Bibliografías temáticas / Models of Ageing

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Literatura académica sobre el tema "Models of Ageing"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 15 de febrero de 2022

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Artículos de revistas sobre el tema "Models of Ageing"

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Howlett, Susan E., and Kenneth Rockwood. "Ageing: Develop models of frailty." Nature 512, no. 7514 (2014): 253. http://dx.doi.org/10.1038/512253d.

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Hoylaerts, Marc F. "Animal Models of Aging Research." Blood 126, no. 23 (2015): SCI—4—SCI—4. http://dx.doi.org/10.1182/blood.v126.23.sci-4.sci-4.

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Ageing is associated with increased hypercoagulability, due to a slow rise of several coagulation factors, factor VIII, fibrinogen and thrombin-antithrombin complexes, markers of fibrinolysis and progressively defective Protein C activation, yet compatible with life at very high age. Mice, naturally aged up to 24 months, likewise show a progressive elevation of coagulation factors, triggering enhanced thrombogenicity during acute injury-induced thrombus formation. To overcome the still gradual natural ageing in mice, several mouse models of premature ageing were characterized, in an effort to allow for more rapid ageing-induced manifestations of natural thrombogenicity. Thus, the Klotho gene, encoding a type-I membrane protein, related to beta-glucosidases underlies degenerative processes, including arteriosclerosis and osteoporosis, observed in chronic renal failure. Mutations within this protein are associated with ageing and bone loss. Defective Klotho gene expression in the mouse accelerates degeneration of multiple age-sensitive traits, whereas its overexpression extends murine life span. The multidomain protein kinases Bub1 and BubR1 are central components of the mitotic checkpoint for spindle assembly (SAC) and self-monitor the eukaryotic cell cycle. Despite their amino acid sequence conservation and similar domain organization, BUB1 and BUBR1 perform different functions in the SAC. Various p53 mutant mice with a BubR1 insufficiency display early onset of ageing-associated phenotypes, whereas the BubR1H/H mouse is characterized by simultaneous vascular defects. Progerin mouse models show phenotypes ranging from being largely restricted to the vascular system to models with a broader progeria-like phenotype (severe growth retardation, fragile bones, alopecia, skin defects and reduced viability). The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus, but the most widespread mouse model of premature ageing consists of a circadian clock gene mutant mouse, the brain and muscle arnt like protein-1 (Bmal1). Mice deficient in this circadian transcription factor have impaired circadian behavior and demonstrate loss of rhythmicity in the expression of target genes. Bmal1-/- mice have reduced lifespan (maximum around 50 weeks) and display symptoms of premature ageing, including sarcopenia, cataracts, less subcutaneous fat, organ shrinkage, and others. Their early ageing phenotype correlates with increased levels of reactive oxygen species in some but not all tissues. These findings and data on CLOCK/BMAL1-dependent control of stress responses were evoked to explain the early onset of age-related pathologies in the absence of Bmal1. Their reduced lifespan is still long enough to enable intervention studies on heart function, renal integrity, tissue degeneration and thrombogenicity, including diet feeding and fat composition studies, analysis of the progressive prothrombotic state and anti-oxidant intervention studies for longevity assessment. Combined though, all these studies raise cautiousness, because no single mouse model can phenocopy human ageing perfectly: even when murine alopecia signals premature ageing, p16INK-4A measurements via qPCR do not always rise, as such is the case during natural mouse ageing and some organs deteriorate more slowly than others (e.g. vascular media and smooth muscle cells), coupled to different exposure/sensitivity to oxidative stress or environmental factors. Also, the major advantage of most accelerated ageing models, i.e. their rapid onset of ageing may insufficiently favor several risk factors, i.e. age-related thrombogenicity factors developing chronically, gradullay deteriorating with ageing. The fragile Bmal1-/- mouse model represents a well-studied compromise, its defects in different organs being well-documented, with a life-span, long enough to allow intervention studies. Disclosures No relevant conflicts of interest to declare.
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Toescu, Emil C. "Normal brain ageing: models and mechanisms." Philosophical Transactions of the Royal Society B: Biological Sciences 360, no. 1464 (2005): 2347–54. http://dx.doi.org/10.1098/rstb.2005.1771.

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Normal ageing is associated with a degree of decline in a number of cognitive functions. Apart from the issues raised by the current attempts to expand the lifespan, understanding the mechanisms and the detailed metabolic interactions involved in the process of normal neuronal ageing continues to be a challenge. One model, supported by a significant amount of experimental evidence, views the cellular ageing as a metabolic state characterized by an altered function of the metabolic triad: mitochondria–reactive oxygen species (ROS)–intracellular Ca 2+ . The perturbation in the relationship between the members of this metabolic triad generate a state of decreased homeostatic reserve, in which the aged neurons could maintain adequate function during normal activity, as demonstrated by the fact that normal ageing is not associated with widespread neuronal loss, but become increasingly vulnerable to the effects of excessive metabolic loads, usually associated with trauma, ischaemia or neurodegenerative processes. This review will concentrate on some of the evidence showing altered mitochondrial function with ageing and also discuss some of the functional consequences that would result from such events, such as alterations in mitochondrial Ca 2+ homeostasis, ATP production and generation of ROS.
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Gray, Rosaire P. "Cardiology in the ageing heart: Models." Drug Discovery Today: Disease Models 2, no. 3 (2005): 233–37. http://dx.doi.org/10.1016/j.ddmod.2005.08.003.

