Sunday, September 30, 2012

The Gray Wardens are recruiting, will you save Ferelden.

Dragon age: reckoning
9:30 Dragon, the fifth blight has started in Ferelden.

The land of Ferelden has been thrown into a war with horrid darkspawn, creature born from the pure taint of blood magic.
Image

King Cailen has assembled his army, along with his top military adviser, Loghain?s, army. He has been battling against the darkspawn, and appears to be winning.
Image
(left Cailen, right Loghain)

The king has called upon the grey wardens to help with the war; the grey wardens are a group of incredibly skilled warriors, mages, archers and all other types of warriors you can imagine. They rose in the first blight to save the whole of Thedas from the first blight. Despite this the wardens are desperate to bolster their numbers. You are one these recruits. All recruits are being taken to the ruins of Ostagar to help Cailen with the battle. There are many of you, but all your stories are different. This initiation is the beginning of your new life.

This is a story based on the story of dragon age: origins.it will follow the same story setting as dragon age: origins. Unlike the game though the role-players will choose all the choices. There will be none of the characters from the game unless someone decides to do a canon. Friendships, arguments, love. It will all be played out in this before you make your character you could look to this website for some background info. I can help you with your application if you need any. Also do not worry if your not experienced with the story, me and other experienced players of dragon age.

Dragon Age of Reckoning

Source: http://feedproxy.google.com/~r/RolePlayGateway/~3/JKU0DNHa0ZA/viewtopic.php

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Combination of targeted treatment drugs delays resistance in melanoma patients

Combination of targeted treatment drugs delays resistance in melanoma patients [ Back to EurekAlert! ] Public release date: 29-Sep-2012
[ | E-mail | Share Share ]

Contact: Katie Marquedant
kmarquedant@partners.org
617-726-0337
Massachusetts General Hospital

Combined treatment with two drugs targeting different points in the same growth-factor pathway delayed the development of treatment resistance in patients with BRAF-positive metastatic malignant melanoma. The results of a phase I/II study of treatment with the kinase inhibitors dabrafenib and trametinib will be published in the New England Journal of Medicine and are being released online to coincide with a presentation at the European Society for Medical Oncology meeting in Vienna.

"We investigated this combination because of research we and others have conducted into the molecular underpinnings of resistance to BRAF inhibitor therapy," says Keith Flaherty, MD, of the Massachustts General Hospital (MGH) Cancer Center, lead author of the NEJM report and principal investigator of the study. "We found that adding the MEK inhibitor trametinib to BRAF inhibitor dabrafenib clearly delays the emergence of resistance. In fact, the combination was at least twice as effective as BRAF inhibition alone."

In around half of patients with metastatic melanoma, tumor growth is driven by mutations that keep the BRAF protein part of the MAPK cell growth pathway constantly activated. In recent years, drugs that inhibit BRAF activity have rapidly halted and reversed tumor growth in about 90 percent of treated patients, but most patients' response is temporary, with tumor growth resuming in six or seven months. Investigations into how this resistance emerges have suggested that the MAPK pathway gets turned back on through activation of MEK, another protein further down the pathway. Based on promising results of animal studies, the current investigation was designed to test whether inhibiting both the BRAF and MEK proteins could delay treatment resistance.

Sponsored by GlaxoSmithKline, the study by researchers at 14 sites in the U.S. and Australia tested two of the company's drugs BRAF inhibitor dabrafenib and MEK inhibitor trametinib, both oral medications currently being evaluated by the FDA as single-agent therapeutics in adult patients with BRAF-expressing malignant melanoma. Phase I testing confirmed that there were no drug-to-drug interactions between the two agents and evaluated the safety of different dose combinations. In the open-label phase II portion of the study, 162 patients were randomized into three groups that received different dose combinations: two daily 150 mg doses of dabrafenib plus one 2 mg trametinib dose, the same dabrafenib dose with a 1 mg dose of trametinib, or treatment with dabrafenib alone. Participants receiving dabrafenib alone were able to cross over to the full-dose combination treatment if their cancer resumed progression.

Treatment with both combination regimens led to a significant delay about four months longer than with dabrafenib alone in the emergence of resistance. After one year of treatment, 41 percent of those receiving full-dose combination treatment had no progression of their cancer, compared with only 9 percent of those receiving one drug. The occurrence of side effects such as skin rash and the development of squamous cell carcinoma, a less malignant skin cancer, was similar to that typically seen when only one of the two drugs is used, and some side effects were less frequent with the combination therapy.

Noting that the tested combination, now being tested in a larger Phase III study, delayed but did not prevent resistance in most participants, Flaherty says, "We need to continue focusing on resistance mechnisms occuring with this combination approach so we can better understand how to treat patients once resistance emerges or to develop other combination regimens to further prevent relapse. We also need to see if this approach could serve as an effective adjuvant therapy used following surgery to prevent recurrence. That might have the biggest impact on patients." Flaherty is an associate professor of Medicine at Harvard Medical School.

###

Jeffrey Infante, MD, of the Sarah Cannon Research Institute in Nashville is co-lead author of the NEJM paper and Jeffrey Weber, MD, PhD, of the Moffitt Cancer Center in Tampa is corresponding author. Additional participating institutions are the University of California at San Francisco, University of Colorado, Vanderbilt University, Angeles Clinic and Research Institute, University of Pennsylvania, Dana-Farber Cancer Institute, and M.D. Anderson Cancer Center in the U.S; and the Westmead Institute for Cancer Reearch and Ludwig Institute for Cancer Research in Australia.

Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $750 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine. In July 2012, MGH moved into the number one spot on the 2012-13 U.S. News & World Report list of "America's Best Hospitals."


[ 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.


Combination of targeted treatment drugs delays resistance in melanoma patients [ Back to EurekAlert! ] Public release date: 29-Sep-2012
[ | E-mail | Share Share ]

Contact: Katie Marquedant
kmarquedant@partners.org
617-726-0337
Massachusetts General Hospital

Combined treatment with two drugs targeting different points in the same growth-factor pathway delayed the development of treatment resistance in patients with BRAF-positive metastatic malignant melanoma. The results of a phase I/II study of treatment with the kinase inhibitors dabrafenib and trametinib will be published in the New England Journal of Medicine and are being released online to coincide with a presentation at the European Society for Medical Oncology meeting in Vienna.

"We investigated this combination because of research we and others have conducted into the molecular underpinnings of resistance to BRAF inhibitor therapy," says Keith Flaherty, MD, of the Massachustts General Hospital (MGH) Cancer Center, lead author of the NEJM report and principal investigator of the study. "We found that adding the MEK inhibitor trametinib to BRAF inhibitor dabrafenib clearly delays the emergence of resistance. In fact, the combination was at least twice as effective as BRAF inhibition alone."

