Tuesday, January 29, 2013

Safer way to vaccinate? Polymer film that gradually releases DNA coding for viral proteins may beat traditional vaccines

Jan. 28, 2013 ? Vaccines usually consist of inactivated viruses that prompt the immune system to remember the invader and launch a strong defense if it later encounters the real thing. However, this approach can be too risky with certain viruses, including HIV.

In recent years, many scientists have been exploring DNA as a potential alternative vaccine. About 20 years ago, DNA coding for viral proteins was found to induce strong immune responses in rodents, but so far, tests in humans have failed to duplicate that success.

In a paper appearing in the Jan. 27 online issue of Nature Materials, MIT researchers describe a new type of vaccine-delivery film that holds promise for improving the effectiveness of DNA vaccines. If such vaccines could be successfully delivered to humans, they could overcome not only the safety risks of using viruses to vaccinate against diseases such as HIV, but they would also be more stable, making it possible to ship and store them at room temperature.

This type of vaccine delivery would also eliminate the need to inject vaccines by syringe, says Darrell Irvine, an MIT professor of biological engineering and materials science and engineering. "You just apply the patch for a few minutes, take it off and it leaves behind these thin polymer films embedded in the skin," he says.

Irvine and Paula Hammond, the David H. Koch Professor in Engineering, are the senior authors of the Nature Materials paper. Both are members of MIT's David H. Koch Institute for Integrative Cancer Research. The lead author of the paper is Peter DeMuth, a graduate student in biological engineering.

Gradual vaccine delivery

Scientists have had some recent success delivering DNA vaccines to human patients using a technique called electroporation. This method requires first injecting the DNA under the skin, then using electrodes to create an electric field that opens small pores in the membranes of cells in the skin, allowing DNA to get inside. However, the process can be painful and give varying results, Irvine says.

"It's showing some promise but it's certainly not ideal and it's not something you could imagine in a global prophylactic vaccine setting, especially in resource-poor countries," he says.

Irvine and Hammond took a different approach to delivering DNA to the skin, creating a patch made of many layers of polymers embedded with the DNA vaccine. These polymer films are implanted under the skin using microneedles that penetrate about half a millimeter into the skin -- deep enough to deliver the DNA to immune cells in the epidermis, but not deep enough to cause pain in the nerve endings of the dermis.

Once under the skin, the films degrade as they come in contact with water, releasing the vaccine over days or weeks. As the film breaks apart, the DNA strands become tangled up with pieces of the polymer, which protect the DNA and help it get inside cells.

The researchers can control how much DNA gets delivered by tuning the number of polymer layers. They can also control the rate of delivery by altering how hydrophobic (water-fearing) the film is. DNA injected on its own is usually broken down very quickly, before the immune system can generate a memory response. When the DNA is released over time, the immune system has more time to interact with it, boosting the vaccine's effectiveness.

The polymer film also includes an adjuvant -- a molecule that helps to boost the immune response. In this case, the adjuvant consists of strands of RNA that resemble viral RNA, which provokes inflammation and recruits immune cells to the area.

The ability to provoke inflammation is one of the key advantages of the new delivery system, says Michele Kutzler, an assistant professor at Drexel University College of Medicine. Other benefits include targeting the wealth of immune cells in the skin, the use of a biodegradable delivery material, and the possibility of pain-free vaccine delivery, she says.

"It's an interesting approach that can be applied not just to delivery of DNA-based vaccine antigens, but other small molecules," says Kutzler, who was not part of the research team.

Eliciting immune responses

In tests with mice, the researchers found that the immune response induced by the DNA-delivering film was as good as or better than that achieved with electroporation.

To test whether the vaccine might provoke a response in primates, the researchers applied a polymer film carrying DNA that codes for proteins from the simian form of HIV to macaque skin samples cultured in the lab. In skin treated with the film, DNA was easily detectable, while DNA injected alone was quickly broken down.

"The hope is that that's an indication that this will translate to large animals and hopefully humans," Irvine says.

The researchers now plan to perform further tests in non-human primates before undertaking possible tests in humans. If successful, the vaccine-delivering patch could potentially be used to deliver vaccines for many different diseases, because the DNA sequence can be easily swapped out depending on the disease being targeted.

