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Biomedical subjects

K Hu

Publications and source records attributed to K Hu.

At least 145 records · Page 8Linked to original sources
PubMed1989

Transmitter neurochemistry of the efferent neuron system innervating the labyrinth.

It is likely that several mechanisms contribute to the efferent control of cochlear and vestibular function. Different effects are probably mediated by different neuronal transmitters. In spite of a number of transmitter candidates, it is still widely assumed that the entire efferent system can be globally characterized as cholinergic. We attempted to label retrogradely identified efferent neurons in the brainstem with a monoclonal antibody against choline acetyltransferase (ChAT), the acetylcholine (ACh) synthesizing enzyme. Only a portion of the vestibular efferents could thus be shown to be cholinergic in the rat. Medial cochlear efferents, terminating under outer hair cells, may also be cholinergic since they stain intensely for acetylcholine esterase (AChE) after pre-treatment with the AChE inhibitor diisopropylfluorophosphate (DFP). The lateral cochlear efferents terminating under inner hair cells, as well as more than half of the vestibular efferent neuron population, reacted negatively with either method designed to identify cholinergic neurons. Half of the lateral olivo-cochlear neuron population filled retrogradely with tritiated gamma-amino butyric acid [( 3H]-GABA). These cells were similar in size and distribution to neurons staining for the GABA synthesizing enzyme glutamic acid decarboxylase (GAD). Retrograde transport of [3H]-aspartate from the inner ear to the brainstem was seen in half of the lateral olivocochlear population, as well as in part of the efferent vestibular population in group E and in the caudal pontine reticular nucleus (CPR). Since various peptides have also been located in efferent neurons, this system is chemically diversified. Several distinct mechanisms of efferent control with presumably differing functions must, therefore, exist.

Acetylcholinesterase↗
PubMed1989

Activation of the GM-CSF promoter by HTLV-I and -II tax proteins.

Production of granulocyte-macrophage colony-stimulating factor (GM-CSF) by normal T lymphocytes requires activation by antigen, mitogen or lectin, whereas T-cell lines transformed by human T-cell leukemia virus type I (HTLV-I) or type II (HTLV-II) constitutively produce high levels of GM-CSF. Using transient cotransfection assays, we demonstrate that introduction of the tax gene of either HTLV-I or HTLV-II is sufficient to activate GM-CSF promoter constructs in an unstimulated T-cell line. The GM-CSF 5' flanking sequences previously shown to be sufficient for GM-CSF induction following T-cell activation are also sufficient for activation by the HTLV tax proteins. The sequences required for trans-activation of GM-CSF are distinct from those required for the activation of other T-cell-inducible genes (IL-2R alpha, IL-2) by tax, suggesting that tax can have pleiotropic effects on gene expression in T cells. Constitutive GM-CSF production by HTLV-infected T cells may therefore be due to trans-activation of its promoter by tax. Expression of GM-CSF by HTLV-I infected lymphocytes may be important in the granulocytosis and eosinophilia frequently seen in patients with HTLV-I-induced adult T-cell leukemia/lymphoma.

Animals↗
PubMed1989

Electrophysiology of the electrically and mechanically damaged cochlea.

Electrical and mechanical stimuli were used in an attempt to cause cochlear deafness in a preparation with a rich supply of afferent cochlear neurons. Hearing sensitivity was assessed by electrocochleography and neuron survival was estimated by evaluating electrically induced auditory brainstem responses (EABR). Charge balanced sinusoidal alternating currents between 1 and 30 kHz for up to 15 hours produced a limited high frequency hearing loss when applied through the intact round window. A similar permanent threshold shift (PTS) could be induced by mechanical irritation with a scala tympani electrode through a round window fenestration. There is a summation of electrical and mechanical damage; however, complete deafness never occurred and the EABR provided no evidence for a major retrocochlear damage. These results suggest that deafness associated with perilymph leakage or induced during certain types of ear surgery should not be accepted as inevitable.

