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Biomedical subjects

T T Jung

Publications and source records attributed to T T Jung.

At least 37 records · Page 2Linked to original sources
PubMed1992

Permeability of arachidonic acid metabolites through the round window membrane in chinchillas.

Our previous studies showed that samples of middle ear effusion contain high concentrations of arachidonic acid metabolites (AAMs); both prostaglandins (PGs) and leukotrienes (LTs). Since abnormal levels of AAMs in the perilymph seem to be associated with salicylate ototoxicity and the round window membrane (RWM) is the most likely route of entry from the middle ear to the inner ear, it would be important to know the permeability of AAMs through the RWM. Permeability of AAMs was determined by applying labeled and standard representatives AAMs on the RWM and counting radioactivity or measuring concentrations of AAMs in perilymph at different time intervals. Using chinchillas as experimental animals, samples of perilymph were obtained through a fenestration made at the helicotrema of the cochlea after 0.5, 1, 2, and 4, hours from placing tritiated or standard PGE2, 6-keto-PGF1 alpha, LTB4, LTC4 and 15-hydroxyeicosatetraenoic acid (HETE) over RWMs. Radioactivity in the perilymph was determined by a scintillation counter and concentrations of AAMs were measured by reverse phase high performance liquid chromatography (RP-HPLC) and radioimmunoassay. AAMs, which are twenty carbon fatty acids, were found to cross the RWM readily. Radioactivity and concentrations of AAMs in perilymph were detected in 30 minutes and peaked by one hour from the application of AAMs on the RWM. The results of this study suggest that AAMs such as PGs and LTs present in the middle ear fluid can cross the RWM readily and enter into the perilymphatic space of the cochlea. Sensorineural hearing loss observed in chronic otitis media could be mediated by PGs and LTs in the middle ear effusion crossing over to the inner ear through the RWM.

Adrenal Cortex Hormones↗
PubMed1992

Effect of exogenous arachidonic acid metabolites applied on round window membrane on hearing and their levels in the perilymph.

Our previous studies revealed that treatment with sodium salicylate or indomethacin caused hearing loss, a decrease in prostaglandin (PG) levels, and an increase in leukotriene (LT) levels of the arachidonic acid (AA) cascade in the perilymph. We suspected that decreased PG-levels and/or elevated LT-levels in the inner ear may be responsible for the salicylate ototoxicity. In order to test this hypothesis, effects of exogenous treatments with PGs, PG-analog, LTs, and other lipoxygenase products on hearing and levels of AA metabolites in the perilymph were studied in chinchillas. Cyclooxygenase products, PGI2, 6-keto-PGF1 alpha, Iloprost (PGI2 analog), PGE2, and LTB4, LTC4, and 15-hydroxyeicosatetraenoic acid (15-HETE) in the lipoxygenase products in the dose of 150 ng were applied on the round window membrane (RWM); cochlear function tested by auditory brainstem response (ABR) and samples of perilymph were collected at 0.5, 1, 2, and 4 hours after the application. Samples of perilymph were assayed for all spectra of AA metabolites by high performance liquid chromatography (HPLC) and radioimmunoassay (RIA). PG-treated animals developed minimal or no hearing loss. LT-treated animals exhibited hearing loss of 20 to 40 dB, peaking at one hour after the treatment. Elevated levels of arachidonic acid metabolites were measured in the perilymph of the ears treated with respective AA metabolites, with peak levels at one hour from the application. The findings of this study indicate that hearing loss can be induced by altered levels of PGs or LTs in the perilymph. This is another strong evidence that salicylate induced ototoxicity can be mediated by abnormal arachidonic acid metabolism in the inner ear.

Animals↗
PubMed1992

Effect of round window membrane application of salicylate and indomethacin on hearing and levels of arachidonic acid metabolites in perilymph.

