885 resultados para later life


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Vols. 4-20 are called "New ser., v. 1-17;" v. 21-34, "New ser., v. 18-31, old ser., v. 21-34."

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Later editions appeared under title: Literature and life.

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Crockett's attempt (ghost-written by Thomas Chilton) to correct erroneous impressions produced by Mathew St. Clair Clarke's The life and adventures of Colonel David Crockett of West Tennessee, which was published anonymously in 1833, and later reissued as Sketches and eccentricities of Colonel David Crockett of West Tennessee. Cf. introduction to the facsimile edition of the Narrative, edited by J.A. Shackford and S.J. Folmsbee, and published by the University of Tennessee Press.

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"Later years of General Grant: by Rev. O.H. Tiffany, D.D.": p. [477]-594.

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The proposed third volume was never published, although copyright claim is printed on back of t.-p. ("The Reminiscences copyright 1881 by Henry Stevens of Vermont." The records of the Copyright office do not bear out this statement) The material was later published in Transactions and proceedings of the Library association of the United Kingdom at their seventh annual meeting...1884. London, 1890 (p. 117-124: Twenty years reminiscences of Panizzi and the British museum, 1845-1865)

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The most commonly observed severe lung injuries in early life are the respiratory distress syndrome in premature infants and the acute respiratory distress syndrome in children. Both diseases are characterised by alveolar instability, fluid filled airspace and some degree of airway obstruction. In the acute phase, collapsed alveoli can be reopened with positive end-expiratory pressure and lung recruitment. New insight into the physiology of lung recruitment suggests that the shape of the pressure–volume curve is defined by the change in rate of alveolar opening and closing. Reduced lung volumes and severe ventilation maldistribution are found in the acute phase but may persist during childhood. Any severe lung injury in this early phase of life can cause significant structural and functional damage to the developing lung. Follow-up studies of children with chronic lung disease have shown that the functional abnormalities will improve but may still be present in later childhood.

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Background: The MacDQoL is an individualised measure of the impact of macular degeneration (MD) on quality of life (QoL). There is preliminary evidence of its psychometric properties and sensitivity to severity of MD. The aim of this study was to carry out further psychometric evaluation with a larger sample and investigate the measure's sensitivity to MD severity. Methods: Patients with MD (n = 156: 99 women, 57 men, mean age 79 ± 13 years), recruited from eye clinics (one NHS, one private) completed the MacDQoL by telephone interview and later underwent a clinic vision assessment including near and distance visual acuity (VA), comfortable near VA, contrast sensitivity, colour recognition, recovery from glare and presence or absence of distortion or scotoma in the central 10° of the visual field. Results: The completion rate for the MacDQoL items was 99.8%. Of the 26 items, three were dropped from the measure due to redundancy. A fourth was retained in the questionnaire but excluded when computing the scale score. Principal components analysis and Cronbach's alpha (0.944) supported combining the remaining 22 items in a single scale. Lower MacDQoL scores, indicating more negative impact of MD on QoL, were associated with poorer distance VA (better eye r = -0.431 p < 0.001; worse eye r = -0.350 p < 0.001; binocular vision r = -0.419 p < 0.001) and near VA (better eye r -0.326 p < 0.001; worse eye r = -0.226 p < 0.001; binocular vision r = -0.326 p < 0.001). Poorer MacDQoL scores were associated with poorer contrast sensitivity (better eye r = 0.392 p < 0.001; binocular vision r = 0.423 p < 0.001), poorer colour recognition (r = 0.417 p < 0.001) and poorer comfortable near VA (r = -0.283, p < 0.001). The MacDQoL differentiated between those with and without binocular scotoma (U = 1244 p < 0.001). Conclusion: The MacDQoL 22-item scale has excellent internal consistency reliability and a single-factor structure. The measure is acceptable to respondents and the generic QoL item, MD-specific QoL item and average weighted impact score are related to several measures of vision. The MacDQoL demonstrates that MD has considerable negative impact on many aspects of QoL, particularly independence, leisure activities, dealing with personal affairs and mobility. The measure may be valuable for use in clinical trials and routine clinical care. © 2005 Mitchell et al; licensee BioMed Central Ltd.