"If you're making a protein vaccine, every protein has its little quirks, and there are manufacturing issues that have to be solved to scale it up to humans. If you had a DNA platform, the DNA is going to behave the same no matter what antigen it's encoding," Irvine says.

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Story Source:

The above story is reprinted from materials provided by Massachusetts Institute of Technology. The original article was written by Anne Trafton.

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


Journal Reference:

  1. Peter C. DeMuth, Younjin Min, Bonnie Huang, Joshua A. Kramer, Andrew D. Miller, Dan H. Barouch, Paula T. Hammond, Darrell J. Irvine. Polymer multilayer tattooing for enhanced DNA?vaccination. Nature Materials, 2013; DOI: 10.1038/nmat3550

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

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

Source: http://feeds.sciencedaily.com/~r/sciencedaily/strange_science/~3/S-p9Fg4Dyxo/130128113922.htm

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Chris Brown Wants To Talk To Police Over Frank Ocean Fight

Brown's lawyer says he has evidence his client didn't throw any punches.
By Gil Kaufman


Chris Brown and Frank Ocean
Photo: Getty Images

Source: http://www.mtv.com/news/articles/1700951/chris-brown-frank-ocean-fight-police.jhtml

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Diabetes drug could hold promise for lung cancer patients

Diabetes drug could hold promise for lung cancer patients [ Back to EurekAlert! ] Public release date: 28-Jan-2013
[ | E-mail | Share Share ]

Contact: Andy Hoang
AHoang@salk.edu
619-861-5811
Salk Institute

Salk study suggests metabolism-based cancer therapy may be useful for non-small cell lung cancer

LA JOLLA, CA Ever since discovering a decade ago that a gene altered in lung cancer regulated an enzyme used in therapies against diabetes, Reuben Shaw has wondered if drugs originally designed to treat metabolic diseases could also work against cancer.

The growing evidence that cancer and metabolism are connected, emerging from a number of laboratories around the world over the past 10 years, has further fueled these hopes, though scientists are still working to identify what tumors might be most responsive and which drugs most useful.

Now, in a new study in the journal Cancer Cell, Shaw and a team of scientists at the Salk Institute for Biological Studies found that phenformin, a derivative of the widely-used diabetes drug metformin, decreased the size of lung tumors in mice and increased the animals' survival. The findings may give hope to the nearly 30 percent of patients with non-small cell lung cancer (NSCLC) whose tumors lack LKB1 (also called STK11).

The LKB1 gene turns on a metabolic enzyme called AMPK when energy levels of ATP, molecules that store the energy we need for just about everything we do, run low in cells. In a previous study, Shaw, an associate professor in Salk's Molecular and Cell Biology Laboratory and researcher in the Institute's new Helmsley Center for Genomic Medicine, demonstrated that cells lacking a normal copy of the LKB1 gene fail to activate AMPK in response to low energy levels. LKB1-dependent activation of AMPK serves as a low-energy checkpoint in the cell. Cells that lack LKB1 are unable to sense such metabolic stress and initiate the process to restore their ATP levels following a metabolic change. As a result, these LKB1-mutant cells run out of cellular energy and undergo apoptosis, or programmed cell death, whereas cells with intact LKB1 are alerted to the crisis and re-correct their metabolism.

"The driving idea behind the research is knowing that AMPK serves as a sensor for low energy loss in cells and that LKB1-deficient cells lack the ability to activate AMPK and sense energy loss," says David Shackelford, a postdoctoral researcher at Salk who spearheaded the study in Shaw's lab and is now an assistant professor at UCLA's David Geffen School of Medicine.

That led Shaw and his team to a class of drugs called biguanides, which lower cellular energy levels by attacking the power stations of the cell, called mitochondria. Metformin and phenformin both inhibit mitochondria; however, phenformin is nearly 50 times as potent as metformin. In the study, the researchers tested phenformin as a chemotherapy agent in genetically-engineered mice lacking LKB1 and which had advanced stage lung tumors. After three weeks of treatment, Shaw and his team saw a modest reduction in tumor burden in the mice.