Our previous studies revealed that systemic salicylate-induced ototoxicity is associated with altered levels of arachidonic acid metabolites (AAMs) in the perilymph. In order to eliminate the possibility of systemic toxic effects of salicylate when it is given parenterally, an animal model of salicylate-induced ototoxicity was developed by applying it on the round window membrane (RWM). Using chinchillas as experimental animals, sodium salicylate (150 micrograms) or another nonsteroidal anti-inflammatory drug (NSAID), indomethacin (20 micrograms) was applied on the RWM, cochlear function was determined by auditory brainstem response (ABR) and perilymph assayed for AAMs both prostaglandins (PGs) and leukotrienes (LTs) by high performance liquid chromatography (HPLC) and radioimmunoassay (RIA) at different time intervals. When salicylate or indomethacin was applied on the RWM, dose-dependent ABR threshold losses of 20 to 50 dB was observed in 1 to 2 hours associated with decreased concentrations of 6-keto-PGF1 alpha and elevated levels of LTs. The hearing loss recovered to normal threshold over a period of 8 hours. The control group showed no hearing loss or any change in PG or LT-levels in the prilymph. The results of this study suggest that the method of inducing ototoxicity by applying salicylate or indomethacin on the RWM seems to be a reliable method for avoiding systemic toxicity of the parenteral treatment method and that ototoxicity induced by salicylate or indomethacin may be mediated by decreased PGs and elevated LTs.

Animals↗
PubMed1991

Otolaryngologic approach to the diagnosis and management of otitis media.

Otitis media is a common childhood disease caused by multiple factors. Understanding the pathogenesis of otitis media is important in the diagnosis and management of it. The mode of therapy should be chosen depending on the type and stage of the disease. Treatment options available to an otolaryngologist include antibiotics, tympanocentesis, myringotomy and tympanostomy tube insertions, adenoidectomy with or without tonsillectomy, exploratory tympanotomy, atympanoplasty, and mastoidectomy.

Anti-Bacterial Agents↗
PubMed1990

Effect of prostaglandin, leukotriene, and arachidonic acid on experimental otitis media with effusion in chinchillas.

Although previous studies have shown that prostaglandins (PGs), leukotrienes (LTs), and other arachidonic acid (AA) metabolites play an important role in the pathogenesis of otitis media with effusion (OME), the exact role of each AA metabolite in OME is still unknown. The purpose of this study was to examine the effect of several individual AA metabolites alone or in combination and AA itself on experimental otitis media in chinchillas. Normal chinchillas were inoculated daily with normal saline, PGE2, LTC4, LTC4 + PGE2, and AA through the superior bullae over 7 days. Animals were followed by otoscopy and tympanometry, samples of middle ear effusion were collected for biochemical assay, and temporal bones were processed for histopathology. The highest number of ears that developed OME was in the group inoculated with PGE2 + LTC4. The degree of inflammatory change was more pronounced in groups injected with LTC4 than any other group. The findings of this study suggest that eicosanoids PGE2, LTC4, and AA alone or in combination inoculated into the middle ear can induce OME.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Prostaglandins, leukotrienes, and other arachidonic acid metabolites in the pathogenesis of otitis media.

Among the various inflammatory mediators of otitis media (OM), metabolites of arachidonic acid (AA) such as prostaglandins (PGs) and leukotrienes (LTs) appear to play an important role in the pathogenesis of otitis media. In an effort to investigate the role of AA metabolites on the pathogenesis of otitis media, concentrations of AA metabolites were measured in middle ear effusion (MEE) from human and paralleling animal models of otitis media and the effects of inhibitors of AA metabolism, antibiotics, and tympanostomy tube (TT) on the outcome of animal models of OM were studied. Concentrations of AA metabolites in MEE were higher in the younger age group. Levels of PGE2 and LTB4 in MEE seem to represent the degree of inflammation of OM best. Lipoxygenase products seem to be associated with the mucoid type of MEE. In the study of animal models of OM, combined models and ears with TT showed more inflammation than single models and ears without TT. Study of the therapeutic use of inhibitors of AA metabolism, penicillin, and TT showed that lipoxygenase products may be more important in the pathogenesis of OM than the cyclo-oxygenase products, and that the use of a combination of penicillin and corticosteroid produces the best results. It is clear from these studies that arachidonic acid metabolites are important inflammatory mediators in the pathogenesis of otitis media.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Prostaglandins in human cholesteatoma and granulation tissue.

