The production of 10-hydroxystearic and 10-ketostearic acids is an alternative route of oleic acid transformation by the ruminal microbiota in cattle.

The formation of hydroxystearic acid (HSA) and ketostearic acid (KSA) from oleic acid transformation has been documented in a variety of microbial species, including several isolated from the rumen of domesticated ruminant species. However, their ruminal production rates have not been established as influenced by fatty acid source. Dosing continuous cultures of mixed ruminal microorganisms with 1-(13C)-oleic acid increased the 13C enrichment of both HSA and KSA at 24 h postdosing, and showed that the majority (96 and 85%, respectively) of the HSA and KSA present in the 24-h samples originated from oleic acid. Several experiments using batch cultures of ruminal microorganisms showed that production of HSA and KSA was directly related to oleic acid input but was not affected by elaidic acid input, and that HSA was further metabolized to KSA but not to other fatty acids. When continuous cultures of ruminal microorganisms were supplemented with soybean oil or canola oil, production of 10-HSA + 10-KSA was related to oleic acid input but not to linoleic acid input. Daily production of 10-HSA + 10-KSA across treatments was 14.4 micromol/100 micromol oleic acid input into the cultures or 31.1 micromol/100 micromol oleic acid net loss. The results of this study quantify the formation of 10-HSA and 10-KSA from oleic acid transformation by ruminal microorganisms, and show that their accumulation in ruminal contents is directly related to the extent of oleic acid input and biotransformation by the rumen microbiota.

Cochlear activation at low sound intensities by a fluid pathway.

In order to assess the mechanisms responsible for cochlear activation at low sound intensities, a semi-circular canal was fenestrated in fat sand rats, and in other experiments a hole was made in the bone over the scala vestibuli of the first turn of the guinea-pig cochlea. Such holes, which expose the cochlear fluids to air, provide a sound pathway out of the cochlea which is of lower impedance than that through the round window. This should attenuate the pressure difference across the cochlear partition and thereby reduce the driving force for the base-to-apex traveling wave along the basilar membrane. The thresholds of the auditory nerve brainstem evoked responses (ABR) and of the cochlear microphonic potentials were not affected in the fenestration experiments. In addition, holes in the scala vestibuli of the first turn did not cause ABR threshold elevations. These results contribute further evidence that at low sound intensities the outer hair cells are probably not activated by a base-to-apex traveling wave along the basilar membrane. Instead it is possible that they are excited directly by the alternating condensation/rarefaction fluid pressures induced by the vibrations of the stapes footplate. The activated outer hair cells would then cause the localized basilar membrane movement.

Use of ABR threshold and OAEs in detection of noise induced hearing loss.

OBJECTIVE: To determine which measure is the most sensitive to noise induced hearing loss (NIHL): auditory nerve brainstem response (ABR), distortion product otoacoustic emission (DPOAE) or transient evoked otoacoustic emission (TEOAE), and how to assess possible changes in these responses. SUBJECTS & METHODS: Four groups of rats were exposed to various durations of 113 dB SPL broadband noise: 5 or 10 minutes (temporary changes in cochlear function), and 3 or 4 hours (permanent changes). Group means and data from individual animals were compared before and after exposure. RESULTS: Mean group DPOAE amplitude reduction showed no clear advantage over mean ABR threshold elevation in detection of temporary and permanent NIHL. Data from individual rats, however, indicated a clinical advantage for DPOAEs in detecting slight temporary, but not permanent, changes. TEOAEs were more sensitive in detecting changes in individual rats than as a group measure. CONCLUSIONS: TEOAE and DPOAE monitoring may improve detection of NIHL, though it should be used in conjunction with audiometric threshold monitoring.

Lateralization during the Weber test: animal experiments.

OBJECTIVES/HYPOTHESIS: The objective of this study were to present an assessment of a new theory to explain lateralization during the Weber test using an animal model. This theory is based on the discovery that a major pathway in bone conduction stimulation to the inner ear is through the skull contents (probably the cerebrospinal fluid [CSF]). The placement of a bone vibrator or tuning fork on the skull excites the inner ear by the classic osseous pathway and by the suggested CSF pathway. We assume that there is a phase difference between the stimulation mediated by the ossicular chain (inertial and occlusion mechanisms) and the one mediated by the CSF. The presence of a conductive pathology will decrease the magnitude of the sound energy mediated by the ossicular chain. Thus, the out-of-phase signal arriving through the bony pathways will be decreased, hence increasing the resultant sound intensity stimulating the cochlea. STUDY DESIGN: Prospective animal study. METHODS: The experiment was performed on 10 fat sand rats, which had undergone unilateral cochleostomy and a small craniotomy. The auditory nerve brainstem response (ABR) thresholds were measured to air-conducted stimulation, to stimulation with the bone vibrator applied to the skull, and to stimulation with the bone vibrator applied directly to the brain through the craniotomy. The ossicular chain of the second ear was then fixed to the middle ear walls with cyanoacrylate glue to induce a conductive hearing loss. The ABR thresholds to the same three stimuli were then measured again. RESULTS: After ossicular chain fixation, the ABR threshold to air-conducted stimulation increased, to bone vibrator stimulation on the bone decreased (hearing improvement), and to bone vibrator stimulation directly on the brain remained unchanged. CONCLUSIONS: This experiment confirms the proposed theory. During clinical bone conduction stimulation, there is a phase difference between sound energy reaching the inner ear through the middle ear ossicles and from the CSF. A middle ear conductive pathology removes one of these components, thus increasing the effective sound intensity in the affected ear. On the other hand, when the bone vibrator is applied on the brain, the inner ear is stimulated only through the CSF, so ossicular chain fixation does not change the ABR threshold. Moreover, this study proves that lateralization during the Weber phenomenon is the result, at least in part, of an intensity difference between sound energy reaching the two cochleae.

Bone conduction hearing on the teeth of the lower jaw.

Bone conduction stimulation of the teeth of the lower jaw initiates auditory sensations. However the lower jaw is only loosely coupled to the skull by the temporo-mandibular joint. Therefore the 'classical' bone conduction pathway involving skull vibration transmission entirely along bone to the temporal-petrous bone requires further consideration. Bone conduction hearing thresholds to stimulation at the forehead and at the teeth of the upper and lower jaw were determined in human subjects. Thresholds on the teeth were better than those on the forehead and there was no difference between the thresholds measured following stimulation of the upper and lower teeth. Experiments in guinea-pigs provided evidence that vibration of the teeth leads to transmission of the audio-frequency vibrations by means of soft tissue, through skull foramina, into the skull cavity (brain and CSF) and from there by fluid channels directly into inner ear fluids, exciting the cochlea.