Ballot Initiative Petition Update

From the Rapid City Journal this AM (my bolding):
South Dakotans circulating petitions to force a public vote on whether tobacco taxes should go up say they are more than halfway to their goal.

Jennifer Stalley of the American Cancer Society said the groups supporting a tax increase hope to gather 17,000 signatures to get the issue on the November 2006 ballot.
And as reported before, S.T.O.P. is over the hump for their constitutional measure, now are making efforts to buffer the inevitable petition problems and challenges that arise from any petition circulated.

The Judicial Accountability group claims about 14-15,000 signatures on their constitutional initiative, if I'm reading their thermometer graphic correctly. Which places them a little less than halfway there.

In a prior post, under comments, I had asked Bob Newland where they were on the Medical Marijuana measure. But since I won't agree with him, and one of the anonymous commenters was taking a few shots at him, he said he wasn't going to say.

This morning I figuratively got off my butt to do some digging, and I checked out the petition measure website. According to http://www.sodaksafeaccess.org/, they are claiming about 2496 signatures. 2500 down, 14,500 to go.

(And is that SD entertainer Gordy Pratt circulating petitions for the measure?)

If anyone else knows of other reports on the number of signatures reportedly collected on behalf of the various ballot Questions, drop me a note and let me know.

The reports on most other measures are sketchy - but here's the information on the measures being circulated as noted on Secretary of State Chris Nelson's website.


Initiated Constitutional Amendment to establish a procedure for each class of property detailing the methods that shall be used to value property. View full text of petition.

Initiated Constitutional Amendment to impose a corporate income tax and create in the state treasury a fund named the people's tax relief fund. View full text of petition.

Initiated Measure to provide safe access to medical marijuana for certain qualified persons. View full text of petition.

Initiated Measure to revise certain provisions related to county zoning and conditional use requests. View full text of petition.

Initiated Measure to increase the tax on cigarettes and tobacco products, to dedicate the revenue for tobacco prevention and cessation programs, property tax reduction, education enhancement, and health care, and to make an annual appropriation therefore. View full text of petition.

Initiated Constitutional Amendment to add a new section titled Judicial Accountability Initiative Law (J.A.I.L.). View full text of petition.

Initiative Measure to change the school start date. View full text of petition.

Initiative Measure to impose a consumption fee on the retail sale of alcoholic beverages in the amount of one percent of the gross sales price of the alcoholic beverage. View full text of petition.

Comments

Bob Newland said…
It's not that you won't agree with me, although that is a typical way for folks like you to twist the truth; it's that you won't even answer my questions about your stance. Ditto for the ch*ck*nsh*t, "Anonymous".

At least you didn't condescendingly refer to the petition as a "ditch-weed" measure this time.

So, here's another chance for you to act like an adult: Why do you oppose allowing sick, disabled, and dying people safe legal access to a medicine that alleviates their suffering?
Anonymous said…
I think what was worse--much, much worse--was the way PP turned off the comments after Bob handed him his ass during their short debate on the merits of the petition. That was as weak as anything I've seen here.

With hardly any substance to back up his position (PP's opposition to the medical marijuana petition basically comes down to "I think it should remain illegal because it's currently illegal") PP got in an utterly childish final word (quote: "NOW there's been enough discussion") and turned off the comments, effectively taking his ball and going home.

So much for the "marketplace of ideas."

I don't really have any expectations here, so I can't say I was surprised, but that was just weak.

Here's the whole thread. Read it for yourself:

http://tinyurl.com/7dld8
Bob Newland said…
Well, Todd, I didn't ask, and I don't give a sh*t. I handed you your ass in whatever exchange we had, too. Not much of anyone cares what you think about anything anyway.

Howdy, Will. Nice to make your acquaintance.
PP said…
Actually, it was turned off because it had become tedious, and it had degraded to the point of personal insults on Bob's part directed at me.

Since it's "my party", and I don't need to go on the internet for my abuse; I can get plenty of abuse at home (insert drum rim-shot here), I decided to end it.

I stand by my reasoning (using and selling it is illegal, the measure allows it's prescription for minors, falsification violations are misdemeanors, and where are the quality controls?), and just because Bob doesn't agree with them doesn't make them immaterial.

In fact, if you conducted an opinion poll of the attitudes of South Dakotans towards MM, I'm betting many would have the same concerns.
----------
On another topic - good thought on the ballot initiatives, Todd. I'll be adding them to the WIKI, along with the advocacy websites.
Bob Newland said…
And your reasoning is still as faulty as it was two months ago.
Anonymous said…
PP,

How dare you disagree with 2496 South Dakotans?

