Unknown Heroin Contaminant Causes Leukoencephalopathy May 7, 2002
An unknown contaminant or filler material has killed at least two people and caused brain damage in at least two others in May of 2002, news reports from Vancouver said. There are a number of cases, documented in the literature, of a type of brain damage that seems to be resulting from smoking a contaminant in some batches of heroin. The following is a collection of references and abstracts related to this issue.
Deaths, brain damage tied to bad drugs, The Province, May 07, 2002
The initial symptoms are often difficulty in speaking or walking. Family members or friends who notice such behaviour should advise any user to seek immediate medical attention, said Blatherwick. The four recent cases are the first of the condition recorded in B.C., he said. He appealed to the unknown dealer of the drugs: "You, out there, if you're cutting it [adding non-drug filler to the heroin/cocaine] with something different than you usually do, you should know you are costing yourself customers."
Heroin Inhalation and Progressive Spongiform Leukoencephalopathy N Engl J Med 1997 Feb 20;336(8):589-90 Kriegstein AR, Armitage BA, Kim PY.
The authors report on two cases of a previously unreported progressive spongiform leukoenceph-alopathy occurring after repeated inhalation of heated heroin vapor. Both patients, a 21-year-old woman and a 40 year old man had been "chasing the dragon" for six months and two weeks respectively. The first patient experienced progressive bradykinesia, ataxia, and slurred speech developing over a two-week period. Over the next two weeks, she became mute, spastic, nearly quadriplegic, and unable to stand or sit. The second patient had dysarthric, scanning speech and saccadic-pursuit eye movements with ocular dysmetria, ataxic arm movements with dysmetria, dysdiadochokinesia, and rebound; broad based and ataxic gait. Cerebral T2-weighted MRI findings were similar for both patients. The authors cite several similar cases reported in Europe, all involving heroin heated in aluminum foil and inhaled. So far there is no known treatment for this condition and a 25% mortality rate. The authors suspect that the cause may be contamination of small batches of heroin by an unknown substance activated by heating, and are concerned, given the rise of heroin smoking as a means of avoiding exposure to HIV through needle use.
Leukoencephalopathy and raised brain lactate from heroin vapor inhalation ("chasing the dragon") Neurology 1999 Nov 10;53(8):1765-73 Kriegstein AR, Shungu DC, Millar WS, Armitage BA, Brust JC, Chillrud S, Goldman J, Lynch T.
BACKGROUND: Inhalation of heated heroin vapor ("chasing the dragon"), which is gaining popularity among drug users seeking to avoid the risks of parenteral drug administration, can produce progressive spongiform leukoencephalopathy. METHODS: We studied the clinical phenotype and course, MRI, MRS, and brain pathology in the first American patients described with this syndrome. RESULTS: Two of the three heroin users studied inhaled heroin pyrolysate together daily over the course of 2 weeks. They developed ataxia, dysmetria, and dysarthria. Patient 1 progressed to an akinetic mute state with decorticate posture and subsequent spastic quadriparesis. Patient 2 developed a mild spastic quadriparesis and gait freezing. Patient 3 was asymptomatic following less heroin exposure. Brain MRI showed diffuse, symmetrical white matter hyperintensities in the cerebellum, posterior cerebrum, posterior limbs of the internal capsule, splenium of the corpus callosum, medial lemniscus, and lateral brainstem. MRS showed elevated lactate. Brain biopsy (Patient 1) showed white matter spongiform degeneration with relative sparing of U-fibers; electron microscopy revealed intramyelinic vacuolation with splitting of intraperiod lines. Progressive deterioration occurred in Patients 1 and 2 over 4 weeks. Both were treated with antioxidants including oral coenzyme Q, and clinical improvement occurred. Patient 1 recovered nearly completely over 24 months. Patient 2 improved, but developed a delayed-onset cerebellar hand tremor. Both still have white matter abnormalities on MRI and MRS. CONCLUSIONS: Elevated lactate in white matter and the possible response to antioxidants suggests mitochondrial dysfunction in progressive spongiform leukoencephalopathy following inhalation of heated heroin vapor.
Leukoencephalopathy after inhalation of heroin vapor. J Formos Med Assoc 1997 Sep;96(9):758-60 Chang YJ, Tsai CH, Chen CJ.
A 25-year-old man presented in March 1996 with progressive dysarthria, cerebellar ataxia, and dystonia, which began after he inhaled heroin vapor for a full day 2 months previously. The patient had a 2-year history of heroin inhalation. Magnetic brain stimulation showed waveform dysynchronization suggestive of motor pathway perturbation above the cervical spinal level. Brain computed tomography and magnetic resonance imaging revealed extensive symmetric white matter involvement of bilateral cerebral and cerebellar hemispheres and the brainstem, especially along the corticospinal tract. The clinical features, electrophysiologic manifestations, and imaging studies strongly indicated a lipophilic toxin-induced demyelinating process, mainly involving the central motor system, as the most likely cause of heroin leukoencephalopathy. This is the first reported case of heroin-related leukoencephalopathy in Taiwan.
Vacuolar leucoencephalopathy induced by heroin: 4cases [Article in French] Rev Neurol (Paris) 2002 Feb;158(2):177-82 Koussa S, Zabad R, Rizk T, Tamraz J, Nasnas R, Chemaly R.
We report 4 cases of toxic leucoencephalopathy after heroin inhalation. The clinical features, which usually occur some days or even longer after the last heroin consumption, are dominated by a cerebellar syndrome. The cerebellar hemispheres are almost always affected; the cerebral hemispheres, the cerebellar peduncles and the pyramidal tract may be affected. Vacuolar demyelination is the morphological substract of the lesions, which are symmmetrical, not contrast enhancing, hypodense on CT scan and hyperintense on T2- weighted MRI. The pathophysiology is unknown and seems different from post-anoxic leucoencephalopathy. The disease is usually progressive leading sometimes to death, but some cases show slow recovery.
Ever see those worms in Africa that start out microscopic and live in mud, then they burrow into someone's foot when they walk through the mud, and then they grow larger and larger as they eat their way up the person's leg, until finally they burst out through the skin up around the knee and crawl out?
That's some really fucked up shit right there, I tell you.
