Combined stimulation with Poly(I:C), TNF-alpha and Th2 cytokines induces TARC production by human fibroblasts from the nose, bronchioles and lungs.

BACKGROUND: Th2 cells trigger allergic diseases in the respiratory tract. However, the mechanisms that cause Th2 cell infiltration remain unclear. Viral infections exacerbate allergic diseases in the respiratory tract. Thymus- and activation-regulated chemokine (TARC) recruits Th2 cells to sites of inflammation. Resident fibroblasts are thought to contribute to inflammatory cell infiltration through chemokine production. We compared the abilities of nasal, bronchiolar and lung fibroblasts to produce TARC. METHODS: Expression of TARC mRNA was evaluated by real-time RT-PCR, while the amount of TARC in supernatants was measured by ELISA. RESULTS: Costimulation with TNF-alpha and Th2 cytokines (IL-4, IL-13) or with poly(I:C) and Th2 cytokines (IL-4, IL-13) induced TARC production by nasal (polyp and normal) fibroblasts. Costimulation with TNF-alpha and Th2 cytokines (IL-4, IL-13) also induced TARC production by both bronchiolar and lung fibroblasts, but costimulation with poly(I:C) and Th2 cytokines (IL-4, IL-13) caused no induction. Combined exposure of cells to poly(I:C), TNF-alpha and Th2 cytokines (IL-4, IL-13) resulted in substantial production of TARC by nasal and lung fibroblasts, but much less by bronchiolar fibroblasts. CONCLUSIONS: TARC is directly inducible in diverse fibroblast populations from the respiratory tract (nose, bronchioles and lungs), but the mechanisms and levels of TARC production differ. Fibroblasts in the respiratory tract may contribute to Th2 cell infiltration and viral-induced exacerbation of allergic diseases, such as allergic sinusitis, asthma and allergic lung inflammation.

Expression of cochlin mRNA splice variants in the inner ear.

Proteomic analysis of inner ear proteins revealed unique properties of cochlin, encoded by the COCH gene. We detected 3 cochlin isoforms, p63s, p44s and p40s, in the inner ear tissue and a short 16-kDa isoform, cochlin-tomoprotein (CTP), in the perilymph. The role of the cochlin isoforms has not been elucidated. To improve our understanding of the mechanism of cochlin isoform expression, we investigated rat cochlin mRNA expression in the inner ear and other organs. We performed RNA-ligation-mediated amplification of cDNA ends (RLM-RACE) using RNA isolated from the inner ear and spleen of rats, which are known to express abundant cochlin mRNA. We also examined the expression profile of full-length cochlin mRNA by nested RT-PCR in the cerebrum, cerebellum/brain stem, eye, inner ear, thyroid gland, thymus gland, lung, heart, liver, spleen, adrenal gland, kidney and blood. We verified CTP expression in rat perilymph by Western blot. By RLM-RACE, alternately spliced variants of cochlin mRNA with 3 different lengths were detected (2442, 2008 and 724 bp). The two longer mRNAs encode full-length cochlin with different polyadenylation signals in the 3'-untranslated region, which are expressed both in the ear and spleen. The short variant encodes the limulus factor C, cochlin, late gestation lung protein (LCCL) domain and the N-terminal sequence of the von Willebrand factor A (vWFA1) domain, and this variant was detected only in the ear. All 3 variants have the same transcriptional start site. By RT-PCR, we found that full-length cochlin was expressed in all organs examined, with a splice variant in the heart. By Western blot, we detected short isoforms (11-17 kDa) in the perilymph. Cochlin isoform formation is regulated, at least in part, by alternative splicing at the transcriptional level. The short mRNA was detected only in the inner ear, and this variant may provide a clue to understanding the formation and function of cochlin isoforms.

The performance of Cochlin-tomoprotein detection test in the diagnosis of perilymphatic fistula.

BACKGROUND: Perilymphatic fistula (PLF), defined as an abnormal communication between the inner and middle ear, presents with a symptomatology of hearing loss and vestibular disorder that is indistinguishable from a number of other inner ear diseases. Methods of diagnosis remain controversial. We have previously shown that Cochlin-tomoprotein (CTP) is selectively detected in the perilymph. To establish a definite diagnostic test for PLF using CTP as a biochemical marker, we examined the diagnostic performance of the CTP detection test. METHODS: CTP detection test was performed by Western blot using recombinant human CTP (rhCTP) as a spiked standard. We evaluated the specificity of the CTP detection test by testing non-PLF cases. To describe the limitations of the test, we tested samples from patients with middle ear infection. We also studied the stability of CTP protein by storing the samples at room temperature (25 degrees C) or 4 degrees C for 55 days. The effects of repeated freezing and thawing were also evaluated. Serially diluted perilymph was tested to find out the detection limit of CTP. FINDINGS: We have established a standardized CTP detection test using high (0.27 ng) and low (0.13 ng) spiked standards of rhCTP in Western blotting. Middle ear lavages (MEL) from 54 of 55 non-PLF cases were negative in the CTP detection test, i.e. the specificity of the test is 98.2%. MEL from 43 out of 46 cases with chronic suppurative otitis media or middle ear cholesteatoma were negative for CTP. CTP is a stable protein and detection was not affected by the storage, or freezing and thawing. The detection limit of perilymph was 0.161 microl/lane in an average of 5 samples. INTERPRETATION: CTP is a stable perilymph-specific protein, and this CTP detection could be the first clinically established diagnostic tool to detect PLF with a high specificity. PLF is surgically correctable by sealing the fistula. Appropriate recognition and treatment of PLF can improve hearing and balance in afflicted patients.

