Stondestmanaliv
Member
Oh my GOD! 600mg/kg? That would be more than 2 ounces of pure THC. I know for a fact if I just sat here and ate 3 ounces of 65% THC hash, I would go fucking crazy..
Ya buddy, that psychogenic shock.
Liver issues
- Thread starter slightlysolid
- Start date
Oh my GOD! 600mg/kg? That would be more than 2 ounces of pure THC. I know for a fact if I just sat here and ate 3 ounces of 65% THC hash, I would go fucking crazy..
Ya buddy, that psychogenic shock.
Stondestmanaliv
Member
...knowing the United States of the 1%, I would assume their 8 subjects had a gun pointed to their heads or the threat of life in prison as they "ingested" cannabis.
I would not breath either... Something about the Nazi`s in the room sucking the life out of the people who built this world.
T
Truthman
Where did you get this number from?
It just states 600mg of cannabis extract which is basically over half a gram of hash as hash is a cannabis extract. How did you come up with 2 ounces of pure thc?. If anything it would be at the most, 10.5mg of pure THC, but it was most likely way less then that as most people can't or couldn't in the past, get potent cannabis that is high in thc.
Dr's are idiots... Str8 Drug Dealers...your wrong about the China thing as well...its all about who you deal with....
Doctors are trained to be pill pushers...nothing more
http://www.ncbi.nlm.nih.gov/pubmed/22994543
Am J Transplant. 2012 Sep 20. doi: 10.1111/j.1600-6143.2012.04261.x. [Epub ahead of print]
Tauroursodeoxycholic Acid Affects PPARγ and TLR4 in Steatotic Liver Transplantation.
Jiménez-Castro MB, Elias-Miro M, Mendes-Braz M, Lemoine A, Rimola A, Rodés J, Casillas-Ramírez A, Peralta C.
Source
Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBPAS), Barcelona, Spain Departamento de Patologia e Medicina Legal, Faculdade de Medicina, Universidade de Sao Paulo, Sau Paulo, Brazil APHP, Biochimie et Oncogénétique Moléculaire, Inserm U1004/Université Paris 11, Institut du Foie, Hopital Paul Brousse, Villejuif, France Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Barcelona, Spain Liver Unit, Hospital Clínic, Barcelona, Spain.
Abstract
Numerous steatotic livers are discarded for transplantation because of their poor tolerance to ischemia-reperfusion (I/R). We examined whether tauroursodeoxycholic acid (TUDCA), a known inhibitor of endoplasmic reticulum (ER) stress, protects steatotic and nonsteatotic liver grafts preserved during 6 h in University of Wisconsin (UW) solution and transplanted. The protective mechanisms of TUDCA were also examined. Neither unfolded protein response (UPR) induction nor ER stress was evidenced in steatotic and nonsteatotic liver grafts after 6 h in UW preservation solution. TUDCA only protected steatotic livers grafts and did so through a mechanism independent of ER stress. It reduced proliferator-activated receptor-γ (PPARγ) and damage. When PPARγ was activated, TUDCA did not reduce damage. TUDCA, which inhibited PPARγ, and the PPARγ antagonist treatment up-regulated toll-like receptor 4 (TLR4), specifically the TIR domain-containing adaptor inducing IFNβ (TRIF) pathway. TLR4 agonist treatment reduced damage in steatotic liver grafts. When TLR4 action was inhibited, PPARγ antagonists did not protect steatotic liver grafts. In conclusion, TUDCA reduced PPARγ and this in turn up-regulated the TLR4 pathway, thus protecting steatotic liver grafts. TLR4 activating-based strategies could reduce the inherent risk of steatotic liver failure after transplantation.
© Copyright 2012 The American Society of Transplantation and the American Society of Transplant Surgeons.
surely this argument could be properly solved if either one of you are medical profesionals or whatever.
http://www.ncbi.nlm.nih.gov/pubmed/22972029
Exp Clin Endocrinol Diabetes. 2012 Sep 12. [Epub ahead of print]
Tauroursodeoxycholate, a Chemical Chaperone, Prevents Palmitate-induced Apoptosis in Pancreatic β-cells by Reducing ER Stress.
Zhu Q, Zhong JJ, Jin JF, Yin XM, Miao H.