In around half of patients with metastatic melanoma, tumor growth is driven by mutations that keep the BRAF protein part of the MAPK cell growth pathway constantly activated. In recent years, drugs that inhibit BRAF activity have rapidly halted and reversed tumor growth in about 90 percent of treated patients, but most patients' response is temporary, with tumor growth resuming in six or seven months. Investigations into how this resistance emerges have suggested that the MAPK pathway gets turned back on through activation of MEK, another protein further down the pathway. Based on promising results of animal studies, the current investigation was designed to test whether inhibiting both the BRAF and MEK proteins could delay treatment resistance.

Sponsored by GlaxoSmithKline, the study by researchers at 14 sites in the U.S. and Australia tested two of the company's drugs BRAF inhibitor dabrafenib and MEK inhibitor trametinib, both oral medications currently being evaluated by the FDA as single-agent therapeutics in adult patients with BRAF-expressing malignant melanoma. Phase I testing confirmed that there were no drug-to-drug interactions between the two agents and evaluated the safety of different dose combinations. In the open-label phase II portion of the study, 162 patients were randomized into three groups that received different dose combinations: two daily 150 mg doses of dabrafenib plus one 2 mg trametinib dose, the same dabrafenib dose with a 1 mg dose of trametinib, or treatment with dabrafenib alone. Participants receiving dabrafenib alone were able to cross over to the full-dose combination treatment if their cancer resumed progression.

Treatment with both combination regimens led to a significant delay about four months longer than with dabrafenib alone in the emergence of resistance. After one year of treatment, 41 percent of those receiving full-dose combination treatment had no progression of their cancer, compared with only 9 percent of those receiving one drug. The occurrence of side effects such as skin rash and the development of squamous cell carcinoma, a less malignant skin cancer, was similar to that typically seen when only one of the two drugs is used, and some side effects were less frequent with the combination therapy.

Noting that the tested combination, now being tested in a larger Phase III study, delayed but did not prevent resistance in most participants, Flaherty says, "We need to continue focusing on resistance mechnisms occuring with this combination approach so we can better understand how to treat patients once resistance emerges or to develop other combination regimens to further prevent relapse. We also need to see if this approach could serve as an effective adjuvant therapy used following surgery to prevent recurrence. That might have the biggest impact on patients." Flaherty is an associate professor of Medicine at Harvard Medical School.

###

Jeffrey Infante, MD, of the Sarah Cannon Research Institute in Nashville is co-lead author of the NEJM paper and Jeffrey Weber, MD, PhD, of the Moffitt Cancer Center in Tampa is corresponding author. Additional participating institutions are the University of California at San Francisco, University of Colorado, Vanderbilt University, Angeles Clinic and Research Institute, University of Pennsylvania, Dana-Farber Cancer Institute, and M.D. Anderson Cancer Center in the U.S; and the Westmead Institute for Cancer Reearch and Ludwig Institute for Cancer Research in Australia.

Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $750 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine. In July 2012, MGH moved into the number one spot on the 2012-13 U.S. News & World Report list of "America's Best Hospitals."


[ 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/2012-09/mgh-cot092712.php

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Henry Ford Health to Implement No-Nicotine Hiring Policy ...

Henry Ford Health System announced Friday that they will not hire job applicants who use tobacco products, effective Jan. 1, 2013.

Job applicants for the Dearborn-based health network will be screened for signs of nicotine as part of the hiring process.

"The health and well-being of our patients, employees and visitors is our top priority," Henry Ford CEO Nancy Schlichting said. "The no-nicotine policy strengthens our commitment as role models for providing a healthy environment for everyone at our facilities.?

While the screening and ban on nicotine use only applies to new job applicants, Henry Ford also is enhancing their existing policies that prohibit the use of tobacco at their facilities, launched in 2007. This includes prohibiting employees from using tobacco products or smelling of tobacco at any time during their workday.

Employees who violate these policies are subject to disciplinary action, up to and including termination.

Henry Ford joins a growing number of local and national health care systems that have implemented a no-nicotine hiring policy, including Beaumont and Oakwood health systems.

Oakwood Healthcare?also based on Dearborn?implemented their tobacco-free workplace program as of Oct. 1, 2011.

The program includes any type of nicotine product, and applies to any new hires, but not existing employees.

Source: http://dearborn.patch.com/articles/henry-ford-health-to-implement-no-nicotine-hiring-policy

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Saturday, September 29, 2012

PFT: Referees officially ratify new deal with NFL

350x-1Getty Images

Wayne Elliott has had a wild week.

On Monday night, he wore the white hat as the referee of the crew that bungled the Seahawks-Packers game.? On Friday night, Elliott worked a high school football game.

In the interim, Elliott says his phone has been ringing with calls from angry fans, telling him he should ?commit suicide? and that he ?should die.?

But he still believes it was the right call.

?The replay guy just said there is nothing here that we can use to overturn it. It?s going to stand,? Elliott told FOX7 in Austin.? (This confirm that, when it came to replay reviews during the lockout, non-replacement replay officials were actually usurping the authority of the on-field referees.)

As we recently explained, via the NFL?s rulebook and casebook, there was enough evidence to overturn the ruling on the field, because Packers safety M.D. Jennings had ?control? of the ball before Seahawks receiver Golden Tate, which is the key factor regardless of what happens as they land on the ground and wrestle for the ball.? (Sorry, Seahawks truthers, but that?s the truth.)

Elliott also said he has ?no regrets? about accepting the assignment as a replacement, and that it was ?the most fun I?ve ever had.?

It was the most fun he?s had because he has been working as an official at the lower levels of the sport since 1978.? The fact that he hadn?t risen to the NFL or to a high-end college conference in the past 34 years tells us all we need to know about his overall skills.? As we?ve said time and again, if the replacements were among the best of the best, they would have been among those who were locked out.

Elliott declined to apologize to the fans of the Packers, explaining that if the call had gone the other way people would be asking if he should apologize to the Seahawks fans.

Scheduled to work the Vikings-Lions game in Week Four, Elliott said he wanted to ?get the bad taste out of his mouth? from Monday night?s game ? you know, the one for which he has nothing about which to apologize.

Source: http://profootballtalk.nbcsports.com/2012/09/29/officials-officially-agree-to-new-deal-with-nfl/related

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How can I find a very good online internet marketing services ...

If a recent Internet was used primarily for information retrieval, these days the situation has changed radically. The increasing range of Web users, technology (communication with all the customers throughout the site, payment systems through the Internet, offers on-line, etc.) and a lot of other causes make the Internet the best advertising tool and place for sales simultaneously. For instance, the boom in shopping on the web definitely reveals that skillfully used Internet technology brings a steady income for site owners.

