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RainDog

RainDog's Journal
RainDog's Journal
March 31, 2014

Robert Hooke - 1689 - Royal Society Meeting

via wiki: The Royal Society of London for Improving Natural Knowledge, commonly known as the Royal Society, is a learned society for science, and is possibly the oldest such society still in existence. Founded in November 1660, it was granted a Royal Charter by King Charles II as the "Royal Society of London". The Society today acts as a scientific advisor to the British government, receiving a parliamentary grant-in-aid. The Society acts as the UK's Academy of Sciences, and funds research fellowships and scientific start-up companies.

Robert Hooke, a contemporary of Isaac Newton, was also the curator or experiments for The Royal Society. In 1681 he made friends with a sea captain and writer named Robert Knox. From Knox's sea voyages for the East India Company, he had come into possession of "India Hemp" or ganja.

Knox introduced Hooke to the herb, and in 1689, Hooke recommended it to members of the Royal Society for its curative properties - and said the worst side effect was laughter.

William Brooke O'Shaughnessy, who began work shortly before Queen Vic took the throne, is credited with bringing cannabis medicine to Great Britain, after a stint working in India and experimenting with cannabis and observing its use among the population there at the time.

This is probably in the article - but it's a reality that cannabis was part of medical life until it was made illegal in the 1930s. It wasn't until Mexicans began settling in California that it suddenly became the subject of "reefer madness."

March 25, 2014

"Stoned" Neil Degrasse Tyson LOL

#t=19

via this link - http://www.rawstory.com/rs/2014/03/24/neil-degrasse-tyson-introduces-fans-to-stoned-version-of-himself/

Astrophysicist and Cosmos host Neil deGrasse Tyson introduced his audience at a recent public appearance to the “stoned” version of himself, Gawker reported on Monday.

“That video — basically, time-dilated — is one you would see if it were moving at 85 percent the speed of light, it was later calculated,” deGrasse Tyson explained during his speech on Friday at the Dunlap Institute for Astronomy and Astrophysics in Toronto. “But, someone did this. I didn’t — somebody did this, alright?”


He's so great. He has a sense of humor about himself. And, yes, I did notice that he noted that scientists considered marijuana a beneficial plant throughout history. Robert Hooke - noted sparky.

March 21, 2014

As the biologist noted, Drs. in Spain are ready for human tests

For both breast cancer and gliomas (brain cancer.)

Guzman, et. al already conducted one human test with 10 subjects with gliomas that were considered beyond standard therapy and the cannabinoids shrank cancer cells in those with brain tumors.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673842/

GW Pharma started a series of tests with 20 patients with gliomas - that was announced in Nov. 2013.

http://www.prnewswire.com/news-releases/gw-pharmaceuticals-commences-phase-1b2a-clinical-trial-for-the-treatment-of-glioblastoma-multiforme-gbm-231391971.html

This study follows several years of pre-clinical research conducted by GW in the field of glioma which has demonstrated that cannabinoids inhibit the viability of glioma cells both in vitro and in vivoi,ii via apoptosis or programmed cell death, may also affect angiogenesis, and have demonstrated tumor growth-inhibiting action and an improvement in the therapeutic efficacy of temozolomide, a standard treatment for glioma. In addition, GW has shown tumor response to be positively associated with tissue levels of cannabinoids. GW has identified the putative mechanism of action for our cannabinoid product candidate, where autophagy and programmed cell death are stimulated via stimulation of the TRB3 pathway.

"We are very excited about moving this compound into further human study and the prospects of cannabinoids as new anti-cancer treatments. This is GW's first clinical study of cannabinoids as a potential treatment to inhibit tumor growth," stated Dr. Stephen Wright, Director of Research and Development at GW. "We believe this clinical program demonstrates the flexibility and broad application of GW's cannabinoid platform to treat significant, unmet therapeutic needs."

This study is a 20-patient, multicentre, two part study with an open-label phase to assess safety and tolerability of GW cannabinoids in combination with temozolomide, and a double blind, randomised, placebo-controlled phase with patients randomised to active or placebo, and with a primary outcome measure of 6 month progression free survival. The study objective is to assess the tolerability, safety and pharmacodynamics of a mixture of two principal cannabinoids, THC and CBD in a 1:1 allocation ratio, in combination with temozolomide in patients with recurrent GBM. Secondary endpoints include additional pharmacokinetic and biomarker analyses and additional measurable outcomes of tumor response.
March 21, 2014

Biologist Christina Sánchez: Cannabinoids kill cancer cells

Sánchez (Madrid, Spain, 1971) graduated in Biology at Madrid Complutense University in 1994. Once graduated, she joined Dr. Manuel Guzmán’’s laboratory, where she studied the effect of cannabinoids on lipid and carbohydrate intermediate metabolism first and on cancer cell proliferation later. She obtained her PhD with Honors in Biochemistry and Molecular Biology at Complutense University in 2000.

