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Does cannabinoids quell cytokine storm??
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Please also go through the following useful link.
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We are isolating hemp oil for testing it's neuroprotective effects in neuropathic pain and epilepsy. Anybody did any work on that ?
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To some extend, what is the exact question?
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Hi everyone,
I am currently running CO2 extractions and winterizing the crude material with 200 proof ethanol at -20oC for 12-24 hours. I am interested in speeding this process up by performing the winterization in a -80oC freezer. Does anyone have any experience with this? Does it speed up the process? I would think that cooling faster would speed up the precipitation of the lipids, but I also know that precipitation/crystallizations are hampered by increased viscosity, and that larger crystals form at a lower viscosity. 
Another potential scenario is to use the -80oC freezer to increase the cooling rate, but then filter in stages in order to pull out precipitated lipids, reduce the viscosity of the mixture, and allow the next stage of precipitation to happen more efficiently.
Any insight is appreciated. 
Cheers!
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Old post, thought I'd offer some insight.
Richard Augimeri I'd imagine the sweet spot for winterization is around -40C/F for the solution itself with somewhat diminishing returns from there (something to further consider for scaled commodity production). -80C and agitation certainly speeds up the process as this is a brute force precipitation and we have had similar experience completing the process in 1-2 hours. I would be most focused on the final filtration stage at <1 micron which can be done in-line without a secondary winterization.
Dilution ratios from 3:1 to 10:1 work reliably, depends on the volume of impurities there is to precipitate out. Naturally at 3:1 the mixture is quite viscous and more difficult to filter as well as nearly impossible to filter when impurity volumes are significant. Greater dilution comes at the cost of more time in solvent recovery and handling of greater volumes of volatile solvent, so consider the compromise.
A more non-polar solvent with steep saturation curve per temperature would be far more efficient, but winterization with I-A volatiles is not desirable to everyone.
Also, it has not been my experience that cannabinoids would precipitate out of the solution in a winterization scenario at -80C. This would not be the circumstance for nucleation and the development of isolated solids. Arguably the winterization process, itself, could be described as an 'oiling out.'
Amanda Felske Regarding utilizing a filter reactor for winterization, the cost vs throughput would be difficult to justify outside of a bench research capacity (where it is quite useful for process development). Aside from the volume of the FR vessels themselves, the limited surface area on the filter plate would result in regular blinding which would require draining of the entire vessel from the lid to then replace the blinded filter pad. Bag mechanical filtration to lenticular may be a better choice for production.
For reference, we pre-heat & pre-mix via in-line homogenization and then pre-chill prior to injecting into the chilled holding vessel. The minutes add up when you consider all the actual steps in the process beyond the precipitation itself. Fairly intricate system at scale, whereas a deep freezer and a Buchner is sufficient for cheap, kilo production (though, with a filter reactor being ideal on the bench).
Derek Walley
Yep, no need to winterize when done right. :)
I'm easy to reach whether for turn-key systems or a constructive conversation. Good luck out there everyone!
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I am looking to start cannabinoid research with a focus on neurogenesis in my lab at Roosevelt University in Illinois. I am hoping to be able to connect with other researchers who have already gone through or are going through the process of starting such research from scratch. Any advice that you can give with regard to obtaining the DEA research license for Schedule I as a researcher and how to ensure all of the legal and safety requirements are in place in the lab would be much appreciated. Also, there has been interest expressed in potentially growing our own plants for research purposes. Are you aware of anyone who is able to do this beyond the University of Mississippi? Is there a way we could apply to grow in Illinois at the University itself (for in-house research, if not distribution to other research centers/universities)? Statewide cannabis is set to become legal in Illinois in January 2020, if that makes a difference. All advice is greatly appreciated! Thank you!
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Psychonautic research is too often looked down upon. I'll ask my dad, pharmacy manager at a opioid replacement clinic, what the DEA regulations are concerning this. Glad to see people doing the dirty work of psychiatric research!
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I’m trying to transfect with CB2 receptors in mammalian cells. I bought a commercial vector with CB2 sequence, without tags, and then I cloned the ORF in the pcDNA3(+), and the cloning is supposed to be alright because I’ve sequenced the vector.
I’ve tried to transiently transfect it in 293T cell line with lipofectamine, and as positive control I transfected them also with pEGFP-N1 (separated wells). I obtained green cells, but when I analyzed by mRNA and protein the CB2 levels, I found that there was no CB2 over-expression. The transient transfection with the commercial plasmid, which is supposed ready for transient transfection in mammalian cells, didn’t work.
