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HEALTH CARE NEWS

US Congress extends CHIP, funds opioid crisis response following temporary shutdown

Publish date: February 9, 2018

By 

Gregory Twachtman 

Oncology Practice

 

 

 

 

 

 

 

 

 

Congress, despite a second shutdown in less than a month, was able to pass a number of financial extenders to fund key health care programs.

The bipartisan spending bill (H.R. 1892), passed in the early morning hours on Feb. 9 by a 71-28 vote in the Senate (16 Republicans and 12 Democrats voted against it, and Sen. John McCain [R-Ariz.] was not present) and a 240-186 vote in the House (67 Republicans and 119 Democrats voted against and 5 representatives did not vote). President Trump signed the bill later that morning.

 

The spending bill and continuing resolution to fund the government through March 23 includes $6 billion to fund treatment for opioid addiction and other mental health issues, $2 billion in additional funding for the National Institutes of Health, and 4 additional years of funding for the Children’s Health Insurance Program. The additional CHIP funding extends the program for a total of 10 years.

The funding bill also made a technical correction to the Merit-based Incentive Payment System (MIPS) track of the Medicare Quality Payment Program. It removes Part B drug reimbursement from the MIPS payment adjustment, so any positive or negative change to physician payments based on the MIPS score will only be applied to physician fee schedule payments.

The bill also repeals the Independent Payment Advisory Board, a panel created by the Affordable Care Act that would have the power to slash Medicare spending under certain budget circumstances. That board was never convened.

The funding legislation also accelerates closure of the Medicare Part D “donut hole,” the coverage gap in which beneficiaries must pay 100% of medication costs prior to entering catastrophic coverage.

Just over $7 billion was provided for community health centers and Medicare’s therapy caps were repealed.

While the funding bill was written in the Senate with bipartisan input and received bipartisan support, Sen. Rand Paul (R-Ky.) held up votes over objections to the more than $1 trillion it will add to the nation’s debt, as well as for the fact that there was no opportunity to introduce and vote on amendments, leading to an hours-long government shutdown.

There also were concerns about two issues that could have derailed the vote in the House. Democrats wanted to add language to address immigrants brought to this nation illegally as children, while some Republicans did not want to increase the federal debt. However, there were enough votes to pass the funding legislation.