For the most part, the weekend was rather beautiful. This was the third in a series of multiday, multiple substance experience that a small group of us had engaged upon together, in various combinations. The seven of us are, for the most part, very experienced with psychedelics in general - years and years of experience among us, with only one individual really being a newcomer to the vast majority of the substances we typically do as a group. We started off the evening with amt, a drug that some find annoying, but which every member of our group finds to be quite a wonderful drug - like mdma, but without the mad scramble to squeeze it all in before it wears off. Amt features two hours of nausea up front, which can be mitigated with the less-drowsy formula of dramamine. After that, it's a very very long experience, 12 hours at least, a very leisurely and enjoyable ride.
After the AMT had pretty much wound down completely, we took MDMA. From a safety perspective, some have suggested that combining amt and mdma is an unsafe move, because amt is an mao inhibitor, and mdma does not combine well with maois. My response to that is that we are taking the mdma well after the amt has essentially run its course, not stacking the peaks, and have never noticed any untoward physical effects. Moreover, as some have heard of this weekend, the mistaken impression seems to be that we were stacking many concurrent peaks; the actual technique, which to me seems much more rational and acceptable, was to essentially let one drug finish out its course entirely before starting the next one. This is much less aggressive physically than stacking concurrent peaks; it gives you time to fully enjoy one substance before moving on, and really does manage to avoid bad synergies. However, it's still an aggressive move: You wind up gradually more and more exhausted, and thus more physically and emotionally open to the drugs that are later in the schedule. It's not at all without risk; but it was within the acceptable range for what every member of this group considered comfortable.
After the mdma, some bumps of ketamine occurred, and then a couple people drifted off to sleep. Ketamine at very high doses is dissociative, but at very low doses, it acts as a very mild repotentiator of whatever you happen to be on. It's a very enjoyable state. At the end of the mdma, some folks moved on to 2cb. Most people managed to squeeze in at least a few hours napping after that. As a group, we were all having a wonderful time, eating split pea soup through- out to keep our spirits up, reminding each other to stay very hydrated, etc.
One thing we did *not* do was utilize a sober sitter for the duration of the experience. It's been my experience with this community that sober sitters are rarely particularly encouraged, no matter what the experience. It happens occasionally, but it's not a rigid rule of thumb. I've participated in dozens of experiences, with combinations, with new substances, with new people, where sitters seemed optional due to the experience of the people involved. It's not overconfidence; it's just confidence, which i've noticed is something many ppl in this group seem to have. Not a confidence that nothing can go wrong, but a confidence that if something does go wrong, it can be handled. That was the mindset we were in, for the most part, as we approached day two. I would consider this the first of our small but very serious mistakes.
After getting up from our naps, 2ct7 was on the agenda. One member of our group bowed out, in order to get some sleep. Of the rest of us, only 2 of us had really had a threshold dose of 2ct7 before; the rest were either new to the substance or had not taken a threshold dose previously. A *lot* happened to us from that point on, and i don't intend to comment on all of it. From a safety perspective, i will focus on one individual, whom i'll refer to as melissa (obviously not her real name). Melissa had never taken t7 before. I informed her that people were considering 20mg a good starter dose, and that some ppl were finding 20mg to be an extremely intense dose as well; that you could start with 20mg and boost your way up, if you wanted to. One of the other women in the group told melissa that she had tried 30mg and found it ok, but that she was going to do 40mg this time. Another woman in our group had done 40mg pre- viously and found that to be boring. The men in our group are all very much high dosers, and we were not particularly used as datapoints in her decision, i believe; we were all doing 60 and 70mg. Melissa chose 40 as her dose. In retrospect, i regret not being more forceful about considering 20mg as a starting point; i also feel that melissa didn't spend nearly enough time educating herself about t7. She came to it with very little if any understanding of what others' experiences had been, and she should have done more research. She was essentially trusting all of us, and that was a mistake. It's the kind of mistake you make when you really trust the people you're with, but there's no excuse not to do the research, and we all should have spent more time right at that point discussing what was about to happen.
The first four hours of the t7 were marvelous and wondrous, in many ways. T7 can be an amazing substance, truly beautiful. Melissa was having a wonderful time by her own account, and so none of us were on alert. The one sober person in the house was asleep at that point. Melissa announced that she was going out for a cigarette, something she'd been doing all night. For some reason, none of her usual smoking buddies went with her; in fact, no one went with her. We realized about 15 minutes later that she hadn't come back, and that she'd gone out alone. It was a rather difficult realization to make, a realization of the 'oh my god, we've really fucked up' variety. We went out to do a quick look for her, but she was long gone. We called likely spots that she might have headed to, but she hadn't been sighted. Hours went by. We reasoned that melissa was a pretty hardcore tripper, known to be able to walk the streets of major cities on lsd without much trouble; she knew the neighborhood we were in, she'd taken walks earlier in the day (accompanied) and she perhaps just wanted some time alone to appreciate the experience. But we were all extremely unsettled.
Other things happened while she was gone that lead me to state categorically: 2Ct7 is worth extreme caution. It's wonderful, but it's an extremely strong psychedelic. Be careful!
Approximately four hours later, melissa returned. Her story was chilling. She remembers walking down the street away from my apartment. The next thing she remembers is being in a man's car. She doesn't know how she got in the car. She remembers them stopping at a 7-11, and asking him to pick up some water for her. She remembers him taking her to a friend's apartment. She remembers them asking her if she was drunk, and responding she was on 2ct7, which of course they didn't recognize. She remembers asking for a telephone, and not being given one. They asked her what her name was, and where she lived, and she couldn't remember. She remembers watching cartoons for a period of time. She remembers her pants coming off, and asking 'where's my pants?' Her underwear stayed on, and she believes nothing sexual happened. Eventually they brought her back to my apartment and let her go. She had left the apartment without shoes on, and without her wallet, meaning she had no identification with her at all.
A number of analogues of LSD have maintained the diethylamide group unchanged, but additions or changes have been made in the pyrrole ring. ALD-52. 1-Acetyl-N,N-diethyllysergamide. This material has been explored in the 50-175 microgram range and there are a number of human trials reported, with varying conclusions. One found that there was less visual distortion than with LSD and it seems to produce less anxiety and was somewhat less potent than LSD. Another report claimed it was more effective in increasing blood pressure. Yet another could not tell them apart. ALD- 52 just may have been the drug that was sold as "Orange Sunshine" during the "Summer of Love" in the late '60's. Or "Orange Sunshine" may have been, really, LSD. This was the focus of a fascinating trial where two defendants were accused of distributing LSD, whereas they claimed that it was ALD-52 which was not an illegal drug. The prosecution claimed that as it hydrolyses readily to LSD, for all intents and purposes it was LSD, and anyway, you had to go through the illegal LSD to get to ALD-52 by any of the known chemical syntheses. The defendants were found guilty. And yet, I do not know who has actually measured the speed or ease of that reaction. If ALD-52 hydrolyses so easily to LSD, and the body is indeed a hydrolytic instrument, then these two drugs should be absolutely equivalent in every particular, This is the ergot equivalent of the psilocybin to psilocin argument, except this is an acetamide rather than a phosphate ester.
