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The information that you find below can not only help you to become an expert at home improvement, but may also help to increase the value of your home.

When you are painting your home, try to get no-VOC paints. Not only are they environmentally friendly, but they do not contain harmful chemicals that are in traditional paints. They are just as effective as regular paints are, and are priced just a bit higher than traditional paints.

Exterior window shutters are one the easiest and most cost-effective ways to improve your home?s appearance. If you have carpentry skills, it is very possible to make custom shutters that can be stained or painted to accent your home?s color. For the less handy, prefabricated wood, shutters are attainable at all home-improvement stores and come ready to paint or stain. Shutters are also available in lightweight, recycled plastic in a variety of colors that never need painting.

To properly stain your deck yourself, be sure that you use the proper tools to do so starting with the brushes you use to apply the stain. If you choose a oil based stain, a natural bristle brush is the way to go. When using a stain that is water based use a brush with nylon bristles.

If you have the money then you should try and add a master suite to your home. While having a nice large bedroom is great it will tremendously help during resale if the bedroom area includes a bathroom and/or a sitting area. The majority of buyers tend to lean toward homes that have master suites.

To improve your home, try re-framing your entry. Try replacing things like door knobs and locks on your main door. Try to locate a substantial handle-and-lock set that can be easily installed. Nice and sturdy pieces of hardware on the front door can help express that this is a solid home.

Improving your home yourself in anyway can be a fun, rewarding experience, but this can also be a disaster. Before starting any projects, make sure you research what you?re doing first. Getting halfway through any home improvement project only to find you?re doing something wrong is a nightmare waiting to happen.

Learning how to remove a sink trap is a valuable skill. It can help you remove anything that has been dropped down the drain which is not an uncommon occurrence. If you do drop something down the drain don?t run water in it until you can remove the trap.

Doing a renovation to the home?s entrance can really add value to your home. As far as curb appeal goes, the entrance to your home plays a critical part in actually getting buyers through the door and gives them the first impression overall of the home when entering. Do not neglect this area of home improvement.

Home improvement can be very rewarding, but it can also be a lot of work. Regardless, if you know what to do and how to properly and safely improve your home, you can create the house of your dreams. So, do yourself a favor by doing your research and applying the above tips to your home improvement.

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Source: http://dominbenito.com/2012/03/27/this-central-constructer-pte-ltd-crank-definitely-makes-the-whole-central-constructer-pte-ltd-way-of-thinking-so-exciting/

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Protein 'jailbreak' helps breast cancer cells live

[ Back to EurekAlert! ] Public release date: 28-Mar-2012
[ | E-mail | Share Share ]

Contact: David Orenstein
david_orenstein@brown.edu
401-863-1862
Brown University

PROVIDENCE, R.I. [Brown University] If the fight against breast cancer were a criminal investigation, then the proteins survivin, HDAC6, CBP, and CRM1 would be among the shadier figures. In that vein, a study to be published in the March 30 Journal of Biological Chemistry is the police report that reveals a key moment for keeping cancer cells alive: survivin's jailbreak from the nucleus, aided and abetted by the other proteins. The research highlights that a protein's location in a cell affects its impact on disease, and offers clear new leads for the investigation.

All four proteins were already under suspicion. Researchers, for example, have already tried to assess what levels of HDAC6 in patients with estrogen-receptor positive breast cancer may mean for their prognosis. The results have been inconclusive. The new research suggests that measuring overall levels may not be enough, said the study's senior author Dr. Rachel Altura, associate professor of pediatrics in The Warren Alpert Medical School of Brown University and a pediatric oncologist at Hasbro Children's Hospital.

"We need to look not only at the levels, but also where is it in the cell," she said.

Altura's emphasis on location comes from what her research team found as they tracked and tweaked the comings and goings of survivin in cells. Inside the nucleus, survivin is no problem. Outside the nucleus, but within the cell, it can prevent normal cell death, allowing cancer cells to persist.

In previous work, Altura and her collaborators established that under normal circumstances, CBP chemically regulates survivin, a process called acetylation, and keeps it in the nucleus. The question in the new work was how survivin gets out.