Could the problem be the commercial sequence (but I did a ballast and matched with CB2)? Or is it a problem with the over-expression of CB2 in mammalian cells?
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Esther Martinez-Martinez, Did succeed transfecting CB2 receptor in Mammalian Cell? Can you please send me the protocol? Please.
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CBD and THC are cannabis sourced moleculs. The use is authorised in some countries. Some associations tends to think that these are the future of fibromialgia treatments. What does the current and serious researchs actually says ?
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As the molecular mechanisms are the same in in vulvodynia and fibromyalgia, and the two often are co-morbid, this might be an answer:
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I am a nurse who is researching why some cancer patients are not reporting the same dramatic effectiveness of high-dose cannabinoid extracts on causing tumor regression as some others. Here is the best current article I know of which explains the Anticancer Mechanisms of Cannabinoids and includes the information about THC-resistant glioma cells that overexpressed Midkine (MDK) and became sensitive to the THC after pharmacologic ALK inhibition. Velasco G, Sánchez C, Guzmán M. Anticancer mechanisms of cannabinoids. Current Oncology. 2016;23(Suppl 2):S23-S32. doi:10.3747/co.23.3080.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4791144/
 
We know there are different rates of over-expression of CB1 and CB2 which appear to play at least a partial role but, of course, the various tumor microenvironment factors, mutations and, especially, this information about MDK/ALK as a mechanism of resistance to THC should soon produce much more clarity about this problem.
 
I am intrigued by the knowledge that Non-Small-Cell Lung Cancer and many Breast Cancers often have ALK mutation (and there are significant patients with NSLC and Breast Cancer who do not seem to get as much/any tumor regression yet others get dramatic regression and even No Evidence of Disease with high-doses of THC and CBD). The NSLC patients with ALK mutations are suddenly becoming more treatable after addition of an ALK inhibitor crizotinib, ceritinib, alectinib and others. I have been unable to find any research assessing ALK mutation status and THC resistance or sensitivity for tumors from other tissues than the brain.
 
I can't help but wonder if research could show if there are THC-resistant tumors of lung and breast ++ that are also ALK mutated or Midkine overproducers that may regain their sensitivity to THC as the glioma cells did after pharmacological ALK inhibition.
Thank you for your assistance.
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HA, I know exactly what you mean! Had similar cases and the delusory stuff is widespread thanks to the unethical "cannabiz" b.s. Would love to chat. I'm in a home office these days, based in S.Oregon ie pacific time zone. My cell is 541 326 6082. Afternoons best. Around most of the day tomorrow wed 5th but can call you to suit if you are still a busy onc nurse. Let me know what works. Best JT
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I am working out a double-labeling immunofluorescence protocol.  I want to double label for ERa and cannabinoid receptor-1 in the brain tissue of rats. My ERa antibody is made in a rabbit and I have a protocol that is working for single labeling.  I would like to find an anti-CR1 antibody that is not made in a rabbit (or goat, as my 2º antibody is goat anti-rabbit).    
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We routinely use CB1 antibodies from Frontiers Institute (http://www.frontier-institute.com/wp/antibodies/?lang=en) for IHC/IF and have found them to be among the best commercially available CB1 antibodies.  Their goat version is the best but they also have a guinea pig version.
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This question is specifically asked within the Project called "Treatment of Melanoma Brain Metastases."
Because neurological tissues as well as many forms of skin malignancies will tend to express at least some significant CB1 and CB2 receptors, perhaps using moderate dosing of a safe agonist like Delta 9-THC may be useful?  And consider including evaluation of equivalent to 100-300 mg or oral CBD for humans as well as this is becoming very common among patients.  
I work with both brain cancer patients (mostly Glioblastoma) and many breast cancer patients and they had already chosen to integrate cannabis extracts into their therapies. Because CBD and THC cross the BBB, and does not appear toxic to healthy normal cells, it may be reasonable to consider exploring this with research. I do have one interesting patient who reported using these compounds to treat her ER-PR-HER2+ brain metastases with tremendous success in only 3 months. The Herceptin and Perjeta she was on are too large to cross the BBB, so the situation is dire for her otherwise. Best wishes and thank you for your project!
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OK.  I think it is a good idea.
