Whats your New year resolutions
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emcee child
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1. Stop smoking.
2. Learn to say NO.
3. Make an honest attempt to get fit.
2. Learn to say NO.
3. Make an honest attempt to get fit.
Grime City, Narco.Hz
Myspace nonsense
Myspace nonsense
- perkalerk215
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thank you festa!!! im excited. feels good landing something you really tried for and just something a bit more secure.
and yeah. i know a lot of ppl looking to get fit this upcoming year. i did that this past yr. and then lost my focus the past 4 or 5 months ha...so its back to focusing on that.
and im with you festa about the getting hammered on tuesday nights...or wednesdays or thursdays....
and yeah. i know a lot of ppl looking to get fit this upcoming year. i did that this past yr. and then lost my focus the past 4 or 5 months ha...so its back to focusing on that.
and im with you festa about the getting hammered on tuesday nights...or wednesdays or thursdays....
big up the donut crew!
"it's not about the politics, it's about love of the music"
http://www.twitter.com/perkrecordings
http://www.facebook.com/perkrecordings
perk.recordings@gmail.com
"it's not about the politics, it's about love of the music"
http://www.twitter.com/perkrecordings
http://www.facebook.com/perkrecordings
perk.recordings@gmail.com
it's fun, but it takes a toll on the midsectionperkalerk215 wrote:and im with you festa about the getting hammered on tuesday nights...or wednesdays or thursdays....
my roomie brought home a bottle of absolut for me last night and I was fighting temptation to crack that badbwoy all night.
but I managed to ward off the demons of drink.
gotta get fit so I can find me a weekend hunny!
- step correct
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emcee child
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Every New year i take 6 weeks off from drinking. it only takes 6 weeks for your liver to fully regenerate itself.Step Correct wrote:Dittounklefesta wrote:
I am trying to drink less (but it's so much fun to get smashed on tuesday night)
Can you imagine what our livers already look like? Better quit while we still can.
Grime City, Narco.Hz
Myspace nonsense
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- step correct
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- step correct
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The liver has a remarkable capacity to regenerate after injury and to adjust its size to match its host. Within a week after partial hepatectomy, which, in typical experimental settings entails surgical removal of two-thirds of the liver, hepatic mass is back essentially to what it was prior to surgery. Some additional interesting observations include:
In the few cases where baboon livers have been transplanted into people, they quickly grow to the size of a human liver.
When the liver from a large dog is transplanted into a small dog, it loses mass until it reaches the size appropriate for a small dog.
Hepatocytes or fragments of liver transplanted in extrahepatic locations remain quiescent but begin to proliferate after partial hepatectomy of the host.
These types of observations have prompted considerable research into the mechanisms responsible for hepatic regeneration, because understanding the processes involved will likely assist in treatment of a variety of serious liver diseases and may have important implications for certain types of gene therapy. A majority of this research has been conducted using rats and utilized the model of partial hepatectomy, but a substantial body of confirmatory evidence has accumulated from human subjects.
The Dynamics of Liver Regeneration
Partial hepatectomy leads to proliferation of all populations of cells within the liver, including hepatocytes, biliary epithelial cells and endothelial cells. DNA synthesis is initiated in these cells within 10 to 12 hours after surgery and essentially ceases in about 3 days. Cellular proliferation begins in the periportal region (i.e. around the portal triads) and proceeds toward the centers of lobules. Proliferating hepatocytes initially form clumps, and clumps are soon transformed into classical plates. Similarly, proliferating endothelial cells develop into the type of fenestrated cells typical of those seen in sinusoids.
It appears that hepatocytes have a practically unlimited capacity for proliferation, with full regeneration observed after as many as 12 sequential partial hepatectomies. Clearly the hepatocyte is not a terminally differentiated cell.
Changes in gene expression associated with regeneration are observed within minutes of hepatic resection. An array of transcription factors (NF-kB, STAT3, fos and jun) are rapidly induced and probably participate in orchestrating expression of a group of hepatic mitogens. Proliferating hepatocytes appear to at least partially revert to a fetal phenotype and express markers such as alpha-fetoprotein. Despite what appears to be a massive commitment to proliferation, the regenerating hepatocytes continue to conduct their normal metabolic duties for the host such as support of glucose metabolism.
Stimuli of Hepatic Regeneration
Hepatic regeneration is triggered by the appearance of circulating mitogenic factors. This conclusion was originally supported by experiments demonstrating that quiescent fragments of liver that had been transplanted to extrahepatic sites would begin to proliferate soon after partial hepatectomy, and also that hepatectomy in one of a pair of parabiotic rats led to hepatic proliferation in the other of the pair.
As might be expected, liver regeneration seems to be supported by a group of mitogens and growth factors acting in concert on several cell types. Some of the major and well-studied players that act together in this process include:
Hepatocyte growth factor (scatter factor) levels rise to high levels soon after partial hepatectomy. This is the only factor tested that acts by itself as a potent mitogen for isolated hepatocytes cultured in vitro. This factor is also of critical importance in development of the liver, as target deletions of its gene lead to fetal death due to hepatic insufficiency.
TNF-alpha, which stimulates proliferation of hepatic endothelial cells.
Interleukin-6, which acts as a biliary epithelial mitogen.
Epidermal growth factor.
Norepinephrine potentiates the mitogenic activity of EGF and HGF.