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Gjerde, A. C. "Multifactor ageing models - origin and similarities." IEEE Electrical Insulation Magazine 13, no. 1 (1997): 6–13. http://dx.doi.org/10.1109/57.567392.

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Vermeij, W. P., Monique C. de Waard, R. Brandt, et al. "Neurodegeneration in accelerated ageing mouse models." Experimental Gerontology 48, no. 7 (2013): 686. http://dx.doi.org/10.1016/j.exger.2013.05.017.

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MOCEIKIS, Rimvydas, Asta KIČAITĖ, Gintautas SKRIPKIŪNAS, and Aleksandrs KORJAKINS. "AGEING MODELS AND ACCELERATED AGEING TESTS OF GLASS FIBER REINFORCED CONCRETE." Engineering Structures and Technologies 10, no. 1 (2018): 10–17. http://dx.doi.org/10.3846/est.2018.1467.

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Glass fiber reinforced concrete (GRC) is used for 40 years to create world’s most stunning and complex architectural elements due to its high mechanical properties, particularly flexural strength. Yet it is very important to note that any type of glass fibers in the concrete matrix are undergoing complex ageing processes, resulting to significant decrease of initial mechanical characteristics of this composite material under natural weathering conditions. Aspects of GRC durability are mainly dependent from the properties of fibers and interaction between them and concrete matrix. In this article, long term strength retention of this composite material is discussed, existing experimental data of weathering tests presented, and main corrosion mechanisms explained. Lack of knowledge about freeze- thaw resistance of glass fiber reinforced concrete is addressed. Finally, latest attempts of GRC durability improvement are reviewed, such as adding micro fillers, polymers to the concrete matrix and enhancing surface of fibers in Nano scale.
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Emery Thompson, Melissa, Alexandra G. Rosati, and Noah Snyder-Mackler. "Insights from evolutionarily relevant models for human ageing." Philosophical Transactions of the Royal Society B: Biological Sciences 375, no. 1811 (2020): 20190605. http://dx.doi.org/10.1098/rstb.2019.0605.

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As the world confronts the health challenges of an ageing population, there has been dramatically increased interest in the science of ageing. This research has overwhelmingly focused on age-related disease, particularly in industrialized human populations and short-lived laboratory animal models. However, it has become clear that humans and long-lived primates age differently than many typical model organisms, and that many of the diseases causing death and disability in the developed world are greatly exacerbated by modern lifestyles. As such, research on how the human ageing process evolved is vital to understanding the origins of prolonged human lifespan and factors increasing vulnerability to degenerative disease. In this issue, we highlight emerging comparative research on primates, highlighting the physical, physiological, behavioural and cognitive processes of ageing. This work comprises data and theory on non-human primates, as well as under-represented data on humans living in small-scale societies, which help elucidate how environment shapes senescence. Component papers address (i) the critical processes that comprise senescence in long-lived primates; (ii) the social, ecological or individual characteristics that predict variation in the pace of ageing; and (iii) the complicated relationship between ageing trajectories and disease outcomes. Collectively, this work provides essential comparative, evolutionary data on ageing and demonstrates its unique potential to inform our understanding of the human ageing process. This article is part of the theme issue ‘Evolution of the primate ageing process’.
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Rychtaříková, Jitka. "Perception of population ageing and age discrimination across EU countries." Population and Economics 3, no. 4 (2019): 1–29. http://dx.doi.org/10.3897/popecon.3.e49760.

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Population ageing is the most dominant demographic challenge that the European Union is experiencing in the 21st century. This may create negative attitudes and lead to discrimination against persons of advanced age. Age-related stereotypes and prejudice can result in age discrimination, termed ageism. This research concerns the question of perceived ageism towards older people in 25 EU countries, surveyed in 2015 using the Special Eurobarometer 437. The analytical section includes descriptive findings and the results of three multi-level regression models addressing three domains (explained variables) of perceived ageism: 1) discrimination in general, 2) discrimination during economic crisis, and 3) discrimination when electing an older person as a high official. The two-level regression allowed simultaneous modelling of individual-level (gender, age, partnership status, social class, and life satisfaction) and of country-level (life expectancy at 55, perceived start of old age, and HDI) effects. The personal characteristics impacted much stronger perceived ageism than country contexts. Ageist perception in general has mostly been noted at pre-retirement age, but the age profile has not been the same across three regression models. The East-West gradient, frequently reported, is questioned because the geographical picture of perceived ageism is rather puzzling.
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Durang, Xavier, and Malte Henkel. "Exactly solvable models of growing interfaces and lattice gases: the Arcetri models, ageing and logarithmic sub-ageing." Journal of Statistical Mechanics: Theory and Experiment 2017, no. 12 (2017): 123206. http://dx.doi.org/10.1088/1742-5468/aa9a53.

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Tesis sobre el tema "Models of Ageing"

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Schwämmle, Veit. "Simulations on evolutionary phenomena with ageing models." [S.l. : s.n.], 2006. http://nbn-resolving.de/urn:nbn:de:bsz:93-opus-27556.

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Mitchell, Hannah Jane. "Latent phase-type models for Italy's ageing population." Thesis, Queen's University Belfast, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709549.

