CoP implementation date pushed to 1/13/18

On 07/07/2017 William A.Dombi, Esq. VP for Law with the National Association of Home Care and Hospice (NAHC) shared that CMS just issued the Final Rule setting out an new effective date for CoP compliance.https://s3.amazonaws.com/public-inspection.federalregister.gov/2017-14347.pdf

As proposed, the new compliance deadline is 1/13/18. CMS was not swayed by the recommendations to delay the effective date in line with the issuance of the interpretive guidelines. CMS anticipates an issuance of draft guidelines this Fall with finalization in December. CMS expressed that the regulations can be implemented without the guidelines.[more]

Skin Damage Associated with Moisture and Pressure: Tips for How to Differentiate and Goals for Protection and Management

American Nurse Today Webinars

American Nurse Today is offering a free webinar on skin:

Webinar Objectives

  • Identify how wounds are classified according to wound depth and etiology
  • Describe the etiology of pressure injury and incontinence- associated skin damage (IAD)
  • Understand evidenced-based protocols of care for prevention and management of IAD and pressure injuries
  • Recognize and describe NPUAP-EPUAP Pressure Injury Classification System
  • Understand appropriate ConvaTec products that can be used for prevention and treatment of IAD and pressure injuries

Check the link below for the free webinar:

Convatec Webinar Access – American Nurse Today

 

Home Health New CoPs Status

ARCHIVE    |    WWW.IAHHC.ORG

Home Health New CoPs Status

 Print this Article | Send to Colleague

The latest information from The National Association of Home Care and Hospice (NAHC) on June 30, 2017 is that CMS has informed NAHC that the final rule that will delay the CoPs is at OMB for clearance. For some reason though, it has yet to post to the OMB website. Still, NAHC fully expects the final rule to be issued prior to July 13.

While we do not know the outcome of the final rule, there has been no indication that the delay will be shorter than the proposed January 13, 2018. NAHC recommended that the delay be extended until 6 months following the yet to be released interpretive guidelines.

IAHHC will be diligently watching for the CoP rule and will inform our members promptly.

Back to IAHHC iWeekly

 

Indiana Association for Home & Hospice Care, Inc.
6320-G Rucker Road, Indianapolis, IN, 46220
info@iahhc.org | www.iahhc.org

 

Source: Home Health New CoPs Status

Enzyme drives middle-age weight and fitness changes | National Institutes of Health (NIH)

At a Glance

  • Scientists identified an enzyme in animal studies whose activity promotes weight gain and the loss of exercise capacity starting in mid-life.
  • A drug that inhibits the enzyme prevented weight gain in mice, increased fitness levels, and reduced the incidence of obesity and type 2 diabetes.
  • The findings could lead to more effective weight-loss medications.

  Researchers have long known that losing weight and maintaining the capacity to exercise tend to get harder beginning between ages 30 and 40—the start of mid-life. Scientists have developed new therapies for obesity, including fat-fighting pills. However, many therapies have failed because of a lack of understanding about the biological changes that cause middle-aged people to gain weight, particularly around the abdomen.

Dr. Jay H. Chung, an endocrinologist at NIH’s National Heart, Lung, and Blood Institute (NHLBI), was always puzzled by the aging-weight gain paradox. An average adult in America gains 30 pounds from age 20 to 50, even though food intake usually decreases during this period. Chung and his associates thus searched for biochemical changes in middle-aged animals (human equivalent of 45 years). Their study appeared on May 2, 2017, in Cell Metabolism.

The team focused on an enzyme called DNA-dependent protein kinase, or DNA-PK. This enzyme is activated by a specific kind of DNA damage, but evidence has been mounting that DNA-PK has functions beyond DNA repair. One such function is in metabolism.

The scientists looked at levels of DNA-PK activity in the skeletal muscles of rhesus macaques and mice. These levels were low over time until middle-age, when they rose significantly. Further experiments showed that DNA-PK activity promotes the conversion of nutrients to fat and decreases the number of mitochondria, the tiny organelles in cells that turn fat into energy to fuel the body.

Mitochondria can be found in abundance among young people, but the numbers drop considerably in older people. Researchers know that fewer mitochondria can promote obesity as well as loss of exercise capacity.

The researchers theorized that reducing DNA-PK activity might increase the number of mitochondria and promote fat burning. They tested their theory with a drug that inhibits DNA-PK. Mice that received the inhibitor had a 40% decrease in weight gain when fed a high-fat diet. The drug boosted the number of mitochondria in the skeletal muscle, increased the fitness of obese and middle aged mice, and reduced the incidence of obesity and type 2 diabetes.

The team also examined the role of DNA-PK activity in calorie restriction and aerobic fitness, both of which can delay aging and protect against chronic diseases in animal models. Rhesus macaques on a calorie-restricted diet had lower levels of DNA-PK activity in skeletal muscle. Rats selectively bred to be strong runners also had reduced DNA-PK levels in their skeletal muscle—three-fold lower than poor rat runners.

“Our society attributes the weight gain and lack of exercise at mid-life (approximately 30-60 years) primarily to poor lifestyle choices and lack of will power, but this study shows that there is a genetic program driven by an overactive enzyme that promotes weight gain and loss of exercise capacity at mid-life,” Chung says.

These findings could lead to the development of a new type of weight-loss medication. However, DNA-PK inhibitors have yet to be tested this way in humans. Middle-aged people who are fighting obesity should continue to reduce calories and boost exercise.

Source: Enzyme drives middle-age weight and fitness changes | National Institutes of Health (NIH)

Diagnosing cystic fibrosis with wearable devices | National Institutes of Health (NIH)

 

Diagnosing cystic fibrosis with wearable devices?

Cystic fibrosis is the most common fatal genetic disease nationwide. It causes the body to produce thick, sticky mucus that clogs the lungs, leads to infection, and blocks the pancreas, which stops digestive enzymes from reaching the intestine where they are required in order to digest food. Mutations in a single gene, called the Cystic Fibrosis Transmembrane Regulator (CFTR) gene, cause cystic fibrosis. In normal cells, the CFTR protein acts as a channel that allows cells to release chloride and other ion…[more]

Source: Diagnosing cystic fibrosis with wearable devices | National Institutes of Health (NIH)