Talk:Senescence: Difference between revisions
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|title = Progeria: Senescence, dyskeratosis congenita, Jonathan Hutchinson, scleroderma |
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== |
== Aging can't be beaten? == |
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If I've read the links correctly on my personal discussion page, things have to be sourced and neutral. |
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To quote: "The above categorisation of theories of aging is generally considered obsolete by [[biogerontology|biogerontologists]].{{fact|date=January 2008}}" |
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End quote. |
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If the statement is included, it looks like it would need multiple reliable citations. Otherwise, it is opinion, stated as fact. I looked for a reference, but could not find one. If you reinsert it, can you add the sources? [[User:WordMachine|WordMachine]] ([[User talk:WordMachine|talk]]) 13:10, 23 January 2008 (UTC) |
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:I'll look for a source. In the meantime, you might want to reconsider trying to link the two paragraphs together with a simple "conversely," since its meaning is not very clear at all. Information does have to be sourced on Wikipedia, but I notice that the programmed and stochastic theories of aging are presented without any source whatsoever to indicate that they have scientific merit, or even that they were considered to have had scientific merit in the past. I'll try to get an expert opinion on this. --[[User:SierraSciSPA|SierraSciSPA]] ([[User talk:SierraSciSPA|talk]]) 18:18, 23 January 2008 (UTC) |
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While we're on the topic of sources, we're all aware Aubrey de Grey and the SENS Foundation have basically been denounced to pseudo-science, right? They're being cited here, and I don't know much about citation rules, but that seems like it would be a problem... Those are more like movements with transhumanism and such than legitimate sciences, at least according to the Technology Review and a few other respected scientist who made the point. [[Special:Contributions/76.78.30.85|76.78.30.85]] ([[User talk:76.78.30.85|talk]]) 06:34, 10 October 2014 (UTC) |
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== To-do list: “Add a proper lead section” == |
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{{tick}} I should like to think I have fulfilled the requirement. I will now cross the item off the list. [[User:Everything Is Numbers|Everything Is Numbers]] ([[User talk:Everything Is Numbers|talk]]) 11:05, 28 September 2012 (UTC) |
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== Expansion, structure reform == |
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I'm considering adopting the following as the base arrangement: |
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:1. Cellular senescence |
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:2. Organismal senescence |
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:3. Effects |
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:4. Hypotheses |
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:5. Treatment |
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:6. Differences between taxa |
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:7. Evolution |
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:8. Accelerated aging-disorders |
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:9. Cloning |
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[[User:Everything Is Numbers|Everything Is Numbers]] ([[User talk:Everything Is Numbers|talk]]) 11:33, 28 September 2012 (UTC) |
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== Senescence / Senesce == |
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Can anyone explain the difference between Senescence & Senesce. Is senesce an actual word. It is mentioned once in the article and can be found else where on the net. Are they used interchangeably? [[User:Ctbolt|Ctbolt]] ([[User talk:Ctbolt|talk]]) 04:49, 9 August 2013 (UTC) |
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== Protein Misfolding Theory of Aging == |
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I would like to add the following section to this page. As a biochemistry professor who has studied human aging for 35 years, I am currently beginning a clinical trial on this cause of aging. I have previously worked on slowing the other processes, and think this practical information is likely to greatly reduce human suffering by reducing the development of chronic disease. OR ELSe it could be entered as a separate new article, just linked on the senescence page as 3.7 [[User:Rocordman|Rocordman]] ([[User talk:Rocordman|talk]]) 20:36, 23 November 2014 (UTC) |
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Contents [hide] |
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3.7 Protein Misfolding or Translational Error Theory of Aging |
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3.7.1 The free radical theory of aging |
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3.7.2 Inflammation |
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3.7.3 Telomere shortening |
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3.7.4 Translational infidelity error theory of aging |
