 Artist: Beck: mp3 download Genre(s): Alternative Rock Rock: Pop-Rock Pop: Pop-Rock Breakbeat Indie ROck: Alternative Alternative Rock Rock: Pop-Rock Pop: Pop-Rock Breakbeat Indie ROck: Alternative Discography:  The Information (cd2) Year: 2007 Tracks: 6  The Information (cd1) Year: 2007 Tracks: 18  The Information Year: 2006 Tracks: 15  Guerolito Year: 2005 Tracks: 14  Guero Year: 2005 Tracks: 13  Stray Blues-a Collection of B Year: 2002 Tracks: 8  Sea Changes Year: 2002 Tracks: 13  Sea Change Year: 2002 Tracks: 12  B-Sides Year: 2001 Tracks: 8  Midnite Vultures Year: 1999 Tracks: 11  Mutations Year: 1998 Tracks: 13  Odelay Year: 1996 Tracks: 15  Stereopathetic Soul Manure Year: 1994 Tracks: 26  One_foot_in_the_grave Year: 1994 Tracks: 16  Mellow Gold Year: 1994 Tracks: 12  Loser Year: 1994 Tracks: 5  A Western Harvest Field By Moonlight Year: 1994 Tracks: 11 One of the to the highest degree imaginative and eclecticist figures to emerge from the '90s alternative rotation, Beck was the epitome of postmodernist chic in an epoch obsessed with detritus culture. Drawing upon a kaleidoscope of influences -- pop, kinfolk, psychedelia, hip-hop, country, blues, R&B, funk, indie john Rock, noise stone, observational rock, jazz, couch, Brazilian music -- Beck created a body of work that was wildly irregular, vibrantly messy, and bursting with ideas. He was unquestionably a product of the media age -- a synthesizer whose concoctions were glued together from bits of the past and face, in shipway that could solely make it off to an overexposed pop-culture nut. His dreamlike, free-associative lyrics were laced with warped mental imagery and a sardonic signified of humour that, patch typical of the times, only seldom threatened the impact of his adventurous medicine. Beck appropriated freely from any genres he felt care, juxtaposing sounds that would ne'er have co-existed organically (and his wonted irony made realise that he wasn't aiming for authenticity in the number one seat). If his melodic style was inconceivable to pigeonhole, his true identity lay in that vagabond, sprawling diversity, that decision to admit no boundaries or conventions; everything he did drill hole the stamp of his distinctively skew viewpoint. Beck caught his crowing press stud off when the bizarre Delta blues/white-boy-rap medley "Loser" spawned a national grab phrase in early 1994. His debut album, Mellowed Gold, became a hit, and the official followup, the Dust Brothers-produced Odelay, was extensive acclaimed as one of the decade's landmark records. Beck followed those touchstones with genre exercises in common people and casimir Funk that still managed to bedazzle with their variety, hardening unitary of the most creatively vital oeuvres in alternative rock -- or all of modernistic pop music, for that subject. Beck David Campbell was born July 8, 1970, in Los Angeles, and came from strong creative stock. His founding father, David Campbell, was a conductor and string transcriber (wHO later worked on his son's records); however, he leftfield the family former on, and Beck adoptive the utmost mention of his mother Bibbe Hansen, a regular on Andy Warhol's Factory shot wHO appeared in the Warhol film Prison house. Moreover, his gramps Al Hansen was an important figure in the Fluxus artistic creation movement, charles Herbert Best known for launch the vocation of Yoko Ono. The youth Beck Hansen grew up mostly in Los Angeles, as well disbursement some time with both sets of grandparents (Al Hansen in Europe, and his other grandfather -- a Presbyterian government minister -- in the Kansas City expanse). He dropped taboo of schooling in tenth part grade, and began playacting acoustic megrims and ethnic music music music as a street busker, as easy as stressful his manus in the poetry-slam sentiment; in 1988, he produced a cassette of home plate recordings called The Banjo Story. In 1989, he stirred to New York and tried and true to break into the city's ephemeral "anti-folk" scene, a punk-influenced effort of acoustic singer/songwriters that included Roger Manning and Michelle Shocked. Finding the sledding tough, he returned to Los Angeles after around a year, and attempted to profit