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Search: WFRF:(Berglund M)

  • Result 951-960 of 1189
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951.
  • Leon, D A, et al. (author)
  • Failure to realise growth potential in utero and adult obesity in relation to blood pressure in 50 year old Swedish men.
  • 1996
  • In: BMJ (Clinical Research Edition). - : BMJ. - 0959-8138 .- 1468-5833. ; 312:7028, s. 401-6
  • Journal article (peer-reviewed)abstract
    • OBJECTIVES: To clarify the type of fetal growth impairment associated with increased blood pressure in adult life, and to establish whether this association is influenced by obesity and is mediated through impairment of insulin action.DESIGN: Cross sectional survey with retrospective ascertainment of size at birth from obstetric archives.SUBJECTS: 1333 men resident in Uppsala, Sweden, who took part in a 1970 study of coronary risk factors at age 50 and for whom birth weight was traced.MAIN OUTCOME MEASURES: Systolic and diastolic blood pressure at age 50.RESULTS: In the full study population for a 1000g increase in birth weight there was a small change in systolic blood pressure of -2.2mmHg (95% confidence interval -4.2 to - 0.3mmHg) and in diastolic blood pressure of -1.0mmHg (-2.2 to 0.1mmHg). Much stronger effects were observed among men who were born at term and were in the top third of body mass index at age 50, for whom a 1000g increase in birth weight was associated with a change of -9.1mmHg (-16.4 to-1.9mmHg) systolic and -4.2mmHg (-8.3 to -0.1mmHg) diastolic blood pressure. Men who were light at birth (<3250g) but were above median adult height had particularly high blood pressure. Adjustment for insulin concentrations reduced the associations of birth weight with systolic and diastolic blood pressure.CONCLUSIONS: A failure to realise growth potential in utero (as indicated by being light at birth but tall as an adult) is associated with raised adult blood pressure. Impaired fetal growth may lead to substantial increases in adult blood pressure among only those who become obese. Metabolic disturbances, possibly related to insulin resistance, may provide a pathway through which fetal growth affects blood pressure.
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952.
  • Leon, D A, et al. (author)
  • Reduced fetal growth rate and increased risk of death from ischaemic heart disease : cohort study of 15 000 Swedish men and women born 1915-29.
  • 1998
  • In: BMJ (Clinical Research Edition). - : BMJ. - 0959-8138 .- 1468-5833. ; 317:7153, s. 241-5
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: To establish whether fetal growth rate (as distinct from size at birth) is associated with mortality from ischaemic heart disease.DESIGN: Cohort study based on uniquely detailed obstetric records with 97% follow up over the entire life course and linkage to census data in adult life.SUBJECTS: All 14 611 babies delivered at the Uppsala Academic Hospital, Sweden, during 1915-29 followed up to end of 1995.MAIN OUTCOME MEASURES: Mortality from ischaemic heart disease and other causes.RESULTS: Cardiovascular disease showed an inverse association with birth weight for both men and women, although this was significant only for men. In men a 1000 g increase in birth weight was associated with a proportional reduction in the rate of ischaemic heart disease of 0.77 (95% confidence interval 0.67 to 0.90). Adjustment for socioeconomic circumstances at birth and in adult life led to slight attenuation of this effect. Relative to the lowest fourth of birth weight for gestational age, mortality from ischaemic heart disease in men in the second, third, and fourth fourths was 0.81 (0.66 to 0.98), 0.63 (0.50 to 0.78), and 0.67 (0.54 to 0.82), respectively. The inclusion of birth weight per se and birth weight for gestational age in the same model strengthened the association with birth weight for gestational age but removed the association with birth weight.CONCLUSION: This study provides by far the most persuasive evidence of a real association between size at birth and mortality from ischaemic heart disease in men, which cannot be explained by methodological artefact or socioeconomic confounding. It strongly suggests that it is variation in fetal growth rate rather than size at birth that is aetiologically important.
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953.
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954.
  • Li, LS, et al. (author)
  • Defects in β-cell Ca2+ dynamics in age-induced diabetes
  • 2014
  • In: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 63:12, s. 4100-4114
  • Journal article (peer-reviewed)abstract
    • Little is known about the molecular mechanisms underlying age-dependent deterioration in β-cell function. We now demonstrate that age-dependent impairment in insulin release, and thereby glucose homeostasis, is associated with subtle changes in Ca2+ dynamics in mouse β-cells. We show that these changes are likely to be accounted for by impaired mitochondrial function and to involve phospholipase C/inositol 1,4,5-trisphosphate–mediated Ca2+ mobilization from intracellular stores as well as decreased β-cell Ca2+ influx over the plasma membrane. We use three mouse models, namely, a premature aging phenotype, a mature aging phenotype, and an aging-resistant phenotype. Premature aging is studied in a genetically modified mouse model with an age-dependent accumulation of mitochondrial DNA mutations. Mature aging is studied in the C57BL/6 mouse, whereas the 129 mouse represents a model that is more resistant to age-induced deterioration. Our data suggest that aging is associated with a progressive decline in β-cell mitochondrial function that negatively impacts on the fine tuning of Ca2+ dynamics. This is conceptually important since it emphasizes that even relatively modest changes in β-cell signal transduction over time lead to compromised insulin release and a diabetic phenotype.
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955.
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956.
  • Liang, B. M., et al. (author)
  • Growth rate dispersion in seeded batch sucrose crystallization
  • 1987
  • In: AIChE Journal. - : Wiley. - 0001-1541 .- 1547-5905. ; 33:12, s. 2077-2079
  • Journal article (peer-reviewed)abstract
    • The object of this study was to compare the results of batch suspension and photomicroscopic cell experiments on growth rate dispersion of sucrose seed crystals to determine the relative effects of GRD in the two different environments. This was done by observing the change in CSD of the seed distribution in the batch suspension crystallizer, while simultaneously monitoring the individual growth rates of an identical seed sample in the photomicroscopic cell. It is found that seeds growing in a stirred suspension batch crystallizer also exhibit growth rate dispersion, as evidenced by the increasing width of the CSD with time.