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Quality of care is deemed a concept of immense importance, but also of great difficulty to define and analyse. This study proposes the development of a novel statistical approach to healthcare modelling which overcomes the need to define quality of care by treating it as a hidden layer in a special type of markov model. The study setting for this research is the Italian healthcare system, in particular admissions into geriatric wards of the Lombardy region of Italy during 2009. The Coxian phase-type distribution was applied to this dataset and shown to give the best representation of the flow of patients. Covariates were then incorporated into this distribution and applied to the data. A simulation study of Coxian phase-type distribution with covariates was also undertaken. The main purpose of this research was to develop the theory of the Coxian phase-type distribution by incorporating a hidden layer within it which can represent quality of care. In forming this model novel methodology was presented. A discrete-time and continuous-time version of the model were both applied to the data with the results analysed. A further extension of the continuous-time hidden Markov model with the Coxian phase-type distribution was developed whereby covariates where incorporated into the hidden element. The results of this model, with application to the Lombardy dataset was analysed followed by a simulation study of all the newly developed models presented. In addition to the hidden Markov model with Coxian phase-type distribution the model was extended to introduce a duration component within the hidden layer. This extension formed the hidden semi- Markov model which relaxes the strict Markov assumption. This model was also applied to the Lombardy dataset.
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Calvert, Shaun. "Studies of molecular responses in models of successful ageing." Thesis, University of Liverpool, 2018. http://livrepository.liverpool.ac.uk/3018939/.

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Ageing is a major socioeconomic concern and a risk factor in most diseases. As such, a better understanding of the ageing process could provide major insights into many disease treatments and prognoses. It is still not completely clear why organisms age, though multitudes of theories exist. There is large variation within and between species in lifespan and ageing progression. Superior maintenance of cognitive and physical function with age and avoidance of age-related morbidities is known as successful ageing. Understanding how this successful ageing occurs could be key to manipulating the ageing phenotype and mitigating age-related morbidity. Caloric restriction has been shown to increase lifespan in a number of organisms and delay the ageing phenotype. This is regarded as the most robust intervention for the extension of lifespan to date. Caloric restriction is difficult to implement in humans, so the use of drugs that mimic the effects of caloric restriction are needed to take advantage of this intervention. We performed a microarray analysis of nematode worms (Caenorhabditis elegans) undergoing caloric restriction or being treated with predicted caloric restriction mimetics. These compounds act similarly to caloric restriction, but a large number of differentially expressed genes were observed between treatments and calorically restricted worms. This suggests that these compounds act through distinct mechanisms to caloric restriction. This was principally due to variations in worm development likely caused by varying levels of developmental delay. In addition to this developmental caveat, cell cycle and cell surface genes were found to be differentially expressed in a number of comparisons particularly with worms treated with the caloric restriction mimetic rapamycin. The naked mole rat (Heterocephalus glaber, NMR) is the longest-lived rodent, living over 30 years. It is also cancer resistant. This lifespan is considerably longer than similarly sized mice (Mus musculus) at up to 4 years and comes with a delayed ageing phenotype. NMR cells have been reported to be more resistant to DNA damage, which is thought to be a major contributor to ageing and cancer. We hypothesise that this DNA damage resistance is responsible for the NMR's long-lived and cancer-resistant phenotype. By studying cells derived from these animals, comparative studies can be performed to identify potential causes for the observed differences in lifespan. As DNA damage is thought to be a causative factor in ageing we performed survival assays and calculated LD50 (the dose at which 50% of the cells die, known as the 'lethal dose 50') values for two DNA damaging compounds, camptothecin and chromium (vi) oxide in mouse and NMR cells. NMR cells appear to have higher LD50 values for both compounds and hence are more resistant as has been previously shown. NMR cells surviving treatment were also less prone to become irreversibly senescent. RNAseq was performed on the mouse and NMR primary fibroblast treated with camptothecin or chromium (vi) oxide. NMR skin fibroblasts appear to show reduced expression of DNA damage repair genes, in contrast to what has been reported previously in NMR liver cells. Functional enrichment revealed significant differences at the cell surface between the two species. Cell adhesion genes were found to be expressed significantly greater in the NMR. NMR cells were shown to adhere to a culture plate more slowly than mouse cells after genotoxic treatment, confirming differences in cellular adhesion dynamics. We conclude that differences in mouse and NMR phenotype are not down to differences in DNA damage repair gene expression. Instead, we propose the hypothesis that the observed differences in cell surface chemistry contribute to the NMR's cancer-resistant phenotype.
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Duggett, Natalie Amy. "Photobiomodulation in animal models of ageing and Alzheimer's disease." Thesis, Durham University, 2013. http://etheses.dur.ac.uk/7018/.