Online promotion may be effective for many companies, the possible audience that?s seeking similar services or goods on the web. According to statistics, the sheer number of Online surfers is increasing each and every year. And this also audience is rather irresistible to business, since it carries a high ability to pay. Think, thousands, perhaps hundreds of thousands of men and women everyday are seeking your service and competitors? products, because more agile competitors have taken the best places in search results. You also may take first instance, it takes to start the search engine optimization.

Search engine optimisation just serves to generate your websites out on the top places in the top. In more scientific terms, seo it is just a set of measures to further improve the position of the site in search engine results for the pre-selected queries.

PROFFI SEO is the thing that you need if you would like see your website high in search engines like google, online search marketing services provides professional services worldwide for small and medium size businesses. Everybody is able to take advantage of our services including Keyword research and analysis, Competition analysis, On-page optimization, Top search rankings, Ethical link building, Ranking reports, Web page design, Internet site promotion.

International seo service is an incredible possibility of promote your business to another level, where there tend to be opportunities and prospects. Our international search engine optimization firm is making use of countries including Germany, Denmark, Norway, France, Belgium, Austria, Netherlands, Czech Republic, Finland, Sweden etc. Our team of professionals will do everything possible to keep your site was the first place of search engines like google, all at a surprisingly low price affordable for anyone.

All the information you need about online internet marketing services you?ll find on our internet site http://proffi-seo.com. Really don?t waste the chance and sign up in the ranks of our customers today, seo optimization company joining together top professionals, who know all the substantial and up-to-the-minute methods of seo as a way to improve the ranking of the website.

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Source: http://informative-articles.com/151673/how-can-i-find-a-very-good-online-internet-marketing-services/

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Joanna Krupa Wants More Sex from Fiance

Source: http://www.thehollywoodgossip.com/2012/09/joanna-krupa-wants-more-sex-from-fiance/

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Friday, September 28, 2012

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Swingers: Mentally Healthier Than Monogamous Peers ...

One of the traits that determines happiness and mental health is flexibility: the capacity for creativity, abstract thinking, and adapting to changing circumstances. When it comes to the sex lives of swingers, there?s no question that they are more flexible in their approach to sex than their monogamous peers. But the real question is more complex: Is flexibility toward sex a good thing or a bad thing?

As a therapist who specializes in relationship issues, I can tell you that I have seen scores of men and women over the years who have varied sexual?lifestyles and appetites. I?ve worked with couples who swing and couples who wouldn't dare, and one distinguishing characteristic I have found is that couples who swing have less fear than monogamous couples. What?s more, they cheat less.

In terms of the fear, monogamous couples often fall into the?toxic?jealousy trap, afraid that a particular behavior or gesture might lead to a full-fledged affair and the end of the relationship. Monogamous couples also often fear that their best days are behind them, that they lost the opportunity for sexual excitement in favor of settling down and getting married. On the other hand,?swinging couples are often deeply in love and emotionally connected, but they don?t value sex in the same way their monogamous peers do.

When it comes down to the nitty-gritty, the dividing line is about the values a given couple holds toward sex. In my clinical work, I find that monogamous couples are often judgmental about a sex life that is anything other than monogamous, while swinging couples often espouse more of a live-and-let-live attitude. In other words, they?re often less judgmental of couples who choose to live a monogamous lifestyle. Is one better? No, because people are different, with different emotional and sexual needs. It makes perfect sense, for example, that someone who isn?t very sexual in the first place wouldn?t care?to have a more liberal sex life: they already don?t have much interest in sex to begin with!

Where problems arise in monogamous relationships is when one or both members of a couple have a?sexual appetite that the relationship isn?t able to satiate. What happens? Couples who are monogamous often stray and seek sex outside of the relationship. The hypocritical part is that many cheaters would never agree to a swinging relationship!

It?s never a therapist?s job to tell a client what kind of lifestyle to live as long as the client isn?t causing harm to himself or anyone else. Even listening to a man tell me about having an affair, it would be out of line for me to tell him to stop it. I would, however, encourage him to tell his wife and come clean about his deceptive behavior. But when it comes to the type of relationship he seeks, it?s not a therapist?s job to prescribe a set of values a client should have and hold onto.

One consideration that any couple should take relates to safety: physical safety if you're having sex with people you don't know, and sexual safety to the point that you make sure to always practice safe sex. A flexible approach to sex is one thing; putting yourself in serious jeopardy is, of course, another.

Ultimately, infidelity is a rampant problem in relationships because men and women are often too afraid to be honest with themselves about what they want, and terrified to make the changes in their relationship that they secretly crave. I?m not suggesting that most monogamous couples secretly want to swing. I am, however, suggesting that men and women often judge those who?swing but could actually learn something about themselves and human nature if they take a moment to reflect on the reasons why others?swingers, included?choose a different lifestyle.

PLUS: Check out my book, Overcome Relationship Repetition Syndrome, about how to stop repeating the same bad patterns in your relationships over and over again.

Source: http://www.psychologytoday.com/blog/insight-is-2020/201209/swingers-mentally-healthier-monogamous-peers

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World hockey chief expects NHL players in Sochi

TOKYO (AP) ? The International Ice Hockey Federation is operating on the assumption that NHL players will take part in the 2014 Sochi Olympics.

"We've prepared everything with the idea that NHL players will be there," IIHF President Rene Fasel said Friday. "We've decided about the format and expect them to be there."

Fasel was re-elected to another four-year term as president at the IIHF's general congress in Tokyo.

Just 16 months before the 2014 Sochi Games, NHL players are not certain to compete in the two-week tournament in Russia run by the IIHF. Fasel said the tournament will start a day later than the 2010 games in Vancouver.

"We decided to start on Wednesday instead of Tuesday," Fasel said. "In Vancouver, we started on Tuesday but the players will need more time to travel to Russia. It will mean less rest between games but we have to start on Wednesday."

NHL Commissioner Gary Bettman has said no decision is imminent about possibly shutting down for two weeks to accommodate an Olympics in which some games would be played in the middle of the night in North America, thus affecting TV viewership and interest.

Before the NHL makes up its mind, a collective bargaining agreement between owners and players must be negotiated. The NHL locked out its players on Sept. 16 when talks broke down. The two sides plan to meet again Friday.

Russian player Alex Ovechkin, one of the NHL's signature stars, is threatening to play in Sochi no matter what the NHL does.

Fasel said the NHL could decide as late as January not to come but the tournament will go ahead.

"We'll play the tournament anyway," Fasel said. "There are not only 750 NHL players playing hockey in the world."

Associated Press

Source: http://hosted2.ap.org/APDEFAULT/347875155d53465d95cec892aeb06419/Article_2012-09-28-OLY-HKO-Sochi-NHL-Players/id-12798a835ab54382a006f30956230b31

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Thursday, September 27, 2012

Tour In Greece | Faraway Vacation Rentals stay with a local | Blog ...