MLD-41. 1-Methyl-N,N-diethyllysergamide. The 1-methyl homologue of LSD is has more of somatic than sensory effect, has fewer visuals and is less well accepted than LSD, with the range of dosages being from 100 to 300 micrograms. This indicates that it is perhaps a third the potency of LSD which is in accord with both pupilary dilation and reflex action. However, the cardiovascular responses are actually increased. Besides being less potent than LSD, it appears to have a slower onset but it is equally long lived. There is cross-tolerance between MLD-41 and LSD.
BOL-148. 2-Bromo-N,N-diethyllysergamide. This synthetic ergot derivative, along with its 1-methyl homologue MBL-61 (mentioned below) should be used as powerful tools for studying the mechanism of action of LSD in the human animal. It does not have LSD-like effects in man. At 6 to 10 milligrams orally, there are some mental changes noted. But in another study, 20 milligrams was administered a day to a subject for 7 days, and there were no reported effects. And yet it is as potent a serotonin agonist as is LSD. How can serotonin be argued as a neurotransmitter that is a major player in explaining the action of psychedelic drugs, when this compound is nearly without activity.
There are some suggestions that an intervenous route may be more effective. I have heard of effects being noted at maybe a milligram and a short (2-3 hour) intoxicaion following 20 milligrams administered over a 20 minute period. I was involved many years ago in a study of radio-labelled BOL-148 which was made by the bromination of LSD. I was quite sure that the only radioactive material present was BOL-148, but there could well have been some unreacted LSD still present which would, of course, still be psychoactive. The synthesis is not clean -- I was tempted to make an entry for this compound if only to reproduce Albert Hofmann's original published experimental procedure. He reacted 13.2 grams of N-bromosuccinimide (in 400 mL dioxane, with 1.2 liters of dioxane containing 25 grams of LSD. This gave 11 grams of crude produce which had to be recrystallized. The radioactive syntheses uses effectively elemental bromine, and gave yields of from 5 to 15%. Visualize that reaction! A warm flask containing over a quart of warm solvent in which there was maybe half a million doses of LSD.
1-Hydroxymethyl-LSD, 1-dimethylaminomethyl-LSD and 2-iodo-LSD. These three additional compounds are shown here because they were described in a synthetic flurry that followed the discovery the activity of LSD. But at the moment I know neither their internal Sandoz codes nor if they had ever been explored in man. This is a kind of frustrating catch-all entry, in that the long index will send you here, and once here you realize that nothing is known. Well, at least the compounds are known, and perhaps there is something in the Sandoz vaults that might be interesting. I do not have access to them.
MBL-61. 2-Bromo-N,N-diethyl-1-methyllysergamide. This is the compound BOL-148 (mentioned above) with a methyl group attached to the 1- position of the indole ring (LSD has a hydrogen there). This wold be an even more tantalizing challenge to the serotonin theory for centrqal activity of the psuchedelics, in that it is without any activity in man at an oral dose of 14 milligrams (similar to the inactivity of the BOL-61 compound, but it is spome five times more potent as a serotonin agonist. With it, as with the iodiniated analogue MIL, there are many examples of the compromising of scientific integrity in the quest for funds and recognition. Both compounds are as effective as LSD itself in displacing labelled LSD that is bound to the post- synaptic serotonin receptor sites in animal brains. But neither of them show any LSD-like activity. But both have been labelled with 11-C or 122-I to give positrol emitting forms that can be administered to man and localized in a positrom emition tomographt instrument (a PET scanner).
I was at a meeting of a NIDA study section a few years ago, where some one presented some findings with a group of subjects who were complaining of continuing mental problems alledgedly due to LSD exposure. A chart was put up showing the outline of the brain showing the locations of the EEG foci that were observed in one of these subjects. Along side it was a PET scan showing the distribution of radioactive LSD in a subject. The purpose was to discuss the similarities and differences of the coordinates of electrical activity and radio-isotope concentration. I innocently asked what positron isotope had been used, as I did not know of any successful positron labelling of LSD. Carbon 11, I was told. Where in the molecule was the label incorporated, I asked. In the 1-position methyl group. It was finally acknowledged that the compound that had actually been used was 2-iodo-1-methyl- LSD, our MIL compound, which is quite a different world. A pharmacologist might say that they are similar in action (looking at serotonin, not psychedelic action), and achemist might say they are of similar structure (looking at the upper 80% of the moledule. But they are different compounds. This is a most subtle form of deceit. It is, in fact, out and out dishonest, but it looks good up there on the screen at a lecture.
Let me mention in passing, that there are three stereoisomers possible for d-LSD. There are d-iso-LSD, l-LSD, and l-iso-LSD. The inversion of the stereochemistry of the attached diethylcarboxyamido group of d-LSD gives the diastereoisomer (d-iso-LSD) which is a frequent synthetic impurity of d- LSD itself. The corresponding optical antipodes l-LSD and l-iso-LSD are also known and have been tasted. All three are completely inactive: d-iso- LSD shows no psychological changes at an oral dose of 4 milligrams; l-LSD none at up to 10 milligrams orally; and l-iso-LSD none at 500 micrograms orally. These dramatic decreases in potency show both the stereoselectivity of the native LSD molecule in producing its central effects, and the LSD- free purity of these isomers.
The second major location of variations in the structure of LSD has been in the nature of the alkyl groups on the amide nitrogen atom. Some of these are Sandoz syntheses, some are from other research groups, and a few of them are found in nature. Some of these have been studied in man, and some have not. A few of the original clutch of Sandoz compounds have both 1-substituents and amide alkyl (R) group variations:
This listing is not intended to be thorough, but it is shown to suggest the amount of synthetic effort that has been made towards the exploring and understanding the high potency associated with those two remarkably important ethyl groups on the amide nitrogen of LSD. I have given the Sandoz code names, again, as far as I know them. Although none of these really warrant a dedicated recipe, there is sufficient animal and human pharmacology reported to justify listing them below as separate items. Most of these reports appeared in the mid-1950's but some studies are still being done and papers are published even today with new ideas but, sadly, only with animal pharmacology. I have been as guilty as the next person who has tried to mount all these compounds into a table with a "human potency" factor that compares them directly to LSD. This is an uncomfortable simplification. Here are the actual reported observations, and I'll let the reader provide his own potency index.