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3.7.5 Teaberry Trial |
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References |
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Protein Misfolding or Translational Error Theory of Aging[edit] |
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The Translational Error Theory of human aging –“Lost in Translation” |
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There are many theories about why humans age, what causes chronic diseases to develop, and why we eventually die. Below four are highlighted which one can clearly do something about. Understanding the rationale and evidence for each of these theories provides guidance on actions one can take that help increase healthspan. Healthspan is the term used to distinguish lifespan or years of being alive, from years of aging in a pleasant state of health. Most people want their years to be enjoyable, and not a burden for those who care about them. Below are theories of aging for which specific actions can be taken easily. |
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The free radical theory of aging[edit] |
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This theory is well documented. To lessen free radical damage, I consume vitamin C 500 mg twice a day, vitamin E 400IU twice a week, and eat a diet of colorful fruits and vegetables that contain a variety of antioxidants. |
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Inflammation[edit] |
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Also called “Inflammaging” by researchers, this is a cause of chronic disease, including plaque in the arteries, cancer, etc. To reduce inflammation, I consume fish oil, avoid 4-legged meat, reduce stress by exercising and avoiding the media, by treasuring friends, meditating and doing yoga. |
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Telomere shortening[edit] |
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The length of telomeres, which are caps on the end of the DNA in our cells, preserve our genetic information to allow longevity. Actions that shorten telomeres include stress and high metabolic rate. Consuming antioxidants, staying fit, and relaxing are all useful to keep long telomeres. Note that EGCG and quercetin help maintain telomere length [1]. |
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Translational infidelity error theory of aging[edit] |
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The basic mechanism is that mRNA is translated incorrectly, incorporating the wrong amino acids into proteins that then fold improperly (based on the AA error theory of Wolfgang Freist). These proteins are either destroyed, causing a shortage of needed proteins, or worse, remain malfunctioning and accumulating as hazardous waste such as plaque in Alzheimer’s. Processes that will lessen functional proteins being lost in translation include: 1) increasing the availability of needed amino acids, 2) slowing the rate of translation to increase accuracy, 3) providing time for better proofreading, 4) increasing degradation of misfolded proteins, or 5) diluting the accumulated damage by half through cell division. Helpful actions include getting exercise, eating blueberries, drinking green tea, and adjusting the diet to include beneficial foods, such as tomatoes, onions, strawberries, and cabbage. Protein misfolding and translation errors have been documented as a cause of human aging [2]. |
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There's a study from Paul Nelson, professor of ecology and evolutionary biology and at the University of Arizona, and Joanna Masel, a postdoc researcher from the same university, stating that mathematically, it is impossible to beat aging, and their study is titled as "Intercellular competition and the inevitability of multicellular aging" |
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One hypothesis of a major cause of aging is errors in translation. One source of such errors is caused by incorrect binding of amino acids of similar structure to tRNA that are then misincorporated into proteins, which subsequently do not function properly. Another possibility is when translation occurs so rapidly that proteins are not properly proofread or do not fold into the proper three dimensional structure. |
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http://www.pnas.org/content/114/49/12982 |
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The first place errors can occur is when the amino acid (AA) is bound to the transfer RNA. Briefly, deficiency of three AAs (PHE, SER, and GLN) (PSG) and excess of 2 AAs (CYS and MET) (CM) increase the occurrence of errors, so correct protein sequences are lost in translation. For human evidence, a metabolomics study was done of 100 yr old Italians. They had high levels of PSG in their blood, which may have reflected that they ate foods containing high levels of PSG. |
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Should we add this to the article?--[[User:K1234567890y|EPN-001GF IZEN]] [[User_talk:K1234567890y|བཀྲ་ཤིས་བདེ་ལེགས།]] 08:52, 27 January 2018 (UTC) |
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One can search for foods that are particularly rich in PSG, and have less CM. A group of Italians living past 100 were probably eating a Mediterranean diet, which is known to be far superior to the Western diet, and also is high in PSG and low in CM |
