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Biomedical subjects

H Tong

Publications and source records attributed to H Tong.

43 records · Page 3Linked to original sources

No evidence of hearing loss due to fetal acoustic stimulation test.

The fetal acoustic stimulation test is used increasingly for fetal assessment. To evaluate the possibility of acoustic trauma, 465 children who had been exposed to vibroacoustic stimulation in utero were screened at 4 years of age for high-frequency hearing loss. A hand-held audiometer with test tones at 25 dB for 1000 and 4000 Hz was used because responses at this level indicate hearing within normal limits for middle and high frequencies. Thirty-one children failed the test. Failure to respond was followed by inspection of the ear canal for wax, tympanometry, and reflex measurement to assess the tympanic membrane, middle ear, and eustachian tube. Hearing was retested across the full frequency range using conventional audiometric technique, and referral for otolaryngologic examination and treatment was made if necessary. The causes of hearing loss were impacted wax in 12, current or recent upper respiratory tract infection with eustachian tube dysfunction and middle ear effusion in 15, and unresolved middle ear effusion after treatment with antibiotics for otitis media in two. Profound bilateral sensorineural hearing loss of unknown origin was found in one and slight bilateral gently sloping hearing loss in another. Retesting of all children with conductive hearing loss indicated that hearing had returned to normal after treatment. None of the children showed evidence of hearing loss.

Acoustic Stimulation↗

Prostaglandin endoperoxide synthase-2 abundance is increased in brain tissues of late-gestation fetal sheep in response to cerebral hypoperfusion.

OBJECTIVE: To determine the mechanism by which cerebral hypoperfusion enhances prostanoid secretion by fetal brain tissues. METHODS: Studies were performed on five intact and five carotid sinus-denervated sheep fetuses (124-136 days) exposed to 10 minutes of cerebral hypoperfusion. Plasma collected from lingual artery and sagittal sinus, and microdialysates collected from brain stem and hypothalamus were assayed for prostanoid production. Fetal hypothalamus, cerebral cortex, hippocampus, cerebellum, and brain stem were collected from intact animals and 30 minutes after cerebral hypoperfusion for the expression, activity, and distribution of prostaglandin endoperoxide synthase-1 (PGHS-1), PGHS-2, and thromboxane synthase. RESULTS: Thromboxane B2 increased significantly in sagittal sinus compared with arterial blood, but PGE2 did not change. Thromboxane B2 decreased in brain stem and hypothalamus microdialysates, and prostaglandin E2 increased in these regions. PGHS-2 immunoreactive protein levels in brain tissues increased in the cerebral hypoperfusion fetuses compared with those of the intact animals. By contrast, PGHS-1 and thromboxane synthase protein levels did not change between these two groups. Prostaglandin endoperoxide synthase activity in brain tissues decreased with the increased levels of immunoreactive PGHS-2. CONCLUSIONS: 1) Prostanoids are produced in response to cerebral hypoperfusion, 2) the increase in the production of prostanoid responses to cerebral hypoperfusion is associated with the decrease in activity of, and therefore, the "suicide" inactivation of PGHS, and 3) PGHS-2 is the predominant form of PGHS, whose synthesis is induced by cerebral hypoperfusion in the fetal brain.

Animals↗