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Biomedical subjects

H A Hartmann

Publications and source records attributed to H A Hartmann.

At least 55 records · Page 3Linked to original sources
PubMed1978

RNA content and volume of nerve cell bodies in human brain. I. Prefrontal cortex in aging normal and demented patients.

The age-related change in the neuronal RNA content, volume, and the RNA concentration of 2,160 single cell bodies was examined from the prefrontal cortex. Human brains from 15 normal and 3 demented patients of ages ranging from 8 months to 94 years were obtained at post-mortem examination. The neuronal RNA showed an adult level at age 9 years and remained unchanged until age 66; the mean RNA content was 27.15 pg during this period of time. A decline in the RNA content followed with increasing ages, but it leveled off to an average of 17.97 pg after the age of 80 years. A comparative observation of morphological changes of normal and demented patients reveal the quantitative spectrum of senile plaques. In spite of the presence of significantly more senile plaques, patients with senile dementia showed the RNA content and the volume of the cell body like those of normal patients of similar age. There seems to be no criterion which is characteristic of senile dementia in terms of the RNA content in cortical cell bodies.

Adolescent↗
PubMed1975

Generalized gangliosidosis type II (juvenile GM1 gangliosidosis). A pathological, histochemical and ultrastructural study.

Pathological, histochemical and ultrastructural studies on 3 siblings with GM1 gangliosidosis type II are reported. These studies support a biochemical defect with profound deficiency of beta-galactosidases which results in widespread accumulation of the GM1 ganglioside and its asialo derivative in brain and to a lesser extent in viscera, as well as in storage of a keratan sulphate-like mucopolysaccharide. Striking valvular changes in the heart without myocardial involvement were seen in all cases. The histochemical and ultrastructural changes are similar to those seen in GM1 gangliosidosis type I, though less severe. Autosomal recessive inheritance without apparent ethnic predilection seems likely.

Autopsy↗
PubMed1972

An investigation of sodium transport in barnacle muscle fibres by means of the microsyringe technique.

1. The cation composition of single barnacle muscle fibres following damage by axial insertion of a microsyringe has been measured. The Na and Ca contents of these fibres were raised.2. Electronmicroscopic studies of fibres following insertion of a microsyringe indicated that the damage done resulted in tubular obstruction of the T-system.3. Fibres loaded with radiosodium by micro-injection showed that the Na(*) efflux declined exponentially with time, but that in most fibres the slope ratio of d/dt ln [Na(*)](1) to d/dt (ln d[Na(*)](i)/dt) was less than unity. Injections of distilled water deep in the fibre failed to influence the course of the Na(*) efflux.4. K removal reduced the Na efflux by 47%. However, a few fibres displayed very little K-dependence.5. When measured in fibres already soaked in a K-free medium for long periods the sodium efflux consisted of a brief rapid phase, followed by a slow phase of Na loss.6. In the presence of 30 mM-K, there was little or no rise in the Na efflux. Raising the external K to 50 or 100 mM caused a marked rise in the Na efflux. Raising the external K to 30 mM in the absence of external Ca(2+) led to a rise in the Na efflux. A high K solution always caused shortening of these fibres.7. Internal application of 1 M or 1 mM-CaCl(2) often caused a significant rise in the Na efflux.8. Internal application of 2.5 or 5 M saline caused a prompt and large fall in the Na efflux. In the presence of high K saline-loaded fibres failed to contract.9. Internal application of 0.5 M-ATP stimulated the Na efflux. A larger effect was not observed in fibres pre-treated with 2 M-MgCl(2). Internal application of 0.5 M-ArP was without effect.10. The results indicate that the barnacle fibre is a suitable preparation for the study of Na fluxes by means of the micro-injection technique. They also indicate that the mechanism regulating the Na efflux is not quite the same as that found in squid axon or frog muscle.

Adenosine Triphosphate↗