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:Done. Although I am the professor and he is the postdoc :-) [[User:Joannamasel|Joannamasel]] ([[User talk:Joannamasel|talk]]) 21:24, 3 September 2018 (UTC) |
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This paragraph explains why those 5 AAs are so important. For instance, phenylalanine (PHE), an essential aromatic AA, is similar in structure to tyrosine and tryptophan, and when the PHE-tRNA should bind PHE, the wrong AA might be incorporated. So by ensuring there is enough PHE available, this mistake is less likely to occur. The Italian centenarian results suggest this type of error is especially likely for three AAs, PSG, so eating a diet with foods containing more of these is likely to reduce such errors. CYS and MET are 2 AAs that contain highly reactive –SH groups that are likely to crosslink and be oxidized by free radicals. –SH is also likely to bind Al, Cu, and Fe. Those metal atoms generate lots of free radicals, and are suspected to contribute to Alzheimer’s and Parkinson’s diseases. |
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== Hatnote == |
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The second likely source of protein errors is when protein synthesis is too rapid. There are proofreading mechanisms that will catch mistakes as the protein is being synthesized, if translation is going slowly enough. One way to slow the process is by exercising. This depletes the supply of ATP, which is necessary to synthesize proteins. After exercise, your proteins are more likely to be synthesized slowly, allowing proper proofreading so mistakes can be corrected. Another molecule that slows translation is EGCG EGCG inhibits protein synthesis, lipogenesis, and cell cycle progression through activation of AMPK in p53 positive and negative human hepatoma cells [3]. Green tea has much higher levels of EGCG than black tea or other foods. The abundant polyphenols from blueberries such as quercetin help prevent the degradation of EGCG. So eating blueberries, and drinking a single cup of green tea will raise EGCG levels 4 to 8 fold [4]. The EGCG inhibits myosin motors running the cell, slowing key processes that might otherwisse cut short effective proofreading. This may be a key reason that green tea is well known to increase longevity. Healthspan has been shown to increase regularly up to 5 cups of green tea daily [5]. Combined with eating blueberries, only one or two cups of green tea may be needed. |
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Currently the hatnote reads, ''This article is about the aging of whole organisms including animals. For the state of cellular growth arrest and aberrant secretory phenotype, see cellular senescence. For aging specifically in humans, see aging. For the study of aging in humans, see gerontology. For the science of the care of the elderly, see geriatrics. For experimental gerontology, see life extension. For the stress- and age-related developmental aging phenomena in plants, see plant senescence. For premature aging disorders, see Progeroid syndromes.'' This seems excessive and contrary to guidelines. [[MOS:HATNOTE]] says hatnotes are "short notes" and "limit hatnotes to just one at the top of the page". This one is eight sentences disambiguating many different topics. Any suggestions for simplifying this? Are the linked topics suitable for a single disambiguation page? [[User:Deli nk|Deli nk]] ([[User talk:Deli nk|talk]]) 19:05, 15 May 2018 (UTC) |
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Finally, after the protein is made, there may be further checkpoints. Chaperone proteins exist in our bodies to ensure that proteins fold into the proper shape. If they do not fold properly, usually they are degraded by a structure known as the proteasome. However, some mistakes escape this process, especially ones that act as prions. After bacteria and then viruses were discovered, the next disease-causing contagious particles to be discovered were infectious proteins, known as prions. These proteins are improperly folded, and they cause other proteins to misfold as well. An example is the degenerative brain disease scrapie. There is concern that eating brain material from animals that had this disease will cause the disease in other animals, and probably even humans. It is possible Alzheimer’s is a disease of this nature, where plaque in the brain may be caused by beta-amyloid, a misfolded protein that coagulates and then cannot be degraded by proteasomes. |
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:{{reply to|Deli nk}} I agree: the hatnote is unnecessarily long and unduly separates the reader from content. Most of the hatnote references are really more suitable for the See also section, so I have added them there (if they weren't there already). [[Cellular senescence]] is mentioned early in the lead, is in the title of 2 section headings, and has a hatnote already at a section. I have retained 2 redirects so the hatnote now reads "This article is about the aging of whole organisms including animals. For aging specifically in humans, see [[Aging]]. For aging specifically in plants, see [[Plant senescence]].". [[User:Shhhnotsoloud|Shhhnotsoloud]] ([[User talk:Shhhnotsoloud|talk]]) 13:56, 17 August 2018 (UTC) |
