If you can’t find anything that interests you at HM16, check your caffeine level. You might need a cup.

There’s so much in store, you can practically hear the binding of the program straining to contain it all.

If there is a dominant theme at this year’s conference, it’s health information technology (IT), which will be featured in a new track that will span electronic medical records, using IT for documentation and shifting from volume to value, and social media. The keynote address will cover health IT as well.

But even a quick glance captures the diversity of the program: applying for jobs, inpatient management, apps, cost-value questions, ischemic stroke, X-ray, endocrinology, and dying and the counseling of families.

Better buckle up.

Here’s some of what you need to know:

• There will be new tracks on health IT for the hospitalist, the doctor-patient relationship, post-acute care, and perioperative medicine.
• The popular “Young Hospitalist” track is back after a successful debut last year. This track covers, among other things, the application process, how to be a good mentee, how to negotiate a first job, and an introduction to quality improvement projects.

  

• To kick off the meeting, a panel will discuss the field’s expansion, or “hospital medicine at the edges.” It will feature big names, including Laurence Wellikson, MD, MHM, SHM’s chief executive officer.
• Keynote speaker Karen DeSalvo, MD, MPH, MSc, national coordinator for health information technology and acting assistant secretary for the U.S. Department of Health & Human Services, will discuss hospital medicine and technology.
• A series of 90-minute workshops will tackle thought-provoking and relevant topics: “Rule Your Inbox, Rule Your Life”; “Attending 101: Everything You Want and Need to Know”; and “Case-Based Discussion of Essential Issues on Anticoagulation Management.”

Plus, the tracks that form a kind of foundation for the meeting—practice management, academic/research, pediatrics, and quality improvement—will be back.

Get some tips on things to do in San Diego at HM16.

“The annual meeting will have the core content that brings hospitalists back year after year, including something for practice administrators and leaders of practice groups [with] the practice management track, including academics and researchers for the academic and research track, and a quality track for all those [involved in quality projects], and many, many hospitalists are engaged in quality and patient safety efforts across the country,” says Course Director Melissa Mattison, MD, SFHM, assistant professor of medicine at Harvard Medical School in Boston.

The panel on hospital expansion will cover four main areas that are seeing rapid change, according to Dr. Wellikson.

“Hospitalists continue to see their scope of practice evolve and expand,” he says. “In this presentation, we will hear from national leaders about the expanding roles of hospitalists.”

Topics will include palliative care, covered by Steve Pantilat, MD, SFHM, medical director of the University of California at San Francisco School of Medicine palliative care service; alternative payment models, covered by Ron Greeno, MD, MHM, executive vice president for strategy and innovation at Cogent Healthcare; post-acute care, covered by SHM President Bob Harrington, MD, SFHM, CMO at Reliant Post-Acute Care Solutions; and perioperative care, covered by Rachel Thompson, MD, MPH, FHM, associate professor of medicine at the University of Washington.

Dr. Mattison and other organizers thought it was imperative to bring back the “Young Hospitalist” track, which “was wildly successful last year” in both attendance and reviews.

“It’s for people who are aspiring hospitalists—medical students and residents in training—who hope to go on to hospital medicine careers, as well as people who are newly minted hospitalists, people who are probably between one and five years out of their training,” Dr. Mattison explains.

Darlene Tad-y, MD, FHM, assistant professor of medicine at University of Colorado at Denver and chair of SHM’s Physicians in Training Committee, says the offerings for young hospitalists come in response to requests from students, residents, and junior faculty. The track intends to give its audience a sense of how to apply for jobs and start shaping a career path, as well as an understanding of the contours of the hospital medicine field.

Dr. Tad-y says she wants the track to reflect her past experiences at SHM meetings (she’s been to five in a row) of a vibrant, engaged community.

“We wanted our students, residents, and young hospitalists to be able to interact with the whole spectrum of hospitalists—folks who are medical educators, folks who are group leaders, folks who are doing quality and safety work,” she says. “All of our sessions are designed to give them those opportunities.”

Hospitalists, she says, “broadly are game changers.”

“We really want our students, residents, and junior hospitalists to engage with us and see how they can be part of this,” she adds.

Dr. Mattison hopes the annual meeting continues to build on its solid reputation.

“I’ve always enjoyed the annual meeting,” she says. “There are a lot of strengths in SHM’s annual meeting year after year. I think the challenge in planning another annual meeting is building upon that strength and continuing it, and finding new topics and new tracks, and evolving with the times.” TH

Thomas R. Collins is a freelance writer in South Florida.

If you can’t find anything that interests you at HM16, check your caffeine level. You might need a cup.

There’s so much in store, you can practically hear the binding of the program straining to contain it all.

If there is a dominant theme at this year’s conference, it’s health information technology (IT), which will be featured in a new track that will span electronic medical records, using IT for documentation and shifting from volume to value, and social media. The keynote address will cover health IT as well.

But even a quick glance captures the diversity of the program: applying for jobs, inpatient management, apps, cost-value questions, ischemic stroke, X-ray, endocrinology, and dying and the counseling of families.

Better buckle up.

Here’s some of what you need to know:

• There will be new tracks on health IT for the hospitalist, the doctor-patient relationship, post-acute care, and perioperative medicine.
• The popular “Young Hospitalist” track is back after a successful debut last year. This track covers, among other things, the application process, how to be a good mentee, how to negotiate a first job, and an introduction to quality improvement projects.

  

• To kick off the meeting, a panel will discuss the field’s expansion, or “hospital medicine at the edges.” It will feature big names, including Laurence Wellikson, MD, MHM, SHM’s chief executive officer.
• Keynote speaker Karen DeSalvo, MD, MPH, MSc, national coordinator for health information technology and acting assistant secretary for the U.S. Department of Health & Human Services, will discuss hospital medicine and technology.
• A series of 90-minute workshops will tackle thought-provoking and relevant topics: “Rule Your Inbox, Rule Your Life”; “Attending 101: Everything You Want and Need to Know”; and “Case-Based Discussion of Essential Issues on Anticoagulation Management.”

Plus, the tracks that form a kind of foundation for the meeting—practice management, academic/research, pediatrics, and quality improvement—will be back.

Get some tips on things to do in San Diego at HM16.

“The annual meeting will have the core content that brings hospitalists back year after year, including something for practice administrators and leaders of practice groups [with] the practice management track, including academics and researchers for the academic and research track, and a quality track for all those [involved in quality projects], and many, many hospitalists are engaged in quality and patient safety efforts across the country,” says Course Director Melissa Mattison, MD, SFHM, assistant professor of medicine at Harvard Medical School in Boston.

The panel on hospital expansion will cover four main areas that are seeing rapid change, according to Dr. Wellikson.

“Hospitalists continue to see their scope of practice evolve and expand,” he says. “In this presentation, we will hear from national leaders about the expanding roles of hospitalists.”

Topics will include palliative care, covered by Steve Pantilat, MD, SFHM, medical director of the University of California at San Francisco School of Medicine palliative care service; alternative payment models, covered by Ron Greeno, MD, MHM, executive vice president for strategy and innovation at Cogent Healthcare; post-acute care, covered by SHM President Bob Harrington, MD, SFHM, CMO at Reliant Post-Acute Care Solutions; and perioperative care, covered by Rachel Thompson, MD, MPH, FHM, associate professor of medicine at the University of Washington.

Dr. Mattison and other organizers thought it was imperative to bring back the “Young Hospitalist” track, which “was wildly successful last year” in both attendance and reviews.

“It’s for people who are aspiring hospitalists—medical students and residents in training—who hope to go on to hospital medicine careers, as well as people who are newly minted hospitalists, people who are probably between one and five years out of their training,” Dr. Mattison explains.

Darlene Tad-y, MD, FHM, assistant professor of medicine at University of Colorado at Denver and chair of SHM’s Physicians in Training Committee, says the offerings for young hospitalists come in response to requests from students, residents, and junior faculty. The track intends to give its audience a sense of how to apply for jobs and start shaping a career path, as well as an understanding of the contours of the hospital medicine field.

Dr. Tad-y says she wants the track to reflect her past experiences at SHM meetings (she’s been to five in a row) of a vibrant, engaged community.

“We wanted our students, residents, and young hospitalists to be able to interact with the whole spectrum of hospitalists—folks who are medical educators, folks who are group leaders, folks who are doing quality and safety work,” she says. “All of our sessions are designed to give them those opportunities.”

Hospitalists, she says, “broadly are game changers.”

“We really want our students, residents, and junior hospitalists to engage with us and see how they can be part of this,” she adds.

Dr. Mattison hopes the annual meeting continues to build on its solid reputation.

“I’ve always enjoyed the annual meeting,” she says. “There are a lot of strengths in SHM’s annual meeting year after year. I think the challenge in planning another annual meeting is building upon that strength and continuing it, and finding new topics and new tracks, and evolving with the times.” TH

Thomas R. Collins is a freelance writer in South Florida.

If you can’t find anything that interests you at HM16, check your caffeine level. You might need a cup.

There’s so much in store, you can practically hear the binding of the program straining to contain it all.

If there is a dominant theme at this year’s conference, it’s health information technology (IT), which will be featured in a new track that will span electronic medical records, using IT for documentation and shifting from volume to value, and social media. The keynote address will cover health IT as well.

