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Lifespan Development - Science topic

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I want to make connections between the real world and the impact these events have on human development. Just any questions that relate to development and the 3 domains: physical, cognitive, and psychosocial.
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Hi,
Maybe some of these articles be of help to you:
Spinhoven P, Elzinga BM, Hovens JG, Roelofs K, Zitman FG, van Oppen P, Penninx BW. The specificity of childhood adversities and negative life events across the life span to anxiety and depressive disorders. J Affect Disord. 2010 Oct;126(1-2):103-12. doi: 10.1016/j.jad.2010.02.132
Levy O, Buckley LB, Keitt TH, Smith CD, Boateng KO, Kumar DS, Angilletta MJ Jr. Resolving the life cycle alters expected impacts of climate change. Proc Biol Sci. 2015 Aug 22;282(1813):20150837
Krammer S, Kleim B, Simmen-Janevska K, Maercker A. Childhood trauma and complex posttraumatic stress disorder symptoms in older adults: A study of direct effects and social-interpersonal factors as potential mediators. J Trauma Dissociation. 2016 Oct-Dec;17(5):593-607. doi: 10.1080/15299732.2014.991861
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I am currently trying to use FuDR to run a lifespan experiment using C. elegans.
I have a stock solution of FuDR that has been dissolved in water and am trying the determine the concentration of FuDR once it is administered to NGM plates. My question is whether or not the FuDR will dissolve into the plates to dilute the concentration, or if it will simply deposit on the surface.
Thanks!
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In our lab we always calculate the final concentration based on the total volume of the plates, in the expectation that it spreads throughout the entire plate over time. However, I am not sure if this has been tested or if it is just an assumption.
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Lifespan development, personality and aging and so on - who is the best now?
My area is age and personality traits change (like personal autonomy for example).
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Yes! That's one of his core areas! And Mathias Alemand (University of Zurich) together with Patrick Hill (Washington University in St. Louis, USA) are co-editing a book which will appear towards summer this year entitled "Personality and Healthy Aging".
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In order to study aging and test anti-aging interventions (our primary interest is, of course, us) we utilize model animals for obvious ethical and logistical reasons. According to the Nuremberg Code, that animal studies are required by United States’ law prior to human trials (Federal Food, Drug and Cosmetic Act, United States Code). Unfortunately and despite all precautionary measures, accumulated experimental data provide many examples of critical differences even between closely related animals that resulted in spectacular failures. For example, an anti-inflammatory drug, TGN1412, was comprehensively tested in two species (including monkeys!!) before going to a preclinical trial stage. However, the volunteers injected with this drug suffered from catastrophic multiple organs failures within minutes after injection. Overall, the success rate for treatments in Phase 1 clinical testing is estimated to be just around 8%.
Relatively recently, the National Institutes on Aging initiated an Interventions Testing Program that allows scrutiny of proposed lifespan-extending interventions in highly standardized and controlled conditions using uniform protocols and three primary sites for independent survival studies. Since 2004, four to six interventions have been tested every year. So far, only six compounds have been shown to increase lifespan of mice, sometimes, in gender-specific manner, including aspirin, rapamycin, 17αEstradiol, acarbose, nordihydroguaiaretic acid and Protandim. Outbred mice were chosen as the animal model of choice based on several criteria including being inexpensive and easy to maintain.
These considerations in themselves are easy to understand, especially, in the current fiscal environment. Yet, one wonders how such concessions at the design stage can compromise Science and chances for success. There is a kernel of truth in the saying “we are not rich enough to buy cheap things”. If the cheap choices we make preclude any meaningful developments, what is the point of the whole enterprise apart from careers made, salaries received and budget money successfully spent?
Among other criteria for selection of animal model were external validity explained as “relevance to human aging process”, responsiveness to caloric restriction (CR) “because CR is the only proven method to extend lifespan, any useful model should be affected by CR”, and similarity of aging to human aging with the primary stipulation of having “multiple causes of death”. “External validity” and “similarity to human aging” are facets of the same question and should have been bundled together, although it would probably be interesting to analyze them separately.
As far as “similarity to human aging” via “multiple causes of death” clause is concerned, I wish luck to those who will try to discern multiple causes of death in C. elegans and fruit flies. The “relevance to the human aging process” is covered by the virtue of being a mammal, I suppose. It seems fair enough and, yet, it is very far from being enough. There still are fundamental differences in physiology, biochemistry and metabolism that result in the failure of the vast majority of pilot clinical trials for interventions that were successful in mice. Moreover, there is a big chance (or rather certainty) that many aspects of human aging are simply non-existent in short-lived mice.
