Academic literature on the topic 'Premature ageing'
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Journal articles on the topic "Premature ageing"
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Villanueva, M. Teresa. "Slowing premature ageing." Nature Reviews Cancer 15, no. 5 (April 24, 2015): 259. http://dx.doi.org/10.1038/nrc3956.
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Joss, Nicola, J. Michael Boulton‐Jones, and Ian More. "Premature ageing and glomerulonephritis." Nephrology Dialysis Transplantation 16, no. 3 (March 1, 2001): 615–18. http://dx.doi.org/10.1093/ndt/16.3.615.
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Smith, Michael. "Premature Ageing: History and Biology." Journal of the Royal Society of Medicine 87, no. 7 (July 1994): 425–27. http://dx.doi.org/10.1177/014107689408700720.
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Biesalski, H. K., M. Berneburg, T. Grune, M. Kerscher, J. Krutmann, W. Raab, J. Reimann, T. Reuther, L. Robert, and T. Schwarz. "Oxidative and premature skin ageing." Experimental Dermatology 12, s3 (December 2003): 3–15. http://dx.doi.org/10.1111/j.0906-6705.2003.00148.x.
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Dokal, Inderjeet. "A disease of premature ageing." Lancet 358 (December 2001): S27. http://dx.doi.org/10.1016/s0140-6736(01)07040-4.
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Silverstein, Janet H. "Does diabetes cause premature AGEing?" Journal of Pediatrics 172 (May 2016): 1–4. http://dx.doi.org/10.1016/j.jpeds.2016.03.011.
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Testori, Alessandro. "Short telomere syndromes, premature ageing syndromes, and biological ageing." Hong Kong Medical Journal 26, no. 1 (January 22, 2020): 76–77. http://dx.doi.org/10.12809/hkmj187782.
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Lehmann, Alan. "Ageing: Repair and Transcription Keep Us from Premature Ageing." Current Biology 12, no. 16 (August 2002): R550—R551. http://dx.doi.org/10.1016/s0960-9822(02)01050-3.
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DYER, CHRISTOPHER A. E., and ALAN J. SINCLAIR. "The premature ageing syndromes: insights into the ageing process." Age and Ageing 27, no. 1 (1998): 73–80. http://dx.doi.org/10.1093/ageing/27.1.73.
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Swanton, Alexander, and Tim Child. "Reproduction and ovarian ageing." British Menopause Society Journal 11, no. 4 (December 1, 2005): 126–31. http://dx.doi.org/10.1258/136218005775544200.
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Female fertility rates are inherently linked to a woman's age, which is in turn related to ovarian function. Reproductive potential declines gradually until 37–38 years of age, from when the rate of decline hastens. Approximately 1% of women suffer from premature ovarian ageing, and many may not have completed their families. This paper reviews the physiology and fertility consequences of ovarian ageing, premature ovarian failure, measures of ovarian reserve and methods of fertility preservation.
Dissertations / Theses on the topic "Premature ageing"
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Mankouri, Hocine William. "DNA helicases and yeast ageing." Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367550.
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Chau, P. Y. Pauline. "Mechanism of genomic instability in Prelamin A based premature ageing." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557352.
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Chau, P. Y. Pauline, and 周珮然. "Mechanism of genomic instability in Prelamin A based premature ageing." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557352.
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Seager, Anna L. "Molecular and cytogenetic analysis of premature ageing disease Hutchinson-Gilford Progeria Syndrome." Thesis, Swansea University, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.638787.
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The principal aim of this study was to evaluate the underlying cellular mechanisms causing HGPS by using an in depth cytogenetic and molecular approach. Firstly, the total genome karyotype of HGPS lines and clinically normal cell lines was analysed utilising modified, multi-colour fluorescent in situ hybridisation (FISH), dual colour FISH, locus specific FISH, and DNA banding methods. The combinations of assays disclosed a characteristic cytogenetic mosaicsm in HGPS, with a distinctive pattern of complex, chromosome aberrations. In particular, chromosome 11 and X alterations were observed at a high frequency. This data suggested that HGPS displays features of chromosomal instability (CIN). There are several mechanisms which can lead to CIN; one such pathway includes disruption of the apparatus responsible for accurate chromosome division during mitosis. To assess the possibility that abnormalities in mitosis was involved in HGPS associated CIN, two different staining methods were employed to examine the spindles and centrosomes. These experiments were conclusive that mitotic spindle abnormalities were a mode of CIN induction in HGPS. In the second part of the study, the work was aimed at investigating the role of free radical damage in the HGPS premature ageing phenotype. Mitochondrial DNA is hypothesised to be particularly sensitive to the damaging effects of free radicals, and thus the levels mtDNA mutation were examined in HGPS relative to age – matched controls. The results showed that deletions were augmented in HGPS as compared to other children; a finding that was thought to reflect the inefficient antioxidant systems operating in HGPS fibroblasts.
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Chan, Wing Lee [Verfasser]. "Molecular basis of Gerodermia Osteodysplastica, a premature ageing disorder / Wing Lee Chan." Berlin : Freie Universität Berlin, 2014. http://d-nb.info/1046312812/34.
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Lees, Hayley Diane. "Molecular mechanisms of premature ageing in a worm model of human Werner syndrome." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:080df619-828b-4248-b03f-c4aeb31f1672.
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Investigating the biological basis of ageing is both fascinating and medically relevant, as we strive to understand both how organisms age, and how our knowledge might be put to good use in an increasingly long-lived human population. Despite the complexity of ageing biology, it is very striking that longevity, in a wide variety of organisms, can be modified by manipulating single genes. In this thesis, I investigate phenotypes associated with mutations in C. elegans homologues of human WRN, the gene mutated in the progeroid Werner syndrome (WS). Mutant phenotypes in the worm recapitulate aspects of the pathophysiology observed in WS patients, including premature ageing, genomic instability, and sensitivity to DNA damaging agents. wrn-1 overexpression, on the other hand, appears to enhance longevity, suggesting that wrn-1 acts as a bona fide anti-gerontogene. The combination of wrn-1 mutations with mutation in the worm p53 homologue, cep-1, unexpectedly triggers a novel and very striking enhanced lifespan and healthspan phenotype, termed synthetic super-viability (SSV). The SSV phenotype is modulated by various environmental inputs such as temperature stress. The data presented here can be incorporated into a model in which stress sensing (involving p53) is the crucial determinant of longevity outcomes. Several theories of ageing incorporate the idea that 'that which does not kill us, makes us stronger' - encapsulated in a biological sense in the idea of hormesis, a physiological shift in response to stress. Here, this hypothesis is expanded to include the notion that intrinsic responses to stress may themselves act to limit lifespan - too much of a good thing can be bad.