gtwachtman@frontlinemedcom.com

Better Understanding ALS by Looking at How Cells Change

Drotumdi O

 Better Understanding ALS by Looking at How Cells Change     Article ID: 691175  Released: 15-Mar-2018 12:05 PM EDT  Source Newsroom:  Universite de Montreal    Add to Favorites         more news from this source                      Share                     Credit: CRCHUM  hnRNP A1B is expressed in the CNS and forms cytoplasmic aggregates in ALS patient neurons.     MEDIA CONTACT   Available for logged-in reporters only   CITATIONS   Brain, March 2018   CHANNELS   All Journal News ,  Cell Biology ,  Neuro ,  Local - Canada   KEYWORDS   ALS ,  University of Montreal ,  Neuroscience ,  Lou Gehrig disease ,  Cell and Molecular Biology ,   Brain ,  TDP-43 ,  RNA ,  HnRNPA1 ,  SMA ,   Cold Spring Harbor Laboratory ,  nusinersen ,  fundamental research ,  Canada ,  Montreal ,   Hebrew University   + Show More        Newswise — It took eight long years of research, but now an international team led by neuroscientists at Université de Montréal has discovered a basic molecular mechanism that better helps understand how Lou Gehrig's disease, or amyotrophic lateral sclerosis (ALS), works.  And that basic science could someday lead to new therapy for the debilitating disease, which cripples people by removing the brain's ability to communicate with their muscles, eventually leading to paralysis and early death.   "It's a story of fundamental research about what happens normally in the body's cells and what changes in the context of ALS," said  Jade-Emmanuelle Deshaies, a research associate in neurosciences at the UdeM Hospital Research Centre (CRCHUM) and lead author of the joint Canada-Israel study,  published  online today in the journal  Brain.   "While studies such as this do not immediately give rise to new treatments for people living with ALS, they do deepen our understanding of the disease. ALS is very complicated; many cellular functions get mis-regulated. This type of work provides important information for future drug targets and the development of biomarkers aimed at detecting the disease more rapidly and following its progression."  The research began eight years ago when Deshaies and her supervisor, associate professor of neurosciences  Christine Vande Velde , started investigating what happens to various molecules when TDP-43, a protein that binds the 'messengers' in the cell known collectively as RNA and that is central to ALS pathology, is removed from the nucleus.  "Our specific focus was on other types of RNA binding proteins that could be interesting players in the disease," Deshaies recalled. "One of these, hnRNP A1, caught our eye. In particular because there was a second form that is rarely mentioned in the literature."      How the science works   But first, a bit of basic science.  In molecular biology, genes encode RNA and the RNA then gets translated into proteins, the workhorses of cells. There are many different versions of RNA, each encoding many different versions of a protein. TDP-43, for one, binds RNA and can change how it is spliced – in a sequence of ABCD, for example, or of ABCEFG – a process called alternative splicing. Another RNA binding protein is hnRNP A1, and it gets spliced into two variants, both regulated by TDP-43.   Why is this important to understanding ALS? Because TDP-43 is known to be a major component of non-living substances in the cell called cytoplasmic inclusions, which are observed in 97 per cent of ALS cases.  "The data we have show that when TDP-43 is either not there at all, or is just absent from the nucleus, you can change the splicing pattern of hnRNP A1," said Vande Velde. "The big picture is that there is a much more broad spectrum of RNA metabolism mis-regulation than what was previously thought. And with that, we get more understanding of what's going wrong, and given this new knowledge, we can potentially develop a therapy that targets this mechanism."      Another motor neuron disease, SMA   A parallel development is research into another motor neuron disease, spinal muscular atrophy (SMA). Scientists know that hnRNP A1 plays a role in its progress, controlling the splicing of an important gene called SMN, survival motor neuron. Vande Velde and her team don't yet know whether or not the new splice variant they discovered changes SMN levels or function, but they point to a new drug therapy announced last year for SMA that does target the splicing of SMN by hnRNP A1.  "The drug is nusinersen, sold commercially as Spinraza," Vande Velde explained.  "When you give it to babies early enough, you can fix their spinal muscular atrophy. Babies that were not able to roll over, or walk, now can. Babies that would normally die within the first two or three years of life are able to reach the developmental milestones. It's being reported as a real cure for the most severe forms of the disease."  Developed by scientists at Cold Spring Harbor Laboratory and Ionis Pharmaceuticals, nusinersen is an exciting development "because they did the type of work we've been doing, which is to understand how a gene is spliced" said Vande Velde. That's a therapeutic that came out of understanding a molecular mechanism involving alternative splicing.  "It took many years to get to that point, and similarly, our work is just the first cog in the wheel," she added. "Whether or not there really is an influence on the expression or the splicing of the very important gene SMN, or other genes important for motor neuron survival, is something we need to evaluate," Vande Velde said.       Persistence pays off   Her lab's work is also a story of persistence. As Deshaies put it, "science is rarely straightforward. It often takes a winding road before leading to explanations and true understanding of what we observe."  "We're studying a mechanism that's never been reported before," Vande Velde noted. "We had some conflicting results early on, and it took time to figure out what the role of TDP-43 was in all this. It was "a massive team undertaking," she added, “with team members from Israel (at Hebrew University), Quebec (at UdeM and Université de Sherbrooke) and elsewhere in Canada (at Western University) all making key contributions."  More ALS research is done in Quebec than any other province, and the UdeM-led study was supported by grants from NSERC and the non-profit ALS Society of Canada.  Hence the importance of getting the news out, even with no new therapy in sight.  "I think it's an important service to communicate back to patients and their families what discoveries are being made with their donations, like those given via the Ice Bucket Challenge" said Vande Velde. "Many families are eager to learn about the molecular details of the disease and how we get to know them, and understand this is an important step in developing a therapy."   -------------------------   About this study    "TDP-43 regulates the alternative splicing of hnRNP A1 to yield an aggregation-prone variant in amyotrophic lateral sclerosis,"  by Jade-Emmanuelle Deshaies et al, was published March 19, 2018 in the journal Brain. DOI 10.1093/brain/awy062.           Permalink to this article               COMMENTS  |  COMMENTING POLICY   We recommend   Experiments in Mice May Help Boost Newly FDA-Approved Therapy for Spinal Muscular Atrophy   Newswise   Novel Mechanisms Underlying Major Childhood Neuromuscular Disease Identified   Newswise   Researchers Gain New Insights on Spinal Muscular Atrophy   Newswise   ALS: New Clues to the Cause and How Future Drugs Might Reverse Disease   Newswise   Orally Delivered Compounds, Which Selectively Modify RNA Splicing Prevent Deficits in Mouse Models of SMA   Newswise      The Emerging Picture of Autism Spectrum Disorder: Genetics and Pathology   Jason A. Chen et. al.ñagarikano, T. Grant Belgard, Vivek Swarup, and Daniel H. Geschwind, Annual Reviews   Share your Insights and Learn How Readers Discover Content   TrendMD, Renew Publishing Consultants   The forgotten. IV. A man with motor neurone disease.   British Medical Journal Publishing Group, The BMJ   Getting the Most Out of Hepatitis C Treatment   Healthline   From De Novo Mutations to Personalized Therapeutic Interventions in Autism   William M. Brandler and Jonathan Sebat, Annual Reviews

