Cannabinoid Research - Science topic

Does cannabinoids quell cytokine storm??

We are isolating hemp oil for testing it's neuroprotective effects in neuropathic pain and epilepsy. Anybody did any work on that ?

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!

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!

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?

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 ?

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.

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).    

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!

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.

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? 

I normally use anti-CB1 from santacruz (sc-20754).

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?

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.

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.

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 E_max of WIN55,212 - 2?

Thanks! 

EDIT: I'm relatively new to pharmacology research so apologies if I have misused terminology. 

what is the exact pharmacokinesiology

a student specifically asked how marijauna helps glaucoma

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?

I am looking for grey literature, non-published technical reports, or even anecdotal data.  Thanks! 

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?

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!

I'm looking for a specific treatment for cannabinoid hyperemesis syndrome(CHS). Which molecules are used to lower intensity of vomiting?

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.

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.

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!

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?

I am in the process of prospectively following up on medical cannabis consumers for pain treatment

I'm seeking reference to the the total number of known cannabinoids of the C. sativa plant (~109 at this point); 

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!

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.

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?

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

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.

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.

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?

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?

Now that marijuana is legal, as a pain reliever, in some states,  where might I find reliable, long-term studies on this topic?

Few publications showed a limited effect of cannabinoids for epilepsy. Gloss D. Cochrane Database Syst Rev. 2014. but what are your experiences?

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.

Exogenous cannabinoids have a potent effect on human behaviour.

This antibody should be specific.

Do cannabinoids have a trancription-specific effect only or do they also affect other processes in the cell?