess I was wondering if there was any data linking tolerance to the REM suppressing effects of ADs to loss of efficacy. Drugs worked best for me when they suppressed REM. 120mg of Parnate doesn't do it anymore, if you can believe it.
>
>
> - Scott
>
>
J.A. Hobson, in "The Dream Drugstore", discusses how SSRI's can suppress actual REM stage sleep but increase dreaming. He says that since serotonin controls eye movements, the saccadic eye movements typical of REM become prevalent in other stages of sleep, resulting in increased dreaming despite diminished time spent in actual REM stage. This increased dreaming, according to him, does indeed cause 'poopout', since it deprives the brain of restorative sleep (since the eye movements, and presumably the accompanying brain activity are no longer confined to REM). What he says implies that noradrenergic AD's would be less likely to have this effect of increasing dream states, since it is 5-HT that is responsible for the saccadic eye movements. This can't be a global account of poopout, because any class of AD can poopout, unfortunately :(
Posted by Sad Panda on July 7, 2004, at 2:03:04
In reply to Re: Nortriptyline Experiences » Sad Panda, posted by SLS on July 6, 2004, at 21:56:10
I got an ECG done at my GP's, they think it's good to have a baseline for future reference in case something does go wrong. I don't know how much Nort I will end up taking, Effexor is keeping me happy, but I want an NE boost & I am hoping to use the constipation side effect to counteract the diarrhoea that I am getting from metformin. I also got a depot injection of Testosterone today too, so now I am taking seven different drugs.... When I was a kid I use to laugh at the amount of drugs my grandparents consumed & now I'm doing the same thing & I'm only 36 :/
Cheers,
Panda.
Posted by linkadge on July 7, 2004, at 16:27:42
In reply to Re: Nortriptyline Experiences, posted by Sad Panda on July 7, 2004, at 2:03:04
You are going to be taking effexor, remeron and nortriptaline ?? That'll be "california atomic rocket fuel"
Linkadge
Posted by Sad Panda on July 7, 2004, at 22:55:22
In reply to panda, posted by linkadge on July 7, 2004, at 16:27:42
> You are going to be taking effexor, remeron and nortriptaline ?? That'll be "california atomic rocket fuel"
>
> Linkadge
>
LOL @ "california atomic rocket fuel" :D
I am swapping from Remeron to Nortriptyline.Mirtazapine(Remeron) is a:
1. POTENT antihistamine (strongest on the market)
2. Moderate 5-HT2A, 5-HT2C, 5-HT3 antagonist.
3. Mild A-2 antagonist.
4. Weak A-1 & M-1 antagonist.Nortriptyline(Pamelor, Eli Lily's main AD before Prozac) is a:
1. Mild antihistamine
2. Moderate 5-HT2A antagonist.
3. Mild A-2 antagonist.
4. Moderate A-1 & M-1 antagonist.
5. Strong NE Reuptake inhibitor.I am hoping for a motivation boost from NE reuptake & I am hoping for the constipation side effect from M-1 blockade to counter the diarrhoea I have. I won't miss the H1 blocakde & I still think 5-HT2A blockade is the bees knees. :)
Cheers,
Panda.
This is the end of the thread.
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