Wonkblog: Steven Brill: Obamacare wont lower Americas health-care bill, but it was still worth it

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About two years ago, journalist Steven Brill offered a blockbuster story in Time Magazine on why Americans' medical bills are so high. He's now followed that up with a new book released Monday explaining why he doesn't believe Obamacare will change that.

Brill's book, "America's Bitter Pill,"details the backroom deals that allowed the Affordable Care Act to become law, why HealthCare.gov was such a mess when it launched in October, and why he believes the law won't do anything to keep health care costs from running wild. His assessment: the deals Democrats struck with industry to get the law passed ensured that the flawed system would remain intact.

Brill also details in his own frustrations with the health-care system when he underwent open-heart surgery during the reporting of his book, and people who's lives have been changed because of the ACA. And he closes with a vision for what he thinks health-care should look like. Below is a transcript of our conversation Monday morning, edited for brevity and clarity.

JM: This book dives into the process that led to the passage of the Affordable Care Act about five years after it became law. What lessons do you hope can be taken away from this account?

SB: The whole process by which Washington attempted to tackle and fix the largest industry and the most important industry in the country is really emblematic of how Washington works and doesn't work. What I realized as I was doing the first piece for Time Magazine and what I realized in spades as I was reporting this book was that the only way legislation this big, this important can possibly come out of Washington is if the most important group of special interest lobbyists say that it can.

The basic deal that the Obama administration and the Democrats in the Senate had to make was we'll get more coverage for people. But we'll get more coverage for people at the same high prices that allow the drug companies to be so profitable, that allow the non-profit hospitals to be so profitable, that allow the device-makers to be so profitable and that is the result that is Obamacare.

So the good news is this couple I interviewed in Kentucky who hadn't had access to doctors in years suddenly had access to health care. The bad news is that you and I and all the other taxpayers are paying the same high prices for that health care that dominated and completely screwed up the system in the first place.

Is it too cynical to say that deal-making with industry is just what happens when you want to pass major legislation?

When the lobbying behind the industries that are affected by that legislation spends four times as much as the next largest industry when it comes to lobbying, which is the military industrial complex, this is what you get. The second sort of theme through the book is Washington not only is dominated by money, but it's dominated by a kind of partisanship which I think is also the result of too much money going into primaries and gerrymandering and everything else. The third overriding theme of the book is not only is Washington beset by money and by partisan politics, but it's also beset by a lack of attention being paid to the sheer competence of the government. We all missed the story, me included, in the run-up to the [Healthcare.Gov] launch. The Web site was a train wreck two or three years in the making.

Why do you think the administration missed this?

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Wonkblog: Steven Brill: Obamacare wont lower Americas health-care bill, but it was still worth it

Afghan health care at risk as international aid is scaled back

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KABUL, Afghanistan At one of Afghanistans busiest hospitals, signs abound of one of the signature rebuilding successes of Americas longest war.

Afghans hobble into a spotless emergency room and are quickly seen by trauma specialists, including orthopedic surgeons. Modern equipment tracks heart rates, and health care professionals are careful to sterilize their equipment.

But everything is not as it appears at Wazir Akbar Khan Hospital.

A closer look at some of the heart-rate monitors reveals they arent working. Whats more, the X-ray technology here is outdated, there is a shortage of oxygen tanks and medicine, and doctors must work punishing hours to keep up with the steady stream of patients.

We dont have time to sleep, said Ahmad Tariq, an orthopedic surgeon.

In key areas, health care in Afghanistan has undeniably improved since the Taliban regime was toppled 13 years ago. But some highly touted gains may have been overstated, and others are at risk as international militaries pull out of the country and aid organizations scale back their efforts.

Improvements in health care are one of the main success stories the international military coalition and aid groups like the U.S. Agency for International Development point to in Afghanistan. Maternal mortality has been reduced by 80 percent and child mortality by 60 percent, according to USAID; life expectancy has risen, and more rural Afghans have access to health care, though the extent of that improvement is debated.