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Photobiomodulation refers to low-intensity light therapy, utilising wavelengths in the near-infrared region of the electromagnetic spectrum to elicit biological effects. The principle aim of this investigation was to explore signalling pathways initiated by IR1072, with particular focus on heat shock proteins (HSPs), a family of proteins known to target cellular aggregates which are involved in the maintenance of cellular homeostasis. This was further examined by exploring the role of age and sex in the magnitude of biological effects induced. Another aim of this study was to explore the cytoprotective potential of IR1072 in conjunction with Alzheimer’s disease-related insults. The results of this study show chronic IR1072 exposure altered the expression of a number of HSPs in both CD-1 and TASTPM mice; including HSP105, HSP70, HSP27, and αB crystallin. The magnitude of effect differed with age and sex of CD-1 and TASTPM mice respectively; these differences coincided with altered endogenous activity of electron transport chain components. Acute exposure of CAD neuronal cultures provided significant neuroprotection against oxidative-stress and β-amyloid insults. Further characterisation of the CD-1 and TASTPM strains during ageing was established. CD-1 mice demonstrated reduced TARP γ2 with age, which may underlie learning deficits that become apparent during ageing. Chronic IR1072 exposure significantly increased TARP γ2 in 7 and 13 month old CD-1 mice, perhaps explaining improved working-memory reported following IR1072 exposure. Acute treatments of CD-1 mice altered Complex I and II activity in mitochondria. Chronic IR1072 exposure Caenorhabditis elegans was shown to consistently extend lifespan. This model system aided in establishing pathways essential for biological effects of IR1072, demonstrating the importance of HSF1 driven pathways, in particular those requiring HSP70. In conclusion, this research revealed mechanisms initiated by photobiomodulation at IR1072 that act to re-establish homeostasis, profoundly reduce amyloid load, prevent cell stress and cell death.
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Hunter, David W. "Synthesis of facial ageing transforms using three-dimensional morphable models." Thesis, St Andrews, 2009. http://hdl.handle.net/10023/763.

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Fenton, Mark. "The role of ageing in atherogenesis : two in vivo models." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445443/.

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Most mammalian cells grown in culture undergo only a limited number of rounds of replicative activity. This exhaustion of proliferative capacity is termed replicative senescence. There is some evidence that replicative senescence may also occur in vivo, and it has been postulated that such cellular ageing may contribute to age-related pathologies such as atherosclerosis, and to organismic ageing itself. The aim of this thesis is to explore the associations between replicative senescence, organismic ageing and atherosclerosis. It was found that a cytochemical assay, senescence-associated P-galactosidase (SA-p- gal), could detect in vitro replicative senescence in human endothelial cells (ECs) and rabbit vascular smooth muscle cells (VSMCs). Endothelial denudation was then undertaken in rabbit carotid arteries, and in some experiments repeated six weeks later. Morphometric analysis of SA-p-gal activity demonstrated mat senescent ECs and VSMCs accumulated in the injured vessel wall, a second denudation augmenting mis accumulation. Further analysis suggested that these senescent cells showed no proliferative or apoptotic activity. An animal model of accelerated organismic ageing, the senescence-accelerated prone mouse (SAM-P), and mice from a related strain showing normal ageing (SAM-R), were fed a Western-type diet. Morphometric analysis of lipid deposition in their aortic roots demonstrated increased lipid deposition in SAM-P compared with SAM-R mice, despite lower serum cholesterol levels in SAM-P mice. Study of telomere lengths and SA-p-gal activity showed no evidence of accelerated cellular ageing in SAM-P mice. It is concluded that cellular ageing can occur in the vasculature, and that a murine strain which ages at an accelerated rate shows a greater susceptibility to atherogenesis. Since no evidence of accelerated cellular ageing was found in this strain, it is postulated that the increased susceptibility of SAM-P mice to atherogenesis, and perhaps also their ageing phenotype, may be attributable to other abnormalities in these mice, such as increased oxidative status.
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Dalle, Pezze Piero. "Dynamical models of the mammalian target of rapamycin network in ageing." Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/2183.

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The mammalian Target of Rapamycin (mTOR)kinase is a central regulator of cellular growth and metabolism and plays an important role in ageing and age- related diseases. The increase of invitro data collected to extend our knowledge on its regulation, and consequently improve drug intervention,has highlighted the complexity of the mTOR network. This complexity is also aggravated by the intrinsic time-dependent nature of cellular regulatory network cross-talks and feedbacks. Systems biology constitutes a powerful tool for mathematically for- malising biological networks and investigating such dynamical properties. The present work discusses the development of three dynamical models of the mTOR network. The first aimed at the analysis of the current literature-based hypotheses of mTOR Complex2(mTORC2)regulation. For each hypothesis, the model predicted specific differential dynamics which were systematically tested by invitro experiments. Surprisingly, nocurrent hypothesis could explain the data and a new hypothesis of mTORC2 activation was proposed. The second model extended the previous one with an AMPK module. In this study AMPK was reported to be activated by insulin. Using a hypothesis ranking approach based on model goodness-of-fit, AMPK activity was insilico predicted and in vitro tested to be activated by the insulin receptor substrate(IRS).Finally,the last model linked mTOR with the oxidative stress response, mitochondrial reg- ulation, DNA damage and FoxO transcription factors. This work provided the characterisation of a dynamical mechanism to explain the state transition from normal to senescent cells and their reversibility of the senescentphenotype.
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Skodras, Angelos A. "Computational approaches and models for ovarian ageing : from 2D to 4D." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/10189.

