Source: gulfnews.com --- Tuesday, July 30, 2013
Agency asks Dubai to fix its budget and avoid another boom-and-bust cycle ...
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বুধবার, ৩১ জুলাই, ২০১৩
IMF: UAE economy recovering, but debt woes linger
[unable to retrieve full-text content]
Live wallpaper brings iOS7-like background effects on Android
1. thephonedude posted on 7
apple hate comments in 3...2....1...
I expected that. there's always a bunch of immature baboons who have no sense of being rational infiltrating P.A Posts relating to apple or Android.. possibly windows phone.
tell me, what's the point of saying "FROFLROOFLFLFLFILFFLOLOLOOOL Apple suksssss! Android ownzzz" or "WOW REVOLUTIONARY! (Old joke, bob.)"? I don't see How you twats would gain from flaming companies. I used androids and iDevices and I must say both are really good. if only someone heroic and brave enough to obliterate bIased rage nerds and geeks off of this website...
3. wendygarett posted on 5
Sorry dude, ios make it wrong, and android just correct that
5. roscuthiii posted on 2
Kinda seems like you're inviting it to happen now though...
I mean, yours is the first comment and it's not even about the article. It's about comments that haven't/hadn't even occurred yet. Ever heard the term: self-fulfilling prophecy?
12. itsdeepak4u2000 posted on 0
Yes +1 to you, I also wanted to comment the same.
6. AmitMajumder posted on 2
Ya, Dude. These people can be divided in 3 categories :-
1) Apple fan - "Android is great but I love iOS"
2) Android fan - "iOS is great but I love Android"
3) Idiots - "Apple sucks, BLA BLA Android is great / Android is copy, Apple is the real one And BLA BLA BLA...."
2. thephonedude posted on 2
BTW good that apple is back into the game......the new ios look shows that cupertino changed their direction. I'm looking forward to what innovations they will make (no sarcasm intended).
BTW here's something for the people who thinks tremendously high specs on a phone is everything- specs are like clothes. Branded clothes. for you to show off. Software and OS is like a person's character- what you are really made off. ;)
4. roscuthiii posted on 0
Normally I would not pay for a wallpaper, but... does look pretty cool for only $0.99. I'll give it some time out on the Play Store first though to see if customer comments confirm or deny it's effect on battery life.
7. E34V8 posted on 6
Such wallpapers were present in Google Play, long ago.
Maybe Apple took a little insPIRATion from them :) . Just joking.
8. Mercenary posted on 0
I'm using it right now..it's nice but doesn't worth to pay for..it must be free.
10. scriptwriter posted on 0
I brought an android smartphone because i dont like apple or apple products. Why would i want to make my phone look like an iphone? Pointless!! Completely!!!
11. bogdancirstea posted on 0
free http : // w w w47.zippyshare.com/v/97324538/file.html
13. itsdeepak4u2000 posted on 0
Nice Live wallpaper of iOS7-like background effects on Android.
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'Cory will forever be in my heart' Lea Michele thanks fans for their suppport via Twitter
The 26-year-old star, who has not been seen in public since Cory passed away on July 13, shared a message as well as a personal photo of them together on her Twitter and Instagram pages.
"Thank you all for helping me through this time with your enormous love & support. Cory will forever be in my heart," she wrote alongside the intimate snap which shows Lea cuddling up to Cory in a beach as they grin for the camera.
It has obviously been a very difficult time for the brunette, who has been spending a lot of time with Cory's mother after helping to organise his funeral.
Lea has also been seeking solace in her grief from her fellow Glee cast and joined them for a memorial service last week "to share memories and music in an emotional celebration of the life of Cory," according to a statement.
Cory, who played Finn Hudson in Glee, was found dead in his hotel room in Vancouver earlier this month.
Results later showed that he had died from a heroin and alcohol overdose - despite having been in rehab earlier on in the year.