Vacation to Greece ? You can get an accommodation depending on your budget on your Greece Vacation but it is best to pre-book and travel so that you don?t become the victim of changing exchange rates or local touts who seem to be a universal breed anywhere on the globe.

Posts related to Tour In Greece | Faraway Vacation Rentals stay with a local

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Source: http://bloginteract.com/stories/tour-in-greece-faraway-vacation-rentals-stay-with-a-local/

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BlackBerry User Base Grows by 2 Million and Three Other Stories You Need to Know

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Wednesday, September 26, 2012

Down syndrome may hold key to new Alzheimer's treatments

CHICAGO (Reuters) - In a new lead on Alzheimer's research, Johnson & Johnson is bankrolling a three-year pilot study of people with Down syndrome to identify the early changes that herald dementia, which afflicts up to 75 percent of adults with the condition.

The aim is to generate support for a much bigger, public-private partnership funded by drugmakers, advocates and government agencies that will study at least 1,000 people with Down syndrome, tracking them from an early age and eventually testing treatments to keep dementia from developing.

"The study we're proposing would provide insight into treating Alzheimer's, but it might help individuals with Down syndrome as well," said Dr. Husseini Manji, J&J's global head of neuroscience drug development.

Experts in Down syndrome and Alzheimer's who gathered in Chicago for a workshop on the idea at the Alzheimer's Association offices this month say it may offer the best scientific model yet for testing drugs to prevent the degenerative brain disease.

The industry has been repeatedly stung by the failure of experimental Alzheimer's treatments, including recent trials of the J&J and Pfizer Inc therapy bapineuzumab. As a result, companies and researchers are looking for ways to test Alzheimer's drugs earlier, before people's brains become too damaged to benefit.

Studies are already planned to enroll people who carry genetic mutations that ensure they will develop Alzheimer's at an early age. One trial backed by the U.S. Department of Health & Human Services will test a drug from Roche Holding AG's Genentech unit called crenezumab in an extended family from Colombia who carry a mutation that causes them to develop Alzheimer's in their 30s.

Only a few hundred families in the world carry these genes, and there is some worry that drugs tested in people with genetic mutations that cause early-onset Alzheimer's may work differently in people who develop the more common late-onset Alzheimer's, which develops after age 65.

AN IMPORTANT DIFFERENCE

The dementia that develops in people with Down syndrome may bear a stronger resemblance to the disease in the broader population because it differs from other forms of early-onset Alzheimer's, researchers say.

People with Down syndrome inherit a third copy of chromosome 21, giving them an extra helping of a gene that makes amyloid precursor protein, or APP, which is linked with the development of plaques in the brains of Alzheimer's patients.

Most early-onset Alzheimer's is caused by mutations in the APP gene or in one of two genes known as presenilin 1 or presenilin 2. People with Down syndrome appear to develop dementia because of their extra copy of an otherwise normal APP gene.

"There is a possibility that the Down syndrome population mimics (late-onset) Alzheimer's disease a little more closely," said Manji, co-author of a commentary this month in Nature Reviews Drug Discovery that laid out plans for the study.

Dementia starts much earlier in people with Down syndrome, who develop brain plaques and tangles by age 30 and signs of dementia by age 40.

The number of potential Down syndrome patients exceeds those with the genetic mutation. There are some 400,000 people in the United States and 6 million people worldwide with Down syndrome.

"These diseases almost certainly have common features," said Dr. William Mobley of the Down Syndrome Center for Research and Treatment at the University of California, San Diego.

While all of the similarities are not yet clear, studies in mice with Down syndrome show that just eliminating just the extra copy of the gene for APP can keep brain cells from dying, he said.

Mobley's center will run the 12-patient pilot study, which aims to lay the foundation for the larger project, dubbed the Down Syndrome Biomarker Initiative.

The larger trial would be patterned after two successful studies: the Alzheimer's Disease Neuroimaging Initiative, a public-private partnership that helped identify biomarkers linked with Alzheimer's, and a breast cancer trial known as I-SPY that pioneered adaptive trial design, in which researchers use biomarkers to match the right drug to the right patient.

What is not yet known is how many parents of people with Down syndrome would be willing to sign up their adult children for such trials. Michelle Whitten of the Global Down Syndrome Foundation thinks many will be.

Whitten, the mother of a 9-year-old with Down syndrome, says the lifespan of people with the condition has increased from 28 years in the 1980s to 60 years today because of better treatment. That means many parents who fought to give their children a good education and a worthwhile job now frequently face their decline into dementia.

"We just want it solved," Whitten said.

Dr. Michael Krems, who heads the neurology franchise at J&J, said the challenge is to develop drugs that offer lots of potential benefit with little risk to patients.

That may rule out the company's drug bapineuzumab, which was shown to cause brain-swelling known as vasogenic edema in several patients.

Krems said one promising approach would be a beta-secretase, or BACE, inhibitor, a drug designed to keep the enzyme beta-secretase from chopping up APP into bits that produce beta amyloid, which forms brain plaques in Alzheimer's patients.

A recent study in the journal Nature hinted that inhibiting beta-secretase might work. A team at deCODE Genetics in Reykjavik discovered a rare mutation in the APP gene that protects against Alzheimer's, and it works by interfering with beta-secretase. Drugmakers who are already developing BACE inhibitors include Eli Lilly and Co, Roche, and Merck & Co.

Krems declined to say if J&J also has a BACE drug, but he said testing such drugs in patients with late-onset Alzheimer's would require very large trials.

"At least conceptually, doing this in a Down's population might be much more efficient."

(Editing by Michele Gershberg and Prudence Crowther)

Source: http://news.yahoo.com/down-syndrome-may-hold-key-alzheimers-treatments-170633270--finance.html

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Foreclosures decline in Rockingham, Strafford counties, report says ...

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September 25, 2012 10:08 AM

PORTSMOUTH ? Foreclosure rates in Rockingham and Strafford counties decreased for the month of July over the same period last year, according to newly released data from CoreLogic, a provider of consumer, financial and property information, analytics and services to business and government.

The CoreLogic data reveals the rate of foreclosures in the two counties among outstanding mortgage loans was 1.43 percent for July, a decrease of 0.23 percentage points compared to July 2011 when the rate was 1.66 percent. Foreclosure activity in Rockingham and Strafford counties was lower than the national foreclosure rate, which was 3.25 percent for July.

The mortgage delinquency rate decreased in the two counties for July. According to CoreLogic data for July, 4.11 percent of mortgage loans were 90 days or more delinquent compared to 4.47 percent for the same period last year, representing a decrease of 0.36 percentage points. The delinquency rate measures the percentage of loans that are more than 90 days delinquent, including those in foreclosure and real estate owned.

Earlier this month, the N.H. Housing Finance Authority reported there were 269 foreclosures in the state in July ? an increase of 13 percent from July of last year. However, the NHHFA reported it was the third month in a row of declining foreclosure numbers. The cumulative total for January through July 2012 is now about 2 percent below the same period in 2011, and 9 percent below the same period in 2010.

