Biomedical subjects

H J Gundersen

Publications and source records attributed to H J Gundersen.

131 records · Page 8Linked to original sources

PubMedDate not supplied

Glomerular basement membrane thickening in streptozotocin diabetic rats despite treatment with an aldose reductase inhibitor.

This study concerns the possible prevention of glomerular basement membrane thickening in experimental diabetes by an aldose reductase inhibitor (ARI), Statil. ARI added to the chow was given to streptozotocin diabetic rats over a period of 6 months. Reference groups were control rats and diabetic rats on the same chow without ARI. The diabetic rats were given insulin two or three times a week, and blood glucose was measured monthly before insulin injections. There was a marked difference in the occurrence of cataracts between the two diabetic groups. ARI treated rats tended to have lower blood glucose than the diabetic reference group, but the difference was not significant. At the termination of the experiment, the left kidney was perfusion fixed, weighed, and prepared for light and electron microscopy. Systematic random sampling from the entire kidney was performed to obtain light microscopic visual fields and ultrathin sections from two glomeruli. Mean glomerular volume was estimated by light microscopy, and glomerular basement membrane thickness, by electron microscopy. Basement membrane thickness was significantly increased in untreated diabetic rats (174 nm, SD = 4.5 nm) as compared to that of controls (Mean: 154 nm, SD = 11.0 nm), and was even more so in ARI treated rats (187 nm, SD = 18.7 nm), although the ARI treated rats showed less renal and glomerular hypertrophy than did untreated diabetic rats. In conclusion, the ARI treatment over an experimental period of 6 months attenuated diabetic renal and glomerular hypertrophy, but had no effect at all on diabetic glomerular basement membrane thickening.

Aldehyde Reductase↗

PubMedDate not supplied

The Conneulor: unbiased estimation of connectivity using physical disectors under projection.

The Euler number and the connectivity of an arbitrary object is defined, and it is illustrated why the connectivity of an n-dimensional object cannot be estimated in an (n-1)-dimensional section. The disector--principle for 3-D counting of the Euler--events is illustrated in cancellous bone. The correct handling for unbiased counting of events at artificial edges is outlined. A nomogram for predicting the precision of an estimate is provided.

Bone and Bones↗

PubMedDate not supplied

Quantification of connectivity in cancellous bone, with special emphasis on 3-D reconstructions.

The connectivity of cancellous bone attracts increasing attention, as it has been hypothesized that a primary reason for decreasing strength and stiffness in osteoporosis is caused by a loss of trabecular elements and consequently a loss in connectivity. The Euler characteristic has in a few previous articles been used to express cancellous bone connectivity, but there are severe problems in using the Euler characteristic uncritically. The Euler characteristic of a three-dimensional structure is a topological invariant, which reports the number of particles of a structure plus the number of enclosed cavities minus the connectivity. As such, one must know the number of components and the number of enclosed cavities in order to use the Euler characteristic as an expression of connectivity. Another difficulty of using the Euler characteristic is that due to edge effects the Euler characteristic of an excised specimen provides a biased estimate of the Euler characteristic of the region from which the specimen was taken. In this article the intuitive concept of connectivity is given a precise mathematical definition, and a basic topological method for quantifying the connectivity of cancellous bone is presented. The method uses the Euler characteristic, but the above-mentioned problems are controlled. The development of the method and the practical implementation is based on a set of topological notes. It must be stressed that the method is free from assumptions concerning trabecular architecture, and that the method is unbiased. This is in contrast to previously presented methods. The unbiased and model-free method is used on a series of 3-D reconstructions of cancellous bone specimens, and it is demonstrated that the connectivity of cancellous bone is not simply related to volume fraction (density), and that biased and model-based 2-D methods aimed at determining connectivity do not have any general relationship to connectivity in cancellous bone.

Bone Density↗

PubMedDate not supplied

Age-induced white matter changes in the human brain: a stereological investigation.

In the present pilot study, age-related white matter changes were investigated by the use of design-based stereological methods. In the brains of elderly subjects, the total volume of the white matter and the total volume of the myelinated fibers therein were lower than in those of young subjects (15% and 17%, respectively), but the differences were not statistically significant. The total length of the myelinated fibers of the white matter in the elderly group of 86,000 km was, statistically, significantly decreased by 27% compared with 118,000 km in the young group. This loss of the total nerve fiber length was accompanied in particular by a decline of the myelinated fibers with a small diameter. The mean diameter of the myelinated fibers in the young group was significantly smaller than in the old group, but the relative size distributions of the myelinated fiber diameters between the young and old groups were similar. Our findings show that the atrophy of the human white matter during ageing is probably caused by a loss of myelinated fibers with a small diameter.

Adult↗

PubMedDate not supplied

Six billion neurons lost in AIDS. A stereological study of the neocortex.

Human immunodeficiency virus type 1 (HIV1) is neurotropic. One of the morphological changes that is seen in patients with acquired immunodeficiency syndrome (AIDS) is cerebral atrophy affecting various structures including the neocortex. The cause of atrophy is not known. The total number of neocortical neurons was estimated in formalin fixed brains of 12 males with AIDS and 12 male controls matched for age and height. The mean number of neocortical neurons was 16.0 x 10(9) (coefficient of variation = 0.11) in the AIDS patients compared with 21.9 x 10(9) (coefficient of variation = 0.22) in the controls, a difference of approximately six billion (p < 0.005, 2-tailed). The global neuronal loss was 37%, and affected all four neocortical lobes. Ten patients did not have a history of central nervous system symptoms; two patients had a history of dementia. The number of neurons in the AIDS cases was not associated with dementia. AIDS is the first disease in which a global loss of neocortical neurons has been demonstrated using unbiased stereological methods. The loss of more than one third of the neurons may partly explain the cortical atrophy. Focal neuron loss has been reported by several authors, but none have been based on unbiased methods. In this group of AIDS patients the severe loss of neurons did not correspond to neurological deficits.

Acquired Immunodeficiency Syndrome↗