The Afghan Public Health Ministry estimates that there are now 2,286 health facilities across Afghanistan, compared with about 500 in 2002, and 60 percent of Afghans are within one hour of a health clinic. But some watchdogs have criticized such numbers as misleading, as facilities vary widely in quality and some cited by both U.S. and Afghan officials may not even be in operation.

It doesnt mean we dont have problems in health were a long way to go to provide quality health care for the people of Afghanistan, Qadir Qadir, director of policy and planning for the Public Health Ministry, said. In terms of quality, we have a lot to do.

Larry Sampler, the chief of Afghanistan and Pakistan operations for USAID, says he understands the concerns of health care professionals. But rather than diminishing support, his organizations biggest challenge may be the uncertainty during this transition period and the fact that the unity government headed by President Ashraf Ghani is still finding its footing. Still, he says he is cautiously optimistic USAID, the biggest aid donor in Afghanistan, can build on the health care gains it has made.

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Afghan health care at risk as international aid is scaled back

Which Path for Health-Care Politics in 2015?

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Yogi Berra said that when you come to a fork in the road, take it. It will be that kind of year for health-care politics. The status quo is not an option.

The key to which path the Affordable Care Acttakes is how the Supreme Court rules in King v. Burwell,the case that concerns whether subsidies in the health law can be provided to millions of low- and middle-income enrollees in states with federally run insurance marketplaces.

The effect on people as well as politics could be substantial. A decision for the plaintiffs would deny insurance subsidies for millions, threaten the viability of the marketplaces, and potentially throw the ACA back into the congressional arena (and onto front pages nationwide). Partisan debate about the health-care law could reignite nationwide.

But if the court sides with the government, the ACA could gradually be transformed from the lightning rod of partisan division it has been since enactment in 2010 to a more ordinary political issue. The upside scenario for the ACA has received much less attention than the downside. Consider:

*After a rough start with the infamous Web site problems in 2013, the ACA is largely working as intended. There is no obvious risk of serious meltdown on the horizon to keep the law at the center of political or media debate. The law faces many implementation challenges, but none of the doomsday predictions have proved accurate: There has been no rate shock. Premium increases in the new marketplaces have been modest. Employers have not dumped coverage, and the ranks of the uninsured are shrinking.

*Efforts by the Republican-controlled Congress to chip away at the ACA could fuel the fire if they gain traction and force presidential vetoes. But congressional debates may turn out to be largely symbolic gestures to satisfy campaign promises to the base. They may also be relatively short-lived as the political world pivots to the 2016 presidential campaign. The majorpresidential candidates who set the tone for the election will want to look forwardnot backand to appeal to the political middle. So will many of the 24 Republicansscheduled to defend Senate seats in 2016 (Democrats will be defending nine).

*The president is likely to veto any legislation he views as striking at the core of the ACA. Vetoes would sustain the political war surrounding the law that has benefited critics by rallying anti-Obamacare partisans to their side. But vetoes would also play into the hands of a president whose poll numbers are going up as he aggressively wields executive authority to advance his policy agenda in his final two years in office.

*The anti-ACA fervor on the right has always been a proxy for anti-Obama sentiment. That sentiment is being redirected to other issues as the president exercises executive authority on immigration and the environment (including toward the presidents use of executive authority itself). When President Barack Obama leaves office, the ACAs role as a proxy for anti-Obama fervor will fade, as will, in all likelihood, the term Obamacare.

Ahead of oral arguments at the Supreme Court this spring, it is far from clear which path ACA politics will take. But as the Supreme Court weighs the ACA once again, its clear that the heat will go either way up or way down in 2015.

Drew Altman is president and chief executive officer of theKaiser Family Foundation. He is on Twitter:@drewaltman.

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Which Path for Health-Care Politics in 2015?

Genetic factors contribute to insomnia in children, teens, twin study suggests

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A new study of twins suggests that insomnia in childhood and adolescence is partially explained by genetic factors.