Continuing the study between Salk and UCLA, Shaw and Shackelford coordinated teams in both locations to perform further testing on mice with earlier stage disease, using cutting-edge imaging technologies just like those used on lung cancer patients in the clinic. They found that early phenformin treatment causes increased survival and slower tumor progression in tumors lacking LKB1, but had no significant benefit for tumors with alterations in other lung cancer genes. This specificity in treatment fits with an emerging approach in cancer treatment nationwide, known as personalized medicine, in which the therapies for each patient are selected based on the genes altered in their tumors.

"This study is a proof-of-principle that drugs of this chemical type cause energy stress and lower ATP levels to where it kills LKB1-deficient cells without damaging normal, healthy cells," says Shaw, senior author of the study.

The Food and Drug Administration took phenformin off the market in 1978 due to a high risk of lactic acid buildup in patients with compromised kidney function, which is not uncommon among diabetics but less of an issue for most cancer patients. The issue of kidney toxicity would also be bypassed in cancer patients because the course of treatment is much shorter, measured in weeks to months compared to years of treatment for diabetes patients.

The next step is to determine if phenformin alone would be a sufficient therapy for certain subsets of NSCLC or if the drug would perform better in combination with existing cancer drugs. Based on their findings, the researchers say that phenformin would be most useful in treating early-stage LKB1-mutant NSCLC, as an adjuvant therapy following surgical removal of a tumor, or in combination with other therapeutics for advanced tumors.

"The good news," says Shackelford, "is that our work provides a basis to initiate human studies. If we can organize enough clinicians who believe in investigating phenforminand many dothen phenformin as an anti-cancer agent could be a reality in the next several years."

###

Other researchers on the study were Laurie Gerken, Debbie S. Vasquez, and Mathias Leblanc of the Salk Institute, and Evan Abt, Atsuko Seki, Liu Wei, Michael C. Fishbein, Johannes Czernin, and Paul S. Mischel, of the David Geffen School of Medicine at the University of California, Los Angeles. The work was supported by the Salk Institute's Dulbecco Center for Cancer Research, the Adler Family Foundation, the Ahmanson Translational Imaging Division at UCLA, the National Center for Advancing Translational Sciences, the National Institutes of Health, the American Cancer Society, the Samuel Waxman Cancer Research Foundation, the Howard Hughes Medical Institute and the Leona M. and Harry B. Helmsley Charitable Trust.

About the Salk Institute for Biological Studies

The Salk Institute for Biological Studies is one of the world's preeminent basic research institutions, where internationally renowned faculty probe fundamental life science questions in a unique, collaborative, and creative environment. Focused on both discovery and on mentoring future generations of researchers, Salk scientists make groundbreaking contributions to our understanding of cancer, aging, Alzheimer's, diabetes and infectious diseases by studying neuroscience, genetics, cell and plant biology, and related disciplines.

Faculty achievements have been recognized with numerous honors, including Nobel Prizes and memberships in the National Academy of Sciences. Founded in 1960 by polio vaccine pioneer Jonas Salk, M.D., the Institute is an independent nonprofit organization and architectural landmark.



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

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


Diabetes drug could hold promise for lung cancer patients [ Back to EurekAlert! ] Public release date: 28-Jan-2013
[ | E-mail | Share Share ]

Contact: Andy Hoang
AHoang@salk.edu
619-861-5811
Salk Institute

Salk study suggests metabolism-based cancer therapy may be useful for non-small cell lung cancer

LA JOLLA, CA Ever since discovering a decade ago that a gene altered in lung cancer regulated an enzyme used in therapies against diabetes, Reuben Shaw has wondered if drugs originally designed to treat metabolic diseases could also work against cancer.

The growing evidence that cancer and metabolism are connected, emerging from a number of laboratories around the world over the past 10 years, has further fueled these hopes, though scientists are still working to identify what tumors might be most responsive and which drugs most useful.