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Wredenberg, Anna. "Mitochondrial dysfunction in ageing and degenerative disease /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-311-5/.
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Chapko, Dorota. "Life-course determinants of resilience to cognitive ageing : empirical evidence and policy implications." Thesis, University of Aberdeen, 2016. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=230978.
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Introduction: Understanding the life-course determinants of resilience to brain ageing could significantly reduce the burden of cognitive impairment and dementia on individuals, heath care providers, and societies. The focus of this work is the concept of cognitive reserve (CR), which implies that some individuals are able to remain cognitively healthy despite the accumulation of age-related neuropathology. Methods: The determinants of brain structure and function were statistically modelled using three ongoing ageing cohort studies [Aberdeen Birth Cohort of 1936 (ABC1936), Aberdeen Children of the 1950s (ACONF), The Three-City French Cohort (3C)]. First, I performed a systematic literature review to identify life-course determinants of CR. Then, I examined whether other potentially modifiable life-course factors such as birth weight, mid-life occupational profile, and late-life social relationships and technology use provided individuals with greater CR. I modelled data in STATA and SPSS/AMOS. Results: I found that the effects of low birth weight and pre-term delivery on cognitive functions persists into mid-life (ACONF). I showed that childhood intelligence at age 11 has almost twice the protective effect on cognitive ageing than mid-life occupation (ABC1936). The quantity and quality of social relationships (3C), and the aspects of technology use in latelife (ABC1936) did not provide greater CR. Conclusion: Early-life factors contribute to later-life brain health. A major implication of this work is that studies and/or programs should consider a life-course perspective (with a focus on early-life) to accurately assess and to improve the brain health of older adults.
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Fontes, Larissa. "Análise da expressão do gene FMR1 no ovário." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/41/41131/tde-25042012-102756/.
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Este estudo teve como objetivo geral a análise do gene FMR1 (Fragile X Mental Retardation gene 1) quanto a sua relação com a insuficiência ovariana primária (Fragile X-related Primary Ovarian Insufficiency, FXPOI). No Capítulo I, apresentamos revisão da literatura sobre FXPOI. A pré-mutação do gene FMR1 constitui a mais frequente causa genética de predisposição para menopausa precoce e entre os casos familiais, cerca de 10% estão associados à pré-mutação do gene FMR1. Entretanto, pouco se conhece sobre a expressão do gene no ovário de mamíferos e os mecanismos pelos quais a pré-mutação causa POI permanecem desconhecidos. O Capítulo II apresenta os resultados do estudo da expressão do gene FMR1 nos ovários adultos, humano e murino. As enormes dificuldades inerentes à obtenção e ao estudo de células germinativas femininas nos levaram a estudar células da granulosa humana (HGC), que são de fácil obtenção, como subprodutos de procedimentos de fertilização in vitro. Também estudamos a expressão do Fmr1 em células da granulosa de camundongos da linhagem CD1 (MGC), coletadas nos ovidutos, após estimulação da ovulação. As células da granulosa interagem intensamente com os ovócitos durante a foliculogênese, transmitindo sinais através do ovário e apoiando o crescimento e a maturação dos ovócitos durante as últimas fases do crescimento folicular. É, portanto, possível que alterações celulares induzidas pela pré-mutação do gene FMR1 nas HGC afetem o crescimento folicular, a taxa de ovulação e a fecundidade. Padronizamos os protocolos de isolamento e de cultivo das HGC do fluido folicular e confirmamos a origem das células isoladas pela expressão de marcadores de HGC, por RT-PCR, e pela natureza lipídica dos grânulos citoplasmáticos, pela coloração com o corante lipofílico DiI. Demonstramos, por RT-PCR que as HGC isoladas do líquido folicular expressam o mRNA do FMR1. Em camundongos, também por RT-PCR, evidenciamos a expressão do mRNA do Fmr1 em ovócitos e nas MGC, coletados do oviduto após hiper-estimulação da ovulação. Por hibridação in situ de RNA em HCG cultivadas, detectamos o mRNA do FMR1 disperso no citoplasma e no núcleo, concentrado em regiões cujas características indicaram ser nucléolos. Essa mesma distribuição foi observada em fibroblastos cultivados. Essa provável localização nucleolar sugere que o transcrito do FMR1, nessas células, constitua ribonucleoproteínas mensageiras, para seu direcionamento do nucléolo para sítios citoplasmáticos específicos, onde ocorre sua tradução. Verificamos, por Western blotting, que as HGC expressam, em níveis elevados, isoformas da FMRP, com massa molecular entre 60 e 95 kDa. Determinamos a localização subcelular da FMRP nas HGC e da Fmrp nas MGC, por imunocoloração. Os sinais de hibridação foram visualizados dispersos, em grânulos finos, no citoplasma das HGC e das MGC, de maneira semelhante ao padrão de distribuição da proteína em neurônios. Nos filopódios das MGC, observamos marcação concentrada em alguns pontos, de forma semelhante ao padrão, previamente descrito, de distribuição da Fmrp em espinhas dendríticas de neurônios de hipocampo de rato, constituindo grânulos de RNA, que promovem o transporte de mRNA e controlam a tradução. O padrão de distribuição semelhante entre neurônios e MGC pode refletir similaridade da função da Fmrp nos dois tecidos. A indução de estresse oxidativo nas HGC por tratamento com arsenito sódico, levou a proteína a deixar de ter distribuição citoplasmática difusa e passar a fazer parte de grânulos de estresse perinucleares, colocalizando-se com TIA-1, marcador dessas estruturas. Resultados semelhantes foram anteriormente obtidos em células HeLa e no hipocampo de rato. Esses resultados apoiam a hipótese de que a FMRP participa do mecanismo transitório de parada da tradução após estresse. No Capítulo III, descrevemos nossas tentativas para obtenção de linhagem de células tronco embrionárias (ESC) de camundongo knockin (KI) quanto a pré-mutação do gene Fmr1. Para a obtenção de embriões KI, fêmeas selvagens (WT; linhagem C57) foram cruzadas com machos KI (linhagem C57/BL6) e fêmeas KI foram cruzadas com machos WT. Pretendíamos comparar a expressão do gene