Results show that clinically significant insomnia was moderately heritable at all stages of the longitudinal study. Genetic factors contributed to 33 to 38 percent of the insomnia ratings at the first two stages of the study, when participants had an average age of 8 to 10 years. The heritability of insomnia was 14 to 24 percent at the third and fourth follow-up points, when the average age of participants was 14 to 15 years. The remaining source of variance in the insomnia ratings was the non-shared environment, with no influence of shared, family-wide factors. Further analysis found that genetic influences around age 8 contributed to insomnia at all subsequent stages of development, and that new genetic influences came into play around the age of 10 years.

"Insomnia in youth is moderately related to genetic factors, but the specific genetic factors may change with age," said study author Philip Gehrman, PhD, assistant professor in the Department of Psychology at the University of Pennsylvania in Philadelphia. "We were most surprised by the fact that the genetic factors were not stable over time, so the influence of genes depends on the developmental stage of the child."

Study results are published in the January issue of the journal Sleep.

Insomnia involves difficulty initiating or maintaining sleep, or waking up earlier than desired, according to the American Academy of Sleep Medicine. Children with insomnia may resist going to bed on an appropriate schedule or have difficulty sleeping without intervention by a parent or caregiver. An insomnia disorder results in daytime symptoms such as fatigue, irritability or behavioral problems.

According to the authors, the results suggest that genes controlling the sleep-wake system play a role in childhood insomnia. Therefore, molecular genetic studies are needed to identify this genetic mechanism, which could facilitate the development of targeted treatments.

"These results are important because the causes of insomnia may be different in teens and children, so they may need different treatment approaches," said Gehrman.

The study group comprised 1,412 twin pairs who were between the ages of 8 and 18 years: 739 monozygotic pairs, 672 dizygotic pairs and one pair with unknown zygosity. Participants were followed up at three additional time points. Average ages at each of the four waves of the study were 8, 10, 14 and 15 years. Results were interpreted in terms of the progression across time, rather than differences between discrete age groups. Clinical ratings of insomnia symptoms were assessed by trained clinicians using the Child and Adolescent Psychiatric Assessment and rated according to the Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition.

Story Source:

The above story is based on materials provided by American Academy of Sleep Medicine. Note: Materials may be edited for content and length.

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Genetic factors contribute to insomnia in children, teens, twin study suggests

UC Davis presents 2015 Benjamin Highman Lecture on genomic medicine

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(PRWEB) January 06, 2015

Sequencing the genomes, or entire DNA codes, of individuals to better diagnose and treat disease is a burgeoning area of research. From identifying specific genetic mistakes highly associated with certain cancers to applying effective treatments to mitigate a wayward genes effects, personalized genomic medicine is increasingly finding its way into patient care.

Harnessing the power of whole genome analysis and further defining the role of pathologists in this new era of medicine is the topic of the 2015 Benjamin Highman Lecture, sponsored by the Department of Pathology and Laboratory Medicine at UC Davis Health System.

The lecture, entitled Moving to Genomic Medicine, will be held from 5 p.m. to 6 p.m. on Thursday, Jan. 22 at the Education Building, 4610 X Street in auditorium #2222 in Sacramento. A reception will follow the presentation. Participants can register at Eventbrite.

The lecture will be presented by Debra G. B. Leonard, a leading expert in molecular pathology and genomic medicine and in applying genomic information for diagnosis and treatment of human diseases, including inherited disorders, cancers and infectious diseases.

During her presentation, Leonard will highlight the current applications for genomics and describe the various online genomic medicine resources for testing and for making patient-care decisions. She has spoken widely on various molecular pathology testing services, the future of molecular pathology and the impact of gene patents on molecular pathology practice. Leonard is professor and chair of pathology and laboratory medicine at the University of Vermont Medical Center and Physician Leader of Pathology and Laboratory Medicine at Fletcher Allen Health Care.

Making use of the massive amount of data that results from whole genome testing is an ongoing challenge for practicing physicians across disciplines, said Lydia Howell, professor and chair of pathology and laboratory medicine at UC Davis Health System. While we have the technology to quickly identify an individuals entire genetic code, which includes some three million genetic sequences, its less easy to know which genetic mistakes actually cause disease. Pathologists, with their expertise in molecular diagnostic testing, are in a unique position to lead the current movement of genomic medicine from the research bench to applications in the clinic.