?The number of foreclosures will decline slowly as overall economic conditions and housing markets improve,? the NHHFA stated. ?Until that time, foreclosed and distressed properties on the housing market will continue to have a negative influence on home sales and prices.?

SEACOAST SALES

For a searchable database of property transfers and real estate transactions for the Portsmouth region and southern York County, visit www.seacoastonline.com/property-transfers.


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Source: http://www.seacoastonline.com/articles/20120925-NEWS-120929847

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Juvenile murderer ruling reopens 'traumatic wounds'

Family photo/Courtesy of Bobbi Jamriska

Kristina Grill, 15, was murdered in 1993 by her ex-boyfriend, who was also 15 at the time of her death and 16 when he was convicted. She's seen in this file photo in Pennsylvania a year before her murder.

By Elizabeth Chuck, NBC News

Nineteen years ago, Bobbi Jamriska's younger sister was found murdered in a Pennsylvania schoolyard. As Jamriska grieved, one thing brought her solace: When a court found her sister's 16-year-old ex-boyfriend guilty and sentenced him to life in prison without parole.

"When you get up every day, you think about what happened, but at least you know that there was that one constant, that life-without-parole was going to make sure that you never had to relive that part of it," said Jamriska, 40, who lives in Pittsburgh.

But three months ago, the Supreme Court struck down mandatory life-without-parole sentences for juveniles as cruel and unusual punishment.?While the June 25 ruling wasn't necessarily designed to be applied retroactively, some youth advocates are trying to use it to free so-called "juvenile lifers," setting?off a series of battles over what to do with the approximately 2,100 convicted murderers who were handed mandatory life-without-parole sentences for acts committed as youths.

For victims' families, the decision has had huge emotional, and in some cases, legal implications.

"After the [Supreme Court] ruling, everyone felt like they were reliving the trial phase and their loved ones' murder," said Jamriska, who traveled to Washington, D.C., with other victims' families to protest the ruling.

She is part of a support group called the National Organization of Victims of Juvenile Lifers.

"There were a lot of families who didn't have any idea that this was even possible," she said. "For them, it was literally one day business as usual, and then the next day, on the news, their whole world got turned upside down."

Pennsylvania, where Jamriska lives, has the biggest concentration of juveniles serving mandatory life sentences -- about 480 of them, the oldest of whom was convicted almost 60 years ago and is now in his 70s, according to the Juvenile Law Center. Earlier this month, the state Supreme Court in Pennsylvania began hearing arguments for why some of the lifers there should be paroled, including the ex-boyfriend who killed Jamriska's sister in 1993.

No one in the legal system told Jamriska that the parole arguments involved her sister's killer. She found out from a reporter's voicemail about three weeks after the Supreme Court ruling that lawyers were trying to get parole for him.

Jamriska was stunned, but she said a lack of communication is somewhat understandable.

Jennifer Bishop-Jenkins / teenkillers.org

Bobbi Jamriska, of Pennsylvania, right, and Jody Robinson, left, of Michigan, another member of the National Organization of Victims of Juvenile Lifers, are seen advocating for victims' families' rights on March 20, 2012, outside of the Supreme Court in Washington, D.C., as the Supreme Court heard arguments on whether mandatory life without parole was cruel and unusual punishment for convicted juvenile murderers.

"There never was a contingency for if this person who was sent to life in prison with no parole is suddenly able to get out," she said. "The DA's office isn't really staffed to manage that influx of appeals and those victims who are trying to get information -- I don't blame them."

The state Supreme Court has put the arguments on hold and didn't give a timeline for a ruling. The Pennsylvania legislature still needs to come up with an appropriate alternative punishment for minors going forward.?

"The sentencing scheme in Pennsylvania currently provides that for any individual, juvenile or adult, convicted of first or second-degree homicide must either receive a sentence of death or a sentence of life without parole. For juveniles, that mandatory sentence of life without parole has been declared unconstitutional," Marsha Levick,?deputy director and chief counsel at the Juvenile Law Center, said. "We think the courts should look to the next most severe sentence that is statutorily available in the state. Here, that means a sentence for third-degree murder, where you have a maximum sentence of 40 years."

Levick suspects lawyers in other states will argue for that too. Since the Supreme Court ruling, North Carolina has passed a law replacing the mandatory life without prison sentence with a 25 years to life sentence; California's governor is currently evaluating a law that sets up two different schemes where parole eligibility comes in at either 15 or 25 years to life, Levick said. In all, 28 states still allow?mandatory life-without-parole sentences for minors, a situation that will have to change.

"States can still impose life without parole," she said. "They just can't make it the only sentence available."

As some juvenile advocates try to undo sentences that have already been imposed, Jennifer Bishop-Jenkins, 54, president of the National Organization of Victims of Juvenile Lifers, worries about the families of their victims.

"Whenever you reopen traumatic wounds or you're triggering a retraumatization, you're talking about something that is going to affect people's work, their sleep, their health, their marriages -- everything," she said.

Victims can only rely on each other for support, Jenkins said.

14 years old: Too young for life in prison?

"They don't register for victim notification and they don't monitor what's happening, and then you get these reactions like what we've been getting in our organization," Bishop-Jenkins said. "We've been trying very hard to find people to let them know that this multi-billion dollar campaign to free their loved ones' killers is going on and they're just shocked."

Family photo/Courtesy of Jennifer Bishop-Jenkins

From left to right: Richard Langert and Nancy Bishop Langert are seen on their wedding day in 1987 in Kenilworth, Ill., with Nancy's parents and sister, Jennifer Bishop-Jenkins, far right. The Langerts were murdered by a 16-year-old in 1990.

There are potential legal issues too: Bishop-Jenkins' pregnant sister and brother-in-law were murdered in their home in Winnetka,?Ill., 22 years ago. It was Bishop-Jenkins' father who found their bodies; his testimony served as crucial evidence in the initial trial. Eight years ago, her father died of cancer. She says the judge from the first trial has also died.

"My father was the best eyewitness to the carnage of the crime scene. We didn't videotape him talking about the crime," Bishop-Jenkins said. "We didn't get the transcript of what the judge said at the sentencing hearing where he gave this speech about if anybody deserved life without parole, he did."

She now fears she and her mom, 83, could have to face her sister's killer in sentencing hearings in court. And while she doubts he will be granted parole, she said she worries lawyers may try again every couple of years.

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Death and recovery after open-heart surgery - Health - Macleans.ca

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A ticking time bomb

Photograph by Cole Garside

?Look, lady, the last time I was in this hospital, I died.?

That was the God?s truth?at least the dying part was. Actually, I?d been back to Toronto General?s emergency unit three times since my heart stopped, the day after I had open-heart surgery in May 2011.