Fmr1 na linhagem de ESC KI e linhagem de ESC WT, inclusive durante a diferenciação Não tivemos sucesso, o que pode ser atribuído às dificuldades inerentes à obtenção de ESC. No acompanhamento dos primeiros quatro dias do desenvolvimento in vitro dos embriões, alterações de clivagem e parada de desenvolvimento foram mais frequentemente observadas nos embriões obtidos de fêmeas KI. Entretanto as taxas médias de sobrevivência de ovócitos para blastocistos e de embriões com 8 a 16 células para blastocistos não diferiram estatisticamente entre as fêmeas KI e selvagens; a grande variabilidade entre o número de blastocistos obtidos por fêmea e o pequeno número delas nos grupos KI (seis) e selvagem (sete) indicam que esses resultados devem ser interpretados com cautela. A análise da proteína Fmrp nos blastocistos, por imunocoloração, mostrou distribuição provavelmente citoplasmática, com padrão granular de marcação, sendo as granulações mais frequentes nos blastocistos de fêmeas WT, porém mais grosseiras nos blastocistos de fêmeas KI. Esse conjunto de dados é sugestivo de efeito da pré-mutação do gene Fmr1 em fêmea murina sobre o início do desenvolvimento de seus embriões. Esse aspecto necessita investigação mais aprofundadaThis study aimed at investigating the FMR1 gene (Fragile X Mental Retardation gene 1), regarding its relationship with primary ovarian insufficiency (Fragile X-related Primary Ovarian Insufficiency, FXPOI). In Chapter I, we present a literature review on FXPOI. The FMR1 premutation is the most frequent genetic cause of predisposition to premature ovary insufficiency (POI) and, among the POI familial cases, about 10% are associated with the FMR1 gene premutation. However, little is known about the gene expression in the mammal ovary, and the mechanisms by which the premutation causes POI remain unknown. Chapter II presents the study of the FMR1 gene expression in the human and murine adult ovaries. The enormous difficulties inherent in obtaining and studying female germ cells led us to study human granulosa cells (HGC), which are easily obtained as byproducts of in vitro fertilization procedures. We also studied the FMR1 expression in granulosa cells of mice of the CD1 strain (MGC), collected from the oviducts after ovulation induction. Granulosa cells interact functionally with oocytes during folliculogenesis, transmitting signals through the ovary and supporting growth and maturation of oocytes during the later stages of follicular growth. It is, therefore, possible that cellular changes induced by the FMR1 premutation in HGCs affect follicular growth, ovulation rate and fecundity. We standardized protocols for isolation and culture of HGCs obtained from follicular fluid and confirmed the origin of the isolated cells by the expression of HGC markers, using RT-PCR, and by the lipid nature of the cytoplasmic granules, as demonstrated by the staining with the lipophilic dye DiI. We demonstrated, by RT-PCR, that HGCs isolated from follicular fluid express the FMR1 mRNA. In mice, also by RT-PCR, we detected the Fmr1 mRNA in oocytes and in the MGCs, collected from the oviduct after ovulation hyperstimulation. Using RNA in situ hybridization on cultured HCGs, we detected the FMR1 mRNA dispersed in the cytoplasm and, in the nucleus, concentrated in regions whose features indicated to be nucleoli. This same distribution was observed in cultured fibroblasts. This probable nucleolar localization of the FMR1 transcript in these cells suggests that it constitutes messenger ribonucleoproteins for further targeting to specific cytoplasmic sites where translation occurs. We verified, by Western blotting, that HGCs express high levels of the main FMRP isoforms, with molecular mass between 60 and 95 kDa. We determined the FMRP subcellular localization in HGCs and that of Fmrp in MGCs, by immunostaining. The hybridization signals were seen scattered in fine granules in the cytoplasm of both HGCs and MGCs, in a pattern of distribution similar to that observed in neurons. In the MGC filopodia, the protein labeling was concentrated at some sites, similar to the previously described pattern of Fmrp distribution in neuronal dendritic spines of rat hippocampus, where it is part of RNA granules, promoting mRNA transport and translation control. The similar distribution pattern between neurons and MGC may reflect the similarity of FMRP function in both tissues. The induction of oxidative stress in the HGC by treatment with sodium arsenite led the protein to leave its diffuse cytoplasmic distribution to become part of perinuclear stress granules, co-localized with TIA-1, a marker of these structures. Similar results were previously obtained in HeLa cells and in rat hippocampus. These results support the hypothesis that FMRP participates in the mechanism of the transient translation arrest after stress. In Chapter III, we describe our attempts to obtain an embryonic stem cell line (ESC) from knock-in mice (KI) for the FMR1 premutation. To obtain KI embryos, wild females (WT, strain C57) were crossed with males KI (strain C57/BL6), and KI females were crossed with WT males. We planned to compare the expression of the fmr1 gene in the ESCs from the KI and WT strains, including during differentiation. We did not succeed in obtaining an ESC KI line, which can be attributed to difficulties inherent to the procedure. At follow-up of the first four days of in vitro development of embryos, changes in cleavage and developmental arrest were more frequently observed in embryos obtained from KI females. Meanwhile, the average survival rates of oocytes to blastocysts, and 8-16 cell embryos to blastocysts were not statistically different between the KI and WT females. The great variability among the numbers of blastocysts obtained per female and the small size of the KI (six females) and WT (seven females) groups indicate that these results should be interpreted with caution. Immunostaining analysis of the Fmrp in blastocysts showed a probably cytoplasmic distribution, with a granular pattern of labeling, the grains being more common in blastocysts from WT females, but coarser in blastocysts from KI females. These data are suggestive that the Fmr1 premutation in murine females affects the early development of their embryos. This aspect needs further investigation
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Urli, Laureline. "Les cellules sénescentes sont-elles des caractéristiques communes à la maladie d'Alzheimer et à l'apnée du sommeil ?" Electronic Thesis or Diss., Sorbonne université, 2024. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2024SORUS085.pdf.