Now, in a new study in the journal Cancer Cell, Shaw and a team of scientists at the Salk Institute for Biological Studies found that phenformin, a derivative of the widely-used diabetes drug metformin, decreased the size of lung tumors in mice and increased the animals' survival. The findings may give hope to the nearly 30 percent of patients with non-small cell lung cancer (NSCLC) whose tumors lack LKB1 (also called STK11).

The LKB1 gene turns on a metabolic enzyme called AMPK when energy levels of ATP, molecules that store the energy we need for just about everything we do, run low in cells. In a previous study, Shaw, an associate professor in Salk's Molecular and Cell Biology Laboratory and researcher in the Institute's new Helmsley Center for Genomic Medicine, demonstrated that cells lacking a normal copy of the LKB1 gene fail to activate AMPK in response to low energy levels. LKB1-dependent activation of AMPK serves as a low-energy checkpoint in the cell. Cells that lack LKB1 are unable to sense such metabolic stress and initiate the process to restore their ATP levels following a metabolic change. As a result, these LKB1-mutant cells run out of cellular energy and undergo apoptosis, or programmed cell death, whereas cells with intact LKB1 are alerted to the crisis and re-correct their metabolism.

"The driving idea behind the research is knowing that AMPK serves as a sensor for low energy loss in cells and that LKB1-deficient cells lack the ability to activate AMPK and sense energy loss," says David Shackelford, a postdoctoral researcher at Salk who spearheaded the study in Shaw's lab and is now an assistant professor at UCLA's David Geffen School of Medicine.

That led Shaw and his team to a class of drugs called biguanides, which lower cellular energy levels by attacking the power stations of the cell, called mitochondria. Metformin and phenformin both inhibit mitochondria; however, phenformin is nearly 50 times as potent as metformin. In the study, the researchers tested phenformin as a chemotherapy agent in genetically-engineered mice lacking LKB1 and which had advanced stage lung tumors. After three weeks of treatment, Shaw and his team saw a modest reduction in tumor burden in the mice.

Continuing the study between Salk and UCLA, Shaw and Shackelford coordinated teams in both locations to perform further testing on mice with earlier stage disease, using cutting-edge imaging technologies just like those used on lung cancer patients in the clinic. They found that early phenformin treatment causes increased survival and slower tumor progression in tumors lacking LKB1, but had no significant benefit for tumors with alterations in other lung cancer genes. This specificity in treatment fits with an emerging approach in cancer treatment nationwide, known as personalized medicine, in which the therapies for each patient are selected based on the genes altered in their tumors.

"This study is a proof-of-principle that drugs of this chemical type cause energy stress and lower ATP levels to where it kills LKB1-deficient cells without damaging normal, healthy cells," says Shaw, senior author of the study.

The Food and Drug Administration took phenformin off the market in 1978 due to a high risk of lactic acid buildup in patients with compromised kidney function, which is not uncommon among diabetics but less of an issue for most cancer patients. The issue of kidney toxicity would also be bypassed in cancer patients because the course of treatment is much shorter, measured in weeks to months compared to years of treatment for diabetes patients.

The next step is to determine if phenformin alone would be a sufficient therapy for certain subsets of NSCLC or if the drug would perform better in combination with existing cancer drugs. Based on their findings, the researchers say that phenformin would be most useful in treating early-stage LKB1-mutant NSCLC, as an adjuvant therapy following surgical removal of a tumor, or in combination with other therapeutics for advanced tumors.

"The good news," says Shackelford, "is that our work provides a basis to initiate human studies. If we can organize enough clinicians who believe in investigating phenforminand many dothen phenformin as an anti-cancer agent could be a reality in the next several years."

###

Other researchers on the study were Laurie Gerken, Debbie S. Vasquez, and Mathias Leblanc of the Salk Institute, and Evan Abt, Atsuko Seki, Liu Wei, Michael C. Fishbein, Johannes Czernin, and Paul S. Mischel, of the David Geffen School of Medicine at the University of California, Los Angeles. The work was supported by the Salk Institute's Dulbecco Center for Cancer Research, the Adler Family Foundation, the Ahmanson Translational Imaging Division at UCLA, the National Center for Advancing Translational Sciences, the National Institutes of Health, the American Cancer Society, the Samuel Waxman Cancer Research Foundation, the Howard Hughes Medical Institute and the Leona M. and Harry B. Helmsley Charitable Trust.