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I am interested in understanding the actions of SERMs such as Tamoxifen and its metabolite 4OHT on GPR55, especially in the breast cancer cells which express GPR55. Since exploring CBD as an antagonist on GPR55 in breast cancer as an antiproliferative agent, we must understand how other substances interact with it. Since SERMs show great affinity for CB1 and CB2, I must wonder about GPR55. Thank you for your consideration.
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1) Has anyone done a study to detect the bio-availability of cannabidiol (CBD) and tetrahydrocannabinol (THC) from different delivery systems and formulations (i.e. smoked, intravenous, transdermal, etc.) in animals or humans?
2) What are the metabolites of CBD?
3) If we can see metabolite and we can see the active, can we see at what point the body won't process it? 
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I would check the FDA to see what they got. Next check chemical databases like chemspider that provide all sorts of info in that regard. maybe check these stats for the proprietary analogs of cannabidiols that have been recently produced...those should have PD/PK profiles.
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I normally use anti-CB1 from santacruz (sc-20754).
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Hello,
I recommend a free antibody database available at labome.com. For antibodies to CB1R you can check the following link: https://www.labome.com/review/gene/human/CNR1-antibody.html. Invitrogen has CNR1 antibody (Thermo Fisher, PA1-745) used in western blot (Freund et al, PLoS One. 2016). Also, Abcam offers CNR1 antibody (Abcam, ab23703) used in western blot on human samples at 1:100 (Borsani et al, Histol Histopathol. 2014). EMD Millipore has rabbit polyclonal AB5636P anti-CB1R abs for western blot (Hebert-Chatelain et al, Mol Metab. 2014).
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To make some standard solutions to quantitative methods, we extract THC and THC-A with absolute ethanol but with de cannabis extracts we have a mixture of oil and some fat components.
Does somebody known a method, not chromatography method, to isolate the fat and oil mixture from the cannabis extractions?
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Please advise if there are any options for individual patients or their doctors to submit biopsy specimens for cannabinoid receptor expression or activity? This seems critically important and I have had no luck finding a resource yet. Thank you for any assistance you may provide.
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well, actually it seems that most (if not all) commercial CB1/2 tests suffer with cross-sensitivity. this is an important issue and i am eager to see the reactions of ther colleagues.
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The Israeli Medical Cannabis Authority plans to make available to patients only a mixture that is "standardized" and not the natural strains. I wish to enquire whether there is any parctical experience with such a move.
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Can you clarify a bit? Your question says you're interested in mixing strains (creating a new, hybrid strain?), but the explanation says that you aren't interested in natural strains.
If you are looking for a whole plant: Even when you have a consistent genotype, you will most likely get some variability in each crop, based on variable growing conditions. The only way I'm aware of to get exactly the same ratio of cannabinoids in a given product every single time you produce it is to extract the cannabinoids of interest, purify, and combine into some formulation (such as Marinol or Sativex).
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Continuing on from a previously posted question where the half-life of WIN55,212 - 2 was discussed, (see: https://www.researchgate.net/post/Does_any_one_know_the_WIN55_212-2_half-life_in_rats),
does anyone know the Emax of WIN55,212 - 2?
Thanks! 
EDIT: I'm relatively new to pharmacology research so apologies if I have misused terminology. 
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Hello,
This is a pretty hard question to answer when discussing cannabinoids. When you're reffering to Emax, which particular effect of WIN55,212-2 are you referring to? Because cannabinoids can have many different effects (many of which are going to be incredibly hard to measure in rodents, as more of them are psychological than are physiological). So could you give me a bit more context - do you have a specific response that you are interested in?
Cheers
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what is the exact pharmacokinesiology
a student specifically asked how marijauna helps glaucoma
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You can find a good review of cannabanoids (including proposed mechanisms) and glaucoma in Tomida, I., Pertwee, R. G., & Azuara-Blanco, A. (2004). Cannabinoids and glaucoma. British journal of ophthalmology, 88(5), 708-713.
Here is a general overview of cannabinoid mechanisms in health and disease:
Pacher, P., Bátkai, S., & Kunos, G. (2006). The endocannabinoid system as an emerging target of pharmacotherapy. Pharmacological reviews, 58(3), 389-462.