In a series of experiments, what they observed was that in human and mouse breast cancer cells, HDAC6 gathers at the boundary between the nucleus and the rest of the cell, becomes activated by CBP, then binds survivin and undoes its acetylation. This deacetylation allows survivin to then be shuttled out of the nucleus by CRM1.

In the classic jailbreak, CBP is a corrupt guard who looks the other way as HDAC6, the shovel, is smuggled in. The final accomplice, CRM1, is the tunnel with a getaway car on the other end.

Working the new leads

Altura said the research suggests a clear strategy to keep survivin in the nucleus and two leads to pursue it, both of which she has already begun working on with collaborators in academia and in the pharmaceutical industry.

One idea is to inhibit HDAC6 in an attempt to prevent it from misregulating the acetylation of survivin. While general HDAC inhibitors are in clinical trials, Altura is optimistic that blocking just HDAC6, using specific inhibitors developed by a colleague in Japan, would have fewer complications.

"You always have to worry about all the things you don't know that you are targeting," she said. "If we can target HDAC6, we can maybe block survivin from coming out of the nucleus and maintain it in its good state."

The other strategy is to block CRM1, Altura said, an idea she is pursuing with a pharmaceutical company in breast cancer cells in the lab. She said preliminary experiments look promising in keeping survivin inside the nucleus and making cancer cells more susceptible to dying.

###

The study's lead author was Brown graduate student Matthew Riolo. Other authors are Zachary Cooper, Michael Holloway, Yan Cheng, Cesario Bianchi, Evgeny Yakirevich, Li Ma, and Eugene Chin.

The National Institutes of Health's Center for Research Resources funded the study.



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?


AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.


[ Back to EurekAlert! ] Public release date: 28-Mar-2012
[ | E-mail | Share Share ]

Contact: David Orenstein
david_orenstein@brown.edu
401-863-1862
Brown University

PROVIDENCE, R.I. [Brown University] If the fight against breast cancer were a criminal investigation, then the proteins survivin, HDAC6, CBP, and CRM1 would be among the shadier figures. In that vein, a study to be published in the March 30 Journal of Biological Chemistry is the police report that reveals a key moment for keeping cancer cells alive: survivin's jailbreak from the nucleus, aided and abetted by the other proteins. The research highlights that a protein's location in a cell affects its impact on disease, and offers clear new leads for the investigation.

All four proteins were already under suspicion. Researchers, for example, have already tried to assess what levels of HDAC6 in patients with estrogen-receptor positive breast cancer may mean for their prognosis. The results have been inconclusive. The new research suggests that measuring overall levels may not be enough, said the study's senior author Dr. Rachel Altura, associate professor of pediatrics in The Warren Alpert Medical School of Brown University and a pediatric oncologist at Hasbro Children's Hospital.

"We need to look not only at the levels, but also where is it in the cell," she said.

Altura's emphasis on location comes from what her research team found as they tracked and tweaked the comings and goings of survivin in cells. Inside the nucleus, survivin is no problem. Outside the nucleus, but within the cell, it can prevent normal cell death, allowing cancer cells to persist.

In previous work, Altura and her collaborators established that under normal circumstances, CBP chemically regulates survivin, a process called acetylation, and keeps it in the nucleus. The question in the new work was how survivin gets out.

In a series of experiments, what they observed was that in human and mouse breast cancer cells, HDAC6 gathers at the boundary between the nucleus and the rest of the cell, becomes activated by CBP, then binds survivin and undoes its acetylation. This deacetylation allows survivin to then be shuttled out of the nucleus by CRM1.

In the classic jailbreak, CBP is a corrupt guard who looks the other way as HDAC6, the shovel, is smuggled in. The final accomplice, CRM1, is the tunnel with a getaway car on the other end.

Working the new leads

Altura said the research suggests a clear strategy to keep survivin in the nucleus and two leads to pursue it, both of which she has already begun working on with collaborators in academia and in the pharmaceutical industry.

One idea is to inhibit HDAC6 in an attempt to prevent it from misregulating the acetylation of survivin. While general HDAC inhibitors are in clinical trials, Altura is optimistic that blocking just HDAC6, using specific inhibitors developed by a colleague in Japan, would have fewer complications.

"You always have to worry about all the things you don't know that you are targeting," she said. "If we can target HDAC6, we can maybe block survivin from coming out of the nucleus and maintain it in its good state."