LA-111, ergine, d-lysergamide. This is an active compound and has been established as a major component in morning glory seeds. It was assayed for human activity, by Albert Hofmann in self-trials back in 1947, well before this was known to be a natural compound. An i.m. administration of a 500 microgram dose led to a tired, dreamy state with an inability to maintain clear thoughts. After a short period of sleep, the effects were gone and normal baseline was recovered within five hours. Other observers have confirmed this clouding of consciousness leading to sleep. The epimer, inverted at C-8, is isoergine or d-isolysergamide, and is also a component of morning glory seeds. Hofmann tried a 2 milligram dose of this amide, and as with ergine, he experienced nothing but tiredness, apathy, and a feeling of emptiness. Both compounds are probably correctly dismissed as not being a contributor to the action of these seeds. It is important to note that ergine, as well as lysergic acid itself, is listed as a Schedule III drug in the Controlled Substances Act, as a depressant. This is, in all probability, a stratagem to control them as logical precursors to LSD.
LAE-32, N-ethyllysergamide. Different people have observed and reported different effects, with different routes of administration. Subcutaneous administrations of from 500 to 750 micrograms have been said to produce a state of apathy and sedation. Clinical studies with dosages of 500 micrograms i.m. were felt to be less effective than the control use of 100 micrograms of LSD. And yet, oral doses of twice this amount, 1.6 milligrams, have been said to produce a short-lived LSD-like effect with none of these negatives.
LPD-824, N-Pyrrolidyllysergamide. Five trials at a dosage of 800 micrograms orally led to the reporting of a fleeting effect that was similar to one tenth this amount of LSD.
LSM-775, N-Morpholinyllysergamide. There are conflicting reports; one states that 75 micrograms is an effective dose, comparable to a similar dose of LSD, and the other stated that between 350 and 700 micrograms was needed to elicit this response, and that there were fewer signs of cardiovascular stimulation and peripheral toxicity.
DAM-57, N,N-Dimethyllysergamide. This compound did induce autonomic disturbances at oral levels of some ten times the dosage required for LSD, presumably in the high hundreds of micrograms. There is some disagreement as to whether there were psychic changes observed.
DAL, N,N-Diallyllysergamide. As the tartrate salt, there is at best a touch of sparkle seen at 600 micrograms orally, but there is a sedation also reported. It is certainly an order of magnitude less potent than LSD itself.
UML-491, Methysergide, Sansert. This is the synthetic homologue of methergine (1-methyl) and is employed clinically as a treatment for migraine headaches. When the usual therapeutic dosage of two milligrams is scaled up by a factor of ten, there is a profound LSD-like response described by most subjects. A number of these ergot analogues from nature can be considered as potential precursors for the preparation of LSD. But here, there is a 1-methyl group that is effectively permanently attached, so it cannot play this role.
I can't stand it I know you planned it But i'm gonna set it straight, this watergate I can't stand rockin' when i'm in here Because your crystal ball ain't so crystal clear So while you sit back and wonder why I got this fuckin' thorn in my side Oh my, it's a mirage I'm tellin' y'all it's sabotage
So listen up 'cause you can't say nothin' You'll shut me down with a push of your button? But i'm out, and i'm gone I'll tell you now I keep it on and on
Cause what you see you might not get And we can't bet so don't you get souped yet You're schmeing on a thing that's a mirage I'm trying to tell you now it's sabotage
Why; our backs are now against the wall Listen all of y'all it's a sabotage
I can't stand it, I know you planned it But i'm gonna set it straight this watergate I can't stand rockin' when i'm in this place Because I feel disgrace because you're all in my face But make no mistakes and switch up my channel I'm buddy rich when I fly off the handle What could it be, it's a miracle You're scheming on a thing; that's sabotage
Re: if we didn't, they sure had NASA fooled
on
China Plans Moonbase
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Quick question: When constructing a foil hat, does the shiny side go on the inside (to keep the brainwaves in) or outside (to keep the satellite mind-rays out)?
"Hamidi" sounds vaguely Arabic to me. Has the FBI investigated this guy yet? These so-called "mass emailings" may be part of a larger terrorist operation.
Einstein was not a handsome fellow Nobody ever called him Al He had a long moustache to pull on, it was yellow I don't believe he ever had a girl One thing he missed out in his theory Of time and space and relativity Is something that makes it very clear; He was never gonna score like you and me
He didn't know about Quark, Strangeness and Charm Quark, Strangeness and Charm Quark, Strangeness and Charm
I had a dangerous liaison To have been found out would've been a disgrace We had to rendezvous some days on the corner of an undiscovered place We got sick of chat chat chatter And the look upon everybody's face But all that doesn't anti-matter now We've found ourselves a black hole out in space
And we're talking about Quark, Strangeness and Charm Quark, Strangeness and Charm Quark, Strangeness and Charm
Copernicus had those Renaissance ladies Crazy about his telescope And Galileo had a name that made his Reputation higher than his hopes Did none of those astronomers discover While they were staring out into the dark That what a lady looks for in her lover Is Charm, Strangeness and Quark
And we're talking about Quark, Strangeness and Charm Quark, Strangeness and Charm Quark, Strangeness and Charm
I'm not sure if Mr. Salvatore was entirely faithful to the movie. At least, none of the previews I've seen show Anakin fighting with two curved lightsabers.
No, I'll tell you what they need... A Secret Society, sworn to protect the area and kill all who may tresspass, like in Indiana Jones and The Holy Grail or The Mummy.
Slashdot Mirror
Unknown Heroin Contaminant Causes Leukoencephalopathy
May 7, 2002
An unknown contaminant or filler material has killed at least two people and caused brain damage in at least two others in May of 2002, news reports from Vancouver said. There are a number of cases, documented in the literature, of a type of brain damage that seems to be resulting from smoking a contaminant in some batches of heroin. The following is a collection of references and abstracts related to this issue.
Deaths, brain damage tied to bad drugs, The Province, May 07, 2002
The initial symptoms are often difficulty in speaking or walking. Family members or friends who notice such behaviour should advise any user to seek immediate medical attention, said Blatherwick. The four recent cases are the first of the condition recorded in B.C., he said. He appealed to the unknown dealer of the drugs: "You, out there, if you're cutting it [adding non-drug filler to the heroin/cocaine] with something different than you usually do, you should know you are costing yourself customers."