About the Salk Institute for Biological Studies

The Salk Institute for Biological Studies is one of the world's preeminent basic research institutions, where internationally renowned faculty probe fundamental life science questions in a unique, collaborative, and creative environment. Focused on both discovery and on mentoring future generations of researchers, Salk scientists make groundbreaking contributions to our understanding of cancer, aging, Alzheimer's, diabetes and infectious diseases by studying neuroscience, genetics, cell and plant biology, and related disciplines.

Faculty achievements have been recognized with numerous honors, including Nobel Prizes and memberships in the National Academy of Sciences. Founded in 1960 by polio vaccine pioneer Jonas Salk, M.D., the Institute is an independent nonprofit organization and architectural landmark.



[ 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/2013-01/si-ddc012813.php

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About South Africa | Otimized Mini web page | Advertise Online

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Source: http://blog.webdesignspecialist.co.za/mini-web-pages-optimized-google/

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Report: Japan to air ultra-high-def TV in 2014

7 hrs.

TOKYO???The Japanese government is set to launch the world's first 4K TV broadcast in July 2014, roughly two years ahead of schedule, to help stir demand for ultra high-definition televisions, the Asahi newspaper reported on Sunday without citing sources.

The service will begin from communications satellites, followed by satellite broadcasting and ground digital broadcasting, the report said.

The 4K TVs, which boast four times the resolution of current high-definition TVs, are now on sale by Japanese makers including Sony, Panasonic and Sharp. Other manufacturers include South Korea's LG Electronics.

Japan's Ministry of Internal Affairs and Communications had aimed to kick-start the 4K TV service in 2016. That has been brought forward to July 2014, when the final match of the 2014 football World Cup is set to take place in Brazil, the Asahi report said.

In Japan, the development of super high-definition 8K TVs is in progress, and the Ministry of Internal Affairs and Communications plans to launch the test 8K TV broadcast in 2016, two years ahead of schedule, it said.

Copyright 2013 Thomson Reuters.

Source: http://www.nbcnews.com/technology/gadgetbox/japan-reportedly-targets-2014-worlds-first-ultra-high-def-4k-1C8135106

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Military suicides show signs of spreading in families

Erin Trieb for NBC News

Monica Velez, pictured in Austin, Texas, had two brothers, Jose "Freddy" Velez and Andrew Velez, both of whom served the U.S. military and both are now dead -- Freddy was killed in action in Iraq, and Andrew took his own life.

By Bill Briggs, NBC News contributor

Before Army Spc. Andrew Velez left Texas for the final time, he asked his fragile sister to write him a promise ? a vow he could carry with him to Afghanistan.

Monica Velez knew she owed him that much. In the horrid weeks after each had lost their beloved brother, Freddy Velez, to enemy fire in Iraq, Monica tried to end her life with pills and alcohol. Now, she put pen to paper: ?I will not hurt myself. I will not do anything crazy. I know that Andrew loves me. I know that Freddy loved me.? Andrew folded her note and slipped it into his pocket.

?Don?t break your word to me,? he told her before heading back to war.

Seven months later, Andrew, 22, sat alone in an Army office at a base in Afghanistan. He put a gun to his head and committed suicide. Back in Texas, word reached Monica Velez who, once again, found herself in a dangerous place. Only now, she was alone. Days of alcohol and anti-depressants. Nights of dark thoughts: ?It would just be better if I was gone.?


'The storm' is coming
As the U.S. military suicide rate soared to record heights?during 2012, the families of service members say they, too, are witnessing a silent wave of self-harm occurring within their civilian ranks: spouses, children, parents and siblings.?

Some suicides and suicide attempts ? like those that ravaged the Velez family???are spurred by combat losses.

Others?may be?triggered by exhaustion and despair: As some veterans return debilitated by anxiety, many spouses realize it's now up to them???and will be for decades???to hold the family together.

Specific figures are lacking as no agency tracks civilian suicides within military families.