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Background: Food allergy is associated with psychological distress in both child and parent. It is unknown whether parental distress is present prior to clinical diagnosis or whether experiences at clinic can reduce any distress present. This study aimed to assess anxiety and depression in parents and the impact of suspected food allergy on the lives of families before and after a visit to an allergy clinic. Methods: One hundred and twenty-four parents visiting an allergy clinic for the first time to have their child assessed for food allergy completed a study-specific questionnaire and the Hospital Anxiety and Depression Scale; 50 parents completed these 4-6 wk later in their own home. Results: Most parents (86.4%) reported suspected food allergy had an impact on their family life prior to clinic attendance; 76% had made changes to their child's diet. 32.5% of parents had mild-to-severe anxiety before their clinic visit; 17.5% had mild-to-moderate depression. Post-clinic, 40% had mild-to-severe anxiety; 13.1% had mild-to-moderate depression. There were no significant differences in anxiety (p = 0.34) or depression scores (p = 0.09) before and after the clinic visit. Conclusions: Anxiety and depression is present in a small proportion of parents prior to diagnosis of food allergy in their child and this does not reduce in the short term after the clinic visit. Identification of parents at risk of suffering from distress is needed and ways in which we communicate allergy information before and at clinic should be investigated to see if we can reduce distress. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

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Previously, we have shown that a maternal low protein diet, fed exclusively during the preimplantation period of mouse development (Emb-LPD), is sufficient to induce by the blastocyst stage a compensatory growth phenotype in late gestation and postnatally, correlating with increased risk of adult onset cardiovascular disease and behavioural dysfunction. Here, we examine mechanisms of induction of maternal Emb-LPD programming and early compensatory responses by the embryo. Emb-LPD induced changes in maternal serum metabolites at the time of blastocyst formation (E3.5), notably reduced insulin and increased glucose, together with reduced levels of free amino acids (AAs) including branched chain AAs leucine, isoleucine and valine. Emb-LPD also caused reduction in the branched chain AAs within uterine fluid at the blastocyst stage. These maternal changes coincided with an altered content of blastocyst AAs and reduced mTORC1 signalling within blastocysts evident in reduced phosphorylation of effector S6 ribosomal protein and its ratio to total S6 protein but no change in effector 4E-BP1 phosphorylated and total pools. These changes were accompanied by increased proliferation of blastocyst trophectoderm and total cells and subsequent increased spreading of trophoblast cells in blastocyst outgrowths. We propose that induction of metabolic programming following Emb-LPD is achieved through mTORC1signalling which acts as a sensor for preimplantation embryos to detect maternal nutrient levels via branched chain AAs and/or insulin availability. Moreover, this induction step associates with changes in extra-embryonic trophectoderm behaviour occurring as early compensatory responses leading to later nutrient recovery. © 2012 Fleming et al.

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Background/Aims: To develop and assess the psychometric validity of a Chinese language Vision Health related quality-of-life (VRQoL) measurement instrument for the Chinese visually impaired. Methods: The Low Vision Quality of Life Questionnaire (LVQOL) was translated and adapted into the Chinese-version Low Vision Quality of Life Questionnaire (CLVQOL). The CLVQOL was completed by 100 randomly selected people with low vision (primary group) and 100 people with normal vision (control group). Ninety-four participants from the primary group completed the CLVQOL a second time 2 weeks later (test-retest group). The internal consistency reliability, test-retest reliability, item-internal consistency, item-discrimination validity, construct validity and discriminatory power of the CLVQOL were calculated. Results: The review committee agreed that the CLVQOL replicated the meaning of the LVQOL and was sensitive to cultural differences. The Cronbach's α coefficient and the split-half coefficient for the four scales and total CLVQOL scales were 0.75-0.97. The test-retest reliability as estimated by the intraclass correlations coefficient was 0.69-0.95. Item-internal consistency was >0.4 and item-discrimination validity was generally <0.40. The Varimax rotation factor analysis of the CLVQOL identified four principal factors. the quality-of-life rating of four subscales and the total score of the CLVQOL of the primary group were lower than those of the Control group, both in hospital-based subjects and community-based subjects. Conclusion: The CLVQOL Chinese is a culturally specific vision-related quality-of-life measure instrument. It satisfies conventional psychometric criteria, discriminates visually healthy populations from low vision patients and may be valuable in screening the local community as well as for use in clinical practice or research. © Springer 2005.