It took the Medical Marijuana people 6 months to gather those signatures.

Why, at that rate they'll have the signatures they need to place the measure on the 2006 ballot by 2008.
Anonymous said…
PP wrote:
"...it had degraded to the point of personal insults on Bob's part directed at me."

Please refer me to the personally insulting comment(s) which motivated you to shut down the thread. I've read them all, more than once, and I can't find anything that even comes close. In fact, the only insults I've seen have been uttered by that anonymous dude who thinks that anyone who supports the medical marijuana ballot measure is a "druggie."

Yes, it's your "party" and you can do what you want. But if being analytically outmatched is akin to "abuse" maybe you shouldn't even open the door. It's not like you're engaging in any sort of honest debate anyhow. You said it yourself: "The Author of the SD War College is not going to change his mind anytime soon." That pretty much says it all, no? You might as well turn off the comments right from the start with that kind of attitude.

I care more about the debate than either side's position on it. If you're going to enter the ring, you ought to play fair. What you did--posting your reasons for being opposed to the ballot measure and then stifling the critique of those reasons--was extraordinarily weak.

We can at least agree on something, though: this ballot measure is unpopular in SD; it's not likely to get on the ballot; and even if it does it's even less likely to pass. Sorry, Bob. You're in the wrong state for this.

But you don't have to travel too far: marijuana is legal for medicinal purposes in Montana (which actually borders SD) and Colorado. That's why I find SD's apparent reluctance so fascinating.

My take: 1) an extremely conservative electorate (SD is one of the few states which would outlaw abortion if Roe were overturned), and 2) lack of political courage.
Bob Newland said…
While Will is correct in my not insulting anyone in the previous thread about medical cannabis, I have devolved into personal attacks here. But I'm not sorry for them.

Anyone who would wilfully and knowingly deprive sick people of medicine that improves their conditions is of too lesser a character to even acknowledge, really.

And you can't say you don't know it's therapeutic. So, following the rest of the syllogism...
PP said…
(PP tries to resist urge to close discussion thread)

Does anyone have anything to say about the other 8 or so ballot measures?
Bob Newland said…
Hell, if it weren't for me, nobody seems to have much to say about anything you or Epp post. Kinda makes me wonder about me.
Anonymous said…
Bob:
The drugs are going to your head! You aren't the reason I visit this site, but you sure are entertaining. Thank you for your contributions to my amusements and good luck with that petition drive. It appears to me you should spend less time abusing and more time collecting.
Bob Newland said…
It's hard to imagine why else you would come to this site.
Bob Newland said…
Dr. Dean Edell weighs in....

[Q from a listener/website visitor) I'm Getting Treatment For Hepatitis C. Will Marijuana Help Me Or Harm Me?


Ernie: I have hepatitis C and I'm getting ready to start the interferon ribarvirin therapy. As an occasional marijuana user, I was hoping to continue smoking it to help me get through the loss of appetite, and restlessness at night. Is there any danger in the way that it is metabolized?

Dr. Dean: Good question.

Marijuana, like most medications, is metabolized in the liver. With active liver disease, a little dose of marijuana may go a long way. In addition, street marijuana has such variability, predicting its effect is difficult.

I know of no contraindication and you know that I'm in favor of medical marijuana, but I'm uncomfortable recommending an illegal substance to you, a person with a serious illness.

This is a very specific question that I think you should ask your doctors. You won't be the first person to ask it.

People with worse illnesses than yours have used marijuana to fight nausea with no negative consequences and any anti-nausea drug that the doctor gives you will also be metabolized by the liver. I feel more secure with your liver trying to handle marijuana. Marinol, the FDA-approved pill form of marijuana has shown no toxicity to the liver.

I would estimate marijuana to be as safe as anything else. Interferon and ribarvirin is a pretty hefty combination that can be curative in a significant percentage of cases. It's basically all we have for hepatitis C. Interferon can make you pretty sick, but ribarvirin is fairly easy on you. They are both antiviral drugs.

This article can be accessed directly at:
http://www.healthcentral.com/
drdean/408/45186.html

You have to copy the two lines above and conjoin them.
Anonymous said…
Isn't the order you campaign - "First, Get measure on Ballot", THEN "propagandize?"