 
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It has been known for a long time now that cotinine, a metabolite of nicotine, is a nootropic and more importantly, is somewhat neuroprotective for PD and AD.  It is also known that cotinine is well tolerated by human subjects and has none of the negative side effects of nicotine itself.  Given today's great concern regarding both PD and AD, how can it be that research on this compound, very closely approximating a "silver bullet" if you will, is not being conducted with great intensity by NIH and/or the pharma industry?  Why does this seemingly magical solution to so many problems sit on the side while less practicable molecules get to dance?  
I don't get it. There is tons of research supporting this but not much is happening.  Why?
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Yes, Paul, I agree.  I was being a bit hyperbolic and put "silver bullet" in quotes for that very reason.  Thanks for the links; I read one of them previously.  I have read much on this and chatted with someone very active in research in this area.  The question still stands:  Why is this going nowhere?
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I am looking for grey literature, non-published technical reports, or even anecdotal data.  Thanks! 
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While marijuana might reduce symptoms, it is not a treatment for PTSD.  Therapy is a treatment for PTSD. Anyone who advocates for the use of Marijuana or MDMA does not take into account the changes in brain chemistry brought on by chronic use.  The VA does not recommend the use of Benzodiazepines for the same reason.  Of course people would report improvement, they feel temporary relief.  I would want to know if their PTSD got better, worse or stayed the same in the long run.
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The primary effects of Cannabis are caused by the chemical compounds in the plant, including cannabinoids such as tetrahydrocannabinol (THC), which is only one of about 400 different cannabinoids. Cannabis has psychological and physiological effects on the human body.  Cannabidiol: from an inactive cannabinoid to a drug with wide spectrum of action. So what is the colateral effects? What about the medical use?
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There are now numerous studies reporting both positive and negative side effects of CBD. for example, Hussain, S. A., Zhou, R., Jacobson, C., Weng, J., Cheng, E., Lay, J., et al. (2015). Perceived efficacy of cannabidiol-enriched cannabis extracts for treatment of pediatric epilepsy: A potential role for infantile spasms and Lennox-Gastaut syndrome. Epilepsy & Behavior, 47, 138-141.
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I would like to have an idea about the half-life of the mixed synthetic cannabinoid receptor CB1/2 agonist WIN55,212-2 half-life in rats. Thanks!
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I just came across a paper titled 'The cannabinoid antagonist SR144528 enhances the acute effect of WIN 55,212-2 on gastrointestinal motility in the rat', which says that the half-life of WIN55,212-2 is 24-36 hours. The two papers it references are titled:
'Spontaneous and precipitated withdrawal with a synthetic cannabinoid, WIN 55212-2'
and
'Repeated cannabinoid administration increases indices of noradrenergic activity in rats.' 
Hope this helps!
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I'm looking for a specific treatment for cannabinoid hyperemesis syndrome(CHS). Which molecules are used to lower intensity of vomiting?
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I would double check CHS, it's like to be a side effect of pesticide usage not cannabinoid overuse.  CHS is not documented in any mammalian cannabinoid tests. And many CHS sufferers have many other health problems that can be attributable to the symptoms. 
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For a long time now, I have been trying to figure out how marijuana enables me to gain some access to vision, even though I am ordinarily totally blind with light perception. This involves translating the subjective experience into language others can understand, and pinpointing the difference between my experience with and without cannabinoids. Recently, I have arrived at the insight that while under the influence of cannabinoids, I am able to maintain momentum of my eye movements. When I move my eyes, they seem to obey the laws of Newtonian physics, in that if I build up the velocity of my eye movements, they will maintain that velocity. when I "push" or "throw" my eyes forward, the effort needed for that push or throw gives me information about my surroundings (i.e. white or reflective objects require very little effort, and my eyes slide across them with very little friction). When I am not under the influence of cannabinoids, I don't feel the kickback or reverberation when I move my eyes, so they feel numb and heavy and impossible to control.  Currently, I am developing an interactive eye training program that gives me auditory feedback about my gaze direction. However, this is just a start, and I am very much thinking that some sort of  wearable device is needed. I am starting to think that the function of this device would be to increase my ability to maintain this sense of momentum, without the influence of marijuana, but what would that look like on a practical level? Any thoughts are welcome.
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A couple of issues.
There is always a problem trying to understand a first-hand experience (perceptual/cognitive/emotional) from a third-person perspective. So it's not clear to me what you mean by momentum. This is particularly important for nystagmus as the evidence is that how and what nystagmus sufferers feel, think, experience, can have a material effect on the nystagmus itself. So for example, if cannabinoids have the general effect of calming someone, this is likely to damp the nystagmus waveform (at least to some extent). But of course, in these circumstances, it may also alter the perception of what's going on, independent of any effect on the nystagmus.
