Psycho-Babble Medication Thread 1121402

Shown: posts 1 to 21 of 21. This is the beginning of the thread.

 

Tentative remission on ketamine

Posted by beckett2 on December 29, 2022, at 20:53:47

About seven months in, ketamine is working well. Decades of depression and untreated BP variations left behavioral scaring and maladaptive behavior, and I'll never be good as new. But I don't expect that.

This is the only thing that has worked. I'm in my first maintenance phase, taking 200 mg every 7-10 days. Someday, maybe, once a month would be nice. The sessions are a bit of a chore.

PS, people report good results for alcoholism, and I can see why. My sweet tooth is a life-long issue, and last month I realized I don't want chocolate. In fact, I had some that sat around for a month that I threw away. Maybe this is related? Idk.

 

Re: Tentative remission on ketamine beckett2

Posted by SLS on December 29, 2022, at 21:35:24

In reply to Tentative remission on ketamine, posted by beckett2 on December 29, 2022, at 20:53:47

> About seven months in, ketamine is working well. Decades of depression and untreated BP variations left behavioral scaring and maladaptive behavior, and I'll never be good as new. But I don't expect that.
>
> This is the only thing that has worked. I'm in my first maintenance phase, taking 200 mg every 7-10 days. Someday, maybe, once a month would be nice. The sessions are a bit of a chore.
>

Have you considered the intranasal administration of ketamine? I think one dose every 5 days works best. It's dirt-cheap. My doctor prescribed the ketamine, and I went to a compounding pharmacy to have the prescription filled. My guess is that a greater percentage of people will respond to I.V. Nevertheless, intranasal administration might be worth trying as a short-term experiment. A friend of mine reported a large improvement within 3 days of her first dose. She described her response to ketamine as being remission. One dose every 7 days was not sufficient to maintain the improvement. She has been stable taking one dose every 5 days.

> PS, people report good results for alcoholism, and I can see why. My sweet tooth is a life-long issue, and last month I realized I don't want chocolate. In fact, I had some that sat around for a month that I threw away. Maybe this is related? Idk.

For people with the "atypical" subtype of depression - which is actually the more typical presentation of depression - having a sweet-tooth, cravings for carbohydrates, increased appetite, and weight gain are common while in the depressed state. These represent the "reverse vegetative symptoms" of atypical depression (as compared to the "positive vegetative symptoms" of melancholic / endogenous depression.

The disappearance of your sweet-tooth might be an artifact of the remission of depression. This is a good sign, especially when one recovers sex-drive and feels less fatigued.

Are there any other vegetative symptoms that have disappeared since your response to ketamine?


Symptoms that resemble dysautonomia / sympathetic system dominance:

Increased heart rate.
The sensation of heart-palpitations.
Sweating.
Dry mouth.
Blurry vision.
Changes in bowels.
Teeth-clenching
Global, non-localized aches and pains.
Cold tip of the nose.
Cold hands or feet.
Headaches.
Light or disrupted sleep.
Sensitivity to light.
Sensitivity to sound.
Decreased libido.
Vivid dreams.
Frequent infections.


- Scott

 

Re: Tentative remission on ketamine

Posted by Jay2112 on December 30, 2022, at 15:37:31

In reply to Tentative remission on ketamine, posted by beckett2 on December 29, 2022, at 20:53:47

Interesting....there is some new research discussing how the dissociative affects of ketamine, which bring it's therapeutic effects, as well as THC, are those we find in Scizophrenia. I find that too, with mid-dose THC, I get a fairly high dissociative feeling going. Dissociation is not always figured with Scizophrenia, but new studies are showing different: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964156/

I'd take a stab at possible high dopamine levels with something like high GABA levels as well, play a part in this. The serotonin and GABA, along with norepinephrine and dopamine, are said to be increased much by Nardil, in particular, GABA.