Bone resorption is a common finding in chronic otitis media with or without cholesteatoma. The etiology of bone resorption in chronic otitis media is still not clear. Bone-resorbing activity of prostaglandins (PGs) has been well known. PGE-like material has been detected in granulation tissue. However, there have been no reports on the comprehensive study of PGs in cholesteatomas or granulation tissue. The purpose of this study is to show that PGs are synthesized in the middle ear tissue and to report concentrations of PGs in cholesteatomas and granulation tissue. Samples of cholesteatoma and granulation tissues were obtained at the time of tympanomastoidectomies. Prostaglandin synthesizing activity was determined by incubating tissue with labeled arachidonic acid (precursor of PGs) and radiochromatography. Levels of PGs were determined by radioimmunoassay. Arachidonic acid metabolites produced in cholesteatoma and granulation tissue included PGE2; 6-keto-PGF1 alpha; PGF2 alpha; PGD2; and 5-, 12-, and 15-hydroxy-eicosatetraenoic acid (HETE). Levels of PGE2 were 2.6 times higher in cholesteatoma (106.8 +/- 46 ng/g) than in granulation tissue (41.0 +/- 14.3 ng/g). Levels of 6-keto-PGF1 alpha were two times higher in granulation tissue (89.0 +/- 27.0 ng/g) than in cholesteatoma. Levels of thromboxane B2 were two times higher in cholesteatoma than in granulation tissue. The results of this study demonstrate that cholesteatoma and granulation tissues actively synthesize PGs and contain high concentrations of them. Since PGs are locally active hormones, the presence of PGs indicates an active role for PGs in the pathogenesis of chronic otitis media with bone resorption.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Prostaglandins, leukotrienes, and other arachidonic acid metabolites in nasal polyps and nasal mucosa.

Prostaglandins (PGs) and leukotrienes (LTs) are known to play an important role in allergic inflammatory reactions. The triad of aspirin sensitivity, nasal polyposis, and asthma led us to suspect that PGs, LTs and other arachidonic acid metabolites may be involved in the pathogenesis of nasal polyps. The purpose of this study was to determine arachidonic acid metabolites and to measure concentrations of PGs and LTs in nasal polyps and nasal mucosa. Samples of nasal polyps and nasal mucosa were obtained at the time of polypectomies and nasal procedures. Metabolites of arachidonic acid in tissue were determined by incubation of tissue-homogenates with 14C-arachidonic acid and analyses with thin-layer chromatography and high performance liquid chromatography (HPLC). Levels of PGE2, 6-keto-PGF1 alpha, thromboxane (Tx)B2, 15-hydroxyeicosatetraenoic acid (HETE), LTC4, LTB4 were measured by radioimmunoassay. The predominant arachidonic acid metabolite in both nasal polyps and mucosa with 15-HETE. The HPLC analysis showed that the predominant metabolite in nasal polyp was 15-HETE, especially in polyps from aspirin sensitive patients. Levels of 15-HETE and PGE2 were higher in polyps from patients with a history of allergy than from nonallergic patients. Levels of LTC4 and LTB4 in nasal polyps were determined. The findings of this study will help to explain biochemical basis of the pathogenesis of aspirin-sensitive nasal polyps and to develop better medical treatment for them.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Cochleovestibular nerve sections in labyrinthectomized patients.

Labyrinthectomy is indicated for a patient who has unilateral peripheral labyrinthine disease with unserviceable hearing loss. For most patients, labyrinthectomy provides complete relief from intractable vertigo. Some patients continue to have persistent vertigo, however, even after a complete destructive labyrinthectomy. Only after cochleovestibular nerve sections were these patients relieved of intractable vertigo. Representative cases of cochleovestibular nerve sections in labyrinthectomized patients are presented. The reason why the cochleovestibular nerve section relieves the symptom of vertigo in labyrinthectomized patients is not clear. Labyrinthectomy destroys vestibular sense organs, while cochleovestibular nerve section eliminates spontaneous activity and prevents the possibility of nerve regeneration by excision of the ganglion. For those patients who required vestibular nerve sections, there may have been abnormal excitation of vestibular nerve fibers. This might be explained by incomplete labyrinthectomy, regeneration of vestibular nerve fibers, contribution from vestibular ganglia or nonfunctioning cochlea, and vascular loop syndrome.