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Background: Environmental conditions early in life may imprint the circadian system and influence response to environmental signals later in life. We previously determined that a large springtime increase in solar insolation at the onset location was associated with a younger age of onset of bipolar disorder, especially with a family history of mood disorders. This study investigated whether the hours of daylight at the birth location affected this association. Methods: Data collected previously at 36 collection sites from 23 countries were available for 3896 patients with bipolar I disorder, born between latitudes of 1.4N and 70.7N, and 1.2S and 41.3S. Hours of daylight variables for the birth location were added to a base model to assess the relation between the age of onset and solar insolation. Results: More hours of daylight at the birth location during early life was associated with an older age of onset, suggesting reduced vulnerability to the future circadian challenge of the springtime increase in solar insolation at the onset location. Addition of the minimum of the average monthly hours of daylight during the first 3 months of life improved the base model, with a significant positive relationship to age of onset. Coefficients for all other variables remained stable, significant and consistent with the base model. Conclusions: Light exposure during early life may have important consequences for those who are susceptible to bipolar disorder, especially at latitudes with little natural light in winter. This study indirectly supports the concept that early life exposure to light may affect the long term adaptability to respond to a circadian challenge later in life.

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A life-course perspective is committed to the proposition that from conception to death, all human outcomes are the result of a continual interaction between the indi- vidual and all of the environments that he or she inhabits at any given point in time. Early development is a critical period, a window of time during the life course when a given exposure can have a critical or permanent in uence on later outcomes. But the impact of exposures upon outcomes does not end at any speci c point in time, inasmuch as life is a continuing interactive and adaptive process. We now know that what applies to human beings also applies to their genomes. The “outcome” of any gene at any given point in time (whether or not it is used to transcribe a particular protein, what form of that protein, and how much) is a product of the interaction between the gene and the multiple environments of which it is a part, which include the epigenome, the cell, the biological human, and the assorted environments he or she occupies (e.g., geographical, socioeconomic, ethnic, etc.). Early life experiences can permanently “reprogram” the epigenome and gene transcription with life-long behavioral consequences. At the same time, the epigenome as well as the genome continue to be environmentally responsive throughout the life course.

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Background. Individual trajectories toward aggression originate in early infancy, before there is intent to harm. We focused on infants who were contentious, i.e., prone to engage in anger and use of physical force with other people, and examined change in levels of contentiousness between 6 and 12 months of age with reference to later aggressive conduct problems.
Sample. The CCDS is a nationally representative sample of 321 firstborn children whose families were recruited from antenatal clinics in two National Health Service Trusts.
Method. Mothers, fathers, and a third family member or friend who knew infants well completed the Cardiff Infant Contentiousness Scale (CICS) at 6 months, which was stable form 6 to 12 months, and validated by direct observation of infants’ use of force against peers. Primary caregivers again completed the CICS at 12 months, and up to three informants completed the Child Behaviour Check List at mean ages of 36 and 84 months. We used Latent Transition Analysis to identify different groups of infants in respect to their patterns of contentiousness from 6 to 12 months.
Results
Three ordered classes of contentiousness from low to high were found at 6 and 12 months. Infants exposed to greater family adversity were more likely to move into the high-contentious class from 6 to 12 months. Higher contentiousness in infancy predicted more aggressive conduct problems at 33 months and thereafter.
Conclusions
Infants exposed to family adversity are already at disadvantage by 6 months and likely to escalate in their anger and aggressiveness over time.