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মঙ্গলবার, ১৮ জুন, ২০১৩
North Korea changes tack and tells US: Let's talk
PYONGYANG, North Korea (AP) ? After months of threatening to wage a nuclear war, North Korea did an about-face Sunday and issued a surprise proposal to the United States, its No. 1 enemy: Let's talk.
But the invitation from North Korea's National Defense Commission, the powerful governing body led by leader Kim Jong Un, comes with caveats: No preconditions and no demands that Pyongyang give up its prized nuclear assets unless Washington is willing to do the same ? ground rules that make it hard for the Americans to accept.
Washington responded by saying that it is open to talks ? but only if North Korea shows it will comply with U.N. Security Council resolutions and live up to its international obligations.
"As we have made clear, our desire is to have credible negotiations with the North Koreans, but those talks must involve North Korea living up to its obligations to the world, including compliance with U.N. Security Council resolutions, and ultimately result in denuclearization," U.S. National Security Council spokeswoman Caitlin Hayden said in a statement. "We will judge North Korea by its actions, and not its words and look forward to seeing steps that show North Korea is ready to abide by its commitments and obligations."
North Korea's call for "senior-level" talks between the Korean War foes signals a shift in policy in Pyongyang after months of acrimony.
Pyongyang ramped up the anti-American rhetoric early this year after its launch of a long-range rocket in December and a nuclear test in February drew tightened U.N. and U.S. sanctions. Posters went up across the North Korean capital calling on citizens to "wipe away the American imperialist aggressors," slogans that hadn't been seen on city streets in years.
The U.S. and ally South Korea countered the provocations and threats by stepping up annual springtime military exercises, which prompted North Korea to warn of a "nuclear war" on the Korean Peninsula.
But as tensions began subsiding in May and June, Pyongyang began making tentative, if unsuccessful, overtures to re-establish dialogue with Seoul and Washington.
Earlier this month, it proposed high-level talks with South Korea ? the first in six years. But plans for two days of meetings last week in Seoul dramatically fell apart even before they began amid bickering over who would lead the two delegations.
Meanwhile, the virulent anti-American billboards plastered across the city were taken down. And on Sunday, as scores of people fanned out across Pyongyang to help carry out the latest urban renewal projects in the capital ? landscaping and construction ? the National Defense Commission issued a statement through state media proposing talks with the U.S. to ease tensions and discuss a peace treaty formally ending the Korean War.
North Korea fought against U.S.-led United Nations and South Korean troops during the three-year Korean War in the early 1950s, and Pyongyang does not have diplomatic relations with either government. The Korean Peninsula remains divided by a heavily fortified border.
Reunifying the peninsula was a major goal of North Korea's two late leaders, Kim Il Sung and Kim Jong Il, and is a legacy inherited by current leader Kim Jong Un. North Korea is expected to draw attention to Korea's division in the weeks leading up to the 60th anniversary in July marking the close of the Korean conflict, which ended in an armistice. A peace treaty has never been signed formally ending the war.
Across Pyongyang, signboards at construction sites are marked with a countdown to July 27, giving laborers a deadline for retiling the roof of the People's Palace of Culture, renovating the Korean War museum, and planting trees and grass meant to beautify the city for the milestone anniversary.
For the nation's leaders, July 27 may well be their deadline for drawing the United States to the negotiating table to discuss a peace treaty.
But for Washington, there will be no talks just for talks' sake, officials say.
Speaking on CBS television's "Face the Nation" show Sunday, President Barack Obama's chief of staff, Denis McDonough, said Washington has been "quite clear" that officials support dialogue and have engaged Pyongyang in talks in the past.
But "those talks have to be real. They have to be based on them living up to their obligations, to include on proliferation, on nuclear weapons, on smuggling and other things," he said. "And so we'll judge them by their actions, not by the nice words that we heard yesterday."
He said smooth talk will not help Pyongyang evade U.N. sanctions supported by Moscow and Beijing, North Korea's two traditional allies. U.N. Security Council resolutions ban North Korea from developing its nuclear and ballistic missile programs.