But even a quick glance captures the diversity of the program: applying for jobs, inpatient management, apps, cost-value questions, ischemic stroke, X-ray, endocrinology, and dying and the counseling of families.

Better buckle up.

Here’s some of what you need to know:

• There will be new tracks on health IT for the hospitalist, the doctor-patient relationship, post-acute care, and perioperative medicine.
• The popular “Young Hospitalist” track is back after a successful debut last year. This track covers, among other things, the application process, how to be a good mentee, how to negotiate a first job, and an introduction to quality improvement projects.

  

• To kick off the meeting, a panel will discuss the field’s expansion, or “hospital medicine at the edges.” It will feature big names, including Laurence Wellikson, MD, MHM, SHM’s chief executive officer.
• Keynote speaker Karen DeSalvo, MD, MPH, MSc, national coordinator for health information technology and acting assistant secretary for the U.S. Department of Health & Human Services, will discuss hospital medicine and technology.
• A series of 90-minute workshops will tackle thought-provoking and relevant topics: “Rule Your Inbox, Rule Your Life”; “Attending 101: Everything You Want and Need to Know”; and “Case-Based Discussion of Essential Issues on Anticoagulation Management.”

Plus, the tracks that form a kind of foundation for the meeting—practice management, academic/research, pediatrics, and quality improvement—will be back.

Get some tips on things to do in San Diego at HM16.

“The annual meeting will have the core content that brings hospitalists back year after year, including something for practice administrators and leaders of practice groups [with] the practice management track, including academics and researchers for the academic and research track, and a quality track for all those [involved in quality projects], and many, many hospitalists are engaged in quality and patient safety efforts across the country,” says Course Director Melissa Mattison, MD, SFHM, assistant professor of medicine at Harvard Medical School in Boston.

The panel on hospital expansion will cover four main areas that are seeing rapid change, according to Dr. Wellikson.

“Hospitalists continue to see their scope of practice evolve and expand,” he says. “In this presentation, we will hear from national leaders about the expanding roles of hospitalists.”

Topics will include palliative care, covered by Steve Pantilat, MD, SFHM, medical director of the University of California at San Francisco School of Medicine palliative care service; alternative payment models, covered by Ron Greeno, MD, MHM, executive vice president for strategy and innovation at Cogent Healthcare; post-acute care, covered by SHM President Bob Harrington, MD, SFHM, CMO at Reliant Post-Acute Care Solutions; and perioperative care, covered by Rachel Thompson, MD, MPH, FHM, associate professor of medicine at the University of Washington.

Dr. Mattison and other organizers thought it was imperative to bring back the “Young Hospitalist” track, which “was wildly successful last year” in both attendance and reviews.

“It’s for people who are aspiring hospitalists—medical students and residents in training—who hope to go on to hospital medicine careers, as well as people who are newly minted hospitalists, people who are probably between one and five years out of their training,” Dr. Mattison explains.

Darlene Tad-y, MD, FHM, assistant professor of medicine at University of Colorado at Denver and chair of SHM’s Physicians in Training Committee, says the offerings for young hospitalists come in response to requests from students, residents, and junior faculty. The track intends to give its audience a sense of how to apply for jobs and start shaping a career path, as well as an understanding of the contours of the hospital medicine field.

Dr. Tad-y says she wants the track to reflect her past experiences at SHM meetings (she’s been to five in a row) of a vibrant, engaged community.

“We wanted our students, residents, and young hospitalists to be able to interact with the whole spectrum of hospitalists—folks who are medical educators, folks who are group leaders, folks who are doing quality and safety work,” she says. “All of our sessions are designed to give them those opportunities.”

Hospitalists, she says, “broadly are game changers.”

“We really want our students, residents, and junior hospitalists to engage with us and see how they can be part of this,” she adds.

Dr. Mattison hopes the annual meeting continues to build on its solid reputation.

“I’ve always enjoyed the annual meeting,” she says. “There are a lot of strengths in SHM’s annual meeting year after year. I think the challenge in planning another annual meeting is building upon that strength and continuing it, and finding new topics and new tracks, and evolving with the times.” TH

Thomas R. Collins is a freelance writer in South Florida.

Unlike the crowded Republican primary field heading into this year’s presidential election, just three candidates seek the Democratic nomination: former First Lady and former New York Sen. Hillary Clinton, former Maryland Gov. Martin O’Malley, and U.S. Sen. Bernie Sanders of Vermont.

Although they share numerous ideas, the candidates also differ fundamentally in how they believe the American healthcare system should be run. And they stand in stark contrast to their Republican opponents.

“There really is a philosophical difference between the parties,” says Robert Blendon, professor of health policy and political analysis at the Harvard T.H. Chan School of Public Health and Harvard Kennedy School of Government. “Republicans really feel that if people themselves controlled more of the financial wherewithal, they would shop more and ask more questions.”

Democrats, however, “tend to believe that when people are ill, they are not in particularly good shape to shop,” Blendon says. Nor are they particularly fit to decide what costs are worth incurring or what procedures they may or may not need, he adds.

Listen to more of our interview with Dr. Blendon.

In general, Democrats believe the healthcare system should provide patients structure to make appropriate choices. They do not support reliance on high-deductible health plans and health savings accounts to lower healthcare costs.

“This is why the outcome of the election will matter,” Blendon says, “because it’s a very different view of what the future should look like.”

In 1993, as First Lady, Clinton undertook a failed but massive healthcare reform effort that would have created a universal healthcare system based on private insurance. Today, she supports the Affordable Care Act and says she will continue to build upon and support it, which includes making changes to the law such as repealing the Cadillac tax and further lowering out-of-pocket healthcare costs for most Americans.

Clinton’s view “is that many people have too large deductibles and copays, and for moderate-income people, it’s really deterring care,” Blendon says. “She’s likely to try to see if they can actually increase the government subsidies so the plans offer a wider range of benefits.”

Bradley Flansbaum, DO, MPH, MHM, hospitalist and SHM Public Policy Committee member, says changes must be made.

“We can’t say the direction we’re moving in is the right direction,” he says. “There is a desperate sense in America that what we have been doing is wrong and we need to change … whether the experiments now lead to a system more Americans would prefer remains to be seen.”

Sanders believes in a much bolder shift in direction. He does not think the Affordable Care Act goes far enough and wants to move to a single-payor system.

“I want to end the international embarrassment of the United States of America being the only major country on Earth that doesn’t guarantee healthcare to all people as a right, not a privilege,” he said at the second Democratic debate on Nov. 14, 2015.

However, his vision is unlikely to come to quick fruition if elected, Blendon says. “There’s not going to be—anywhere in the short term—the votes in the U.S. Congress to move in that direction.

“But it would change the level of discussion.”

O’Malley, on the other hand, wants to expand the ACA and envisions an “all-payor system” like that in Maryland, where the state sets medical costs and caps what hospitals can charge. He has vowed to continue to move away from a fee-for-service healthcare system and has said that reform should “eliminate the profit motive” for hospitals CEOs to keep beds filled.

“Regardless of who is elected, I would like to believe they would build off of what already exists,” says Joshua Lenchus, DO, RPh, SFHM, a member of SHM’s Public Policy Committee and a hospitalist at the University of Miami Jackson Memorial Hospital. “The populace doesn’t have the stomach for going through healthcare reform again.”

One of the biggest issues to emerge in the Democratic primaries is drugs: the pricing set by and regulations governing the pharmaceutical industry. Sanders wants to see a higher level of transparency, Clinton wants to require companies receiving federal support to invest in research, and both want to see the skyrocketing costs of prescription drugs reduced dramatically. This includes allowing Medicare to negotiate drug prices and allowing the sale of drugs from other countries that meet FDA standards.

“That resonates with the general public,” Blendon says, “because it’s very hard for people to understand that if we’re free trade in everything, why aren’t we for free trade in pharmaceuticals?”

Dr. Lenchus believes Democrats are going to “double-down” on health reform.

“To ensure the financial underpinnings and some of the partisan concerns are addressed,” he says. “I think with respect to hospitalists, the thing that impacts us the most is how medicine is going to get paid for doing what it does.” TH

Kelly April Tyrrell is a freelance writer in Madison, Wis.

Unlike the crowded Republican primary field heading into this year’s presidential election, just three candidates seek the Democratic nomination: former First Lady and former New York Sen. Hillary Clinton, former Maryland Gov. Martin O’Malley, and U.S. Sen. Bernie Sanders of Vermont.

Although they share numerous ideas, the candidates also differ fundamentally in how they believe the American healthcare system should be run. And they stand in stark contrast to their Republican opponents.

“There really is a philosophical difference between the parties,” says Robert Blendon, professor of health policy and political analysis at the Harvard T.H. Chan School of Public Health and Harvard Kennedy School of Government. “Republicans really feel that if people themselves controlled more of the financial wherewithal, they would shop more and ask more questions.”

Democrats, however, “tend to believe that when people are ill, they are not in particularly good shape to shop,” Blendon says. Nor are they particularly fit to decide what costs are worth incurring or what procedures they may or may not need, he adds.

Listen to more of our interview with Dr. Blendon.