Didn't the STOP measure start at the same time as Bob rode his bike around the state?

I think they have 30,000 plus signatures and counting now, isn't it?

The MM advocates are pretty cocky for 2500 signatures.
Bob Newland said…
As I muse upon the taunts thrown out by someone too spineless to write under a real name, someone who also has no compassion for people in pain or nausea, it occurs to me that..., well, he/she should simply suck my d*k.
Bob Newland said…
An academic paper written by Robert Melamede, Ph.D, which compares tobacco and cannabis smoke in regards to their carcinogenicity.



Cannabis and Tobacco Smoke are not Equally Carcinogenic

Robert Melamede, PhD.
1 Biology Department, 1420 Austin Bluffs Parkway, University of Colorado, Colorado Springs, 80918, USA

2 Bioenergetics Institute, 1420 Austin Bluffs Parkway, University of Colorado, Colorado Springs, 80918, USA


ABSTRACT

More people are using the cannabis plant as modern basic and clinical science reaffirms and extends its medicinal uses. Concomitantly, concern and opposition to smoked medicine has occurred, in part due to the known carcinogenic consequences of smoking tobacco. Are these reactions justified?

While chemically very similar, there are fundamental differences in the pharmacological properties between cannabis and tobacco smoke. Cannabis smoke contains cannabinoids whereas tobacco smoke contains nicotine. Available scientific data, that examines the carcinogenic properties of inhaling smoke and its biological consequences, suggests reasons why tobacco smoke, but not cannabis smoke, may result in lung cancer. Keywords: marijuana, tobacco, cancer, smoke, cannabinoids, carcinogens, nicotine

Tobacco has dramatic negative consequences for those who smoke it. In addition to its high addiction potential [1], tobacco is causally associated with over 400,000 deaths yearly in the United States, and has a significant negative effect on health in general [2]. More specifically, over 140,000 lung-related deaths in 2001 were attributed to tobacco smoke [3]. Comparable consequences would naturally be expected from cannabis smoking since the burning of plant material in the form of cigarettes generates a large variety of compounds that possess numerous biological activities [4]. While cannabis smoke has been implicated in respiratory dysfunction, including the conversion of respiratory cells to what appears to be a pre-cancerous state [5], it has not been causally linked with tobacco related cancers [6] such as lung, colon or rectal cancers.

Recently, Hashibe et al [7] carried out an epidemiological analysis of marijuana smoking and cancer. A connection between marijuana smoking and lung or colorectal cancer was not observed. These conclusions are reinforced by the recent work of Tashkin and coworkers [8] who were unable to demonstrate a cannabis smoke and lung cancer link, despite clearly demonstrating cannabis smoke-induced cellular damage. Furthermore, compounds found in cannabis have been shown to kill numerous cancer types including: lung cancer [9], breast and prostate [10], leukemia and lymphoma [11], glioma [12], skin cancer [13], and pheochromocytoma [14].

The effects of cannabinoids are complex and sometimes contradicting, often exhibiting biphasic responses. For example, in contrast to the tumor killing properties mentioned above, low doses of THC may stimulate the growth of lung cancer cells in vitro [15]. The genotoxic effects of partially oxidized hydrocarbons created by burning either cannabis or tobacco have been widely examined as the likely source of genetic changes that lead to the carcinogenic state [16].

As a result, the medical potential of cannabis has been obscured by the potential negative impact of using a smoked medicine [17]. Those who deny the validity of ©¯medical marijuana,©˜ cite that marijuana smoke contains four fold more tars than does tobacco smoke [18]. Nevertheless, smoking is often the preferred route of intake by medical cannabis users because rapid action allows self- titration [19]. Are the biological consequences of smoking cannabis and tobacco similar? Smoke from tobacco and cannabis contains many of the same carcinogens and tumor promoters [20][21]. However, cannabis and tobacco have additional pharmacological activities, both receptor-dependent and independent, that result in different biological endpoints. Polycyclic aromatic hydrocarbons found in smoke are pro- carcinogens that are converted to carcinogens by the enzymatic activity of the cytochrome P4501A1 oxidase protein (CYP1A1 gene product). Benzo [a] pyrene is converted to its carcinogenic metabolite diol epoxide, which binds to specific hyper- mutable nucleotide sequences in the K-ras oncogene and p53 tumor suppressor [22]. Recent work by Roth et al. demonstrates that THC treatment of murine hepatoma cells caused a dose dependent increase in CYP1A1 gene transcription, while at the same time directly inhibiting the enzymatic activity of the gene product [23]. Thus, despite potentially higher levels of polycyclic aromatic hydrocarbons found in cannabis smoke compared to tobacco smoke (dependent on what part of the plant is smoked), the THC present in cannabis smoke should exert a protective effect against pro-carcinogens that require activation. In contrast, nicotine activates some CYP1A1 activities, thus potentially increasing the carcinogenic effects of tobacco smoke [24].