Earlier this year, Kim Jong Un enshrined the drive to build a nuclear arsenal, as well as expand the economy, in North Korea's constitution. Pyongyang, estimated to have a handful of crude nuclear devices, says it needs to build atomic weapons to defend itself against what it sees as a U.S. nuclear threat in Korea and the region.
The National Defense Commission reiterated its refusal to give up its nuclear ambitions until the entire Korean Peninsula is free of nuclear weapons, a spokesman said in a statement carried by the Korean Central News Agency.
"The denuclearization of the Korean Peninsula does not only mean 'dismantling the nuclear weapons of the North'" but also should involve "denuclearizing the whole peninsula, including South Korea, and aims at totally ending the U.S. nuclear threats" to North Korea, the spokesman said.
The U.S. denies having nuclear bombs in South Korea, saying they were removed in 1991. However, the U.S. military keeps nuclear submarines in the region and has deployed them for military exercises with South Korea.
After blaming Washington for raising tensions by imposing "gangster-like sanctions" on North Korea, the spokesman called on the U.S. to propose a venue and date for talks ? but warned against setting preconditions.
Washington has been burned in the past by efforts to reach out to Pyongyang.
Months of behind-the-scenes negotiations yielded a significant food-for-disarmament deal in February 2012, but that was scuttled by a failed North Korean long-range rocket launch just weeks later.
___
Associated Press writers Youkyung Lee in Seoul, South Korea, and Tom Strong in Washington, contributed to this report. Follow AP's Korea bureau chief on Twitter at twitter.com/newsjean.
Source: http://news.yahoo.com/north-korea-changes-tack-tells-us-lets-talk-164523908.html
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সোমবার, ১৭ জুন, ২০১৩
NYSCF and Columbia researchers demonstrate use of stem cells to analyze causes, treatment of diabetes
![[ Back to EurekAlert! ]](https://lh3.googleusercontent.com/blogger_img_proxy/AEn0k_uySfgZtWV3CrN-1B6E8NzDanBB0WQ-oPqXZFyQD5yTVQvgdyY79EoyFI0ZhFjIRMRGQJu_dwjiy82invPlg2B-IDHJsGTCqKOH81z5Gbc=s0-d){kind=small}
Public release date: 17-Jun-2013[ | E-mail |
Share ] Contact: David McKeon
dmckeon@nyscf.org
212-365-7440
New York Stem Cell Foundation
Using patient-specific stem cells to correct deficient insulin-producing cells
NEW YORK, NY (June 17, 2013) A team from the New York Stem Cell Foundation (NYSCF) Research Institute and the Naomi Berrie Diabetes Center of Columbia University has generated patient-specific beta cells, or insulin-producing cells, that accurately reflect the features of maturity-onset diabetes of the young (MODY).
The researchers used skin cells of MODY patients to produce induced pluripotent stem (iPS) cells, from which they then made beta cells. Transplanted into a mouse, the stem cell-derived beta cells secreted insulin in a manner similar to that of the beta cells of MODY patients. Repair of the gene mutation restored insulin secretion to levels seen in cells obtained from healthy subjects. The findings were reported today in the Journal of Clinical Investigation.
Previous studies have demonstrated the ability of human embryonic stem cells and iPS cells to become beta cells that secrete insulin in response to glucose or other molecules. But the question remained as to whether stem cell-derived beta cells could accurately model genetic forms of diabetes and be used to develop and test potential therapies.
"We focused on MODY, a form of diabetes that affects approximately one in 10,000 people. While patients and other models have yielded important clinical insights into this disease, we were particularly interested in its molecular aspectshow specific genes can affect responses to glucose by the beta cell," said co-senior author Dieter Egli, PhD, Senior Research Fellow at NYSCF, who was named a NYSCFRobertson Stem Cell Investigator in 2012.