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Roc Ordman has developed a nutritional supplement, Mito-C, containing 11 ingredients specifically selected to reduce the rate of protein misfolding. He recently submitted a scientific article to the Journal of Nutrition and Supplements describing how the ingredients work. Among them are EGCG from green tea and quercetin from blueberries which slow the rate of mRNA translation. Also included are two amino acids which are deficient in most people's diets, causing improper amino acids to be substituted during translation. Read the paper at the link at TriumphHealthCorp.com. Email roc@ordman.net for further information. [[User:Rocordman|Rocordman]] ([[User talk:Rocordman|talk]]) 17:16, 27 September 2019 (UTC) |
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Once we are adults, cell division is rare, so misfolded proteins that are not degraded will accumulate. It is likely this is especially damaging for proteins that adhere to chromosomal DNA causing errors in gene expression that can cause cancer. Those proteins on chromosomes are often not repaired. However, during mitosis the cell divides so faulty proteins are diluted from one cell to two. So newly divided cells, including stem cells, stay much healthier than “senescent” cells that no longer divide. |
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== Gingko == |
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Dr. Martin is arranging internet-based studies that can be completed at home to determine whether food choices, including consumption of blueberries and green tea, may be able to partially reverse damage caused by the accumulation of misfolded proteins and deficiency of proper folding. Senescent cells with adequate levels of polyphenols and EGCG may continue to degrade misfolded proteins and produce functional ones, and such recovery may be measurable by tests of abilities like memory that can be conducted online. To receive email notices when such trials have been authorized, please email Roc Ordman at ordman@beloit.edu, SUBJ: Healthspan trial. |
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[[User:Zefr]] placed a sentence on gingko that I edited to blend into the rest of the section, and then has repeatedly reverted my edits and restored that sentence without doing anything to improve it in response to in-line comments. I am moving the dispute here to talk. |
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Here is an index of healthspan activities[6]. |
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The section is on variation in senescence among species. The sentence talks about senescence being slow (but positive) in ginkgo. The sentence placement was right after to a sentence on negative senescence, suggesting a link but not providing the evidence that senescence is negative. It contained non-notable information eg year of publication and place that gingkos grow, that is disproportionate with treatment of other species - this in a vital article that has repeatedly suffered from bloat. I have moved the reference and the ginkgo example to the sentence that contains other species with positive senescence, creating a direct comparison between mice, men, and gingkos, with the most words given to the last of these. |
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Teaberry Trial[edit] |
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The Teaberry Trial is a clinical trial to develop a nutraceutical method to reduce the risk for what may be a major cause of human aging, or senecense, and the development of chronic disease. For other efforts, see Strategies for Engineered Negligible Senescence. The trial has been approved by the Beloit College IRB, is being managed by Roc Ordman, and analyzed by Rolf Martin. Professor Ordman, nicknamed Nutrition Investigator , is interested in extending human healthspan. The goal of Nutrition Investigator is to help people achieve the maximum healthspan based on current nutrition research. Here is current information to extend healthspan with convenient actions. The first key to the Teaberry Trial is the health benefits of blueberries. This is based on results of a clinical trial since 2002. The benefits found from this trial for which Rolf Martin has been responsible for analysis, has resulted in the popularity of blueberries. The emails which indicate and reference the potential benefits of consuming blueberries and green tea appropriately are shown [1]. Our new trial extends the benefits of the polyphenols in blueberries by combining their action with the active ingredient in green tea, EGCG. |
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In the last edit, details on mechanism were given. They do not belong in this section unless they are rewritten to relate to variation among species, not just to ginkgo. |
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If you are interested in further information about the trial, here is the announcement that has been authorized: |
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[[User:Joannamasel|Joannamasel]] ([[User talk:Joannamasel|talk]]) 22:03, 21 January 2020 (UTC) |
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:The sentence and source had been edited substantially [https://en.wikipedia.org/enwiki/w/index.php?title=Senescence&diff=936781330&oldid=936618138 here.] I can see the reasoning for moving addition to the paragraph on the speed of aging, but am adding back information on why this occurs from a strong source: gene expression associated with adaptable defense mechanisms that would be unique to local environmental conditions, such as climate, erosion, pests, etc., so the location is notable. Further punctuation edit for the negligent editor who chooses to ignore a simple WP style rule, [[WP:REFPUNCT]]. --[[User:Zefr|Zefr]] ([[User talk:Zefr|talk]]) 18:20, 23 January 2020 (UTC) |