For these reasons, trying to draw any conclusions without an actual recording of the nystagmus (ie an objective recording) is probably unwise.
Secondly, the balance of evidence is that we have little or no conscious perception of what our eyes are actually doing from moment to moment. Intramuscular signals from the extraocular muscles that move the eyes in the orbits are available to the central nervous system, but it remains unclear what these are used for - over the years there's been lots of suggestions (including suggestions about their role in nystagmus as it happens). But what you feel you are doing with your eyes, and what's actually happening to them, may be two very different things. Again a decent recording will help clarify things.
None of this is to say that your insights are unimportant, or that some form of biofeedback might not enable you to change the pattern of your nystagmus.
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I've heard anecdotal reports of the effectiveness of marijuana oil in the cure or shrinking of tumors.
What I read in the research has to do,primarily with pain, nausea control and weight gain.
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I found nothing about cannabis and medulloblastoma, but there are several findings about cannabis and other brain tumors like glioblastoma and gliom as well as non-brain cancer. Maybe these references could be helpfull
Glioblastoma
Guzman M, Duarte MJ, Blazquez C, Ravina J, Rosa MC, Galve-Roperh I, Sanchez C, Velasco G, Gonzalez-Feria L. A pilot clinical study of Delta(9)-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. Br J Cancer, 27. Juni 2006
California Pacific Medical Center Research Institute, San Francisco, USA. Singer E, et al. Cell Death 2015;6:e1601. http://www.ncbi.nlm.nih.gov/pubmed/25590811
Marcu JP, Christian RT, Lau D, Zielinski AJ, Horowitz MP, Lee J, Pakdel A, Allison J, Limbad C, Moore DH, Yount GL, Desprez PY, McAllister SD.Cannabidiol enhances the inhibitory effects of Delta9-tetrahydrocannabinol on human GLIOBLASTOMa cell proliferation and survival. Mol Cancer Ther 2010;9(1):180-9.)
Schley M, et al. Brain Res Bull 2009;79(5):333-7.
GW commenced a Phase 1b/2a clinical trial for the treatment of Recurrent Glioblastoma Multiforme (GBM).
Gliom
Oncology - GW Pharmaceuticals
Cancer: Do cannabinoids cure cancer?
other expert: Dr. med. Franjo Grotenhermen
International Association for Cannabinoid Medicines
National Cancer Institute of the US
Cancer Research UK website
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I am blind, but marijuana gives me access to some visual information, as described in my paper. using an eye tracker, I will be conducting some experiments to determine whether the affects on my vision have to do with an increase in the fidelity of the retinal image, increased proprioception/control of my eye muscles, or a combination of the two. I have anecdotal evidence that different strains affect my vision differently. Sometimes, I am more aware of using eye movements to interact with my environment, and sometimes I am more aware of having an intuitive knowledge that I am seeing an object that I am unable to localize. Roughly, these effects break down into what pathway vs. where pathway effects. I don't have empirical evidence that these effects are strain-dependent; maybe they are dosage dependent, or dependent on the type of stimuli I am looking at. But I wanted to make sure there wasn't any sort of established findings about different strains affecting the dorsal vs. the ventral streams before proceeding with my experiments. Thanks!
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Dear Tasha,
      I have researched the effects of THC and CBD on night vision, which THC improves, presumably at the retinal level. Please see attached article. I would be happy to follow-up with you on additional corroboratory studies.
Cheers,
Ethan Russo, MD
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It is now a known fact that marijuana (medical or otherwise) actually has positive effects on the human brain.  Even more amazing is the effects of the drug on children with autism.  Marinol and Dronabinol are both derivatives of marijuana, and seemingly just as effective in combating the symptoms of autism.  Can someone direct me to parent testimonials concerning the positive effects of medical marijuana and its derivatives on children with autism?
