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Biomedical subjects

R Gothe

Publications and source records attributed to R Gothe.

At least 145 records · Page 8Linked to original sources
PubMed1979

The erythrocytic entry- and exit-mechanism of Aegyptianella pullorum Carpano, 1928.

The erythrocytic entry- and exit-mechanisms of Aegyptianella pullorum were investigated and characterized by scanning (SEM) and transmission electron microscopy (TEM) using for TEM ruthenium red as a marker of the red cell plasmalemma. The scanned Aegyptianella preparations produced static evidence of an endocytosis followed by an erythrocytic vesiculation as the possible mode of entrance of initial bodies into erythrocytes. The presence of ruthenium red only coating the membrane around the parasitophorous vacuole during the whole invasive process and the complete absence of the stain inside the host cell indicate that the entry of aegyptianellas is accomplished by invagination of the host cell plasmalemma and is not preceded nor followed by its breakage, furthermore unequivocally proving the intracellular parasitism of A. pullorum during its reproductive cycle. One possible mode of exit of initial bodies from parasitized erythrocytes appeared to be the invasive mechanism in reverse order, an exocytosis. Generally, however, the affected erythrocytes are parasitogenically injured, resulting in release of the parasites into the plasma and, subsequently, in host cell lysis.

Animals↗
PubMed1978

[The vulnerability of peripheral nerves and the somatic toxin linkage in tick paralysis of chickens, caused by Argas (Persicargas) walkerae (author's transl)].

Investigations on the impulse propagation and the pattern of amplitudes of toxically by Argas (Persicargas) walkerae larvae impaired peripheral nerves were carried out under oxygen saturated and anoxic conditions. It was demonstrated, that the maximum nerve conduction velocities of the isolated N. ischiadicus were slightly lowered in the first carbogenic and anoxic phase, in comparison with normal nerves. After the second incubation the conduction velocities were, however, almost the same or even higher. The survival times of the nerves after anoxic exposure, which were determined by the temporal persistence of the potentials, revealed that this neurophysiological parameter always resulted in a higher value for the damaged nerves after every two anoxic phases. The diseased nerves therefore tolerate anoxia longer and better than do healthy nerves in respect to their excitability and in their function of impulse propagation. From these in vitro investigations it is concluded that the noxious substance responsible for the paralysis is not cell-bound, but circulates humorally. The toxin possesses membranophilic properties, but its somatic linkage is very labile.

Animals↗