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La maladie d'Alzheimer (MA), maladie neurodégénérative, progressive et incurable entraînant un déclin cognitif est caractérisée par l'accumulation extracellulaire de plaques amyloïdes et d'agrégats intracellulaires de protéines Tau dans les neurones. Ces deux types de lésions apparaissent initialement dans l'hippocampe et se répandent progressivement dans les autres régions du cerveau. L'âge est le principal facteur de risque de la MA, mais d'autres facteurs de risque tels que les troubles du sommeil sont également mis en cause dans le développement de cette pathologie. Le syndrome d'apnée du sommeil (SAS), caractérisé par une fragmentation du sommeil et une hypoxie intermittente (HI) est fréquemment retrouvé chez les patients atteints de la MA et les personnes souffrant de SAS sont plus enclines à développer de troubles cognitifs et des pathologies neurodégénératives. Expérimentalement, l'HI provoque du stress oxydant et une neuroinflammation, en particulier au niveau de l'hippocampe, pouvant entrainer et/ou être le corollaire d'une sénescence cellulaire et d'un vieillissement précoce.Au cours de ce travail de thèse, nous nous sommes intéressés à l'HI chronique comme inducteur potentiel de la sénescence dans l'hippocampe en analysant les marqueurs de sénescence et du secrétome inflammatoire associé à la sénescence (SASP) chez des souris sauvages soumises à une HI chronique pendant six semaines. Afin de déterminer l'impact de la sénescence induite par l'HI sur le développement de la MA, nous avons également travaillé sur des cohortes de souris PS1Ki, modèles de la MA.Nous montrons des effets délétères de l'exposition à l'HI chronique chez des souris adultes par la mise en évidence de l'altération de la mémoire de reconnaissance d'objet, de l'induction d'un stress oxydant et de l'augmentation de marqueurs de sénescence cellulaire et du SASP dans l'hippocampe, notamment dans le gyrus denté et la région CA3 de la corne d'Ammon. Les effets sont graduels avec l'âge des souris et les neurones semblent être particulièrement impactés par cet état de sénescence. Chez les souris PS1Ki, les altérations, déjà révélées dans des conditions de normoxie sont exacerbées par l'HI chronique. En effet, en plus d'être présentes dans l'hippocampe, les cellules sénescentes s'accumulent dans les cortex entorhinal et préfrontal en fonction de l'âge des souris.L'ensemble de nos résultats suggèrent que le processus de sénescence cellulaire serait un facteur clé de la transition du vieillissement cérébral physiologique vers la pathologie neurodégénérative. Un traitement sénolytique visant à éliminer les cellules sénescentes pourrait être envisagé pour améliorer les traitements actuels du SAS et prévenir un vieillissement cérébral prématuré accélérant la physiopathologie et les symptômes de la MAAlzheimer's disease (AD), a neurodegenerative, progressive and incurable diseaseleading to cognitive decline is characterized by extracellular Aβ plaques and intracellular neuronal tau-containing neurofibrillary tangles.Both of these lesions appear in the hippocampus and spread to other regions of the brain. Age is the primary risk factor, but other risk factors such as sleep disorders are also implicated in the development of AD. Obstructive sleep apnea syndrome (OSAS), characterized by sleep fragmentation and intermittent hypoxia (IH), is frequently found in AD patients, and people with OSAS are more prone to developing cognitive disorders and neurodegenerative pathologies. Experimentally, IH induces oxidative stress and neuroinflammation, specially, in the hippocampus, which may lead to and/or be a consequence of cellular senescence and premature aging.In this thesis work, we focused on chronic IH as a potential inducer of senescence in the hippocampus by analyzing senescence markers and the senescence-associated secretory phenotype (SASP) in mice subjected to chronic IH for six weeks. To determine the impact of IH-induced senescence on the development of AD, we also worked on cohorts of PS1Ki mice, AD models.We demonstrate detrimental effects of chronic IH exposure in adult mice by showing impairment in object recognition memory, induction of oxidative stress, and increased markers of cellular senescence and SASP in the hippocampus, particularly in the dentate gyrus and CA3. These effects are age-dependent and neuronal cells appear to be particularly affected by this state of senescence. In PS1Ki mice, alterations, already revealed under normoxic conditions, are exacerbated by chronic IH. Indeed, in addition to being present in the hippocampus, senescent cells accumulate in the entorhinal and prefrontal cortices depending on the age of the mice.Collectively, our results suggest that the process of cellular senescence may be a key factor in the transition from physiological brain ageing to neurodegenerative pathology. Senolytic treatment targeting senescent cells could be considered to improve current OSAS treatments and to prevent premature brain ageing, thereby accelerating the pathophysiology and symptoms of AD
Books on the topic "Premature ageing"
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Goodrum, Glen. Premature Ageing: Premature Aging Facts You Wish You Knew. Independently Published, 2019.
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Goodrum, Glen. Stop or Reverse Premature Ageing: Knowledge Is Golden. Independently Published, 2019.
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Ferreira, Isabel, and Jos WR Twisk. Physical activity, cardiorespiratory fitness, and cardiovascular health. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0017.