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I agree, but the general consensus is that long term use has detrimental effects on cognition and memory. We have to be careful that this doesn't become adderall/Ritalin part 2, where pts can become dependent. For example, with anorexia I am not surprised at the short-term efficacy - my concern is long term dependency and tolerance.  Opioids are great antidepressants and anxiolytics yet most clinicians do not prescribe them for psychiatric patients except in very special cases, eg extreme OCD.  This is all a risk/benefit analysis, but in the case of THC we often don't know the long term effects but we do know that tolerance will develop that will erode efficacy (in some patients, quite quickly)
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I am in the process of prospectively following up on medical cannabis consumers for pain treatment
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I did a recent paper on this general topic of cannabis and pain/headache. You may find some useful info to think about in terms of formulating questions in it. I would say amount consumed, smoked, etc, for what kinds of pain, what degree of pain decrease, improvement in daily functions, and ability to decrease opiate use (seems to be some synergistic effects) would be good topics to start with.
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I'm seeking reference to the the total number of known cannabinoids of the C. sativa plant (~109 at this point); 
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I have been reading a lot about cannabis and it's impact on human brain and body since quite long time. Now, the pineal gland is in the middle of my interest. I'm wondering if there are any effects of cannabis on pineal gland in human. I've found very poor info about that, if you know something more about that please share!
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I recommend that you review the Journal of Pineal Research, you could find some good answers to your question.
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Is anybody researching the impact of legalisation of cannabis in Colorado and Washington, US on mental health?
A study in UK (Hamilton et al., 2014) found that in the UK, reclassifying cannabis from a class 'B' to a class 'C' drug lead to a reduction in cannabis related psychosis hospital admissions.
However in Portugal and Holland, legalisation has not increased prevalence of use. In UK studies have also found no overall relationship between increase in use in a population overtime and changes in prevalence of psychotic illness.
It would be interesting to see whether this legalisation has an impact on mental health problems. A lot of variables to consider. I'm wondering whether anybody is planning to do this? Happy to share thoughts on the issue.
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I'm working on similar research topic in Poland now - how cannabis impact on human cognitive functioning. If you could send me some of this information as well it would be great!
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I suppose what I am trying to get at is; if there is an endogenous antagonist or reverse agonist produced during certain events, wouldn't this cause a rise in eCB levels (i.e. anandamide), leaving the only "signalling" to the antagonist or reverse agonist?
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I would interpret the data with cannabidiol as a weak antagonist with caution. Cannabidiol is also a potent inhibitor of FAAH and anandamide transporter so the possible rise in endocannabinoids after cannabidiol may not be only due to weak CB1 antagonism. See file FAAH+AT.pdf attached.
I will add some papers on the functioning of the endocannabinoid system where you may find interesting information.
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I am trying to propose a proiect that will measure brain PO2 using a PO2 sensor (licox or oxylite) in awake unrestrained Rat´s brian
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I'm not sure if this is exactly what you're looking for, but there are a number of papers which measure changes in O2 after cannabinoid administration. Below is a small selection of studies which take a look at O2 one way or another in brain homogenates or in vivo as is the case with the Cheer paper.
Effects of 1-delta9-tetrahydrocannabinol, dl-amphetamine and pentobarbital on oxygen consumption by mouse brain and heart homogenates.
Dembert ML, Harclerode J.
The influence of delta9-tetrahydrocannabinol, cannabinol and cannabidiol on tissue oxygen consumption.
Chiu P, Karler R, Craven C, Olsen DM, Turkanis SA.
Changes in body temperature and oxygen consumption rate of conscious mice produced by intrahypothalamic and intracerebroventricular injections of delta 9-tetrahydrocannabinol.
Fitton AG, Pertwee RG.
Cannabinoid modulation of electrically evoked pH and oxygen transients in the nucleus accumbens of awake rats.
Cheer JF1, Wassum KM, Wightman RM.
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I have been virtually totally blind since birth, due to Leber's Congenital Amaurosis. In my paper, Mending The Mirror, I describe how marijuana  gives me some access to vision by stimulating the endocannabinoid system found in the retina  and brain. I would  like to know if marijuana has improved the vision of others with retinal blinding diseases. So I am interested in collaborating with any researchers who are studying this topic. The effects are not related to reductions in intraocular pressure and seem to have to do with stimulation of the cones, rods, and visual cortex.
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Before even thinking to look at the possibility of a new drug derived from cannabis, you'll need to demonstrate out of any doubt that Marijuana itself improves vision in LCA patients.  Such a study, if it passes REB, would need to be against a placebo formula (not necessarily easy to formulate but naive subjects, contrary to long standing users,  may probably be fooled by other smokes (french tobacco, for instance), in a randomized, blinded study using standardized, widely used clinical tests investigating visual acuity, contrast and movement perception... etc...   This is the first step.  You have to demonstrate that what YOU are experiencing, can be first documented by scientific methodology and second, that it can be reproduced on others.