It is worth noting that cytochrome P4501A1 oxidase has numerous substrates including biologically active lipid metabolites such as arachidonic acid, and eicosinoids [25]. These molecules are components of metabolic pathways that are interwoven with the synthesis and degradation of endocannabinoids such as arachidonylethanolamine (anandamide) [26]. Hence, the inhibition of cytochrome P4501A1 oxidase by THC is likely to have multiple biological effects such as possibly enhancing cannabinoid activities by decreasing their catabolism. The need to better understand the biological consequences of tobacco compared to cannabis smoke has been underscored by recent studies that demonstrate a unique role for nicotine in the pathogenesis of lung cancer [27]. In order to appreciate potential biological differences between tobacco and cannabis smoke, the molecular basis of signal transduction must be considered with respect to the life and death of cells. Evolution has provided cells with biochemical feedback loops, checkpoints that monitor genetic integrity and the overall state of the cell. Under conditions of sufficient cellular damage, apoptotic cell death is induced [28]. While a variety of different biochemical states are consistent with a cell either living or dying, constant communication between a cell and its environment is critical for survival of the cell and ultimately the organism. Cells communicate with each other via specific cell surface receptors. When bound with their appropriate ligand, the receptors initiate signaling cascades that alter cellular biochemistry [29]. THC found in cannabis [30] and nicotine found in tobacco [31] both have specific receptors by which their corresponding ligands modulate cellular functions. Interestingly, both cannabinoid [32] and nicotine receptors [27] are coupled to the AKT (PKB) signaling pathway. Activation of either receptor type can induce an anti- apoptotic state that prevents cell death. However, it is the context in which the AKT pathway is activated that determines whether an organism benefits or is harmed by this anti-apoptotic activity. Nicotine receptors are widely distributed and are found in the epithelial cells lining respiratory passages. Cannabinoid receptors are also widely distributed, but have not been reported in respiratory epithelial cells. The differential expression of receptors may account for the apparent difference in carcinogenic activity that results from smoking tobacco compared to cannabis. Both types of smoke contain a complex mixture of compounds, some of which are carcinogenic. They both contain hot gasses and irritating particulate matter (tars). However, the anti-apoptotic response that results from the stimulation of the nicotine receptors, under mutagenic conditions, creates a worst- case scenario. The very cells that have accumulated sufficient genetic damage to normally initiate the apoptotic cascade are prevented from going down this suicidal path [33] even though it would be best for the organism as a whole. In contrast, when the AKT pathway is activated in the brain after head injury [34] or stroke, [35] cannabinoids protect against cell death to the organism©Ë†s benefit. Likewise, nicotine can also activate the AKT pathway in the brain in a beneficial manner. For example, activation of the nicotine receptors, as is also true of cannabinoid receptors [36], can prevent the brain cell death that results from exposure to beta amyloid protein [37] as occurs in Alzheimer©Ë†s disease. The impact of receptor and downstream activation is complicated. Both nicotine and cannabinoids have been shown to effect angiogenesis in a receptor-mediated manner [13]. However, nicotine and tobacco have opposite effects on angiogenesis. Nicotine promotes neo-vacularization along with associated tumor growth, atheroma, up- regulation of VEGF, and cell migration [38]. In contrast, cannabinoids promote tumor regression in rodents and inhibit pro-angiogenic factors [39]. In fact, clinical trials to treat human glioma with THC have resulted in decreased levels of VEGF [40]. The signal transduction pathway described above represents one means by which the carcinogenic affects of tobacco are amplified in a contrasting manner to what occurs with cannabis. The immunological effects resulting from smoking tobacco or cannabis are also distinctive and result in opposite end-points. Again, the carcinogenic potential of smoke is increased by tobacco, whereas it is uniquely reduced by the specific immune regulatory activity of cannabinoids in cannabis smoke. The introduction of hot gaseous material containing both carcinogens and particulate material into the respiratory passages produces pro-inflammatory immune responses [41]. The inflammatory state is a double-edged sword that can serve to protect or kill an organism. A functional characteristic of the pro-inflammatory state is the production of free radicals [42]. These reactive chemical species are essential armaments in the body©Ë†s defense against various pathogens, in particular against intracellular parasites and bacteria. Free radicals are thought to be contributing etiological agents behind a number of pathological states [43] including cardiovascular and neuro-degenerative diseases [44], cancers, and aging in general [45]. Endocannabinoids are specific immunological homeostatic modulators when acting on ©¯peripheral©˜ CB2 receptors [30]. Both endo- and exo-cannabinoids push the immune system towards the relatively anti-inflammatory Th2 cytokine profile [46]. Thus, cannabinoids inhaled in cannabis smoke physiologically reduce the potential amplification of carcinogens in smoke that results from biologically produced free radicals. This response is not induced by tobacco smoke. In conclusion, while both tobacco and cannabis smoke have similar properties chemically, their pharmacological activities differ greatly. Components of cannabis smoke minimize some carcinogenic pathways whereas tobacco smoke enhances some. Both types of smoke contain carcinogens and particulate matter that promotes inflammatory immune responses that may enhance the carcinogenic effects of the smoke. However, cannabis typically down-regulates immunologically-generated free radical production by promoting a Th2 immune cytokine profile. Furthermore, THC inhibits the enzyme necessary to activate some of the carcinogens found in smoke. In contrast, tobacco smoke increases the likelihood of carcinogenesis by overcoming normal cellular checkpoint protective mechanisms through the activity of respiratory epithelial cell nicotine receptors. Cannabinoids receptors have not been reported in respiratory epithelial cells (in skin they prevent cancer), and hence the DNA damage checkpoint mechanism should remain intact after prolonged cannabis exposure. Furthermore, nicotine promotes tumor angiogenesis whereas cannabis inhibits it. It is possible that as the cannabis-consuming population ages, the long-term consequences of smoking cannabis may become more similar to what is observed with tobacco. However, current knowledge does not suggest that cannabis smoke will have a carcinogenic potential comparable to that resulting from exposure to tobacco smoke. It should be noted that with the development of vaporizers, that use the respiratory route for the delivery of carcinogen-free cannabis vapors, the carcinogenic potential of smoked cannabis has been largely eliminated [47][48].

