Melanoma erysipeloides: successful treatment by chemoimmunotherapy.
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Adult↗
Biomedical subjects
U Hillen
Publications and source records attributed to U Hillen.
[Ruptured aneurysm of an aberrant subclavian artery].
An X-ray film of the thorax in a 76-year-old man with recurrent dyspnoea and haemoptysis showed a widened upper mediastinum. Computed tomography demonstrated an aneurysm of an aberrant right subclavian artery as the cause of the symptoms and the mediastinal widening. The patient died 5 days after hospitalization and before a planned operation, another episode of severe haemoptysis having been followed by haematemesis. Autopsy revealed a 13 cm-long aneurysm which had ruptured into the right upper lobe of the lung with bleeding into the bronchial system. No further cases of an aneurysm of an aberrant right subclavian artery with ruptures into the lung parenchyma have been reported so far. But it should be included as a rare cause in the differential diagnosis of recurrent haemoptysis.
Aged↗
Increase by tubocurarine of [3H]acetylcholine release from the rat phrenic nerve after desensitization of nicotine receptors.
Tubocurarine reduced the neurally evoked [3H]acetylcholine release in the absence of nicotine, indicating positive nicotinic feedback. Tubocurarine, however, enhanced [3H]acetylcholine release after pretreatment with nicotine, a condition which causes desensitization of nicotine autoreceptors. After a nicotine-free period (15-60 min) during which the facilitatory autoreceptors could recover from desensitization, tubocurarine again reduced [3H]acetylcholine release. Protection of facilitatory nicotine autoreceptors from desensitization could explain the tubocurarine-induced increase in transmitter release.
Acetylcholine↗
Effects of (+)-tubocurarine on [3H]acetylcholine release from the rat phrenic nerve at different stimulation frequencies and train lengths.
The effect of (+)-tubocurarine (TC) on the release of [3H]acetylcholine from the rat phrenic nerve-hemidiaphragm preincubated with [3H]choline was investigated at different stimulation frequencies and train lengths. At 0.5 Hz (100 pulses) TC failed to modulate the evoked acetylcholine release. A slight (30%) inhibition was observed at 1 Hz (100 pulses). Release of acetylcholine evoked at 5, 25 and 50 Hz (100 pulses) or 100 Hz (200 pulses) was markedly reduced by TC. The degree of inhibition (60%) was similar between 5 Hz and 100 Hz. A concentration of 1 mumol/l TC was a maximal effective concentration at 5 Hz whilst at all higher stimulation frequencies a 10-fold higher concentration was necessary for the maximal effect. When 300 pulses were continuously applied at 5 Hz or 50 Hz TC caused only a slight inhibition (20%). Additionally, the phrenic nerve was stimulated intermittently. Trains of 15 pulses were repeated 10 times with an interval of 3 s between each train. Under this latter stimulation condition TC failed to reduce acetylcholine release. It is concluded that nicotinic autofacilitation of acetylcholine release from the motor nerve operates at frequencies and stimulation conditions similar to the pattern of nerve activity under in vivo conditions. At least more than 15 pulses are required before the nicotinic autofacilitation becomes apparent. It appears unlikely that the TC induced fading of end-organ responses can only be attributed to a blockade of the presynaptic nicotine receptors.
Acetylcholine↗