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I have had no success with straight methanol (1mL/5mg) , methanol and DMSO (5uL), or heating the solution to increase dissolving. I am using it as a standard for LC/MS.
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I agree with Bruno and have had success with Tween. A drop (it's very viscous) of tween 80 suspends lipophilic molecules, like cannabinoids, in suspension. In the past, I have used a 1cc syringe to place a drop in a test-tube with the cannabinoid already in the test-tube. Vortex a bit, reconstitute with saline, and vortex until there are no visible components.
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G'day,
The synthetic cannabinoids (SC) currently being marketed as alternatives to plant cannabis have a higher risk of adverse outcomes than phyto (plant) cannabinoids.
The SC products on the market are much stronger agonists at the CB1 receptor than THC, and none contain a synthetic equivalent to the phyto-cannabinoid CBD, but is part of the increased risk also due to SC substances acting at other receptor sites?
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It is an important question but, unfortunatelly, but there is no published data on effects on non-cannabinoid targets. None. Anything that has been mentioned here in the comments is mere speculation. In vitro studies, such as receptor profiling or enyzme screeing, are urgently needed. At a meeting organized by the European drug agency EMCDDA last year I gave a talk on new and some anticipated SCs as well as some similar structures but with different mode of action. Selected slides relevant to this topic can be found in the downloadable pdf file. Note that the list of structurally related substances such as etonitazene or indibuline, is incomplete. Furthermore, it would be interesting to test these latter 'non-cannnabinoid' compounds for CB receptor effect.
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I have two data sets of different cannabinoids on Caco2 cell lines. I used DMSO as a vehicle, and it seems that my vehicle affects cell activity. Im not too sure how to account for my vehicle when it comes to my data set. Can anyone help me with this?
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Your response is "cell count". Since these are counts, a Poisson model should be appropriate. If there is overdispersion (the variance > mean) you should consider a negative binomial model.
I suppose you have data (cell counts from several independent experiments) of cells
- [N] completely untreated
- [D] treated with DMSO alone (no cannabinoid)
- [A] treated with cannabinoid A
- [B] treated with cannabinoid B
- ...
You expected the groups N and D to behave similar, but as I understood D behaves different to N, so DMSO seems to have an effect.
Since DMSO is contained as vehicle in all canabinoid-groups (A,B,...), group D is the appropriate control group to study the effect of the cannabinoids - when cannabinoid-effect is independent of the DMSO effect. This independence can here only be assumed. There is no data available to study the interaction of DMSO and cannabinol effects. This would require groups where the cannabinoids are given without DMSO, but this is biologically/technically impossible. (a workaround might be to use different vehicles to estimate a crossed effect, but I would only do this if I has good reasons to assume an interaction between the vehicle and the cannabinoid)
So the group N can (should) not be used to evaluate the effect of the cannabinoids. What you want are the comparisons of the groups A vs. D, B vs. D and so on.
Written as model formula, your model is simple:
Cellcount ~ Group
where "Group" is a categorical variable with the categories "D", "A", "B"...
If the contrasts are coded all against D, the linear model is
log(Cellcount) = b0 + b1*X[A] + b2*X[B] + ... + error
where b0, b1, b2, ... are the coefficients and X[A], X[B], ... are indicator variables that are 1 for the values belonging to the respective group (A, B, ...) and 0 otherwise, and error are the residuals with error ~ Poisson or NegBinom.
The coefficient b0 will then be the mean (log) Cellcount of "D", b1 will be the (log fold-)change in Cellcount induced by Cannabinoid A, and so on.
Any statistics software you use should provide an option to perform "Poisson regression" or "Analysis of count data" or "Generalized linear models".
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Now that marijuana is legal, as a pain reliever, in some states,  where might I find reliable, long-term studies on this topic?
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Contact Dr. Carl Hart of Columbia, he has run clinical studies on users of all types of drugs including marijuana. Most studies that showed "damage" to brain or health were not run well. Cannabinoids boost neurogenesis, the growth of new brain cells in the adult brain.
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Few publications showed a limited effect of cannabinoids for epilepsy. Gloss D. Cochrane Database Syst Rev. 2014. but what are your experiences?