In general, Democrats believe the healthcare system should provide patients structure to make appropriate choices. They do not support reliance on high-deductible health plans and health savings accounts to lower healthcare costs.

“This is why the outcome of the election will matter,” Blendon says, “because it’s a very different view of what the future should look like.”

In 1993, as First Lady, Clinton undertook a failed but massive healthcare reform effort that would have created a universal healthcare system based on private insurance. Today, she supports the Affordable Care Act and says she will continue to build upon and support it, which includes making changes to the law such as repealing the Cadillac tax and further lowering out-of-pocket healthcare costs for most Americans.

Clinton’s view “is that many people have too large deductibles and copays, and for moderate-income people, it’s really deterring care,” Blendon says. “She’s likely to try to see if they can actually increase the government subsidies so the plans offer a wider range of benefits.”

Bradley Flansbaum, DO, MPH, MHM, hospitalist and SHM Public Policy Committee member, says changes must be made.

“We can’t say the direction we’re moving in is the right direction,” he says. “There is a desperate sense in America that what we have been doing is wrong and we need to change … whether the experiments now lead to a system more Americans would prefer remains to be seen.”

Sanders believes in a much bolder shift in direction. He does not think the Affordable Care Act goes far enough and wants to move to a single-payor system.

“I want to end the international embarrassment of the United States of America being the only major country on Earth that doesn’t guarantee healthcare to all people as a right, not a privilege,” he said at the second Democratic debate on Nov. 14, 2015.

However, his vision is unlikely to come to quick fruition if elected, Blendon says. “There’s not going to be—anywhere in the short term—the votes in the U.S. Congress to move in that direction.

“But it would change the level of discussion.”

O’Malley, on the other hand, wants to expand the ACA and envisions an “all-payor system” like that in Maryland, where the state sets medical costs and caps what hospitals can charge. He has vowed to continue to move away from a fee-for-service healthcare system and has said that reform should “eliminate the profit motive” for hospitals CEOs to keep beds filled.

“Regardless of who is elected, I would like to believe they would build off of what already exists,” says Joshua Lenchus, DO, RPh, SFHM, a member of SHM’s Public Policy Committee and a hospitalist at the University of Miami Jackson Memorial Hospital. “The populace doesn’t have the stomach for going through healthcare reform again.”

One of the biggest issues to emerge in the Democratic primaries is drugs: the pricing set by and regulations governing the pharmaceutical industry. Sanders wants to see a higher level of transparency, Clinton wants to require companies receiving federal support to invest in research, and both want to see the skyrocketing costs of prescription drugs reduced dramatically. This includes allowing Medicare to negotiate drug prices and allowing the sale of drugs from other countries that meet FDA standards.

“That resonates with the general public,” Blendon says, “because it’s very hard for people to understand that if we’re free trade in everything, why aren’t we for free trade in pharmaceuticals?”

Dr. Lenchus believes Democrats are going to “double-down” on health reform.

“To ensure the financial underpinnings and some of the partisan concerns are addressed,” he says. “I think with respect to hospitalists, the thing that impacts us the most is how medicine is going to get paid for doing what it does.” TH

Kelly April Tyrrell is a freelance writer in Madison, Wis.

Unlike the crowded Republican primary field heading into this year’s presidential election, just three candidates seek the Democratic nomination: former First Lady and former New York Sen. Hillary Clinton, former Maryland Gov. Martin O’Malley, and U.S. Sen. Bernie Sanders of Vermont.

Although they share numerous ideas, the candidates also differ fundamentally in how they believe the American healthcare system should be run. And they stand in stark contrast to their Republican opponents.

“There really is a philosophical difference between the parties,” says Robert Blendon, professor of health policy and political analysis at the Harvard T.H. Chan School of Public Health and Harvard Kennedy School of Government. “Republicans really feel that if people themselves controlled more of the financial wherewithal, they would shop more and ask more questions.”

Democrats, however, “tend to believe that when people are ill, they are not in particularly good shape to shop,” Blendon says. Nor are they particularly fit to decide what costs are worth incurring or what procedures they may or may not need, he adds.

Listen to more of our interview with Dr. Blendon.

In general, Democrats believe the healthcare system should provide patients structure to make appropriate choices. They do not support reliance on high-deductible health plans and health savings accounts to lower healthcare costs.

“This is why the outcome of the election will matter,” Blendon says, “because it’s a very different view of what the future should look like.”

In 1993, as First Lady, Clinton undertook a failed but massive healthcare reform effort that would have created a universal healthcare system based on private insurance. Today, she supports the Affordable Care Act and says she will continue to build upon and support it, which includes making changes to the law such as repealing the Cadillac tax and further lowering out-of-pocket healthcare costs for most Americans.

Clinton’s view “is that many people have too large deductibles and copays, and for moderate-income people, it’s really deterring care,” Blendon says. “She’s likely to try to see if they can actually increase the government subsidies so the plans offer a wider range of benefits.”

Bradley Flansbaum, DO, MPH, MHM, hospitalist and SHM Public Policy Committee member, says changes must be made.

“We can’t say the direction we’re moving in is the right direction,” he says. “There is a desperate sense in America that what we have been doing is wrong and we need to change … whether the experiments now lead to a system more Americans would prefer remains to be seen.”

Sanders believes in a much bolder shift in direction. He does not think the Affordable Care Act goes far enough and wants to move to a single-payor system.

“I want to end the international embarrassment of the United States of America being the only major country on Earth that doesn’t guarantee healthcare to all people as a right, not a privilege,” he said at the second Democratic debate on Nov. 14, 2015.

However, his vision is unlikely to come to quick fruition if elected, Blendon says. “There’s not going to be—anywhere in the short term—the votes in the U.S. Congress to move in that direction.

“But it would change the level of discussion.”

O’Malley, on the other hand, wants to expand the ACA and envisions an “all-payor system” like that in Maryland, where the state sets medical costs and caps what hospitals can charge. He has vowed to continue to move away from a fee-for-service healthcare system and has said that reform should “eliminate the profit motive” for hospitals CEOs to keep beds filled.

“Regardless of who is elected, I would like to believe they would build off of what already exists,” says Joshua Lenchus, DO, RPh, SFHM, a member of SHM’s Public Policy Committee and a hospitalist at the University of Miami Jackson Memorial Hospital. “The populace doesn’t have the stomach for going through healthcare reform again.”

One of the biggest issues to emerge in the Democratic primaries is drugs: the pricing set by and regulations governing the pharmaceutical industry. Sanders wants to see a higher level of transparency, Clinton wants to require companies receiving federal support to invest in research, and both want to see the skyrocketing costs of prescription drugs reduced dramatically. This includes allowing Medicare to negotiate drug prices and allowing the sale of drugs from other countries that meet FDA standards.

“That resonates with the general public,” Blendon says, “because it’s very hard for people to understand that if we’re free trade in everything, why aren’t we for free trade in pharmaceuticals?”

Dr. Lenchus believes Democrats are going to “double-down” on health reform.

“To ensure the financial underpinnings and some of the partisan concerns are addressed,” he says. “I think with respect to hospitalists, the thing that impacts us the most is how medicine is going to get paid for doing what it does.” TH

Kelly April Tyrrell is a freelance writer in Madison, Wis.

Lab mouse

The protein kinase CHK1 may be a therapeutic target for Fanconi anemia (FA), according to researchers.

They studied induced pluripotent stem cells (iPSCs) derived from FA patients and found the FA DNA repair pathway was essential for the cells’ proliferation and survival.

The team also discovered that CHK1 played a “crucial” role in iPSCs’ sensitivity to accrued DNA damage, and inhibiting CHK1 allowed FA-deficient iPSCs to grow

normally.

The team relayed these findings in Stem Cell Reports.

“This study provides an experimental platform to test new therapies that could prevent pre- and post-natal Fanconi anemia conditions, which have no cure and limited treatment options,” said study author Susanne Wells, PhD, of the Cincinnati Children’s Hospital Medical Center in Ohio.

“Our findings also raise a number of important questions, so there is a lot more to be done.”

For this study, Dr Wells and her colleagues used iPSCs reprogrammed from mature skin and connective tissue cells donated by FA patients. The cells had a defective FA DNA repair pathway.

The researchers studied the iPSCs in culture and injected them into humanized mouse models, monitoring their genetic, molecular, and developmental progression.

Even with defective FA DNA repair, the iPSCs retained their ability to transform into different tissues, and humanized mice injected with the defective cells started to form teratomas.

However, the DNA repair defect started to kill off the iPSCs by blocking cell division and causing apoptosis.

The researchers noticed that CHK1, which serves as a DNA regulatory checkpoint during cell division, was hyperactive in the iPSCs, which hastened their death.

So the team used pharmacologic inhibitors of CHK1 to block the hyperactive enzyme at a critical stage of the stem cell cycle. This allowed them to override what are usually unfixable errors in the FA repair pathway.

After targeted treatment, FA-pathway-deficient iPSCs resumed dividing and expanding normally.

The researchers said that, to their surprise, the resumption of cell growth occurred without what they had expected to be massive chromosome abnormalities. Because of this, they speculate that a compensating DNA repair process is engaged in the reinvigorated cells.