Competing Interests: The author has no competing interests to declare.

References 1. Khurana S, Batra V, Patkar AA, Leone FT: Twenty-first century tobacco use: it is not just a risk factor anymore. Respir Med. 2003, 97(4):295-301.

2. Thun MJ, Henley SJ, Calle EE: Tobacco use and cancer: an epidemiologic perspective for geneticists. Oncogene. 2002, 21(48):7307-7325.

3. Alavanja MC: Biologic damage resulting from exposure to tobacco smoke and from radon: implication for preventive interventions. Oncogene. 2002, 21(48):7365-7375.

4. Novotny, M., Merli F, Weisler D, Fencl M, Saeed T: Fractionation and capillary gas chromatographic-mass spectrometric characterization of the neutral components in marijuana and tobacco smoke condensates. J Chromatogr. 1982, 238:141-150.

5. Tashkin DR, Baldwin GC, Sarafian T, Dubinett S, Roth MD: Respiratory and immunologic consequences of marijuana smoking. J Clin Pharmacol. 2002, 42(11 Suppl):71S-81S.

6. Sidney S, Beck JE, Tekawa IS, Quesenberry CP, Friedman GD: Marijuana use and mortality. Am J Public Health. 1997, 87:585-590. 7. Hashibe M, Straif K, Tashkin DP, Morgenstern H, Greenland S, Zhang ZF: Epidemiologic review of marijuana use and cancer risk. Alcohol. 2005, 35:265- 275.

8. Tashkin DP: Smoked marijuana as a cause of lung injury. Monaldi Arch Chest Dis. 2005, 63:93-100.

9. Munson AE, Harris LS, Friedman MA, Dewey WL, Carchman RA: Antineoplastic activity of cannabinoids. J Natl Cancer Inst. 1975, 55:597-602.

10. Sanchez C, de Ceballos ML, del Pulgar TG, Rueda D, Corbacho C, Velasco G, Galve-Roperh I, Huffman JW, Ramon y Cajal S, Guzman M: Inhibition of glioma growth in vivo by selective activation of the CB(2) cannabinoid receptor. Cancer Res. 2001, 61:5784-5789.