During her postdoc at Dr. Piomelli’’s laboratory (University of California Irvine, 2000-2003) she studied the involvement of another group of bioactive lipids (lysophosphatidic acid and related compounds) on pain initiation. In 2004, Cristina returned to Spain and she started coordinating a new line of research within Dr. Guzmán’’s laboratory. The goal of her research is to understand and exploit cannabinoids as potential antitumoral agents in breast cancer. More recently, she has also focused her attention on new cannabinoid receptors and their possible involvement in cannabinoid antitumoral action in breast cancer and other type of tumors.


http://vimeo.com/83094404#embed
March 20, 2014

Marijuana researchers: Access to research reefer limited by politics

http://www.rawstory.com/rs/2014/03/19/marijuana-researchers-accuse-feds-of-using-only-legal-u-s-pot-batch-for-anti-legalization-studies/

Researchers looking to study the potential health benefits of medical marijuana use are accusing the government of steering its own supply of the drugs toward probes favoring keeping the drug illegal on the federal level, McClatchy Newspapers reported on Wednesday.

“Nobody could explain it — it’s indefensible,” University of Arizona assistant professor Suzanne Sisley told McClatchy. “The only thing we can assume is that it is politics trumping science.”

Sisley said officials at the Health and Human Services Department (HHS) waited three years before approving a university study into whether veterans suffering from post-traumatic stress disorder benefitted more from smoked or vaporized marijuana, despite the Food and Drug Administration signing off on the project.

...The government’s “stash” is located in a 12-acre garden on the campus of the University of Mississippi. University researchers grow about 13 pounds of the drug per year, with much of it distributed for use in projects approved by both HHS and the National Institute on Drug Abuse (NIDA). The institute reported providing more than $30 million in federal funding for 69 studies related to the drug in 2012.
March 12, 2014

Two articles on phytocannabnoids

Cannabis was used to illustrate 4 features of synergistic plant medical action not obtained by isolating and synthetically reproducing a naturally-occurring multi-molecular interaction. There are over a hundred different cannabinoids in the cannabis plant - which were discovered before we knew we had an endocannabinoid regulatory system in the human body. Some plants other than cannabis do act upon endocannabinoids, however.

At present, the only phytocannabinoid that has been discovered to also exist in plants other than Cannabis is ?-caryophyllene, which is among the most abundant plant essential oil components.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2931553/


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165946/

...‘This type of synergism may play a role in the widely held (but not experimentally based) view that in some cases plants are better drugs than the natural products isolated from them’. Support derives from studies in which cannabis extracts demonstrated effects two to four times greater than THC (Carlini et al., 1974); unidentified THC antagonists and synergists were claimed (Fairbairn and Pickens, 1981), anticonvulsant activity was observed beyond the cannabinoid fraction (Wilkinson et al., 2003), and extracts of THC and CBD modulated effects in hippocampal neurones distinctly from pure compounds (Ryan et al., 2006). Older literature also presented refutations: no observed differences were noted by humans ingesting or smoking pure THC versus herbal cannabis (Wachtel et al., 2002); pure THC seemed to account for all tetrad-type effects in mice (Varvel et al., 2005); and smoked cannabis with varying CBD or CBC content failed to yield subjective differences combined with THC (Ilan et al., 2005). Explanations include that the cannabis employed by Wachtel yielded 2.11% THC, but with only 0.3% cannabinol (CBN) and 0.05% CBD (Russo and McPartland, 2003), and Ilan's admission that CBN and CBD content might be too low to modulate THC. Another factor is apparent in that terpenoid yields from vaporization of street cannabis were 4.3–8.5 times of those from US National Institute on Drug Abuse cannabis (Bloor et al., 2008). It is undisputed that the black market cannabis in the UK (Potter et al., 2008), Continental Europe (King et al., 2005) and the USA (Mehmedic et al., 2010) has become almost exclusively a high-THC preparation to the almost total exclusion of other phytocannabinoids. If – as many consumers and experts maintain (Clarke, 2010) – there are biochemical, pharmacological and phenomenological distinctions between available cannabis ‘strains’, such phenomena are most likely related to relative terpenoid contents and ratios. This treatise will assess additional evidence for putative synergistic phytocannabinoid-terpenoid effects exclusive of THC, to ascertain whether this botanical may fulfil its promise as, ‘a neglected pharmacological treasure trove’ (Mechoulam, 2005).