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The theme of the work presented in this multi-disciplinary PhD is the development of new computational tools and techniques to study and understand spatio-temporal follicle growth in neonatal mouse ovaries. The female ovary is endowed at birth with a finite, non-renewable supply of oocytes, each enclosed in a layer of supporting somatic (granulosa) cells to form a quiescent follicle. From birth, a steady trickle of follicles initiate growth to maintain a supply of mature oocytes for regular ovulation. Disruption in the regulation of initiation of follicle growth can result in various pathologies, such as premature ovarian failure and polycystic ovary syndrome. The mechanism of regulation of the initiation of follicle growth remains unclear, but may involve inter-follicle signaling via paracrine growth factors. To investigate this hypothesis, a new technique for quantifying and analyzing spatial distributions of quiescent and growing follicles in the adult human has been developed, as an extension of a novel technique previously developed in neonatal mice in our laboratory. As in the mouse study, we have found evidence that in the human ovary neighbouring quiescent follicles inhibit follicle growth, at a small range. This approach has been further extended to cultured neonatal mouse ovaries, which in vitro lack a systemic blood supply, to investigate the relative contributions of inter-follicle paracrine signaling and endocrine growth factor/nutrient signaling to the regulation of initiation of follicle growth. Accurate counts of the numbers of follicles in ovaries are important for a wide variety of studies of ovarian physiology, including investigating the effects of age, toxins, chemotherapeutics, endocrine disruptors and specific genes (knock out/transgenic studies) on follicle formation, endowment and development. Many published studies use frequent sampling of a small number of ovaries (often as few as three) to obtain estimates of the number of follicles. We have tested the validity of this approach by generating 3D spherical simulated ovaries which contain realistic numbers of follicles at different stages and which are realistically positioned within these ovaries. The number and position of follicles is based on real biological data. This model enables us to rapidly ‘virtually’ section the ovary in silico and obtain computer-generated counts of the numbers of follicles in sections at different frequencies, such as one every fifth section (1/5), 1/20 or 1/50. As we know precisely how many follicles each simulated ovary contains, we can compare the accuracy using different sampling frequencies of varying numbers of ovaries. This has enabled us to demonstrate that the error is smaller when infrequent sampling of a large number of ovaries (≥8) is carried out, and that this actually involves analyzing fewer sections overall. We have gone on to generate simulated ovaries from knockout mice, with more or fewer follicles, and can predict how many ovaries are required to make robust comparisons between knockout and control animals. This has shown that biological variability contributes more to counting error than the method of sampling. These simulated ovaries provide a unique resource to model large studies. Currently follicle counts are obtained by fixing and serially sectioning ovaries, and manually counting the follicles in sections. This is laborious and time-consuming. Faster methods of obtaining follicle estimates are required. With the use of confocal microscopy and immunohistochemistry for an oocyte-specific protein, we were able to establish a protocol that allows us to image and computationally reconstruct a whole neonatal mouse ovary in 3D. Follicle number can be estimated rapidly using a stereologic method. The stereologic technique error was estimated using the simulated ovary model, leading to the conclusion that the method can be safely used to obtain rapid estimates of follicle number. The time required can be further reduced by using image processing to detect the stained follicles on the sections. We have developed an algorithmic technique that can instantaneously identify stained oocytes, count them, and calculate their spatial distribution. A fundamental unanswered question is whether follicles move in the ovary, particularly as they grow. This question has arisen from the observation that small follicles tend to be situated close to the ovarian surface, while large ones are closer to the medulla. This question has implications for interfollicle signaling. We have developed a protocol to image the ovary while in culture using timelapse confocal and live lipid stains to visualize the follicles. Results show that small follicles are not moving significantly over a period of 12h. This project can be extended in the future with the use of transgenic mice for GFP tagging, to accurately monitor changes in structures of interest within cultured ovaries.
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Gibson, Paul Martyn. "The application of hybrid neural network models to archaeofaunal ageing and interpretation." Thesis, University of York, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296383.

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Duncombe, Jessica. "Imaging cerebrovascular alterations in experimental models of ageing and vascular cognitive impairment." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28828.