The other strategy is to block CRM1, Altura said, an idea she is pursuing with a pharmaceutical company in breast cancer cells in the lab. She said preliminary experiments look promising in keeping survivin inside the nucleus and making cancer cells more susceptible to dying.

###

The study's lead author was Brown graduate student Matthew Riolo. Other authors are Zachary Cooper, Michael Holloway, Yan Cheng, Cesario Bianchi, Evgeny Yakirevich, Li Ma, and Eugene Chin.

The National Institutes of Health's Center for Research Resources funded the study.



[ Back to EurekAlert! ] [ | E-mail | Share Share ]

?


AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.


Source: http://www.eurekalert.org/pub_releases/2012-03/bu-ph032812.php

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Harry Potter e-books now available to muggles

Image
The Hunger Games may have had a heck of an opening weekend, but let's not forget who the top box office spot belongs to: a certain bespectacled boy wizard. Roughly a decade and half after the publication of the first book in the series -- and after several months of promises -- the ultra-popular series has finally made its way onto e-readers like the Kindle and Nook. A couple of days after announcing the rather pricey Wizard's Collection, J.K. Rowling's books have hit the Pottermore site, priced at $8 to $10. The books are currently available in English, with French, German, Italian and Spanish versions coming soon. "Enhanced" versions are on their way as well. Check our some relevant press info after the break.

Continue reading Harry Potter e-books now available to muggles

Harry Potter e-books now available to muggles originally appeared on Engadget on Tue, 27 Mar 2012 10:07:00 EDT. Please see our terms for use of feeds.

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The way to Give Your easiest Nutrition Business presentation in 2012

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Source: http://marmarisnyc.com/?p=1309

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Hawks beat Jazz in NBA's first 4OT game since 1997

ATLANTA (AP) ? Joe Johnson was exhausted by the time the Hawks and Utah Jazz had dragged each other into a fourth overtime ? in Atlanta's third game in three nights, no less.

"It was unbelievable," he said. "I just had to laugh it off. I've never played in a game like that."

Johnson scored 37 points, Josh Smith added 22 and the Hawks ended Utah's six-game winning streak with a 139-133 victory Sunday night in the NBA's first quadruple-overtime game since 1997.

The four overtimes tied for the third-longest game in NBA history. It was the ninth NBA game to go four OTs and the first since Phoenix beat Portland 140-139 on Nov. 14, 1997.

Al Jefferson finished with 28 points and 17 rebounds, and Paul Millsap had 25 points and 13 boards for the Jazz before both players fouled out in the final overtime.

"We'll take a moral victory out of this one," Millsap said. "This was a good ball team we played tonight. They played excellent defense. We just didn't get it done."

Atlanta has won four straight and six of seven. The Hawks improved to 30-20 and moved one-half game ahead of Indiana for fifth place in the Eastern Conference.

"It would happen on the third (straight night), but it shows the toughness of this ballclub to be able to push through that many overtimes and come out victorious," said Smith, who fouled out with 1:57 left in the first overtime. "It was a special win, and I think we'll probably appreciate this win more so than any other win during the season thus far."

Johnson ended the first quarter with 18 points after going 8 of 8 in the period. He missed eight of his next nine shots, including a potential game-winning runner with 3 seconds left in regulation, before hitting a 3-pointer that forced the third overtime.

With 16.9 seconds remaining in the fourth OT, Johnson's 20-foot jumper over C.J. Miles gave the Hawks a 135-131 lead.

"I got some great looks in that first quarter," Johnson said. "I got into a rhythm early and for whatever reason it took me a little while to get that rhythm back, but other guys stepped up and made plays."

Jeff Teague, who had 18 points and nine assists, added a pair of free throws with 13 seconds to go to make it 137-133. Johnson's two free throws sealed the victory with 5.5 seconds remaining.

Zaza Pachulia, who pulled down 20 rebounds, hit a short jumper in the final seconds of the second quarter that gave the Hawks a 17-point lead, their biggest of the game.

Utah rallied with a 27-9 run, giving the Jazz their first lead since early in the opening period. Millsap's 16-footer made it 65-64 with 3:23 left in the third.