MODY is a genetically inherited form of diabetes. The most common form of MODY, type 2, results in a loss-of-function mutation in one copy of the gene that codes for the sugar-processing enzyme glucokinase (GCK). With type 2 MODY, higher glucose levels are required for GCK to metabolize glucose, leading to chronic, mildly elevated blood sugar levels and increased risk of vascular complications.
MODY patients are frequently misdiagnosed with type 1 or 2 diabetes. Proper diagnosis can not only change the patient's course of treatment but affect family members, who were previously unaware that they, too, might have this genetic disorder.
NYSCF scientists took skin cells from two Berrie Center type 2 MODY patients and "reprogrammed"or revertedthem to an embryonic-like state to become iPS cells. To examine the effect of the GCK genetic mutation, they also created two genetically manipulated iPS cell lines for comparison: one fully functional (two correct copies of the GCK gene) and one with complete loss of function (two faulty copies of the GCK gene). They then generated beta cell precursors from the fully functional and loss-of-function iPS cell lines and transplanted the cells for further maturation into immune-compromised mice.
"Our ability to create insulin-producing cells from skin cells, and then to manipulate the GCK gene in these cells using recently developed molecular methods, made it possible to definitively test several critical aspects of the utility of stem cells for the study of human disease," said Haiqing Hua, PhD, lead author on the paper, a postdoctoral fellow in the Division of Molecular Genetics, Department of Pediatrics and Naomi Berrie Diabetes Center at Columbia University and the New York Stem Cell Foundation Research Institute.
When given a glucose tolerance test three months later, mice with MODY beta cells had decreased sensitivity to glucose but a normal response to other molecules that stimulate insulin secretion. This is the hallmark of MODY. Mice with two faulty copies of the GCK gene secreted no additional insulin in response to glucose. When the researchers repaired the GCK mutation using molecular techniques, cells with two restored copies of GCK responded normally to the glucose stress test. Unlike other reported techniques, the researchers' approach efficiently repaired the GCK mutation without introducing any potentially harmful additional DNA.
"Generation of patient-derived beta cells with gene correction could ultimately prove to be a useful cell-replacement therapy by restoring patients' ability to regulate their own glucose. This result is truly exciting," said Susan L. Solomon, Chief Executive Officer of The New York Stem Cell Foundation.
The researchers also used an electron microscope to assess beta cells for insulin content by counting granulespackages that store insulin for release. Even though all beta cell types had a similar number of granules, complete loss of function of the GCK gene was associated with decreased beta-cell production.
"These studies provide a critical proof-of-principle that genetic characteristics of patient-specific insulin-producing cells can be recapitulated through use of stem cell techniques and advanced molecular biological manipulations. This opens up strategies for the development of new approaches to the understanding, treatment, and, ultimately, prevention of more common types of diabetes," said co-senior author Rudolph Leibel, MD, Christopher Murphy Memorial Professor of Diabetes Research, Columbia University Medical Center, and Director, Division of Molecular Genetics, and Co-Director of the Naomi Berrie Diabetes Center.
The other authors are: Linshan Shang and Hector Martinez of the New York Stem Cell Foundation Research Institute; and Matthew Freeby, Mary Pat Gallagher, Thomas Ludwig, Liyong Deng, Ellen Greenberg, Charles LeDuc, Wendy K. Chung, and Robin Goland of the Division of Molecular Genetics, Department of Pediatrics, and Naomi Berrie Diabetes Center at Columbia University.
###
Funding for this study was provided by: The New York Stem Cell Foundation; the Russell Berrie Foundation; the Leona M. and Harry B. Helmsley Charitable Trust; the Hunter Eastman Scholar Award in Translational Diabetes Research; the James and Irene Hunter Charitable Fund; an ADA-Mentored Fellowship to H. Hua; and NIH Grants RO1 DK52431 and P30DK063608.
The authors report no financial or other conflict of interest.
