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  • Articles: DFG German National Licenses  (7)
  • 1990-1994  (7)
  • 1994  (7)
  • 1
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objective To examine the relation between indices of maternal nutrition during pregnancy, including haemoglobin concentration, skinfold thickness and body weight, and the child's blood pressure at 10 to 12 years of age.Design Follow up study of children whose mothers had haemoglobin estimations, weights and skinfold thicknesses recorded during pregnancy.Setting Kingston, Jamaica.Subjects Seventy-seven children whose mothers took part in a prospective study of nutrition during pregnancy in relation to fetal growth.Main outcome measure Blood pressure at 10 to 12 years of age.Results The child's mean systolic pressure adjusted for current weight rose by 2.6 mmHg (95 % CI 0.5–4.6, P= 0.01) for each 1 g/dl fall in the mother's lowest haemoglobin during pregnancy. Mothers with a lower haemoglobin had thinner skinfold thicknesses, especially over the triceps (P= 0.005). In multiple regression analyses, taking account of the child's sex and current weight, there was a strong association between thin maternal triceps skinfold thickness at 15 weeks of gestation and raised blood pressure in the offspring. Taking account of the mother's triceps skinfold thickness abolished the relation between lower haemoglobin and raised blood pressure in the child. Lower weight gain between 15 and 35 weeks of gestation was independently associated with raised children's blood pressure. Systolic pressure rose by 10.7 mmHg (95 % CI 5.7 to 15.6, P= 0.0001) for each log mm decrease in the mother's triceps skinfold thickness, and by 0.6 mmHg (95% CI 0.1 to 1.0, P= 0.02) for each 1 kg decrease in the mother's weight gain during pregnancy.Conclusions These results parallel animal experiments suggesting that impaired maternal nutrition may underlie the programming of adult hypertension during fetal life.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Plant, cell & environment 17 (1994), S. 0 
    ISSN: 1365-3040
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Two direct but independent approaches were developed to identify the average δ18O value of the water fraction in the chloroplasts of transpiring leaves. In the first approach, we used the δ18O value of CO2 in isotopic equilibrium with leaf water to reconstruct the δ18O value of water in the chloroplasts. This method was based on the idea that the enzyme carbonic anhydrase facilitates isotopic equilibrium between CO2 and H2O predominantly in the chloroplasts, at a rate that is several orders of magnitude faster than the non-catalysed exchange in other leaf water fractions. In the second approach, we measured the δ18O value of O2 from photosynthetic water oxidation in the chloroplasts of intact leaves. Since O2 is produced from chloroplast water irreversibly and without discrimination, the δ18O value of the O2 should be identical to that of chloroplast water. In intact, transpiring leaves of sunflower (Helianthus annuus cv. giant mammoth) under the experimental conditions used, the average δ18O value of chloroplasts water was displaced by 3—10 % (depending on relative humidity and atmospheric composition) below the value predicted by the conventional Craig & Gordon model. Furthermore, this δ18O value was always lower than the δ18O value that was measured for bulk leaf water. Our results have implications for a variety of environmental studies since it is the δ18O value of water in the chloroplasts that is the relevant quantity in considering terrestrial plants influence on the δ18O values of atmospheric CO2 and O2, as well as in influencing the δ18O of plant organic matter.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 24 (1994), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary. A follow-up study was carried out to determine whether either impaired or disproportionate fetal growth are associated with a raised total serum IgE concentration in men and women aged 50 years. The serum IgE concentration was measured in 146 men and 134 women born in Preston (Lancashire, UK) between 1935 and 1943, whose size at birth had been measured in detail.Sixty-two subjects were found to have an IgE concentration above 80 IU/ml. Compared with subjects with a normal IgE on average they had a 0.30 inch larger head circumference at birth (P -0.004) and weighed 5.6 ounces more at birth (P= 0.04). People with a raised and with a normal IgE were of similar crown-heel length at birth, indicating that in utero those with a raised IgE had had disproportionate growth of the head in relation to the trunk and limbs. The prevalence of a raised IgE rose from 14% in subjects whose head circumference at birth was 13 inches or less to 37% in those whose head circumference was more than 14 inches. This association was independent of gestational age at birth and of the mother's pelvic size and parity. It was also independent of adult physique, social class and smoking, and was similar in men and women. In multiple logistic regression analyses odds ratios of a raised IgE rose progressively to more than 4 as head circumference at birth increased from 13 inches or less to more than 14 inches.One possibility is that these associations reflect the long-term effects of sustaining fetal brain growth at the expense of the trunk, in particular the thymus. This may be a consequence of fetal under-nutrition in late gestation.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Oecologia 97 (1994), S. 297-307 
    ISSN: 1432-1939
    Keywords: Photoinhibition ; Rainforest disturbance Photosynthesis ; Leaf turnover
