Lily Allen abashed herself by flashing her breasts to photographers this past weekend, but denies her actions were a publicity stunt.
Ranting on her MySpace blog, the LDN singer explains: "I wore a loose fitting T-shirt. It was very red-hot in London and it's no secret I don't like wearing bras.
"My boob fell out doubly and people on the blogs are saying it was a publicity stunt.
"Can I just say, I have been keeping myself very much to myself recently. I've been gardening, decorating my new flat and looking at after my grieving grandfather.
"If I precious publicity, I'd be accepting invitations, non to reference money, for turning up to glamorous events."
Should Lily force herself to bear bras? See support-free photos here and judge for yourself.
Tuesday, 12 August 2008
Lily Allen: 'My Boob Flash Was Not Publicity Stunt'
...more Lily Allen �
Wednesday, 6 August 2008
Kim Mitchell
Artist: Kim Mitchell
Genre(s):
Rock
Discography:
Shakin' Like a Human Being
Year: 2007
Tracks: 10
Ain't Life Amazing
Year: 2007
Tracks: 11
Kimosabe
Year: 2000
Tracks: 10
Itch
Year: 1998
Tracks: 11
Born in 1952 in Ontario, Canada, Kim Mitchell formed the dance banding Max Webster in 1973. After rending from the mathematical
Brideshead Revisited
First promulgated just as World War II was ending, Evelyn Waugh�s weighty literary masterpiece was turned into a wildly successful British mini-series in 1981. For some strange reason, however, Brideshead Revisited has never been given a motion picture adaptation--until today. Although the story essentially remains the same, much of plot threads have been dropped or truncate and some liberty has been taken with at least unitary major character. Set in the pre-World War II era, this romantic story spans a couple of decades notification the saga of atheist Charles Ryder (Matthew Goode) and his fascination, even obsession, with the very regal and very catholic Marchmain family--now led by ultra-stiff matriarch Lady Marchmain (Emma Thompson), whose husband (Michael Gambon) is AWOL with his Italian schoolma'am (Greta Scacchi). Centering about his �friendship� with the charming and adventurous son, Sebastian (Ben Whishaw), Charles� affections and apparent sexual confusion discover new cannon fodder with Sebastian�s beautiful baby Julia (Hayley Atwell). When the terzetto take off for Venice to call patriarch Lord Marchmain, the romance 'tween Charles and Julia takes off causation numerous complications for everyone involved.Rising star Goode, so fine in Woody Allen�s Match Point, meets his promise hither making the ideal Charles, a brigham Young man dalliance with his own sexual and religious identity in the fallow period 'tween World Wars. His good luck charm quotient is so hard, it�s easy to see how he could appeal both Sebastian and Julia, equally well-played by Whishaw and Atwell. Whishaw (I'm Not There) nails the unwarranted side of his character, taking Sebastian much further into merry territory than suggested in either the book or the mini-series. Atwell�s Julia also takes a going from previous versions, specially when she joins the guys in Venice--a plot turn entirely invented for this film adaptation. It has the effect of increasing the tension, sexual and otherwise, between the three primary characters and allows the film to fully focus on this aspect of Waugh�s original story. Atwell is a real find wHO fully explores the disordered but charmed journey Julia must necessitate. Sprightly two-time Oscar winner Thompson is at first glance an odd choice to play the rigid Lady Marchmain but she proves her worth, giving the woman an duplicate dimension of humanity she doesn�t appear to have when we first forgather her. Gambon is superb as the family�s anxious patriarch with fine support from the still-beautiful Scacchi as his mistress.Young British director Julian Jarrold followed his feature of speech debut, the refreshing upbeat comedy Kinky Boots with last summer�s vapid and drilling Jane Austen period composition Becoming Jane. With the hot-blooded Brideshead adjustment, he is on his game over again, clearly demonstrating complete control over the sprawling account and intertwined relationships that are key to Waugh�s novel. Choosing to focus on the central triangle of Sebastian, Charles and Julia more fully than ever earlier is a wise decision and brings the interview right in to the thick of things, instead than taking the many side trips of the mini-series. Of course, with only deuce hours alternatively of 12, painful decisions had to be made, and Jarrold, with screenwriters Andrew Davies and Jeremy Brock, have delivered a version that meets our expectations, without dashing them. Unless, of course, you are a Waugh purist in which case it�s probably best to revisit the mini-series. There crapper be no argument about the ocular splendors provided here though, particularly the location filming at Castle Howard, 1 of England�s oldest and most hitting estates. Waugh�s extensive descriptions of the splendors of Brideshead Manor are perfectly realized through the spot-on choice of locales and the film�s superb motion-picture photography and product design.