Heroin Inhalation and Progressive Spongiform Leukoencephalopathy N Engl J Med 1997 Feb 20;336(8):589-90 Kriegstein AR, Armitage BA, Kim PY.
The authors report on two cases of a previously unreported progressive spongiform leukoenceph-alopathy occurring after repeated inhalation of heated heroin vapor. Both patients, a 21-year-old woman and a 40 year old man had been "chasing the dragon" for six months and two weeks respectively. The first patient experienced progressive bradykinesia, ataxia, and slurred speech developing over a two-week period. Over the next two weeks, she became mute, spastic, nearly quadriplegic, and unable to stand or sit. The second patient had dysarthric, scanning speech and saccadic-pursuit eye movements with ocular dysmetria, ataxic arm movements with dysmetria, dysdiadochokinesia, and rebound; broad based and ataxic gait. Cerebral T2-weighted MRI findings were similar for both patients. The authors cite several similar cases reported in Europe, all involving heroin heated in aluminum foil and inhaled. So far there is no known treatment for this condition and a 25% mortality rate. The authors suspect that the cause may be contamination of small batches of heroin by an unknown substance activated by heating, and are concerned, given the rise of heroin smoking as a means of avoiding exposure to HIV through needle use.
Leukoencephalopathy and raised brain lactate from heroin vapor inhalation ("chasing the dragon") Neurology 1999 Nov 10;53(8):1765-73 Kriegstein AR, Shungu DC, Millar WS, Armitage BA, Brust JC, Chillrud S, Goldman J, Lynch T.
BACKGROUND: Inhalation of heated heroin vapor ("chasing the dragon"), which is gaining popularity among drug users seeking to avoid the risks of parenteral drug administration, can produce progressive spongiform leukoencephalopathy. METHODS: We studied the clinical phenotype and course, MRI, MRS, and brain pathology in the first American patients described with this syndrome. RESULTS: Two of the three heroin users studied inhaled heroin pyrolysate together daily over the course of 2 weeks. They developed ataxia, dysmetria, and dysarthria. Patient 1 progressed to an akinetic mute state with decorticate posture and subsequent spastic quadriparesis. Patient 2 developed a mild spastic quadriparesis and gait freezing. Patient 3 was asymptomatic following less heroin exposure. Brain MRI showed diffuse, symmetrical white matter hyperintensities in the cerebellum, posterior cerebrum, posterior limbs of the internal capsule, splenium of the corpus callosum, medial lemniscus, and lateral brainstem. MRS showed elevated lactate. Brain biopsy (Patient 1) showed white matter spongiform degeneration with relative sparing of U-fibers; electron microscopy revealed intramyelinic vacuolation with splitting of intraperiod lines. Progressive deterioration occurred in Patients 1 and 2 over 4 weeks. Both were treated with antioxidants including oral coenzyme Q, and clinical improvement occurred. Patient 1 recovered nearly completely over 24 months. Patient 2 improved, but developed a delayed-onset cerebellar hand tremor. Both still have white matter abnormalities on MRI and MRS. CONCLUSIONS: Elevated lactate in white matter and the possible response to antioxidants suggests mitochondrial dysfunction in progressive spongiform leukoencephalopathy following inhalation of heated heroin vapor.
Leukoencephalopathy after inhalation of heroin vapor. J Formos Med Assoc 1997 Sep;96(9):758-60 Chang YJ, Tsai CH, Chen CJ.
A 25-year-old man presented in March 1996 with progressive dysarthria, cerebellar ataxia, and dystonia, which began after he inhaled heroin vapor for a full day 2 months previously. The patient had a 2-year history of heroin inhalation. Magnetic brain stimulation showed waveform dysynchronization suggestive of motor pathway perturbation above the cervical spinal level. Brain computed tomography and magnetic resonance imaging revealed extensive symmetric white matter involvement of bilateral cerebral and cerebellar hemispheres and the brainstem, especially along the corticospinal tract. The clinical features, electrophysiologic manifestations, and imaging studies strongly indicated a lipophilic toxin-induced demyelinating process, mainly involving the central motor system, as the most likely cause of heroin leukoencephalopathy. This is the first reported case of heroin-related leukoencephalopathy in Taiwan.
Vacuolar leucoencephalopathy induced by heroin: 4cases [Article in French] Rev Neurol (Paris) 2002 Feb;158(2):177-82 Koussa S, Zabad R, Rizk T, Tamraz J, Nasnas R, Chemaly R.
We report 4 cases of toxic leucoencephalopathy after heroin inhalation. The clinical features, which usually occur some days or even longer after the last heroin consumption, are dominated by a cerebellar syndrome. The cerebellar hemispheres are almost always affected; the cerebral hemispheres, the cerebellar peduncles and the pyramidal tract may be affected. Vacuolar demyelination is the morphological substract of the lesions, which are symmmetrical, not contrast enhancing, hypodense on CT scan and hyperintense on T2- weighted MRI. The pathophysiology is unknown and seems different from post-anoxic leucoencephalopathy. The disease is usually progressive leading sometimes to death, but some cases show slow recovery.
Ever see those worms in Africa that start out microscopic and live in mud, then they burrow into someone's foot when they walk through the mud, and then they grow larger and larger as they eat their way up the person's leg, until finally they burst out through the skin up around the knee and crawl out?
That's some really fucked up shit right there, I tell you.
For the most part, the weekend was rather beautiful. This was the third in a series of multiday, multiple substance experience that a small group of us had engaged upon together, in various combinations. The seven of us are, for the most part, very experienced with psychedelics in general - years and years of experience among us, with only one individual really being a newcomer to the vast majority of the substances we typically do as a group. We started off the evening with amt, a drug that some find annoying, but which every member of our group finds to be quite a wonderful drug - like mdma, but without the mad scramble to squeeze it all in before it wears off. Amt features two hours of nausea up front, which can be mitigated with the less-drowsy formula of dramamine. After that, it's a very very long experience, 12 hours at least, a very leisurely and enjoyable ride.
