February 1, 2007
"You'll love it. They are both real petit and design all their clothes for smaller framed girls..." said Jessica Kay, close friend to the designer duo, as she shopped in Steve Madden on Walnut St. last Friday afternoon adorning her friends' designs of dozens of gold chains on her neck.
Drexel University COMAD graduates, Abby Kessler, 26 and Katie Loftus, 25 are the proud owners of the trendy boutique, Smak Parlour in Olde City.
Located at 219 Market Street, this quaint shop with an urban outfitters (http://www.urbanoutfitters.com/) meets Betsey Johnson (http://www.betseyjohnson.com) vibe, is 100 percent girl.
From the pink decorations, walls and flowers, to the vintage glam chandeliers and dozens and dozens of customized furniture inside, the shop could not be decorated to better stand for their brand.
Tanks and tee-shirts emphasizing prissy details, metal chains, pendants, vintage inspired jackets and accessories are this boutiques specialties and are made in their workplace behind the front of the store.
As adorable as the pair who run this hidden secret in Philadelphia's Olde City district, the shop has continued to thrive for over a year now.
http://profile.myspace.com/index.cfm?fuseaction=user.viewprofile&friendid=63938181
Smak Parlour
219 Market Street
Philadelphia, PA 19106
215.625.4551
www.smakparlour.com
Wednesday, January 31, 2007
Monday, January 29, 2007
Online Article Evaluation
Jennifer Kramer
On-line News Source
Com 300
January 29, 2007
Progeria, a premature aging disease affecting an estimated one in four million to one in eight million live births is the subject of the online article, “Cellular Defects in Premature Aging Disease are Reversible. This same fatal, rare disease was the topic of Wall Street Journal’s front page article on Monday, January, 29, 2007 print edition, entitled, “With Just 42 Known Cases, A Precarious Clinical Trial - Fatal Condition Causes Heart Attacks in Children; Push from Sam’s parents by Amy Dockser Marcus.
The online article was published on website, www. scienceblog.com, a general science and technology news blog.
The online article explains the disease in detail. It points out when it occurs, how frequently, the physical symptoms, as well as average life expectancy for those affected with it.
The sources in the online article are extremely welll known, and well trusted medical organizations. Sources such as the National Cancer Institute (NCI) scientists, a part of the National Institutes of Health and Nature Medicine online article is referenced. The names of scientists involved in research studies are published and their findings are outlined showing much credibility to this article. The possiblity of a cancer drug to stop premature aging is included which interests readers especially those with children affected showing hope and a sense of security that one day this fatal disease might have a cure.
The Wall Street Journal published a more personal article on the disease with focus on Dr. Leslie Gore, a parent who's son is affected with progeria and her journey dealing with his diagnosis and how her family goes about their daily lives. Sources used are Francis Collins, director of the NIH's National Human Genome Research Institute and Mark Kieran, a pediatric oncologist at the Dana Farber Cancer Institute in Boston. The Progeria Research Foundation is almost publicized in the article but it does provide that knowledge for those wanting to get more involved and raise money and awareness, that the online articled does not even mention. The online article does not show families affected as the Wall Street Journal shows and does not have the same emotional draw one gains from reading about the constant struggle each child affected with progeria goes through.
If I were editor of scienceblog.com I would stress including a quote from a parent with a child afflicted with the disease and some photos as the Wall Street Journal has done to show a personal side of those affected and to increase awareness and instill a need for parents of newborns to watch for symptoms so the disease is diagnosed as early as possible.
The medical jargon is very well defined in this article but in my paper I might include less of it as my readers would probably be more of the general public and not scientists and might be scared of such big medical language such as “chemicall stable DNA nucleotide.”
In my paper, I would add less of the specifics fo the tests being done to associated cellular changes with progeria and briefly explain that testing is being done continuously by researchers at the Center for Cancer Research in Bethesda and that it is productive and being done by experienced, credible scientists.
I thought it was excellent at the end of the online article to include a link about where to turn for more information on progeria. I would definely put this in my paper and also include a local support group for children and parents associated with the disease and hospitals who specialize in treatment.
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Cellular Defects in Premature Aging Disease are Reversible
Mon, 2005-03-07 09:03 — BJS
Cells affected by Hutchinson-Gilford Progeria Syndrome (HGPS) -- a disease associated with premature aging -- can be made healthy again, according to findings by scientists at the National Cancer Institute (NCI), part of the National Institutes of Health (NIH). Using specially modified segments of DNA, NCI researchers Paola Scaffidi, PhD, and Tom Misteli, PhD, reversed the abnormalities seen in HGPS cells by correcting defects associated with the key protein, lamin A. By demonstrating that HGPS cellular characteristics are reversible, this study, appearing in Nature Medicine online on March 6, 2005*, brings scientists one step closer to understanding this devastating childhood disease and might provide insights into the normal aging process.