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It is now recognized that cardiovascular disease (CVD) is partly a paediatric problem, i.e. the onset begins in childhood, although clinical symptoms may not become apparent until later in life. Therefore, from a primary prevention point of view, the extent to which physical activity or physical fitness in childhood may deter this process is of utmost importance. Although physical activity and CRF at a young age have not been directly linked to the incidence of CVD, evidence thus far supports cardiovascular health benefits of early higher physical activity and CRF levels on cardiometabolic risk factors like obesity, blood pressure, insulin resistance, and their maintenance throughout the course of life. By affecting these intermediary pathways, lifelong (high-intensity) physical activity may also deter the age-related decreases in CRF and related signs of premature arterial ageing.
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Raggi, Paolo, and Luis D’Marco. Imaging for detection of vascular disease in chronic kidney disease patients. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0116.
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The well-known severity of cardiovascular disease in patients suffering from chronic kidney disease (CKD) requires an accurate risk stratification of these patients in several clinical situations. Imaging has been used successfully for such purpose in the general population and it has demonstrated excellent potential among CKD patients as well. Two main forms of arterial pathology develop in patients with CKD: atherosclerosis, with accumulation of inflammatory cells, lipids, fibrous tissue and calcium in the subintimal space, and arteriosclerosis. The latter is characterized by accumulation of deposits of hydroxyapatite and amorphous calcium crystals in the muscular media of the vessel wall, and is believed to be more closely associated with alterations of mineral metabolism than with traditional atherosclerosis risk factors. The result is the development of what appears to be premature arterial ageing, with loss of elastic properties, increased stiffness, and increased overall fragility of the arterial system. Despite intensifying research and increasing awareness of these issues, the underlying pathophysiology of the aggressive vasculopathy of CKD remains largely unknown. As a consequence, there are currently very limited pathways to prevent progression of vascular damage in CKD. The indications, strengths and weaknesses of several imaging modalities employed to evaluate vascular disease in CKD are described, focusing on coronary arterial circulation and the peripheral arteries, with the exclusion of the intracranial arteries.
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Abhishek, Abhishek, and Michael Doherty. Investigations of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0051.
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Joint aspiration and microscopic examination of the aspirated synovial fluid remains the gold standard for the diagnosis of calcium pyrophosphate crystal deposition (CPPD). If synovial fluid aspiration is not feasible, plain radiography and/or ultrasound scanning may be used to detect chondrocalcinosis (CC) which predominantly occurs due to calcium pyrophosphate (CPP) crystals, and this can be used as a diagnostic surrogate for CPPD as suggested by the EULAR Task Force. Acute CPP crystal arthritis often associates with a brisk acute phase response (elevated C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR), plasma viscosity) and neutrophilia. A mildly raised CRP and/or ESR may be present in chronic CPP crystal inflammatory arthritis. On the contrary, asymptomatic CC, or CPPD with osteoarthritis does not cause raised acute phase reactants. As CPPD most commonly occurs due to increasing age and osteoarthritis, investigations to screen for underlying metabolic abnormalities should be carried out in those with early-onset CPPD (under 55 years), or in those with florid polyarticular CC. As hyperparathyroidism gets more common with ageing its presence should be specifically sought in all age groups. Tests for other predisposing metabolic conditions should only be carried out in the presence of specific clinical features. Genotyping for mutations, especially in the ANKH gene, may be warranted in those with a family history of premature CPPD and no evidence of inherited metabolic predisposition, but such testing is unavailable to most clinicians.
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Hunt, Beverley J. Haemostatic agents in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0052.
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Antifibrinolytics can prevent excessive bleeding during surgery and are also used to reduce established bleeding. By blocking the effects of plasmin, they prevent premature clot breakdown and enhance clot stability. The CRASH-2 trial showed that use of tranexamic acid in those with or at high risk of traumatic haemorrhage reduced mortality by 9%. Importantly for a drug that affects haemostasis, there appears to be no increased risk of either arterial or venous thromboembolism. Aprotinin while an excellent agent in reducing bleeding disproves previous assumption that reducing bleeding improves outcome, for the BART study demonstrated an increased mortality compared with tranexamic acid and EACA. It is still used occasionally in very high risk cardiac surgery patients. DDAVP (desmopressin) stimulates platelet function and is of use in patients with uraemia, although needs to be given with an antifibrinolytics, because it does also stimulate fibrinolytic activity. Off-license use of rVIIa is waning, clinical trials have as yet failed to show major benefit. Moreover, there is a high rate of arterial thrombosis after using rVIIA.
Book chapters on the topic "Premature ageing"
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Toriello, Helga V. "Premature Ageing Syndromes." In Harper's Textbook of Pediatric Dermatology, 134.1–134.19. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444345384.ch134.
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Debacq-Chainiaux, Florence, Randa Ben Ameur, Emilie Bauwens, Elise Dumortier, Marie Toutfaire, and Olivier Toussaint. "Stress-Induced (Premature) Senescence." In Cellular Ageing and Replicative Senescence, 243–62. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26239-0_13.
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Du, Hong-Yan, Monica Bessler, and Philip J. Mason. "Telomerase Mutations and Premature Ageing in Humans." In Telomeres and Telomerase in Ageing, Disease, and Cancer, 77–107. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-73709-4_5.
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Pascual-Castroviejo, Ignacio, and Martino Ruggieri. "Progeria and Progeroid Syndromes (Premature Ageing Disorders)." In Neurocutaneous Disorders Phakomatoses and Hamartoneoplastic Syndromes, 847–78. Vienna: Springer Vienna, 2008. http://dx.doi.org/10.1007/978-3-211-69500-5_54.
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Hartwig, W. "Lifespan of Cattle and Horses Under Various Climatic Conditions and the Reasons for Premature Culling." In Ciba Foundation Symposium - The Lifespan of Animals (Colloquia on Ageing, Vol. 5), 57–71. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470715253.ch5.
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Gittenberger-de Groot, Adriana C., Regina Bokenkamp, Vered Raz, Conny van Munsteren, Robert E. Poelmann, Nimrat Grewal, and Marco C. DeRuiter. "Progerin Expression during Normal Closure of the Human Ductus Arteriosus: A Case of Premature Ageing?" In Etiology and Morphogenesis of Congenital Heart Disease, 245–51. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-54628-3_34.