Source
Department of Endocrinology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Abstract
Free fatty acids (FFA) can have deleterious effects on β-cells and promote type 2 diabetes, a process known as lipotoxicity. Recently, the induction of endoplasmic reticulum (ER) stress is one mechanism proposed to contribute to the detrimental effects of FFA on β-cells. Tauroursodeoxycholic acid (TUDCA) has been reported to show cytoprotective effects by alleviating ER stress induced by some cytotoxic stimuli. The aim of this study was to investigate the effects of TUDCA on FFA (palmitate)-induced apoptosis and ER stress in rat islet β-cells.The rat pancreatic β-cell line INS-1 was cultured with palmitate (0.5 mM), or cultured togther with TUDCA (100 μM), Annexin V-fluorescein-isothiocyanate/propidium iodide flow cytometry was used to assess apoptosis in INS-1 cells. Cell viability was evaluated with MTT reduction conversion assay. The expressions of ER stress marker GRP78, ER stress-associated pro-apoptotic effectors CHOP and ATF4 were detected by Western blotting.TUDCA significantly reduced palmitate-induced cell apoptosis and growth inhibition in INS-1 cells. TUDCA also attenuated palmitate-induced expressions of GRP78, CHOP and ATF4 in INS-1 cells.Our results thus suggested that TUDCA could protect INS-1 cells from palmitate-induced injury, which might be due to the amelioration of ER stress and blocking the ATF4/CHOP signaling pathway.
© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York.
Exp Clin Endocrinol Diabetes. 2012 Sep 12. [Epub ahead of print]
Tauroursodeoxycholate, a Chemical Chaperone, Prevents Palmitate-induced Apoptosis in Pancreatic β-cells by Reducing ER Stress.
Zhu Q, Zhong JJ, Jin JF, Yin XM, Miao H.
Source
Department of Endocrinology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Abstract
Free fatty acids (FFA) can have deleterious effects on β-cells and promote type 2 diabetes, a process known as lipotoxicity. Recently, the induction of endoplasmic reticulum (ER) stress is one mechanism proposed to contribute to the detrimental effects of FFA on β-cells. Tauroursodeoxycholic acid (TUDCA) has been reported to show cytoprotective effects by alleviating ER stress induced by some cytotoxic stimuli. The aim of this study was to investigate the effects of TUDCA on FFA (palmitate)-induced apoptosis and ER stress in rat islet β-cells.The rat pancreatic β-cell line INS-1 was cultured with palmitate (0.5 mM), or cultured togther with TUDCA (100 μM), Annexin V-fluorescein-isothiocyanate/propidium iodide flow cytometry was used to assess apoptosis in INS-1 cells. Cell viability was evaluated with MTT reduction conversion assay. The expressions of ER stress marker GRP78, ER stress-associated pro-apoptotic effectors CHOP and ATF4 were detected by Western blotting.TUDCA significantly reduced palmitate-induced cell apoptosis and growth inhibition in INS-1 cells. TUDCA also attenuated palmitate-induced expressions of GRP78, CHOP and ATF4 in INS-1 cells.Our results thus suggested that TUDCA could protect INS-1 cells from palmitate-induced injury, which might be due to the amelioration of ER stress and blocking the ATF4/CHOP signaling pathway.
© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York.
http://www.ncbi.nlm.nih.gov/pubmed/22994399
Hepatol Res. 2012 Sep 20. doi: 10.1111/j.1872-034X.2012.01085.x. [Epub ahead of print]
Cannabinoid 1 receptor in fatty liver.
Regnell SE.
Source
Lund University, Lund, Sweden.
Abstract
The role of cannabinoids in fatty liver disease has been increasingly acknowledged in recent years, and it has been suggested that drugs targeting peripheral cannabinoid receptors could have therapeutic use. Development of such drugs would require a good understanding of the mechanisms of fat accumulation caused by cannabinoid receptor activation. This review describes in detail the enzymatic steps that lead from the stimulation of cannabinoid 1 receptor to steatosis. It identifies several signaling pathways that activate sterol regulatory element-binding protein 1c (SREBP-1c), the key transcription factor causing fatty liver. The downstream effects of SREBP-1c leading to increased fatty acid synthesis and decreased fatty acid oxidation are also described.
© 2012 The Japan Society of Hepatology.
Hepatol Res. 2012 Sep 20. doi: 10.1111/j.1872-034X.2012.01085.x. [Epub ahead of print]
Cannabinoid 1 receptor in fatty liver.
Regnell SE.
Source
Lund University, Lund, Sweden.
Abstract
The role of cannabinoids in fatty liver disease has been increasingly acknowledged in recent years, and it has been suggested that drugs targeting peripheral cannabinoid receptors could have therapeutic use. Development of such drugs would require a good understanding of the mechanisms of fat accumulation caused by cannabinoid receptor activation. This review describes in detail the enzymatic steps that lead from the stimulation of cannabinoid 1 receptor to steatosis. It identifies several signaling pathways that activate sterol regulatory element-binding protein 1c (SREBP-1c), the key transcription factor causing fatty liver. The downstream effects of SREBP-1c leading to increased fatty acid synthesis and decreased fatty acid oxidation are also described.