About The New York Stem Cell Foundation
The New York Stem Cell Foundation (NYSCF) is an independent organization founded in 2005 to accelerate cures and better treatments for patients through stem cell research. NYSCF employs over 40 researchers at the NYSCF Research Institute, located in New York, and is an acknowledged world leader in stem cell research and in developing pioneering stem cell technologies, including the NYSCF Global Stem Cell Array. Additionally, NYSCF supports another 60 researchers at other leading institutions worldwide through its Innovator Programs, including the NYSCF Druckenmiller Fellowships and the NYSCF-Robertson Investigator Awards. NYSCF focuses on translational research in a model designed to overcome the barriers that slow discovery and replaces silos with collaboration.
NYSCF researchers have achieved four major discoveries in the field, including: the discovery of a clinical cure to prevent transmission of maternal mitochondrial diseases in December 2012; the derivation of the first-ever patient specific embryonic stem cell line (#1 Medical Breakthrough of 2011 by Time magazine); the discovery of a new way to reprogram stem cells; and the creation of the first disease model from induced pluripotent stem cells (also named the #1 Medical Breakthrough by Time magazine in 2008). More information is available at http://www.nyscf.org.
About the Naomi Berrie Diabetes Center
Upon its official opening in October 1998, the Naomi Berrie Diabetes Center at Columbia University Medical Center established a new standard of care for the 1.6 million people with diabetes in the New York areacombining world-class diabetes research and education programs with unprecedented family-oriented patient care. Founded with support from the Russell Berrie Foundation and other friends, and named in honor of the mother of the late Russell Berrie, founder of RUSS Toys, the center is today recognized as the most comprehensive diabetes research and treatment center in the tri-state region and has been designated a national "Diabetes Center of Excellence" one of only three in the state of New York. Approximately one hundred and fifty clinicians and scientists, affiliated with the Center, conduct basic and clinical research related to the pathogenesis and treatment of all forms of diabetes and its complications. For more information, visit nbdiabetes.org.
Drs. Chung and Leibel are also members of the Columbia Stem Cell Initiative (http://www.ColumbiaStemCell.org), which brings together the many scientists and clinicians at Columbia focused on tapping the potential of stem cells for human health.
About Columbia University Medical Center
Columbia University Medical Center provides international leadership in basic, preclinical, and clinical research; medical and health sciences education; and patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest faculty medical practices in the Northeast. For more information, visit cumc.columbia.edu or columbiadoctors.org.
[ | E-mail | 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.
Public release date: 17-Jun-2013[ | E-mail |
Share ] Contact: David McKeon
dmckeon@nyscf.org
212-365-7440
New York Stem Cell Foundation
Using patient-specific stem cells to correct deficient insulin-producing cells
NEW YORK, NY (June 17, 2013) A team from the New York Stem Cell Foundation (NYSCF) Research Institute and the Naomi Berrie Diabetes Center of Columbia University has generated patient-specific beta cells, or insulin-producing cells, that accurately reflect the features of maturity-onset diabetes of the young (MODY).
The researchers used skin cells of MODY patients to produce induced pluripotent stem (iPS) cells, from which they then made beta cells. Transplanted into a mouse, the stem cell-derived beta cells secreted insulin in a manner similar to that of the beta cells of MODY patients. Repair of the gene mutation restored insulin secretion to levels seen in cells obtained from healthy subjects. The findings were reported today in the Journal of Clinical Investigation.
Previous studies have demonstrated the ability of human embryonic stem cells and iPS cells to become beta cells that secrete insulin in response to glucose or other molecules. But the question remained as to whether stem cell-derived beta cells could accurately model genetic forms of diabetes and be used to develop and test potential therapies.
"We focused on MODY, a form of diabetes that affects approximately one in 10,000 people. While patients and other models have yielded important clinical insights into this disease, we were particularly interested in its molecular aspectshow specific genes can affect responses to glucose by the beta cell," said co-senior author Dieter Egli, PhD, Senior Research Fellow at NYSCF, who was named a NYSCFRobertson Stem Cell Investigator in 2012.