Because this unidentified repair process may also rescue the DNA repair defect in the different tissue types affected by FA, Dr Wells and her colleagues believe their study may point to an approach that treats all clinical manifestations of the disease, including anemia and cancer.

“A key question for us is, ‘What type of DNA repair kicks in under these conditions, and is it error-free or error-prone?’” Dr Wells explained. “A novel mode of emergency DNA repair might indeed be discovered in the [iPSCs]. We believe some type of compensatory DNA repair must be driven by CHK1 inhibition when cells have FA pathway loss. Otherwise, the cells would have died off very quickly.”

The researchers plan to follow up this study with additional testing in humanized and genetic mouse models. They said they will attempt to improve embryonic development and post-birth fitness in FA-pathway-deficient mice with timed application of a CHK1 inhibitor.

The team will monitor the mice as they age and use genetic sequencing to screen for disease-causing mutations. And they will look for evidence of a DNA repair process (either novel or existing) in the FA-deficient mice.

Lab mouse

The protein kinase CHK1 may be a therapeutic target for Fanconi anemia (FA), according to researchers.

They studied induced pluripotent stem cells (iPSCs) derived from FA patients and found the FA DNA repair pathway was essential for the cells’ proliferation and survival.

The team also discovered that CHK1 played a “crucial” role in iPSCs’ sensitivity to accrued DNA damage, and inhibiting CHK1 allowed FA-deficient iPSCs to grow

normally.

The team relayed these findings in Stem Cell Reports.

“This study provides an experimental platform to test new therapies that could prevent pre- and post-natal Fanconi anemia conditions, which have no cure and limited treatment options,” said study author Susanne Wells, PhD, of the Cincinnati Children’s Hospital Medical Center in Ohio.

“Our findings also raise a number of important questions, so there is a lot more to be done.”

For this study, Dr Wells and her colleagues used iPSCs reprogrammed from mature skin and connective tissue cells donated by FA patients. The cells had a defective FA DNA repair pathway.

The researchers studied the iPSCs in culture and injected them into humanized mouse models, monitoring their genetic, molecular, and developmental progression.

Even with defective FA DNA repair, the iPSCs retained their ability to transform into different tissues, and humanized mice injected with the defective cells started to form teratomas.

However, the DNA repair defect started to kill off the iPSCs by blocking cell division and causing apoptosis.

The researchers noticed that CHK1, which serves as a DNA regulatory checkpoint during cell division, was hyperactive in the iPSCs, which hastened their death.

So the team used pharmacologic inhibitors of CHK1 to block the hyperactive enzyme at a critical stage of the stem cell cycle. This allowed them to override what are usually unfixable errors in the FA repair pathway.

After targeted treatment, FA-pathway-deficient iPSCs resumed dividing and expanding normally.

The researchers said that, to their surprise, the resumption of cell growth occurred without what they had expected to be massive chromosome abnormalities. Because of this, they speculate that a compensating DNA repair process is engaged in the reinvigorated cells.

Because this unidentified repair process may also rescue the DNA repair defect in the different tissue types affected by FA, Dr Wells and her colleagues believe their study may point to an approach that treats all clinical manifestations of the disease, including anemia and cancer.

“A key question for us is, ‘What type of DNA repair kicks in under these conditions, and is it error-free or error-prone?’” Dr Wells explained. “A novel mode of emergency DNA repair might indeed be discovered in the [iPSCs]. We believe some type of compensatory DNA repair must be driven by CHK1 inhibition when cells have FA pathway loss. Otherwise, the cells would have died off very quickly.”

The researchers plan to follow up this study with additional testing in humanized and genetic mouse models. They said they will attempt to improve embryonic development and post-birth fitness in FA-pathway-deficient mice with timed application of a CHK1 inhibitor.

The team will monitor the mice as they age and use genetic sequencing to screen for disease-causing mutations. And they will look for evidence of a DNA repair process (either novel or existing) in the FA-deficient mice.

Lab mouse

The protein kinase CHK1 may be a therapeutic target for Fanconi anemia (FA), according to researchers.

They studied induced pluripotent stem cells (iPSCs) derived from FA patients and found the FA DNA repair pathway was essential for the cells’ proliferation and survival.

The team also discovered that CHK1 played a “crucial” role in iPSCs’ sensitivity to accrued DNA damage, and inhibiting CHK1 allowed FA-deficient iPSCs to grow

normally.

The team relayed these findings in Stem Cell Reports.

“This study provides an experimental platform to test new therapies that could prevent pre- and post-natal Fanconi anemia conditions, which have no cure and limited treatment options,” said study author Susanne Wells, PhD, of the Cincinnati Children’s Hospital Medical Center in Ohio.

“Our findings also raise a number of important questions, so there is a lot more to be done.”

For this study, Dr Wells and her colleagues used iPSCs reprogrammed from mature skin and connective tissue cells donated by FA patients. The cells had a defective FA DNA repair pathway.

The researchers studied the iPSCs in culture and injected them into humanized mouse models, monitoring their genetic, molecular, and developmental progression.

Even with defective FA DNA repair, the iPSCs retained their ability to transform into different tissues, and humanized mice injected with the defective cells started to form teratomas.

However, the DNA repair defect started to kill off the iPSCs by blocking cell division and causing apoptosis.

The researchers noticed that CHK1, which serves as a DNA regulatory checkpoint during cell division, was hyperactive in the iPSCs, which hastened their death.

So the team used pharmacologic inhibitors of CHK1 to block the hyperactive enzyme at a critical stage of the stem cell cycle. This allowed them to override what are usually unfixable errors in the FA repair pathway.

After targeted treatment, FA-pathway-deficient iPSCs resumed dividing and expanding normally.

The researchers said that, to their surprise, the resumption of cell growth occurred without what they had expected to be massive chromosome abnormalities. Because of this, they speculate that a compensating DNA repair process is engaged in the reinvigorated cells.

Because this unidentified repair process may also rescue the DNA repair defect in the different tissue types affected by FA, Dr Wells and her colleagues believe their study may point to an approach that treats all clinical manifestations of the disease, including anemia and cancer.

“A key question for us is, ‘What type of DNA repair kicks in under these conditions, and is it error-free or error-prone?’” Dr Wells explained. “A novel mode of emergency DNA repair might indeed be discovered in the [iPSCs]. We believe some type of compensatory DNA repair must be driven by CHK1 inhibition when cells have FA pathway loss. Otherwise, the cells would have died off very quickly.”

The researchers plan to follow up this study with additional testing in humanized and genetic mouse models. They said they will attempt to improve embryonic development and post-birth fitness in FA-pathway-deficient mice with timed application of a CHK1 inhibitor.

The team will monitor the mice as they age and use genetic sequencing to screen for disease-causing mutations. And they will look for evidence of a DNA repair process (either novel or existing) in the FA-deficient mice.

T cells

Image courtesy of NIAID

A protein called diacylglycerol kinase alpha (DGKα) could be a therapeutic target for X-linked lymphoproliferative disease (XLP-1), according to research published in Science Translational Medicine.

Researchers have known for some time that XLP-1 is a heritable disorder caused by germline mutations in SH2D1A.

When this gene is affected, it leads to defects in an adaptor molecule known as SAP (signaling lymphocytic activation molecule-associated protein), which regulates T-cell receptor signaling and triggers cytotoxic T cells to self-destruct when they are no longer needed.

Without an effective SAP adaptor molecule, apoptosis is impaired, and DGKα is activated.

With the current study, researchers wanted to determine whether the over-activation of DGKα might contribute to the reduced apoptosis observed in T cells in patients with XLP-1 and the accumulation of T cells that occurs following infection with Epstein-Barr virus.

“Patients with X-linked lymphoproliferative disease are prone to severe Epstein-Barr virus infection due to a weakened immune system,” explained study author Kim Nichols, MD, of St. Jude Children’s Research Hospital in Memphis, Tennessee.

“Infection with Epstein-Barr virus can have potentially fatal consequences for these patients. This severe disease is a double-edged sword. On the one hand, the immune system is significantly weakened. However, detrimental side effects occur due to the expansion and hyper-activation of T cells.”

“[W]e wanted to establish the biochemical mechanism underlying these changes so that we could develop better treatments for X-linked lymphoproliferative disease patients experiencing hyper-inflammation.”

Studying T cells from XLP-1 patients, the researchers found that SAP and DGKα are both crucial for the regulation of T-cell death. Loss of SAP, which normally inhibits DGKα, led to unrestrained DGKα activity, resulting in impaired T-cell receptor signaling and resistance to apoptosis.

Pharmacologic inhibition of DGKα restored the sensitivity of XLP-1 T cells to cell death. Using small interfering RNA to knockout DGKα in cultured XLP-1 T cells had the same results.

And pharmacologic inhibition of DGKα curtailed the expansion of T cells in virus-infected mice that served as a model organism to study XLP-1.

Treating the mice with a DGKα inhibitor restored T cells’ sensitivity to cell death by boosting the expression of pro-apoptotic proteins, which prevented excessive T-cell buildup and reduced the severity of the disease.

“Our findings suggest that inhibition of DGKα could reverse some of the life-threatening effects linked to Epstein-Barr virus infection of patients with X-linked lymphoproliferative disease,” Dr Nichols concluded.