Animals↗
PubMed1989

Analogue signal representation in the medial superior olive of the cat.

Temporal sound processing is likely to depend upon a delay line at a low level in the auditory pathways. We searched for such a delay line in the medial superior olivary nucleus of anesthetized cats. A remarkably pure sinusoidal neurophonic field potential could be recorded in the center of the MSO which was localized electrophysiologically as the point of the field potential polarity reversal and histologically by microinjection WGA-HRP through the recording microelectrode. Fourier analysis of the neurophonic potentials revealed increasing degradation by distortion products with distance from the MSO center. Neurophonic tuning curves indicated a similar frequency selectivity for individual recording sites as predicted by cochlear filter functions. Cross correlation of neurophonics recorded at different positions along the medio-lateral axis demonstrated the presence of a delay line, extending to over 0.6 ms. It is concluded that delay lines required for directional hearing and complex tone identification exist in the MSO.

Acoustic Stimulation↗
PubMed1988

Retrograde transport of [3H]-GABA by lateral olivocochlear neurons in the rat.

Injection of [3H]-gamma aminobutyric acid (GABA) into the perilymphatic space of the rat's inner ear resulted in retrograde labeling of a portion of the small efferent olivocochlear neurons within the lateral superior olivary nucleus (LSO). These cells were of similar size as LSO neurons stained immunohistochemically with antibodies to the GABA synthesizing enzyme glutamic acid decarboxylase (GAD). They were of fusiform shape, but smaller than principal LSO cells, which did not stain for GAD and did not accumulate [3H]-GABA. Other efferent cochlear and vestibular neurons were not labeled.

Animals↗
PubMed1988

Histopathology of chloroform-induced inner ear damage.

Inner ear function loss was caused in guinea pigs and rats by injecting chloroform into the middle ear. After symptoms for cochlear and vestibular deficit had been registered, the animals were permitted to survive for one day to five months. Ear histopathology was then studied in celloidin sections. In both species, hair cells and afferent nerve fibers were intact at all survival times. The acute stage of functional loss in guinea pigs was associated with inner ears of normal histological appearance. Within days after chloroform injection a severe otitis media developed which led to fibrous occlusion of the round window and eventually to new bone growth in the middle ear space around the otic capsule. A secondary labyrinthitis was also observed, resulting in endolymphatic hydrops at longer survival times. Different histopathological changes were seen in rats. The tectorial membrane appeared swollen in all cases, the swelling being more severe in more apical turns at longer survival times. It is concluded that only secondary sequela of the initial functional insult can be detected by standard light microscopic histopathology. Chloroform does not cause a chemical labyrinthectomy as previously assumed, although it is severely ototoxic.

Animals↗
PubMed1987

Electrophysiological evaluation of chloroform-induced inner ear damage.

Local placement of chloroform in either the external or the middle ear has been previously reported to induce a chemical labyrinthectomy. In order to examine the value of this effect as a research tool, we injected chloroform into the middle ears of guinea pigs and rats. Cochlear damage was assessed by electrocochleography (ECochG) and auditory brainstem response (ABR) audiometry. Both species developed complete deafness within a few hours after instillation of the chloroform. The deafness was permanent in the guinea pigs, whereas there was a partial recovery of auditory function in the rats. The survival rate of the auditory nerve fibers was estimated by measuring the ABR evoked by electrical stimulation via the scala tympani (EABR). A normal EABR recruitment pattern suggested that the main chloroform effect was located peripheral to the afferent axons. In conclusion, chloroform must be considered a severely ototoxic agent when applied locally.

Animals↗
PubMed1986

Cholinergic innervation of the rat's labyrinth.