MODY is a genetically inherited form of diabetes. The most common form of MODY, type 2, results in a loss-of-function mutation in one copy of the gene that codes for the sugar-processing enzyme glucokinase (GCK). With type 2 MODY, higher glucose levels are required for GCK to metabolize glucose, leading to chronic, mildly elevated blood sugar levels and increased risk of vascular complications.
MODY patients are frequently misdiagnosed with type 1 or 2 diabetes. Proper diagnosis can not only change the patient's course of treatment but affect family members, who were previously unaware that they, too, might have this genetic disorder.
NYSCF scientists took skin cells from two Berrie Center type 2 MODY patients and "reprogrammed"or revertedthem to an embryonic-like state to become iPS cells. To examine the effect of the GCK genetic mutation, they also created two genetically manipulated iPS cell lines for comparison: one fully functional (two correct copies of the GCK gene) and one with complete loss of function (two faulty copies of the GCK gene). They then generated beta cell precursors from the fully functional and loss-of-function iPS cell lines and transplanted the cells for further maturation into immune-compromised mice.
"Our ability to create insulin-producing cells from skin cells, and then to manipulate the GCK gene in these cells using recently developed molecular methods, made it possible to definitively test several critical aspects of the utility of stem cells for the study of human disease," said Haiqing Hua, PhD, lead author on the paper, a postdoctoral fellow in the Division of Molecular Genetics, Department of Pediatrics and Naomi Berrie Diabetes Center at Columbia University and the New York Stem Cell Foundation Research Institute.
When given a glucose tolerance test three months later, mice with MODY beta cells had decreased sensitivity to glucose but a normal response to other molecules that stimulate insulin secretion. This is the hallmark of MODY. Mice with two faulty copies of the GCK gene secreted no additional insulin in response to glucose. When the researchers repaired the GCK mutation using molecular techniques, cells with two restored copies of GCK responded normally to the glucose stress test. Unlike other reported techniques, the researchers' approach efficiently repaired the GCK mutation without introducing any potentially harmful additional DNA.
"Generation of patient-derived beta cells with gene correction could ultimately prove to be a useful cell-replacement therapy by restoring patients' ability to regulate their own glucose. This result is truly exciting," said Susan L. Solomon, Chief Executive Officer of The New York Stem Cell Foundation.
The researchers also used an electron microscope to assess beta cells for insulin content by counting granulespackages that store insulin for release. Even though all beta cell types had a similar number of granules, complete loss of function of the GCK gene was associated with decreased beta-cell production.
"These studies provide a critical proof-of-principle that genetic characteristics of patient-specific insulin-producing cells can be recapitulated through use of stem cell techniques and advanced molecular biological manipulations. This opens up strategies for the development of new approaches to the understanding, treatment, and, ultimately, prevention of more common types of diabetes," said co-senior author Rudolph Leibel, MD, Christopher Murphy Memorial Professor of Diabetes Research, Columbia University Medical Center, and Director, Division of Molecular Genetics, and Co-Director of the Naomi Berrie Diabetes Center.
The other authors are: Linshan Shang and Hector Martinez of the New York Stem Cell Foundation Research Institute; and Matthew Freeby, Mary Pat Gallagher, Thomas Ludwig, Liyong Deng, Ellen Greenberg, Charles LeDuc, Wendy K. Chung, and Robin Goland of the Division of Molecular Genetics, Department of Pediatrics, and Naomi Berrie Diabetes Center at Columbia University.
###
Funding for this study was provided by: The New York Stem Cell Foundation; the Russell Berrie Foundation; the Leona M. and Harry B. Helmsley Charitable Trust; the Hunter Eastman Scholar Award in Translational Diabetes Research; the James and Irene Hunter Charitable Fund; an ADA-Mentored Fellowship to H. Hua; and NIH Grants RO1 DK52431 and P30DK063608.
The authors report no financial or other conflict of interest.