11. McKallip RJ, Lombard C, Fisher M, Martin BR, Ryu S, Grant S, Nagarkatti PS, Nagarkatti M: Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease. Blood. 2002, 100:627-634.

12. Sanchez C, Galve-Roperh I, Canova C, Brachet P, Guzman M: Delta9- tetrahydrocannabinol induces apoptosis in C6 glioma cells. FEBS Lett. 1998, 436:6-10.

13. Casanova ML, Blazquez C, Martinez-Palacio J, Villanueva C, Fernandez-Acenero MJ, Huffman JW, Jorcano JL, Guzman M: Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. J Clin Invest. 2003, 111:43-50.

14. Sarker KP, Obara S, Nakata M, Kitajima I, Maruyama I: Anandamide induces apoptosis of PC-12 cells: involvement of superoxide and caspase-3. FEBS Lett. 2000, 472:39-44.

15. Hart S, Fischer OM, Ullrich A: Cannabinoids induce cancer cell proliferation via tumor necrosis factor alpha-converting enzyme (TACE/ADAM17)-mediated transactivation of the epidermal growth factor receptor. Cancer Res. 2004, 64:1943-1950.

16. Godschalk R, Nair J, van Schooten FJ, Risch A, Drings P, Kayser K, Dienemann H, Bartsch H: Comparison of multiple DNA adduct types in tumor adjacent human lung tissue: effect of cigarette smoking. Carcinogenesis. 2002, 23:2081- 2086.

17. Watson SJ, Benson JAJ, Joy JE: Marijuana and medicine: assessing the science base: a summary of the 1999 Institute of Medicine report. Arch Gen Psychiatry. 2000, 57(6):547-552.

18. Wu TC, Tashkin DP, Djahed B, Rose JE: Pulmonary hazards of smoking marijuana as compared with tobacco. N Engl J Med. 1988, 318:347-351.

19. Grotenhermen F: Pharmacokinetics and pharmacodynamics of cannabinoids. Clin Pharmacokinet. 2003, 42(4):327-360.

20. Nebert DW, Gonzalez FJ: P450 genes: structure, evolution, and regulation. Annu Rev Biochem. 1987, 56:945-993.

21. Hecht SS, Carmella SG, Murphy SE, Foiles PG, Chung FL: Carcinogen biomarkers related to smoking and upper aerodigestive tract cancer. J Cell Biochem Suppl. 1993, 17F:27-35.

22. Tretyakova N, Matter B, Jones R, Shallop A: Formation of benzo[a]pyrene diol epoxide-DNA adducts at specific guanines within K-ras and p53 gene sequences: stable isotope-labeling mass spectrometry approach. Biochemistry. 2002, 41:9535-9544.

23. Roth MD, Marques-Magallanes JA, Yuan M, Sun W, Tashkin DP, Hankinson O: Induction and regulation of the carcinogen-metabolizing enzyme CYP1A1 by marijuana smoke and delta (9)-tetrahydrocannabinol. Am J Respir Cell Mol Biol. 2001, 24:339-344.

24. Price RJ, Renwick AB, Walters DG, Young PJ, Lake BG: Metabolism of nicotine and induction of CYP1A forms in precision-cut rat liver and lung slices. Toxicol In Vitro. 2004, 18:179-185.

25. Nebert DW, Russell DW: Clinical importance of the cytochromes P450. Lancet. 2002, 360(9340):1155-1162.

26. Devane WA, Hanus L, Breuer A, Pertwee RG, Stevenson LA, Griffin G, Gibson D, Mandelbaum A, Etinger A, Mechoulam R: Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science. 1992, 258:1946- 1949.

27. West KA, Brognard J, Clark AS, Linnoila IR, Yang X, Swain SM, Harris C, Belinsky S, Dennis PA: Rapid Akt activation by nicotine and a tobacco carcinogen modulates the phenotype of normal human airway epithelial cells. J Clin Invest. 2003, 111:81-90.

28. Woo RA, Poon RY: Cyclin-Dependent Kinases and S Phase Control in Mammalian Cells. Cell Cycle. 2003, 2:316-324.

29. Bockaert J, Pin JP: Molecular tinkering of G protein-coupled receptors: an evolutionary success. EMBO J. 1999, 18(7):1723-1729.