Jefferson gave the Jazz their biggest lead of the game when his turnaround 12-footer made it 109-104 in the third OT, but Utah never went ahead in the final two periods.

"It's over with," Jefferson said. "We've just got to get ready for tomorrow. That's why you get in shape. We can't make any excuses. It was their third game in three nights. They found a way to pull it out in the end."

The Jazz, who have won only one road game when they trailed after three quarters, fell to 7-17 away from home. They began the day as one of six teams separated by only 1 1/2 games for the final five playoff spots in the Western Conference.

"We showed a lot of character and fight," Utah coach Tyrone Corbin said. "That's what we need on the road in the second half to win. We've got to make sure we understand that's what's going to make us have a chance."

Utah's biggest lead in regulation came when Gordon Hayward's two free throws made it 93-89 with 5:31 left in the fourth.

Hayward scored 19 points and Devin Harris handed out 10 assists for the Jazz.

Not surprisingly, Johnson was delighted when Jefferson and Millsap both picked up their sixth foul in the last OT.

"I was so happy when they fouled out, man, you wouldn't even believe it," Johnson said with a smile.

Notes: The teams were a combined 2 of 16 from the field in the first OT, and their combined four points tied for 2nd-fewest in NBA history in an overtime period. ... Utah dropped to 1-16 when trailing on the road after three periods. ... The lead changed hands 14 times. ... The score was tied 19 times. ... Jazz coach Tyrone Corbin said that G Raja Bell is still waiting for results of a second opinion on a strained left adductor that's sidelined him for the last six games.

Source: http://news.yahoo.com/hawks-beat-jazz-nbas-first-4ot-game-since-015216052--spt.html

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Genetics of flu susceptibility: Why the flu is life-threatening for some, and quite mild for others

ScienceDaily (Mar. 25, 2012) ? A genetic finding could help explain why influenza becomes a life-threating disease to some people while it has only mild effects in others. New research led by the Wellcome Trust Sanger Institute has identified for the first time a human gene that influences how we respond to influenza infection.

People who carry a particular variant of a gene called IFITM3 are significantly more likely to be hospitalised when they fall ill with influenza than those who carry other variants, the team found. This gene plays a critical role in protecting the body against infection with influenza and a rare version of it appears to make people more susceptible to severe forms of the disease. The results are published in the journal Nature.

A central question about viruses is why some people suffer badly from an infection and others do not. IFITM3 is an important protein that protects cells against virus infection and is thought to play a critical role in the immune system's response against such viruses as H1N1 pandemic influenza, commonly known as 'swine flu'. When the protein is present in large quantities, the spread of the virus in lungs is hindered, but if the protein is defective or absent, the virus can spread more easily, causing severe disease.

"Although this protein is extremely important in limiting the spread of viruses in cells, little is known about how it works in lungs," explains Aaron Everitt, first author from the Wellcome Trust Sanger Institute. "Our research plays a fundamental part in explaining how both the gene and protein are linked to viral susceptibility."

The antiviral role of IFITM3 in humans was first suggested by studies using a genetic screen, which showed that the protein blocked the growth of influenza virus and dengue virus in cells. This led the team to ask whether IFITM3 protected mice from viral infections. They removed the IFITM3 gene in mice and found that once they contracted influenza, the symptoms became much more severe compared to mice with IFITM3. In effect, they found the loss of this single gene in mice can turn a mild case of influenza into a fatal infection.

The researchers then sequenced the IFITM3 genes of 53 patients hospitalised with influenza and found that some have a genetic mutant form of IFITM3, which is rare in normal people. This variant alters the IFITM3 gene and makes cells more susceptible to viral infection.

"Since IFITM3 appears to be a first line defender against infection, our efforts suggest that individuals and populations with less IFITM3 activity may be at increased risk during a pandemic and that IFITM3 could be vital for defending human populations against other viruses such as avian influenza virus and dengue virus" says Dr. Abraham Brass, co-senior author and Assistant Professor at the Ragon Institute of MGH, MIT and Harvard and the Gastrointestinal Unit of Massachusetts General Hospital.

This research was a collaboration between institutes in the United States and the United Kingdom. The samples for this study were obtained from the MOSAIC consortium in England and Scotland, co-ordinated from the Centre for Respiratory Infection (CRI) at Imperial College London, and the GenISIS consortium in Scotland at the Roslin Institute of University of Edinburgh. These were pivotal for the human genetics component of the work.