The Highman Symposium is an annual lectureship in honor of Benjamin Highman, who spent almost 40 years in the U.S. Public Health Service as medical director and as chief of Pathologic Anatomy at the National Institutes of Health. He was awarded the Willey Medallion and a special citation by the U.S. Food and Drug Administration. In 1985, Highman retired and joined the volunteer faculty at the UC Davis School of Medicine.

The Department of Pathology and Laboratory Medicine includes 40 faculty and 400 academic and clinical staff who develop and deliver comprehensive diagnostic services in the fields of pathology and laboratory medicine through established and novel diagnostic modalities. Its Clinical Laboratory is home to one of the most technologically advanced testing facilities in California, providing many unique diagnostic tests unavailable elsewhere. The department processes 5 million clinical tests and 20,000 surgical pathology and 20,000 cytology specimens each year.

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UC Davis presents 2015 Benjamin Highman Lecture on genomic medicine

Researchers identify new genetic and epigenetic contributors to diabetes

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Comparison of fat cells in mice and men hints at how genes and environment conspire to produce disease

IMAGE:Researchers compared epigenetic "tags " on fat cells of lean and obese mice. view more

Credit: Oak Ridge National Laboratory

An analysis of the genomes and epigenomes of lean and obese mice and humans has turned up a wealth of clues about how genes and the environment conspire to trigger diabetes, Johns Hopkins researchers say. Their findings reveal that obesity-induced changes to the epigenome -- reversible chemical "tags" on DNA -- are surprisingly similar in mice and humans, and might provide a new route to prevention and treatment of the disease, which affects hundreds of millions worldwide. A report on the study appears Jan. 6 in the journal Cell Metabolism.

"It's well known that most common diseases like diabetes result from a combination of genetic and environmental risk factors. What we haven't been able to do is figure out how, exactly, the two are connected," says Andrew Feinberg, M.D., M.P.H. , Gilman Scholar and director of the Center for Epigenetics in the Institute for Basic Biomedical Sciences at the Johns Hopkins University School of Medicine. "This study takes a step in that direction."

Feinberg has long studied the epigenome, which he compares to "software" that runs on DNA's "hardware." Epigenetic chemical tags affect whether and how much genes are used without changing the genetic code itself.

Feinberg wondered whether epigenetics might partly explain the skyrocketing worldwide incidence of type 2 diabetes. Obesity is a well-established risk factor for the disease, so Feinberg's research group teamed with that of a group led by G. William Wong, Ph.D. , an associate professor of physiology in the Center for Metabolism and Obesity Research at Johns Hopkins, to study the epigenetics of otherwise identical mice that were fed either normal or high-calorie diets.

Analyzing epigenetic marks at more than 7 million sites in the DNA of the mice's fat cells, the researchers found clear differences between the normal and obese mice. Some sites that bore chemical tags called methyl groups in the lean mice were missing them in the obese mice, and vice versa. The methyl groups prevent genes from making proteins.

With colleagues at Sweden's Karolinska Institutet, Feinberg and his team then tested whether the same pattern of differences held in fat cells from lean and obese people, and found, to their surprise, that it did. "Mice and humans are separated by 50 million years of evolution, so it's interesting that obesity causes similar epigenetic changes to similar genes in both species," Feinberg says. "It's likely that when food supplies are highly variable, these epigenetic changes help our bodies adapt to temporary surges in calories. But if the high-calorie diet continues over the long term, the same epigenetic pattern raises the risk for disease."

The research team also found that some of the epigenetic changes associated with obesity affect genes already known to raise diabetes risk. Others affect genes that had not been conclusively linked to the disease, but that turned out to have roles in how the body breaks down and uses nutrients, a process called metabolism. "This study yielded a list of genes that previously have not been shown to play a role in diabetes," says Wong. "In further tests, we showed that at least some of these genes indeed regulate insulin action on sugar uptake; they offer insights into new potential targets for treating type 2 diabetes."