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Disturbance or rainforest is often followed by mass mortality of understorey seedlings. Transitions of shade grown plants to full sunlight can cause reductions in the efficiency with which light is used in photosynthesis, called photoinhibition. In order to assess the influence of photoinhibition on mortality and growth after rainforest disturbance this study examined photoinhibition in both simulated and real forest disturbances in northern Papua New Guinea. In an experiment simulating rainforest disturbance, exposure of shade-grown plants to full sunlight resulted in abrupt decreases in the chlorophyll fluorescence parameter F v/F m that is characteristic of photoinhibition. However, in the well-watered plants used in these experiments there were no fatalities during 3 weeks after exposure to full sunlight. Thus, it is unlikely that photoinhibition, alone, is responsible for seedling fatalities after rainforest disturbances, but more likely that fatalities are due to photoinhibition in conjunction with other environmental stress. There were differences between the response of species to the simulated disturbance that concurred with their preferred habitats. For example, species form the genus Barringtonia, which is commonly found in shaded understorey environments, underwent greater reductions in F v/F m and were slower to recover than species that usually inhabit high solar radiation environments. The extent of photoinhibition and the rate of recovery appeared to be dependent on avoidance of direct solar radiation by altering leaf angles and on increasing maximum photosynthetic rates. A field survey of photoinhibition in man-made rainforest gaps corroborated the findings of the simulated disturbance experiment showing that plant species commonly found in shaded environments showed a greater degree of photoinhibition in forest gaps at midday than those species which are classified as species that benefit from gaps or specialist gap inhabitors.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 37 (1994), S. 592-596 
    ISSN: 1432-0428
    Keywords: NIDDM ; insulin secretion ; fetal growth ; programming
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent studies suggest that NIDDM is linked with reduced fetal and infant growth. Observations on malnourished infants and studies of experimental animals exposed to protein energy or protein deficiency in fetal or early neonatal life suggest that the basis of this link could lie in the detrimental effects of poor early nutrition on the development of the beta cells of the islets of Langerhans. To test this hypothesis we have measured insulin secretion following an IVGTT in a sample of 82 normoglycaemic and 23 glucose intolerant subjects who were born in Preston, England, and whose birthweight and body size had been recorded at birth. The subjects with impaired glucose tolerance had lower first phase insulin secretion than the normoglycaemic subjects (mean plasma insulin concentrations 3 min after intravenous glucose 416 vs 564 pmol/l, p=0.04). Insulin secretion was higher in men than women (601 vs 457 pmol/l, P=0.02) and correlated with fasting insulin level (p=0.04). However, there was no relationship between insulin secretion and the measurements of prenatal growth in either the normoglycaemic or glucose intolerant subjects. These results argue against a major role for defective insulin secretion as a cause of glucose intolerance in adults who were growth retarded in pre-natal life.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 37 (1994), S. 592-596 
    ISSN: 1432-0428
    Keywords: Key words NIDDM, insulin secretion, fetal growth, programming.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent studies suggest that NIDDM is linked with reduced fetal and infant growth. Observations on malnourished infants and studies of experimental animals exposed to protein energy or protein deficiency in fetal or early neonatal life suggest that the basis of this link could lie in the detrimental effects of poor early nutrition on the development of the beta cells of the islets of Langerhans. To test this hypothesis we have measured insulin secretion following an IVGTT in a sample of 82 normoglycaemic and 23 glucose intolerant subjects who were born in Preston, England, and whose birthweight and body size had been recorded at birth. The subjects with impaired glucose tolerance had lower first phase insulin secretion than the normoglycaemic subjects (mean plasma insulin concentrations 3 min after intravenous glucose 416 vs 564 pmol/l, p =0.04). Insulin secretion was higher in men than women (601 vs 457 pmol/l, p =0.02) and correlated with fasting insulin level (p =0.04). However, there was no relationship between insulin secretion and the measurements of prenatal growth in either the normoglycaemic or glucose intolerant subjects. These results argue against a major role for defective insulin secretion as a cause of glucose intolerance in adults who were growth retarded in prenatal life. [Diabetologia (1994) 37: 592–596]
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 37 (1994), S. 150-154 
    ISSN: 1432-0428
    Keywords: Key words Type 2 (non-insulin-dependent) diabetes mellitus, insulin resistance, fetal growth, metabolic programming.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Type 2 (non-insulin-dependent) diabetes mellitus may originate through impaired development in fetal life. Both insulin deficiency and resistance to the action of insulin are thought to be important in its pathogenesis. Although there is evidence that impaired fetal development may result in insulin deficiency, it is not known whether insulin resistance could also be a consequence of reduced early growth. Insulin resistance was therefore measured in 81 normoglycaemic subjects, and 22 subjects with impaired glucose tolerance, who were born in Preston, UK, between 1935 and 1943. Their birth measurements had been recorded in detail. Insulin resistance was measured by the insulin tolerance test which uses the rate of fall in blood glucose concentrations after intravenous injection of insulin as an index of insulin resistance. Men and women who were thin at birth, as measured by a low ponderal index, were more insulin resistant. The association was statistically significant (p =0.01) and independent of duration of gestation, adult body mass index and waist to hip ratio and of confounding variables including social class at birth or currently. Thinness at birth and in adult life has opposing effects such that resistance fell with increasing ponderal index at birth but rose with increasing adult body mass index. It is concluded that insulin resistance is associated with impaired development in fetal life. [Diabetologia (1994) 37: 150–154]
    Type of Medium: Electronic Resource
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