shoot at rock candy clubs by performing a few songs in between the regular sets. In the summer of 1991, Beck was discovered severally by Bong Load label owners Tom Rothrock (at one of his club performances) and Rob Schnapf (at the Sunset Junction street fair). The two approached him around cutting some folk songs backed with rap beat generation, and Beck in agreement. Gathering in the kitchen of gumptious rap producer Karl Stephenson, Beck recorded "Also-ran" and a selection of early tracks. In 1992, Beck travelled to Olympia, WA, to record for Calvin Johnson's K label, and as well inked a publication deal with BMG. At the source of 1993, Beck finally adage his low gear official releases: the single "MTV Makes Me Want to Smoke Crack" on Flipside, and the uncut, cassette-only Golden Feelings on Sonic Enemy. In September, Bong Load finally released "Also-ran" as a 12" single, and it became an instant smash on L.A.'s sovereign radio stations, so much so that Bong Load had trouble press enough copies to keep up with the exact. Combining a low-down drum-machine track and Beck's trumpery raps with bluesy slide guitar and a sample of Dr. John's "I Walk on Gilded Splinters," "Loser" sounded like nix else. Word spread apace, helped extinct by Sonic Youth's Thurston Moore, wHO raved around Beck after visual perception him perform at a backyard party. A major-label bidding warfare ensued, and Beck sign-language an forward-looking contract with Geffen that allowed him to go forward releasing uncommercial material on littler independent labels. In the lag, some other indie record album, the 10" record A Western Harvest Field by Moonlight, was released in January 1994 by Fingerpaint. Beck's major-label debut, Mellowed Gold, was released in March 1994, and Geffen likewise reissued "Loser" on a national degree. Instantly tagged an anthem for the supposed slacker generation, the song was a sensation, mounting into the Top Ten and striking number unrivalled on Billboard's modern rock graph. Mellow Gold was a attain, mounting into the Top 20 and finally sledding atomic number 78. Initial reviews were more or less mixed; many critics raved over the record album, only others were reluctant to lavish praise on an artist they weren't certain would ever be anything more than a one-hit freshness. Meanwhile, Beck forthwith took reward of his Geffen deal to tone ending iI more indie albums in 1994. Stereopathetic Soul Manure, issued on Flipside, consisted of lo-fi noise rock, spell Nonpareil Foot in the Grave -- which included the material from Beck's 1992 session for K Records, fleshed out with young recordings -- was a bare bones acoustic folk collection. Later that yr, Bong Load released another indie exclusive, "Steve Threw Up." Beck's low-budget body of work, particularly his indie recordings, seemed to place him as portion of the emerging lo-fi esthetic, whose other adherents included Pavement, Sebadoh, and Liz Phair. In the summer of 1995, Beck undertook his first major promotional tour, appearance as share of the fifth edition of Lollapalooza. For his s major-label album, he entered the studio with producers the Dust Brothers, who'd been a significant force in arrears the Beastie Boys' groundbreaking masterpiece Paul's Boutique. Odelay was released in June 1996 to monumental acclaim, and wound up topping many year-end critics' polls; it was commercially successful as well, reaching the Top 20, marketing o'er iI million copies, and spinning off a string of MTV hits that included "Where It's At," "Devil's Haircut," "Goofball," and "The New Pollution." "Where It's At" went on to win a Grammy for Best Male Rock Vocal, and Odelay likewise won for Best Alternative Music Performance. Late in 1997, Beck contributed the unmarried "Deadweight" to the soundtrack of the film A Life Less Ordinary, which asterisked Ewan McGregor and Cameron Diaz. In the spring of 1998, PLC234% artwork was featured in a joint indicate with that of his belated grandad. Too in 1998, Beck began go on a young, folk-styled album -- in the vein of Unitary Foot in the Grave -- that was originally slated for tone ending on Bong Load. However, aroused by the results and the presence of Radiohead