About The New York Stem Cell Foundation
The New York Stem Cell Foundation (NYSCF) is an independent organization founded in 2005 to accelerate cures and better treatments for patients through stem cell research. NYSCF employs over 40 researchers at the NYSCF Research Institute, located in New York, and is an acknowledged world leader in stem cell research and in developing pioneering stem cell technologies, including the NYSCF Global Stem Cell Array. Additionally, NYSCF supports another 60 researchers at other leading institutions worldwide through its Innovator Programs, including the NYSCF Druckenmiller Fellowships and the NYSCF-Robertson Investigator Awards. NYSCF focuses on translational research in a model designed to overcome the barriers that slow discovery and replaces silos with collaboration.
NYSCF researchers have achieved four major discoveries in the field, including: the discovery of a clinical cure to prevent transmission of maternal mitochondrial diseases in December 2012; the derivation of the first-ever patient specific embryonic stem cell line (#1 Medical Breakthrough of 2011 by Time magazine); the discovery of a new way to reprogram stem cells; and the creation of the first disease model from induced pluripotent stem cells (also named the #1 Medical Breakthrough by Time magazine in 2008). More information is available at http://www.nyscf.org.
About the Naomi Berrie Diabetes Center
Upon its official opening in October 1998, the Naomi Berrie Diabetes Center at Columbia University Medical Center established a new standard of care for the 1.6 million people with diabetes in the New York areacombining world-class diabetes research and education programs with unprecedented family-oriented patient care. Founded with support from the Russell Berrie Foundation and other friends, and named in honor of the mother of the late Russell Berrie, founder of RUSS Toys, the center is today recognized as the most comprehensive diabetes research and treatment center in the tri-state region and has been designated a national "Diabetes Center of Excellence" one of only three in the state of New York. Approximately one hundred and fifty clinicians and scientists, affiliated with the Center, conduct basic and clinical research related to the pathogenesis and treatment of all forms of diabetes and its complications. For more information, visit nbdiabetes.org.
Drs. Chung and Leibel are also members of the Columbia Stem Cell Initiative (http://www.ColumbiaStemCell.org), which brings together the many scientists and clinicians at Columbia focused on tapping the potential of stem cells for human health.
About Columbia University Medical Center
Columbia University Medical Center provides international leadership in basic, preclinical, and clinical research; medical and health sciences education; and patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest faculty medical practices in the Northeast. For more information, visit cumc.columbia.edu or columbiadoctors.org.
[ | E-mail | 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/2013-06/nysc-nc061713.php
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Self-esteem - ADD Forums - Attention Deficit Hyperactivity Disorder ...
I also struggle with this from time to time. Right now I am doing great again. Some things that help me:
- Being conscious that no one is perfect and that everyone needs a lot of practice to become good at something. Practice requires failure. Failure requires courage. Courage simply means being conscious of what could go wrong but believing you could conquer something... sooner or later!
- It's better to learn something late then never (a recent example for me: I just started to learn to keep my room organized. I have never been able to, and while I am not perfect I'm already a lot better at this then I was)
- A lot of quality time with friends and family, open heartedly discussing what goes on within you, has helped me a lot. Knowing that there are people who love me, who know me. Connecting to them in this way gives me a huge boost of self confidence. Hearing that they believe in me. Saying to them that it's sometimes hard, but that I will keep on going for it! Hearing that they love whatever happens. No substitute for that! (It's quite special to have such good relations with people, but I hope that if you have these people, treasure them, or invest in them! Or find them.)
- Have patience with yourself and focus on one issue at the time. All other issues should be irrelevant, something for later that you accept at the time. And have plenty of fun and relaxing time. You need that to be fit to conquer the issue you're focussing on.
For me, I've always see that I need a 3:1 ratio, or better, for positive:negative thoughts/experiences. If I have a 5:1 ratio, I am in a positive cycle and changing something is really easy. If I have a 1:5 ratio, then I can really get stuck and totally lose my self esteem.