"Collectively, these data reveal that the action of a single antiviral protein, IFITM3, can profoundly alter the course of the flu and potentially other viruses in both human and mouse," explains Professor Paul Kellam, co-senior author from the Wellcome Trust Sanger Institute. "To fully understand how both the protein and gene control our susceptibility to viral infections, we need to study the mechanisms of the gene variant more closely.

"Our research is important for people who have this variant as we predict their immune defences could be weakened to some virus infections. Ultimately as we learn more about the genetics of susceptibility to viruses, then people can take informed precautions, such as vaccination to prevent infection."

Sir Mark Walport, director of the Wellcome Trust, said: "During the recent swine flu pandemic, many people found it remarkable that the same virus could provoke only mild symptoms in most people, while, more rarely, threatening the lives of others. This discovery points to a piece of the explanation: genetic variations affect the way in which different people respond to infection.

"This important research adds to a growing scientific understanding that genetic factors affect the course of disease in more than one way. Genetic variations in a virus can increase its virulence, but genetic variations in that virus's host -- us -- matter greatly as well."

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The above story is reprinted from materials provided by Wellcome Trust Sanger Institute.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Aaron R. Everitt, Simon Clare, Thomas Pertel, Sinu P. John, Rachael S. Wash, Sarah E. Smith, Christopher R. Chin, Eric M. Feeley, Jennifer S. Sims, David J. Adams, Helen M. Wise, Leanne Kane, David Goulding, Paul Digard, Verneri Anttila, J. Kenneth Baillie, Tim S. Walsh, David A. Hume, Aarno Palotie, Yali Xue, Vincenza Colonna, Chris Tyler-Smith, Jake Dunning, Stephen B. Gordon, K. Everingham, H. Dawson, D. Hope, P. Ramsay, T. S. Walsh (Local Lead Investigator), A. Campbell, S. Kerr, D. Harrison, K. Rowan, J. Addison, N. Donald, S. Galt, D. Noble, J. Taylor, N. Webster (Local Lead Investigator), I. Taylor (Local Lead Investigator), J. Aldridge (Local Lead Investigator), R. Dornan, C. Richard, D. Gilmour, R. Simmons (Local Lead Investigator), R. White (Local Lead Investigator), C. Jardine, D. Williams (Local Lead Investigator), M. Booth (Local Lead Investigator), T. Quasim, V. Watson, P. Henry, F. Munro, L. Bell, J. Ruddy (Local Lead Investigator), S. Cole (Local Lead Investigator), J. Southward, P. Allcoat, S. Gray, M. McDougall (Local Lead Investigator), J. Matheson, J. Whiteside (Local Lead Investigator), D. Alcorn, K. Rooney (Local Lead Investigator), R. Sundaram, G. Imrie (Local Lead Investigator), J. Bruce, K. McGuigan, S. Moultrie (Local Lead Investigator), C. Cairns (Local Lead Investigator), J. Grant, M. Hughes, C. Murdoch (Local Lead Investigator), A. Davidson (Local Lead Investigator), G. Harris, R. Paterson, C. Wallis (Local Lead Investigator), S. Binning (Local Lead Investigator), M. Pollock, J. Antonelli, A. Duncan, J. Gibson, C. McCulloch, L. Murphy, C. Haley, G. Faulkner, T. Freeman, D. A. Hume, J. K. Baillie (Principal Investigator), D. Chaussabel, W. E. Adamson, W. F. Carman, C. Thompson, M. C. Zambon, P. Aylin, D. Ashby, W. S. Barclay, S. J. Brett, W. O. Cookson, L. N. Drumright, J. Dunning, R. A. Elderfield, L. Garcia-Alvarez, B. G. Gazzard, M. J. Griffiths, M. S. Habibi, T. T. Hansel, J. A. Herberg, A. H. Holmes, T. Hussell, S. L. Johnston, O. M. Kon, M. Levin, M. F. Moffatt, S. Nadel, P. J. Openshaw, J. O. Warner, S. J. Aston, S. B. Gordon, A. Hay, J. McCauley, A. O?Garra, J. Banchereau, A. Hayward, P. Kellam, J. K. Baillie, D. A. Hume, P. Simmonds, P. S. McNamara, M. G. Semple, R. L. Smyth, J. S. Nguyen-Van-Tam, L.-P. Ho, A. J. McMichael, P. Kellam, Rosalind L. Smyth, Peter J. Openshaw, Gordon Dougan, Abraham L. Brass, Paul Kellam. IFITM3 restricts the morbidity and mortality associated with influenza. Nature, 2012; DOI: 10.1038/nature10921