30. Howlett AC, Barth F, Bonner TI, Cabral G, Casellas P, Devane WA, Felder CC, Herkenham M, Mackie K, Martin BR, Mechoulam R, Pertwee RG: International Union of Pharmacology. XXVII. Classification of cannabinoid receptors. Pharmacol Rev. 2002, 54(2):161-202.

31. Itier V, Bertrand D: Neuronal nicotinic receptors: from protein structure to function. FEBS Lett. 2001, 504(3):118-125.

32. Gomez del Pulgar T, Velasco G, Guzman M: The CB1 cannabinoid receptor is coupled to the activation of protein kinase B/Akt. Biochem J. 2000, 347:369- 373.

33. Minna JD: Nicotine exposure and bronchial epithelial cell nicotinic acetylcholine receptor expression in the pathogenesis of lung cancer. J Clin Invest. 2003, 111(1):31-33.

34. Panikashvili D, Simeonidou C, Ben-Shabat S, Hanus L, Breuer A, Mechoulam R, Shohami E: An endogenous cannabinoid (2-AG) Is neuroprotective after brain injury. Nature. 2001, 413:527-531.

35. Leker RR, Shohami E, Abramsky O, Ovadia H: Dexanabinol; a novel neuroprotective drug in experimental focal cerebral ischemia. J Neurol Sci. 1999, 162:114-119.

36. Iuvone T, Esposito G, Esposito R, Santamaria R, Di Rosa M, Izzo AA: Neuroprotective effect of cannabidiol, a non-psychoactive component from Cannabis sativa, on beta-amyloid-induced toxicity in PC12 cells. J Neurochem. 2004, 89:134-141.

37. Kihara T, Shimohama S, Sawada H, Honda K, Nakamizo T, Shibasaki H, Kume T, Akaike A: alpha 7 nicotinic receptor transduces signals to phosphatidylinositol 3-kinase to block A beta-amyloid-induced neurotoxicity. J Biol Chem. 2001, 276:13541-13546.

38. Heeschen C, Jang JJ, Weis M, Pathak A, Kaji S, Hu RS, Tsao PS, Johnson FL, Cooke JP: Nicotine stimulates angiogenesis and promotes tumor growth and atherosclerosis. Nat Med. 2001, 7:833-839.

39. Galve-Roperh I, Sanchez C, Cortes ML, del Pulgar TG, Izquierdo M, Guzman M: Anti-tumoral action of cannabinoids: involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation. Nat Med. 2000, 6:313-319.

40. Blazquez C, Gonzalez-Feria L, Alvarez L, Haro A, Casanova ML, Guzman M: Cannabinoids inhibit the vascular endothelial growth factor pathway in gliomas. Cancer Res. 2004, 64:5617-5623.

41. Sarafian TA, Magallanes JA, Shau H, Tashkin D, Roth MD: Oxidative stress produced by marijuana smoke. An adverse effect enhanced by cannabinoids. Am J Respir Cell Mol Biol. 1999, 20:1286-1293.

42. Chung HY, Kim HJ, Kim JW, Yu BP: The inflammation hypothesis of aging: molecular modulation by calorie restriction. Ann N Y Acad Sci. 2001, 928:327- 335.

43. Raha S, Robinson BH: Mitochondria, oxygen free radicals, and apoptosis. Am J Med Genet. 2001, 106:62-70.

44. Halliwell B: Role of free radicals in the neurodegenerative diseases: therapeutic implications for antioxidant treatment. Drugs Aging. 2001, 18:685-716.

45. Drew B, Leeuwenburgh C: Aging and the role of reactive nitrogen species. Ann N Y Acad Sci. 2002, 959:66-81.

46. Yuan M, Kiertscher SM, Cheng Q, Zoumalan R, Tashkin DP, Roth MD: Delta 9- Tetrahydrocannabinol regulates Th1/Th2 cytokine balance in activated human T cells. J Neuroimmunol. 2002, 133:124-131.

47. Mirken B. Vaporizers for medical marijuana. Aids Treat News No 327 1999; Sect. 1, 5.

48. Gieringer D, St. Laqurent J, Goodrich S. Cannabis Vaporizer Combines Efficient Delivery of THC with Effective Suppression of Pyrolytic

-end- Compounds. In: Journal of Cannabis Therapeutics. Russo, ed. 4. 2004:7-27.
PP said…
Okay. Here's the deal guys. When the discussion degrades into nasty insults, goes way off topic, and brings up suggestions of fellatio, that's when I consider bothing to turn it off because I don't want to read the comments (as e-mailed).

