Talk:Purinergic signalling

Original research

A recent addition of this particular edit is not found in any of the cited sources. Removed per WP:OR. -A1candidate (talk) 02:01, 7 May 2014 (UTC)

Mainstream scientific view

Needle stimulation by acupuncture releases adenosine

The New England Journal of Medicine

Acupuncture also has effects on local tissues, including mechanical stimulation of connective tissue, release of adenosine at the site of needle stimulation, and increases in local blood flow

Berman, Brian M. (29 July 2010). "Acupuncture for Chronic Low Back Pain". New England Journal of Medicine. 363 (5): 454–461. doi:10.1056/NEJMct0806114. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)

Acupuncture and purinergic signaling

Critical Reviews in Eukaryotic Gene Expression

Although considerable controversy surrounds the legitimacy of acupuncture as a treatment, a growing literature on the physiological effects of acupuncture needling in animals and humans is providing new insights into basic cellular mechanisms including connective tissue mechanotransduction and purinergic signaling.

Langevin, Helene. "Acupuncture, Connective Tissue and Peripheral Sensory Modulation". Critical Reviews in Eukaryotic Gene Expression. doi:10.1615/CritRevEukaryotGeneExpr.2014008284.

Anti-nociceptive effect of acupuncture is mediated by the adenosine A1 receptor

European Journal of Physiology

It was found that insertion and manual rotation of acupuncture needles triggered a general increase in the extracellular concentration of purines, including the transmitter adenosine and ATP metabolites. Anti-nociceptive effect of acupuncture requires A1 receptors, and acupuncture failed to reduce pain in A1 knockout mice.

Yang, Edward S. (26 August 2011). "Ancient Chinese medicine and mechanistic evidence of acupuncture physiology". Pflügers Archiv - European Journal of Physiology. 462 (5): 645–653. doi:10.1007/s00424-011-1017-3. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)

European Journal of Pain

The role of peripheral adenosine systems, and specifically activation of A1Rs on peripheral sensory nerves in inhibiting pain, is now receiving renewed attention. This reflects several developments including: (1) identification of nucleotidases (CD73, PAP) that generate endogenous adenosine from nucleotides in nociceptive circuits (Zylka et al., 2008; Sowa et al., 2010b); (2) implication of peripheral adenosine (and nucleotides) in acupuncture analgesia in mice (Goldman et al., 2010) and in humans (Takano et al., 2012); (3) peripheral administration of PAP into acupoints leads to long-lasting antinociception (several days) that is dependent on A1Rs (Hurt and Zylka, 2012); (4) exercise regimens that produce analgesia in a model of neuropathic pain involve A1Rs (peripheral adenosine levels increase due to increased ATP utilization in muscle) (Martins et al., 2013).

Sawynok, J. "Topical analgesics for neuropathic pain: Preclinical exploration, clinical validation, future development". European Journal of Pain. 18 (4): 465–481. doi:10.1002/j.1532-2149.2013.00400.x.

Anesthesiology (journal)

Manual acupuncture or a local injection of the adenosine A1 receptor agonist 2-chloro-N(6)-cyclopentyladenosine at acupoint ST36 significantly inhibits mechanical allodynia and thermal hyperalgesia in wild-type but not in adenosine A1 receptor knockout mice with inflammatory and neuropathic pain.

Zhang, Ruixin. "Mechanisms of Acupuncture–Electroacupuncture on Persistent Pain". Anesthesiology. 120 (2): 482–503. doi:10.1097/ALN.0000000000000101. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)

Antinociceptive effects of acupuncture require A1R activation

Trends in Molecular Medicine

These antinociceptive effects of acupuncture were entirely dependent on A1R activation, suggesting a link between antinociception and extracellular adenosine. Although not directly tested, this suggests that ectonucleotidases convert nucleotides to adenosine in skeletal muscle. In addition, local injection of an A1R agonist into an acupuncture point had antinociceptive effects in inflammatory and neuropathic pain models, consistent with studies showing that peripheral A1R activation is antinociceptive [4, 74]. Therefore, it might be possible to treat pain in patients by locally injecting adenosine or A1R agonists. Local injections are unlikely to have cardiovascular side effects, which are associated with systemic A1R activation (Box 1) [1].

