A Great Example of the Latest Gobbledegook from Current Medical Science

Warning : If you attempt to understand this, you may damage brain cells. TT.

http://www.eurekalert.org/pub_releases/2016-06/uoc--dcd060716.php (Disjointed: Cell differences may explain why rheumatoid arthritis varies by location)

Disjointed: Cell differences may explain why rheumatoid arthritis varies by location
Findings point to new approaches in targeted therapies so that what works for arthritic hands may not be the same for ailing hips

UNIVERSITY OF CALIFORNIA - SAN DIEGO

Researchers at the University of California San Diego School of Medicine, with colleagues in Pennsylvania and China, report that not only are there distinct differences in key cellular processes and molecular signatures between rheumatoid arthritis (RA) and osteoarthritis (OA) but, more surprisingly, there are joint-specific differences in RA. The findings help explain, in part, why drugs treating RA vary in effect -- why, for example, a treatment that might work in arthritic knees isn't effective in an arthritic hip - and provide a potential new template for precisely targeting treatment for each and every ailing joint.

The results are published in the June 10 online issue of Nature Communications and represent a collaborative project that combined the power of computational science with modern biology and a deep understanding of the causes of arthritis.

At least 50 million adults and 300,000 children in the United States have some type of arthritis, which includes more than 100 different diseases, according to the Centers for Disease Control. Osteoarthritis is the most common type and involves damage to and ultimately the loss of cartilage -- the cushion inside joints that permits them to move smoothly and painlessly. Rheumatoid arthritis is the most common chronic inflammatory arthritis and also affects joints. It can rapidly damage joints and, in the days before effective therapy, routinely put patients in a wheelchair after a few years.

While OA tends to localize in weight-bearing joints where cartilage is specifically worn away, RA is distributed more symmetrically -- both hands may be affected equally, for example -- and often evolves from the small joints of the hands and wrists to the larger weight-bearing joints. Why some joints are affected early, some late and some not at all has remained unknown.

In their new study, co-corresponding authors Wei Wang, PhD, professor in the departments of Chemistry and Biochemistry and Cellular and Molecular Medicine, and Gary S. Firestein, MD, professor in the Department of Medicine, investigated epigenetic patterns in fibroblast-like synoviocytes (FLS) -- a specialized type of cell that lines the inside of joints.

"We hypothesized that changes in epigenetic modifications and gene expression between FLS in different joints might potentially contribute to differences in synovial inflammation and responses to clinical treatment," said Wang.

The researchers discovered that DNA methylation -- a fundamental, life-long process in which a methyl group is added or removed from the cytosine molecule in DNA to promote or suppress gene activity and expression -- does in fact vary between FLS from the knees and hips of RA patients.

"We showed that the epigenetic marks vary from joint to joint in diseases like rheumatoid arthritis," said Firestein. "Even more importantly, the differences involved key genes and pathways that are designed to be blocked by new RA treatments. This might provide an explanation as to why some joints improve while others do not, even though they are exposed to the same drug."

Firestein, who is also director of the Clinical and Translational Research Institute at UC San Diego, said the work "opens up the potential for precision medicine approaches that allow us to target all of the joints, not just a subset. It has broad implications for how we evaluate new drugs in clinical trials as well."

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Co-authors include: Rizi Ai, Deepa Hammaker, David L. Boyle, and Rachel Morgan, all at UC San Diego; Alice Walsh, Janssen Research & Development, Spring House, PA; and Shicai Fan, University of Electronic Science and Technology of China and UC San Diego.

Funding for this research came, in part, from the Rheumatology Research Foundation, the Arthritis Foundation, the National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01 AR065466) and the National Science Foundation (NSFC61503061).



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slafee@ucsd.edu
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@UCSanDiego

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Hi,Tom. Thanks for sharing the mindboggling article. I'm 86 and not in pain, thanks to TMS healing my severe back pain more than two years ago. My secret in staying healthy all these years is believe in TMS and the MindBody connection.

I think I've stayed healthy all these years because I have had dogs, am on my fourth now after more than 16 years with each, I keep mentally busy, and I laugh as much as I can. I laugh at articles like the one from San Diego and stay away from doctors, professors, and anyone else with initials before or after their name.

 

Then, how come all my pain centers in my left leg (the same one where I shattered my calcaneous back in 1989-90)? Sounds like neurological programming to me that only flares up whenever I'm badly stressed or experiencing a major life stress event like the death of my mother in 2001. If you throw all that genetic determinism gobbledygook out the window, it sure sounds to me like my TMS is caused by emotions, memory and neurological programming. I think Bruce Lipton is absolutely correct when he insists that the "DNA-RNA-Protein" dogma should really be revised to read "DNA-RNA-Environment! Environment! Environment!" And not just physical environment; you have to factor in emotional environment too.

 

It's probably no coincidence that this report originates from UC San Diego, which has about 400 pharmaceutical development companies nearby. Arthritis is a general term for more then 100 different dis-eases, as the article states. The "experts" don't know what causes them, how to cure them or how to treat them. Perhaps some NIH research money should be put towards researching the emotional/mind part of the arthritis equation that Dr. Sarno has theorized in his books and life long clinical practice. 100 different dis-eases, lumped under the umbrella term "arthritis", sounds suspiciously like TMS, with it's myriad of physical symptoms. A recent meta-study from the LANCET, came out stating that the medications that most hip and knee joint pain sufferers have been using for decades, doesn't do much good for those conditions, and that another medication, dicolfenac (Voltaran) is much better. I'm not opposed to meds, but some "scientific" thought and research should go towards the "thinking" part of the pain equation--the mind--where as the Good Doctor has proven, the majority of humanity's pain emanates from.

 

Arthritis, osteoarthritis, etc. is also caused by bad nutrition (too much sugar/glucose/carbs) and toxins everywhere, besides emotional stress.

 

Probably 10% nutrition and 90% stressful emotions.

 

I agree completely, it's our emotions that ultimately define what decisions we make and food we crave.

 

I think the wife of a doctor (double-hearsay evidence of course) once told me that everyone over 35 years of age has osteoarthritis to some degree, no exceptions. However, I would add that it's whether you feel it or not that really matters. And the perception of pain is very subjective and subject to the influence of psychological set, setting and emotions. Interesting in this context how Queen Victoria's arthritis came on right after the death of her husband Prince Albert in 1861. Couldn't attend Parliament to officiate at the opening, but could dance the quadrille in private back at Windsor. Went away almost completely when Benjamin Disraeli had her crowned Empress of India. Out and about in public again. I'd say Victoria's extreme depression after the death of her beloved Albert either caused her arthritis or intensified her perception of its pain. You can argue that one for days and weeks.

 

All pain that is NOT structural in nature….is TMS PERIOD.