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Researchers identify new genetic and epigenetic contributors to diabetes

The 'Berlin patient,' first and only person cured of HIV, speaks out

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IMAGE:AIDS Research and Human Retroviruses, published monthly in print and online, presents papers, reviews, and case studies documenting the latest developments and research advances in the molecular biology of HIV... view more

Credit: Mary Ann Liebert, Inc., publishers

New Rochelle, NY, January 6, 2015--Timothy Ray Brown, long known only as the "Berlin Patient" had HIV for 12 years before he became the first person in the world to be cured of the infection following a stem cell transplant in 2007. He recalls his many years of illness, a series of difficult decisions, and his long road to recovery in the first-person account, "I Am the Berlin Patient: A Personal Reflection," published in AIDS Research and Human Retroviruses, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is part of a special issue on HIV Cure Research and is available free on the AIDS Research and Human Retroviruses website.

Brown's Commentary describes the bold experiment of using a stem cell donor who was naturally resistant to HIV infection to treat the acute myeloid leukemia (AML) diagnosed 10 years after he became HIV-positive. The stem cell donor had a specific genetic mutation called CCR5 Delta 32 that can protect a person against HIV infection. The virus is not able to enter its target, the CD4 cells. After the stem cell transplant, Brown was able to stop all antiretroviral treatment and the HIV has not returned.

"This is the first time that we get to read this important story written by the man who lived it," says Thomas Hope, PhD, Editor-in-Chief of AIDS Research and Human Retroviruses and Professor of Cell and Molecular Biology at Northwestern University, Feinberg School of Medicine, Chicago, IL. "It is a unique opportunity to share in the human side of this transformative experience."

###

About the Journal

AIDS Research and Human Retroviruses, published monthly in print and online, presents papers, reviews, and case studies documenting the latest developments and research advances in the molecular biology of HIV and SIV and innovative approaches to HIV vaccine and therapeutic drug research, including the development of antiretroviral agents and immune-restorative therapies. The content also explores the molecular and cellular basis of HIV pathogenesis and HIV/HTLV epidemiology. The Journal features rapid publication of emerging sequence information and reports on clinical trials of emerging HIV therapies. Tables of content and a sample issue may be viewed on the AIDS Research and Human Retroviruses website.

About the Publisher

Mary Ann Liebert, Inc., publishers/ is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including AIDS Patient Care and STDs, Viral Immunology, and Journal of Interferon & Cytokine Research. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 80 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc., publishers website.

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The 'Berlin patient,' first and only person cured of HIV, speaks out

Gene Therapys Hemophilia Promise Is Tempered by Memories of Past Tragedies

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History explains why people with the malady, and their physicians, are cautious to believe that a cure is in sight

HEATHER VAN UXEM LEWIS

In 2011, a remarkable study in the New England Journal of Medicine detailed the successful treatment of six adults with haemophilia B, which is caused by a deficiency in the coagulation protein known as factor IX. All of the participants were able to eliminate or reduce the frequency of clotting-factor-replacement injections the current standard treatment for the disease after their livers began producing functional levels of factor IX. The experimental therapy came in the form of an adeno-associated virus (AAV) carrying a gene that encodes instructions for production of normal levels of human factor IX. Three trials of AAV-mediated gene transfer in patients with haemophilia B are ongoing, with high expectations.

After more than 20 years of research on gene transfer, it is a promising time for haemophilia therapies. It now seems likely that a single-dose treatment for haemophilia B using an AAV or another gene-transfer technique will be a viable option for many people in the next decade or two.

Yet haemophilia researchers are not inclined to speak enthusiastically of a cure. Part of that caution comes from recognition that there are still problems to solve. For example, some 40% of people with haemophilia B would find no refuge in an AAV treatment because they produce antibodies that attack and neutralize this virus.

And even if that problem were solved, the treatment would apply only to those with haemophilia B. The more common form of the condition, haemophilia A, stems from a deficit in another protein factor VIII and the gene for that protein is a more difficult target. Regardless of the type of haemophilia, researchers remain hesitant about gene therapy owing to the unresolved ethical issues that arose decades ago.

