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Biomedical subjects

R Meyer

Publications and source records attributed to R Meyer.

At least 361 records · Page 20Linked to original sources

Epithelial cell-cell and cell substrate contacts.

An epithelial sheet maintains its normal morphology by an appropriate balance between cell to cell and cell to substrate contacts which must be adjusted as proliferation occurs. We review our studies which attempts to analyze some of these problems by recombining cell and matrix tissue components, or by analyzing developmental changes in intact tissue. Epithelial and mesenchymal cells placed on tissue matrices which have been denuded of their normal tissue components behave distinctively, suggesting that this procedure could reveal inherent differences. When chick epiblast is grown on the outer surface of the vitelline membrane, the mode of expansion changes from that seen in the normal site, the vitelline membrane inner surface. Dispersed skin and corneal cells studied during subsequent aggregation show that one cell can influence desmosome formation in another. Finally, recent studies on developing chick liver indicate a correlation between the percent of lateral cell surface in the junctional domain and the proliferative rate of these cells.

Animals↗

[Diagnosis and treatment of pericardial effusions with the aid of 2-dimensional Doppler echo cardiography (author's transl)].

In a case of a large acute pericardial effusion the diagnosis and the following pericardiocentesis under visible control by means of 2-dimensional echocardiography (2 D-E) are described. The effusion coat around the heart can clearly be localised. Furthermore, a new echocardiographic system is used combining 2 D-E and range-gated pulsed Doppler technique that allows the registration of flow-velocity curves in the superior vena cava and the recognition of a beginning cardiac tamponade. If indicated, the following pericardiocentesis can be done under direct ultrasonic control avoiding any risk of heart perforation.

Adolescent↗

Regions of broad-host-range plasmid RK2 which are essential for replication and maintenance.

The sites of cleavage on the map of the broad-host-range plasmid RK2 (56 kilobases) were determined for the BglII, PstI, and SmaI restriction enzymes, and the determinants for tetracycline and ampicillin resistance were localized. The cleavage sites were clustered at or near the drug resistance genes. To localize regions required for plasmid replication and maintenance in Escherichia coli, we deleted nonessential regions of RK2 by partial digestion with the restriction endonuclease HaeII to produce small derivatives. The smallest stable replicon obtained contained five HaeII fragments of RK2 which total 5.4 kilobases. These fragments were derived from three regions of RK2 that are separated from each other by antibiotic resistance genes. One of these HaeII fragments (0.75 kilobases) has the properties expected of the origin of replication. The outer four fragments, located in two separate regions of RK2, were found to provide, in trans, functions that permit the replication of the HaeII fragment carrying the origin of the replication. These results indicate that at least two plasmid-encoded genes, capable of acting in trans, and a replication origin are required for RK2 replication and maintenance.

Anti-Bacterial Agents↗

[Ultrastructural-morphometric characterization of adaptive and compensatory myocardial changes using heart enlargement as an example].

A morphometric analysis of the heart muscle cell shows significant differences in the reaction of different cellular structures in different experimental stress models of the myocardium (swimming exercise and ligature infarction) in the rat. For instance, the number of mitochondria is 44% higher only 2 days after infarction than after 45 h of swimming exercise over a period of 4 weeks. The mitochondria/myofibrils ratio is higher than in the case of training. But later on in the course of the experiment the number of mitochondria and their membrane surface density diminishes compared with training. The differences in the rate of formation and in the kind and intensity of the changes are probably attributable to different adaptive mechanisms by means of which the heart reacts to acute and chronic loads.

Adaptation, Physiological↗

Morphometric analysis of myocardial mitochondria in rats during adaptation to exercise.

Comparative morphometric studies of the mitochondria of muscle cells and of interstitial cells of rat hearts were carried out in order to obtain more information about changes in mitochondrial parameters during adaptation of the myocardium to physical training of different durations (45, 180, 360 hours of swimming) and intensities. On the basis of the results the authors conclude that the mitochondrial biogenesis of heart muscle cells occurs in dependence on the intensity of training at two morphometrically different stages. Some parameters of the mitochondria of the interstitial cells reacted in a manner similar to that of the muscle cells, but opposite reactions were also observed. The biogenesis of mitochondria and the absence of a decrease in the mitochondria/myofibrils ratio in muscle cells may be regarded as an improvement in cell metabolism in the training-induced hypertrophy of the rat heart.

Adaptation, Physiological↗

[Comparative quantitative-cytochemical and ultrastructura-morphometric studies for the characterization of the rat heart in experimental myocardial infarct].

Some oxidative enzymes of undamaged sites of the left ventricle were examined with the aid of ultrastructural morphometric and quantified cytochemical methods 1, 2, 7 and 14 days after the ligature of the descending branch of the left coronary artery. A comparison of the ultrastrastructural morphometric data with the densitometric data showed that increases in the activities of some oxidative enzymes are accompanied by enlargements of the mitochondria.

Animals↗

[Morphometric studies of rat myocardium during early postnatal period].

The mass development of heart ventricle (right and left with septum) was investigated with histologic-morphometric methods on rats from 1...14 days of live. The increase (twice) of myocard area is caused by increase of myocards of the left ventricle. Growth is the result of hyperplasie, in the second week it is the result of hypertrophy of heart muscle cells. The number of interstitiell cells enlarges to more than once. The perinatal change of circulation is the decisive factor for postnatal heart growth.

Animals↗