Aged↗
PubMed1986

Primary and secondary tumors of the facial nerve. A temporal bone study.

Of 1400 temporal bones in the collection at the University of Minnesota, Minneapolis, 17 temporal bones from 15 patients were found to have tumors involving the facial nerve. The findings were as follows: one case of facial nerve schwannoma; two cases of invasion of the facial nerve by contiguous tumor; and 14 cases of metastatic tumors involving the facial nerve. Facial nerve paralysis was present in half of the cases (nine of 17). Facial nerve paralysis was present in the case of facial nerve schwannoma, in both cases of invasion of the facial nerve by contiguous tumor, and in six of 14 cases of metastatic tumors involving the facial nerve. The presence of the facial nerve paralysis correlated well with the degree of tumor infiltration into the nerve fibers and the segment of the tumor involvement in the facial nerve. In the patients with metastatic tumors, facial nerve paralysis was a sign of extensive intracranial tumor involvement and was usually accompanied by other cranial nerve palsies, most commonly involving the fifth nerve.

Cranial Nerve Neoplasms↗
PubMed1986

The kinetics of penicillin diffusion in serum and middle ear effusions in experimentally induced otitis media.

The kinetics of penicillin diffusion in serum and middle ear effusions (MEE) was studied in experimentally induced serous otitis media (SOM) and purulent otitis media (POM) after systemic injection of procaine-penicillin G. A higher rate of diffusion of penicillin into the middle ear cavity was found in POM than in SOM. The time to reach peak concentrations in MEE was also shorter in POM. Elimination of penicillin from the middle ear cavity was slower in SOM than in POM.

Animals↗
PubMed1986

Biochemical aspects of inner ear fluids and possible implications for pharmacological treatment.

Inner ear fluids are in dynamic equilibrium with surrounding fluids, namely blood and cerebrospinal fluid. It is known that substances injected into the blood stream or cerebrospinal fluid are transported into the inner ear fluids. The rate of transport from blood into perilymph is inversely related to the molecular weight or molecular size. There appears to exist a blood-labyrinth barrier. In general, the morphology of capillaries in the spiral ligament and stria vascularis is similar to that of brain capillaries which contribute to formation of the blood-brain barrier. Information on the volume of the inner ear fluids is necessary for estimating the toxicity of the drugs as well as the effective concentration of systemically injected substances. Recently, alteration of the levels of arachidonic acid metabolites, especially the prostaglandins, in perilymph under experimental conditions has been reported. The responses of prostaglandin levels in perilymph to these experimental conditions (aspirin injection, antidiuretic hormone or epinephrine infusion) suggest that prostaglandins may play an important role under physiological conditions. Possible mechanisms of auditory dysfunction due to abnormal prostaglandin metabolism in the auditory system are discussed.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Inflammatory changes reflected in middle ear effusion in otitis media.

Otitis media (OM) is an extremely wide-spread disease, and the presence of middle ear effusion (MEE) is a common phenomena in OM. The analyses of MEE provide important information for better understanding of etiology and evaluation of inflammatory stages of the middle ear cavity. Well investigated etiologic factors of OM have included negative pressures within the middle ear cavity secondary to Eustachian tube dysfunction, and bacterial or viral infection. It is quite conceivable that the biochemical, cytological and immunochemical products found in the middle ear mucosa (MEM) and MEE during OM may contribute to the clinical course of the disease. The sources of these inflammatory components include: inflamed epithelial cells of MEM, cells of the subepithelial space, vasogenic origins, bacterial and/or inflammatory cell products in MEE. In animal studies (serous otitis media [SOM] and purulent otitis media [POM]), interesting correlations between sequential biochemical and cytological findings have been observed. The vasodilation, increased blood vessel permeability, and the release of intracellular products both from inflamed middle ear mucosa and inflammatory cells are determining factors for the biochemical changes of MEE. Recently, the importance of the role of the subepithelial space (SES) in the pathogenesis of various types of OM has been emphasized in human studies. A strong cellular-immune response with proliferation of fibroblasts, collagen fibers, plasma cells, lymphocytes, macrophages, along with an increase in capillary networks have been characterized with SES changes in OM. Analysis of MEE by biochemical and immunochemical markers (prostaglandins, immunoglobulins, intracellular enzymes) have reflected inflammatory changes in the MEM of various types and stages of OM.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Prostaglandins and other arachidonic acid metabolites in the middle ear fluids.