T cells

Image courtesy of NIAID

A protein called diacylglycerol kinase alpha (DGKα) could be a therapeutic target for X-linked lymphoproliferative disease (XLP-1), according to research published in Science Translational Medicine.

Researchers have known for some time that XLP-1 is a heritable disorder caused by germline mutations in SH2D1A.

When this gene is affected, it leads to defects in an adaptor molecule known as SAP (signaling lymphocytic activation molecule-associated protein), which regulates T-cell receptor signaling and triggers cytotoxic T cells to self-destruct when they are no longer needed.

Without an effective SAP adaptor molecule, apoptosis is impaired, and DGKα is activated.

With the current study, researchers wanted to determine whether the over-activation of DGKα might contribute to the reduced apoptosis observed in T cells in patients with XLP-1 and the accumulation of T cells that occurs following infection with Epstein-Barr virus.

“Patients with X-linked lymphoproliferative disease are prone to severe Epstein-Barr virus infection due to a weakened immune system,” explained study author Kim Nichols, MD, of St. Jude Children’s Research Hospital in Memphis, Tennessee.

“Infection with Epstein-Barr virus can have potentially fatal consequences for these patients. This severe disease is a double-edged sword. On the one hand, the immune system is significantly weakened. However, detrimental side effects occur due to the expansion and hyper-activation of T cells.”

“[W]e wanted to establish the biochemical mechanism underlying these changes so that we could develop better treatments for X-linked lymphoproliferative disease patients experiencing hyper-inflammation.”

Studying T cells from XLP-1 patients, the researchers found that SAP and DGKα are both crucial for the regulation of T-cell death. Loss of SAP, which normally inhibits DGKα, led to unrestrained DGKα activity, resulting in impaired T-cell receptor signaling and resistance to apoptosis.

Pharmacologic inhibition of DGKα restored the sensitivity of XLP-1 T cells to cell death. Using small interfering RNA to knockout DGKα in cultured XLP-1 T cells had the same results.

And pharmacologic inhibition of DGKα curtailed the expansion of T cells in virus-infected mice that served as a model organism to study XLP-1.

Treating the mice with a DGKα inhibitor restored T cells’ sensitivity to cell death by boosting the expression of pro-apoptotic proteins, which prevented excessive T-cell buildup and reduced the severity of the disease.

“Our findings suggest that inhibition of DGKα could reverse some of the life-threatening effects linked to Epstein-Barr virus infection of patients with X-linked lymphoproliferative disease,” Dr Nichols concluded.

T cells

Image courtesy of NIAID

A protein called diacylglycerol kinase alpha (DGKα) could be a therapeutic target for X-linked lymphoproliferative disease (XLP-1), according to research published in Science Translational Medicine.

Researchers have known for some time that XLP-1 is a heritable disorder caused by germline mutations in SH2D1A.

When this gene is affected, it leads to defects in an adaptor molecule known as SAP (signaling lymphocytic activation molecule-associated protein), which regulates T-cell receptor signaling and triggers cytotoxic T cells to self-destruct when they are no longer needed.

Without an effective SAP adaptor molecule, apoptosis is impaired, and DGKα is activated.

With the current study, researchers wanted to determine whether the over-activation of DGKα might contribute to the reduced apoptosis observed in T cells in patients with XLP-1 and the accumulation of T cells that occurs following infection with Epstein-Barr virus.

“Patients with X-linked lymphoproliferative disease are prone to severe Epstein-Barr virus infection due to a weakened immune system,” explained study author Kim Nichols, MD, of St. Jude Children’s Research Hospital in Memphis, Tennessee.

“Infection with Epstein-Barr virus can have potentially fatal consequences for these patients. This severe disease is a double-edged sword. On the one hand, the immune system is significantly weakened. However, detrimental side effects occur due to the expansion and hyper-activation of T cells.”

“[W]e wanted to establish the biochemical mechanism underlying these changes so that we could develop better treatments for X-linked lymphoproliferative disease patients experiencing hyper-inflammation.”

Studying T cells from XLP-1 patients, the researchers found that SAP and DGKα are both crucial for the regulation of T-cell death. Loss of SAP, which normally inhibits DGKα, led to unrestrained DGKα activity, resulting in impaired T-cell receptor signaling and resistance to apoptosis.

Pharmacologic inhibition of DGKα restored the sensitivity of XLP-1 T cells to cell death. Using small interfering RNA to knockout DGKα in cultured XLP-1 T cells had the same results.

And pharmacologic inhibition of DGKα curtailed the expansion of T cells in virus-infected mice that served as a model organism to study XLP-1.

Treating the mice with a DGKα inhibitor restored T cells’ sensitivity to cell death by boosting the expression of pro-apoptotic proteins, which prevented excessive T-cell buildup and reduced the severity of the disease.

“Our findings suggest that inhibition of DGKα could reverse some of the life-threatening effects linked to Epstein-Barr virus infection of patients with X-linked lymphoproliferative disease,” Dr Nichols concluded.

Erik Malmström

Photo by Ingela Björck

Researchers have reported using mass spectrometry to measure hundreds of proteins in a single blood sample.

And they used the resulting protein patterns to determine the severity of sepsis in animal models. They were also able to determine which organs had been damaged in these mice.

The researchers said they’ve been able to map the majority of proteins found in vital organs and list which proteins are specific to each organ.

“If you see in a blood sample that the amount of proteins from a specific organ increases, it indicates damage to this organ,” explained study author Erik Malmström, of Lund University in Sweden.

“The method provides an understanding of the molecular events that take place during the course of a disease and the possibility, using the same analysis, to study how different organs are affected.”

The researchers described this work in Nature Communications.

The group believes their study of hundreds of different proteins could eventually be used to select other important proteins that can serve as biomarkers for different aspects of sepsis.

First and foremost, however, they think their method will be an important research tool.

“There is so much we don’t know about sepsis,” Malmström said. “Why do not all patients react the same way? Why do some organs suffer the most damage in some patients and not in others? Do different bacteria cause the disease to progress? Can you divide patients into different subgroups, or bacteria, or does each new combination of patients and bacteria lead to a specific form of sepsis?”

The current study was conducted in animals, but the researchers are now moving on to human tissue. They have obtained samples of healthy tissue from various organs and are comparing protein patterns of these samples with patterns in corresponding tissues from sepsis patients.

Erik Malmström

Photo by Ingela Björck

Researchers have reported using mass spectrometry to measure hundreds of proteins in a single blood sample.

And they used the resulting protein patterns to determine the severity of sepsis in animal models. They were also able to determine which organs had been damaged in these mice.

The researchers said they’ve been able to map the majority of proteins found in vital organs and list which proteins are specific to each organ.

“If you see in a blood sample that the amount of proteins from a specific organ increases, it indicates damage to this organ,” explained study author Erik Malmström, of Lund University in Sweden.

“The method provides an understanding of the molecular events that take place during the course of a disease and the possibility, using the same analysis, to study how different organs are affected.”

The researchers described this work in Nature Communications.

The group believes their study of hundreds of different proteins could eventually be used to select other important proteins that can serve as biomarkers for different aspects of sepsis.

First and foremost, however, they think their method will be an important research tool.

“There is so much we don’t know about sepsis,” Malmström said. “Why do not all patients react the same way? Why do some organs suffer the most damage in some patients and not in others? Do different bacteria cause the disease to progress? Can you divide patients into different subgroups, or bacteria, or does each new combination of patients and bacteria lead to a specific form of sepsis?”

The current study was conducted in animals, but the researchers are now moving on to human tissue. They have obtained samples of healthy tissue from various organs and are comparing protein patterns of these samples with patterns in corresponding tissues from sepsis patients.

Erik Malmström

Photo by Ingela Björck

Researchers have reported using mass spectrometry to measure hundreds of proteins in a single blood sample.

And they used the resulting protein patterns to determine the severity of sepsis in animal models. They were also able to determine which organs had been damaged in these mice.

The researchers said they’ve been able to map the majority of proteins found in vital organs and list which proteins are specific to each organ.

“If you see in a blood sample that the amount of proteins from a specific organ increases, it indicates damage to this organ,” explained study author Erik Malmström, of Lund University in Sweden.

“The method provides an understanding of the molecular events that take place during the course of a disease and the possibility, using the same analysis, to study how different organs are affected.”

The researchers described this work in Nature Communications.

The group believes their study of hundreds of different proteins could eventually be used to select other important proteins that can serve as biomarkers for different aspects of sepsis.

First and foremost, however, they think their method will be an important research tool.

“There is so much we don’t know about sepsis,” Malmström said. “Why do not all patients react the same way? Why do some organs suffer the most damage in some patients and not in others? Do different bacteria cause the disease to progress? Can you divide patients into different subgroups, or bacteria, or does each new combination of patients and bacteria lead to a specific form of sepsis?”

The current study was conducted in animals, but the researchers are now moving on to human tissue. They have obtained samples of healthy tissue from various organs and are comparing protein patterns of these samples with patterns in corresponding tissues from sepsis patients.

