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Fonsy74 (talk) 18:16, 12 March 2016 (UTC)[reply]

@JytDog: Hello, I finded this official web who says all of the information about the homotaurine subreceptors

http://naturaldatabase.therapeuticresearch.com/nd/PrintVersion.aspx?id=1251&AspxAutoDetectCookieSupport=1 Can I use it to sourcing my actual article? Fonsy74 (talk) 00:46, 12 March 2016 (UTC)[reply]

@JytDog: Under any circunstance I can use primary sources? ReallY? There are A LOT OF articles in wikipedia that has primary sources ... Can I erase all and explain this in the log?

Thanks so much JytDog. Fonsy74 (talk) 00:50, 12 March 2016 (UTC)[reply]

There is a lot of bad content in Wikipedia. See WP:OTHERSTUFFEXISTS. Here is the deal with primary sources. I avoid them like the plague, as do most of the high quality editors that I respect. There are people who will use primary sources from the biomedical literature and will argue like crazy for them. They are crappy editors. There are arguments you can make to use them. But if you are going to use them, they have to be as a fallback, and you have to be really, really careful with them. Do not treat them like they are True. Do not give a lot of WP:WEIGHT to them and never build a whole article out of them. OK? What you have done below, is crappy editing - you are giving way too much credence to sources that are just unreliable - they may be unreplicable, and that may have been abandoned by the field. This is a bad way to edit. But it is very good that you are not removing the good sources anymore! that is progress. :) I mean that. Jytdog (talk) 00:59, 12 March 2016 (UTC)[reply]
Here is what I think about your draft below - there is this interesting link between homotaurine and Acamprosate, which is an actual drug. I think your use of primary sources in the fourth paragraph, linking homotaurine and Acamprosat by describing the preclinical work (yes using primary sources) is valuable. I think the third paragraph, where you load up a bunch of detail based on primary sources, is bad. The detail is based on primary sources that we shouldn't trust. And we have higher level, less specific content, in that paragraph based on better sources. So I would be OK with this if we killed the stuff in the third paragraph based on primary sources (keeping the content based on secondary sources) but kept the fourth which is all based on primary sources. This is what i mean about being careful, and only using them if there is some good reason. Jytdog (talk) 01:08, 12 March 2016 (UTC)[reply]

I try to put secondary sources to the third paragraph! Thanks :) Fonsy74 (talk) 13:06, 12 March 2016 (UTC)[reply]

Fonzyn74 thank you so much for really trying to work with the policies and guidelines now! So happy!! This is the right direction for sure. You are going a bit too far in what we call original research (abbreviated as WP:OR) with the "bridging language" you are using... I will implement this and tweak that, so you can see how to do it without overstepping WP:OR... but thank you so much. With such a short article we don't need the section headers, btw.. Implemented here. Jytdog (talk) 21:52, 12 March 2016 (UTC)[reply]
Thanks to you Joydog for teaching and for opening my mind, the article looks great. Now I'm going to register with another username to start from scratch, and to contribute in an appropriate manner

I will also write articles on wikipedia Spain. Thanks so much:) Fonsy74 (talk) 20:04, 13 March 2016 (UTC)[reply]

As you will. there is no need to abandon this account though. Everybody starts somewhere! And I am really happy that you find the article to be good enough now. Jytdog (talk) 00:34, 14 March 2016 (UTC)[reply]

HomoTaurine Article

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Homotaurine (3-amino-1-propanesulfonic acid (3-APS) or tramiprosate (INN)) is a synthetic organic compound. It is analogous to taurine, but with an extra carbon in its chain. It has GABAergic activity, apparently by mimicking GABA, which is it resembles;[1]

Clinical Trials

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Homotaurine was investigated in a Phase III clinical trial as a potential treatment for Alzheimer's disease that did not show efficacy in its primary endpoints.[2] In preclinical studies it had been found to bind to soluble amyloid beta and inhibit the formation of neurotoxic aggregates.[2][3] homotaurine has shown anticonvulsant activities, reduction in skeletal muscle tonus, and hypothermic activity too.[4]

Possible Mechanism of Action

[edit]

Homotaurine has been reported as a GABA antagonist[1] as well as a GABA agonist.[5][4]. This conflicting information may be due to some research papers saying that Homotaurine is a GABAA partial agonist [6] and a GABAB receptor partial agonist with low efficacy, becoming an antagonist and displacing full agonist as GABA or baclofen at this receptor[7].

