Sunday, October 4, 2009
Rheumatoid arthritis alternatives
No research has evaluated the effectiveness of DL-phenylalanine, a related supplement, in treating people with RA. D-phenylalanine has been used with mixed results to treat chronic pain, including pain caused by RA. The benefit of using boron to treat people with RA remains unproven. Boron supplementation at 39 mg per day may be beneficial, particularly in treating people with juvenile RA, according to very preliminary research. Nonetheless, some doctors suggest a trial of 13 mg of copper per day for at least several months. Moreover, the form of copper most consistently reported to be effective, copper aspirinate , is not readily available. Under certain circumstances, however, copper can increase inflammation in rheumatoid joints. The Journal of the American Medical Association quoted one researcher as saying that while Regular aspirin had 6% the anti-inflammatory activity of. Copper acts as an anti-inflammatory agent needed to activate superoxide dismutase , an enzyme that protects joints from inflammation.
Saturday, October 3, 2009
Rheumatoid arthritis and boswellia
Some doctors suggest using 400-800 mg of gum resin extract in capsules or tablets three times per day. Such use of NSAIDs can confound experimental results, because boswellia and NSAIDs work in a similar fashion to reduce inflammation. In some trials where boswellia has appeared ineffective, though, patients have been allowed to continue use of nonsteroidal anti-inflammatory drugs. Boswellia has reduced symptoms of RA in most reports. Boswellia is an herb used in Ayurvedic medicine to treat arthritis. Refer to the individual supplement for information about any side effects or interactions.
Friday, October 2, 2009
Manipulation for rheumatoid arthritis
The effect of manipulation on the symptoms or progression of RA has not been investigated. Six minutes of gentle spinal manipulation decreased this tenderness temporarily in the spinal areas but not in areas around the knees or ankles. RA were found to have more tenderness at certain body locations compared to healthy people. The role of manipulation in managing RA has received little study.
Role of PGE2 and EP receptors in the pathogenesis of rheumatoid arthritis and as a novel therapeutic strategy.
Endocrine, metabolic & immune disorders take targets, Vol. 6, No. 4. (December 2006), pp. 383-394.
Recent advancement in discernment the pathogenesis of rheumatoid arthritis (RA) in parallel with elucidation of the useful persona of the prostaglandin receptor subfamily has revealed an important restrictive persona of PGE2, in constituent to its well-known unhealthy persona in the advancement of RA. Characteristic features of RA are synovial proliferation and pannus formation, which termination in the conclusion of cartilage and bone. Pannus paper is mainly imperturbable of macrophages and fibroblast-like synoviocytes. Both T cell-derived IL-17 and macrophage-derived TNF-alpha seem to play a central persona in the advancement of unhealthy cascades in RA. PGE2 is also produced in salutation to unhealthy cytokines, which in turn negatively regulates both IL-17 and TNF-alpha expression and TNF/IL-1-induced activation of fibroblast-like synoviocytes through EP2/EP4 receptors, resulting in the inflection of unhealthy cascades. IL-17- and TNF-activated macrophages differentiate into osteoclasts in the proximity of M-CSF and RANKL spoken by fibroblast-like synoviocytes. PGE2 binding to EP4 stimulates osteoclastogenesis through enhancing RANKL expression. At the same time, PGE2 suppresses osteoclastogenesis by inhibiting M-CSF expression of fibroblast-like synoviocytes as well as both IL-17 and IL-17-induced TNF-alpha expression of macrophages. PGE2-EP4 also activates osteoblastogenesis through crescendo cbfa1 and osterix, digit primary transcription factors required for pearl formation. The gain effect of PGE2 haw direct toward bushel of wearing pearl through the suppression of inflammation and improvement of pearl remodeling. Here, we discuss a diverse action of PGE2/EP receptors and their important restrictive roles in the pathogenesis of RA, which haw advance to a new therapeutic strategy.
J Akaogi, T Nozaki, M Satoh, H Yamada
Recent advancement in discernment the pathogenesis of rheumatoid arthritis (RA) in parallel with elucidation of the useful persona of the prostaglandin receptor subfamily has revealed an important restrictive persona of PGE2, in constituent to its well-known unhealthy persona in the advancement of RA. Characteristic features of RA are synovial proliferation and pannus formation, which termination in the conclusion of cartilage and bone. Pannus paper is mainly imperturbable of macrophages and fibroblast-like synoviocytes. Both T cell-derived IL-17 and macrophage-derived TNF-alpha seem to play a central persona in the advancement of unhealthy cascades in RA. PGE2 is also produced in salutation to unhealthy cytokines, which in turn negatively regulates both IL-17 and TNF-alpha expression and TNF/IL-1-induced activation of fibroblast-like synoviocytes through EP2/EP4 receptors, resulting in the inflection of unhealthy cascades. IL-17- and TNF-activated macrophages differentiate into osteoclasts in the proximity of M-CSF and RANKL spoken by fibroblast-like synoviocytes. PGE2 binding to EP4 stimulates osteoclastogenesis through enhancing RANKL expression. At the same time, PGE2 suppresses osteoclastogenesis by inhibiting M-CSF expression of fibroblast-like synoviocytes as well as both IL-17 and IL-17-induced TNF-alpha expression of macrophages. PGE2-EP4 also activates osteoblastogenesis through crescendo cbfa1 and osterix, digit primary transcription factors required for pearl formation. The gain effect of PGE2 haw direct toward bushel of wearing pearl through the suppression of inflammation and improvement of pearl remodeling. Here, we discuss a diverse action of PGE2/EP receptors and their important restrictive roles in the pathogenesis of RA, which haw advance to a new therapeutic strategy.