But on this particular morning, three months later, I was lying on a gurney waiting to go into an operating room for yet another heart procedure when the anaesthetist said: ?Mr. Ramsay, we?re going to give you something to relax you.? She unwrapped the needle before inserting it into a vein in my wrist. But she missed the vein, and since I was on blood thinners, my wrist began to bleed all over the sheets. The doctor quickly stepped back and asked a nurse to get my ?line? going. By now, the sedative was having its effect and I began to feel light-headed. But I was ever watchful. That?s when I told her about dying the last time I was here. It was an inauspicious start.

Cardioverting is a little like being tasered. Big wire patches are taped onto your chest and back. Then you?re zapped with 100 joules of electricity in the hope that your heart will be converted back into a normal thub-thub, thub-thub rhythm. Mine was beating all over the place, sometimes fast, sometimes slow, sometimes skipping a beat. This is called atrial fibrillation. You can have it and not feel it, and it can usually be controlled by drugs. But in my case, A-fib made it impossible for me to work, to sleep, to function at all without huge fear that it would send me, as it had many times following my surgery, into what felt like having a heart attack and a stroke at the same time. So by this time I would have done anything to stop the chaos that had taken over my life.

My open-heart surgery three months earlier had lasted for five hours, so I asked my cardiologist, Dr. John Ross, how long this procedure would take.

?A few milliseconds.?

?Will I feel anything??

?I hope not, for your sake.?

He smiled.

Five years before, I?d finished running my 10th marathon and was in the best shape of my life. Indeed, my wife, Jean Marmoreo, and I had founded the women?s marathon group Jean?s Marines that had taken hundreds of women off the couch and trained them to do the Marine Corps Marathon in Washington. Years later, Jean had gone on to be the fastest woman in her age group in the Boston Marathon. We?d trekked to Mount Everest, hiked 1,000 miles of the Appalachian Trail, mushed huskies in the Arctic. I wore my street cred in the world of adventure like a medal.

Then one day in 2005 I asked my family doctor if I could have a stress echocardiogram. I did it more out of cockiness than caution. Sure, it made sense that a 57-year-old man whose mother had died of arteriosclerosis at 59 would have his heart tested to see if anything was amiss. In truth, I just wanted to have proof of how fit my heart was. But as I was to find out, fit doesn?t mean healthy. That test and the events that followed would teach me some painful lessons about what we can and can?t control in our lives.

The cardio imaging revealed that I had a heart murmur caused by my faulty aortic valve. It seems that one in 100 Canadians is born with it and, like fully half the cases, I?d need to come back in 10 to 15 years and get a new aortic valve. My only concern was if I?d be able to run after I got that new valve. ?Of course you can run,? my cardiologist assured me. That was in 2006.

By January 2011, I was barely able to walk up stairs without stopping for breath. I?d ?nap? for an hour in the morning at work, and for another hour in the afternoon. One day I went to a gym to do some spinning on a bike and had to quit after a minute.

My wife, who?s a physician, grew alarmed.

More tests came in fast order. It seemed my aortic valve was wearing out much sooner than expected. Dr. Ross said I needed valve replacement surgery. So on May 3, 2011, my rib cage was cut open and a team of surgeons at the Peter Munk Cardiac Centre at Toronto General Hospital replaced my aging aortic valve with a shiny new titanium one.

All went well. Right after surgery, I was taken to the intensive care unit for 24 hours. I was expected to remain in hospital for another four or five days. Then I?d be sent home, and for the next six weeks or so I?d recuperate and try to walk a little further each day. I could look forward to being back at work in a couple of months. When I was feeling up to it, I could ride my bike or even run.

That day in intensive care I drifted in and out of consciousness. The nurses asked me endlessly if I knew what day it was and could I spell the word ?world? backwards. Jean was by my side. Once when I woke up, she looked teary. I asked her what was wrong. She said: ?I?ll tell you when they take you to your room.?

They did that the next day.

?I think it?s time we told you what happened yesterday,? said Jean.

?Sure, what happened??

?Well, honey, you didn?t have a near-death experience.?

What was she talking about?

?You had a death experience.?

?What do you mean??

She was looking steadily into my eyes. ?Your heart stopped.?

?What??

I first thought it was a bad joke. My next thought was: ?Wow, I?m invincible!? Then, after a few seconds, as I absorbed the impact of what Jean had said, I burst into tears.

Jean told me I?d had sudden ?heart block? (not to be confused with heart blockage). She explained what had happened.

?How long was I dead??

?A little over two minutes.?

?How did they restart my heart??

?Just like on TV.?

So the next day a pacemaker was inserted below my collarbone to kick-start my heart should it ever ?block? again.

F. Scott Fitzgerald once said that in the real dark night of the soul, it is always 3 o?clock in the morning. For me, it was 5 o?clock. At that hour, when everything in the hospital is dark and quiet, I would wake from my drugged sleep and cry.

I know people die on the operating table. For every 100 Canadians who undergo aortic replacement surgery, 2.7 will not make it (although at the Munk Cardiac Centre, the rate is 0.9 per cent). Our parents can die in surgery, maybe. Not us. And certainly not me. Besides, I?d survived the open-heart surgery with flying colours. Mind you, I couldn?t remember a single thing about dying or coming back from the dead. No flashing lights or smiling loved ones. Nothing. In fact, I had to take it entirely on faith that any of this had happened. I told myself that my job right now was to get better physically.

Over the next six weeks, I tried to do precisely that. At home, I read a lot of books, watched a ton of TV and walked further each day.

A couple of times in the months before surgery, I?d felt dizzy and had to sit down, and when my wife would take my pulse, she?d declare I was in A-fib. In other words, I had that occasional irregular heartbeat, with resulting palpitations and shortness of breath.

The doctors had said they couldn?t fix my A-fib until they replaced my valve. It turns out my heart remained in A-fib after surgery. But not to worry, there were drugs that could regulate it. One of them was a beta blocker called Metoprolol. Unfortunately, it also made me tired and lethargic, pretty much how I had felt before surgery.

Two months after surgery, I had a post-operative meeting with my cardiac surgeon who pronounced the valve replacement a total success. So there was a bounce in my step as I headed out of his office and down University Avenue to a client meeting. I had been back at work as a communications consultant for a month. I ducked into the Hilton Hotel to go to the men?s room on the lower floor. Suddenly, my legs buckled. I grabbed ahold of the railing. What the hell was that?

I felt light-headed. My hands and jaw started to tingle. My lips grew numb. I turned around and pulled myself up the stairs to the main floor. I was damned if I was going to die alone in the men?s room in the basement of a hotel.