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/~3/zC1sVOCkMUE/120325173138.htm

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Economical Prices For Decorative Concrete - Tallahassee,

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Trayvon, my son and the Black Male Code

I thought my son would be much older before I had to tell him about the Black Male Code. He's only 12, still sleeping with stuffed animals, still afraid of the dark. But after the Trayvon Martin tragedy, I needed to explain to my child that soon people might be afraid of him.

We were in the car on the way to school when a story about Martin came on the radio. "The guy who killed him should get arrested. The dead guy was unarmed!" my son said after hearing that neighborhood watch captain George Zimmerman had claimed self-defense in the shooting in Sanford, Fla.

We listened to the rest of the story, describing how Zimmerman had spotted Martin, who was 17, walking home from the store on a rainy night, the hood of his sweatshirt pulled over his head. When it was over, I turned off the radio and told my son about the rules he needs to follow to avoid becoming another Trayvon Martin ? a black male who Zimmerman assumed was "suspicious" and "up to no good."

As I explained it, the Code goes like this:

Always pay close attention to your surroundings, son, especially if you are in an affluent neighborhood where black folks are few. Understand that even though you are not a criminal, some people might assume you are, especially if you are wearing certain clothes.

Never argue with police, but protect your dignity and take pride in humility. When confronted by someone with a badge or a gun, do not flee, fight, or put your hands anywhere other than up.

Please don't assume, son, that all white people view you as a threat. America is better than that. Suspicion and bitterness can imprison you. But as a black male, you must go above and beyond to show strangers what type of person you really are.

I was far from alone in laying out these instructions. Across the country this week, parents were talking to their children, especially their black sons, about the Code. It's a talk the black community has passed down for generations, an evolving oral tradition from the days when an errant remark could easily cost black people their job, their freedom, or sometimes their life.

After Trayvon Martin was killed, Al Dotson Jr., a lawyer in Miami and chairman of the 100 Black Men of America organization, told his 14-year-old son that he should always be aware of his surroundings, and of the fact that people might view him differently "because he's blessed to be an African-American."

"It requires a sixth sense that not everyone needs to have," Dotson said.

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Dotson, 51, remembers receiving his own instructions as a youth, and hearing those instructions evolve over time.

His grandparents told Dotson that when dealing with authority figures, make it clear you are no threat at all ? an attitude verging on submissive. Later, Dotson's parents told him to respond with respect and not be combative.

Today, Dotson tells his children that they should always be respectful, but should not tolerate being disrespected ? which would have been recklessly bold in his grandparents' era.

Yet Dotson still has fears about the safety of his children, "about them understanding who they are and where they are, and how to respond to the environment they are in."

Bill Stephney, a media executive who lives in a New Jersey suburb that is mostly white and Asian, has two sons, ages 18 and 13. The Martin killing was an opportunity for him to repeat a longtime lesson: Black men can get singled out, "so please conduct yourself accordingly."

Like Dotson, Stephney mentioned an ultra-awareness ? "a racial Spidey sense, a tingling" ? that his sons should heed when stereotyping might place them in danger.

One night in the early 1980s, while a student at Adelphi University on Long Island, Stephney and about a dozen other hip-hop aficionados went to White Castle after their late-night DJ gig. They were gathered in the parking lot, eating and talking, when a squadron of police cars swooped in and a helicopter rumbled overhead.

"We got a report that a riot was going on," police told them.

Stephney and his crew used to talk late into the night about how black men in New York were besieged by violence ? graffiti artist Michael Stewart's death after a rough arrest in 1983; Bernhard Goetz shooting four young black men who allegedly tried to mug him on the subway in 1984; Michael Griffith killed by a car while being chased by a white mob in 1986; the crack epidemic that rained black-on-black violence on the city. They felt under attack, as if society considered them the enemy.