HGPS is a rare inherited disease affecting about one in eight million children. While appearing normal at birth, infants with HGPS age rapidly after their first 18 months, and physical symptoms include stunted growth, loss of hair and body fat, joint stiffness, osteoporosis, and heart problems. The condition is fatal, with heart disease being the leading killer, and affected children usually die before they reach their late teens.
Less than two years ago, NIH-led researchers discovered that the genetic basis for HGPS is a single mutation in the gene encoding lamin A. Lamin A is a critical structural protein that acts as the scaffolding which holds a cell's nucleus together. Lamin A is defective in HGPS cells because the mutation creates an aberrant splice site in the lamin A gene; the aberrant splicing, or joining the separate parts of the gene together, results in synthesis of a truncated lamin protein. Without lamin A holding them together, the nuclei of progeria cells become wrinkled and misshapen. In addition, numerous other nuclear proteins show reduced expression.
"Our NCI team at the Center for Cancer Research in Bethesda set out to ask whether these cellular changes associated with progeria are permanent or reversible," said Scaffidi. First, the investigators added DNA encoding normal lamin A into cells taken from patients affected with progeria, but observed that increased synthesis of normal lamin A did not correct any of the progeria-associated defects. In addition, they found that introduction of the mutant protein into healthy human cells was sufficient to produce the disease characteristics. "These results made it clear that in order to achieve a potential therapeutic effect, we needed to completely eliminate the mutant protein," said Scaffidi.
The NCI researchers designed a chemically stable DNA oligonucleotide — a short DNA sequence that the cell wouldn't be able to degrade — that would bind to the mutant splice site and prevent the splicing machinery from cutting in the wrong place. "You can think of it as a molecular Band-Aid®," said Misteli. The researchers inserted their oligonucleotides into the progeria cells and observed that after four days almost all the mutant lamin A transcripts had been eliminated and replaced with the properly spliced counterpart. The oligonucleotide was highly specific to the mutated region and did not cover-up other splicing locations. One week after correcting the splicing defect, the mutant lamin A protein had been eliminated and more than 90 percent of progeria cells were restored to normal; visually, the nuclei lost their wrinkles and lobes and returned to a natural ellipsoid shape, and the expression of other nuclear proteins was also restored to normal levels.
"It's amazing that we could take a cell that looked about ready to die, and a few days later it was healthy and ready to divide again," said Misteli.
Misteli noted that these results demonstrate a proof-of-principle that the cellular effects of progeria can be reversed, meaning his laboratory's method could be used some day in the future as a therapeutic strategy. The fact that a progeria reversal can be achieved in multiple cell types, and that the cells can return to normal, independent of cell division, bolsters this possibility. "Some tissues in our body do not divide," Misteli pointed out. "So demonstrating that we can rescue the normal phenotype without cell division means this procedure could be effective in all tissues." Misteli and his group will also look more closely at healthy cells to determine how similar progeria is to the normal aging process.
For more information about progeria, please visit the NHGRI Web site at http://www.genome.gov/11007255.
On-line News Source
Com 300
January 29, 2007
Progeria, a premature aging disease affecting an estimated one in four million to one in eight million live births is the subject of the online article, “Cellular Defects in Premature Aging Disease are Reversible. This same fatal, rare disease was the topic of Wall Street Journal’s front page article on Monday, January, 29, 2007 print edition, entitled, “With Just 42 Known Cases, A Precarious Clinical Trial - Fatal Condition Causes Heart Attacks in Children; Push from Sam’s parents by Amy Dockser Marcus.
The online article was published on website, www. scienceblog.com, a general science and technology news blog.
The online article explains the disease in detail. It points out when it occurs, how frequently, the physical symptoms, as well as average life expectancy for those affected with it.
The sources in the online article are extremely welll known, and well trusted medical organizations. Sources such as the National Cancer Institute (NCI) scientists, a part of the National Institutes of Health and Nature Medicine online article is referenced. The names of scientists involved in research studies are published and their findings are outlined showing much credibility to this article. The possiblity of a cancer drug to stop premature aging is included which interests readers especially those with children affected showing hope and a sense of security that one day this fatal disease might have a cure.
The Wall Street Journal published a more personal article on the disease with focus on Dr. Leslie Gore, a parent who's son is affected with progeria and her journey dealing with his diagnosis and how her family goes about their daily lives. Sources used are Francis Collins, director of the NIH's National Human Genome Research Institute and Mark Kieran, a pediatric oncologist at the Dana Farber Cancer Institute in Boston. The Progeria Research Foundation is almost publicized in the article but it does provide that knowledge for those wanting to get more involved and raise money and awareness, that the online articled does not even mention. The online article does not show families affected as the Wall Street Journal shows and does not have the same emotional draw one gains from reading about the constant struggle each child affected with progeria goes through.
If I were editor of scienceblog.com I would stress including a quote from a parent with a child afflicted with the disease and some photos as the Wall Street Journal has done to show a personal side of those affected and to increase awareness and instill a need for parents of newborns to watch for symptoms so the disease is diagnosed as early as possible.