This was meant to be a discussion of where people are on their petition efforts. Not a request for people to justify the pros and cons.

Bob - if you want to deviate from saying how many signatures you have and take the liberty to post what you consider as your supportive evidence, it would be preferable for you to use your own site for the bulk of it, and provide a link for those who choose to read them.

Thanks for your consideration.
Bob Newland said…
Was fun, though. Was it good for you, too, Anon?
Anonymous said…
PP wrote:
"Here's the deal guys. When the discussion degrades into nasty insults, goes way off topic, and brings up suggestions of fellatio..."

Guys? Plural? Pat, I've been nothing but respectful here. Harsh maybe, but I certainly haven't issued any "nasty insults" or "suggestions of fellatio." My criticism--not excessive in light of the offense--was of your actions and not of your character. I stand by it. You've done nothing to disprove it. Other than threaten to, once again, shut down the comments.

Again I say: if you're going to offer your opinion on a political topic--ANY political topic, not just this one--you ought to play fair and allow an unlimited amount of substantive responses. Either that or do it the SDP way and don't allow any comments at all. Turning the comments off because you're tired of responding to them is a middle ground which satisfies no one.

I agree with you that insulting and offensive comments warrant closure of the thread. That's not what happened earlier. I called you on it. You've done nothing to alter my thinking. (Unlike you, I *am* willing to change my mind.)

I asked you to please "refer me to the personally insulting comment(s) which motivated you to shut down the [earlier] thread." My request went unheeded and unacknowledged.

I'm sorry for wasting your time. And mine. I think I've learned my lesson.
PP said…
Will, Did I say you was nasty? No. Opinionated, yes, but otherwise there was plenty of snippiness to go around.

If you don't care for my throwing out a caution sign when I think it's getting a little off topic, personal, or the discussion starts moving towards sex acts instead of politics, go to http://www.blogger.com and start your own blog.

If it's South Dakota politics related, I'll even link to it.
Anonymous said…
If I mention SD every once in a while, does that count? ;)

I have been thinking about starting a blog, but it seems like blog-burnout is something to be concerned about. Seems like this takes a lot of effort, especially if you want to do it right. Epp has had to change his style, Jer Bear shut down entirely, Eddie did too. The last thing I want to do is start up only to find I don't have the time, energy, or desire to keep it running.

I admire you for that: you put effort into your blog, and it's reader friendly. SDWC is my home-base blog, partly to read what you write, and partly because of your RSS feeds. I'm more interested in the political issues than the campaign advice, but I do think you have a lot of knowledge in that area.

You didn't say I was nasty, but you addressed your post to the "guys," and since me and Bob were pretty much the only ones commenting on this thread, I thought you were referring to me too. Sorry for the misunderstanding.

Bob, I admire you too. I think you are driven by compassion, not self-interest. Unlike probably everyone else here (other than Bob and PP) I've actually read the proposed legislation -- it's for people who are truly sick, not for stoners looking for a backdoor way to get it legalized.

If someone who is ailing feels better from smoking pot--and they do, I've met them--who am I to deny them that right? Who am I to say what they can and cannot use to make themselves feel better? Who are YOU to say?

Does anyone really think Angela Raich (the CA woman who recently lost the Sup Ct case) is selling her home-grown marijuana to people in the black market? No. She's smoking it to feel better. Because it's the only thing that makes her feel better. I don't doubt her veracity.

I suggest you all read the proposed legislation for yourselves before coming to any conclusions about Bob's motivations.
PP said…
Will, actually that's kind of funny. I've had people compliment me because I do focus on the campaign related stuff.

The difference for the other coverage is that I pretty much ignore the federal level stuff in favor of State Level politics.

It's my bread and butter.

And if you talk about SD, I'd still link you.
Bob Newland said…
Will says, "Bob, I think you are driven by compassion, not self-interest."

I appreciate your saying that, and I still am mystified by the reasoning of those who say I am in this struggle for self-interested reasons. (actually, I am, because there is a growing chance I will contract a medical condition wherein I would be a candidate for therapeutic use, but that's not the self-interest Anon has in mind, I think).

So, Anonymous, once more I'd ask you to explain how you think I could benefit (in a different way from that which I mention above) if South Dakota allows sick people access to cannabis as one alternative among many therapies.
Bob Newland said…
C'mon, Anon.

Chicken, Mon?

Sitting upon
the Anon con.

Or maybe just stupid-san?

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