Jay

 

Re: Tentative remission on ketamine Jay2112

Posted by beckett2 on December 30, 2022, at 15:59:15

In reply to Re: Tentative remission on ketamine, posted by Jay2112 on December 30, 2022, at 15:37:31

> Interesting....there is some new research discussing how the dissociative affects of ketamine, which bring it's therapeutic effects, as well as THC, are those we find in Scizophrenia. I find that too, with mid-dose THC, I get a fairly high dissociative feeling going. Dissociation is not always figured with Scizophrenia, but new studies are showing different: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964156/
>
> I'd take a stab at possible high dopamine levels with something like high GABA levels as well, play a part in this. The serotonin and GABA, along with norepinephrine and dopamine, are said to be increased much by Nardil, in particular, GABA.
>
> Jay

I don't know my chemicals very well. So GABA is (perhaps) increased with ketamine?

 

Re: Tentative remission on ketamine SLS

Posted by beckett2 on December 30, 2022, at 16:09:35

In reply to Re: Tentative remission on ketamine beckett2, posted by SLS on December 29, 2022, at 21:35:24

Hi, Scott,

Generally, my physical health is better all around. I 'think' my depression, etc, is heavily weighted toward sleep disturbance and inflammation. With more study, we might find ketamine is effective for certain types of depression and less so for others. A few years from now there will be new treatments from psychedelics and dissociative that will help a suite of MH ailments.

 

Re: Tentative remission on ketamine beckett2

Posted by Jay2112 on December 30, 2022, at 16:54:04

In reply to Re: Tentative remission on ketamine Jay2112, posted by beckett2 on December 30, 2022, at 15:59:15

> > Interesting....there is some new research discussing how the dissociative affects of ketamine, which bring it's therapeutic effects, as well as THC, are those we find in Scizophrenia. I find that too, with mid-dose THC, I get a fairly high dissociative feeling going. Dissociation is not always figured with Scizophrenia, but new studies are showing different: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964156/
> >
> > I'd take a stab at possible high dopamine levels with something like high GABA levels as well, play a part in this. The serotonin and GABA, along with norepinephrine and dopamine, are said to be increased much by Nardil, in particular, GABA.
> >
> > Jay
>
> I don't know my chemicals very well. So GABA is (perhaps) increased with ketamine?
>

Yes, GABA is the main nt affected by ketamine. https://www.karger.com/Article/Fulltext/493425

The NMDA antagonism is part of that, as glutamine is a part of GABA.(GABA works the opposite of glutamine.) I have taken high dose benzo Xanax (5-6mg) and with a wee bit of an SRI, it's like almost heaven! But, it doesn't last long and you just fall asleep. Now, the side effects, in particular disassociation, to me, feel nice, because it takes me "out" of my depression and anxiety. I *love* that feeling. I think I may positively react to ketamine and possibly other psychedelics. Funny that edible cannabis has a similar effect on me, in low doses with CBD and CBG. I am working at trying ketamine through the CAMH here in Canada.

Jay

 

Re: Tentative remission on ketamine Jay2112

Posted by beckett2 on December 30, 2022, at 17:48:58

In reply to Re: Tentative remission on ketamine beckett2, posted by Jay2112 on December 30, 2022, at 16:54:04

Jay, thank you. This makes a bit of sense to me. I had been on a decent dose of xanax for maybe ten years, and withdrawing was hell. And it takes much longer than people often credit because my anxiety was through the roof for a number of years afterward.

What's very cool about ketamine is I have zero cravings or rebound as I did with xanax. In fact, I take it much less often than the starting protocol.

In addition to depression and BPii, I have fibromyalgia which is tied up with GABA (theoretically, I guess).

You may respond to ketamine. Sadly, about 40% (or so) do not.

Btw, cannibis and I do NOT get along. I ave increased anxiety to the point panic :( also worse pain!

I think it's great people get relief from it.

(Is ketamine available in Canada?)

 

Re: Tentative remission on ketamine

Posted by SLS on December 30, 2022, at 22:11:11

In reply to Re: Tentative remission on ketamine, posted by Jay2112 on December 30, 2022, at 15:37:31

> Interesting....there is some new research discussing how the dissociative affects of ketamine, which bring it's therapeutic effects, as well as THC, are those we find in Scizophrenia. I find that too, with mid-dose THC, I get a fairly high dissociative feeling going. Dissociation is not always figured with Scizophrenia, but new studies are showing different: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964156/
>
> I'd take a stab at possible high dopamine levels with something like high GABA levels as well, play a part in this. The serotonin and GABA, along with norepinephrine and dopamine, are said to be increased much by Nardil, in particular, GABA.
>
> Jay


I find Nardil to be much more of a "mood-brightener" and anti-anhedonic than Parnate is. Parnate never made me feel motivated and *want* to do things like Nardil does. I have fun with Nardil and look forward to having rewarding experiences rather than manufacturing reasons to avoid them. Parnate leaves me lacking, although it helps increase mental energy. Nardil also has pro-social effects and promotes more confidence and assertiveness in social situations. Social inhibition had been a symptom identified in France as a symptom of depression. It was for me.


