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Technology Stocks : Nokia (NOK) -- Ignore unavailable to you. Want to Upgrade?

To: Eric L who wrote (28584)	4/17/2008 11:16:42 AM
From: Eric L	Read Replies (10) \| Respond to of 34857

Quote of the Day ... ... from the "Take" by MacDailyNews: Kallasvuo is either incapable of applying the lessons of iPod to iPhone and understanding what's coming his way or, much more likely, he understands perfectly and, since he has no answer, is saying just what many now-defunct (if they aren't making iPod accessories) MP3-makers said a few years ago. Candybars and way-too-late, fake 1st generation iPhones with craptastic UI's aren't going to cut it from here on out, Nokia boy. This June, the bloodbath really begins, and Kallasvuo sounds like he knows it. macdailynews.com This from a fanboy of a 2.5G dumbphone that is trying to morph into a 3G smartphone with Apple finally releasing an iPhone SDK and promising a 3G device shortly. OPK announced today that Nokia shipped 14.6 million "converged devices" (smartphones) this quarter of which almost 10 million were NSeries 'multimedia computers.' A little disaponting to me. I expected 15.5m to 16m. Not to demean the iPhone UI (and its VERY good display), which is darned good if one can adjust to its craptastic 2-handed operation. <ggg> - Eric -

To: Eric L who wrote (28584)	4/17/2008 11:20:13 AM
From: 49thMIMOMander	Respond to of 34857

I am slightly worried about Kuitti-Kuittinen., and my worst sister (who just moved in downstairs, the good chemist and my first worst better guerilla sister than my finnish military guerilla explosive bomb education, we got it better than them, just we two, using just regular household chemicals, that was the rule) ECS changes induced by cannabis consumption [edit] Memory Mice treated with tetrahydrocannabinol show suppression of long-term potentiation in the hippocampus - a process that is essential for the formation and storage of long-term memory[20]. These results concur with anecdotal evidence suggesting that smoked preparations of Cannabis Sativa attenuates short-term memory[21]. Indeed, mice without the CB1 receptor show enhanced memory and long-term potentiation indicating that the endocannabinoid system may play a pivotal role in the extinction of old memories. Interestingly, recent research reported in a 2005 Journal Of Clinical Investigation article[22] indicate that the high-dose treatment of rats with the synthetic cannabinoid, HU-210 over a period of a few weeks resulted in stimulation of neural growth in the rats' hippocampus region, a part of the limbic system playing a part in the formation of declarative and spatial memories. [edit] Appetite Those who use cannabis are familiar with its appetite-enhancing effects. Emerging data suggests that THC act via CB1 receptors on hypothalamic nuclei, thus directly increasing appetite[23]. It is thought that hypothalamic neurons tonically produce endocannabinoids that work to tightly regulate hunger. Interestingly, the amount of endocannabinoids produced is inversely correlated with the amount of leptin in the blood[24]. For example, mice without leptin not only become massively obese but have higher-than-normal levels of hypothalamic endocannabinoids[25]. Similarly, when these mice were treated with an endocannabinoid antagonist, such as Rimonabant, food intake was reduced[25]. When the CB1 receptor is knocked out in mice, these animals tend to be leaner and less hungry than wild-type (or "normal") mice While there is need for more research, these results (and others) suggest that exogenous cannabinoids (as from smoking marijuana) in the hypothalamus activates a pathway responsible for food-seeking behavior[26]. [edit] ECS and multiple sclerosis Historical records from ancient China and Greece suggest that preparations of Cannabis Sativa were commonly prescribed to ameloriate multiple sclerosis-like symptoms such as tremors and muscle pain; unfortunately, however, treatment with marinol hasn’t shown the same efficacy as inhaled Cannabis [27][28]. Due to the illegality of Cannabis and rising incidence of multiple sclerosis patients who self-medicate with the drug, there has been much interest in exploiting the endocannabinoid system in the cerebellum to provide a legal and effective relief (reviewed in Pertwee, 2001). In mouse models of multiple sclerosis, there is a profound reduction and reorganization of CB1 receptors in the cerebellum (Cabranes et al., 2006). Serial sections of cerebellar tissue subjected to immunohistochemistry revealed that this aberrant expression occurred during the relapse phase but returned to normal during the remitting phase of the disease (Cabranes et al., 2006). There is recent data indicating that CB1 agonists promote the in vitro survival of oligodendrocytes, specialized support glia that are involved in axonal myelination, in the absence of growth and trophic factors; in addition, these agonist have been shown to promote mRNA expression of myelin lipid protein. (Kittler et al., 2000; Mollna-Holgado et al., 2002). Taken together, these studies point to the exciting possibility that cannabinoid treatment may not only be able to attenuate the symptoms of multiple sclerosis but also improve oligodendrocyte function (reviewed in Pertwee, 2001; Mollna-Holgado et al., 2002). 2-arachidonylglycerol stimulates proliferation of a microglial cell line by a CB2 receptor dependent mechanism, and the number of microglial cells is increased in multiple sclerosis.[29] [edit] Role in human female reproduction