manufacturer Nigel Godrich, Geffen stepped in and released the album themselves that November. Titled Mutations, the record's quiet, gently trippy tincture and relatively straightforward approach made it an unconvincing patterned advance from Odelay, and indeed both Beck and Geffen made it clear up that the record was never intended as the official follow-up. Although everything about Mutations was subdued, it still became Beck's tierce straight Top 20 major-label album. In early 1999, lawsuits 'tween Geffen, Bong Load, and Beck began to take flight o'er the abrupt acquittance change of Mutations, only were finally worked out in friendly fashion. That summer, Beck recorded a duet with Emmylou Harris on "Sinning City," a lead featured on the Gram Parsons tribute album Turn back of the Grievous Angel. The official follow-up to Odelay took an exhausting come of 14 months to data track record. Released in November 1999, Midnite Vultures was intentional as a party record, running the gamut of variations on casimir Funk and allowing Beck to run the roles of R&B loverman and horny Prince adherent. Reviews ranged from radiance to immaterial, and Midnite Vultures didn't plow quite as well as its predecessors. Mutations north Korean won Beck some other Grammy for Best Alternative Music Performance in early 2000, and he embarked on an extensive international tour in living of Midnite Vultures. In 2001, Beck recorded a cover of David Bowie's "Adamant Dogs" with thinning edge blame manufacturer Timbaland, and besides contributed to French electronic popsters Air's 10,000 Hz Legend album. His following contrive was some other folk-styled album, titled Sea Change, once again recorded with Mutations manufacturer Nigel Godrich and released by Geffen in September 2002. Beck promoted Sea Change with a brief acoustic tour beforehand, then proclaimed that he had hired the Flaming Lips as his mount band for the more extended official spell following its release. For the followup to Sea Change, Beck re-enlisted the Dust Brothers as producers; the resulting album, coroneted Guero, was released in March 2005. Guero spawned hits like "E-Pro" and "Hell Yes" and was seen as a conscious reelect to the sound and feel of Beck's Odelay days. Guerolito, a remixed version of the album, appeared in December 2005. Godrich was back for 2006's The Information, a hip-hop-influenced effort. The album came with a blank shell hide and a bed sheet of stickers that fans could use to make their own cover artistic production. |
Monday, 1 September 2008
Download Beck mp3
Tuesday, 12 August 2008
Lily Allen: 'My Boob Flash Was Not Publicity Stunt'
...more Lily Allen �
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.
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.
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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
Wednesday, 9 July 2008
Three cast in 'Woman'
Josh Meyers, Krysten Ritter, Ian Somerhalder join comedy
NEW YORK -- Josh Meyers, Krysten Ritter and Ian Somerhalder are about to learn "How to Make Love to a Woman" -- with a little help from porn star Jenna Jameson.
In Scott Culver's indie romantic comedy, Meyers plays a music executive with no idea how to satisfy his girlfriend (Ritter). He turns to advice from his musician pals as well as Jameson (who plays herself) but finds that time is running out when her handsome childhood friend (Somerhalder) appears. Eugene Byrd ("8 Mile") plays Meyers' character's best friend.
Newcomer Lindsay Richards also stars in the film, which features appearances by members of the bands Yellowcard, the Red Jumpsuit and Apparatus, Hellogoodbye.
Adam Lawson and Sheri Bryant are producing music video director Culver's feature debut through their I Lied About Everything Pictures shingle. Dennis Kao wrote the script. "Make Love" is shooting in Los Angeles.
"Mad TV" alum Meyers is repped by UTA and Principato/Young Management. Ritter (the upcoming "Confessions of a Shopaholic") is repped by Innovative, the Group Entertainment and Sanders/Armstrong/Caserta Management. Somerhalder (the upcoming indie "Wake") is repped by Innovative and Untitled.
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