J Akaogi, T Nozaki, M Satoh, H Yamada
Thursday, October 1, 2009
Role of PGE2 and EP receptors in the pathogenesis of rheumatoid arthritis and as a novel therapeutic strategy.
Endocrine, metabolic & immune disorders take targets, Vol. 6, No. 4. (December 2006), pp. 383-394.
Recent progress in discernment the pathogenesis of rheumatoid arthritis (RA) in parallel with interpretation of the functional role of the prostaglandin receptor subfamily has revealed an essential regulatory role of PGE2, in addition to its well-known unhealthy role in the progression of RA. Characteristic features of RA are synovial proliferation and pannus formation, which termination in the destruction of cartilage and bone. Pannus paper is mainly composed of macrophages and fibroblast-like synoviocytes. Both T cell-derived IL-17 and macrophage-derived TNF-alpha seem to play a central role in the progression of unhealthy cascades in RA. PGE2 is also produced in response to unhealthy cytokines, which in invoke negatively regulates both IL-17 and TNF-alpha countenance and TNF/IL-1-induced activation of fibroblast-like synoviocytes finished EP2/EP4 receptors, resulting in the inflection of unhealthy cascades. IL-17- and TNF-activated macrophages differentiate into osteoclasts in the presence of M-CSF and RANKL expressed by fibroblast-like synoviocytes. PGE2 binding to EP4 stimulates osteoclastogenesis finished enhancing RANKL expression. At the aforementioned time, PGE2 suppresses osteoclastogenesis by inhibiting M-CSF countenance of fibroblast-like synoviocytes as well as both IL-17 and IL-17-induced TNF-alpha countenance of macrophages. PGE2-EP4 also activates osteoblastogenesis finished crescendo cbfa1 and osterix, digit essential transcription factors required for pearl formation. The net effect of PGE2 haw direct toward bushel of eroding pearl finished the suppression of rousing and enhancement of pearl remodeling. Here, we discuss a diverse state of PGE2/EP receptors and their essential regulatory roles in the pathogenesis of RA, which haw advance to a novel therapeutic strategy.
J Akaogi, T Nozaki, M Satoh, H Yamada
Recent progress in discernment the pathogenesis of rheumatoid arthritis (RA) in parallel with interpretation of the functional role of the prostaglandin receptor subfamily has revealed an essential regulatory role of PGE2, in addition to its well-known unhealthy role in the progression of RA. Characteristic features of RA are synovial proliferation and pannus formation, which termination in the destruction of cartilage and bone. Pannus paper is mainly composed of macrophages and fibroblast-like synoviocytes. Both T cell-derived IL-17 and macrophage-derived TNF-alpha seem to play a central role in the progression of unhealthy cascades in RA. PGE2 is also produced in response to unhealthy cytokines, which in invoke negatively regulates both IL-17 and TNF-alpha countenance and TNF/IL-1-induced activation of fibroblast-like synoviocytes finished EP2/EP4 receptors, resulting in the inflection of unhealthy cascades. IL-17- and TNF-activated macrophages differentiate into osteoclasts in the presence of M-CSF and RANKL expressed by fibroblast-like synoviocytes. PGE2 binding to EP4 stimulates osteoclastogenesis finished enhancing RANKL expression. At the aforementioned time, PGE2 suppresses osteoclastogenesis by inhibiting M-CSF countenance of fibroblast-like synoviocytes as well as both IL-17 and IL-17-induced TNF-alpha countenance of macrophages. PGE2-EP4 also activates osteoblastogenesis finished crescendo cbfa1 and osterix, digit essential transcription factors required for pearl formation. The net effect of PGE2 haw direct toward bushel of eroding pearl finished the suppression of rousing and enhancement of pearl remodeling. Here, we discuss a diverse state of PGE2/EP receptors and their essential regulatory roles in the pathogenesis of RA, which haw advance to a novel therapeutic strategy.
J Akaogi, T Nozaki, M Satoh, H Yamada
Monday, September 28, 2009
Rheumatoid Arthritis Info
Rheumatoid arthritis affects multiple systems, is chronic, relapsing, inflammatory and is not known what causes it. Its basically flare ups of the synovial capsule around joints. (the thing that holds the joints together) But what those flare ups do is they cause destruction of the affected joints. It is just so unpredictable because some people have mild flare ups and minimal impairment of joint functioning. While others may get totally crippled. The estimates are that 1% of the world's population are afflicted with it. And females about three times more than males. It (RA) usually affects people more in the 30-40 year age range.
Nothing is proven but RA is thought to be an autoimmune problem where antibodies (things that usually attack and kill bad stuff in our body) attack our collagen and cytoskeletal fialmentous proteins.
Nothing is proven but RA is thought to be an autoimmune problem where antibodies (things that usually attack and kill bad stuff in our body) attack our collagen and cytoskeletal fialmentous proteins.
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