Researchers from The Netherlands report that patients with rheumatoid arthritis (RA) who have higher levels of self-efficacy for physical activity are more likely to achieve their physical activity goals. According to the study now available in Arthritis Care & Research, a journal of the American College of Rheumatology (ACR), achievement of physical activity goals is associated with lower self-reported arthritis pain and increased health-related quality of life (HRQOL).

The World Health Organization (WHO) estimates that RA, a chronic autoimmune disease causing inflammation in the lining of joints, affects nearly 1% of the world population. In the U.S., the ACR reports 1.3 million adults suffer with RA. Studies indicate that RA patients cite pain and stiffness as the most limiting factors of their illness, and report lower HRQOL than healthy individuals. RA patients who do not engage in regular physical activity have a more pronounced effect from the disease.

For the current study, Keegan Knittle, MSc, from Leiden University in The Netherlands and colleagues surveyed 106 patients with RA to assess physical activity, motivation and self-efficacy for physical activity, level of arthritis pain, and quality of life. After six months, participants were surveyed again and asked to indicate the extent to which they achieved their baseline physical activity goal. Previous research has shown that self-efficacy, described as one's belief in his or her own capabilities to perform a specific behavior, is associated with increased physical activity participation among RA patients.

Results showed that 75% of participants rated their physical activity goal achievement at 50% or more. Higher levels of self-efficacy for physical activity increased the likelihood that patients would achieve their physical activity goals, and goal achievement had a direct positive effect upon quality of life outcomes. Researchers found that patients who achieved their physical activity goal reported less arthritis pain and greater quality of life. No differences were found between men and women who completed the surveys, or between patients newly diagnosed versus those with RA for 10 years or more.

Knittle concluded, "Our results suggest that an increased focus on self-efficacy enhancement, realistic goal-setting, and techniques that increase the likelihood of goal achievement will assist clinicians and researchers develop interventions that have a positive impact on pain reduction and quality of life outcomes for RA patients."

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A gene responsible for regulating chronic pain, called HCN2, has been identified by scientists at the University of Cambridge.

The Biotechnology and Biological Sciences Research Council (BBSRC) and EU funded research, published today (09 September) in the journal Science, opens up the possibility of targeting drugs to block the protein produced by the gene in order to combat chronic pain.

Approximately one person in seven in the UK suffers from chronic, or long-lasting, pain of some kind, the commonest being arthritis, back pain and headaches. Chronic pain comes in two main varieties. The first, inflammatory pain, occurs when a persistent injury (e.g. a burn or arthritis) results in an enhanced sensitivity of pain-sensitive nerve endings, thus increasing the sensation of pain.

More intractable is a second variety of chronic pain, neuropathic pain, in which nerve damage causes on-going pain and a hypersensitivity to stimuli. Neuropathic pain, which is often lifelong, is a surprisingly common condition and is poorly treated by current drugs. Neuropathic pain is seen in patients with diabetes (affecting 3.7m patients in Europe, USA and Japan) and as a painful after-effect of shingles, as well as often being a consequence of cancer chemotherapy. Neuropathic pain is also a common component of lower back pain and other chronic painful conditions.

Professor Peter McNaughton, lead author of the study and Head of the Department of Pharmacology at the University of Cambridge, said: "Individuals suffering from neuropathic pain often have little or no respite because of the lack of effective medications. Our research lays the groundwork for the development of new drugs to treat chronic pain by blocking HCN2."

The HCN2 gene, which is expressed in pain-sensitive nerve endings, has been known for several years, but its role in regulating pain was not understood. Because a related gene, HCN4, plays a critical role in controlling the frequency of electrical activity in the heart, the scientists suspected that HCN2 might in a similar way regulate the frequency of electrical activity in pain-sensitive nerves.

For the study, the researchers engineered the removal of the HCN2 gene from pain-sensitive nerves. They then carried out studies using electrical stimuli on these nerves in cell cultures to determine how their properties were altered by the removal of HCN2.