Mick Bhatia, PhD

Photo courtesy of

McMaster University

Research published in Cancer Cell suggests a molecular signature can be used to predict which patients with myelodysplastic syndromes (MDS) will develop acute myeloid leukemia (AML).

Investigators found that progressive removal of glycogen synthase kinase-3 (GSK-3) signaling via GSK-3β deletion in hematopoietic stem cells (HSCs) results in an MDS-like state.

And when both GSK-3β and GSK-3α are deleted, AML develops.

“We’ve found that the transition from healthy to cancerous blood stem cells happens in clear, compartmentalized steps,” said study author Mick Bhatia, PhD, of McMaster University in Hamilton, Ontario, Canada. “We’ve identified 2 steps in that staircase.”

Specifically, the investigators found that deleting GSK-3β in HSCs led to the generation of self-renewing cells dubbed MDS-initiating cells. These cells proved capable of sustaining MDS in vivo.

Next, the team found that GSK-3β deletion drives Wnt/Akt/mTOR signaling and can induce AML in the absence of GSK-3α.

They noted that GSK-3α has no biological impact on hematopoiesis, but GSK-3α deletion is necessary for the evolution of MDS to AML that occurs in the absence of GSK-3β.

The investigators then defined a molecular signature of GSK-3β-deficient HSCs that could predict transformation to AML in patients with MDS.

The team tested the utility of this 63-gene signature using blood samples that were previously collected from patients with MDS, some of whom ultimately developed AML. The results showed the signature could accurately predict which patients would develop AML and which would not.

“[O]ur next step is to go beyond better predictive measures for the development of a blood cancer and use this predictive gene expression as a target for drugs to prevent AML from developing altogether,” Dr Bhatia said. “This will be part of a new era of genetic-based drug discovery.”

Mick Bhatia, PhD

Photo courtesy of

McMaster University

Research published in Cancer Cell suggests a molecular signature can be used to predict which patients with myelodysplastic syndromes (MDS) will develop acute myeloid leukemia (AML).

Investigators found that progressive removal of glycogen synthase kinase-3 (GSK-3) signaling via GSK-3β deletion in hematopoietic stem cells (HSCs) results in an MDS-like state.

And when both GSK-3β and GSK-3α are deleted, AML develops.

“We’ve found that the transition from healthy to cancerous blood stem cells happens in clear, compartmentalized steps,” said study author Mick Bhatia, PhD, of McMaster University in Hamilton, Ontario, Canada. “We’ve identified 2 steps in that staircase.”

Specifically, the investigators found that deleting GSK-3β in HSCs led to the generation of self-renewing cells dubbed MDS-initiating cells. These cells proved capable of sustaining MDS in vivo.

Next, the team found that GSK-3β deletion drives Wnt/Akt/mTOR signaling and can induce AML in the absence of GSK-3α.

They noted that GSK-3α has no biological impact on hematopoiesis, but GSK-3α deletion is necessary for the evolution of MDS to AML that occurs in the absence of GSK-3β.

The investigators then defined a molecular signature of GSK-3β-deficient HSCs that could predict transformation to AML in patients with MDS.

The team tested the utility of this 63-gene signature using blood samples that were previously collected from patients with MDS, some of whom ultimately developed AML. The results showed the signature could accurately predict which patients would develop AML and which would not.

“[O]ur next step is to go beyond better predictive measures for the development of a blood cancer and use this predictive gene expression as a target for drugs to prevent AML from developing altogether,” Dr Bhatia said. “This will be part of a new era of genetic-based drug discovery.”

Mick Bhatia, PhD

Photo courtesy of

McMaster University

Research published in Cancer Cell suggests a molecular signature can be used to predict which patients with myelodysplastic syndromes (MDS) will develop acute myeloid leukemia (AML).

Investigators found that progressive removal of glycogen synthase kinase-3 (GSK-3) signaling via GSK-3β deletion in hematopoietic stem cells (HSCs) results in an MDS-like state.

And when both GSK-3β and GSK-3α are deleted, AML develops.

“We’ve found that the transition from healthy to cancerous blood stem cells happens in clear, compartmentalized steps,” said study author Mick Bhatia, PhD, of McMaster University in Hamilton, Ontario, Canada. “We’ve identified 2 steps in that staircase.”

Specifically, the investigators found that deleting GSK-3β in HSCs led to the generation of self-renewing cells dubbed MDS-initiating cells. These cells proved capable of sustaining MDS in vivo.

Next, the team found that GSK-3β deletion drives Wnt/Akt/mTOR signaling and can induce AML in the absence of GSK-3α.

They noted that GSK-3α has no biological impact on hematopoiesis, but GSK-3α deletion is necessary for the evolution of MDS to AML that occurs in the absence of GSK-3β.

The investigators then defined a molecular signature of GSK-3β-deficient HSCs that could predict transformation to AML in patients with MDS.

The team tested the utility of this 63-gene signature using blood samples that were previously collected from patients with MDS, some of whom ultimately developed AML. The results showed the signature could accurately predict which patients would develop AML and which would not.

“[O]ur next step is to go beyond better predictive measures for the development of a blood cancer and use this predictive gene expression as a target for drugs to prevent AML from developing altogether,” Dr Bhatia said. “This will be part of a new era of genetic-based drug discovery.”

The increase in nonmedical prescription opioid use in the United States does not appear to be strongly related to the concurrent increase in heroin use, according to a review by Dr. Wilson Compton of the National Institute on Drug Abuse, Bethesda, Md., and his associates.

While heroin users are 3.9 times more likely to have used nonmedical prescription opioids than are those who haven’t used heroin, heroin use only occurs in a small number of nonmedical prescription opioid users. The researchers cited studies showing that 3.6% of opioid users began using heroin within 5 years of beginning opioid use, and 4.2% of opioid users reported also using heroin in the past year.

©PaulPaladin/thinkstockphotos.com

A more likely driver for the increased use of heroin and heroin death rate is decreased cost and increased availability, the investigators wrote. For every $100 decrease in price per gram of heroin, hospitalizations for heroin overdose increase by 2.9%. In addition, heroin use has grown significantly in areas of the United States that were not typically centers for heroin distribution, the researchers reported.

“Fundamentally, prescription opioids and heroin are each elements of a larger epidemic of opioid-related disorders and death. Viewing them from a unified perspective is essential to improving public health. The perniciousness of this epidemic requires a multipronged interventional approach that engages all sectors of society,” the investigators wrote.

Dr. Compton has ties with General Electric, 3M, and Pfizer. No other conflicts were reported. Find the study in the New England Journal of Medicine (doi: 10.1056/NEJMra1508490).

lfranki@frontlinemedcom.com

The increase in nonmedical prescription opioid use in the United States does not appear to be strongly related to the concurrent increase in heroin use, according to a review by Dr. Wilson Compton of the National Institute on Drug Abuse, Bethesda, Md., and his associates.

While heroin users are 3.9 times more likely to have used nonmedical prescription opioids than are those who haven’t used heroin, heroin use only occurs in a small number of nonmedical prescription opioid users. The researchers cited studies showing that 3.6% of opioid users began using heroin within 5 years of beginning opioid use, and 4.2% of opioid users reported also using heroin in the past year.

©PaulPaladin/thinkstockphotos.com

A more likely driver for the increased use of heroin and heroin death rate is decreased cost and increased availability, the investigators wrote. For every $100 decrease in price per gram of heroin, hospitalizations for heroin overdose increase by 2.9%. In addition, heroin use has grown significantly in areas of the United States that were not typically centers for heroin distribution, the researchers reported.

“Fundamentally, prescription opioids and heroin are each elements of a larger epidemic of opioid-related disorders and death. Viewing them from a unified perspective is essential to improving public health. The perniciousness of this epidemic requires a multipronged interventional approach that engages all sectors of society,” the investigators wrote.

Dr. Compton has ties with General Electric, 3M, and Pfizer. No other conflicts were reported. Find the study in the New England Journal of Medicine (doi: 10.1056/NEJMra1508490).

lfranki@frontlinemedcom.com

The increase in nonmedical prescription opioid use in the United States does not appear to be strongly related to the concurrent increase in heroin use, according to a review by Dr. Wilson Compton of the National Institute on Drug Abuse, Bethesda, Md., and his associates.

While heroin users are 3.9 times more likely to have used nonmedical prescription opioids than are those who haven’t used heroin, heroin use only occurs in a small number of nonmedical prescription opioid users. The researchers cited studies showing that 3.6% of opioid users began using heroin within 5 years of beginning opioid use, and 4.2% of opioid users reported also using heroin in the past year.

©PaulPaladin/thinkstockphotos.com

A more likely driver for the increased use of heroin and heroin death rate is decreased cost and increased availability, the investigators wrote. For every $100 decrease in price per gram of heroin, hospitalizations for heroin overdose increase by 2.9%. In addition, heroin use has grown significantly in areas of the United States that were not typically centers for heroin distribution, the researchers reported.

“Fundamentally, prescription opioids and heroin are each elements of a larger epidemic of opioid-related disorders and death. Viewing them from a unified perspective is essential to improving public health. The perniciousness of this epidemic requires a multipronged interventional approach that engages all sectors of society,” the investigators wrote.