See Also
See Also
Turned-off Cannabinoid Receptor Turns On Colorectal Tumor Growth - CB1 Suppresses Tumors, A New Potential Path For Treatment, Prevention
�New preclinical research shows that cannabinoid cell surface receptor CB1 plays a tumor-suppressing role in human colorectal cancer, scientists report in the Aug. 1 edition of the journal Cancer Research.
CB1 is well-established for relieving pain and nausea, elevating mood and stimulating appetite by serving as a docking station for the cannabinoid group of signaling molecules. It now may serve as a new path for cancer prevention or treatment.
"We've found that CB1 expression is lost in most colorectal cancers, and when that happens a cancer-promoting protein is free to inhibit cell death," said senior author Raymond DuBois, M.D., Ph.D., provost and executive vice president of The University of Texas M. D. Anderson Cancer Center.
DuBois and collaborators from Vanderbilt-Ingram Cancer Center also show that CB1 expression can be restored with an existing drug, decitabine. They found that mice prone to developing intestinal tumors that also have functioning CB1 receptors develop fewer and smaller tumors when treated with a drug that mimics a cannabinoid receptor ligand. Ligands are molecules that function by binding to specific receptors. Agonists are synthetic molecules that mimic the action of a natural molecule.
"Potential application of cannabinoids as anti-tumor drugs is an exciting prospect, because cannabinoid agonists are being evaluated now to treat the side-effects of chemotherapy and radiation therapy," DuBois said. "Turning CB1 back on and then treating with a cannabinoid agonist could provide a new approach to colorectal cancer treatment or prevention."
Cannabinoids are a group of ligands that serve a variety of cell-signaling roles. Some are produced by the body internally (endocannabinoids). External cannabinoids include manmade versions and those present in plants, most famously the active ingredient in marijuana (THC).
Receptor shutdown by methylation
Endocannabinoid signaling is important to the normal functioning of the digestive system and has been shown to protect the colon against inflammation. Since chronic inflammation is a known risk factor for colorectal cancer, the researchers decided to look into the role of cannabinoid receptors in a mouse model of colon cancer.
"People have looked at cannabinoids in cancer earlier, mainly in cell culture experiments," DuBois said. "The molecular mechanisms for loss of the receptor and its effect on cancer have not been previously shown."
First, the team found that CB1 was largely absent in 18 of 19 human tumor specimens and in 9 of 10 colorectal cancer cell lines. Further experimentation showed that the gene that encodes the CB1 protein was not damaged, but shut down chemically by the attachment of methyl groups - a carbon atom surrounded by three hydrogen atoms - to the gene encoding CB1.
Treating cell lines with decitabine, a demethylating agent approved for some types of leukemia, removed the methyl groups, restoring gene expression in 7 of 8 cell lines and full expression of CB1 protein in three lines.
Next, the group found that deletion of the CB1 gene in a strain of mice that spontaneously develops precancerous polyps resulted in a 2.5-to-3.8-fold increase in the number of polyps and a 10-fold increase in the number of large growths, those most likely to develop into cancer.
Treating mice that had the CB1 receptor with an endocannabinoid agonist resulted in a decline in polyps ranging from 16.7 percent to 50 percent. The reduction was greater for larger polyps.