Better Understanding ALS by Looking at How Cells Change

Article ID: 691175

Released: 15-Mar-2018 12:05 PM EDT

Source Newsroom: Universite de Montreal

Add to Favorites

more news from this source

 

 

 

 

Share

 

 

Credit: CRCHUM

hnRNP A1B is expressed in the CNS and forms cytoplasmic aggregates in ALS patient neurons.

MEDIA CONTACT

Available for logged-in reporters only

CITATIONS

Brain, March 2018

CHANNELS

All Journal News, Cell Biology, Neuro, Local - Canada

KEYWORDS

ALS, University of Montreal, Neuroscience, Lou Gehrig disease, Cell and Molecular Biology,

Brain, TDP-43, RNA, HnRNPA1, SMA,

Cold Spring Harbor Laboratory, nusinersen, fundamental research, Canada, Montreal,

Hebrew University

+ Show More

 

Newswise — It took eight long years of research, but now an international team led by neuroscientists at Université de Montréal has discovered a basic molecular mechanism that better helps understand how Lou Gehrig's disease, or amyotrophic lateral sclerosis (ALS), works.

And that basic science could someday lead to new therapy for the debilitating disease, which cripples people by removing the brain's ability to communicate with their muscles, eventually leading to paralysis and early death. 

"It's a story of fundamental research about what happens normally in the body's cells and what changes in the context of ALS," said  Jade-Emmanuelle Deshaies, a research associate in neurosciences at the UdeM Hospital Research Centre (CRCHUM) and lead author of the joint Canada-Israel study, published online today in the journal Brain.

"While studies such as this do not immediately give rise to new treatments for people living with ALS, they do deepen our understanding of the disease. ALS is very complicated; many cellular functions get mis-regulated. This type of work provides important information for future drug targets and the development of biomarkers aimed at detecting the disease more rapidly and following its progression."

The research began eight years ago when Deshaies and her supervisor, associate professor of neurosciences Christine Vande Velde, started investigating what happens to various molecules when TDP-43, a protein that binds the 'messengers' in the cell known collectively as RNA and that is central to ALS pathology, is removed from the nucleus.

"Our specific focus was on other types of RNA binding proteins that could be interesting players in the disease," Deshaies recalled. "One of these, hnRNP A1, caught our eye. In particular because there was a second form that is rarely mentioned in the literature."

