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Just over $7 billion was provided for community health centers and Medicare’s therapy caps were repealed.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

In BRCA Mutation Carriers, Obesity Is Linked with Increased DNA Damage in Normal Breast Gland Cells

Drotumdi O

In BRCA Mutation Carriers, Obesity Is Linked with Increased DNA Damage in Normal Breast Gland Cells

Article ID: 691265

Released: 16-Mar-2018 10:05 AM EDT

Source Newsroom: Endocrine Society

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CITATIONS

ENDO 2018, Mar-2018

CHANNELS

Cancer, Cell Biology, Obesity, Women's Health, Local - DC, Local - DC Metro, Medical Meetings

KEYWORDS

 

Newswise — CHICAGO—Being obese or having a higher body mass index (BMI) while carrying a BRCA (BReast CAncer gene) mutation is positively linked with higher levels of damage to the DNA in normal breast gland cells, new research suggests. The results of the study will be presented Sunday, March 18, at ENDO 2018, the 100th annual meeting of the Endocrine Society in Chicago, Ill.

Obesity is a known risk factor for breast cancer, and breast cancer has been shown to occur more frequently in BRCA mutation carriers who are obese than in those who are lean.

"These data show for the first time that obesity is associated with increased DNA damage in breast epithelium of BRCA mutation carriers," lead study author Priya Bhardwaj, a Ph.D. student at Weill Cornell Medicine in New York, N.Y., and colleagues write in their abstract.

Bhardwaj and her colleagues analyzed archival breast tissue from 82 BRCA mutation carriers. Using immunofluorescence to stain the gamma-H2AX foci, which occur as a result of DNA damage, they examined the normal breast epithelium for DNA damage.

The researchers counted the number of gamma-H2AX foci and found a significant positive link between BMI and the number of gamma-H2AX foci in the tissue.

Obesity was positively associated with DNA damage in the breast epithelial cells of individuals whether or not they were BRCA mutation carriers, but the stronger effect was seen in the tissue of those who were BRCA mutation carriers.

"Women who carry a mutation in BRCA genes have an increased risk of developing breast and ovarian cancer,” Kristy A. Brown, Ph.D., study principal investigator, said. “Obesity is a well-established risk factor for breast cancer in the general population and some studies suggest that maintaining a healthy lifestyle by exercising or avoiding obesity may decrease the likelihood of developing cancer in BRCA mutation carriers."

"This research provides biological evidence for cells of the breast being susceptible to the effects of obesity," she noted. "Maintaining a healthy weight may be associated with a decreased likelihood of developing breast cancer by limiting the amount of DNA damage in the breast glands."

The National Institutes of Health (National Cancer Institute), the Breast Cancer Research Foundation and the National Breast Cancer Foundation funded this study.

# # #

Endocrinologists are at the core of solving the most pressing health problems of our time, from diabetes and obesity to infertility, bone health, and hormone-related cancers. The Endocrine Society is the world’s oldest and largest organization of scientists devoted to hormone research and physicians who care for people with hormone-related conditions.

The Society has more than 18,000 members, including scientists, physicians, educators, nurses and students in 122 countries. To learn more about the Society and the field of endocrinology, visit our site at www.endocrine.org. Follow us on Twitter at @TheEndoSociety and @EndoMedia.

 

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