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Biomedical subjects

T J Yoo

Publications and source records attributed to T J Yoo.

At least 55 records · Page 3Linked to original sources
PubMed1990

Binding of platelet activating factor by isolated membranes from U937 cells.

Platelet activating factor (PAF), 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (1-O-alkyl-2-acetyl-GPC) has been known to have biological effect on cells. The mechanisms of the effect of the potent phospholipid on cells has not been established. We have used 1-O-[3H]alkyl-2-acetyl-GPC [( 3H]PAF) to study the interaction on the isolated membranes of U937 cells. The binding process was time, protein concentration, temperature dependent and reversible. The binding of [3H]PAF to the U937 cell membranes was slightly inhibited by the addition of PAF analogue, 3-O-Hexadecyl-2-acetyl-sn-glycerol-1-phosphorylcholine. U937 cell membranes showed high affinity binding sites for PAF with equilibrium dissociation constant (Kd) of 5 x 10(-9) M. The displacement of bound [3H]PAF with 500-fold excess of nonlabeled PAF was not altered suggesting that the bound [3H]PAF was not degraded during the binding. Binding of [3H]PAF on U937 cell membranes was inhibited by PAF antagonist, 59227RP. The kinetic of the inhibition by PAF antagonist is competitive suggesting that PAF and PAF antagonist bind at the same site.

Cell Line↗
PubMed1990

Type II collagen distribution in the monkey ear.

A possible role for type II collagen autoimmunity in the pathogenesis of Meniere's disease and otosclerosis was recently suggested by studies demonstrating anti-type II collagen antibody in the serum of humans with these disorders and by the induction of similar lesions in animals immunized with type II collagen. In light of these findings, we studied the anatomic distribution of type II collagen in the nonhuman primate ear by immunohistochemical techniques using defined monoclonal antibodies to type II collagen. Type II collagen was observed in the cartilage plate of the auricle and external auditory meatus, tympanic annulus, lamina propria of tympanic membrane (pars tensa), interossicular joints, stapes footplate, eustachian tube cartilage, enchondral layer and globuli interossei of the otic capsule, Rosenthal canal, cribriform base, osseous spiral lamina, spiral ligament, limbus, tectorial membrane, semicircular canal membrane and subepithelial layer of the ampullary crista, utricular and saccular maculae, and the endolymphatic duct and proximal part of the sac. Thus, type II collagen should be considered an important component of ear tissue.

Animals↗
PubMed1989

Type II collagen distribution in the ear of the guinea pig fetus.

By using monoclonal antibodies to type II collagen and immunohistochemical techniques, we studied the distribution of type II collagen in the developing guinea pig ear. Type II collagen appearance and disappearance corresponded to cartilage development and resorption. Type II collagen was identified in Meckel's and Reichert's cartilages, the cartilage plate of the auricle and external acoustic meatus, the ossicles, eustachian tube cartilage, and the otic capsule. Type II collagen also appeared with the development of structures in noncartilaginous parts including the tympanic membrane, tympanic annulus, basilar membrane, spiral limbus, spiral ligament, and osseous spiral lamina, Rosenthal's canal, the maculae of the utricle and saccule, and the semicircular canal membrane, crista ampullaris, and endolymphatic duct. Type II collagen is distributed widely in the ear after the early stages of development. Thus, type II collagen should be considered an important structural component of the ear.

Animals↗
PubMed1989

Type II collagen distribution in the ear of the developing chick embryo.

The localization of type II collagen was immunohistochemically studied in the developing chick ear using monoclonal antibodies. Type II collagen appeared under the basal lamina of the otocyst from developmental stages 14 to 16. In the otic capsule, endolymphatic duct, and semicircular canal membrane, type II collagen appeared in stage 23 or 24. From stages 28 to 29, type II collagen appeared in the primitive columella, endolymphatic sac, and fibrocartilaginous plate. Type II collagen was first observed in the crista ampullaris, basilar membrane, macula sacculi, and utriculi in stages 30 and 31. Type II collagen was not detected in the endolymphatic sac beyond developmental stage 37 and the amount of type II collagen in the otic capsule and columella decreased after stage 40. The wide distribution of type II collagen in the inner ear throughout the development of the chick embryo suggests that this collagen may act as a basic structural component of the ear.

Animals↗
PubMed1988

Induction of arthritis in monkeys by immunization with type II collagen.