Dr. Compton has ties with General Electric, 3M, and Pfizer. No other conflicts were reported. Find the study in the New England Journal of Medicine (doi: 10.1056/NEJMra1508490).

lfranki@frontlinemedcom.com

ORLANDO – Hypertensive persons who sleep 5 hours or less per night have a significantly higher all-cause mortality rate than those who get more shut-eye, according to an analysis from the Penn State Adult Cohort Study.

“We found that the odds of all-cause mortality associated with hypertension increased in a dose-response manner as a function of the degree of objective short sleep duration, even after adjusting for a multitude of factors,” Julio Fernandez-Mendoza, Ph.D., reported at the American Heart Association scientific sessions.

©Bruce Jancin/Frontline Medical News

The Penn State Adult Cohort consists of a random, general population sample of 1,741 men and women who enrolled in the study back in the 1990s, at a mean age of 48.7 years. As part of their comprehensive evaluation they were studied in the overnight sleep laboratory. The cohort has been followed for 15.5 years, during which 20% of subjects died.

As expected, hypertension was associated with increased risk of all-cause mortality in the Penn State Adult Cohort. But Dr. Fernandez-Mendoza and coinvestigators further dissected this association by incorporating the subjects’ objective sleep lab data, something that hadn’t been done in other studies. They found that while as a group the roughly 35% of study participants with hypertension had an adjusted 2.54-fold increased risk of all-cause mortality, compared with normotensive subjects, those who slept 6 or more hours at night – placing them at or above the 50th percentile for sleep duration – had a 1.75-fold increased risk, which just barely reached statistical significance.

In contrast, those who slept 5-6 hours per night were at 2.36-fold increased risk of all-cause mortality, while hypertensives in the bottom quartile for sleep duration with 5 hours or less of sleep had an even more robust 4.04-fold increased risk. All risk figures were determined in a multivariate logistic regression analysis extensively adjusted for age, gender, race, diabetes, obesity, smoking, depression, insomnia, sleep apnea, and history of heart disease or stroke.

This finding of an inverse association between sleep duration and all-cause mortality was consistent with the investigators’ study hypothesis that short sleep duration in hypertensive patients may be a marker of the severity of autonomic dysfunction. After all, it is known that the autonomic nervous system not only controls cardiovascular function, it also regulates sleep, explained Dr. Fernandez-Mendoza, a behavioral psychologist at Pennsylvania State University in Hershey.

Other possible explanations for the findings are that short sleep duration in hypertensive patients might be genetically driven or behaviorally induced, but he considers these less plausible.

In an interview, Dr. Fernandez-Mendoza said he and his coinvestigators have found the same relationship between short sleep duration and increased all-cause mortality in Penn State Adult Cohort members with diabetes or dyslipidemia, although he didn’t present those data at the AHA meeting.

If indeed short sleep duration is a marker of autonomic dysfunction, it would have important clinical implications: “Objective sleep duration may allow for refinement of estimates of mortality risk. I predict that someday cardiovascular risk calculators will incorporate sleep duration,” he said.

The Penn State Adult Cohort findings bring a measure of clarity to what has been a somewhat cloudy area, Dr. Fernandez-Mendoza said. Most prior epidemiologic studies of sleep’s impact on health have relied upon self-reported sleep duration, which is considerably less reliable than objectively measured sleep lab data. And many studies have looked at sleep duration as an isolated variable in relation to morbidity and mortality risk. This, he said, has contributed to public misunderstanding.

“We have people coming into the sleep lab thinking, ‘If I don’t get 7 hours of sleep I’m going to die,’ ” according to the sleep scientist. “But the paradigm we’ve developed, tied to what we know about autonomic control, is that the cardiovascular system and the sleep system are connected to each other. It doesn’t mean that short sleep kills you, it’s that the combination of the traditional cardiometabolic risk factors and short sleep increases risk of morbidity and mortality.”

Dr. Fernandez-Mendoza’s study was funded by an AHA Scientist Development Grant. He reported having no financial conflicts of interest.

bjancin@frontlinemedcom.com

ORLANDO – Hypertensive persons who sleep 5 hours or less per night have a significantly higher all-cause mortality rate than those who get more shut-eye, according to an analysis from the Penn State Adult Cohort Study.

“We found that the odds of all-cause mortality associated with hypertension increased in a dose-response manner as a function of the degree of objective short sleep duration, even after adjusting for a multitude of factors,” Julio Fernandez-Mendoza, Ph.D., reported at the American Heart Association scientific sessions.

©Bruce Jancin/Frontline Medical News

The Penn State Adult Cohort consists of a random, general population sample of 1,741 men and women who enrolled in the study back in the 1990s, at a mean age of 48.7 years. As part of their comprehensive evaluation they were studied in the overnight sleep laboratory. The cohort has been followed for 15.5 years, during which 20% of subjects died.

As expected, hypertension was associated with increased risk of all-cause mortality in the Penn State Adult Cohort. But Dr. Fernandez-Mendoza and coinvestigators further dissected this association by incorporating the subjects’ objective sleep lab data, something that hadn’t been done in other studies. They found that while as a group the roughly 35% of study participants with hypertension had an adjusted 2.54-fold increased risk of all-cause mortality, compared with normotensive subjects, those who slept 6 or more hours at night – placing them at or above the 50th percentile for sleep duration – had a 1.75-fold increased risk, which just barely reached statistical significance.

In contrast, those who slept 5-6 hours per night were at 2.36-fold increased risk of all-cause mortality, while hypertensives in the bottom quartile for sleep duration with 5 hours or less of sleep had an even more robust 4.04-fold increased risk. All risk figures were determined in a multivariate logistic regression analysis extensively adjusted for age, gender, race, diabetes, obesity, smoking, depression, insomnia, sleep apnea, and history of heart disease or stroke.

This finding of an inverse association between sleep duration and all-cause mortality was consistent with the investigators’ study hypothesis that short sleep duration in hypertensive patients may be a marker of the severity of autonomic dysfunction. After all, it is known that the autonomic nervous system not only controls cardiovascular function, it also regulates sleep, explained Dr. Fernandez-Mendoza, a behavioral psychologist at Pennsylvania State University in Hershey.

Other possible explanations for the findings are that short sleep duration in hypertensive patients might be genetically driven or behaviorally induced, but he considers these less plausible.

In an interview, Dr. Fernandez-Mendoza said he and his coinvestigators have found the same relationship between short sleep duration and increased all-cause mortality in Penn State Adult Cohort members with diabetes or dyslipidemia, although he didn’t present those data at the AHA meeting.

If indeed short sleep duration is a marker of autonomic dysfunction, it would have important clinical implications: “Objective sleep duration may allow for refinement of estimates of mortality risk. I predict that someday cardiovascular risk calculators will incorporate sleep duration,” he said.

The Penn State Adult Cohort findings bring a measure of clarity to what has been a somewhat cloudy area, Dr. Fernandez-Mendoza said. Most prior epidemiologic studies of sleep’s impact on health have relied upon self-reported sleep duration, which is considerably less reliable than objectively measured sleep lab data. And many studies have looked at sleep duration as an isolated variable in relation to morbidity and mortality risk. This, he said, has contributed to public misunderstanding.

“We have people coming into the sleep lab thinking, ‘If I don’t get 7 hours of sleep I’m going to die,’ ” according to the sleep scientist. “But the paradigm we’ve developed, tied to what we know about autonomic control, is that the cardiovascular system and the sleep system are connected to each other. It doesn’t mean that short sleep kills you, it’s that the combination of the traditional cardiometabolic risk factors and short sleep increases risk of morbidity and mortality.”

Dr. Fernandez-Mendoza’s study was funded by an AHA Scientist Development Grant. He reported having no financial conflicts of interest.

bjancin@frontlinemedcom.com

ORLANDO – Hypertensive persons who sleep 5 hours or less per night have a significantly higher all-cause mortality rate than those who get more shut-eye, according to an analysis from the Penn State Adult Cohort Study.

“We found that the odds of all-cause mortality associated with hypertension increased in a dose-response manner as a function of the degree of objective short sleep duration, even after adjusting for a multitude of factors,” Julio Fernandez-Mendoza, Ph.D., reported at the American Heart Association scientific sessions.

©Bruce Jancin/Frontline Medical News

The Penn State Adult Cohort consists of a random, general population sample of 1,741 men and women who enrolled in the study back in the 1990s, at a mean age of 48.7 years. As part of their comprehensive evaluation they were studied in the overnight sleep laboratory. The cohort has been followed for 15.5 years, during which 20% of subjects died.

As expected, hypertension was associated with increased risk of all-cause mortality in the Penn State Adult Cohort. But Dr. Fernandez-Mendoza and coinvestigators further dissected this association by incorporating the subjects’ objective sleep lab data, something that hadn’t been done in other studies. They found that while as a group the roughly 35% of study participants with hypertension had an adjusted 2.54-fold increased risk of all-cause mortality, compared with normotensive subjects, those who slept 6 or more hours at night – placing them at or above the 50th percentile for sleep duration – had a 1.75-fold increased risk, which just barely reached statistical significance.