Zylka, Mark J. "Pain-relieving prospects for adenosine receptors and ectonucleotidases". Trends in Molecular Medicine. 17 (4): 188–196. doi:10.1016/j.molmed.2010.12.006.

Discussion

So, a textbook case of WP:SYN. Alexbrn ^{talk|contribs|COI} 19:59, 7 May 2014 (UTC)

Could you please be more specific about what you think is wrong? -A1candidate (talk) 20:17, 7 May 2014 (UTC)

You're stringing together sources to imply a conclusion that isn't directly stated by any one of them. Alexbrn ^{talk|contribs|COI} 20:23, 7 May 2014 (UTC)

At least two sources have stated that "Anti-nociceptive effect of acupuncture requires A1 receptors" and "Antinociceptive effects of acupuncture require A1R activation". I'm quoting them directly. -A1candidate (talk) 20:29, 7 May 2014 (UTC)

By all means reflect what the sources say (if on topic) but don't bundle multiple sources together to synthesize a conclusion (the three-cites-per-sentence is a big red flag). If purinergic signalling has a role in acupuncture it will be plainly stated in a good source we can use. If it isn't then it's synthesis. Alexbrn ^{talk|contribs|COI} 20:42, 7 May 2014 (UTC)

I hope you've read the sources, because I did not go through all that effort to quote them if they do not directly support a finding. I'm asking you again: Can you be more specific about which "conclusion" you have an issue with? Because I cannot find anything that's not directly supported. -A1candidate (talk) 20:59, 7 May 2014 (UTC)

Taking the last sentence, the source used concludes:

"There is no question that adenosine receptors have been validated in the setting of chronic pain [5], although whether these receptors inhibit spontaneous pain in humans is still an open question (Box 3). The recent findings linking adenosine to the antinociceptive effects of acupuncture in mice suggest that peripheral engagement of A1R could underlie the pain-relieving effects of this procedure in humans. Localized activation of adenosine receptors, either spinally or in peripheral tissues, might be the key to unlocking the therapeutic potential of these receptors. Localized activation could minimize or eliminate cardiovascular side effects when compared to systemic drug delivery while providing non-addictive treatment options for patients with chronic pain." (my bolds)

yet you seem to have swerved past this tentative musing and plucked out something incidental from the article body to weave into the less tentative argument you are advancing (which appears to part of a TCM-boosting POV-push). Putting this in a "therapeutic intervention" section is also rather misleading, since lab work and hypotheses are being discussed, not "therapy" (this also applies to the table of herbs you have constructed later in the section). Alexbrn ^{talk|contribs|COI} 07:18, 8 May 2014 (UTC)

Source is from 2011, acupuncture analgesia in humans was demonstrated in 2012 (see source 4th source). Eliminating cardiovascular side effects has nothing to do with acupuncture analgesia -A1candidate (talk) 10:11, 8 May 2014 (UTC)

Huh? The point is you are citing a source and misrepesenting its conclusion. Raising arguments from other sources as justification for this is part of the synthesis problem we have here. Alexbrn ^{talk|contribs|COI} 10:19, 8 May 2014 (UTC)

I've asked you to state which part of the section you have an issue with, and you still refuse to do so. We can't fix a problem without identifying the problem -A1candidate (talk) 10:24, 8 May 2014 (UTC)

Um, read what I wrote ("Taking the last sentence ..."). We have an incorrect section title that implies this is content about (human) "therapy", and I have specifically singled-out the last sentence of it as being a misrepresentation of its cited source's conclusion. Alexbrn ^{talk|contribs|COI} 10:30, 8 May 2014 (UTC)

A paper's conclusion is a summary of its main points, not a reproduction of the entire paper. The source's conclusion does not contradict what's already stated the body. Acupuncture analgesia via A1 receptor activation was demonstrated in humans in 2012. -A1candidate (talk) 10:44, 8 May 2014 (UTC)

You have summarized it differently than the author, which is a big clue there's a problem. You have cherry-picked a portion of the article in support of your text, and omitted key pertinent information (this is about mice & speculative lab work, not human "therapy"). This is blatant misrepesentation. Alexbrn ^{talk|contribs|COI} 10:49, 8 May 2014 (UTC)

As a compromise, we could add "in humans" after the 1st sentence and "in mice" before the last sentence. But apparently, you choose to continue edit-warring instead. -A1candidate (talk) 10:53, 8 May 2014 (UTC)