Immunization of two cynomolugus and three rhesus monkeys with purified type II collagen resulted in the development of polyarthritis. Arthritis first became clinically apparent 7 wk after primary immunization and persisted for 16 mo. Radiologic examination of the limbs demonstrated soft tissue swelling with severe joint destruction including loss of cartilage and bone. Involved joints eventually became ankylosed with permanent loss of some motion. All of the monkeys developed a response to the immunizing collagen as determined by ELISA of serum for antibodies. Arthritis was associated with weight loss and constitutional symptoms, including lethargy and refusal to eat. One monkey became so debilitated that it was necessary to euthanize it. Histologic examination of the joints showed synovial hypertrophy with pannus formation. A control monkey immunized with type I collagen suffered no apparent ill effects.

Animals↗
PubMed1988

Type II collagen distribution in rodents.

The anatomical distribution of type II collagen in animal ears was studied by immunohistochemical techniques, using defined monoclonal antibodies to type II collagen. Type II collagen was observed in the cartilage plate of the auricle and external auditory meatus, tympanic annulus, lamina propria of tympanic membrane (pars tensa), interossicular joints, stapes footplate, eustachian tube cartilage, enchondral layer and globuli interossei of the otic capsule, Rosenthal canal, cribriform base, osseous spiral lamina, spiral ligament, limbus, tectorial membrane, semicircular canal membrane and subepithelial layer of the ampullary crista, utricular and saccular maculae, and the endolymphatic duct and proximal part of the sac.

Animals↗
PubMed1988

Prostaglandins in type II collagen-induced ear diseases.

This study examines the role of prostaglandins in type II collagen-induced inner ear disease. Hartley guinea pigs were immunized with type II collagen in complete Freund's adjuvant. Auditory brain stem response was measured initially and at 2, 3, 4, and 6 months after immunization. The presence of PGE2 and 6-keto-PGF1 alpha in the perilymph was determined by radioimmunoassay. Perilymph from immunized animals contained about five times more PGE2 and about three times more 6-keto-PGF1 alpha than the perilymph from control animals. However, the two groups showed no difference in the level of either PGE2 or 6-keto-PGF1 alpha in cerebrospinal fluid and serum. Immunized guinea pigs also showed evidence of hearing loss. The temporal bones showed the following changes: spiral ganglion degeneration; mild to moderate degeneration in the organ of Corti; and infrequent and very mild endolymphatic hydrops. Thus, prostaglandins might play an important role in the pathogenesis of type II collagen-induced inner ear disease.

Animals↗
PubMed1986

The use of methacholine inhalation, methacholine skin testing, distilled water inhalation challenge and eosinophil counts in the evaluation of patients presenting with cough and/or nonwheezing dyspnea.

Twenty-four patients presenting with cough and/or nonwheezing dyspnea were evaluated with methacholine inhalation challenge (MC), distilled water inhalation challenge (DC), intracutaneous tests to varying concentrations of methacholine, total eosinophil counts (TEC), sinus and chest x-rays. We found a statistically significant difference (P less than .005) in the mean TEC in those patients with a positive MC test and those with a negative test. Hyperreactivity of the airways to methacholine in asthmatics is not found in the skin. Distilled water inhalation did not serve to substitute for MC as a test of hyperreactive airways. The TEC is an excellent screening test as a predictor of patients with cough or dyspnea who have hyperreactive airways.

Adolescent↗
PubMed1985

Mediator release in local heat urticaria: protection with combined H1 and H2 antagonists.

Two patients with local heat urticaria were examined for evidence of histamine release and for changes in mast cell morphology after local heat challenge. Both patients demonstrated significant release of histamine into the draining venous blood in the challenged arm. Biopsy specimens revealed mucosal edema after 30 min, followed by a mononuclear, perivascular infiltrate by 6 hr, and increasing in intensity by 24 hr. Degranulated mast cells were observed by electron microscopy. Heat challenge was repeated after treatment with hydroxyzine, cimetidine, or a combination of both drugs. Neither hydroxyzine nor cimetidine alone affected the clinical response to challenge, but both drugs together completely abolished the clinical response. In addition, the combination of both drugs taken regularly completely prevented symptoms. This observation suggests that histamine is one of the major mediators of this disorder and that both H1 and H2 receptors are operative.

Adult↗
PubMed1985

Type II collagen mediated autoimmune middle ear disease: eustachian tube disease, otitis media with effusion and tympanosclerosis.

Intact Eustachian tube and tympanic cavity functions are essential for normal middle ear physiology. Type II collagen is an essential component of ear tissue. Autoimmune response to this type II collagen produces sensorineural hearing loss, vestibular dysfunction, endolymphatic hydrops, otospongiosis-like lesions, Eustachian tube inflammation and Eustachian tube chondritis. In addition, these autoimmune responses occasionally produce otitis media with effusion (not infectious). Tympanosclerosis, which is a frequent sequelae of otitis media with effusions, was also induced by type II collagen immunization together with surgical incision of the tympanic membrane. The exact mechanisms of this type II collagen autoimmune mediated middle ear disease are not clear. However, the animals thus induced have higher antibody titers and cell mediated immune responses to type II collagen. The tympanic membrane showing tympanosclerosis also had C3 and Ig deposits. All the animals with otitis media with effusion induced by type II collagen immunization also had Eustachian tube disease. This could be due to a malfunction of the Eustachian tube. Thus, this model might provide a rational approach for the study of otitis media with effusion associated with vasculitis. Further studies are needed to elucidate the immunologic mechanism involved in the pathogenesis of otitis media with effusion.