After the AMT had pretty much wound down completely, we took MDMA. From a safety perspective, some have suggested that combining amt and mdma is an unsafe move, because amt is an mao inhibitor, and mdma does not combine well with maois. My response to that is that we are taking the mdma well after the amt has essentially run its course, not stacking the peaks, and have never noticed any untoward physical effects. Moreover, as some have heard of this weekend, the mistaken impression seems to be that we were stacking many concurrent peaks; the actual technique, which to me seems much more rational and acceptable, was to essentially let one drug finish out its course entirely before starting the next one. This is much less aggressive physically than stacking concurrent peaks; it gives you time to fully enjoy one substance before moving on, and really does manage to avoid bad synergies. However, it's still an aggressive move: You wind up gradually more and more exhausted, and thus more physically and emotionally open to the drugs that are later in the schedule. It's not at all without risk; but it was within the acceptable range for what every member of this group considered comfortable.
After the mdma, some bumps of ketamine occurred, and then a couple people drifted off to sleep. Ketamine at very high doses is dissociative, but at very low doses, it acts as a very mild repotentiator of whatever you happen to be on. It's a very enjoyable state. At the end of the mdma, some folks moved on to 2cb. Most people managed to squeeze in at least a few hours napping after that. As a group, we were all having a wonderful time, eating split pea soup through- out to keep our spirits up, reminding each other to stay very hydrated, etc.
One thing we did *not* do was utilize a sober sitter for the duration of the experience. It's been my experience with this community that sober sitters are rarely particularly encouraged, no matter what the experience.
It happens occasionally, but it's not a rigid rule of thumb. I've participated in dozens of experiences, with combinations, with new substances, with new people, where sitters seemed optional due to the experience of the people involved. It's not overconfidence; it's just confidence, which i've noticed is something many ppl in this group seem to have. Not a confidence that nothing can go wrong, but a confidence that if something does go wrong, it can be handled. That was the mindset we were in, for the most part, as we approached day two. I would consider this the first of our small but very serious mistakes.
After getting up from our naps, 2ct7 was on the agenda. One member of our group bowed out, in order to get some sleep. Of the rest of us, only 2 of us had really had a threshold dose of 2ct7 before; the rest were either new to the substance or had not taken a threshold dose previously. A *lot* happened to us from that point on, and i don't intend to comment on all of it. From a safety perspective, i will focus on one individual, whom i'll refer to as melissa (obviously not her real name). Melissa had never taken t7 before. I informed her that people were considering 20mg a good starter dose, and that some ppl were finding 20mg to be an extremely intense dose as well; that you could start with 20mg and boost your way up, if you wanted to. One of the other women in the group told melissa that she had tried 30mg and found it ok, but that she was going to do 40mg this time. Another woman in our group had done 40mg pre- viously and found that to be boring. The men in our group are all very much high dosers, and we were not particularly used as datapoints in her decision, i believe; we were all doing 60 and 70mg. Melissa chose 40 as her dose. In retrospect, i regret not being more forceful about considering 20mg as a starting point; i also feel that melissa didn't spend nearly enough time educating herself about t7. She came to it with very little if any understanding of what others' experiences had been, and she should have done more research. She was essentially trusting all of us, and that was a mistake. It's the kind of mistake you make when you really trust the people you're with, but there's no excuse not to do the research, and we all should have spent more time right at that point discussing what was about to happen.
The first four hours of the t7 were marvelous and wondrous, in many ways. T7 can be an amazing substance, truly beautiful. Melissa was having a wonderful time by her own account, and so none of us were on alert. The one sober person in the house was asleep at that point. Melissa announced that she was going out for a cigarette, something she'd been doing all night. For some reason, none of her usual smoking buddies went with her; in fact, no one went with her. We realized about 15 minutes later that she hadn't come back, and that she'd gone out alone. It was a rather difficult realization to make, a realization of the 'oh my god, we've really fucked up' variety. We went out to do a quick look for her, but she was long gone. We called likely spots that she might have headed to, but she hadn't been sighted. Hours went by. We reasoned that melissa was a pretty hardcore tripper, known to be able to walk the streets of major cities on lsd without much trouble; she knew the neighborhood we were in, she'd taken walks earlier in the day (accompanied) and she perhaps just wanted some time alone to appreciate the experience. But we were all extremely unsettled.
Other things happened while she was gone that lead me to state categorically: 2Ct7 is worth extreme caution. It's wonderful, but it's an extremely strong psychedelic. Be careful!
Approximately four hours later, melissa returned. Her story was chilling. She remembers walking down the street away from my apartment. The next thing she remembers is being in a man's car. She doesn't know how she got in the car. She remembers them stopping at a 7-11, and asking him to pick up some water for her. She remembers him taking her to a friend's apartment. She remembers them asking her if she was drunk, and responding she was on 2ct7, which of course they didn't recognize. She remembers asking for a telephone, and not being given one. They asked her what her name was, and where she lived, and she couldn't remember. She remembers watching cartoons for a period of time. She remembers her pants coming off, and asking 'where's my pants?' Her underwear stayed on, and she believes nothing sexual happened. Eventually they brought her back to my apartment and let her go. She had left the apartment without shoes on, and without her wallet, meaning she had no identification with her at all.
A number of analogues of LSD have maintained the diethylamide group unchanged, but additions or changes have been made in the pyrrole ring.
ALD-52. 1-Acetyl-N,N-diethyllysergamide. This material has been explored in the 50-175 microgram range and there are a number of human trials reported, with varying conclusions. One found that there was less visual distortion than with LSD and it seems to produce less anxiety and was somewhat less potent than LSD. Another report claimed it was more effective in increasing blood pressure. Yet another could not tell them apart. ALD- 52 just may have been the drug that was sold as "Orange Sunshine" during the "Summer of Love" in the late '60's. Or "Orange Sunshine" may have been, really, LSD. This was the focus of a fascinating trial where two defendants were accused of distributing LSD, whereas they claimed that it was ALD-52 which was not an illegal drug. The prosecution claimed that as it hydrolyses readily to LSD, for all intents and purposes it was LSD, and anyway, you had to go through the illegal LSD to get to ALD-52 by any of the known chemical syntheses. The defendants were found guilty. And yet, I do not know who has actually measured the speed or ease of that reaction. If ALD-52 hydrolyses so easily to LSD, and the body is indeed a hydrolytic instrument, then these two drugs should be absolutely equivalent in every particular, This is the ergot equivalent of the psilocybin to psilocin argument, except this is an acetamide rather than a phosphate ester.