The medical jargon is very well defined in this article but in my paper I might include less of it as my readers would probably be more of the general public and not scientists and might be scared of such big medical language such as “chemicall stable DNA nucleotide.”
In my paper, I would add less of the specifics fo the tests being done to associated cellular changes with progeria and briefly explain that testing is being done continuously by researchers at the Center for Cancer Research in Bethesda and that it is productive and being done by experienced, credible scientists.
I thought it was excellent at the end of the online article to include a link about where to turn for more information on progeria. I would definely put this in my paper and also include a local support group for children and parents associated with the disease and hospitals who specialize in treatment.
Archives
Navigation
about
contact
forums
reader blogs
register
science gifts
Home
Cellular Defects in Premature Aging Disease are Reversible
Mon, 2005-03-07 09:03 — BJS
Cells affected by Hutchinson-Gilford Progeria Syndrome (HGPS) -- a disease associated with premature aging -- can be made healthy again, according to findings by scientists at the National Cancer Institute (NCI), part of the National Institutes of Health (NIH). Using specially modified segments of DNA, NCI researchers Paola Scaffidi, PhD, and Tom Misteli, PhD, reversed the abnormalities seen in HGPS cells by correcting defects associated with the key protein, lamin A. By demonstrating that HGPS cellular characteristics are reversible, this study, appearing in Nature Medicine online on March 6, 2005*, brings scientists one step closer to understanding this devastating childhood disease and might provide insights into the normal aging process.
HGPS is a rare inherited disease affecting about one in eight million children. While appearing normal at birth, infants with HGPS age rapidly after their first 18 months, and physical symptoms include stunted growth, loss of hair and body fat, joint stiffness, osteoporosis, and heart problems. The condition is fatal, with heart disease being the leading killer, and affected children usually die before they reach their late teens.
Less than two years ago, NIH-led researchers discovered that the genetic basis for HGPS is a single mutation in the gene encoding lamin A. Lamin A is a critical structural protein that acts as the scaffolding which holds a cell's nucleus together. Lamin A is defective in HGPS cells because the mutation creates an aberrant splice site in the lamin A gene; the aberrant splicing, or joining the separate parts of the gene together, results in synthesis of a truncated lamin protein. Without lamin A holding them together, the nuclei of progeria cells become wrinkled and misshapen. In addition, numerous other nuclear proteins show reduced expression.
"Our NCI team at the Center for Cancer Research in Bethesda set out to ask whether these cellular changes associated with progeria are permanent or reversible," said Scaffidi. First, the investigators added DNA encoding normal lamin A into cells taken from patients affected with progeria, but observed that increased synthesis of normal lamin A did not correct any of the progeria-associated defects. In addition, they found that introduction of the mutant protein into healthy human cells was sufficient to produce the disease characteristics. "These results made it clear that in order to achieve a potential therapeutic effect, we needed to completely eliminate the mutant protein," said Scaffidi.
The NCI researchers designed a chemically stable DNA oligonucleotide — a short DNA sequence that the cell wouldn't be able to degrade — that would bind to the mutant splice site and prevent the splicing machinery from cutting in the wrong place. "You can think of it as a molecular Band-Aid®," said Misteli. The researchers inserted their oligonucleotides into the progeria cells and observed that after four days almost all the mutant lamin A transcripts had been eliminated and replaced with the properly spliced counterpart. The oligonucleotide was highly specific to the mutated region and did not cover-up other splicing locations. One week after correcting the splicing defect, the mutant lamin A protein had been eliminated and more than 90 percent of progeria cells were restored to normal; visually, the nuclei lost their wrinkles and lobes and returned to a natural ellipsoid shape, and the expression of other nuclear proteins was also restored to normal levels.
"It's amazing that we could take a cell that looked about ready to die, and a few days later it was healthy and ready to divide again," said Misteli.
Misteli noted that these results demonstrate a proof-of-principle that the cellular effects of progeria can be reversed, meaning his laboratory's method could be used some day in the future as a therapeutic strategy. The fact that a progeria reversal can be achieved in multiple cell types, and that the cells can return to normal, independent of cell division, bolsters this possibility. "Some tissues in our body do not divide," Misteli pointed out. "So demonstrating that we can rescue the normal phenotype without cell division means this procedure could be effective in all tissues." Misteli and his group will also look more closely at healthy cells to determine how similar progeria is to the normal aging process.
For more information about progeria, please visit the NHGRI Web site at http://www.genome.gov/11007255.
Tuesday, January 23, 2007
purpose of blog
The purpose of this blog is to inform the fashionably advanced about up and coming hip places to shop and spend that all too small paycheck us students receive on fashions you simply cannot live without.
Trendy new boutiques and hidden fashion treasures Philly has to offer will be explored in full on my blog and available to all
Trendy new boutiques and hidden fashion treasures Philly has to offer will be explored in full on my blog and available to all
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