This is how the legendary rap group Public Enemy was born. Their logo: A young black man in the crosshairs of a gun sight.

"Fast forward 25 years later," Stephney said. "We've come a long way to get nowhere."

Trayvon's death: Young, black, wearing a hoodie

But what about that long road traveled, which took a black man all the way to the White House? I can hear some of my white friends now: What evidence is there that Trayvon Martin caught George Zimmerman's attention ? and his bullet ? because of his race? Lynching is a relic of the past, so why are you teaching your son to be so paranoid?

There is a difference between paranoia and protection. Much evidence shows that black males face unique risks: Psychological studies indicate they are often perceived as threatening; here in Philadelphia, police stop-and-frisk tactics overwhelmingly target African-Americans, according to a lawsuit settled by the city; research suggests that people are more likely to believe a poorly seen object is a gun if it's held by a black person.

Yes, it was way back in 1955 when 14-year-old Emmitt Till was murdered in Mississippi for flirting with a white woman. But it was last Wednesday when a white Mississippi teenager pleaded guilty to murder for seeking out a black victim, coming across a man named James Craig Anderson, and running him over with his pickup truck.

Obama: 'If I had a son, he'd look like Trayvon'

Faced with this information, I'm doing what any responsible parent would do: Teaching my son how to protect himself.

Still, it requires a delicate balance. Steve Bumbaugh, a foundation director in Los Angeles, encourages his 8- and 5-year-old sons to talk to police officers, "and to otherwise develop a good relationship with the people and institutions that have the potential to give them trouble. I think this is the best defense."

"I don't want them to actually think that they are viewed suspiciously or treated differently," Bumbaugh said. "I think that realization breeds resentment and anger. And that can contribute to dangerous situations."

Video: Attorney defends Martin shooter (on this page)

His sons are large for their age, however.

"I'm probably naive to think that they won't realize they're viewed differently when they're 6-4 and 200 pounds," Bumbaugh said, "but I'm going to try anyway."

I am 6-4 and more than 200 pounds, son. You probably will be too. Depending on how we dress, act and speak, people might make negative assumptions about us. That doesn't mean they must be racist; it means they must be human.

Let me tell you a story, son, about a time when I forgot about the Black Male Code.

One morning I left our car at the shop for repairs. I was walking home through our quiet suburban neighborhood, in a cold drizzle, wearing an all-black sweatsuit with the hood pulled over my head.

From two blocks away, I saw your mother pull out of our driveway and roll towards me. When she stopped next to me and rolled down the window, her brown face was full of laughter.

"When I saw you from up the street," your mother told me, "I said to myself, what is that guy doing in our neighborhood?"

___

Jesse Washington covers race and ethnicity for The Associated Press. He is reachable at http://twitter.com/jessewashington or jwashington(at)ap.org

Source: http://www.msnbc.msn.com/id/46843826/ns/us_news-life/

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Organ recipient testifies at trial in Kosovo

FILE - In this Jan. 12, 2011 file photo, police escort Turkish doctor Yusuf Sonmez, 53, to a local court in Istanbul, Turkey. Sonmez, who allegedly performed transplants at a clinic in Kosovo said to be used by an international organ trafficking network for dozens of illegal operations, remains at large and is being sought by European Union prosecutors in charge of an organ trafficking case. (AP Photo/Ibrahim Usta, File)

FILE - In this Jan. 12, 2011 file photo, police escort Turkish doctor Yusuf Sonmez, 53, to a local court in Istanbul, Turkey. Sonmez, who allegedly performed transplants at a clinic in Kosovo said to be used by an international organ trafficking network for dozens of illegal operations, remains at large and is being sought by European Union prosecutors in charge of an organ trafficking case. (AP Photo/Ibrahim Usta, File)

(AP) ? A Canadian man testified Friday that he paid $105,000 (?80,000) to an Israeli citizen in 2008 to organize a kidney transplant in a Kosovo clinic allegedly used by an international organ trafficking network for dozens of illegal operations.

Raul Fain, 66, of Toronto, told an EU-run panel of three judges that he sought foreign organ donors after doctors told him he could wait up to 12 years for such an operation in Canada.