Efferent vestibular and cochlear neurons were identified in the rat's brain stem by retrograde labelling with True Blue (TB) or wheat germ agglutinin - horseradish peroxidase (WGA-HRP) injected into the utricle. Such cells were found at the same locations described in 1983 by White and Warr (ipsilateral superior olivary nucleus (LSO), bilateral latero-ventral nucleus of the trapezoid body (LTz) bilateral group E medial and lateral to the genu facialis) and, in addition, bilaterally in the caudal pontine reticular nucleus (CPR) at the level of the descending facial nerve. Cholinergic neurons were identified by counterstaining sections containing TB filled perikarya for acetylcholinesterase (AChE) following pretreatment with diisopropylfluorophosphate (DFP) or choline acetyltransferase (ChAT), by immunohistochemistry with highly specific monoclonal antibodies. Many, but not all, vestibular efferent cell bodies located in group E were shown to be cholinergic. These and other recently published data suggest that the efferent octavus system may consist of a number of chemically distinct cell groups.

Acetylcholinesterase↗
PubMed1986

A procedure of vestibular decompensation for clinical diagnosis. I. Animal experiments.

Vestibular lesions are often so effectively compensated that their diagnosis may be difficult. Certain chemicals can decompensate the central vestibular system and thus uncover symptoms present before compensation. This study attempts to devise a procedure which can utilize such decompensation for the benefit of clinical diagnosis. Unilateral labyrinthectomies were performed in rats. Pathological movements and body positions due to the vestibular loss were compensated within about one week. Systemic application of cholinomimetic drugs (physostigmine and nicotine) led to consistent decompensation which lasted, however, too long and was accompanied by too severe side effects to be considered for clinical diagnostic purposes. Local application of these drugs into the middle ear of the healthy side were without effect. Brief inhalation of nitrous oxide (up to 79 vol.%) caused decompensation during the first four postoperative weeks but not consistently at longer survival times. Inhalation of halothane in N2O and O2 for 90 seconds caused a reliable decompensation at all times during the six month postoperative observation period. It is concluded that a brief halothane-N2O anesthesia may prove to be useful in a diagnostic search for compensated vestibular deficits.

Adaptation, Physiological↗
PubMed1984

Cochlear implant: our preliminary experience.

We have performed cochlear implants on 16 patients (12 cases with the plug type electrodes and 4 cases with the coil type electrodes) with analogue single channel electroacoustic stimulators. The follow-up period was 8 months to 3 years. The selection of patients, operative approach and the results of these cases are presented. Our present cochlear implant can bring the totally sensory deaf patient back to the world of sound but the sounds heard are distorted so they are unable to discriminate speech, although it improves their lipreading capacity and sense of safety. The results are encouraging but much more is to be desired and further research and investigation are required.

Adolescent↗
PubMedDate not supplied

Chronic effects of ACE-inhibition (quinapril) and angiotensin-II-type-1 receptor blockade (losartan) on atrial natriuretic peptide in brain nuclei of rats with experimental myocardial infarction.

Alterations of the central nervous system may be important for imbalance of cardiovascular and fluid regulation in heart failure. The central renin-angiotensin and atrial natriuretic peptide (ANP) systems act as mutual antagonists. The effects of angiotensin converting enzyme (ACE) inhibition (quinapril, 6 mg/kg/day) and angiotensin II type 1 (AT1) receptor blockade (losartan, 10 mg/kg/day) on ANP levels in 18 selected, microdissected brain nuclei were determined in sham-operated rats and rats with left ventricular dysfunction 8 weeks after myocardial infarction (MI). Plasma ANP tended to increase in MI rats and was further increased by quinapril. ANP was decreased in 12 brain areas of MI rats. ANP concentration was also significantly decreased by quinapril in six brain nuclei including subfornical organ and organum vasculosum laminae terminalis (areas lacking blood-brain barrier), and by losartan in 16 brain nuclei outside and within the blood-brain barrier in sham operated rats. However, both quinapril and losartan prevented a further reduction of central ANP as a result of myocardial infarction. These data suggest that there are effects on central ANP that result from chronic left ventricular dysfunction as well as an ACE-inhibitor and AT1-antagonist. Mechanisms and consequences of central ANP depression remain unclear. They could, however, support systemic vasoconstriction and sodium and fluid retention.

Angiotensin Receptor Antagonists↗