- Scott

 

Re: Tentative remission on ketamine beckett2

Posted by Jay2112 on December 31, 2022, at 3:42:16

In reply to Re: Tentative remission on ketamine Jay2112, posted by beckett2 on December 30, 2022, at 17:48:58

> Jay, thank you. This makes a bit of sense to me. I had been on a decent dose of xanax for maybe ten years, and withdrawing was hell. And it takes much longer than people often credit because my anxiety was through the roof for a number of years afterward.
>
> What's very cool about ketamine is I have zero cravings or rebound as I did with xanax. In fact, I take it much less often than the starting protocol.
>
> In addition to depression and BPii, I have fibromyalgia which is tied up with GABA (theoretically, I guess).
>
> You may respond to ketamine. Sadly, about 40% (or so) do not.
>
> Btw, cannibis and I do NOT get along. I ave increased anxiety to the point panic :( also worse pain!
>
> I think it's great people get relief from it.
>
> (Is ketamine available in Canada?)

Hey, thanks! It does make sense that a benzodiazepine user would greatly benefit from ketamine, and I actually didn't realize the strong GABA agonism of ketamine until doing some serious research a few months ago. I wanted to undertake ketamine therapy. Yes, it is available in Canada, and at low cost for low income people like me, thankfully. We do have both the infusions and spray, and like methadone therapy, it is strictly managed. I am still trying to find cheap sources on the side, and my doctors are all uptight people..lol

I am very glad this is *working* for you!!! Do you take any meds with this? Any other types of therapy, or psychedelics?

Thanks,
Jay

 

Re: Tentative remission on ketamine

Posted by undopaminergic on December 31, 2022, at 14:03:45

In reply to Re: Tentative remission on ketamine, posted by Jay2112 on December 30, 2022, at 15:37:31

> Interesting....there is some new research discussing how the dissociative affects of ketamine, which bring it's therapeutic effects, as well as THC, are those we find in Scizophrenia. I find that too, with mid-dose THC, I get a fairly high dissociative feeling going. Dissociation is not always figured with Scizophrenia, but new studies are showing different: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964156/
>
> I'd take a stab at possible high dopamine levels with something like high GABA levels as well, play a part in this. The serotonin and GABA, along with norepinephrine and dopamine, are said to be increased much by Nardil, in particular, GABA.
>
> Jay

In my view, NMDA-glutamatergic receptor antagonists, like ketamine or memantine, enhance the *functional* dopaminergic tone, without necessarily elevating dopamine concentrations at all. They achieve stimulant-like or even manic-like effects by a mechanism of action that is distinct from the way stimulants like cocaine or Ritalin do.

-undopaminergic

 

Re: Tentative remission on ketamine undopaminergic

Posted by SLS on December 31, 2022, at 17:28:38

In reply to Re: Tentative remission on ketamine, posted by undopaminergic on December 31, 2022, at 14:03:45

Hi, UD.

> In my view, NMDA-glutamatergic receptor antagonists, like ketamine or memantine, enhance the *functional* dopaminergic tone, without necessarily elevating dopamine concentrations at all.

What is "dopaminergic tone"?

How does blocking NMDA receptors result in increased dopaminergic tone?

Thanks.

I am clueless as to what NMDA receptors are all about, other than their endogenous ligand is glutamate.