© 2012 The Japan Society of Hepatology.
no thats the case in the usa only where you pay for all your health care. for example in the uk we get free health care so pills are not sold to us and they will diagnose rather than sell.
Cha Ching
http://www.ncbi.nlm.nih.gov/pubmed/21182490
Br J Pharmacol. 2011 Apr;162(7):1650-8. doi: 10.1111/j.1476-5381.2010.01179.x.
Cannabidiol improves brain and liver function in a fulminant hepatic failure-induced model of hepatic encephalopathy in mice.
Avraham Y, Grigoriadis N, Poutahidis T, Vorobiev L, Magen I, Ilan Y, Mechoulam R, Berry E.
Source
Department of Human Nutrition and Metabolism, Braun School of Public Health, Hadassah-Hebrew University Medical School, Jerusalem, Israel. [email protected]
Abstract
BACKGROUND AND PURPOSE:
Hepatic encephalopathy is a neuropsychiatric disorder of complex pathogenesis caused by acute or chronic liver failure. We investigated the effects of cannabidiol, a non-psychoactive constituent of Cannabis sativa with anti-inflammatory properties that activates the 5-hydroxytryptamine receptor 5-HT(1A) , on brain and liver functions in a model of hepatic encephalopathy associated with fulminant hepatic failure induced in mice by thioacetamide.
EXPERIMENTAL APPROACH:
Female Sabra mice were injected with either saline or thioacetamide and were treated with either vehicle or cannabidiol. Neurological and motor functions were evaluated 2 and 3 days, respectively, after induction of hepatic failure, after which brains and livers were removed for histopathological analysis and blood was drawn for analysis of plasma liver enzymes. In a separate group of animals, cognitive function was tested after 8 days and brain 5-HT levels were measured 12 days after induction of hepatic failure.
KEY RESULTS:
Neurological and cognitive functions were severely impaired in thioacetamide-treated mice and were restored by cannabidiol. Similarly, decreased motor activity in thioacetamide-treated mice was partially restored by cannabidiol. Increased plasma levels of ammonia, bilirubin and liver enzymes, as well as enhanced 5-HT levels in thioacetamide-treated mice were normalized following cannabidiol administration. Likewise, astrogliosis in the brains of thioacetamide-treated mice was moderated after cannabidiol treatment.
CONCLUSIONS AND IMPLICATIONS:
Cannabidiol restores liver function, normalizes 5-HT levels and improves brain pathology in accordance with normalization of brain function. Therefore, the effects of cannabidiol may result from a combination of its actions in the liver and brain.
© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.
http://www.ncbi.nlm.nih.gov/pubmed/21182490
Br J Pharmacol. 2011 Apr;162(7):1650-8. doi: 10.1111/j.1476-5381.2010.01179.x.
Cannabidiol improves brain and liver function in a fulminant hepatic failure-induced model of hepatic encephalopathy in mice.
Avraham Y, Grigoriadis N, Poutahidis T, Vorobiev L, Magen I, Ilan Y, Mechoulam R, Berry E.
Source
Department of Human Nutrition and Metabolism, Braun School of Public Health, Hadassah-Hebrew University Medical School, Jerusalem, Israel. [email protected]
Abstract
BACKGROUND AND PURPOSE:
Hepatic encephalopathy is a neuropsychiatric disorder of complex pathogenesis caused by acute or chronic liver failure. We investigated the effects of cannabidiol, a non-psychoactive constituent of Cannabis sativa with anti-inflammatory properties that activates the 5-hydroxytryptamine receptor 5-HT(1A) , on brain and liver functions in a model of hepatic encephalopathy associated with fulminant hepatic failure induced in mice by thioacetamide.
EXPERIMENTAL APPROACH:
Female Sabra mice were injected with either saline or thioacetamide and were treated with either vehicle or cannabidiol. Neurological and motor functions were evaluated 2 and 3 days, respectively, after induction of hepatic failure, after which brains and livers were removed for histopathological analysis and blood was drawn for analysis of plasma liver enzymes. In a separate group of animals, cognitive function was tested after 8 days and brain 5-HT levels were measured 12 days after induction of hepatic failure.
KEY RESULTS:
Neurological and cognitive functions were severely impaired in thioacetamide-treated mice and were restored by cannabidiol. Similarly, decreased motor activity in thioacetamide-treated mice was partially restored by cannabidiol. Increased plasma levels of ammonia, bilirubin and liver enzymes, as well as enhanced 5-HT levels in thioacetamide-treated mice were normalized following cannabidiol administration. Likewise, astrogliosis in the brains of thioacetamide-treated mice was moderated after cannabidiol treatment.