Supporting this, in animals, Homotaurine reversed in rats the catatonia induced by baclofen (The prototypical GABAB agonist) [8] . And was able to produce analgesia via GABAB receptor, effect that was abolished when applied CGP 35348, a GABAB receptor antagonist [9][10] .

Acamprosate

[edit]

Acamprosate, the N-acetyl derivative of homotaurine was approved by the FDA in 2004 to treat alcohol dependence.[1][11]

One study in rats shows Homotaurine suppress ethanol-stimulated dopamine release, ethanol intake and preference in rats similar to acamprosate, howewer the only approvation for this indication is Acamprosate[12][13].

  1. ^ a b c Lednicer D (2008). The Organic Chemistry of Drug Synthesis (7th ed.). Hoboken: John Wiley & Sons. p. 15. ISBN 978-0-470-18066-2.
  2. ^ a b Caltagirone C et al. The potential protective effect of tramiprosate (homotaurine) against Alzheimer's disease: a review. Aging Clin Exp Res. 2012 Dec;24(6):580-7. PMID 22961121
  3. ^ Aisen PS, Gauthier S, Vellas B, Briand R, Saumier D, Laurin J, Garceau D (2007). "Alzhemed: a potential treatment for Alzheimer's disease". Current Alzheimer Research. 4 (4): 473–8. doi:10.2174/156720507781788882. PMID 17908052.
  4. ^ a b Oja SS and Kontro P. Taurine. Chapter 18 in Metabolism in the Nervous System, Ed. Lajtha ANS. Springer Science & Business Media, 2013. ISBN 9781468443677. Page 520
  5. ^ Armen H. Tashjian and Ehrin J. Armstrong. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. Edited by David E. Golan. Lippincott Williams & Wilkins, 2011 ISBN 9781451118056. Page 308
  6. ^ Reyes-Haro D1, Cabrera-Ruíz E, Estrada-Mondragón A, Miledi R, Martínez-Torres A. "Modulation of GABA-A receptors of astrocytes and STC-1 cells by taurine structural analogs". PMID 25119985. {{cite journal}}: Cite journal requires |journal= (help)CS1 maint: multiple names: authors list (link) CS1 maint: numeric names: authors list (link)
  7. ^ Giotti A, Luzzi S, Spagnesi S, Zilletti L. "Homotaurine: a GABAB antagonist in guinea-pig ileum". PMID 6652358. {{cite journal}}: Cite journal requires |journal= (help)CS1 maint: multiple names: authors list (link)
  8. ^ Mehta AK1, Ticku MK. "Baclofen induces catatonia in rats". PMID 2823166. {{cite journal}}: Cite journal requires |journal= (help)CS1 maint: numeric names: authors list (link)
  9. ^ Serrano MI1, Serrano JS, Fernández A, Asadi I, Serrano-Martino MC. "GABA(B) receptors and opioid mechanisms involved in homotaurine-induced analgesia". PMID 9510095. {{cite journal}}: Cite journal requires |journal= (help)CS1 maint: multiple names: authors list (link) CS1 maint: numeric names: authors list (link)
  10. ^ Serrano MI1, Serrano JS, Asadi I, Fernández A, Serrano-Martino MC. "Role of K+ -channels in homotaurine-induced analgesia". PMID 11468027. {{cite journal}}: Cite journal requires |journal= (help)CS1 maint: multiple names: authors list (link) CS1 maint: numeric names: authors list (link)
  11. ^ Reyes-Haro D, Cabrera-Ruíz E, Estrada-Mondragón A, Miledi R, Martínez-Torres A (Nov 2014). "Receptors of astrocytes and STC-1 cells by taurine structural analogs". Amino Acids. 46 (11): 2587–93. doi:10.1007/s00726-014-1813-0. PMID 25119985.
  12. ^ Olive MF, Nannini MA, Ou CJ, Koenig HN, Hodge CW. "Effects of acute acamprosate and homotaurine on ethanol intake and ethanol-stimulated mesolimbic dopamine release". PMID 11864639. {{cite journal}}: Cite journal requires |journal= (help)CS1 maint: multiple names: authors list (link)
  13. ^ Berton F, et al. Alcohol Clin Exp Res. 1998. . "Acamprosate reduces ethanol drinking behaviors and alters the metabolite profile in mice lacking ENT1". PMID 21172405. {{cite journal}}: Cite journal requires |journal= (help); line feed character in |author= at position 45 (help)CS1 maint: numeric names: authors list (link)
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