Prostaglandins (PGs) and other arachidonic acid (AA) metabolites have been recognized as mediators of inflammation and bone resorption, chemotactic agent to polymorphonuclear leukocytes (PMN), and regulators of inflammatory response. Although assays of some PGs in the middle ear fluid (MEF) were reported, there has been no report on comprehensive assay of PGs and other AA metabolites in MEF. Concentrations of PGs were measured by radioimmunoassay in human MEF. The data on human MEF were analyzed according to age group. In addition, levels of lipoxygenase-products, 5- and 15-hydroxyeicosatetraenoic acid (HETE) and leukotriene (LT)C4 were measured in human MEF. Levels of PGE2 in MEF from human serous otitis media (SOM) were highest in younger age group (below the age of 10) then the levels drop down to lower level in older age group. In human mucoid otitis media (MOM) the levels of PGE2 are lower than SOM in younger age group then become higher than SOM in older age group. Levels of 6-keto-PGF1 alpha were higher in SOM than in MOM overall. The age breakdown of data showed progressive increase in the 6-keto-PGF1 alpha levels with older age group. Levels of TxB2 in SOM were higher than in MOM overall. The age breakdown of SOM data remained almost the same in all the age groups but the MOM data showed lowest levels in 6-10 year-old group and highest in 11-15 year-old group. Concentrations of 15-HETE in human MOM were over two times higher than in SOM. LTC4 levels in MOM were higher than SOM.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Prostaglandins in squamous cell carcinoma of the head and neck: a preliminary study.

It has already been demonstrated in human and animal systems that PGE2 is a suppressor signal for many immune functions. These include T-lymphocyte blastogenesis, natural killer cell activity, and cytolytic T-lymphocyte activity. These functions are important for destruction of tumor cells. Conceivably, suppression of these functions by excessive PGE2 restricts tumor cell kill, and reversal of suppression by an inhibitor of prostaglandin synthesis such as indomethacin could increase tumor cell kill. The purpose of this study was to determine the kind of prostaglandins (PGs) produced by tissues with squamous cell carcinoma of head and neck and to measure the concentrations of PGE2, 6-keto-PGF1 alpha, and thromboxane (Tx) B2 in the tumor tissue and in the corresponding control tissue. Tumor and normal control tissues at the margin of the resection were obtained from surgical specimens. The production of PGs was determined by incubation of tissue homogenates with 14C-arachidonic acid, by thin layer chromatography, autoradiography, and scintillation counting. Concentrations of PGs were measured by radioimmunoassay. Tumor tissues produced PGD2, E2, TxB2, F2 alpha, and 6-keto-F1 alpha, and 15-, 12-, and 5-monohydroxyeicosatetraenoic acid (HETE). Concentrations of PGE2 were four times higher in the tumor tissues compared to those in control tissues. There was no difference between the levels of TxB2 and 6-keto-PGF1 alpha in the tumor tissues and those in control tissues. The results of this study will serve as basic information necessary for the potential use of inhibitors of PG-synthesis in the treatment of head and neck carcinoma.

Adult↗
PubMed1985

Subepithelial space in otitis media.

The role of the subepithelial space (SES) has not received sufficient attention in assessing pathogenesis, pathology, and therefore, clinical diagnosis and treatment of the various forms of otitis media (OM). Temporal bones from patients with OM were classified as cases of acute purulent (POM), serous (SOM), mucoid or secretory (MOM), or chronic otitis media (COM). Controlled morphometric studies were made of cellular components of the SES, along with studies of the epithelium and middle ear space. Corollary studies of biochemistry, cellular components, and prostaglandins (PGs) were done on fluid from the human middle ear. Middle ear effusions (MEE) from animal models of SOM, MOM, and POM were analyzed biochemically. Findings are surprising in that the SES was more actively involved in all forms of OM than had been thought, especially in MOM and COM. Implications are discussed.

Animals↗