I walked unsteadily into the lobby and sat down. By this time, I was feeling dizzy, but I had to get out of there. So I got up and walked, one foot slowly in front of the other, outside. The doorman looked at me oddly. I was walking like a drunken sailor. When I walked smack into a building, hitting my arm on the marble wall, I knew I was in trouble. I was having a stroke. I had to get to the hospital. It had to be Toronto General. They had all my records. It was six blocks away.

Somehow, I managed to walk out onto the street and into oncoming traffic. I raised my hand and a taxi stopped right away. I got into the back and said: ?Toronto General Emerg.?

The driver looked at me in his mirror: ?Are you okay, mister??

?I?m not sure.?

Five minutes later, we were at the front door of one of the largest emergency units in Canada. I struggled out of the cab and walked up to the reception. I blurted out: ?I?m having a stroke.? I was pouring sweat and barely able to stand. Within a minute, two triage nurses got me into an examining room. There, they asked me if I could talk, if I was in pain, if I felt numb and where (?My hands, my jaw!?) and even the old standby, if I could spell ?world? backwards. By now the waves of dizziness forced me to prop my head on the top of my chair as I tried to answer their questions. The nurses moved me into an acute-care cardio bed in the ER. They called Jean, who rushed over. Over the next three hours, doctors, nurses and technicians poked, probed and questioned me. I felt better lying down, but the waves of dizziness and rapid heartbeat kept coming every 15 minutes. I was terrified.

After an hour, I was struck by the fact that no one was using the word ?stroke? anymore, so I assumed I wasn?t having one. It seems I had had a particularly virulent A-fib attack that had broken through the Metoprolol and sent my heartbeat racing?irregularly?to 140 beats per minute. All the doctors could do for now was give me more Metoprolol.

Six hours later, feeling exhausted and relieved, I left the ER with Jean. We took a cab home and I crawled into bed. I was well and truly gorked on Metoprolol.

The next morning, Jean told me the new prescription for Metoprolol would double the dose of what I?d been taking. Although it would make me feel even more lethargic, I should stay on the high dosage until they figured out what to do. Clearly, my A-fib was no longer a benign condition. I learned that a third of all strokes are caused by it.

While I?d hoped to be back to work full-time, it became obvious that it would take me longer to recover. Just writing a brief email took enormous energy. My concentration was shot, and my memory, well, it leaked everywhere. Jean said a lot of this was because of the drugs. Talking was tiring; a 10-minute conversation would leave me drained. And though I gradually got my strength and focus back over those weeks, if someone had asked me to write a 30-minute speech, as I?d routinely done before, I no longer had it in me.

After awhile, I knew that I really couldn?t work, so I had to lay off my two staff. This left me alone in the office, where I puttered with paperwork. But frankly, my big daytime activity last June and July was snoozing. I?d bought an air mattress and a blanket and would doze off for an hour each morning and two hours each afternoon.

A week after my first A-fib attack, it struck again. This time, I had a foreboding. Walking along Bay Street in midtown Toronto, I suddenly felt very light-headed. I knew right away I?d have to lie down, so I walked as fast as I could back to my office. I unlocked the door and bolted to the air mattress. My heart raced, my head spun. This time, lying down didn?t help. I was alone on the floor thinking: ?What if this isn?t A-fib, but that stroke I?m at risk of having?? I stood up unsteadily and called Jean, who was at work a block away. I told her I had to come over to her clinic. She told me to go to emerg. I made it downstairs and out onto Bay Street where a friend saw me clinging to a lamppost as I yelled for a cab. I didn?t want to call 911 because the ambulance might take too long. Besides, what if I was taken to the wrong hospital?

At Toronto General, the routine was much like my first visit, and I was discharged that night. Two weeks later, it happened again. Over the course of the month between my first A-fib attack and my third, I went into a profound physical and psychological free fall. When I wasn?t in A-fib, I was in terror of it. I stopped taking the subway for fear I?d be trapped underground during an attack. Each morning, I would map out which streets I would walk on. They couldn?t be side streets. They had to have lots of people, day and night, and most of all, lots of cabs.

By this time, I was avoiding even the few client meetings I needed to attend. Not just because I didn?t want my clients to call 911, but because there were two occasions when I was in the middle of a meeting and I simply burst into tears. So I stopped meeting clients in person as much as I could. But even the phone couldn?t shield me. I took calls from friends, and again I couldn?t stop weeping, and I?d hang up.

The fact is, I rarely went to the office anymore. I?d still do my daily walks. But why do anything that would get my heart rate higher and risk flipping into A-fib? So I stayed at home, slept and ate a lot. I gained 20 lb., filling the holes left by my anxiety.

I gave up reading books because I couldn?t remember what I?d read even as I was reading it. I stuck to magazines and newspapers (I remember getting through the entire front section of the Globe and Mail one day before I realized it was yesterday?s edition). I would lie in bed and watch half a dozen hour-long episodes of MI-5 in a row.

Three or four days would go by and there would be no attacks. I would think, ?Phew, they?re over.? But now, even a mild one brought the same terror as a major attack. Jean thought I should see my cardiologist.

Dr. Ross expressed some surprise that I was on such large doses of Metoprolol. I told him I was always tired. What I didn?t tell him was that I thought the Metoprolol was starting to make me crazy. He suggested I switch to a different kind of beta blocker, one called Sotolol. We talked about what could be done to stop the attacks. It was clear they were not just running my life, they were ruining it.

He said there were three ways out when it came to stopping A-fib. The first was drugs. Well, that clearly wasn?t working. The second was cardioversion, where your heart is shocked back into normal rhythm. But cardioversion only works on a third of patients. The same with drugs and the third option: ablation. They?d open up my heart again and ablate, or destroy, the areas of abnormal heart tissue that were causing the heart?s electrical system to short-circuit. The last thing I wanted was another round of open-heart surgery. Besides, you often had to wait three to six months after ablation for your heart to move back into normal rhythm.

I left Dr. Ross?s office feeling angry and helpless. When I talked to Jean, she admitted that whenever one medical problem had three solutions, generally none of them was really good. I told her that if each of these procedures only worked a third of the time, then the odds were against me ever beating A-fib. She suggested I was getting ahead of myself.

The next morning, a Friday in early August, I went to the drugstore to have my prescription filled for that new beta blocker. The pharmacist explained how often I had to take the pills and suggested I read the product description he had printed off.

I did. It said: ?Sotolol should only be taken in a hospital environment under the direct supervision of a cardiologist.?

What was this? ?Side effects include heart attack, stroke and sudden death.?

What the hell? I read it over and over.

By the time I got home, there was only one conclusion I could logically draw: my doctors were trying to kill me. This wasn?t just some angry fantasy. I truly believed I could no longer trust my cardiologist, my family doctor, or even my wife. So I called a friend who?s a doctor, Elaine Chin, and told her that my new beta blocker would surely kill me.

She suggested I go to the drugstore and buy a bottle of Tylenol and read the product description. ?It will say pretty much the same thing. They all do because they have to mention every conceivable bad outcome. So Bob: take the Sotolol!?

