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Two Ballot Measures In The Works To Counter Restrictive San Jose Medical Marijuana Policy


Medical MarijuanaActivists organize to educate San Jose at the ballot box

By David Burton

When they passed their medical marijuana ordinance in September, San Jose city council members had hoped to finally put a lid on what one member called “the problem” of cannabis dispensaries in the community. What they got instead was a medical marijuana community galvanized against them as never before.

Outraged by a laundry list of regulations they see as unworkable and unfair, compassionate-use activists have launched two signature-gathering efforts to qualify a pair of measures to put before city voters. One is a referendum, spearheaded by the grassroots group Citizens Coalition for Patient Care (CCPC), to repeal the ordinance. The other, a ballot initiative organized by the Cannabis Patient Alliance (CPA), would ask residents to approve what proponents say would be a vastly better ordinance than the existing one.

“We’re not saying there shouldn’t be guidelines,” says Matthew Witemyre, co-chair of the Citizens Coalition for Patient Care, which is working to qualify the referendum. “We just believe there should be reasonable guidelines that actually reflect what’s happening in the industry right now.”

In November 2010, local voters passed Measure U, which placed a 7-percent tax on the gross receipts of all dispensaries. A May 27 internal city memo shows that San Jose gained about $1.12 million in business tax revenue from dispensaries in the last four months of fiscal year 2010-11.

The new regulations include requiring all cannabis and edibles to be grown/prepared on site, requiring dispensaries to have an on-site doctor or nurse and limiting dispensaries allowed in the city to 10–meaning about 130 medical marijuana shops currently operating in San Jose must go, at the loss of an estimated 1,500 jobs.

City officials did not return calls for comment. About 40,000 signatures must be collected by the end of October to qualify for the ballot.

“That’s where it’s important for the community to get together and educate the public about medical cannabis, what’s needed for patients to have the access they need, and for the general community’s rights to be respected,” CPA president and local cannabis activist Sean Cambern says.

Article from Culture Magazine and republished with special permission


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  1. Wow how you can you tax marijuana when most states dont even want it? and if they are taxing on it they should make it legal in all states.. Dumbasses

  2. The following text is taken directly from the US government’s National Cancer Institute website: http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page4


    One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors. During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepatic adenoma tumors and hepatocellular carcinoma was observed in the mice. Decreased incidences of benign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, and pancreas) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lung adenocarcinoma cells in vitro and in vivo. In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.

    Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis and metastasis. Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. These compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats. Cannabinoids protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.

    In an in vivo model using severe combined immunodeficient mice, subcutaneous tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines. Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects.


    In addition, both plant-derived and endogenous cannabinoids have been studied for anti- inflammatory effects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation. As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the prevention and treatment of colorectal cancer has been developed.


    Another study has shown delta-9-THC is a potent and selective antiviral agent against Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8. The researchers concluded that additional studies on cannabinoids and herpesviruses are warranted, as they may lead to the development of drugs that inhibit the reactivation of these oncogenic viruses. Subsequently, another group of investigators reported increased efficiency of KSHV infection of human dermal microvascular epithelial cells in the presence of low doses of delta-9-THC.


    Many animal studies have previously demonstrated that delta-9-THC and other cannabinoids have a stimulatory effect on appetite and increase food intake. It is believed that the endogenous cannabinoid system may serve as a regulator of feeding behavior. The endogenous cannabinoid anandamide potently enhances appetite in mice. Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.


    Understanding the mechanism of cannabinoid-induced analgesia has been increased through the study of cannabinoid receptors, endocannabinoids, and synthetic agonists and antagonists. The CB1 receptor is found in both the central nervous system (CNS) and in peripheral nerve terminals. Similar to opioid receptors, increased levels of the CB1 receptor are found in sections of the brain that regulate nociceptive processing. CB2 receptors, located predominantly in peripheral tissue, exist at very low levels in the CNS. With the development of receptor-specific antagonists, additional information about the roles of the receptors and endogenous cannabinoids in the modulation of pain has been obtained.

    Cannabinoids may also contribute to pain modulation through an anti-inflammatory mechanism; a CB2 effect with cannabinoids acting on mast cell receptors to attenuate the release of inflammatory agents, such as histamine and serotonin, and on keratinocytes to enhance the release of analgesic opioids has been described.

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