Following promising results from the in vitro studies in cell cultures, the researchers studied genetically modified mice in which the HCN2 gene had been deleted. By measuring the speed the mice withdrew from different types of painful stimuli, the scientists were able to determine that deleting the HCN2 gene abolished neuropathic pain. Interestingly, they found that deleting HCN2 does not affect normal acute pain (the type of pain produced by a sudden injury - such as biting one's tongue).

Professor McNaughton added: "Many genes play a critical role in pain sensation, but in most cases interfering with them simply abolishes all pain, or even all sensation. What is exciting about the work on the HCN2 gene is that removing it - or blocking it pharmacologically- eliminates neuropathic pain without affecting normal acute pain. This finding could be very valuable clinically because normal pain sensation is essential for avoiding accidental damage."

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I spent a lot of time playing in my tree house, that the trees in.....

By measuring the speed the mice withdrew from different types of painful stimuli, the scientists were able to determine that deleting the HCN2 gene abolished neuropathic pain. RA patients who do not engage in regular physical activity have a more pronounced effect from the disease.For the current study, Keegan Knittle, MSc, from Leiden University in The Netherlands and colleagues surveyed 106 patients with RA to assess physical activity, motivation and self-efficacy for physical activity, level of arthritis pain, and quality of life. According to the study now available in Arthritis Care & Research, a journal of the American College of Rheumatology (ACR), achievement of physical activity goals is associated with lower self-reported arthritis pain and increased health-related quality of life (HRQOL).The Biotechnology and Biological Sciences Research Council (BBSRC) and EU funded research, published today (09 September) in the journal Science, opens up the possibility of targeting drugs to block the protein produced by the gene in order to combat chronic pain. After six months, participants were surveyed again and asked to indicate the extent to which they achieved their baseline physical activity goal. What is exciting about the work on the HCN2 gene is that removing it - or blocking it pharmacologically- eliminates neuropathic pain without affecting normal acute pain.g. Interestingly, they found that deleting HCN2 does not affect normal acute pain (the type of pain produced by a sudden injury - such as biting one's tongue). The first, inflammatory pain, occurs when a persistent injury (e." Additional References Citations . Neuropathic pain is seen in patients with diabetes (affecting 3. They then carried out studies using electrical stimuli on these nerves in cell cultures to determine how their properties were altered by the removal of HCN2. Our research lays the groundwork for the development of new drugs to treat chronic . It's a beautiful painting but it's just too depressing to hang anywhere. It's of a swamp house on a bayou and has a Louisiana feel to it. It's called Alligator Fisher and I'm thinking about getting because it reminds me of my cajun heritage, most of my family is from Louisiana. I saw a painting he did of a fishing scene but I chose not to buy it. When she died, she left me the painting and it hangs in a place of honor over my fireplace mantle. It is done in vibrant colors and also depicts the buildings in the market like an ice cream parlor and the Hotel Van Nuys.There is a water scene that I really like painted in 1940. I don't particularly care for his art.Another painting that I admire is called Howard in 1944. She looked so relaxed, that I could imagine what it felt like to lie there myself. Still, they are a joy to behold. Now we're very close. It's pretty funny to me that when we were growing up, she'd cry because she wasn't allowed to play football with the boys and I used to tease her relentlessly and pull her pigtails whenever I got the chance. I spent a lot of time playing in my tree house, that the trees in the picture appealed to me so much. It's too bad

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Researchers from The Netherlands report that patients with rheumatoid arthritis (RA) who have higher levels of self-efficacy for physical activity are more likely to achieve their physical activity goals. According to the study now available in Arthritis Care & Research, a journal of the American College of Rheumatology (ACR), achievement of physical activity goals is associated with lower self-reported arthritis pain and increased health-related quality of life (HRQOL).

The World Health Organization (WHO) estimates that RA, a chronic autoimmune disease causing inflammation in the lining of joints, affects nearly 1% of the world population. In the U.S., the ACR reports 1.3 million adults suffer with RA. Studies indicate that RA patients cite pain and stiffness as the most limiting factors of their illness, and report lower HRQOL than healthy individuals. RA patients who do not engage in regular physical activity have a more pronounced effect from the disease.