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::Thank you for fixing the punctuation. As for the other sentence, it does not pertain to the topic of variation among species, because it does not involve comparisons among species. I am moving the sentence to the more appropriate and specialized page [[negligible senescence]], where it is a better fit.[[User:Joannamasel|Joannamasel]] ([[User talk:Joannamasel|talk]]) 20:37, 23 January 2020 (UTC) |
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== Please update with: "Clonal dynamics of haematopoiesis across the human lifespan" & missing and/or recent findings about aging == |
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Drs. Rolf Martin and Alfred “Roc” Ordman plan to conduct a clinical trial to determine whether consuming blueberries and/or green tea on a daily basis may affect cognitive functions of decision making, memory, and hearing. This is the first part of our investigation of a new theory of why people develop chronic diseases associated with aging. If you are interested in further information about the study, please email teaberrystudy@gmail.com, SUBJ: clinical trial. |
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I think it would be good to also list or mention or maybe briefly inform about the conclusions/findings from this study. It's currently included in [[2022 in science]] like so: |
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References[edit] |
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Jump up ^ Nutr Cancer. 2012;64(4):580-7. doi: 10.1080/01635581.2012.661514. Epub 2012 Mar 27. Quercetin increased the antiproliferative activity of green tea polyphenol (-)-epigallocatechin gallate in prostate cancer cells. Wang P1, Heber D, Henning SM |
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Jump up ^ Ribosome rescue and neurodegeneration Jennifer C. Darnell Science 25 July 2014: 378-379 |
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Jump up ^ Huang C et al, Molecular Nutrition & Food Research Volume 53, Issue 9, pages 1156–1165, September 2009 |
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Jump up ^ Nutr Cancer. 2012;64(4):580-7. doi: 10.1080/01635581.2012.661514. Epub 2012 Mar 27. Quercetin increased the antiproliferative activity of green tea polyphenol (-)-epigallocatechin gallate in prostate cancer cells. Wang P1, Heber D, Henning SM |
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Jump up ^ Green Tea Consumption and Mortality Due to Cardiovascular Disease, Cancer, and All Causes in Japan, The Ohsaki Study, S. Kuriyama et al, JAMA. 2006;296(10):1255-1265 |
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Jump up ^ http://chemistry.beloit.edu/Ordman/nutrition/indices/ihealthspan.htm |
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<blockquote>A study shows the clonal diversity of [[stem cell]]s that [[haematopoiesis|produce blood cells]] gets drastically reduced around age 70 {{tooltip|2=from 20,000–200,000 HSC/MPPs contributing evenly to 10–20 expanded clones accounting for 30–60% of haematopoiesis due to mutations that occurred decades earlier that make them grow faster|to a faster-growing few}}, substantiating [[Stem cell theory of aging#Hematopoietic stem cell diversity aging|a novel]] [[Senescence|theory of ageing]] which could enable [[life extension|healthy aging]].<ref>{{cite news |title=Research may reveal why people can suddenly become frail in their 70s |url=https://www.theguardian.com/science/2022/jun/01/research-may-reveal-why-people-can-suddenly-become-frail-in-their-70s |access-date=18 July 2022 |work=The Guardian |date=1 June 2022 |language=en}}</ref><ref>{{cite journal |last1=Mitchell |first1=Emily |last2=Spencer Chapman |first2=Michael |last3=Williams |first3=Nicholas |last4=Dawson |first4=Kevin J. |last5=Mende |first5=Nicole |last6=Calderbank |first6=Emily F. |last7=Jung |first7=Hyunchul |last8=Mitchell |first8=Thomas |last9=Coorens |first9=Tim H. H. |last10=Spencer |first10=David H. |last11=Machado |first11=Heather |last12=Lee-Six |first12=Henry |last13=Davies |first13=Megan |last14=Hayler |first14=Daniel |last15=Fabre |first15=Margarete A. |last16=Mahbubani |first16=Krishnaa |last17=Abascal |first17=Federico |last18=Cagan |first18=Alex |last19=Vassiliou |first19=George S. |last20=Baxter |first20=Joanna |last21=Martincorena |first21=Inigo |last22=Stratton |first22=Michael R. |last23=Kent |first23=David G. |last24=Chatterjee |first24=Krishna |last25=Parsy |first25=Kourosh Saeb |last26=Green |first26=Anthony R. |last27=Nangalia |first27=Jyoti |last28=Laurenti |first28=Elisa |last29=Campbell |first29=Peter J. |title=Clonal dynamics of haematopoiesis across the human lifespan |journal=Nature |date=June 2022 |volume=606 |issue=7913 |pages=343–350 |doi=10.1038/s41586-022-04786-y |pmid=35650442 |pmc=9177428 |language=en |issn=1476-4687}}</ref></blockquote> |
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[[User:Rocordman|Rocordman]] ([[User talk:Rocordman|talk]]) 20:36, 23 November 2014 (UTC) |