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Ziegenhain, Patrick. "Getting Old Before Getting Rich (and not Fully Realizing It): Premature Ageing and the Demographic Momentum in Southeast Asia." In Global Political Demography, 167–93. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-73065-9_7.
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van Oostwaard, Marsha, and Andréa Marques. "Osteoporosis and the Nature of Fragility Fracture: An Overview." In Perspectives in Nursing Management and Care for Older Adults, 17–34. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-33484-9_2.
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AbstractOsteoporosis is a common, chronic, systemic skeletal disease that is characterised by low bone mass and deterioration of the microarchitecture of bone tissue, with a consequent increase in bone fragility and risk of fracture. The number of people suffering from osteoporosis and high risk of fractures is increasing globally, probably as a result of global ageing and longer life expectancy.Typically, fractures in patients with osteoporosis occur at the following locations: vertebral (spine), proximal femur (hip), distal forearm (wrist) and proximal humerus (upper arm). Bone loss occurs silently and progressively without signs or symptoms until fractures occur, so patients are often unaware that they may have osteoporosis and are at risk of fractures.Osteoporosis is a devastating condition that can lead to pain, severe disability and premature death from fracture. Nurses, alongside other practitioners, play a key role in the prevention of osteoporosis and fragility fractures and can be envisaged in case finding, risk assessment and management and education after diagnosis. The aim of this chapter is to provide an overview of the link between osteoporosis and fractures and explore the diagnosis and treatment of osteoporosis.
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De Pauw, Ines, Carolien Boeckx, and An Wouters. "Mechanisms of Cetuximab Resistance and How to Overcome It." In Critical Issues in Head and Neck Oncology, 21–51. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_3.
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AbstractDeregulated or increased signalling of the epidermal growth factor receptor (EGFR) plays an integral role in the development of various cancer types, including head and neck squamous cell carcinoma (HNSCC), making it a compelling drug target. However, after initially promising results of EGFR-targeted therapies, such as the monoclonal antibody cetuximab, it became clear that both intrinsic and acquired therapeutic resistance are major roadblocks in the field of personalised cancer treatments.In order to unravel and overcome resistance to cetuximab, at least two strategies can be adopted.Firstly, therapeutic resistance to anti-EGFR therapy may arise from mechanisms that can compensate for reduced EGFR signalling and/or mechanisms that can modulate EGFR-dependent signalling. In this chapter, we discuss which mechanisms of cetuximab resistance are already known and which ones deserve further investigation. This enhanced knowledge will guide us to rationally design and test novel combination therapies that overcome resistance to EGFR-targeting agents in cancer treatment.Secondly, an urgent need remains to develop novel targeted treatments for single-agent or combined therapy use. In this view, due to the particular mode of activation of the EGFR receptor, involving ligand-induced homo- and heterodimerization of the four HER receptors, an increased inhibition scope of HER receptors most likely results in a more potent blockade of the HER network, preventing premature emergence of resistance and leading to a more pronounced therapeutic benefit. We discuss two multitargeted compounds, being MEHD7945A (duligotuzumab) and afatinib, in this chapter.Despite the huge efforts to unravel the molecular landscape of HNSCC, the main clinically validated target remains EGFR. However, immune checkpoints, like programmed cell death protein 1 (PD-1), are gaining clinical approvals as well. We underscore the importance of adopting rational drug combinations to enhance the therapeutic effect of the EGFR-inhibitor cetuximab and highlight the ongoing search for predictive biomarkers, with the ultimate goal of delivering individualized cancer therapy to HNSCC patients.
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Davis, Colin J., and Gerard S. Conway. "Premature ovarian failure and ovarian ageing." In Paediatric and Adolescent Gynaecology, 373–88. Cambridge University Press, 2004. http://dx.doi.org/10.1017/cbo9780511527036.031.
Full textConference papers on the topic "Premature ageing"
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Clements, David, and Pierluigi Mancarella. "Risk of cable overheating and premature ageing due to load control measures." In 2017 IEEE Manchester PowerTech. IEEE, 2017. http://dx.doi.org/10.1109/ptc.2017.7981024.
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Wang, Kun, Avinash Das, Zheng-Mei Xiong, Kan Cao, and Sridhar Hannenhalli. "Identification of gene clusters with phenotype-dependent expression with application to normal and premature ageing." In BCB'13: ACM-BCB2013. New York, NY, USA: ACM, 2013. http://dx.doi.org/10.1145/2506583.2506652.
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Aljaroudi, Alireda, Premkumar Thodi, Ayhan Akinturk, Faisal Khan, and Mike Paulin. "Application of Probabilistic Methods for Predicting the Remaining Life of Offshore Pipelines." In 2014 10th International Pipeline Conference. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/ipc2014-33431.
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When offshore pipelines are approaching the end of their design life or have gone beyond their design life, their condition could possibly threaten oil flow continuity (through leak or rupture) as well as become a potential safety or environmental hazard. Some of the pipelines may show signs of deterioration and ageing due to corrosion, cracking or other damage mechanisms. Any assets, such as the pipeline, may be desired to continue transporting hydrocarbons beyond its design life due to increased oil and gas demand, due to unforeseen increased oil and gas reserves, or due to upgrade where additional assets are tied-into the existing pipeline system. Other situations may force operators to maintain the pipeline’s design life in spite of premature ageing of the pipe wall caused by the increased corrosion growth or other anomalies. Hence, there may be a need to assess the remaining life of pipeline in order to determine if it is capable of coping with current and future operational demand. The first task in the assessment process is to identify degradation mechanisms and their rate of growth, then estimate uncertainties in the collected data concerning pipeline flaw geometry, pipeline mechanical properties and operating characteristics. Based on the collected data and the assessment, the probability and consequence of failure can be determined. The remaining life of a pipeline is the time it takes the pipeline to fail or exceed the target failure probability. This paper presents a methodology for assessing the condition of ageing pipelines and determining the remaining life that supports extended operation without compromising safety and reliability. Applying this methodology would facilitate a well-informed decision that enables decision makers to determine the best strategy or adequate course of action for assessing and maintaining the integrity of ageing pipelines.