MLD-41. 1-Methyl-N,N-diethyllysergamide. The 1-methyl homologue of LSD is has more of somatic than sensory effect, has fewer visuals and is less well accepted than LSD, with the range of dosages being from 100 to 300 micrograms. This indicates that it is perhaps a third the potency of LSD which is in accord with both pupilary dilation and reflex action. However, the cardiovascular responses are actually increased. Besides being less potent than LSD, it appears to have a slower onset but it is equally long lived. There is cross-tolerance between MLD-41 and LSD.
BOL-148. 2-Bromo-N,N-diethyllysergamide. This synthetic ergot derivative, along with its 1-methyl homologue MBL-61 (mentioned below) should be used as powerful tools for studying the mechanism of action of LSD in the human animal. It does not have LSD-like effects in man. At 6 to 10 milligrams orally, there are some mental changes noted. But in another study, 20 milligrams was administered a day to a subject for 7 days, and there were no reported effects. And yet it is as potent a serotonin agonist as is LSD. How can serotonin be argued as a neurotransmitter that is a major player in explaining the action of psychedelic drugs, when this compound is nearly without activity.
There are some suggestions that an intervenous route may be more effective. I have heard of effects being noted at maybe a milligram and a short (2-3 hour) intoxicaion following 20 milligrams administered over a 20 minute period. I was involved many years ago in a study of radio-labelled BOL-148 which was made by the bromination of LSD. I was quite sure that the only radioactive material present was BOL-148, but there could well have been some unreacted LSD still present which would, of course, still be psychoactive. The synthesis is not clean -- I was tempted to make an entry for this compound if only to reproduce Albert Hofmann's original published experimental procedure. He reacted 13.2 grams of N-bromosuccinimide (in 400 mL dioxane, with 1.2 liters of dioxane containing 25 grams of LSD. This gave 11 grams of crude produce which had to be recrystallized. The radioactive syntheses uses effectively elemental bromine, and gave yields of from 5 to 15%. Visualize that reaction! A warm flask containing over a quart of warm solvent in which there was maybe half a million doses of LSD.
1-Hydroxymethyl-LSD, 1-dimethylaminomethyl-LSD and 2-iodo-LSD. These three additional compounds are shown here because they were described in a synthetic flurry that followed the discovery the activity of LSD. But at the moment I know neither their internal Sandoz codes nor if they had ever been explored in man. This is a kind of frustrating catch-all entry, in that the long index will send you here, and once here you realize that nothing is known. Well, at least the compounds are known, and perhaps there is something in the Sandoz vaults that might be interesting. I do not have access to them.
MBL-61. 2-Bromo-N,N-diethyl-1-methyllysergamide. This is the compound BOL-148 (mentioned above) with a methyl group attached to the 1- position of the indole ring (LSD has a hydrogen there). This wold be an even more tantalizing challenge to the serotonin theory for centrqal activity of the psuchedelics, in that it is without any activity in man at an oral dose of 14 milligrams (similar to the inactivity of the BOL-61 compound, but it is spome five times more potent as a serotonin agonist. With it, as with the iodiniated analogue MIL, there are many examples of the compromising of scientific integrity in the quest for funds and recognition. Both compounds are as effective as LSD itself in displacing labelled LSD that is bound to the post- synaptic serotonin receptor sites in animal brains. But neither of them show any LSD-like activity. But both have been labelled with 11-C or 122-I to give positrol emitting forms that can be administered to man and localized in a positrom emition tomographt instrument (a PET scanner).
I was at a meeting of a NIDA study section a few years ago, where some one presented some findings with a group of subjects who were complaining of continuing mental problems alledgedly due to LSD exposure. A chart was put up showing the outline of the brain showing the locations of the EEG foci that were observed in one of these subjects. Along side it was a PET scan showing the distribution of radioactive LSD in a subject. The purpose was to discuss the similarities and differences of the coordinates of electrical activity and radio-isotope concentration. I innocently asked what positron isotope had been used, as I did not know of any successful positron labelling of LSD. Carbon 11, I was told. Where in the molecule was the label incorporated, I asked. In the 1-position methyl group. It was finally acknowledged that the compound that had actually been used was 2-iodo-1-methyl- LSD, our MIL compound, which is quite a different world. A pharmacologist might say that they are similar in action (looking at serotonin, not psychedelic action), and achemist might say they are of similar structure (looking at the upper 80% of the moledule. But they are different compounds. This is a most subtle form of deceit. It is, in fact, out and out dishonest, but it looks good up there on the screen at a lecture.
Let me mention in passing, that there are three stereoisomers possible for d-LSD. There are d-iso-LSD, l-LSD, and l-iso-LSD. The inversion of the stereochemistry of the attached diethylcarboxyamido group of d-LSD gives the diastereoisomer (d-iso-LSD) which is a frequent synthetic impurity of d- LSD itself. The corresponding optical antipodes l-LSD and l-iso-LSD are also known and have been tasted. All three are completely inactive: d-iso- LSD shows no psychological changes at an oral dose of 4 milligrams; l-LSD none at up to 10 milligrams orally; and l-iso-LSD none at 500 micrograms orally. These dramatic decreases in potency show both the stereoselectivity of the native LSD molecule in producing its central effects, and the LSD- free purity of these isomers.
The second major location of variations in the structure of LSD has been in the nature of the alkyl groups on the amide nitrogen atom. Some of these are Sandoz syntheses, some are from other research groups, and a few of them are found in nature. Some of these have been studied in man, and some have not. A few of the original clutch of Sandoz compounds have both 1-substituents and amide alkyl (R) group variations:
This listing is not intended to be thorough, but it is shown to suggest the amount of synthetic effort that has been made towards the exploring and understanding the high potency associated with those two remarkably important ethyl groups on the amide nitrogen of LSD. I have given the Sandoz code names, again, as far as I know them. Although none of these really warrant a dedicated recipe, there is sufficient animal and human pharmacology reported to justify listing them below as separate items. Most of these reports appeared in the mid-1950's but some studies are still being done and papers are published even today with new ideas but, sadly, only with animal pharmacology. I have been as guilty as the next person who has tried to mount all these compounds into a table with a "human potency" factor that compares them directly to LSD. This is an uncomfortable simplification. Here are the actual reported observations, and I'll let the reader provide his own potency index.