Fain testified from Canada via a video link to the trial of seven Kosovars suspected of involvement in the criminal network. Kosovo law forbids the removal and transplant of organs.

Fain was shown photos of a building that he identified as the Medicus clinic in Pristina where he was driven for his kidney transplant in June 2008.

The witness said he had been met in Istanbul, Turkey, by Israeli national Moshe Harel, who allegedly organized the transplant, and flown to Kosovo together with an elderly German man also seeking a kidney and two Russian women prepared to each donate one.

Fain said the Russian women appeared between 30 and 40 years old and were busy shopping at the main airport in Istanbul. Upon arrival in Pristina, they were taken in separate cars to the clinic and into separate rooms, he said.

"I was asked to shave and injected with what I believe was a form of anesthetic. After about 15 minutes I was wheeled into the operating room," Fain said. "I was kind of half asleep already, but I remember it was dark and it was cold. I was lying down on a very, very narrow bed."

Harel and Turkish Dr. Yusuf Sonmez, who allegedly performed the operations, remain at large and are being sought by European Union prosecutors in charge of the case.

Prosecutor Jonathan Ratel has said the Russian women were just two of some 20 foreign nationals "recruited with false promises of payments" in 2008.

Victims were promised up to $20,000 (?15,100), while kidney recipients were required to pay between $105,000-$132,000 (?80,000 and ?100,000), according to Ratel.

Fain testified Friday that Sonmez introduced himself before the operation and visited him every day while he was at the clinic, in the room he shared with a German man who also underwent an operation.

"The discussion was about the state of my health. He said there were encouraging signs that the transplant was successful," Fain said.

Fain spent five days recovering at the clinic before flying back to Canada. He said his recovery was "uneventful and faster than expected."

He said he saw the two Russian women at the clinic but did not talk with them.

"I encountered them in the hallway of the clinic. They appeared to be walking, like me," Fain said.

Asked by the prosecution if he had received one of their kidneys, Fain said: "I believe so."

The case began with indictments in November 2010, and the trial began last year. It is providing a stark look at a crime network that allegedly organized organ transplants and included criminals from countries such as Kosovo, Moldova, Ukraine, Turkey, Russia and Israel.

Ratel said Fain's testimony helped "crystalize issues that have been outstanding for some time" by confirming the presence of Russian donors. He said Russian authorities were withholding evidence and access to crucial witnesses and at least three injured parties.

"These three persons have been located, identified and provided statements to investigative authorities within the Russian Federation," Ratel said stressing that Russian authorities did not respond to requests for legal assistance from the EU rule of law mission in Kosovo.

"A lot is said and a lot written ... All I have had through diplomatic channels has been definite silence," Ratel said.

Russia does not recognize Kosovo's secession from Serbia, and Russian authorities are calling for an independent inquiry into allegations raised in a 2008 book by former U.N. war crimes prosecutor Carla Del Ponte that ethnic Albanian guerrillas killed Serb captives during the 1998-99 Kosovo war and sold their organs.

The claims led to Council of Europe investigator Dick Marty write a report which said he is in possession of witness statements proving Kosovo Prime Minister Hashim Thaci and other citizens who once served as rebel commanders in the Kosovo Liberation Army had run detention centers on Albania's border with Kosovo where civilian captives, including Serbs, were killed and their organs sold on the black market during Kosovo's war for independence from Serbia.

Thaci and Albania's government have denied those allegations.

Ratel said Friday he will ask Marty to testify at the trial. Ratel is part of a 3,000-strong EU rule of law and police mission in Kosovo ? known as EULEX ? that deals with sensitive cases such as war crimes and organized crime.

The allegations in the Marty report are being investigated by a special EULEX task force.

Associated Press

Source: http://hosted2.ap.org/APDEFAULT/cae69a7523db45408eeb2b3a98c0c9c5/Article_2012-03-23-EU-Kosovo-Organ-Trafficking/id-5edcc8aa6ef54992b63eadca81bda08e

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Food Regulatory and Safety Summit India 2012 (March 21 - 22, 2012)

UBM Asia

Event Organiser

UBM Asia

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Source: http://events.ubm.com/event/1681/food-regulatory-and-safety-summit-india-2012

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