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I ve startet in oneof my patients with Nieman Pick disease with THC. Not because of seizures but because of pain, his muscular spasticity and trouble with sleep. all of this problems improved right from the beginning and most important, the quality of live improved very much. unfortunately is the norwegian health system not willing to pay for the treatment.
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A wide variety of synthetic cannabinoids (SC) are now being marketed as "safer" or "quasi legal" alternatives to plant cannabis.
Anecdotally, it appears that these research chemicals are typically associated with a significantly higher risk of acute adverse responses (such as tachycardia, anxiety attacks and transient psychosis) than smoking "real" plant cannabis.
As the majority of SC products being marketed contain chemicals that are much stronger cannabinoid receptor ligands than THC, (and some contain mixtures of more than one SC), and as these mixtures do not contain any equivalent to CBD, this is perhaps not surprising.
Does anyone know of animal studies or case histories relevant to the potential of these chemicals to induce such acute problems?
I am also keen to find any research that may indicate the potential for dependence, and likely withdrawal profiles upon abrupt abstinence from regular use, of these chemicals.
<<< The intravenous administration of THC may be associated with a range of schizophrenia-like positive and negative symptoms in psychosis-free individuals (D’Souza et al., 2004).
Conversely, the phytocannabinoid CBD presents with anxiolytic and antipsychotic properties (Zuardi et al., 2006), possibly because CBD may displace the binding of THC from CB-rs.
In contrast, spice products contain no CBD, and the SC chemicals are full agonists at CB-rs and are characterized by both a receptors’ higher affinity and higher potency in comparison with THC (Fattore and Fratta, 2011; EMCDDA, 2011).
Forrester et al. (2012) showed that a “cannabis”-associated psychopathological syndrome occurrence was less likely with marijuana than with SC, with 2% in the marijuana and 11.2% in the SC misusers’ group, having been identified as experiencing hallucinations and delusions.
Those experiencing psychotic episodes related to Spice use are also reported to present with higher/more frequent levels of agitation and behavioral dyscontrol in comparison with those psychotic episodes described in marijuana misusers (Brakoulias, 2012). >>>
“Spiceophrenia”: a systematic overview of “Spice”-related psychopathological issues and a case report
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Thanks.
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Dear Paul,
I have performed animal studies on the abuse liability of the synthetic cannabinoid JWH-018, and I'm almost ready with the paper for publication. I'm attaching an abstract of the results recently presented at the Dopamine 2013 Meeting (Alghero, Italy, May 24-28). feel free to contact me for further information.
Best wishes,
Mary De Luca
University of Cagliari (Italy)
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Exogenous cannabinoids have a potent effect on human behaviour.
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The cannabinoid receptors are a class of cell membrane receptors under the G protein-coupled receptor superfamily. As is typical of G protein-coupled receptors, the cannabinoid receptors contain seven transmembrane spanning domains. Cannabinoid receptors are activated by three major groups of ligands, endocannabinoids (produced by the mammalian body), plant cannabinoids (such as THC, CBD etc. produced by the cannabis plant) and synthetic cannabinoids (such as HU-210). All of the endocannabinoids and plant cannabinoids are lipophilic, i.e. fat soluble, compounds.
Cannabinoid receptor type 1 (CB1) receptors are thought to be one of the most widely expressed G protein-coupled receptors in the brain. This is due to endocannabinoid-mediated depolarization-induced suppression of inhibition (retrograde signaling), a very common form of short-term plasticity in which the depolarization of a single neuron induces a reduction in GABA-mediated neurotransmission. Endocannabinoids released from the depolarized post-synaptic neuron bind to CB1 receptors in the pre-synaptic neuron and cause a reduction in GABA release.
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This antibody should be specific.
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None exist, we didn't find anything out there is that selective anyway.
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Do cannabinoids have a trancription-specific effect only or do they also affect other processes in the cell?
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Cannabinoids act at cannabinoid receptors on the membrane, which are G protein-coupled receptors that are coupled generally to the Gi subtype of G protein and the negative regulation of adenylyl cyclase and cAMP. Of the two known cannabinoid receptors, CB1 and CB2, the CB1 receptors are abundant in the brain and are located predominantly, although not exclusively, on axon terminals, where their activation by cannabinoids causes the suppression of neurotransmitter release. This is a rapid action that does not require gene transcription or interaction with transcription factors.