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Biomedical subjects

M Jones

Publications and source records attributed to M Jones.

At least 937 records · Page 52Linked to original sources
PubMed1975

Postnantal cerebellar hypoplasia and dysfunction following methylazoxymethanol acetate treatment (38495).

Swiss albino mice were injected postnatally with 0.05 ul of MAM-ac/g body weight. The mice were sacrificed at 0, 5,10, 15,20, and 25 days. Cerebellar, whole brain and body weights were determined. The treated mice generally showed smaller body weights reflecting the general toxicity of MAM-ac. There was no statistical difference between the whole brain weights of the two groups, when the loss of cerebellar weight was taken into account. Significant differences between the cerebellar weights of control and treated animals were shown at each sacrifice time. It is the conclusion of this study that those differences in weight reflect the destruction induced by MAM-ac during the first 5 days of postnatal life and are not due to a continued degeneration. As for general developmental and behavioral dysfunctions,the treated mice showed delayed eye opening and fur appearance, and by day 25, exhibited a tremorous altered gait.

Age Factors↗
PubMed1975

Lipid composition in postnatal methylazoxymethanol-treated swiss albino mouse cerebellum.

Postnatal Swiss albino mice were treated with with methylazoxymethanol acetate (MAM) or saline and sacrificed at 25 days of age. Granule cell depletion resulted. Significant reduction in the cerebellar weight, protein, ganglioside sialic acid , cerebrosides, sulfatides, and phospholipids were documented. There was not, however, selective reduction of any component known to be associated with the synaptic structures. Specific association of cerebellar ganglioside with its granule cell population was not substantiated. Cerebroside/sulfatide ratios were not different in the two groups, indicating that significant alterations previously observed in spinal cord were not present in the cerebellum. It was concluded that the bulk of cerebellar granule cells and their synaptic connections could be deleted without affecting total ganglioside and phospholipid concentrations.

Animals↗
PubMed1975

The spectrum of degenerative changes in hypertrophied human cardiac muscle cells: an ultrastructural study.

Light and electron microscopic observations were made on cardiac tissues removed at operation from 91 patients with ventricular hypertrophy, including left ventricular myocardium from 16 patients with aortic valvular disease and from 16 patients with asymmetric septal hypertrophy, and crista supraventricularis muscle from 59 patients with congenital heart diseases associated with right ventricular outflow tract obstruction. In all patients the majority of cardiac muscle cells were hypertrophied, had intact myofibrils, and were surrounded by small amounts of fibrous tissue. In 18 (20%) of the 91 patients cardiac muscle cells with a wide spectrum of degenerative changes were present in addition to hyperthrophied, nondegenerated cells. Early degenerative changes consisted of focal myofibrillar lysis, with preferential loss of thick myofilaments, and focal proliferation of tubules of sarcoplasmic reticulum. Cardiac muscle cells with advanced degeneration had extensive myofibrillar damage and a marked decrease in numbers of myofibrils and T-tubules. The most severely degenerated cells showed selective proliferation of organelles, including sarcoplasmic reticulum, mitochondria, and glycogen, which replaced the contractile elements in the cytoplasm. These findings suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with ventricular hypertrophy. These morphological features appear to represent a final common pathway for degeneration of cardiac muscle cells in a variety of cardiac conditions.

Aortic Valve Insufficiency↗
PubMed1975

The nuclear membranes in hypertrophied human cardiac muscle cells.

Nuclear membranes of cardiac muscle cells were studied in 134 patients with cardiac hypertrophy of various causes. Abnormalities observed consisted of: a) increased foldings and convolutions; b) nuclear pseudoinclusions formed by cytoplasmic organelles protruding into saccular invaginations of the nuclear membranes, and c) intranuclear tubules. The increased foldings and convolutions of the nuclear membranes and the nuclear pseudoinclusions appear to result from synthesis of nuclear membranes in excess of that needed to accommodate the increase in nuclear volume which occurs in hypertrophy. Intranuclear tubules were found in 6 patients and consisted of tubular invaginations, 400 to 650 A in diameter, of the inner nuclear membranes into the nucleoplasm. Some of these tubules were straight and cylindrical, and were associated with a peripheral layer of marginated chromatin; others were not associated with chromatin, appeared coiled and followed irregular courses. Intranuclear tubules in cardiac muscle cells probably represent an extreme cellular response to the stimulus of hypertrophy.

Adult↗