 

How the science works

But first, a bit of basic science.

In molecular biology, genes encode RNA and the RNA then gets translated into proteins, the workhorses of cells. There are many different versions of RNA, each encoding many different versions of a protein. TDP-43, for one, binds RNA and can change how it is spliced – in a sequence of ABCD, for example, or of ABCEFG – a process called alternative splicing. Another RNA binding protein is hnRNP A1, and it gets spliced into two variants, both regulated by TDP-43. 

Why is this important to understanding ALS? Because TDP-43 is known to be a major component of non-living substances in the cell called cytoplasmic inclusions, which are observed in 97 per cent of ALS cases.

"The data we have show that when TDP-43 is either not there at all, or is just absent from the nucleus, you can change the splicing pattern of hnRNP A1," said Vande Velde. "The big picture is that there is a much more broad spectrum of RNA metabolism mis-regulation than what was previously thought. And with that, we get more understanding of what's going wrong, and given this new knowledge, we can potentially develop a therapy that targets this mechanism."

 

Another motor neuron disease, SMA

A parallel development is research into another motor neuron disease, spinal muscular atrophy (SMA). Scientists know that hnRNP A1 plays a role in its progress, controlling the splicing of an important gene called SMN, survival motor neuron. Vande Velde and her team don't yet know whether or not the new splice variant they discovered changes SMN levels or function, but they point to a new drug therapy announced last year for SMA that does target the splicing of SMN by hnRNP A1.

"The drug is nusinersen, sold commercially as Spinraza," Vande Velde explained.  "When you give it to babies early enough, you can fix their spinal muscular atrophy. Babies that were not able to roll over, or walk, now can. Babies that would normally die within the first two or three years of life are able to reach the developmental milestones. It's being reported as a real cure for the most severe forms of the disease."

Developed by scientists at Cold Spring Harbor Laboratory and Ionis Pharmaceuticals, nusinersen is an exciting development "because they did the type of work we've been doing, which is to understand how a gene is spliced" said Vande Velde. That's a therapeutic that came out of understanding a molecular mechanism involving alternative splicing.

"It took many years to get to that point, and similarly, our work is just the first cog in the wheel," she added. "Whether or not there really is an influence on the expression or the splicing of the very important gene SMN, or other genes important for motor neuron survival, is something we need to evaluate," Vande Velde said. 

 

Persistence pays off

Her lab's work is also a story of persistence. As Deshaies put it, "science is rarely straightforward. It often takes a winding road before leading to explanations and true understanding of what we observe."

"We're studying a mechanism that's never been reported before," Vande Velde noted. "We had some conflicting results early on, and it took time to figure out what the role of TDP-43 was in all this. It was "a massive team undertaking," she added, “with team members from Israel (at Hebrew University), Quebec (at UdeM and Université de Sherbrooke) and elsewhere in Canada (at Western University) all making key contributions."

More ALS research is done in Quebec than any other province, and the UdeM-led study was supported by grants from NSERC and the non-profit ALS Society of Canada.  Hence the importance of getting the news out, even with no new therapy in sight.

"I think it's an important service to communicate back to patients and their families what discoveries are being made with their donations, like those given via the Ice Bucket Challenge" said Vande Velde. "Many families are eager to learn about the molecular details of the disease and how we get to know them, and understand this is an important step in developing a therapy." 

-------------------------

About this study

"TDP-43 regulates the alternative splicing of hnRNP A1 to yield an aggregation-prone variant in amyotrophic lateral sclerosis," by Jade-Emmanuelle Deshaies et al, was published March 19, 2018 in the journal Brain. DOI 10.1093/brain/awy062.

 

 

Permalink to this article

 

 

COMMENTS | COMMENTING POLICY

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ALS: New Clues to the Cause and How Future Drugs Might Reverse Disease

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Orally Delivered Compounds, Which Selectively Modify RNA Splicing Prevent Deficits in Mouse Models of SMA

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