It's not totally up to us to determine how this ratio is for use. There can be negative and stressful circumstances and events in our lives. But there are things that we can control and these are the number of goals we set for ourselves (which should never exceed 2, preferably 1 - I am talking about new goals, about changing stuff, which causes stress and perhaps shame and guilt) and the time and activities we allow ourselves to have fun and relax.
So, to summarize: for me, the keys are: reflection, courage, patience, meaningful relations with people (quality time), balancing and fun and relaxing.
Source: http://www.addforums.com/forums/showthread.php?t=146704
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Woods matches his worst US Open round as a pro
ARDMORE, Pa. (AP) ? Tiger Woods made birdie at the first hole, only to watch his day go racing downhill from there.
By the time it was over, Woods skidded to seven bogeys and a 6-over-par 76 Saturday, tumbling down the leaderboard and matching his worst round as a pro at the U.S. Open. That left him 10 strokes behind third-round leader Phil Mickelson, the only player under par at the short but devilishly tough Merion Golf Club.
Despite leading the PGA Tour in putting in recent weeks, Woods needed 36 putts on the severely undulating greens. He blamed his inability to gauge the speed of those baffling putting surfaces for his three days of uneven play ? and he was right.
Woods is tied for third in fairways hit and 22nd in reaching the greens in regulation. But he's averaged 32 putts per round, which left him tied for 53rd in the field of 73 players.
"It's certainly frustrating because I was feeling like I was playing well this week and I just didn't make the putts I needed to make," he said afterward.
"The first two days, I had, like, three 3-putts and I was four shots off the lead, and I missed a boatload of putts within 10 feet. So I really wasn't that far off. If I clean up the round and don't 3-putt, I'm one shot back starting out today. ..." Woods added.
"Basically, I just didn't have the speed right this week and it certainly showed."
Woods' toughest stretch came at Nos. 3-6, where he made three bogeys in a four-hole stretch. He blamed the last of those for setting the negative tone that hung over his round like the storm clouds that rolled over Merion throughout Thursday's opening round. His troubles at No. 6 included a tee shot that finished up in another player's divot in the fairway, as well as a delicate greenside chip that rolled back and left him facing his next shot from farther back.
"I think the (bogey) 5 really turned my round around," Woods said. "I drove it right in the middle of the fairway and I end up in a ball mark from somebody else's ball mark, so it was kind of the way it went."
This U.S. Open marks exactly five years since Woods won his last major, at Torrey Pines, which he captured in a playoff against Rocco Mediate, despite hobbling around with ligament damage. His pursuit of Jack Nicklaus' career record of 18 majors remains stalled at 14.
Woods also shot a 76 in the final round at Shinnecock Hills in 2004, as well as two rounds of 76 at Winged Foot in 2006 when he missed the cut.
Woods' worst round ever at an Open was a 77 at Oakland Hills in 1996, when he was a 19-year-old amateur.
What made his performance here perhaps even more surprising is that Woods has already won four times this season, including The Players Championship ? sometimes called golf's fifth major ? and three of his last five starts. Most recently, however, Woods stumbled to an 8-over-par finish and a tie for 65th at the Memorial, a tournament he'd won five times.
Woods said several tough pin placements chosen by the U.S. Golf Association's course set up compounded his problems trying to figure out the speed of the greens.
"Look at what they did at (Nos.) 7 and 8 today. Couple short holes, but 7 is one step and a half over the top of the ridge. Eight is on the down slope a little bit, and it's a pretty steep slope. So they got some really tough ones out there," he said.
But Woods' also conceded he rarely put his approach shots into those greens where he should have.
"If you put the ball in the right spots you've got uphill putts and you can be really aggressive," Woods said.
Woods now faces the prospect of beginning the final day of yet another major with only the longest of shots to contend. What little consolation he could muster came when someone asked, "Tough day?"
"Yeah," Woods replied. "At least I started well."
Source: http://news.yahoo.com/woods-matches-worst-us-open-round-pro-003419332.html
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