Animals↗
PubMed1985

Type II collagen induced autoimmune salpingitis in the rat.

Previous studies showed type II collagen induced autoimmune salpingitis in Wistar rats. In this study we increased the number of animals and investigated whether or not type II collagen induced salpingitis is transferable by immune sera. Histopathological observations of salpingitis in the serum transferred rats were similar to those observed in the immunized rats but the degree of otopathological changes was less than that of immunized rats. Electronmicroscopic findings indicate an increased permeability in the capillaries and intercellular space and cellular infiltration in the submucosa of the immunized rats.

Animals↗
PubMed1985

Immunologic aspects of otologic disease: an overview.

The immunologic explosion has now reached the field of otology. By having better techniques to measure the changes at cellular and molecular levels, it is now possible to devise experiments to show morphologic anatomic changes as well as functional changes. The demonstration in 1980 (M.S.) that tympanosclerosis could be induced immunologically represents a concrete advancement in immunologic thinking in conceptualization of otologic disease. In 1974, one of the authors (M.S.) published work dealing with the treatment of vasculitis of immunologic origin for sudden hearing loss. This was aimed at inhibiting the complement cascade from starting its destructive action. Recently, the immunologic challenge in animals demonstrated by changes in the inner ear was shown by one of the authors (T.J.Y.). Such changes were compatible with labyrinthine hydrops, or Meniere's disease, otosclerosis, and sensorineural hearing loss and vestibular dysfunction.

Cholesteatoma↗
PubMed1985

The incidence and clinical implications of hypersensitivity to papain in an allergic population, confirmed by blinded oral challenge.

Five hundred allergy clinic patients were prick skin tested with papain, 1 mg/mL, in addition to usual local aeroallergens. Five of 475 subjects with seasonal allergic disease had positive skin tests to both papain and local pollens. None of the 25 individuals with negative skin test to pollens had skin reactivity to papain. The five subjects with positive skin tests to papain underwent double-blind placebo-papain challenges. All papain challenges were positive. Placebo challenges were negative. Papain-induced symptoms included palatal itching, watering itchy eyes, sneezing, rhinorrhea, abdominal cramps, diarrhea, and diaphoresis. Circulating papain-specific IgE was detected in all the papain-sensitive individuals, but not in control subjects. Confirmed papain sensitivity occurred in 1.05% of allergic subjects. In the papain-sensitive patients, cross-reacting antibodies with chymopapain were found. The small number of non-allergic subjects did not show any papain or chymopapain sensitivity in vitro.

Administration, Oral↗
PubMed1984

Evolution to eosinophilic leukemia with a t(5:11) translocation in a patient with idiopathic hypereosinophilic syndrome.

The idiopathic hypereosinophilic syndrome (HES) comprises a diverse group of diseases that may ultimately lead to multiorgan dysfunction and death. We present a case of a man who was followed for over 9 years with HES that underwent malignant transformation to acute leukemia with eosinophilic features. The patient's clinical acceleration was accompanied by the development of a malignant clone that was identified with banding techniques as 46,XY,t(5:11)(p15;q13). Electron microscopy reaffirmed findings reported in earlier cases of eosinophilic leukemia. At no time during his illness were cytotoxic drugs administered. In addition to delineating the natural evolution and cytostructural details of the case, we emphasize the role of cytogenetics in the predicting of malignant variants of the hypereosinophilic syndrome and in identifying eosinophilic leukemia.

Aged↗
PubMed1984

Protease inhibition of natural killer (NK) and antibody-dependent cell-mediated cytoxicity (ADCC) activities.

The ability of protease inhibitors to modulate NK and ADCC cell activities was studied. NK and ADCC cell activities were suppressed by 1,10 phenanthroline (PHE), N-alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK), L-1-tosylamide-2-phenylethylchoromethyl ketone (TPCK), N-benzoyl-DL-tyrosine ethyl ester (BTEE), and phenylethylchoromethyl fluoride (PMSF). The effect of these protease inhibitors on ADCC was not mediated through the early phase of cytotoxicity involving Fc-receptor binding, since they failed to alter EoxA rosetting of effector cells. The results suggest that an activated esterase system might play a role in the later phase of the cytotoxic mechanism by ADCC cells and perhaps NK cells.

Animals↗