- Scott

 

Re: Tentative remission on ketamine

Posted by SLS on December 31, 2022, at 23:07:42

In reply to Re: Tentative remission on ketamine SLS, posted by beckett2 on December 30, 2022, at 16:09:35

> Hi, Scott,
>
> Generally, my physical health is better all around. I 'think' my depression, etc, is heavily weighted toward sleep disturbance and inflammation. With more study, we might find ketamine is effective for certain types of depression and less so for others. A few years from now there will be new treatments from psychedelics and dissociative that will help a suite of MH ailments.
>
>


Ketamine is confusing to some researchers. It is thought to increase neuroplasticity acutely, but makes cells more vulnerable to hypoxic stress. Fortunately, hypoxic conditions aren't something likely to be encountered. Perhaps you have already seen the following abstract. It posits that it is neuroinflammation that is the common denominator between depression and the ability of ketamine and several other psychoactive substances to treat it.

One drug that has been used to reduce inflammation in the brain is monocycline. It is marketed as an antibiotic in the tetracycline class. My doctor has been focusing on brain inflammation for quite awhile. Monocycline reduces the secretion of pro-inflammatory cytokines from microglia. It gave me enough of an improvement to remain on it for over a year. However, a black-and-blue hyperpigmentation emerged on my feet and shins. Although benign, it looked like hell. It took perhaps two years to completely disappear. For many people, there is a residual that never disappears.

From what you've read, does depression cause inflammation or does inflammation cause depression?

My intuition suggest to me that it is the depression that starts first. Once triggered, perhaps depression places enough stress on the brain and CNS to cause an inflammatory reaction facilitated by increased microglial activity. I get the feeling that the core depressive disorder and the inflammation begin to feed off each other once both are established. I never researched the matter.

The immune system is probably the second most complicated system in the body to understand, with the brain being the first.


Abstract:

"Neuroinflammation and neuroprogression in depression: Effects of alternative drug treatments"

https://pubmed.ncbi.nlm.nih.gov/36388140/


- Scott

 

Re: Tentative remission on ketamine beckett2

Posted by SLS on January 1, 2023, at 3:18:43

In reply to Re: Tentative remission on ketamine SLS, posted by beckett2 on December 30, 2022, at 16:09:35

> Hi, Scott,
>
> Generally, my physical health is better all around. I 'think' my depression, etc, is heavily weighted toward sleep disturbance and inflammation. With more study, we might find ketamine is effective for certain types of depression and less so for others.

Undoubtedly.

Major Depressive Disorder is really just a set of hetergenous presentations; each with a different gestalt of etiologies.

> A few years from now there will be new treatments from psychedelics and dissociative that will help a suite of MH ailments.

Once, a friend of mine encouraged me to look into intranasal ketamine. It sounded like a whacky idea to me at first, but the idea grew on me. She is an old-timer of Psycho-Babble, but hasn't posted in over a decade. Treatment-resistent. Tried all of the available "traditionally-defined" antidepressants. She decided to take a 8 hour trip to see her old psychiatrist, who happened to be an associate of my doctor in Princeton. The doctor had just begun to treat people with intranasal ketamine. Long story short... My friend, who had spent the better part of her life chasing remission by ingesting all sorts of substances was offered something very different - intranasal ketamine. 3 days after her first dose, she described herself as being in remission. Huh? Same person?

The second phase of using intranasal ketamine to treat depression is to discover the best dosing frequency to maintain remission. Some people dose every day. Some people dose once per week. I think a schedule of one dose every 5 days is showing itself to be the sweet-spot for dosing frequency.

The clinical rule of thumb for establishing the optimal therapeutic dosing for any method of ketamine administration is that the dosage be high enough to produce a mild dissociative state. If, however, the magnitude of the dissociative state is too great, ketamine will fail to exert an antidepressant effect. Check the work of John Krystal from Yale. His work helped to foster the use of ketamine in psychiatry - for both mood and schizoid disorders.

Ketamine is dirt-cheap. Your doctor prescribes the concentration of the ketamine solution and the amount to be administered per nostril. I had my prescription filled at an apothecary in Princeton.

Intra-nasal - Quick, Cheap, Convenient, Effective, Lower rate of response(?), but full remission is possible.

Intra-veneous I.V. - Not quick, Not cheap, Not convenient, Higher rate of response (?).


Optimal schedule for dosing: One treatment every 3-7 days. I am under the impression that one dose every 5 days most often hits the bullseye.