In contrast, those who slept 5-6 hours per night were at 2.36-fold increased risk of all-cause mortality, while hypertensives in the bottom quartile for sleep duration with 5 hours or less of sleep had an even more robust 4.04-fold increased risk. All risk figures were determined in a multivariate logistic regression analysis extensively adjusted for age, gender, race, diabetes, obesity, smoking, depression, insomnia, sleep apnea, and history of heart disease or stroke.

This finding of an inverse association between sleep duration and all-cause mortality was consistent with the investigators’ study hypothesis that short sleep duration in hypertensive patients may be a marker of the severity of autonomic dysfunction. After all, it is known that the autonomic nervous system not only controls cardiovascular function, it also regulates sleep, explained Dr. Fernandez-Mendoza, a behavioral psychologist at Pennsylvania State University in Hershey.

Other possible explanations for the findings are that short sleep duration in hypertensive patients might be genetically driven or behaviorally induced, but he considers these less plausible.

In an interview, Dr. Fernandez-Mendoza said he and his coinvestigators have found the same relationship between short sleep duration and increased all-cause mortality in Penn State Adult Cohort members with diabetes or dyslipidemia, although he didn’t present those data at the AHA meeting.

If indeed short sleep duration is a marker of autonomic dysfunction, it would have important clinical implications: “Objective sleep duration may allow for refinement of estimates of mortality risk. I predict that someday cardiovascular risk calculators will incorporate sleep duration,” he said.

The Penn State Adult Cohort findings bring a measure of clarity to what has been a somewhat cloudy area, Dr. Fernandez-Mendoza said. Most prior epidemiologic studies of sleep’s impact on health have relied upon self-reported sleep duration, which is considerably less reliable than objectively measured sleep lab data. And many studies have looked at sleep duration as an isolated variable in relation to morbidity and mortality risk. This, he said, has contributed to public misunderstanding.

“We have people coming into the sleep lab thinking, ‘If I don’t get 7 hours of sleep I’m going to die,’ ” according to the sleep scientist. “But the paradigm we’ve developed, tied to what we know about autonomic control, is that the cardiovascular system and the sleep system are connected to each other. It doesn’t mean that short sleep kills you, it’s that the combination of the traditional cardiometabolic risk factors and short sleep increases risk of morbidity and mortality.”

Dr. Fernandez-Mendoza’s study was funded by an AHA Scientist Development Grant. He reported having no financial conflicts of interest.

bjancin@frontlinemedcom.com

ORLANDO – Venetoclax monotherapy achieved an overall response rate of 79% in a high-risk population of 107 patients with relapsed or refractory del(17p) chronic lymphocytic leukemia, Dr. Stephan Stilgenbauer reported in a late-breaking abstract at the annual meeting of the American Society of Hematology.

Of the 85 responders, the response was maintained at 1 year in 85%. Of the 45 patients assessed for minimal residual disease in the blood, 18 achieved MRD negativity. Ten of these 18 patients also had bone marrow assessments and six were MRD negative.

Dr. Stilgenbauer of the University of Ulm (Germany), discussed the implications of the phase II study findings in our exclusive interview at ASH, as well as phase III study plans and the use of venetoclax in combination therapies.

He receives honoraria or research funding from a wide range of companies, including AbbVie and Genentech, the companies collaborating on the development of venetoclax.

mdales@frontlinemedcom.com

On Twitter @maryjodales

ORLANDO – Venetoclax monotherapy achieved an overall response rate of 79% in a high-risk population of 107 patients with relapsed or refractory del(17p) chronic lymphocytic leukemia, Dr. Stephan Stilgenbauer reported in a late-breaking abstract at the annual meeting of the American Society of Hematology.

Of the 85 responders, the response was maintained at 1 year in 85%. Of the 45 patients assessed for minimal residual disease in the blood, 18 achieved MRD negativity. Ten of these 18 patients also had bone marrow assessments and six were MRD negative.

Dr. Stilgenbauer of the University of Ulm (Germany), discussed the implications of the phase II study findings in our exclusive interview at ASH, as well as phase III study plans and the use of venetoclax in combination therapies.

He receives honoraria or research funding from a wide range of companies, including AbbVie and Genentech, the companies collaborating on the development of venetoclax.

mdales@frontlinemedcom.com

On Twitter @maryjodales

ORLANDO – Venetoclax monotherapy achieved an overall response rate of 79% in a high-risk population of 107 patients with relapsed or refractory del(17p) chronic lymphocytic leukemia, Dr. Stephan Stilgenbauer reported in a late-breaking abstract at the annual meeting of the American Society of Hematology.

Of the 85 responders, the response was maintained at 1 year in 85%. Of the 45 patients assessed for minimal residual disease in the blood, 18 achieved MRD negativity. Ten of these 18 patients also had bone marrow assessments and six were MRD negative.

Dr. Stilgenbauer of the University of Ulm (Germany), discussed the implications of the phase II study findings in our exclusive interview at ASH, as well as phase III study plans and the use of venetoclax in combination therapies.

He receives honoraria or research funding from a wide range of companies, including AbbVie and Genentech, the companies collaborating on the development of venetoclax.

mdales@frontlinemedcom.com

On Twitter @maryjodales

Ibrutinib may prove useful for patients whose chronic lymphocytic leukemia (CLL) relapses after allogeneic stem cell transplantation, Dr. C. S. Link and colleagues reported.

Ibrutinib has shown efficacy in patients with high-risk CLL, but there are few data from patients who relapsed after allogeneic stem cell transplantation, wrote Dr. Link of the Medizinische Klinik und Poliklinik I, Universitätsklinikum Carl Gustav Carus and the DFG Research Center for Regenerative Therapies, both at the Technische Universität Dresden (Germany).

The researchers performed analyses on cytokine levels and direct measuring of CD4 Th1 and CD4 Th2 cells in a study of five CLL patients treated with ibrutinib for relapse after allogeneic transplants. All patients had partial responses to ibrutinib and one had a minimal residual disease–negative remission.

At 1 year, none of the patients had relapsed; however, one patient died of pneumonia while on ibrutinib treatment. No other unexpected adverse events were observed, the researchers reported in the study, which was published online on Jan. 11.

No substantial changes in T-cell distribution in favor of a CD4 Th1 T-cell shift were noted based on flow cytometry and analyses of T cell–mediated cytokine levels. No acute exacerbations of graft-versus-host disease occurred.

Click here to read the study (Bone Marrow Transplant. 2016 Jan 11. doi: 10.1038/bmt.2015.339).

mdales@frontlinemedcom.com

On Twitter @maryjodales

Ibrutinib may prove useful for patients whose chronic lymphocytic leukemia (CLL) relapses after allogeneic stem cell transplantation, Dr. C. S. Link and colleagues reported.

Ibrutinib has shown efficacy in patients with high-risk CLL, but there are few data from patients who relapsed after allogeneic stem cell transplantation, wrote Dr. Link of the Medizinische Klinik und Poliklinik I, Universitätsklinikum Carl Gustav Carus and the DFG Research Center for Regenerative Therapies, both at the Technische Universität Dresden (Germany).

The researchers performed analyses on cytokine levels and direct measuring of CD4 Th1 and CD4 Th2 cells in a study of five CLL patients treated with ibrutinib for relapse after allogeneic transplants. All patients had partial responses to ibrutinib and one had a minimal residual disease–negative remission.

At 1 year, none of the patients had relapsed; however, one patient died of pneumonia while on ibrutinib treatment. No other unexpected adverse events were observed, the researchers reported in the study, which was published online on Jan. 11.

No substantial changes in T-cell distribution in favor of a CD4 Th1 T-cell shift were noted based on flow cytometry and analyses of T cell–mediated cytokine levels. No acute exacerbations of graft-versus-host disease occurred.

Click here to read the study (Bone Marrow Transplant. 2016 Jan 11. doi: 10.1038/bmt.2015.339).

mdales@frontlinemedcom.com

On Twitter @maryjodales

Ibrutinib may prove useful for patients whose chronic lymphocytic leukemia (CLL) relapses after allogeneic stem cell transplantation, Dr. C. S. Link and colleagues reported.

Ibrutinib has shown efficacy in patients with high-risk CLL, but there are few data from patients who relapsed after allogeneic stem cell transplantation, wrote Dr. Link of the Medizinische Klinik und Poliklinik I, Universitätsklinikum Carl Gustav Carus and the DFG Research Center for Regenerative Therapies, both at the Technische Universität Dresden (Germany).

The researchers performed analyses on cytokine levels and direct measuring of CD4 Th1 and CD4 Th2 cells in a study of five CLL patients treated with ibrutinib for relapse after allogeneic transplants. All patients had partial responses to ibrutinib and one had a minimal residual disease–negative remission.

At 1 year, none of the patients had relapsed; however, one patient died of pneumonia while on ibrutinib treatment. No other unexpected adverse events were observed, the researchers reported in the study, which was published online on Jan. 11.

No substantial changes in T-cell distribution in favor of a CD4 Th1 T-cell shift were noted based on flow cytometry and analyses of T cell–mediated cytokine levels. No acute exacerbations of graft-versus-host disease occurred.

Click here to read the study (Bone Marrow Transplant. 2016 Jan 11. doi: 10.1038/bmt.2015.339).

mdales@frontlinemedcom.com

On Twitter @maryjodales