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Moreover, it seems like the article needs a lot of updates / improvements beyond that. It seems to focus too much on the initial 2013 [[hallmarks of aging]] without integrating expansions/revisions of/additions to these. This doesn't mean the article should grow much larger or that sections should be long – each section should be as brief as possible and have a fitting headline, various things could be listed via brief bullet-points with further info only at the respective wikilinked article, and so on – the article just shouldn't be very incomplete and outdated. Maybe you can find some relevant info/content at [[Timeline of senescence research]] and recently expanded (imo a v1.0 now) [[Life extension#Strategies]]. |
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:Hi [[User:Rocordman|Rocordman]]! Thanks for your suggestions - it's always great when I see a professor taking the time to edit Wikipedia. This is very interesting, but unfortunately I think a lot of it is probably too detailed for this article. Since Wikipedia's organization is closer to traditional encylopedias than to scientific literature, the idea of an article on a topic as large as senescence is to give the reader a broad overview of the subject and put more specific details in more specific articles. |
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Maybe [[Help:Transclusion|transclusions]] could be used in good ways with articles like [[Ageing]] so that each article is up-to-date, brief, complete and doesn't duplicate content more than needed.<br/> [[User:Prototyperspective|Prototyperspective]] ([[User talk:Prototyperspective|talk]]) 11:44, 3 August 2022 (UTC) |
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:Also, not all of the proposed content is cited. Since the reader won't know who wrote any particular sentence, they need to know how to confirm that it's correct. Ideally the majority of the content should be cited to secondary sources (that is, review papers). |
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{{reflist-talk}} |
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:There are also a couple of other things but those are the most important points I would emphasize. Let me know if I can help. Cheers, '''''[[User:Sunrise|<font color="FF6600"><font face="Times New Roman">Sunrise</font></font>]]''''' ''<font size="1.8">([[User talk:Sunrise|talk]])</font>'' 07:29, 24 November 2014 (UTC) |
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Aging can't be beaten?
[edit]There's a study from Paul Nelson, professor of ecology and evolutionary biology and at the University of Arizona, and Joanna Masel, a postdoc researcher from the same university, stating that mathematically, it is impossible to beat aging, and their study is titled as "Intercellular competition and the inevitability of multicellular aging"
http://www.pnas.org/content/114/49/12982
Should we add this to the article?--EPN-001GF IZEN བཀྲ་ཤིས་བདེ་ལེགས། 08:52, 27 January 2018 (UTC)
- Done. Although I am the professor and he is the postdoc :-) Joannamasel (talk) 21:24, 3 September 2018 (UTC)
Hatnote
[edit]Currently the hatnote reads, This article is about the aging of whole organisms including animals. For the state of cellular growth arrest and aberrant secretory phenotype, see cellular senescence. For aging specifically in humans, see aging. For the study of aging in humans, see gerontology. For the science of the care of the elderly, see geriatrics. For experimental gerontology, see life extension. For the stress- and age-related developmental aging phenomena in plants, see plant senescence. For premature aging disorders, see Progeroid syndromes. This seems excessive and contrary to guidelines. MOS:HATNOTE says hatnotes are "short notes" and "limit hatnotes to just one at the top of the page". This one is eight sentences disambiguating many different topics. Any suggestions for simplifying this? Are the linked topics suitable for a single disambiguation page? Deli nk (talk) 19:05, 15 May 2018 (UTC)
- @Deli nk: I agree: the hatnote is unnecessarily long and unduly separates the reader from content. Most of the hatnote references are really more suitable for the See also section, so I have added them there (if they weren't there already). Cellular senescence is mentioned early in the lead, is in the title of 2 section headings, and has a hatnote already at a section. I have retained 2 redirects so the hatnote now reads "This article is about the aging of whole organisms including animals. For aging specifically in humans, see Aging. For aging specifically in plants, see Plant senescence.". Shhhnotsoloud (talk) 13:56, 17 August 2018 (UTC)
Roc Ordman has developed a nutritional supplement, Mito-C, containing 11 ingredients specifically selected to reduce the rate of protein misfolding. He recently submitted a scientific article to the Journal of Nutrition and Supplements describing how the ingredients work. Among them are EGCG from green tea and quercetin from blueberries which slow the rate of mRNA translation. Also included are two amino acids which are deficient in most people's diets, causing improper amino acids to be substituted during translation. Read the paper at the link at TriumphHealthCorp.com. Email roc@ordman.net for further information. Rocordman (talk) 17:16, 27 September 2019 (UTC)
Gingko
[edit]User:Zefr placed a sentence on gingko that I edited to blend into the rest of the section, and then has repeatedly reverted my edits and restored that sentence without doing anything to improve it in response to in-line comments. I am moving the dispute here to talk.