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Vascular cognitive impairment describes a heterogeneous condition in which cognitive decline is precipitated by underlying cerebrovascular dysfunction. Ageing, as well as vascular diseases such as hypertension, stroke, cerebral small vessel disease and cerebral amyloid angiopathy, are risk factors for vascular cognitive impairment. The precise mechanisms by which these conditions impact the cerebral vasculature to drive cognitive decline, however, are unknown. Previous research has indicated that vascular risk factors can lead to microvascular oxidative stress, inflammation and endothelial dysfunction that can lead to tissue hypoperfusion, the development of white and grey matter vascular lesions (microinfarcts and microbleeds) and cognitive impairment. It was hypothesised that ageing, a prominent risk factor for cognitive decline, would induce impairments on neurovascular coupling resulting from neurovascular unit disruption. It was further hypothesised that induction of chronic cerebral hypoperfusion would mediate neurovascular dysfunction and vascular lesion development through increased oxidative stress, resulting in cognitive decline. Finally, it was also hypothesised that neurovascular impairments resulting from ageing and chronic cerebral hypoperfusion would be exacerbated in the presence of amyloid deposition. Four studies were performed in order to test these hypotheses. Vascular risk factors can be reproduced using experimental mouse models and provide a valuable basis in which to test hypotheses and therapeutic interventions. As such, a primary aim of this thesis was to develop and validate sensitive MRI approaches that would allow the detection of vascular alterations in vivo. In the first series of studies, MRI techniques to assess resting cerebral blood flow, vessel number, vascular lesions and inflammation in experimental mice were validated using established in vivo and ex vivo techniques, so that these techniques could be used in subsequent studies for vascular assessments in vivo. Arterial spin labelling was developed to assess resting cerebral blood flow, and was able to detect reductions in blood flow following cerebral hypoperfusion that correlated well with those obtained from laser speckle imaging. Q-map imaging was able to detect reductions in vessel number in acute lesions, and in non-lesioned mice measures of vessel number correlated well with histopathological measures. Structural T2 imaging was performed in order to detect ischaemic and haemorrhagic lesions in chronically hypoperfused mice, and was validated using H&E and Perls’ staining. Finally, contrast-enhanced T2* imaging was used to detect iron oxide uptake by macrophages in the brains of hypoperfused mice, which was further validated by the identification of iron-containing macrophages in immunostained brain sections. The second study was conducted to test the hypothesis that ageing would impair neurovascular unit function and structure, and that these impairments would be exacerbated in the presence of amyloid pathology. The aim of the study was to incorporate previously developed in vivo imaging approaches in the assessment of vascular function and alterations in neurovascular unit structure in both wild type and TgSwDI mice. As predicted, ageing caused a pronounced deficit on measures of neurovascular coupling, however this was not exacerbated by accumulation of amyloid in TgSwDI mice and was not associated with alterations in baseline blood flow measured by arterial spin labelling. Structural assessment of the neurovascular unit revealed a loss of contact between astrocytic endfeet and vasculature, which was significantly associated with the impairment on neurovascular coupling, in addition to other markers of breakdown of the neurovascular unit such as loss of pericyte coverage and microglial activation. Age and thalamic vascular amyloid accumulation were also associated with an increase in the NADPH oxidase (NOX) subunit p47, indicative of increased oxidative stress. Data from this experiment indicate that ageing can profoundly impair neurovascular coupling, mediated by gliosis and loss of astrocytic contacts with vasculature. The third study aimed to test the hypothesis that chronic cerebral hypoperfusion (a prominent early feature of vascular cognitive impairment) would impair vascular function and induce the development of vascular lesions and cognitive decline. The impact of hypoperfusion on neurovascular coupling, ischaemic and haemorrhagic lesion burden and cognition was investigated in wild type and TgSwDI mice. Hypoperfusion induced deficits on neurovascular coupling, increased lesion burden and inflammation assessed with T2 and contrast-enhanced T2* imaging, and caused impairment on measures of learning and memory. Hypoperfusion was also associated with an increase in the levels of NOX2, NOX4 and 3-NT at 3 months following surgery, indicating persistent reactive oxygen species production and oxidative damage in hypoperfused mice. The findings from this study indicate that vascular dysfunction and cognitive impairment following hypoperfusion may be mediated by increased NADPH oxidase activity and resulting oxidative stress. The previous studies indicated that markers of oxidative stress were induced in response to ageing, vascular amyloid accumulation and cerebral hypoperfusion. The final study sought to determine whether increased NOX activity mediates downstream pathological effects on vascular function, vascular lesion development and cognitive decline following hypoperfusion. NOX activity was inhibited pharmacologically by administration of apocynin to hypoperfused TgSwDI mice for 3 months following surgery. Treatment with apocynin significantly restored neurovascular coupling to a level similar to sham-operated mice, and there was a trend toward reduction of ischaemic vascular lesions. However, it was unable to rescue the prominent inflammatory response or decline in cognitive ability, as apocynin-treated mice were no different on these measures to non-treated hypoperfused mice. The data indicate that whilst inhibiting NOX may have potential therapeutic value in improving vascular function, additional interventions, for example to reduce inflammation, may also be required in order to prevent cognitive decline. Overall, the work outlined within the thesis indicate that vascular risk factors of ageing, cerebral amyloid angiopathy and cerebral hypoperfusion may converge on common pathways involving oxidative stress and increased inflammation in order to drive vascular dysfunction and lead to cognitive decline. Inhibition of NOX activity was able to rescue vascular function, however the results indicate that this was not sufficient to protect against cognitive impairment, suggesting additional therapeutic targets may need to be sought in order to fully preserve vascular health and prevent cognitive decline.
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Libros sobre el tema "Models of Ageing"

1

Winkelmann, Rainer. Ageing, migration and labourmobility. Centre for Economic Policy Research, 1992.

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Oxydative ageing of polymers. ISTE, 2012.

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Ageing, a biomedical perspective. John Wiley & Sons, 1995.

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Roel M. W. J. Beetsma. The budgetary and economic consequences of ageing in the Netherlands. Research Centre for Economic Policy, 1999.

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Pensions and population ageing: An economic analysis. Northampton, MA, 1998.

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Coggins, Lewis G. Effects of sample size and ageing error on estimates of sustained yield. State of Alaska, Dept. of Fish and Game, 1997.

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Broer, D. P. Growth and welfare distribution in an ageing society: An applied general equilibrium analysis for the Netherlands. Research Centre for Economic Policy, 1999.

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Hviding, Ketil. Macroeconomic effects of pension reforms in the context of ageing populations: Overlapping generations model simulations for seven OECD countries. OECD, 1998.

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Agent-based models. Sage Publications, 2008.

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Gilbert, Nigel. Agent-Based Models. SAGE Publications, Inc., 2008. http://dx.doi.org/10.4135/9781412983259.

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Capítulos de libros sobre el tema "Models of Ageing"

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Iparraguirre, José Luis. "Perpetual Youth and Dynastic Models." In Economics and Ageing. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-93248-4_10.

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Iparraguirre, José Luis. "Models and Time in Economics." In Economics and Ageing. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-93248-4_7.