For the current study, Keegan Knittle, MSc, from Leiden University in The Netherlands and colleagues surveyed 106 patients with RA to assess physical activity, motivation and self-efficacy for physical activity, level of arthritis pain, and quality of life. After six months, participants were surveyed again and asked to indicate the extent to which they achieved their baseline physical activity goal. Previous research has shown that self-efficacy, described as one's belief in his or her own capabilities to perform a specific behavior, is associated with increased physical activity participation among RA patients.

Results showed that 75% of participants rated their physical activity goal achievement at 50% or more. Higher levels of self-efficacy for physical activity increased the likelihood that patients would achieve their physical activity goals, and goal achievement had a direct positive effect upon quality of life outcomes. Researchers found that patients who achieved their physical activity goal reported less arthritis pain and greater quality of life. No differences were found between men and women who completed the surveys, or between patients newly diagnosed versus those with RA for 10 years or more.

Knittle concluded, "Our results suggest that an increased focus on self-efficacy enhancement, realistic goal-setting, and techniques that increase the likelihood of goal achievement will assist clinicians and researchers develop interventions that have a positive impact on pain reduction and quality of life outcomes for RA patients."

  • Additional
  • References
  • Citations

A gene responsible for regulating chronic pain, called HCN2, has been identified by scientists at the University of Cambridge.

The Biotechnology and Biological Sciences Research Council (BBSRC) and EU funded research, published today (09 September) in the journal Science, opens up the possibility of targeting drugs to block the protein produced by the gene in order to combat chronic pain.

Approximately one person in seven in the UK suffers from chronic, or long-lasting, pain of some kind, the commonest being arthritis, back pain and headaches. Chronic pain comes in two main varieties. The first, inflammatory pain, occurs when a persistent injury (e.g. a burn or arthritis) results in an enhanced sensitivity of pain-sensitive nerve endings, thus increasing the sensation of pain.

More intractable is a second variety of chronic pain, neuropathic pain, in which nerve damage causes on-going pain and a hypersensitivity to stimuli. Neuropathic pain, which is often lifelong, is a surprisingly common condition and is poorly treated by current drugs. Neuropathic pain is seen in patients with diabetes (affecting 3.7m patients in Europe, USA and Japan) and as a painful after-effect of shingles, as well as often being a consequence of cancer chemotherapy. Neuropathic pain is also a common component of lower back pain and other chronic painful conditions.

Professor Peter McNaughton, lead author of the study and Head of the Department of Pharmacology at the University of Cambridge, said: "Individuals suffering from neuropathic pain often have little or no respite because of the lack of effective medications. Our research lays the groundwork for the development of new drugs to treat chronic pain by blocking HCN2."

The HCN2 gene, which is expressed in pain-sensitive nerve endings, has been known for several years, but its role in regulating pain was not understood. Because a related gene, HCN4, plays a critical role in controlling the frequency of electrical activity in the heart, the scientists suspected that HCN2 might in a similar way regulate the frequency of electrical activity in pain-sensitive nerves.

For the study, the researchers engineered the removal of the HCN2 gene from pain-sensitive nerves. They then carried out studies using electrical stimuli on these nerves in cell cultures to determine how their properties were altered by the removal of HCN2.

Following promising results from the in vitro studies in cell cultures, the researchers studied genetically modified mice in which the HCN2 gene had been deleted. By measuring the speed the mice withdrew from different types of painful stimuli, the scientists were able to determine that deleting the HCN2 gene abolished neuropathic pain. Interestingly, they found that deleting HCN2 does not affect normal acute pain (the type of pain produced by a sudden injury - such as biting one's tongue).

Professor McNaughton added: "Many genes play a critical role in pain sensation, but in most cases interfering with them simply abolishes all pain, or even all sensation. What is exciting about the work on the HCN2 gene is that removing it - or blocking it pharmacologically- eliminates neuropathic pain without affecting normal acute pain. This finding could be very valuable clinically because normal pain sensation is essential for avoiding accidental damage."

  • Additional
  • References
  • Citations