...Phytocannabinoids are exclusively produced in cannabis (vide infra for exception), but their evolutionary and ecological raisons d'être were obscure until recently. THC production is maximized with increased light energy (Potter, 2009). It has been known for some time that CBG and CBC are mildly antifungal (ElSohly et al., 1982), as are THC and CBD against a cannabis pathogen (McPartland, 1984). More pertinent, however, is the mechanical stickiness of the trichomes, capable of trapping insects with all six legs (Potter, 2009). Tetrahydrocannabinolic acid (THCA) and cannabichromenic acid (Morimoto et al., 2007), as well as cannabidiolic acid and cannabigerolic acid (CBGA; Shoyama et al., 2008) produce necrosis in plant cells. Normally, the cannabinoid acids are sequestered in trichomes away from the flower tissues. Any trichome breakage at senescence may contribute to natural pruning of lower fan leaves that otherwise utilize energy that the plant preferentially diverts to the flower, in continued efforts to affect fertilization, generally in vain when subject to human horticulture for pharmaceutical production. THCA and CBGA have also proven to be insecticidal in their own right (Sirikantaramas et al., 2005).

THC (Table 1) is the most common phytocannabinoid in cannabis drug chemotypes, and is produced in the plant via an allele co-dominant with CBD (de Meijer et al., 2003). THC is a partial agonist at CB1 and cannabinoid receptor 2 (CB2) analogous to AEA, and underlying many of its activities as a psychoactive agent, analgesic, muscle relaxant and antispasmodic (Pacher et al., 2006). Additionally, it is a bronchodilator (Williams et al., 1976), neuroprotective antioxidant (Hampson et al., 1998), antipruritic agent in cholestatic jaundice (Neff et al., 2002) and has 20 times the anti-inflammatory power of aspirin and twice that of hydrocortisone (Evans, 1991). THC is likely to avoid potential pitfalls of either COX-1 or COX-2 inhibition, as such activity is only noted at concentrations far above those attained therapeutically (Stott et al., 2005).

CBD is the most common phytocannabinoid in fibre (hemp) plants, and second most prevalent in some drug chemotypes. It has proven extremely versatile pharmacologically (Table 1) (Pertwee, 2004; Mechoulam et al., 2007), displaying the unusual ability to antagonize CB1 at a low nM level in the presence of THC, despite having little binding affinity (Thomas et al., 2007), and supporting its modulatory effect on THC-associated adverse events such as anxiety, tachycardia, hunger and sedation in rats and humans (Nicholson et al., 2004; Murillo-Rodriguez et al., 2006; Russo and Guy, 2006). CBD is an analgesic (Costa et al., 2007), is a neuroprotective antioxidant more potent than ascorbate or tocopherol (Hampson et al., 1998), without COX inhibition (Stott et al., 2005), acts as a TRPV1 agonist analogous to capsaicin but without noxious effect (Bisogno et al., 2001), while also inhibiting uptake of AEA and weakly inhibiting its hydrolysis. CBD is an antagonist on GPR55, and also on GPR18, possibly supporting a therapeutic role in disorders of cell migration, notably endometriosis (McHugh et al., 2010). CBD is anticonvulsant (Carlini and Cunha, 1981; Jones et al., 2010), anti-nausea (Parker et al., 2002), cytotoxic in breast cancer (Ligresti et al., 2006) and many other cell lines while being cyto-preservative for normal cells (Parolaro and Massi, 2008), antagonizes tumour necrosis factor-alpha (TNF-? in a rodent model of rheumatoid arthritis (Malfait et al., 2000), enhances adenosine receptor A2A signalling via inhibition of an adenosine transporter (Carrier et al., 2006), and prevents prion accumulation and neuronal toxicity (Dirikoc et al., 2007). A CBD extract showed greater anti-hyperalgesia over pure compound in a rat model with decreased allodynia, improved thermal perception and nerve growth factor levels and decreased oxidative damage (Comelli et al., 2009). CBD also displayed powerful activity against methicillin-resistant Staphylococcus aureus (MRSA), with a minimum inhibitory concentration (MIC) of 0.5–2 µg·mL?1 (Appendino et al., 2008). In 2005, it was demonstrated that CBD has agonistic activity at 5-hydroxytryptamine (5-HT)1A at 16 µM (Russo et al., 2005), and that despite the high concentration, may underlie its anti-anxiety activity (Resstel et al., 2009; Soares Vde et al., 2010), reduction of stroke risk (Mishima et al., 2005), anti-nausea effects (Rock et al., 2009) and ability to affect improvement in cognition in a mouse model of hepatic encephalopathy (Magen et al., 2009). A recent study has demonstrated that CBD 30 mg·kg?1 i.p. reduced immobility time in the forced swim test compared to imipramine (P < 0.01), an effect blocked by pre-treatment with the 5-HT1A antagonist WAY100635 (Zanelati et al., 2010), supporting a prospective role for CBD as an antidepressant. CBD also inhibits synthesis of lipids in sebocytes, and produces apoptosis at higher doses in a model of acne (vide infra). One example of CBD antagonism to THC would be the recent observation of lymphopenia in rats (CBD 5 mg·kg?1) mediated by possible CB2 inverse agonism (Ignatowska-Jankowska et al., 2009), an effect not reported in humans even at doses of pure CBD up to 800 mg (Crippa et al., 2010), possibly due to marked interspecies differences in CB2 sequences and signal transduction. CBD proved to be a critical factor in the ability of nabiximols oromucosal extract in successfully treating intractable cancer pain patients unresponsive to opioids (30% reduction in pain from baseline), as a high-THC extract devoid of CBD failed to distinguish from placebo (Johnson et al., 2010). This may represent true synergy if the THC–CBD combination were shown to provide a larger effect than a summation of those from the compounds separately (Berenbaum, 1989).
March 7, 2014