CB1 thwarts survivin, a protein that protects cancer
Cannabinoids previously had been shown to kill cancer cells in lab experiments by inducing apoptosis - programmed cell death. The team confirmed the role of CB1 in apoptosis, showing that tumor cells with high CB1 expression were sensitive to apoptosis when treated by a cannabinoid agonist. Cell lines with silenced CB1 resisted cell death.
A series of experiments showed that CB1 increases cancer cell death by stifling a protein called survivin. Survivin is overexpressed in nearly every human tumor but is barely detectable in normal tissue, DuBois noted. Overexpression of survivin is associated with poor outcome and reduced apoptosis in colorectal cancer patients. The researchers pinpointed a cell signaling pathway by which activated CB1 cuts down survivin.
"Just increasing the levels of cannabinoids to treat colorectal cancer won't work if the CB1 receptor is not present," DuBois said. This suggests that treating first with a demethylating agent, such as decitabine, to reactivate CB1 in the tumor and following up with a cannabinoid might be an effective attack on colorectal cancer.
Scarcity of CB1 also is associated with Huntington's disease, Alzheimer's disease and multiple sclerosis. Further investigation, the researchers note, is needed to define its role in those diseases and other types of cancer. The team also analyzed the other main cannabinoid receptor, CB2, and found no role for it in colorectal cancer.
They also treated the mice with a CB1 antagonist, a compound that binds to the receptor but does not activate it. Mice with CB1 blocked in this manner also showed an increase in the number and size of polyps. A CB1 antagonist called rimonabant is currently marketed overseas for weight loss. The researchers note that a patient's risk for colorectal cancer should be assessed when use of such drugs is being considered.
The study was funded by grants from the National Cancer Institute and the National Colorectal Cancer Research Alliance.
"Loss of Cannabinoid Receptor 1 Accelerates Intestinal Tumor Growth"
Dingzhi Wang, Haibin Wang, Wei Ning, Michael G. Backlund, Sudhansu K. Dey and Raymond N. DuBois
Cancer Research 68, 6468-6476, August 1, 2008. doi: 10.1158/0008-5472.CAN-08-0896
Click here to view Abstract online
The University of Texas M. D. Anderson Cancer Center in Houston ranks as one of the world's most respected centers focused on cancer patient care, research, education and prevention. M. D. Anderson is one of only 39 Comprehensive Cancer Centers designated by the National Cancer Institute. For five of the past eight years, M. D. Anderson has ranked No. 1 in cancer care in "America's Best Hospitals," a survey published annually in U.S. News and World Report.
Source - Scott Merville
University of Texas M. D. Anderson Cancer Center
More info
CB1 is well-established for relieving pain and nausea, elevating mood and stimulating appetite by serving as a docking station for the cannabinoid group of signaling molecules. It now may serve as a new path for cancer prevention or treatment.
"We've found that CB1 expression is lost in most colorectal cancers, and when that happens a cancer-promoting protein is free to inhibit cell death," said senior author Raymond DuBois, M.D., Ph.D., provost and executive vice president of The University of Texas M. D. Anderson Cancer Center.
DuBois and collaborators from Vanderbilt-Ingram Cancer Center also show that CB1 expression can be restored with an existing drug, decitabine. They found that mice prone to developing intestinal tumors that also have functioning CB1 receptors develop fewer and smaller tumors when treated with a drug that mimics a cannabinoid receptor ligand. Ligands are molecules that function by binding to specific receptors. Agonists are synthetic molecules that mimic the action of a natural molecule.
"Potential application of cannabinoids as anti-tumor drugs is an exciting prospect, because cannabinoid agonists are being evaluated now to treat the side-effects of chemotherapy and radiation therapy," DuBois said. "Turning CB1 back on and then treating with a cannabinoid agonist could provide a new approach to colorectal cancer treatment or prevention."
Cannabinoids are a group of ligands that serve a variety of cell-signaling roles. Some are produced by the body internally (endocannabinoids). External cannabinoids include manmade versions and those present in plants, most famously the active ingredient in marijuana (THC).
