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Powerful. Marijuana saves child's life. (Original Post)
peoli
Dec 2014
OP
A lot of the opposition to legalization is a firmly held belief that civilization is fragile....
Spitfire of ATJ
Dec 2014
#2
????? this is either bullshit of or brilliant but I know the oppoinents agenda is ignorant greed .
Spitfire of ATJ
(32,723 posts)2. A lot of the opposition to legalization is a firmly held belief that civilization is fragile....
And that people shouldn't be allowed to "run wild".
It's classic imposition of a perceived morality based upon the mistaken belief that being a fucking PRUDE is a virtue.
Pastiche423
(15,406 posts)4. It is not bullshit
I can personally testify that it works.
For 18 years I could not drive due to fears of a grand mal seizures. Thanks to cannabis oil, I am now seizure free and can drive again.
- I personally know that it works.
Smoking Weed with the President of Uruguay
ABSTRACT
Autophagy can promote cell survival or cell death, but the molecular basis underlying its dual role in cancer remains obscure. Here we demonstrate that ?9-tetrahydrocannabinol (THC), the main active component of marijuana, induces human glioma cell death through stimulation of autophagy. Our data indicate that THC induced ceramide accumulation and eukaryotic translation initiation factor 2a ( eIF2a ) phosphorylation and thereby activated an ER stress response that promoted autophagy via tribbles homolog 3dependent (TRB3-dependent) inhibition of the Akt/mammalian target of rapamycin complex 1 (mTORC1) axis. We also showed that autophagy is upstream of apoptosis in cannabinoid-induced human and mouse cancer cell death and that activation of this pathway was necessary for the anti-tumor action of cannabinoids in vivo. These findings describe a mechanism by which THC can promote the autophagic death of human and mouse cancer cells and provide evidence that cannabinoid administration may be an effective therapeutic strategy for targeting human cancers.
Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells
Friends of Charlie
Oregons Youngest Medical Cannabis Patient Is Now Cancer Free
Autophagy can promote cell survival or cell death, but the molecular basis underlying its dual role in cancer remains obscure. Here we demonstrate that ?9-tetrahydrocannabinol (THC), the main active component of marijuana, induces human glioma cell death through stimulation of autophagy. Our data indicate that THC induced ceramide accumulation and eukaryotic translation initiation factor 2a ( eIF2a ) phosphorylation and thereby activated an ER stress response that promoted autophagy via tribbles homolog 3dependent (TRB3-dependent) inhibition of the Akt/mammalian target of rapamycin complex 1 (mTORC1) axis. We also showed that autophagy is upstream of apoptosis in cannabinoid-induced human and mouse cancer cell death and that activation of this pathway was necessary for the anti-tumor action of cannabinoids in vivo. These findings describe a mechanism by which THC can promote the autophagic death of human and mouse cancer cells and provide evidence that cannabinoid administration may be an effective therapeutic strategy for targeting human cancers.
Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells
Friends of Charlie
Oregons Youngest Medical Cannabis Patient Is Now Cancer Free
Smoking Weed with the President of Uruguay
DeSwiss
(27,137 posts)5. Here's another one I found today:
The potential therapeutic effects of THC on Alzheimer's disease.
Abstract
The purpose of this study was to investigate the potential therapeutic qualities of ?9-tetrahydrocannabinol (THC) with respect to slowing or halting the hallmark characteristics of Alzheimer's disease. N2a-variant amyloid-? protein precursor (A?PP) cells were incubated with THC and assayed for amyloid-? (A? ) levels at the 6-, 24-, and 48-hour time marks. THC was also tested for synergy with caffeine, in respect to the reduction of the A? level in N2a/A?PPswe cells. THC was also tested to determine if multiple treatments were beneficial. The MTT assay was performed to test the toxicity of THC. Thioflavin T assays and western blots were performed to test the direct anti-A? aggregation significance of THC. Lastly, THC was tested to determine its effects on glycogen synthase kinase-3? (GSK-3? ) and related signaling pathways. From the results, we have discovered THC to be effective at lowering A? levels in N2a/A?PPswe cells at extremely low concentrations in a dose-dependent manner. However, no additive effect was found by combining caffeine and THC together. [font color=red]We did discover that THC directly interacts with A? peptide, thereby inhibiting aggregation. Furthermore, THC was effective at lowering both total GSK-3? levels and phosphorylated GSK-3? in a dose-dependent manner at low concentrations. At the treatment concentrations, no toxicity was observed and the CB1 receptor was not significantly upregulated. Additionally, low doses of THC can enhance mitochondria function and does not inhibit melatonin's enhancement of mitochondria function. These sets of data strongly suggest that THC could be a potential therapeutic treatment option for Alzheimer's disease through multiple functions and pathways.[/font]
MORE
US National Library of Medicine
National Institutes of Health
Abstract
The purpose of this study was to investigate the potential therapeutic qualities of ?9-tetrahydrocannabinol (THC) with respect to slowing or halting the hallmark characteristics of Alzheimer's disease. N2a-variant amyloid-? protein precursor (A?PP) cells were incubated with THC and assayed for amyloid-? (A? ) levels at the 6-, 24-, and 48-hour time marks. THC was also tested for synergy with caffeine, in respect to the reduction of the A? level in N2a/A?PPswe cells. THC was also tested to determine if multiple treatments were beneficial. The MTT assay was performed to test the toxicity of THC. Thioflavin T assays and western blots were performed to test the direct anti-A? aggregation significance of THC. Lastly, THC was tested to determine its effects on glycogen synthase kinase-3? (GSK-3? ) and related signaling pathways. From the results, we have discovered THC to be effective at lowering A? levels in N2a/A?PPswe cells at extremely low concentrations in a dose-dependent manner. However, no additive effect was found by combining caffeine and THC together. [font color=red]We did discover that THC directly interacts with A? peptide, thereby inhibiting aggregation. Furthermore, THC was effective at lowering both total GSK-3? levels and phosphorylated GSK-3? in a dose-dependent manner at low concentrations. At the treatment concentrations, no toxicity was observed and the CB1 receptor was not significantly upregulated. Additionally, low doses of THC can enhance mitochondria function and does not inhibit melatonin's enhancement of mitochondria function. These sets of data strongly suggest that THC could be a potential therapeutic treatment option for Alzheimer's disease through multiple functions and pathways.[/font]
MORE
US National Library of Medicine
National Institutes of Health
See also:
Could magic mushrooms become a new drug for hospice care?