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Robitaille, Annie, and Graciela Muniz Terrera. "Considerations when using longitudinal statistical models to study ageing." In Researching Ageing. Routledge, 2020. http://dx.doi.org/10.4324/9781003051169-12.

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Farazdaghi, Elham, Farnaz Majid Zadeh Heravi, and Amine Nait-Ali. "Lifestyle Facial Ageing Models." In Biometrics under Biomedical Considerations. Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1144-4_5.

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Gillon, Renaud, Aarnout Wieers, Frederik Deleu, et al. "Ageing Models and Reliability Prediction." In Mathematics in Industry. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-30726-4_19.

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Brock, Alistair J., Ari Sudwarts, Matthew O. Parker, and Caroline H. Brennan. "Zebrafish Behavioral Models of Ageing." In The rights and wrongs of zebrafish: Behavioral phenotyping of zebrafish. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-33774-6_11.

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Panchenko, Andrey V., Ekaterina A. Gubareva, and Vladimir N. Anisimov. "Circadian System and Aging in Rodent Models." In Healthy Ageing and Longevity. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-64543-8_5.

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Khan, Parvez, Aarfa Queen, Md Imtaiyaz Hassan, and Sher Ali. "Genetics, Ageing and Human Health." In Models, Molecules and Mechanisms in Biogerontology. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-3585-3_10.

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Lahoud, Nadine, Laurent Boudou, Christian Mayoux, and Juan Martinez-Vega. "Models for Ageing of Electrical Insulation." In Dielectric Materials for Electrical Engineering. John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118557419.ch09.

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Pathak, Sen. "Healthy Ageing and Cancer in Humans." In Models, Molecules and Mechanisms in Biogerontology. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-3585-3_18.

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Actas de conferencias sobre el tema "Models of Ageing"

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Wang, Bing, Tuan D. Pham, Tuan D. Pham, et al. "Estimating Neuronal Ageing with Hidden Markov Models." In 2011 INTERNATIONAL SYMPOSIUM ON COMPUTATIONAL MODELS FOR LIFE SCIENCES (CMLS-11). AIP, 2011. http://dx.doi.org/10.1063/1.3596633.

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Requena, Carmen, Paula Álvarez-Merino, and María Plaza-Carmona. "Educational Models against ageism in higher education." In Fourth International Conference on Higher Education Advances. Universitat Politècnica València, 2018. http://dx.doi.org/10.4995/head18.2018.7986.

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There have allways been old persons, but their number has unprecedentedly grown and it is expected to overtake any other age group in contemporary developed societies. Instead of taking this process as a success of mankind, ageism grows on a par with ageing. It is well documented how standard educational models fail to correct implicit ageistic stereotypes, thus new emerging theoretical models such as generational intelligence and identity in old age put forward experiential methodologies designed to educate both explicit and implicit ageistic stereotypes. Both theoretical models incorporate the subjective first-person perspective on ageing, which complements the standard university curriculum for ageing-related professsionals in health, social or educational sectors. The practical implementation of these educational models involve experiential methodologies such as life stories. A crucial educational element in the practical success of this methodology lies in understanding intergenerational education not only as a gathering of generations, but as the intentional production and evaluation of educational ends. The paper exemplifies these methodologies and contrasts their success in dealing with the complexities involved in educating against explicit and implicit agesitic stereotypes in intergenerational relations. Therefore, the key to intergenerationality lies less in its "generational" element as in its "inter" element.
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Poghosyan, Shahen, Armen Amirjanyan, and Albert Malkhasyan. "Approach on Component Selection for Ageing-Trend Analysis Within PSA Models." In 17th International Conference on Nuclear Engineering. ASMEDC, 2009. http://dx.doi.org/10.1115/icone17-75029.

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The major advantage of PSA is the possibility of in-depth qualitative and quantitative analysis of NPP actual configuration with definition of factors introducing a significant contribution to the general risk of reactor core damage. However main lack of the PSA current models is neglect of equipment ageing effects. Neglecting of ageing effects in PSA could lead to incorrectness of risk profile and influent on risk-informed decision making process. To solve this issue incorporation of ageing aspects into PSA models for Armenian NPP Unit 2 was initiated. Implementation of ageing trend analysis for all PSA components is insuperable effort, so the first step of the analysis is component selection activity. This paper is addressing the approach on component selection for ageing-trend analysis within PSA models. Presented approach is based on ageing effect and risk importance data. The procedure was developed and implemented in the framework of ageing aspects incorporation into PSA level 1 model for Armenian NPP Unit 2.
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Cvijovic, Marija, Hayssam Soueidan, David James Sherman, Edda Klipp, and Macha Nikolski. "Exploratory simulation of cell ageing using hierarchical models." In Proceedings of the 19th International Conference. IMPERIAL COLLEGE PRESS, 2008. http://dx.doi.org/10.1142/9781848163324_0010.

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German, R., P. Venet, A. Sari, O. Briat, and J. M. Vinassa. "Comparison of EDLC impedance models used for ageing monitoring." In 2012 First International Conference on Renewable Energies and Vehicular Technology (REVET). IEEE, 2012. http://dx.doi.org/10.1109/revet.2012.6195275.

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Banerjee, B., D. Jayaweera, and S. M. Islam. "Wind power forecasting with dynamic regression models and ageing considerations." In 2011 IEEE PES Innovative Smart Grid Technologies (ISGT Australia). IEEE, 2011. http://dx.doi.org/10.1109/isgt-asia.2011.6167131.