I did, half convinced I was going to drop dead right there.

That same evening, in another desperate effort to exert some control over my life, I told Jean that I was going to check into a hotel, which was just a block from the Toronto General ER. Jean carefully asked me why. I told her?or rather snapped?that I never wanted to be more than 100 yards from the hospital. My barking was one part anger at anyone who was listening, because they couldn?t solve my problem, and one part anger at myself that I was unable to help myself.

Over the last few weeks, my A-fib attacks had occurred more often, with greater force, and lasted longer. My memory had become even worse. I painstakingly entered every appointment in my Outlook calendar, checking to make sure I had the right time and date and place?and three times in a week I turned up for meetings 24 hours ahead of time, or at the wrong place. I tried to cling to my work, but I was way too jumpy to write anything more than a page at most.

Finally, on Aug. 3, I found myself lying on a gurney waiting to be cardioverted. I awoke an hour later to find my heart?thub-thub, thub-thub?beating normally. Days later, it was still fine. Those terrible days of A-fib were in the past. I could pick up where I?d left off in recovering from my valve replacement. I did that; I started to walk to the office. I was even willing to walk down side streets. I took the subway. I noticed that I could walk up more stairs without getting out of breath. I actually started to ride my bike.

But I felt highly anxious. I couldn?t understand why my psyche hadn?t returned to normal when my heart had. A friend called me one night from Chicago. She asked how I was. I burst into tears. I hung up and sent her a text message saying I was fine, really.

Then one evening after dinner, Jean and I went for a walk. Jean idly mentioned that most of the 12 doctors in her office had had a meeting that afternoon. ?Oh, what was that about?? I asked.

?It was about you.?

?Really??

?Yes. It took us 10 seconds to determine you?re depressed and 15 minutes to figure out which antidepressant you should go on.?

I was enraged. I turned to her, practically yelling: ?I?m not depressed. I?m just sad!?

?Right, darling . . . So the antidepressant is safe with all your meds and is called Remeron. Here?s the prescription. You can get it filled in the morning.?

After my flash of anger, I suddenly felt relieved. Someone cared! The cavalry was coming! But could I really be depressed? I?d forgotten the warning before my operation that one in three patients who has open-heart surgery will suffer from depression.

It takes a few weeks for any antidepressant to kick in, and weeks longer to fiddle with the right dosage. But I have to tell you, the next morning, after I picked up my prescription, taking care not to read the product description, I took my first dose of Remeron and felt better within 30 seconds. As Jean said, so great was my need to feel in control that the placebo effect likely sped me on my way.

Today, 16 months after I got a new valve and died, almost a year after my A-fib attacks fell away and a year after I was diagnosed with depression, I marvel at a number of things I?d taken for granted before. I?m amazed that the doctors at the Munk Cardiac Centre were right: I could run after I got my new valve. It?s three times a week at a plodding pace. But I?ll go further tomorrow than I did yesterday, and that counts for something, too.

I marvel at my heart and the new life it has given me. I?m back at work. I rarely cry. My clients have returned and Jean and I have just come home from trekking in the mountains of Bhutan. I marvel that our hearts sit quietly in our chests, beating 100,000 times a day in the seven billion of us who walk the Earth, with only a few of us giving it a second?s thought. Maybe that?s why heart disease doesn?t get the fear and loathing that cancer does, even though it will kill almost as many of us.

But the greatest marvel for me is that I finally realized that for three months last year I?d been living my life as if each day was my last. So now I?m happiest when I?m doing incredibly ordinary things, like having dinner with Jean, or reading a book, or even just going for a walk, one foot consciously in front of the other.

Source: http://www2.macleans.ca/2012/09/24/a-ticking-time-bomb/

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Tuesday, September 25, 2012

NASA's Orion spacecraft: Crew access arm reaches for new and heritage technologies

ScienceDaily (Sep. 24, 2012) ? NASA Kennedy Space Center's Ground Systems Development and Operations Program engineers in Florida are combining heritage technology and new innovations to design the crew access arm for the tower on the mobile launcher that will be used for NASA's Orion spacecraft atop the Space Launch System (SLS) rocket.

Orion will be the most advanced spacecraft ever designed and carry astronauts farther into space than ever before. SLS is designed to be flexible for launching spacecraft for crew and cargo missions and will enable new missions of exploration and expand human presence across the solar system. It will first launch Orion in 2017.

According to Kelli Maloney, a mechanical design engineer in the center's Engineering Directorate, the mobile launcher's new 60-foot-long hydraulic arm will be similar in length and speed to the arm used during the Apollo missions. It will have two levels and incorporate hardware from NASA's Apollo and Space Shuttle Programs.

Located at about the 270 feet high on the 355-foot-tall tower, the upper level will include a new "White Room" that provides access to the Orion crew module. The White Room will contain a six-foot-long access platform, also nicknamed the "diving board," that will extend through Orion's outer door to the crew module door. Refurbished Apollo era control console and accumulators also will be part of the new arm.

The lower-level walkway will provide access to two panels on the spacecraft's service module.

Maloney said design elements from the inflatable dock seal on the shuttle's orbiter access arm will be reused, as well as storage cabinets and safety equipment from the shuttle-era White Room.

The access arm will rotate out to the crew module on giant Apollo-era hinges. The hinges will be refurbished and retrofitted with new digital encoders to accurately obtain the arm's position.

"This information will be fed back to the Program Logic Controllers in an electrical room on the Mobile Launcher tower in order to achieve precise control of arm position," Maloney said.

Platforms from Launch Pad 39B's fixed service structure will be installed on the mobile launcher tower and provide access to the hinges for inspection and repair.

Maloney said new 3-D design visualization tools are being used to view the concept throughout the design process.

"It's a challenge, because you have to think about every detail," Maloney said. "It's very diverse."

During the process, heritage parts planned for reuse, such as Apollo-era control consoles, are scanned and then uploaded into a special 3-D design software program. Maloney said this process saves time and costs to modeling existing components.

"Having access to 3-D scanning capabilities is very helpful so that we can see how the design will fit into the existing structures, such as the mobile launcher, the Vehicle Assembly Building and Launch Pad 39B," Maloney said.

Another innovation for the future is that the White Room can be removed and replaced on the upper level of the arm to accommodate access to larger, planned SLS cargo vehicles and future launch vehicles.

The design team, comprising NASA and Engineering Services Contract engineers, is working toward a 60 percent design review in January 2013. Design work on the crew access arm, as well as other access arms and umbilicals, will continue through 2013. Fabrication of the access arm could begin in 2014, with testing in the Launch Equipment Test Facility at Kennedy in 2015.

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Source: http://feeds.sciencedaily.com/~r/sciencedaily/~3/rQ8Q3S5e8kQ/120924094129.htm

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