LA-111, ergine, d-lysergamide. This is an active compound and has been established as a major component in morning glory seeds. It was assayed for human activity, by Albert Hofmann in self-trials back in 1947, well before this was known to be a natural compound. An i.m. administration of a 500 microgram dose led to a tired, dreamy state with an inability to maintain clear thoughts. After a short period of sleep, the effects were gone and normal baseline was recovered within five hours. Other observers have confirmed this clouding of consciousness leading to sleep. The epimer, inverted at C-8, is isoergine or d-isolysergamide, and is also a component of morning glory seeds. Hofmann tried a 2 milligram dose of this amide, and as with ergine, he experienced nothing but tiredness, apathy, and a feeling of emptiness. Both compounds are probably correctly dismissed as not being a contributor to the action of these seeds. It is important to note that ergine, as well as lysergic acid itself, is listed as a Schedule III drug in the Controlled Substances Act, as a depressant. This is, in all probability, a stratagem to control them as logical precursors to LSD.
LAE-32, N-ethyllysergamide. Different people have observed and reported different effects, with different routes of administration. Subcutaneous administrations of from 500 to 750 micrograms have been said to produce a state of apathy and sedation. Clinical studies with dosages of 500 micrograms i.m. were felt to be less effective than the control use of 100 micrograms of LSD. And yet, oral doses of twice this amount, 1.6 milligrams, have been said to produce a short-lived LSD-like effect with none of these negatives.
LPD-824, N-Pyrrolidyllysergamide. Five trials at a dosage of 800 micrograms orally led to the reporting of a fleeting effect that was similar to one tenth this amount of LSD.
LSM-775, N-Morpholinyllysergamide. There are conflicting reports; one states that 75 micrograms is an effective dose, comparable to a similar dose of LSD, and the other stated that between 350 and 700 micrograms was needed to elicit this response, and that there were fewer signs of cardiovascular stimulation and peripheral toxicity.
DAM-57, N,N-Dimethyllysergamide. This compound did induce autonomic disturbances at oral levels of some ten times the dosage required for LSD, presumably in the high hundreds of micrograms. There is some disagreement as to whether there were psychic changes observed.
DAL, N,N-Diallyllysergamide. As the tartrate salt, there is at best a touch of sparkle seen at 600 micrograms orally, but there is a sedation also reported. It is certainly an order of magnitude less potent than LSD itself.
UML-491, Methysergide, Sansert. This is the synthetic homologue of methergine (1-methyl) and is employed clinically as a treatment for migraine headaches. When the usual therapeutic dosage of two milligrams is scaled up by a factor of ten, there is a profound LSD-like response described by most subjects. A number of these ergot analogues from nature can be considered as potential precursors for the preparation of LSD. But here, there is a 1-methyl group that is effectively permanently attached, so it cannot play this role.
Salute me!
Dammit bitch, you better have dinner ready when I get home, or you'll be explaining your theories about successful movies to the back of my hand.
Not only that, I think this Obi-Wan guy might be Ben Kenobi in Episode IV. Not 100% sure, though.
I can't stand it I know you planned it
But i'm gonna set it straight, this watergate
I can't stand rockin' when i'm in here
Because your crystal ball ain't so crystal clear
So while you sit back and wonder why
I got this fuckin' thorn in my side
Oh my, it's a mirage
I'm tellin' y'all it's sabotage
So listen up 'cause you can't say nothin'
You'll shut me down with a push of your button?
But i'm out, and i'm gone
I'll tell you now I keep it on and on
Cause what you see you might not get
And we can't bet so don't you get souped yet
You're schmeing on a thing that's a mirage
I'm trying to tell you now it's sabotage
Why; our backs are now against the wall
Listen all of y'all it's a sabotage
I can't stand it, I know you planned it
But i'm gonna set it straight this watergate
I can't stand rockin' when i'm in this place
Because I feel disgrace because you're all in my face
But make no mistakes and switch up my channel
I'm buddy rich when I fly off the handle
What could it be, it's a miracle
You're scheming on a thing; that's sabotage
I hear there's vast deposits of MSG.
Quick question: When constructing a foil hat, does the shiny side go on the inside (to keep the brainwaves in) or outside (to keep the satellite mind-rays out)?
"Hamidi" sounds vaguely Arabic to me. Has the FBI investigated this guy yet? These so-called "mass emailings" may be part of a larger terrorist operation.
No, if he was a K5'er he would have said "USian" instead of "American".
I thought priests were more into assraping?
If the .com I worked for had these, they would have saved so much money they could have laid me off on Thursday instead of Wednesday!
Einstein was not a handsome fellow
Nobody ever called him Al
He had a long moustache to pull on, it was yellow
I don't believe he ever had a girl
One thing he missed out in his theory
Of time and space and relativity
Is something that makes it very clear;
He was never gonna score like you and me
He didn't know about
Quark, Strangeness and Charm
Quark, Strangeness and Charm
Quark, Strangeness and Charm
I had a dangerous liaison
To have been found out would've been a disgrace
We had to rendezvous some days on
the corner of an undiscovered place
We got sick of chat chat chatter
And the look upon everybody's face
But all that doesn't anti-matter now
We've found ourselves a black hole out in space
And we're talking about
Quark, Strangeness and Charm
Quark, Strangeness and Charm
Quark, Strangeness and Charm
Copernicus had those Renaissance ladies
Crazy about his telescope
And Galileo had a name that made his
Reputation higher than his hopes
Did none of those astronomers discover
While they were staring out into the dark
That what a lady looks for in her lover
Is Charm, Strangeness and Quark
And we're talking about
Quark, Strangeness and Charm
Quark, Strangeness and Charm
Quark, Strangeness and Charm
I'm not sure if Mr. Salvatore was entirely faithful to the movie. At least, none of the previews I've seen show Anakin fighting with two curved lightsabers.
Last month I ordered myself an Russian mail-order bride. She arrived yesterday. Dumbasses forgot to poke airholes in the box.
Yeah, Christina Aquilera mixes well with my Strokes, if you know what I mean...
FIrst drunken post motherfucker! woooooaaaahH!!!!! nigggaaaaaaaaaHHhhhhh!!!
No, I'll tell you what they need... A Secret Society, sworn to protect the area and kill all who may tresspass, like in Indiana Jones and The Holy Grail or The Mummy.
She's having another of those tonight btw, if you want to stop by. She's raised her price to $5, though, since the price of crack went up again.
Strange, her ass is tight enough for me. Perhaps you just have an abnormally small penis.
Do you have to buy her a ticket, or do you just deflate her before you go in?
Good gig.
So what if they want to share information. Isn't that what the whole Free Software Revolution is about? Information wants to be free, right?
Or do they have to encode your personal information into MP3 form before it's okay to distribute it?