Vanwa71

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Hello, Vanwa71, and welcome to Wikipedia! Thank you for your contributions. I hope you like the place and decide to stay. Here are some pages that you might find helpful:

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Your recent edits

Hello. In case you didn't know, when you add content to talk pages and Wikipedia pages that have open discussion, you must sign your posts by typing four tildes ( ~~~~ ) at the end of your comment. You may also click on the signature button located above the edit window. This will automatically insert a signature with your username or IP address and the time you posted the comment. This information is useful because other editors will be able to tell who said what, and when. Thank you. --SineBot (talk) 02:14, 14 January 2011 (UTC)

A Thank You

		The Barnstar of Good Humor
		Whether or not this passes FPC, I just wanted to thank you for your determination with the Barnstar of Good Humor. The folks at FPC can be rather demanding at times, but it's their job! Please feel welcome to contribute further excellent images to this encyclopedia. NauticaShades 17:23, 15 January 2011 (UTC)

		The Resilient Barnstar
		I'm glad that you managed to convert your gastric acid secretion diagram into a wonderful SVG. Good job! I look forward to seeing more quality work from you in the future! I wish my profs made awesome graphics like you. Purpy Pupple (talk) 23:30, 15 January 2011 (UTC)

Regulation of Gastric Acid Secretion

Pharmacological Regulation

There are several neuronal, endocrine, and paracrine determinants of gastric acid secretion. Parietal cells in the fundus and body of the stomach are responsible for secretion of acid into the stomach. Major receptors on parietal cells that trigger acid release when activated include the M3 muscarinic, the H2 histaminic, and the CCK-B or gastrin receptor. The respective ligands for these receptors are acetylcholine, histamine, and gastrin. Acetylcholine is released from enteric neurons, histamine is released from enterochromaffin-like cells, and gastrin is released from G cells which are generally found in the antrum, or lower portion, of the stomach. Enterochromaffin-like (ECL) cells are generally found below the epithelial cell layer of the stomach lumen. ECL cells express M3 muscarinic, ST2 somatostatin, and CCK-B gastrin receptors. While M3 and CCK-B receptors trigger histamine release when activated, the ST2 somatostatin receptor inhibits histamine release. Thus, gastrin is pro-acid, and somatostatin is anti-acid secretion. Both somatostatin and gastrin are released primarily from cells in the antrum. G cells secrete gastrin, and D cells secrete somatostatin. D cells have a regulatory role over G cells in that the somatostatin that they release has an inhibitory influence on gastrin secretion from G cells. This serves to reduce futile simultaneous pro-acid and anti-acid signals to the fundus and body of the stomach. A major trigger for gastrin release is the presence of protein in the antrum: this serves to enhance acid secretion, which is necessary for the activity of pepsin, a major digestive enzyme in the stomach which is important for protein breakdown. In addition, D cells are also subject to regulation by gastric luminal contents. In particular, D cells release more somatostatin when the antral pH is low (i.e., when a highly acidic condition exists). This serves as a negative feedback when acid levels are high, as somatostatin will be secreted, enter the gastric bloodstream, and signal to ECL cells to reduce histamine release. Reduced histamine release will, in turn, reduce acid secretion from parietal cells. Finally, our gastric cells would be susceptible to damage from acid and pepsin if they had no protection. Protection of the gastric mucosal cells is in two forms, a physical barrier of viscous mucus, and a chemical defense of bicarbonate, which neutralizes acid. Protective prostaglandins, i.e., PGE2 and PGI2 activate EP3 receptors on non-parietal mucosal cells to enhance mucus and bicarbonate secretion. At the same time, EP3 receptors are activated on parietal cells to inhibit acid secretion. This is primarily a result of EP3's coupling to the G-protein, Gi, which reduces cyclic adenosine monophosphate (cAMP) levels. The proton pump in parietal cells is an exchanger of potassium and protons. Many portions of the physiology of gastric acid secretion are influenced by drugs, especially those used to treat peptic ulcer disease (PUD) and gastroesophageal reflux disease (GERD). The drug classes and sites of action are denoted by numbers. Note: non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and ibuprofen inhibit the production of protective prostaglandins by inhibiting cyclooxygenase 1 (COX1). For this reason, NSAIDs can promote ulcer formation, and their antiplatelet effects also make patients more susceptible to excessive bleeding if a gastric ulcer becomes severe.