The section is on variation in senescence among species. The sentence talks about senescence being slow (but positive) in ginkgo. The sentence placement was right after to a sentence on negative senescence, suggesting a link but not providing the evidence that senescence is negative. It contained non-notable information eg year of publication and place that gingkos grow, that is disproportionate with treatment of other species - this in a vital article that has repeatedly suffered from bloat. I have moved the reference and the ginkgo example to the sentence that contains other species with positive senescence, creating a direct comparison between mice, men, and gingkos, with the most words given to the last of these.
In the last edit, details on mechanism were given. They do not belong in this section unless they are rewritten to relate to variation among species, not just to ginkgo. Joannamasel (talk) 22:03, 21 January 2020 (UTC)
- The sentence and source had been edited substantially here. I can see the reasoning for moving addition to the paragraph on the speed of aging, but am adding back information on why this occurs from a strong source: gene expression associated with adaptable defense mechanisms that would be unique to local environmental conditions, such as climate, erosion, pests, etc., so the location is notable. Further punctuation edit for the negligent editor who chooses to ignore a simple WP style rule, WP:REFPUNCT. --Zefr (talk) 18:20, 23 January 2020 (UTC)
- Thank you for fixing the punctuation. As for the other sentence, it does not pertain to the topic of variation among species, because it does not involve comparisons among species. I am moving the sentence to the more appropriate and specialized page negligible senescence, where it is a better fit.Joannamasel (talk) 20:37, 23 January 2020 (UTC)
Please update with: "Clonal dynamics of haematopoiesis across the human lifespan" & missing and/or recent findings about aging
[edit]I think it would be good to also list or mention or maybe briefly inform about the conclusions/findings from this study. It's currently included in 2022 in science like so:
A study shows the clonal diversity of stem cells that produce blood cells gets drastically reduced around age 70 to a faster-growing few, substantiating a novel theory of ageing which could enable healthy aging.[1][2]
Moreover, it seems like the article needs a lot of updates / improvements beyond that. It seems to focus too much on the initial 2013 hallmarks of aging without integrating expansions/revisions of/additions to these. This doesn't mean the article should grow much larger or that sections should be long – each section should be as brief as possible and have a fitting headline, various things could be listed via brief bullet-points with further info only at the respective wikilinked article, and so on – the article just shouldn't be very incomplete and outdated. Maybe you can find some relevant info/content at Timeline of senescence research and recently expanded (imo a v1.0 now) Life extension#Strategies.
Maybe transclusions could be used in good ways with articles like Ageing so that each article is up-to-date, brief, complete and doesn't duplicate content more than needed.
Prototyperspective (talk) 11:44, 3 August 2022 (UTC)
References
- ^ "Research may reveal why people can suddenly become frail in their 70s". The Guardian. 1 June 2022. Retrieved 18 July 2022.
- ^ Mitchell, Emily; Spencer Chapman, Michael; Williams, Nicholas; Dawson, Kevin J.; Mende, Nicole; Calderbank, Emily F.; Jung, Hyunchul; Mitchell, Thomas; Coorens, Tim H. H.; Spencer, David H.; Machado, Heather; Lee-Six, Henry; Davies, Megan; Hayler, Daniel; Fabre, Margarete A.; Mahbubani, Krishnaa; Abascal, Federico; Cagan, Alex; Vassiliou, George S.; Baxter, Joanna; Martincorena, Inigo; Stratton, Michael R.; Kent, David G.; Chatterjee, Krishna; Parsy, Kourosh Saeb; Green, Anthony R.; Nangalia, Jyoti; Laurenti, Elisa; Campbell, Peter J. (June 2022). "Clonal dynamics of haematopoiesis across the human lifespan". Nature. 606 (7913): 343–350. doi:10.1038/s41586-022-04786-y. ISSN 1476-4687. PMC 9177428. PMID 35650442.
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