Absolute numbers do matter. For example, one of the remarkable features of human aging is appearance of cells with clonally expanded mutations in mtDNA starting from the fifth decade of life. These cells comprise a sizable fraction of all cells (up to 30%) in non-renewable tissues like muscles and brains in older individuals. Clearly, clonal expansion of detrimental mutations in mtDNA is important to human aging and lifespan but its development takes a very considerable time which is not afforded to relatively short-lived model animals. Compared to old human brains, the accumulation of deletions in mtDNA in the brains of old mice is at least 10-times lower. Another example is cardiovascular diseases. Mouse aging is not accompanied with the development of cardiovascular pathologies because of the differences in lipid metabolism (blood of mice is practically solidly packed with “good” cholesterol) and lack of sufficient time for plaque buildup during normal aging. In short, although the “external validity” clause fulfills its function of ruling out microscopic worms and fruit flies as models of human aging (thank you very much), it still remains a very shaky concept.
The “responsiveness to caloric restriction” clause is interesting in its own right. First, all animals under consideration were shown to be responsive to CR which makes this condition unnecessary (authors conceded as much). Second, it is like running an employment opportunity ad at a ski resort with the compulsory requirement of being able to swim. How responsiveness to caloric restriction is supposed to guarantee that successful intervention - whether related or not related to energy metabolism - is transferable to humans? Does it imply that there is only one pathway to longevity? What these people were thinking? It is also curious that the requirement for a relatively short lifespan was not mentioned at all, although it was the most likely underlying reason for ruling out dogs and primates along with the fact that, with few exceptions, the entire experimental biology is based on mice models and it is much easier to utilize existing infrastructure. Be as it may, there is no easy alternative solution to this problem. We are beholden to mice and such simply because experimental studies on humans are a big fat unsurmountable taboo.
Perhaps our strategy needs to be revised. Perhaps we should allow that animal studies for validation of anti-aging interventions are not always a decisive factor. Maybe in some cases interventions could be conceived based on cell culture experiments and then very cautiously eased into relatively short term clinical trials. There is, of course, an option of genetically modified mice that allegedly mimic aging process in humans. Unfortunately, many of these models are also a departure from human aging due to oversimplification, significant side effects, or as an embodiment of the dominant schools of thought (which may be right but, judging from the historical trends, is more likely be wrong).
To summarize, although it is indisputable that the basic mechanisms of aging contribute to the aging process of all species, the aging of every species is a unique mixture of relative contributions. It, therefore, remains possible that what we see as leading determinants of lifespan in model animals have almost nothing to do with us and - vice versa – our very own leading determinants of the lifespan play no discernable role in aging of short-lived animals we use as our proxies. As the results of clinical trials show, there is less than one in ten chance for anti-aging interventions based on model animals to succeed in humans. The negative results also do not mean much for there is similar or perhaps greater probability that interventions that did not result in lifespan extension in mice might have worked in humans. All this means that applied gerontology has a problem and that the currently accepted model-animals-to-humans sequence for our search of the fountain of youth is deeply flawed.
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Do the animals suffer because of manipulation, or is your approach purely observational?
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The incidence of Total knee replacement is on a rise. In another decade the incidence of revisions will rise too. Is there any way to predict the lifespan of implants nowadays so that we can prepare for the inevitable tomorrow
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I agree completely with Mr Vaishya's opinion about the registries' limitations and their statistical interpretations, but registries are the "crude" way to understand behaviour of a prosthesis when this is implanted by the "general population" of Mr Average of the surgeons.
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I have been exploring Perry’s epistemological stages of development into adulthood.  The Learning Context Questionnaire (LCQ) by Griffith and Chapman (1982) seems to be the most common quantitative measure.  Unfortunately I have not been able to locate a copy.  Do you have a copy you could share? Are there other existing measures of Perry stages or other measures of how individuals understand truth/knowledge?  Thank you for your help. ~ Kevin
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I believe LCQ co-developer John Griffith now lives in or around Greenville, SC or Charlotte NC. His profile is on LinkedIn https://www.linkedin.com/in/john-griffith-870b6545/. I corresponded with him several years back and he provided me with copies of the questionnaire. Hope this helps!
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Rusty grain beetle is one of the common insect pests in stored grains worldwide. I am curious of the lifespan of this pest. Anybody here in RG knows it?
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We are running a study where we measure grip strength to older patients in acute medical wards to flag up those with low levels who might be at risk of poor healthcare outcomes. We know that grip strength vary according to age, gender, and dominant hand, but I am not aware that there is any research on whether the grip strength of a patient vary when it is being tested before and after meals. It would be helpful if anyone can share their experiences or refer me to any useful references. 
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I can't see the relevance of this study. If the client has the motivation to eat and the skills involved - what is the significance of grip strength after meals? How will your study provide information that is meaningful to clients healthcare outcomes? What are the assumptions/hypotheses underpinning your study?
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Can anyone recommend a good abbreviated life-span development text book? I am teaching a 100-level general developmental psychology course which will primarily be freshman and have to choose a text immediately. 
I am looking for a relatively inexpensive text that briefly covers essential topics to Lifespan development (since it is so expansive). I will expand upon relevant topics in my lecture, but just need a solid foundation of the many concepts for my students to read and reference before my lectures. 
I would even appreciate recommendations for longer texts! 
Thanks so much! 
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I used all of the books mentioned above and found them appropriate. The Berk text is the one we used when I directed the online BS program for the Penn State World Campus.