CONCLUSIONS AND IMPLICATIONS:
Cannabidiol restores liver function, normalizes 5-HT levels and improves brain pathology in accordance with normalization of brain function. Therefore, the effects of cannabidiol may result from a combination of its actions in the liver and brain.
© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.
man do you know why they do trials on humans before they release drugs? i like pubmed its about as good as your gonna get on line. but studies on mice?? lol
Damn, sorry dude i didn't mean to neg rep ur post, twas funny but my dang ol fingers slipped
Stondestmanaliv
Member
600mg/kg is what was given to the rats.. Dang, I don`t think you are qualified to understand.. 600mg/kg = 60g/100kg ...I am 100kg... What are you failing to understand? Basic math?
T
Truthman
I'm done because I can't rationalize with you if you can even understand something that is in your face. Where did you get 600mg/kg=60g/100kg?.
What that meant was 600mg per 1 kilogram which means the extract was .60 grams.
WOW
Stondestmanaliv
Member
I would never ask you to attempt treatment based on the information hypothesized upon trial studies from rats and no further.
I would ask you to relay your information to a medical doctor if you have any concerns regarding cannabis usage. I wished I could help more but I am not currently a medical doctor, therefor, I am not fully qualified to answer your questions. I can offer 2 years of medical school information and 8 years as an EMT-1. ....but, if there is pain in the liver, I suggest a check-up asap.
Stondestmanaliv
Member
No... I don`t know why you are trying to answer VERY serious problems with the health of human beings if you don`t even understand how medical dosage is measured. ANYONE who knows ANYTHING about medicine knows EXACTLY what 600mg/kg means as a dosage. Dang..
600mg/kg means they give 600mg of THC per 1/kg of BODY WEIGHT.
a rat weighs less than 1kg so i assume they give the rat less than 0.6grams of THC.
T
Truthman
First of all, you don't read right because the op stated he got his liver checked and his numbers were good so he couldn't understand why his friend kept getting pain the HIGHER her got, and I gave him an answer that MAY help. If it didn't I told him to get back at me because I wanted to know what they issue may be.
Secondly, you are right in the dosage now that I read it again, but it still doesn't negate the fact that cannabis effects liver glycogen which is why they gave the right a high amount. The same would happen if you were low in glucose and puffed herb. If you are puffing on some potent herb and your glucose levels are low, your liver will use up the glycogen stored in the liver to make glucose to use for fuel. Look man, you can debate all you want, I just want to see what is wrong with the kid. If I'm wrong, I want to see what the issue is. If I'm right I want you to say sorry and kiss the ring because "WE ARE THE BEST". LOL.
Secondly, you are right in the dosage now that I read it again, but it still doesn't negate the fact that cannabis effects liver glycogen which is why they gave the right a high amount. The same would happen if you were low in glucose and puffed herb. If you are puffing on some potent herb and your glucose levels are low, your liver will use up the glycogen stored in the liver to make glucose to use for fuel. Look man, you can debate all you want, I just want to see what is wrong with the kid. If I'm wrong, I want to see what the issue is. If I'm right I want you to say sorry and kiss the ring because "WE ARE THE BEST". LOL.
man i agree with everything you have said. theres obviously people here who wish to put their health in the hands of an internet qualified doctor like storm shadow. anyone who does that must be insane
Stondestmanaliv
Member
These are his quotes on the same post.. One was edited less than 1 min later.
~Last~
First
Are you going to call me a liar or are you going to rethink your stage-name? No offense, but I took an oath to perform a Duty To Act when needed and to help a patient or a person in need. What exactly are you doing?
~Last~
First
Are you going to call me a liar or are you going to rethink your stage-name? No offense, but I took an oath to perform a Duty To Act when needed and to help a patient or a person in need. What exactly are you doing?
T
Truthman
EDIT
T
Truthman
Man, I'm doing a shitload of things which is why I'm editing my post as I realize what I'm writing. There is a reason why there is an edit button my little friend. Try again.
BTW, I have helped MANY people from people passed out from suicide attempts, to people who needed help to enjoy cannabis again while everyone was telling them NO answers, such as yourself, that would help them. I gave simple thought out answers that helped even though damn near everyone try to prove me wrong. Hopefully the same happens in this situation, if it doesn't that is more for me to learn. What will you do, still give answers that don't help?. Don't get me wrong, I appreciate your evaluation, and input BUT give an answer that can be done, and not just posting to post to remind yourself what you learned. Give real world answers.
Again, why did you post an article that didn't prove anything you claimed?.