As an aside, both ketamine and memantine block NMDA receptors. I haven't looked into the variability in the binding affinities of both drugs to the NMDA receptor. Whereas ketamine produces an immediate and robust antidepressant when administered as monotherapy, memantine does not. Clinically, ketamine is clearly a more effective tool to treat depression than memantine is.


- Scott4

 

Re: Tentative remission on ketamine beckett2

Posted by SLS on January 1, 2023, at 6:34:09

In reply to Re: Tentative remission on ketamine SLS, posted by beckett2 on December 30, 2022, at 16:09:35

Hi, Beckett2.

I was thinking about you and your ketamine treatment earlier today.

http://www.dr-bob.org/babble/20220917/msgs/1121438.html

Happy New Year!

I hope you find something helpful in my hunch.


- Scott

 

Re: Tentative remission on ketamine SLS

Posted by undopaminergic on January 1, 2023, at 10:33:00

In reply to Re: Tentative remission on ketamine undopaminergic, posted by SLS on December 31, 2022, at 17:28:38

> Hi, UD.
>
> > In my view, NMDA-glutamatergic receptor antagonists, like ketamine or memantine, enhance the *functional* dopaminergic tone, without necessarily elevating dopamine concentrations at all.
>
> What is "dopaminergic tone"?
>

Tonic is in contrast to phasic. I meant it, approximately, as the dopaminergic "background" or "baseline" signal. It adapts to stimuli slowly, but is sustained. Phasic signals react fast, but are also more ephemeral.

> How does blocking NMDA receptors result in increased dopaminergic tone?
>

I think it is about the balance between dopamine and glutamate. Increasing dopamine would affect the balance similarly to decreasing glutamate. It's just my theory, though, so you probably shouldn't quote me on it.

> Thanks.
>
> I am clueless as to what NMDA receptors are all about, other than their endogenous ligand is glutamate.
>

NMDA receptors are ligand-gated ion channels. When activated, they are permeable to Ca2+ ions. They are named after the excitatory amino acid N-methyl-D-aspartate that binds selectively to these channels.

-undopaminergic

 

Re: Tentative remission on ketamine SLS

Posted by undopaminergic on January 1, 2023, at 10:56:53

In reply to Re: Tentative remission on ketamine beckett2, posted by SLS on January 1, 2023, at 3:18:43

>
> As an aside, both ketamine and memantine block NMDA receptors. I haven't looked into the variability in the binding affinities of both drugs to the NMDA receptor. Whereas ketamine produces an immediate and robust antidepressant when administered as monotherapy, memantine does not. Clinically, ketamine is clearly a more effective tool to treat depression than memantine is.
>

You are mostly correct. There can be a lag between memantine initiation and an antidepressant response, but this lag is at most a few days. I would say it doesn't produce remission, but a state similar to (hypo)mania. And the required dose escalates -- I went from 10 mg to about 60 mg/dose. Then I deliberately overdosed with a few *grams*, and that's another story.

-undopaminergic

 

Re: Tentative remission on ketamine

Posted by Jay2112 on January 1, 2023, at 14:49:09

In reply to Re: Tentative remission on ketamine undopaminergic, posted by SLS on December 31, 2022, at 17:28:38

> Hi, UD.
>
> > In my view, NMDA-glutamatergic receptor antagonists, like ketamine or memantine, enhance the *functional* dopaminergic tone, without necessarily elevating dopamine concentrations at all.
>
> What is "dopaminergic tone"?
>
> How does blocking NMDA receptors result in increased dopaminergic tone?
>
> Thanks.
>
> I am clueless as to what NMDA receptors are all about, other than their endogenous ligand is glutamate.
>
>
> - Scott

Don't know about tone. But, possibly the way this GABA agonist pregabalin is considered "addictive" explains the relation:

https://www.nature.com/articles/s41598-019-51556-4

Jay

 

Re: Tentative remission on ketamine Jay2112

Posted by beckett2 on January 1, 2023, at 18:51:59

In reply to Re: Tentative remission on ketamine beckett2, posted by Jay2112 on December 31, 2022, at 3:42:16

I don't take other psychedelics or weed, but I'm curious about microdosing mushrooms.

My ketamine comes through the mail by a provider licensed in most states. He's a psych, but I still have my regular psychiatrist who manages my other meds. This regular psych does approve of ketamine and in fact, suggested it because I've suffered for many years. He's such a good guy.