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Bartonicek, Jaroslav, Lubomir Junek, Milan Vrana, and Stanislav Vejvoda. "Safety Approach and Ageing Management in Czech Rules and Standards." In ASME 2009 Pressure Vessels and Piping Conference. ASMEDC, 2009. http://dx.doi.org/10.1115/pvp2009-77653.
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There are basic technical (protection) objectives determined for assurance of nuclear power plant safety and the following generally belong among them: - Reactor pressure vessel shut down, - Long term maintenance of sub-critical state, - Long term cooling, - Prevention of radioactivity leakage. To ensure these objectives multi-step concept of deep protection is used for the design of a nuclear power plant and it includes: - Prevention of failures during normal and abnormal operation, - Control of failures and their consequences, - Minimizing of risks during accidents. Failure of operating systems is conservatively postulated for determination of systems requirements using for failure ensure as piping breaks. Ensure of these postulated failures come under multilevel safety approach. Failure consequences should be mainly ensured by design measures as separation of high energy piping, whip piping restrains etc. Efficiency of design measures have to be demonstrated. This passive safety procedure during design of new NPP can be applied. Application of this passive procedure for operating NPP can lead to technical and economical problems. It can be done by non precise and non sufficient requirements, current standards and documents. Leak before break concept (LBB) is very often out due to break operation conditions for successful concept usage. Beak preclusion concept was defined in Germany thirty years ago. The concept is developed from this time. Required quality of SSC is basic of this concept. The quality has to be received during manufacturing and assembly of new components to system or the quality passport has to be documented for SSC in operation before enlistment to the concept. During next operation they are sufficient and redundant measures necessary to control and to manage ageing phenomena (conceptual, technological, and physical) for exclusion of premature ageing. This proactive approach is also basic of documents from the last year’s required ageing and lifetime management. In Czech NPPs postulated failures and their consequences in accord with producer knowledge state at that time were insured. Postulated failures and their consequences were insured partly design measures and partly design supposed quality too. It is very difficult to realize new requirements on needed design provision on NPP in operation. It is impracticable in any cases. Needed national law for approach application exists in Czech from 1997. Regulation on lifetime management and national nuclear standards with specific requirements exist in Czech too. There are backgrounds for application proactive approach as it is used in Germany NPPs. New safety approach was provided in Czech NPPs. SSC are separated into three groups on the base safety approach: - SSC must not fail (guarantee of quality), - SSC may fail in rare case (preventative maintenance), - SSC may fail (failure orientated maintenance). The contribution deals about new Czech safety concept aspects, boundary conditions, needed document and proactive measures.
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Fan, Zimo, Andrew Steptoe, and Olesya Ajnakina. "OP55 The effect of high polygenic propensity for ADHD and socioeconomic factors on increasing timing to premature mortality: evidence from English Longitudinal Study of Ageing." In Society for Social Medicine Annual Scientific Meeting Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jech-2022-ssmabstracts.54.
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De Cristofaro, Sarah, Luca Rizzi, Dario Cardone, Lisa Berti, and Ubaldo Spina. "Smart Relax Armchair - a solution for active and safe ageing at home." In 15th International Conference on Applied Human Factors and Ergonomics (AHFE 2024). AHFE International, 2024. http://dx.doi.org/10.54941/ahfe1004896.
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The fact that people are living longer is a social and economic challenge for developed countries in the 21st century. An ageing society leads to an increase in the number of people living with multiple chronic conditions, facing the loss of independence and autonomy in daily activities and suffering social isolation caused by the pandemic or by the necessity of long-term care at home. The increasing incidence of sedentarism as well as prolonged immobility caused by long-stay settings (care home) is also a growing health concern. Indeed, spending too much time sitting daily could increase the incidence of postural changes and pressure ulcer formation, further reducing the physical, social, and emotional well-being of older adults.These problems are countable as significant contributors among many threats to elderly health and well-being leading to morbidity, disability, and premature death. In this view, Ambient Assisted Living solutions to monitor house routines of elderly patients and offer simple and healthy exercises daily are essential.This paper reports the results of the research activity conducted by the authors in collaboration with a well-known Italian sofa and armchair producer and health experts to develop an innovative solution for promoting active and safe ageing at home using a Smart Relax Armchair. The goal of the study was to introduce new smart functions to a Relax Armchair to help maintain a correct posture as well as to reduce the formation of bedsores by inducing frequent repositioning.To reach the goal, firstly the authors conducted a benchmarking analysis to identify the smart functions dedicated to health and wellbeing purposes already available on the market in the home furniture sector. A user-centred design methodology has been implemented to identify the Smart Relax Armchair functionalities, by involving industry experts, researchers in active ageing, biomedical engineers, and potential users since the early design stage. A dedicated design thinking tool has been used for users’ needs identification and translation into metrics (i.e. technical features). The Quality Function Deployment (QFD) method and tool have been used to rank such metrics and drive the design of the final product to meet users’ needs at best.3D virtual manikins, technical standards, ergonomic manuals, and the know-how of biomedical engineers and experts in Functional Recovery and Rehabilitation have been used to identify postural misbehaviour in daily life and potential intervention areas on a commercial Relax Armchair. Several active and passive solutions have been identified and tested to help maintain the correct posture and reduce the formation of bedsores. A sensorised mat has been used to assess changes in pressure distribution with respect to different layers of cushioning materials and to help select the specific pressure relief mattresses for bedsore prevention to be integrated into the final design.At the same time, an innovative protocol (anti-decubitus function) has been developed and implemented via ARDUINO to automatically induce a repositioning of the Smart Relax Armchair and thus changing the pressure distribution on the body, if the APP detects prolonged sitting.The protocol of the anti-decubitus function has been validated on a preliminary prototype thanks to a sensorised mat which demonstrated the effectiveness on pressure distribution variation, thus allowing the patenting of the idea.In order to promote active ageing at home, a set of simple rehabilitation exercises to be performed with the help of the Smart Relax Armchair has been designed and implemented in the APP specifically developed to control the product via a Smartphone or a vocal assistant.A final prototype including all the selected and developed solutions has been produced and a clinical trial will be conducted in the next months for the final validation of the product.The solutions developed and implemented on the Smart Relax Armchair have the potential to be applied to any model of Armchair or Sofa by the producer, thus changing the conventional paradigm of expensive products for active ageing only available for residential care facilities which cannot be afforded by those willing to age in place.