September 2023

Please do not add or change content, as you did at Cannabigerol, without citing a reliable source. Please review the guidelines at Wikipedia:Citing sources and take this opportunity to add references to the article. Do not use Youtube as a source, WP:YT. Follow WP:MEDRS for medical content. Zefr (talk) 19:09, 6 September 2023 (UTC)

I added the appropriate reference to back up the statement. Furthermore, I made it clear that the studies were done in rodents, and what will happen in humans is inconclusive. Vanwa71 (talk) 19:19, 6 September 2023 (UTC)

I have a PhD in toxicology and a Pharm.D.. I also teach physiology, pharmacology, toxicology, pharmacokinetics, pharmacogenomics, and am a full professor. Vanwa71 (talk) 19:22, 6 September 2023 (UTC)

Very good for you. Lab animal studies are not reliable sources for medical content in an encyclopedia. Follow MEDRS sources and see WP:MEDASSESS, left pyramid, for where animal studies fall as unreliable, primary evidence. We're here to write for an encyclopedia, not a journal, WP:NOTJOURNAL. Zefr (talk) 19:36, 6 September 2023 (UTC)

I disagree. I clearly stated that it was animal studies, which avoids any confusion from the reader. I specifically saif there is not enough evidence in humans, so how is that not making it clear? Let me ask you this. Why did you not delete the paragraph before mine? That also refers to animal studies. Vanwa71 (talk) 19:47, 6 September 2023 (UTC)

This statement is directly from the MEDRS guidelines: "Any text that relies on primary sources should usually have minimal weight, only describe conclusions made by the source, and describe these findings so clearly that any editor can check the sourcing without the need for specialist knowledge. Primary sources should never be cited in support of a conclusion that is not clearly made by the authors"

I followed that direction by describing that the study was in rodents, and not humans. I have serious concerns about how this truthful information is being filtered out. Vanwa71 (talk) 19:51, 6 September 2023 (UTC)

Please stop. If you continue to add unsourced or poorly sourced content, as you did at Cannabigerol, you may be blocked from editing. Read WP:MEDRS and use sources from that guide. Do not edit war over animal studies, WP:WAR. Zefr (talk) 19:32, 6 September 2023 (UTC)

I followed the guidelines for describing animal studies. I specifically mentioned that it was in animals, and not humans, and that receptor binding studies have not been performed. I adhered to this guideline exactly:

"In vitro studies and animal models serve a central role in research, and are invaluable in determining mechanistic pathways and generating hypotheses. However, in vitro and animal-model findings do not translate consistently into clinical effects in human beings. Where in vitro and animal-model data are cited on Wikipedia, it should be clear to the reader that the data are pre-clinical, and the article text should avoid stating or implying that reported findings hold true in humans. The level of support for a hypothesis should be evident to a reader." Vanwa71 (talk) 20:19, 6 September 2023 (UTC)

You are extrapolating lab research to suggest an effect similar to approved drugs for which there is far greater evidence for mechanisms in humans. This is WP:SYNTH and is especially discouraged for medical content and even moreso for a discussion on safety for which little is known about cannabigerol. See this discussion for the manual of style when writing medical content. The section and Youtube video you added would do little to educate the general reader. Zefr (talk) 20:50, 6 September 2023 (UTC)

Your recent editing history at Cannabigerol shows that you are currently engaged in an edit war; that means that you are repeatedly changing content back to how you think it should be, when you have seen that other editors disagree. To resolve the content dispute, please do not revert or change the edits of others when you are reverted. Instead of reverting, please use the talk page to work toward making a version that represents consensus among editors. The best practice at this stage is to discuss, not edit-war; read about how this is done. If discussions reach an impasse, you can then post a request for help at a relevant noticeboard or seek dispute resolution. In some cases, you may wish to request temporary page protection.

Being involved in an edit war can result in you being blocked from editing—especially if you violate the three-revert rule, which states that an editor must not perform more than three reverts on a single page within a 24-hour period. Undoing another editor's work—whether in whole or in part, whether involving the same or different material each time—counts as a revert. Also keep in mind that while violating the three-revert rule often leads to a block, you can still be blocked for edit warring—even if you do not violate the three-revert rule—should your behavior indicate that you intend to continue reverting repeatedly. Zefr (talk) 20:44, 6 September 2023 (UTC)