Not sure if Canada has any service like that available. I do telehealth through the ketamine guy.

 

Re: Tentative remission on ketamine SLS

Posted by beckett2 on January 1, 2023, at 19:00:42

In reply to Re: Tentative remission on ketamine beckett2, posted by SLS on January 1, 2023, at 6:34:09

> Hi, Beckett2.
>
> I was thinking about you and your ketamine treatment earlier today.
>
> http://www.dr-bob.org/babble/20220917/msgs/1121438.html
>
> Happy New Year!
>
> I hope you find something helpful in my hunch.
>
>
> - Scott

Happy New Year to you, too, Scott!

Thank you for the information and support. I hadn't seen that article. While looking and it, I went down a little rabbit hole and found something that addresses our conversation and my own symptoms:

https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-021-02245-5

 

Re: Tentative remission on ketamine

Posted by SLS on January 1, 2023, at 20:10:48

In reply to Re: Tentative remission on ketamine SLS, posted by beckett2 on January 1, 2023, at 19:00:42

> > Hi, Beckett2.
> >
> > I was thinking about you and your ketamine treatment earlier today.
> >
> > http://www.dr-bob.org/babble/20220917/msgs/1121438.html
> >
> > Happy New Year!
> >
> > I hope you find something helpful in my hunch.
> >
> >
> > - Scott
>
> Happy New Year to you, too, Scott!
>
> Thank you for the information and support. I hadn't seen that article. While looking and it, I went down a little rabbit hole and found something that addresses our conversation and my own symptoms:
>
> https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-021-02245-5


Great find, Beckett.

I don't recall whether or not I discussed with you my being treated with monocycline quite a few years ago. My doctor chose it specifically to see whether or not a substance known to reduce brain inflammation would produce an improvement in my depression. It did. At a time when almost nothing was helping, I experienced a moderate, but consistent improvement for over a year with monocycline. After about 1 1/2 years, I developed black-and-blue marks on the skin of my feet and shins. This is known as hyperpignentation, and is not an uncommon side effect produced by monocycline. It can grow to be very ugly. It is common that the hyperpigmentation appears with a latency of 1-2 years. In most cases, the discolorations on the lower legs disappear, but this can take years. I still had some residual markings after a year. They are gone now. For some people, the hyperpigmentation is irreversible.

It is important to know that no such improvement in depression occurred while I was taking doxycycline - the analog of monocycline in the tetracycline class of antibiotics. I took doxycycline for three months. My doctor wanted to see if doxycyline would produce an improvement as a sort of challenge to assess the possibility that I might have Lyme Disease.

My doctor keeps himself apprised of the latest discoveries coming from the frontier. He has been incorporating brain inflammation into his conceptualizations of the genesis of depression. If you hadn't provided the motivation to look into ketamine, I wouldn't have learned that:

1. The addition of magnesium to ketamine amplifies the inhibition of NMDA receptors and produces a significantly better antidepressant response and reduction in brain inflammation compared to ketamine alone.

2. Magnesium by itself can reduce the rush of calcium ions into the neuron terminals via blocking the calcium channels. This results in a reduction of the release of neurotransmitter. Perhaps magnesium acts as a buffer to prevent an unrestricted influx of calcium ions rushing through the calcium channels that stimulates the release of neurotransmitter from presynaptic storage vesicles into the synaptic cleft, thereupon to bind to receptors located on the postsynaptic membrane.


- Scott

 

Re: Tentative remission on ketamine beckett2

Posted by SLS on January 2, 2023, at 16:05:34

In reply to Tentative remission on ketamine, posted by beckett2 on December 29, 2022, at 20:53:47

Hi, Beckett.

"Lumateperone normalizes pathological levels of acute *inflammation* through important pathways known to be involved in mood regulation"

https://pubmed.ncbi.nlm.nih.gov/36549907/

I suggested to one person who failed to respond to lurasodone (Latuda) if they might look into lumateperone (Caplyta) for treating depression. I have not seen Latuda have a good track record for treating depression. Caplyta has an FDA indication for Bipolar I and II depression. Regarding inflammation, I found only one article describing inflammation as possibly being involved with the mechanism of action of lumaterpersone.


- Scott


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