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Konrade, Daiga. "Carotenoid extract and oil from pumpkin (cucurbitta spp.) by-products for facial creams with high antioxidant activity." In Research for Rural Development 2023 : annual 29th international scientific conference proceedings. Latvia University of Life Sciences and Technologies, 2023. http://dx.doi.org/10.22616/rrd.29.2023.012.
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Nowadays, different sun protective creams are available in the market, but most of them contain harmful synthetic chemicals and minerals which can induce skin allergies and premature ageing. Usage of sunscreens and photoprotectors of natural origin and natural antioxidants can reduce skin damage caused by excessive sun exposure. The effectiveness of the use of β-carotene – vitamin’s A precursor against excessive irradiation caused by oxidative stress cell damages has been proven of its very good antioxidative properties and leading to sooner regeneration of the skin after several environmental damages. Carotenoids and high value oil can be extracted from pumpkin (Cucurbitta spp.) by-products – peel and seeds with SC CO2. The objective of this study was to incorporate pumpkin seed oil (PSO) and carotenoid extract (CE) from pumpkin by-products in to facial creams for UV protection. Two types of creams with PSO and CE were prepared emulsion o/w and w/o. A cream without extracts and natural ingredients was used as control sample. The sun protection factor values in vitro (SPF = 0.92 to 1.18), total content of carotenoids (TCC = 1.08–17.95 μg mL-1), β-carotene content (0.64–0.72 μg mL-1), total phenolics content (TPC = 62.64–95.82 mg GAE g-1), antiradical scavenging activity (11.26–43.66 %) and rheological behaviour of facial creams were determined. Although creams with CE and PSO show comparatively low SPF values, ß-carotene and phenolic compounds found in samples demonstrated very high antioxidant abilities valuable for skin protection.
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Banerjee, Sarbartha, Rajarshi Maitra, JyotiKamal Das, Abani Satapathy, Tiju Zachariah, Harpreet Singh Sandhu, and Jon Wang Abanikumar. "Assessment of River Mersey Steel Truss Bridge Using Non-Linear Finite Element Analysis." In IABSE Symposium, Istanbul 2023: Long Span Bridges. Zurich, Switzerland: International Association for Bridge and Structural Engineering (IABSE), 2023. http://dx.doi.org/10.2749/istanbul.2023.0480.
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<p>United Kingdom's railway bridges, a majority of which are more than 150 years old, is owned, managed, and maintained by Network Rail (NR). For the safe and efficient administration of the rail network, it is essential to have up-to-date capability information, for these ageing assets.</p><p>One example of its kind is River Mersey Bridge (SDJ2/38A). It was initially built in 1853 (Fig1) as a wrought iron tubular structure, later rebuilt with steel, except the central box girder, in the year 1908.</p><p>As per NR/GN/CIV/025, Level 1 assessment would not adequately depict the interaction between the main structural parts as expected for a structure of this age due to its known conservative nature. Therefore, it was beneficial to perform non-linear analysis as part of Level 2 assessment.</p><p>To properly simulate the structure and account for the potential failure modes of the structural components, this study took the complete structure into account. The paper also gives an insight into the mathematical model developed to capture all the section losses obtained from inspection for assessment report (IFA). The critical mode shape obtained from Eigen value buckling analysis was used as an input for initial imperfection to carry out the non-linear analysis (geometric and material). Discussions were carried out on the use of model to calculate the Von Mises stresses in Ultimate Limit State (ULS) and Service Limit State (SLS), areas of material yield, and the tendency of local premature buckling.</p><p>A comparison between linear and nonlinear analysis revealed a significant improvement in the stress distribution near the connection points, consequently the member stresses were found to be within acceptable limits. A continuous mesh improvement process was also followed to converge the analysis with successively coarser to finer meshes.</p><p>If any structural elements had shown material yield further recommendations have been made based on engineering judgement and modelling constraints. The non-linear assessment subsequently found the structure to be able to accommodate current load rating which was a betterment from the previous linear assessment.</p>
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Geurts, J., S. Nasi, T. A. Prolla, G. C. Kujoth, U. A. Walker, and T. Hügle. "SAT0071 Subchondral osteopenia but not cartilage damage is prevalent in knee joints of prematurely ageing mitochondrial dna mutator mice." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.1065.
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Prasad, Romesh, Matthew K. Swanson, and Young Moon. "Recovering From Cyber-Manufacturing Attacks by Reinforcement Learning." In ASME 2022 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/imece2022-93982.
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Abstract A Cyber-Manufacturing systems (CMS) is an integration of informational and operational entities that are synchronized with manufacturing processes to increase productivity. However, this integration enlarges the scope for cyber attackers to intrude manufacturing processes, which are called cyber-manufacturing attacks. They can have significant impacts on physical operations within a CMS, such as shutting down plants, production interruption, premature failure of products, and fatal accidents. Although research activities in this emerging problem have been increased recently, existing research has been limited to detection and prevention solutions. However, these strategies cannot ensure a continuous function of an attacked CMS. To ensure continuous functioning of a CMS, a robust recovery strategy must be developed and employed. Current research in recovery has been limited to feedback controllers with an assumption of a complete knowledge of a system model. To overcome this limitation, a recovery agent augmented by reinforcement learning was developed. This is to utilize the ability of reinforcement learning to handle sequential decisions and to proceed even without a complete knowledge of a system model. A virtual environment for recovery agents has been developed to assist efforts needed to obtain sample data, experiment various scenarios, and explore with reinforcement learning. Two cyber-manufacturing attack scenarios have been developed: (i) spoofing a stepper motor controlling additive manufacturing processes, (ii) disrupting the sequence of the pick and place robot. The recovery agent takes random actions by exploring its environment and receives rewards from the actions. After many iterations, it learns proper actions to take.