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Biomedical subjects

R Jung

Publications and source records attributed to R Jung.

At least 127 records · Page 7Linked to original sources
PubMed1980

Comparison of three methods of respiratory care following upper abdominal surgery.

Incentive spirometry, as a method for preventing postoperative atelectasis, was compared with intermittent positive-pressure breathing (IPPB) and resistance breathing in 126 patients undergoing upper-abdominal surgery, most of whom had cholecystectomy. There was no statistically significant difference in the incidence of atelectasis among the three groups, who were matched for age, sex, smoking history, previous respiratory disease, and duration of surgery. There was a significantly higher incidence of atelectasis in patients over the age of 50 years (P = 0.004) than in younger subjects, where the incidence was not different among the three groups. Incentive spirometric therapy, as used in this study, offered no advantage over the other methods of treatment.

Abdomen↗
PubMed1979

[Fiftieth anniversary of Hans Berger's publication of the electroencephalogram. His first records in 1924--1931 (author's transl)].

For the fiftieth anniversary of Berger's first EEG publication, some of his early recordings obtained between 1924 and 1931 are discussed and illustrated. Examples of his protocols from the Freiburg Berger Archives are reproduced. Three types of Berger's early investigations are described: (1) String-galvanometer recordings obtained between 1924 and 1926, mainly from trephined patients with cerebral diseases, which usually showed brain waves slowed to 6--8 per second; (2) Direct recordings from the cortex and white matter proving the cortical origin of the EEG in 1930; (3) Typical unpublished EEG recordings of epileptics and of petit-mal attacks obtained in 1930 and 1931. Berger's first six papers published between 1929 and 1933 described nearly all the main EEG findings of cerebral diseases and the EEG alterations of normals during attention, sleep, and narcosis, but they did not report on convulsive potentials in the EEGs of epileptics. Berger had, however, obtained excellent records of epileptic EEG features, here depicted in Figs. 4 through 7. These remained unpublished until 1933 and 1938, because Berger suspected that they contained artifacts caused by blinks and facial movements which he had recorded in his controls (Fig. 4). Only in 1933, after other authors had described large amplitudes of convulsive potentials in the cortex of animals, did Berger publish parts of the EEGs of a petit-mal attack and of focal attacks in progressive paresis. In 1938, Berger presented the EEG of the beginning of a petit-mal attack with large 3/s spikes and waves recorded in 1931 which were similar to those described by Gibbs and coworkers in 1935. In 1933 and 1938, Berger interpreted the abnormal brain potentials of epileptics as signs of a preconvulsive state of the forebrain and suggested that the periods of 3/s waves were cortical correlates of an epileptic absence.

Electroencephalography↗
PubMed1979

Influence of microwave irradiation on cultured glioma cells I. An enzymatic and scanning electron microscopy study.

Temperature-induced variations in the surface morphology of cultured glioma cells were evaluated by scanning electron microscopy. Furthermore, after irradiation by microwave power, plasminogen activator activity was measured in cell cultures. The data suggest that heating of glioma cells to about 51 degrees C causes thermotropic protein transitions of cell surface together with an irreversible loss of plasminogen activator activity.

Cells, Cultured↗
PubMed1976

[Training and dominance in human voluntary movements. Right-left-comparisons of putting and throwing programs (author's transl)].

1. Muscle action potentials and efficiency were measured during shot putting and ball throwing in right and left handed normals. The dominant and the nondominant side were compared in trained and untrained persons in order to investigate motor learning effects. 2. Trained shot putters show a coordinated sequence of activation of trunk, leg and arm muscles of both sides which precedes the final arm extension. After turning the body from an initially inclined and twisted position the final arm extension transfers the force of the accelerated body mass to the shot. 3. When shot putting or throwing is performed by the nondominant arm in subjects trained for the dominant arm the coordination of the contralateral dominant arm is lacking, in contrast to the performance by the trained arm. 4. In untrained persons the shot putting is effected mainly by arm extension on either side. The preceding trunk and leg action is very incomplete and without coordination of the contralateral arm, whereas the shot putting arm shows stronger triceps brachii innervation. The distances achieved by untrained shot putters reach only one-fifth or one-third of those of highly trained persons. 5. In ball throwing the throwing arm shows final coactivation of the biceps and triceps muscles coordinated with trunk and contralateral arm movements. The distances reached by throwing with the untrained arm are about half of those of the trained dominant arm. 6. Trained sportsmen put the shot with the untrained nondominant arm to 73% of the distance achieved by the trained arm. Untrained persons, however, show an approximately equal, smaller range of shot with the dominant and nondominant arm (8% side difference). 7. A biomechanical factor causing different performances of trained and untrained persons in shot putting is the different force of the energy transferring mass: the untrained person thrusts mainly with the arm which has barely 1/20 of the mass of the whole body, used by the trained shot putter. 8. That bilateral training and not hemispheric dominance is the decisive factor producing the improved efficiency is demonstrated by three observations: a) the maximal efficiency and bilateral coordination of shot putting in trained persons, b) the lack of contralateral activation of the dominant arm in shot putting and throwing by the nondominant arm, and c) the minimal left and right side differences in performance of untrained persons.

Action Potentials↗
PubMed1975

[Delayed initiation of voluntary movements after pyramidal lesions in man (author's transl)].

The reaction times for rapid movements in muscles of arm and leg were measured in 20 patients with unilateral lesions of the motor cortex and the internal capsule. Rapid unilateral and bilateral movements after an acoustic signal (click) on the pyramidally paretic side were compared with the normal side. In these patients and in 10 normal subjects, electromyographic and mechanical recordings from symmetrical muscles of both sides were compared. 2. All patients with pyramidal lesions showed in the case of unilateral movements a marked prolongation of motor latency in the affected muscles: compared to the normal side, the movement started 30-160 msec later in muscles contralateral to the lesion of the motor cortex. In contrast, normal subjects showed equal latencies on both sides with maximal differences of 10-20 msec. 3. When movements were executed bilaterally the latency prolongation in the pyramidally paretic muscles was markedly diminished or disappeared in later stages. In most patients the bilateral movements started simultaneously in the normal and the paretic muscles, except in 5 recent lesions of the contralateral motor cortex. 4. The significance of the findings is discussed in terms of the function of the human motor cortex in starting and controlling voluntary movements. It is assumed that the disappearance of latency prolongation when movements are executed bilaterally in patients with unilateral pyramidal lesions can be best explained by homolateral projections of uncrossed pyramidal fibres to the motoneurones. 5. These results, and other observations, suggest that the motor cortex starts and controls voluntary movements via rapidly conducting pyramidal fibres to the motoneurones. This occurs after a preprogramming and a readiness posture is established by other cerebral structures. The prolongation of motor latencies after motor cortex lesions is probably due to a disturbance in the rapidly conducting cortico-spinal projections to spinal motoneurones and interneurones.

Adult↗