However, Kristina Kaufmann, a long-time Army wife, knows of three other Army wives, all friends, who took their lives in recent years.

Courtesy Kristina Kaufmann

"When you know that you are the anchor ? and if you go down, the family's going down ? the problem is that you can only do that for so long," said Kristina Kaufmann.

One was Faye Vick, described by Kaufmann as ?the perfect picture of an Army wife???pretty, nice, always with a smile.? Vick and her family lived around the corner from Kaufmann and near Fort Bragg, N.C. In 2006, when Kaufmann?s husband was in Afghanistan and Vick?s husband was deployed overseas, the 39-year-old mother placed herself, her infant and her 2-year-old son in a car inside a closed garage and started the engine, asphyxiating all three with carbon monoxide, according to Kaufmann and to local news reports at the time.

?And I know of too many others through the grapevine,? said Kaufmann, executive director of Code of Support, an Alexandria, Va.-based nonprofit that seeks to bridge the gap between civilians and military America.

?When you know that you are the anchor???and if you go down, the family?s going down???the problem is that you can only do that for so long,? said Kaufmann. ?That population (of spouses) is at the most risk. Because the storm is going to happen when everybody comes home. That?s where we are, unfortunately, going to see an uptick in lots of negative outcomes, including suicide, including suicide among the spouses.?

On Jan. 14, Department of Defense officials acknowledged that during 2012, service members committed suicide at a record pace as more than 349 people took their own lives across the four branches.?The military suicide rate is slightly lower than that of the general public. However, one active-duty member died by suicide every 25 hours last year.?

The Army sustained the heaviest branch toll at 182 suicides, which ??as NBC News reported Jan. 3?? meant that soldier suicides outpaced combat deaths for the first time, according to Pentagon officials.

Defense Secretary Leon Panetta informed Congress last July that American armed forces are in the grip of a suicide "epidemic."?

One of the darkest undercurrents of the glaring statistics is that one suicide in a family boosts future suicide risks for everyone else inside the home.?They can be contagious, say experts like Dr. Barbara Van Dahlen, a psychologist in the Washington, D.C., area and the founder of Give an Hour, which develops networks of mental-health volunteers who respond to both acute and chronic situations.

Numerous researchers have explored the so-called contagion effect of suicides within families and ?there?s no question the data supports there?s at least a doubling of risk,? among surviving family members, said Dr. Alan L. Berman, Ph.D., executive director of the American Association of Suicidology. The organization strives to better understand and prevent suicide.

?It?s understood that risk, in part, is biological,"?Berman said, given that disorders like depression have a genetic component.?

?But it?s also based on social modeling behavior: The suicide of a parent presents a model (for children in that family) of how to deal with problems, and that?s no less true for a spouse.?

Added Van Dahlen: "The closer that family member is to you, the greater risk you?re at. We believe, psychologically, it opens the possibility and ends a taboo."

?The thousands of service members who have killed themselves,? she added, ?they leave in their wake thousands of family members who are now at risk for that same kind of decision."

'I completely lost myself'
The cascade of Velez family tragedies began with pure valor.

On Nov. 13, 2004, Army Cpl. Jose ?Freddy? Velez, 23, sprayed bullets at insurgent forces???covering fire to allow other U.S. soldiers time to retreat from an enemy strong point in Fallujah, Iraq. After his ammo ran dry, Freddy Velez was shot and killed. The Army awarded him the Bronze Star and Silver Star.

Courtesy Monica Velez

"There are days I'm still overwhelmed. And if I sit and think about it, I feel like I wouldn't have to live through all this pain if I just let myself go," said Monica Velez, who shared family photos of brothers Freddy and Andrew.

Andrew, then serving with another unit in Iraq, told Monica of escorting his brother?s body home to Lubbock, Texas ? a job, he said, that required unzipping his brother?s body bag at every stop to re-verify Freddy?s identity.

During the trip, Andrew called his sister repeatedly while en route home and screamed into the phone for nearly two consecutive hours, ?like somebody was killing him,? she said.

?There was nothing I could do,? Monica Velez recalled. ?The operator kept cutting in (to request additional payment for the call) and I just said, ?Add it to my credit card.? He just wailed. That travel home, I think is what eventually broke him.?