The Republican Party's Pot Dilemma

A panel at the recent CPAC convention turned into an argument for legalization. So, the left and the right are in agreement that marijuana laws need to change. Are Republicans ignoring the will of their base?

All the more reason for Democrats to make this an issue on state ballots in 2014, imo.

http://www.theatlantic.com/politics/archive/2014/03/the-republican-partys-pot-dilemma/284289/

In recent years, American public opinion has shifted rapidly in favor of legalizing marijuana. The percentage of adults who support it has gone from 12 percent in 1969 to 58 percent as of last fall, according to Gallup; in the past decade alone, support for legalization has increased by 24 percentage points. The shift has powered a wave of political victories for marijuana advocates, from the 20 states where medical marijuana is now legal to the unprecedented ballot measures legalizing the drug in Colorado and Washington in 2012. Three more states expect to put pot to a popular vote this year, with referenda on medical marijuana in Florida and full legalization in Oregon and Alaska.

What opposition remains is concentrated among Republicans. According to Gallup, only about a third of Democrats and independents now oppose legalization, compared to nearly two-thirds of Republicans. Opponents of legalization are also disproportionately elderly. The situation closely parallels the party's predicament on gay marriage, which most Republicans still oppose even as widening majorities of the broader public support it.

It adds up to a quandary for the GOP: Should it embrace the unpopular position still disproportionately favored by its members and risk marginalization as a result? Or will the burgeoning conservative voices in favor of legalization win out? Simply put, do Republicans want to be on the losing side of yet another culture war?

...The tide, (Beach, producer for Morning in America) believes, could still turn back against legalization—if the opponents' dark predictions come true and states like Colorado and Washington experience serious consequences from their embrace of marijuana. "The beauty of America is that the states can experiment with this and we will see what happens," Beach said. "But I am afraid of the effects it's going to have on society."


Yes. So far it's caused 37 fake deaths, cited by a police chief more than a month after the hoax was revealed, CNN correspondents giggling on air, sales of Girl Scout Cookies,1 million to Colorado tax coffers, and the exodus of families from Texas, New Jersey, Utah, Florida, South Carolina, Virginia, New York, and other states without legal marijuana laws to seek help for family members who might benefit from cannabis oil for various medical conditions.
March 4, 2014

D.C. Just Decriminalized Marijuana!

The Washington D.C. city council just voted to decriminalize according to MPP.

Congrats!

March 4, 2014

The Yes Men - WTO pranksters

...and members of the BLO (Barbie Liberation Front!)

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