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957.
  • Lilja, Hans, et al. (author)
  • Long-term prediction of prostate cancer up to 25 years before diagnosis of prostate cancer using prostate kallikreins measured at age 44 to 50 years.
  • 2007
  • In: Journal of Clinical Oncology. - 1527-7755. ; 25:4, s. 431-436
  • Journal article (peer-reviewed)abstract
    • Purpose We examined whether prostate-specific antigen (PSA) forms and human kallikrein 2 (hK2) measured at age 44 to 50 years predict long-term risk of incident prostate cancer. Methods From 1974 to 1986, 21,277 men age <= 50 years in Malmo, Sweden, enrolled onto a cardiovascular study (74% participation). The rate of PSA screening in this population is low. According to the Swedish Cancer Registry, 498 were later diagnosed with prostate cancer. We measured hK2, free PSA, and total PSA (tPSA) in archived blood plasma from 462 participants later diagnosed with prostate cancer and from 1,222 matched controls. Conditional logistic regression was used to test for association of prostate cancer with hK2 and PSA forms measured at baseline. Results Median delay between venipuncture and prostate cancer diagnosis was 18 years. hK2 and all PSA forms were strongly associated with prostate cancer (all P < .0005). None of the 90 anthropometric, lifestyle, biochemical, and medical history variables measured at baseline was importantly predictive. A tPSA increase of 1 ng/mL was associated with an increase in odds of cancer of 3.69 (95% CI, 2.99 to 4.56); addition of other PSA forms or hK2 did not add to the predictive value of tPSA. tPSA remained predictive for men diagnosed >= 20 years after venipuncture, and the predictive value remained unchanged in an analysis restricted to palpable disease. Conclusion A single PSA test at age 44 to 50 years predicts subsequent clinically diagnosed prostate cancer. This raises the possibility of risk stratification for prostate cancer screening programs.
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958.
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959.
  • Lindberg, Terese, et al. (author)
  • Prevalence of unknown and untreated arrhythmias in an older outpatient population screened by wireless long-term recording ECG
  • 2016
  • In: Clinical Interventions in Aging. - 1176-9092 .- 1178-1998. ; 11, s. 1083-1090
  • Journal article (peer-reviewed)abstract
    • Purpose: With longer life expectancies, the prevalence of arrhythmias is increasing; thus, there is a need for new methods to screen the older outpatient population. This population-based study describes the prevalence of arrhythmias in 200 outpatients aged ≥66 years. We also investigated the feasibility of wireless long-term recording (LTR) using the ECG-BodyKom®. Methods: Two hundred elderly persons aged 66–93 years were recruited from the Swedish National Study on Aging and Care in 2010–2013, and data were collected via wireless LTR ECG-BodyKom. Results: Screening with the LTR ECG revealed that persistent atrial fibrillation (AF) occurred in 10% of the outpatient population aged ≥66 years. Paroxysmal AF occurred in 5.5% of the population, with no difference between younger (60–80 years) and older (≥80 years) elderly participants. Furthermore, all patients with paroxysmal AF had a CHA2DS2VASc score of ≥2 and were therefore potential candidates for follow-up and medical examination. LTR ECG-BodyKom can be considered a feasible method to screen for arrhythmias in older outpatient populations. This simple method requires little of the user, and there was high satisfaction with the equipment and a good overall experience wearing it. Conclusion: The increasing occurrence of arrhythmias in the older population, as well as the high number of untreated cases of arrhythmias such as persistent AF and paroxysmal AF, poses a challenge for health care. Therefore, it is essential to develop effective strategies for their prevention and treatment.
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960.
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  • Result 951-960 of 1189
Type of publication
journal article (862)
conference paper (153)
other publication (13)
book chapter (9)
reports (7)
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doctoral thesis (6)
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Type of content
peer-reviewed (980)
other academic/artistic (200)
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Author/Editor
Abi, B. (316)
Abramowicz, H. (316)
Adelman, J. (316)
Adye, T. (316)
Akimov, A. V. (316)
Aleksa, M. (316)
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Alexandre, G. (316)
Amelung, C. (316)
Anastopoulos, C. (316)
Antonaki, A. (316)
Antonelli, M. (316)
Arai, Y. (316)
Arguin, J-F. (316)
Arnaez, O. (316)
Asquith, L. (316)
Assamagan, K. (316)
Azuma, Y. (316)
Bachacou, H. (316)
Bachas, K. (316)
Backes, M. (316)
Baker, O. K. (316)
Banas, E. (316)
Barillari, T. (316)
Barisonzi, M. (316)
Barklow, T. (316)
Beau, T. (316)
Beck, H. P. (316)
Bella, G. (316)
Beltramello, O. (316)
Benary, O. (316)
Benekos, N. (316)
Benhammou, Y. (316)
Bentvelsen, S. (316)
Berger, N. (316)
Beringer, J. (316)
Berry, T. (316)
Biesiada, J. (316)
Bilokon, H. (316)
Blumenschein, U. (316)
Boehler, M. (316)
Boisvert, V. (316)
Boonekamp, M. (316)
Borisov, A. (316)
Borissov, G. (316)
Bulekov, O. (316)
Burckhart, H. (316)
Burke, S. (316)
Busato, E. (316)
Butler, B. (316)
Calderini, G. (316)
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Swedish University of Agricultural Sciences (11)
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Natural sciences (282)
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