Weeks later, Monica broke.

She doesn?t know how close she came to death the first time she tried to end her life. She never was told how slow her pulse became that night. She just remembers regaining consciousness at a hospital in Killeen, Texas???home to Fort Hood, where Freddy was based. She awoke with an IV plugged into her arm. A doctor handed her a list of local psychiatrists then discharged her.

Velez tried, she said, to seek help for her deepening depression but was told that her health insurance would not cover counseling.

Her grief was rooted in a difficult childhood, she said, that forged "tighter than tight" emotional bonds between Velez and her two brothers, turning the siblings into a mutual support group.

?When Freddy passed away, I went through a really hard depression,? she said. ?I went to the emergency room for anxiety attacks. I couldn?t breathe. But nobody knew how to deal with me so they just gave me Ativan (an anti-anxiety drug) and Hydrocodone (a pain killer).

?I started drinking heavily and taking the prescriptions. And one day, I just felt it would be better off if I wasn?t around and decided to take all of the pills. Grief can bring you to that breaking moment.?

Soon after, in February 2005, Andrew sent his older sister (then 25) an email: ?We need to be stronger. We need to protect each other.?

Though he was the youngest of the siblings, Andrew always was ?the strong one,? his sister said. ?But he and Freddy were inseparable.? Near the end of 2005, Andrew told his sister he was redeploying to Afghanistan because, she said, ?I think he felt closer to Freddy there.?

From March through July of 2006, the two swapped calls and emails. In Afghanistan, Andrew grew increasingly despondent, she said, over the unraveling of his marriage and family in Lubbock. He had three children. But he worried, too, about his sister?s state of mind.

?We could both hear it in each other?s voices. He was scared I was going to do something. I was scared he was going to do something.?

He did. Andrew?s suicide on July 25, 2006, drove Monica, at first, into 20-hour workdays at a domestic violence shelter. She wasn?t sleeping or eating. Eventually, she was drinking again, ?from the morning until I passed out,? she said. ?Then, doing it again the next day.

?I completely lost myself. I resigned my job. I stopped paying my bills. I got evicted. I was prescribed anti-depressants. I noticed taking the pills and drinking got me out of the emotions. So I found myself in a dangerous place very quickly.

?Again???several trips to the ER (for overdoses). I?m not sure why I wasn?t ever held there. In my down periods, I would tell myself it would just be better off if I was gone.?

In 2008, a friend at Fort Hood, Texas, connected Velez with the Tragedy Assistance Program For Survivors (TAPS), a resource for anyone who suffers the loss of a military loved one.

?That was the first time anybody had offered to help me with the depression and the grief.? she said.

'Family units breaking down'
Kaufmann, who lost three Army-spouse friends to suicide, argues that military-family suicides should be tracked and researched by the Department of Defense to help mental-health experts begin to slow or stop the problem. She knows, however, such an accounting is not likely.?

?I get the sense that people in the military think that by including families into this kind of discussion ? particularly when you?re talking about the (broader) mental-health impacts on family members ? they look at that as something that will only add to the problem. Whereas, we believe that it would prove to be a solution,? Kauffman said.

?We?ve approached this very myopically. More than half of soldiers are married. Soldiers come with families. And the military has a maddening way of both dismissing families and holding them accountable at the same time. It?s frustrating for us, not only when we?re trying to get our husbands help, but also when you have the family units breaking down,? she added.?

NBC News requested to speak with officials at the newly formed Department of Defense suicide-prevention office about the issue of suicides within military families and whether tracking is needed. A DOD spokeswoman said, however, that the office is only working to address active-duty suicides. The interview request was not granted.

Van Dahlen, meanwhile, believes that asking DOD to track military families is an unreasonable expectation to place on the agency when it already is facing budget cuts.

Even if the DOD wants to ? and many of my colleagues there desperately would want to devote resources to this???those resources are not going to be there,? she said. Rather than putting "the screws to DOD" and doing "even more with even less," Van Dahlen believes public-private partnerships should be encouraged "to figure out how we can (address) this together."