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Florescu, Gheorghe, and Mihail Cojan. "Identification of CSSC Caused by Ageing and Degradation." In 14th International Conference on Nuclear Engineering. ASMEDC, 2006. http://dx.doi.org/10.1115/icone14-89286.

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PSA studies, that were developed for some NPPs, permit the using of the created models to perform many research tests, in order to optimize the structures, systems and components (SSCs) operation or to identify the NPP or systems weaknesses, due to specific or special factors. SSCs that influence decisively the NPP reliability are considered as critical. Also, for the accident conditions, the SSC, which have a major influence to the system availability or operability, are considered as critical. Many worldwide NPPs reached the life time or are very close to do that. Several SSCs have shorter life times than NPP’s life time. Ageing is one of the factors that decrease the SSC life time. Due to ageing, if are not replaced, some SSCs, or groups of redundant SSCs, become critical looking to safety. Some questions for what to do in the situation when a SSC must be replaced and the SSC specific manufacturer doesn’t exist, could also be put. The paper tried to solve the problem of SSC modeling by introducing of an ageing factor in SSC model. Fault tree (F/T) modeling approach is assumed. There are two possibilities for modeling: failure rates that are changed or specific MCS (minimal cut set) term modified by ageing. Risk analysis and PSA techniques are used as a basis for analysis. The paper includes: the steps to establish the systems or components that suffer ageing; methods to identify CSSC taking into account ageing; the events associated to ageing/degradation and presentation of method to determine the ageing related events, selection of the SSCs that are important for analyses; selection of the most significant ageing events; ranking of ageing events; association of events to these components in order to decide for the CSSC detailed analyses; ranking / ordering of the ageing related events; optimization of NPP systems design and operation considering ageing; impact of ageing to NPP operation/safety/safety margins and to manufacturer technical specifications. The paper presents a brief description of the most important aspects of the methods, used to analyze the ageing effects on appearing of CSSCs, taking into account the previous developed NPP PSA models and PSA modeling tools.
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Sugier, Jaroslaw, and George J. Anders. "Modifying Markov Models of Ageing Equipment for Modeling Changes in Maintenance Policies." In 2009 Fourth International Conference on Dependability of Computer Systems. IEEE, 2009. http://dx.doi.org/10.1109/depcos-relcomex.2009.23.

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Fielding, Suzanne M. "Fluctuation-dissipation relations in ageing and driven non-mean field glass models." In SLOW DYNAMICS IN COMPLEX SYSTEMS: 3rd International Symposium on Slow Dynamics in Complex Systems. AIP, 2004. http://dx.doi.org/10.1063/1.1764243.

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Timmermans, Jean-Marc, Alexandros Nikolian, Joris De Hoog, et al. "Batteries 2020 — Lithium-ion battery first and second life ageing, validated battery models, lifetime modelling and ageing assessment of thermal parameters." In 2016 18th European Conference on Power Electronics and Applications (EPE'16 ECCE Europe). IEEE, 2016. http://dx.doi.org/10.1109/epe.2016.7695698.

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Informes sobre el tema "Models of Ageing"

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Lakkaraju, Kiran, Jonathan H. Whetzel, Jina Lee, Asmeret Brooke Bier, Rogelio E. Cardona-Rivera, and Jeremy Ray Rhythm Bernstein. Validating agent based models through virtual worlds. Office of Scientific and Technical Information (OSTI), 2014. http://dx.doi.org/10.2172/1147200.

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Backus, David, Mikhail Chernov, and Stanley Zin. Sources of Entropy in Representative Agent Models. National Bureau of Economic Research, 2011. http://dx.doi.org/10.3386/w17219.

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Geller, Armando, Claudio Cioffi-Revilla, Maciej M. Latek, et al. Forecasting Irregular Warfare via Agent-Based Network Models. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada546483.

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Pelechano, Nuria, Kevin O'Brien, Barry Silverman, and Norman Badler. Crowd Simulation Incorporating Agent Psychological Models, Roles and Communication. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada522128.

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Bonhomme, Stéphane, and Manuel Arellano. Nonlinear panel data methods for dynamic heterogeneous agent models. The IFS, 2016. http://dx.doi.org/10.1920/wp.cem.2016.5116.

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Fonoberova, Maria, Vladimir A. Fonoberov, Igor Mezic, and Jadranka Mezic. MetaModel Analysis for Agent-Based Models: Scales, Uncertainty, Data Analysis. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada563753.

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Kocherlakota, Narayana. Public Debt Bubbles in Heterogeneous Agent Models with Tail Risk. National Bureau of Economic Research, 2021. http://dx.doi.org/10.3386/w29138.

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Agha, Gul, and Koushik Sen. A Parametric Model for Large Scale Agent Systems. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada434354.

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Riddle, Matthew E., Eric Tatara, Charles M. Olson, Diane J. Graziano, Braeton J. Smith, and Allison Bennett Irion. Argonne’s global critical materials agent-based model (GCMat). Office of Scientific and Technical Information (OSTI), 2020. http://dx.doi.org/10.2172/1631454.

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Wheaton, William, James Cajka, Bernadette Chasteen, et al. Synthesized population databases: A US geospatial database for agent-based models. RTI Press, 2009. http://dx.doi.org/10.3768/rtipress.2009.mr.0010.0905.

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