Infant growth is associated with parental education but not with parental adiposity - Early Stockholm Obesity Prevention Project.

AIM: To explore the simultaneous impact of parental adiposity and education level on infant growth from birth to 12 months, adjusting for known early-life risk factors for subsequent childhood obesity. METHODS: Baseline data for 197 one-year-old children and their parents, participating in a longitudinal obesity intervention, were used. Obesity risk groups, high/low, were defined based on parental body mass index (n = 144/53) and parental education (n = 57/139). Observational data on infant growth between 0 and 12 months were collected. The children's relative weight (body mass index standard deviation score) at 3, 6 and 12 months and rapid weight gain 0-6 months were analysed in regression models, with obesity risk as primary exposure variables, adjusting for gestational weight gain, birth weight, short exclusive breastfeeding and maternal smoking. RESULTS: Relative weight at 3, 6 and 12 months was associated with low parental education but not with parental adiposity. No significant associations were observed with rapid weight gain. None of the early-life factors could explain the association with parental education. CONCLUSION: Low parental education level is independently associated with infant growth, whereas parental obesity does not contribute to a higher weight or to rapid weight gain during the first year.

Vascular permeability in acute triethyltin-induced brain edema studied with FITC-dextrans, sodium fluorescein and horseradish peroxidase as tracers.

In golden hamsters, a study was made on the vascular permeability changes which might take place during the formation of triethyltin (TET)-induced brain edema. For this purpose, the animals received a single intravenous (i.v.) injection of TET sulphate (5-10 mg/kg b.wt) and groups of animals were studied 4 to 24 h thereafter. By the use of a new density gradient technique based on polyvinylcoated silica particles (1), it was shown that white matter edema was present already at 4 h after the TET injection. The edema then progressed during the following 20 h. Electron microscopy revealed that fluid accumulated in myelin vacuoles of the hamsters in the same way as has been described in other animal species. The macromolecular tracer, horseradish peroxidase mol.wt 40,000 injected i.v., did not leak out of the cerebral vessels during the period when edema developed. In order to find out if the formation of edema is associated with a vascular permeability increase to other and smaller markers, we used several fractions of FITC-dextrans varying from mol.wt 3,000 to 70,000 and determined their intracerebral localization with a histotechnical procedure. FITC-dextrans, mol.wt 70,000, did not leak out of the cerebral vessels in any of the TET intoxicated hamsters during the observation period of 24 h. The same was true for most animals given the other dextran fractions. However, FITC-dextrans, mol.wt 3,000-20,000 were present outside the vessels in the edematous optic nerves and corpus callosum in a few TET treated animals taken 16-24 h after the TET injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Distribution of exudated FITC-dextrans in experimental vasogenic brain edema produced by a focal cryogenic injury.

Mice were subjected to cortical cryogenic brain injury, and FITC-dextrans (mol. wt. 20,000 or 150,000) were injected intravenously (i.v.). After a survival period of 4 h the distribution of the FITC-dextrans was determined by a histotechnical procedure described recently ( Hultstr öm et al. 1982a ). This technique is based on freeze-drying and vapor fixation to immobilize the tracer and to provide tissue fixation. In and around the cryogenic injury both tracers leaked out of the cortical and the leptomeningeal vessels and spread into the brain parenchyma. They were seen as multiple, closely apposed droplets of fluorescent material best recognized by fluorescence microscopy under high magnification. The tracers were also taken up by neuronal perikarya and in glial cell nuclei of, presumably, astrocytic origin. Our study shows that the FITC-dextran technique can be used for experimental studies on the vasogenic form of brain edema. The patterns formed by the extravasated tracers have qualitative similarities to those produced by other more commonly used tracers, such as fluorochrome-labeled serum proteins and peroxidase.

Measurement of edema in the nervous system. Use of Percoll density gradients for determination of specific gravity in cerebral cortex and white matter under normal conditions and in experimental cytotoxic brain edema.

A method is presented by which density measurements can be performed on samples from cerebral cortex and white matter of normal and intoxicated animals using nontoxic ingredients as an alternative to the bromobenzene-kerosene technique described by Nelson et al. (1971). A continuous density gradient is prepared in a calibrated glass cylinder by using a new product, Percoll, which consists of colloidal silica particles coated with polyvinyl pyrrolidone. The gradient is stable and the same column can be used for repeated experiments over a long period of time. Interactions between the gradient media and the samples are evaluated and various methodological aspects concerning removal and handling of the tissue samples are presented. Experiments with acute triethyltin (TET) intoxication in the mouse and the hamster show that the Percoll technique can be used as an alternative to the bromobenzene-kerosene method in quantitative studies on cytotoxic brain edema.