'Like an airborne disease'
More than eight years after Freddy?s combat death, and more than six years removed from Andrew?s suicide, Monica Velez annually runs the Marine Corps Marathon in Washington, D.C., in honor of her fallen brothers.

Matt Slocum / AP file

Monica Velez cleans her brother's name, engraved in a memorial at Fort Hood, Texas.

But, now living in Austin, she acknowledges she still struggles with what she calls, ?those thoughts.?

?There are days I?m still overwhelmed. And if I sit and think about it, I feel like I wouldn?t have to live through all this pain if I just let myself go. It doesn?t just go away. But you learn how to cope. You learn better coping skills,? she said, adding she gained those tools from TAPS.

Army officers at Fort Hood have occasionally asked her, she said, for ideas to help them prevent the rising military suicide rate. She watches that tally, too.

?The numbers take my breath away. I know it can be overwhelming for the Army generals on the other end of the table trying to figure this problem out. Because it?s like an airborne disease going through the building and you?re trying to figure out how to stop it before it gets to you," she said.?

?But it?s coming at a really fast rate, and it?s inevitable.?

Related stories:
Military suicide rate set record high in 2012
The enemy within: Soldier suicides outpace combat deaths in 2012
Some wounded vets shine on 'Alive Day,' others wear black?

Source: http://usnews.nbcnews.com/_news/2013/01/16/16540098-like-an-airborne-disease-concern-grows-about-military-suicides-spreading-within-families?lite

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Philharmonic Society unveils 2013-2014 schedule | orchestra ...

The Philharmonic Society of Orange County announced its 2013-2014 concert schedule today, the 60th season for the presenter and the last for president and artistic director Dean Corey, who will retire in June 2014. A number of events will offer tribute to Corey, who has led the Society since 1993, including a Dean Corey Legacy Concerts series that features a return visit by the Vienna Philharmonic and the publication of a book by Corey, "Beethoven: The Late Great, 33 Personal Essays." The season also includes the performance of a complete opera in concert.

The Vienna Philharmonic, one of the world's most celebrated, returns to Segerstrom Concert Hall on March 3 (2014), with Italian conductor Daniele Gatti leading a program of Schubert's "Unfinished" Symphony and Mahler's Symphony No. 4 (with soprano Juliane Banse as soloist).

Pianist Yuja Wang will perform a recital in October for the Philharmonic Society.

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Other orchestras on the schedule include the Irish Chamber Orchestra, conducted by JoAnn Falletta and featuring flutist James Galway; the Boston Pops Orchestra conducted by Keith Lockhart; the Royal Philharmonic Orchestra, featuring violinist Pinchas Zukerman as both conductor and soloist; the period-instrument English Concert led by Harry Bicket in a performance of Handel's "Theodora," with countertenor David Daniels; the Haifa Symphony Orchestra of Israel; and the annual visit from the Los Angeles Philharmonic, this time conducted by St?phane Den?ve and featuring violinist Gil Shaham.

Three student orchestras also appear on the subscription series. Los Angeles Opera music director James Conlon will lead the Colburn Orchestra and the USC Thorton Symphony in a performance of Britten's "War Requiem" (honoring the composer's centenary), with choirs from USC, Cal State Fullerton and Cal State Long Beach as well as the Los Angeles Children's Chorus.

The season ends with a performance by the Orange County Youth Orchestra under Daniel Alfred Wachs, who will lead a program that includes a new commission (entitled "Frieze") from progressive British composer Mark-Anthony Turnage and Beethoven's Ninth Symphony, with choirs from UCI, Cal State Fullerton and Chapman University.

Recitals by pianists Olga Kern and Yuja Wang are scheduled as well as chamber concerts by Camera Lucida, the Madelring Quartet, the Scharoun Ensemble Berlin and the Myriad Trio.

Subscriptions ranging from four to 12 concerts go on sale Monday. For more information call 949-553-2422 or visit www.philharmonicsociety.org.

Contact the writer: 714-796-6811 or tmangan@ocregister.com


Source: http://www.ocregister.com/entertainment/orchestra-409429-philharmonic-symphony.html

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