The unfettered optimism that characterized the early years of gene-therapy research came to a screeching halt in 1999, when 18-year-old Jesse Gelsinger died in a phase I clinical trial at the University of Pennsylvania in Philadelphia. Gelsinger had undergone an experimental gene transfer for his otherwise treatable metabolic disorder. His death, along with a series of other harmful events in early gene-therapy trials for a variety of diseases, threatened the whole field.

Haemophilia specialists who were engaged in gene-transfer studies were more guarded than most of that era's self-proclaimed gene doctors. The source of their reserve goes beyond the cautious optimism that characterized such research after 1999; it is grounded instead in the long and troubled experience that the haemophilia community has had with technological fixes.

By the late 1970s, a therapeutic revolution had transformed haemophilia from an obscure hereditary malady into a manageable disease. But the glory of this achievement was tragically short-lived. The same clotting-factor-replacement therapies that delivered a degree of normality to the lives of people with haemophilia brought unexpected and fatal results: tens of thousands of people with haemophilia were diagnosed with transfusion-related HIV/AIDS in the 1980s and with hepatitis C virus (HCV) in the 1990s.

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Gene Therapys Hemophilia Promise Is Tempered by Memories of Past Tragedies

Gene Therapys Haemophilia Promise Is Tempered by Memories of Past Tragedies

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See Inside

History explains why people with the malady, and their physicians, are cautious to believe that a cure is in sight

HEATHER VAN UXEM LEWIS

In 2011, a remarkable study in the New England Journal of Medicine detailed the successful treatment of six adults with haemophilia B, which is caused by a deficiency in the coagulation protein known as factor IX. All of the participants were able to eliminate or reduce the frequency of clotting-factor-replacement injections the current standard treatment for the disease after their livers began producing functional levels of factor IX. The experimental therapy came in the form of an adeno-associated virus (AAV) carrying a gene that encodes instructions for production of normal levels of human factor IX. Three trials of AAV-mediated gene transfer in patients with haemophilia B are ongoing, with high expectations.

After more than 20 years of research on gene transfer, it is a promising time for haemophilia therapies. It now seems likely that a single-dose treatment for haemophilia B using an AAV or another gene-transfer technique will be a viable option for many people in the next decade or two.

Yet haemophilia researchers are not inclined to speak enthusiastically of a cure. Part of that caution comes from recognition that there are still problems to solve. For example, some 40% of people with haemophilia B would find no refuge in an AAV treatment because they produce antibodies that attack and neutralize this virus.

And even if that problem were solved, the treatment would apply only to those with haemophilia B. The more common form of the condition, haemophilia A, stems from a deficit in another protein factor VIII and the gene for that protein is a more difficult target. Regardless of the type of haemophilia, researchers remain hesitant about gene therapy owing to the unresolved ethical issues that arose decades ago.

The unfettered optimism that characterized the early years of gene-therapy research came to a screeching halt in 1999, when 18-year-old Jesse Gelsinger died in a phase I clinical trial at the University of Pennsylvania in Philadelphia. Gelsinger had undergone an experimental gene transfer for his otherwise treatable metabolic disorder. His death, along with a series of other harmful events in early gene-therapy trials for a variety of diseases, threatened the whole field.

Haemophilia specialists who were engaged in gene-transfer studies were more guarded than most of that era's self-proclaimed gene doctors. The source of their reserve goes beyond the cautious optimism that characterized such research after 1999; it is grounded instead in the long and troubled experience that the haemophilia community has had with technological fixes.

By the late 1970s, a therapeutic revolution had transformed haemophilia from an obscure hereditary malady into a manageable disease. But the glory of this achievement was tragically short-lived. The same clotting-factor-replacement therapies that delivered a degree of normality to the lives of people with haemophilia brought unexpected and fatal results: tens of thousands of people with haemophilia were diagnosed with transfusion-related HIV/AIDS in the 1980s and with hepatitis C virus (HCV) in the 1990s.

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Gene Therapys Haemophilia Promise Is Tempered by Memories of Past Tragedies

Elon Musk Reveals He Likes Robots and Whiskey

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Hours before his company, SpaceX, was set to launch a rocket to the International Space Station, Elon Musk gave thousands of eager fans the chance to pick his brain in a Reddit "Ask Me Anything" interview.

