How Is the Cochlea Activated in Response to Soft Tissue Auditory Stimulation in the Occluded Ear?

Soft tissue conduction is an additional mode of auditory stimulation which can be initiated either by applying an external vibrator to skin sites not overlying skull bone such as the neck (so it is not bone conduction) or by intrinsic body vibrations resulting, for example, from the heartbeat and vocalization. The soft tissue vibrations thereby induced are conducted by the soft tissues to all parts of the body, including the walls of the external auditory canal. In order for soft tissue conduction to elicit hearing, the soft tissue vibrations which are induced must penetrate into the cochlea in order to excite the inner ear hair cells and auditory nerve fibers. This final stage can be achieved either by an osseous bone conduction mechanism, or, more likely, by the occlusion effect: the vibrations of the walls of the occluded canal induce air pressures in the canal which drive the tympanic membrane and middle ear ossicles and activate the inner ear, acting by means of a more air conduction-like mechanism. In fact, when the clinician applies his stethoscope to the body surface of his patient in order to detect heart sounds or pulmonary air flow, he is detecting soft tissue vibrations.

Inhaled Insulin Forms Toxic Pulmonary Amyloid Aggregates

It is well known that interfaces, such as polar-nonpolar or liquid-air, play a key role in triggering protein aggregation in vitro, in particular the aggregation of peptides and proteins with the predisposition of misfolding and aggregation. Here we show that the interface present in the lungs predisposes the lungs to form aggregation of inhaled insulin. Insulin inhalers were introduced, and a large number of diabetic patients have used them. Although inhalers were safe and effective, decreases in pulmonary capacity have been reported in response to inhaled insulin. We hypothesize that the lung air-tissue interface provides a template for the aggregation of inhaled insulin. Our studies were designed to investigate the harmful potential that inhaled insulin has in pulmonary tissue in vivo, through an amyloid formation mechanism. Our data demonstrate that inhaled insulin rapidly forms amyloid in the lungs causing a significant reduction in pulmonary air flow. Our studies exemplify the importance that interfaces play in protein aggregation in vivo, illustrating the potential aggregation of inhaled proteins and the formation of amyloid deposits in the lungs. These insulin deposits resemble the amyloid structures implicated in protein misfolding disorders, such as Alzheimer’s and Parkinson’s diseases, and could as well be deleterious in nature.

Ventilatory responses to embolization of lung

Marked changes in respiratory rate and volume occurred when anesthetized and spontaneously breathing dogs were subjected to pulmonary embolization with barium sulfate. Following embolization, there was a statistically significant fall in lung compliance, and, although a rise in pulmonary air-flow resistance occurred in the majority of instances, this change was not statistically significant. When the dogs were ventilated in approximately the resting tidal range by means of a pump and embolization was carried out, a statistically significant fall in lung compliance as well as a significant rise in pulmonary resistance was seen. Embolization of spontaneously breathing vagotomized animals in three instances revealed a fall in lung compliance and a rise in pulmonary resistance. The experimental observations of others are reviewed and the clinical implications are discussed. Submitted on October 28, 1960