Insulin is required for regeneration but appears to play a permissive rather than mitogenic role.
The processes and signals involved in shutting down the regenerative response are less well studied than those that stimulate it. TGF-beta1, which is known to inhibit proliferative responses in hepatocytes, is one cytokine involved in this process, but undoubtedly several others participate.
References and Reviews
Michalopoulos GK, DeFrances MC: Liver regeneration. Science 276:60, 1997.
In the few cases where baboon livers have been transplanted into people, they quickly grow to the size of a human liver.
When the liver from a large dog is transplanted into a small dog, it loses mass until it reaches the size appropriate for a small dog.
Hepatocytes or fragments of liver transplanted in extrahepatic locations remain quiescent but begin to proliferate after partial hepatectomy of the host.
These types of observations have prompted considerable research into the mechanisms responsible for hepatic regeneration, because understanding the processes involved will likely assist in treatment of a variety of serious liver diseases and may have important implications for certain types of gene therapy. A majority of this research has been conducted using rats and utilized the model of partial hepatectomy, but a substantial body of confirmatory evidence has accumulated from human subjects.
The Dynamics of Liver Regeneration
Partial hepatectomy leads to proliferation of all populations of cells within the liver, including hepatocytes, biliary epithelial cells and endothelial cells. DNA synthesis is initiated in these cells within 10 to 12 hours after surgery and essentially ceases in about 3 days. Cellular proliferation begins in the periportal region (i.e. around the portal triads) and proceeds toward the centers of lobules. Proliferating hepatocytes initially form clumps, and clumps are soon transformed into classical plates. Similarly, proliferating endothelial cells develop into the type of fenestrated cells typical of those seen in sinusoids.
It appears that hepatocytes have a practically unlimited capacity for proliferation, with full regeneration observed after as many as 12 sequential partial hepatectomies. Clearly the hepatocyte is not a terminally differentiated cell.
Changes in gene expression associated with regeneration are observed within minutes of hepatic resection. An array of transcription factors (NF-kB, STAT3, fos and jun) are rapidly induced and probably participate in orchestrating expression of a group of hepatic mitogens. Proliferating hepatocytes appear to at least partially revert to a fetal phenotype and express markers such as alpha-fetoprotein. Despite what appears to be a massive commitment to proliferation, the regenerating hepatocytes continue to conduct their normal metabolic duties for the host such as support of glucose metabolism.
Stimuli of Hepatic Regeneration
Hepatic regeneration is triggered by the appearance of circulating mitogenic factors. This conclusion was originally supported by experiments demonstrating that quiescent fragments of liver that had been transplanted to extrahepatic sites would begin to proliferate soon after partial hepatectomy, and also that hepatectomy in one of a pair of parabiotic rats led to hepatic proliferation in the other of the pair.
As might be expected, liver regeneration seems to be supported by a group of mitogens and growth factors acting in concert on several cell types. Some of the major and well-studied players that act together in this process include:
Hepatocyte growth factor (scatter factor) levels rise to high levels soon after partial hepatectomy. This is the only factor tested that acts by itself as a potent mitogen for isolated hepatocytes cultured in vitro. This factor is also of critical importance in development of the liver, as target deletions of its gene lead to fetal death due to hepatic insufficiency.
TNF-alpha, which stimulates proliferation of hepatic endothelial cells.
Interleukin-6, which acts as a biliary epithelial mitogen.
Epidermal growth factor.
Norepinephrine potentiates the mitogenic activity of EGF and HGF.
Insulin is required for regeneration but appears to play a permissive rather than mitogenic role.
The processes and signals involved in shutting down the regenerative response are less well studied than those that stimulate it. TGF-beta1, which is known to inhibit proliferative responses in hepatocytes, is one cytokine involved in this process, but undoubtedly several others participate.
References and Reviews
Michalopoulos GK, DeFrances MC: Liver regeneration. Science 276:60, 1997.
- step correct
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- perkalerk215
- Posts: 2422
- Joined: Fri Jul 27, 2007 4:07 am
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i wouldnt be too nice of a person if i stopped drinking for 6 whole weeks....i dont drink ALL the time. but i have been a lot more often. i just try to eat as healthy as i can to balance it out. and exercise.
big up the donut crew!
"it's not about the politics, it's about love of the music"
http://www.twitter.com/perkrecordings
http://www.facebook.com/perkrecordings
perk.recordings@gmail.com
"it's not about the politics, it's about love of the music"
http://www.twitter.com/perkrecordings
http://www.facebook.com/perkrecordings
perk.recordings@gmail.com
- step correct
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le_hardcore_chiefus
- Posts: 1632
- Joined: Wed Feb 07, 2007 5:55 pm
- Location: ellesmere port
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le_hardcore_chiefus
- Posts: 1632
- Joined: Wed Feb 07, 2007 5:55 pm
- Location: ellesmere port
aye it unklefesta..made up with me bike, though i aint rode it yet, its that actual 1, looks very sexy i think.....mum n step dad bought it 4 me, just b4 they purchassed a £14,000 or somet honda, thus now my brother not getting anything near as expensive lol
cant wait fo summer grand ...should be er....grand!
cant wait fo summer grand ...should be er....grand!
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le_hardcore_chiefus
- Posts: 1632
- Joined: Wed Feb 07, 2007 5:55 pm
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