(Today's SpaceX flight was scrubbed due to rocket trouble. Musk said they'll try again Friday at 5 a.m. ET.)

During the interview, no topic was off limits, as Musk addressed everything from his favorite food and drink to his plan to send humans to Mars.

Here's what we learned:

Food and Drink

When inviting the billionaire futurist to a party, be sure to offer him whiskey, his drink of choice. The South African-born Musk also likes French food and BBQ.

Artificial Intelligence

Musk has already warned that machines with artificial intelligence may one day be more dangerous than nuclear weapons, however he doesn't believe we're set for a robot war just yet.

"The timeframe is not immediate, but we should be concerned," he wrote. "There needs to be a lot more work on AI safety."

Mission to Mars

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Elon Musk Reveals He Likes Robots and Whiskey

Cleveland Museum of Art offers glimpse of mechanized sound world with Futurist noise intoners

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CLEVELAND, Ohio -- Part of their vision came true. Music did indeed come to be made by machines.

What they didn't get right: the kind of machines that would make it.

In fact, the Italian Futurists of the early 20th century had something quite different in mind. What they imagined weren't exactly the iPods or synthesizers of today but rather something more like the Intonarumori devices headed this week to the Cleveland Museum of Art.

Part curiosity, part mystery, part sculpture, these 16 box-like "noise intoners" conceived by Luigi Rossolo in 1913 embody the mechanized sound world predicted by our forebears.

PREVIEW

Intonarumori

What: An orchestra of Italian Futurist noise intoners.

When: 7:30 p.m. Friday, Jan. 16.

Where: Cleveland Museum of Art, 11150 East Blvd., Cleveland.

Tickets: $33-$45. Go toclevelandart.org or call 216-421-7350.

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Cleveland Museum of Art offers glimpse of mechanized sound world with Futurist noise intoners

GAO Denies Sierra Nevada's NASA Spacecraft Contract Protest

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Sierra Nevada's Dream Chaser (Credit: Sierra Nevada Corporation)

The Government Accountability Office has denied a legal challenge that was filed by the Sierra Nevada Corporation over a NASA contract award to SpaceX and Boeing for crewed commercial flights.

Sierra Nevada was one of three finalists for the Commercial Crew Transportation Capability (CCtCap) contract, which was ultimately awarded to Boeing and SpaceX. Sierra Nevadas bid was for its Dream Chaser an airplane-like spacecraft thats capable of landing on a runway to deliver astronauts to the ISS.

The company challenged NASAs decision to award a contract to its competitors based on factors including the cost of Boeings proposal and concerns over SpaceXs ability to meet the terms of its proposal to NASA.

In its decision which has not been fully released to the public due because, according to the GAO, it contains proprietary and source selection sensitive information the GAO rejected Sierra Nevadas arguments. In its statement, the GAO stated that it had reviewed the conclusions reached by NASA to determine if they were reasonable, and consistent with the evaluation approach NASA set out in its solicitation but made no conclusions as to the relative merits of each proposal.

In a statement issued earlier today, the Sierra Nevada thanked the GAO for reviewing its proposal, and stated its commitment to continue to develop the Dream Chaser spacecraft.

SNC remains fully committed to being a part of returning world-class human spaceflight and enhanced cargo capabilities to low-Earth orbit, the company said in its statement. In doing so, SNC firmly believes that the Dream Chaser will play a central role in shaping the future of space transportation with its unique capabilities which address a wide spectrum of needs.

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GAO Denies Sierra Nevada's NASA Spacecraft Contract Protest

Freedom Street Medley / Johnny Was King Flashman The Ragga Years 1989 – 1994 – Video

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Freedom Street Medley / Johnny Was King Flashman The Ragga Years 1989 - 1994
Another workout on the New Music riddim. King Flashman @ Rainbow Arch Studio 1992. An improvisation piece containing fragments of Tappa Zukie #39;s "Freedom Street" and Al Tashit Joe #39;s "Ethiopian...

By: KING FLASHMAN

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Freedom Street Medley / Johnny Was King Flashman The Ragga Years 1989 - 1994 - Video