Receptor shutdown by methylation
Endocannabinoid signaling is important to the normal functioning of the digestive system and has been shown to protect the colon against inflammation. Since chronic inflammation is a known risk factor for colorectal cancer, the researchers decided to look into the role of cannabinoid receptors in a mouse model of colon cancer.
"People have looked at cannabinoids in cancer earlier, mainly in cell culture experiments," DuBois said. "The molecular mechanisms for loss of the receptor and its effect on cancer have not been previously shown."
First, the team found that CB1 was largely absent in 18 of 19 human tumor specimens and in 9 of 10 colorectal cancer cell lines. Further experimentation showed that the gene that encodes the CB1 protein was not damaged, but shut down chemically by the attachment of methyl groups - a carbon atom surrounded by three hydrogen atoms - to the gene encoding CB1.
Treating cell lines with decitabine, a demethylating agent approved for some types of leukemia, removed the methyl groups, restoring gene expression in 7 of 8 cell lines and full expression of CB1 protein in three lines.
Next, the group found that deletion of the CB1 gene in a strain of mice that spontaneously develops precancerous polyps resulted in a 2.5-to-3.8-fold increase in the number of polyps and a 10-fold increase in the number of large growths, those most likely to develop into cancer.
Treating mice that had the CB1 receptor with an endocannabinoid agonist resulted in a decline in polyps ranging from 16.7 percent to 50 percent. The reduction was greater for larger polyps.
CB1 thwarts survivin, a protein that protects cancer
Cannabinoids previously had been shown to kill cancer cells in lab experiments by inducing apoptosis - programmed cell death. The team confirmed the role of CB1 in apoptosis, showing that tumor cells with high CB1 expression were sensitive to apoptosis when treated by a cannabinoid agonist. Cell lines with silenced CB1 resisted cell death.
A series of experiments showed that CB1 increases cancer cell death by stifling a protein called survivin. Survivin is overexpressed in nearly every human tumor but is barely detectable in normal tissue, DuBois noted. Overexpression of survivin is associated with poor outcome and reduced apoptosis in colorectal cancer patients. The researchers pinpointed a cell signaling pathway by which activated CB1 cuts down survivin.
"Just increasing the levels of cannabinoids to treat colorectal cancer won't work if the CB1 receptor is not present," DuBois said. This suggests that treating first with a demethylating agent, such as decitabine, to reactivate CB1 in the tumor and following up with a cannabinoid might be an effective attack on colorectal cancer.
Scarcity of CB1 also is associated with Huntington's disease, Alzheimer's disease and multiple sclerosis. Further investigation, the researchers note, is needed to define its role in those diseases and other types of cancer. The team also analyzed the other main cannabinoid receptor, CB2, and found no role for it in colorectal cancer.
They also treated the mice with a CB1 antagonist, a compound that binds to the receptor but does not activate it. Mice with CB1 blocked in this manner also showed an increase in the number and size of polyps. A CB1 antagonist called rimonabant is currently marketed overseas for weight loss. The researchers note that a patient's risk for colorectal cancer should be assessed when use of such drugs is being considered.
The study was funded by grants from the National Cancer Institute and the National Colorectal Cancer Research Alliance.
"Loss of Cannabinoid Receptor 1 Accelerates Intestinal Tumor Growth"
Dingzhi Wang, Haibin Wang, Wei Ning, Michael G. Backlund, Sudhansu K. Dey and Raymond N. DuBois
Cancer Research 68, 6468-6476, August 1, 2008. doi: 10.1158/0008-5472.CAN-08-0896
Click here to view Abstract online
The University of Texas M. D. Anderson Cancer Center in Houston ranks as one of the world's most respected centers focused on cancer patient care, research, education and prevention. M. D. Anderson is one of only 39 Comprehensive Cancer Centers designated by the National Cancer Institute. For five of the past eight years, M. D. Anderson has ranked No. 1 in cancer care in "America's Best Hospitals," a survey published annually in U.S. News and World Report.
Source - Scott Merville
University of Texas M. D. Anderson Cancer Center
More info
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