Nasal polyp fibroblasts produce MIP-3alpha in response to toll-like receptor ligands and cytokine stimulation.

OBJECTIVE: Dendritic cells (DCs) play important roles in the development and perpetuation of immune responses. DCs are present in upper airway diseases such as chronic rhinosinusitis with nasal polyps. However, the mechanisms of how DCs migrate into the upper airway mucosa during upper airway inflammatory diseases remains unclear. Macrophage inflammatory protein-3alpha (MIP-3alpha) is known to be a migratory factor for immature DCs. There have been very few reports regarding cells producing this chemokine in the airways. To investigate this, we stimulated fibroblasts cultured from the nasal polyps with various toll-like receptor (TLR) ligands, which are derived from microorganisms, and IL-beta1 and TNF-alpha, which are proinflammatory cytokines, and analyzed their ability to produce MIP-3alpha. METHODS: Fibroblast lines were established from nasal polyps and stimulated with TLR2, 3, 4, 5, 7/8 and 9 ligands, IL-beta1 and TNF-alpha. MIP-3alpha mRNA expression in nasal polyp fibroblasts (NPF) was evaluated by real-time RT-PCR and the protein levels of MIP-3alpha in the supernatants of stimulated NPF was measured by ELISA. RESULTS: Stimulation with TLR2, 3, 4 and 5 ligands, IL-beta1 and TNF-alpha, induced MIP-3alpha gene expression and protein production in the cultured NPF This response was dose- and time-dependent. CONCLUSION: NPF possibly play an important role in the recruitment of DCs in upper airway diseases such as chronic rhinosinusitis with nasal polyps through the production of MIP-3alpha.

One-year evaluation of combined treatment with an intranasal corticosteroid and montelukast for chronic rhinosinusitis associated with asthma.

OBJECTIVES: Chronic rhinosinusitis associated with asthma is often difficult to treat effectively with intranasal corticosteroids alone. Thus, the aim of this study was to evaluate the effectiveness of combination treatment with an intranasal corticosteroid and a leukotriene-receptor antagonist (montelukast) in reducing the size of nasal polyps. METHODS: The subjects of this study were 20 patients with chronic rhinosinusitis associated with adult-onset asthma, which was being treated with inhaled corticosteroids. All patients were treated with intranasal fluticasone propionate, 200 microg/day, and montelukast, 10 mg/day, for 1 year. The size of nasal polyps and the score of sinus shadows were assessed with nasal endoscopy and computed tomography (CT), respectively, before and after treatment. The peripheral blood eosinophil counts were also evaluated before and after treatment. RESULTS: Nasal polyps were significantly smaller after both 6 months (p<0.01) and 12 months of treatment (p<0.01) than before treatment. The decrease in the shadow score was statistically significant after both 6 months (p<0.01) and 12 months of treatment (p<0.01). Significant reductions in peripheral blood eosinophil counts were also seen after both 6 months (p<0.05) and 12 months of treatment (p<0.01). A significant correlation was found between the rate of change in the peripheral blood eosinophil count and that in the CT score after both 6 months (r=0.578, p=0.012) and 12 months (r=0.625, p=0.007). CONCLUSION: Combined treatment with intranasal fluticasone propionate and montelukast, for at least 1 year, is effective for chronic rhinosinusitis associated with adult-onset asthma.

Cochlin-tomoprotein: a novel perilymph-specific protein and a potential marker for the diagnosis of perilymphatic fistula.

BACKGROUND: Perilymphatic fistula (PLF) is an abnormal connection between the inner and middle ear. A procedure for obtaining definite proof of a PLF remains elusive, and methods of diagnosis remain controversial. To date, there is no clinically relevant biochemical marker for perilymph leakage. Using proteomic analysis of inner ear proteins, we have previously found unique properties of cochlin, encoded by the COCH gene. We detected 3 cochlin isoforms (p63s, p44s and p40s) in the inner ear tissue and a short 16-kDa isoform of cochlin-tomoprotein (CTP) in the perilymph. Since cochlin was found to be highly specific to the inner ear, we speculated that CTP might also be specific to the perilymph. The aim of this study was to determine whether CTP, a novel perilymph-specific protein, could be used as a marker for the diagnosis of PLF. METHODS: By Western blotting, we investigated the specificity of CTP expression in a range of body fluids that included perilymph, serum, saliva and cerebrospinal fluid. To elucidate the detection limit of CTP, serially diluted recombinant human (rh)CTP as well as human perilymph was tested. RESULTS: CTP was selectively expressed in all 20 perilymph samples tested, but not in 77 samples of the other body fluids. The detection limit of rhCTP was 0.27 ng or 0.022 microl of perilymph per well on Western blot analysis. CONCLUSION: The results strongly suggest that CTP can be a specific marker of perilymph leakage. Moreover, CTP has the potential to be a biochemical marker that allows a definitive diagnosis of the etiology of PLF-related hearing loss and vestibular disorders.

Follicular dendritic cell sarcoma with microtubuloreticular structure and virus-like particle production in vitro.

Neoplasm of follicular dendritic cells (FDC), follicular dendritic cell sarcoma (FDCS), is a rare tumor of intermediate to high-grade malignancy in lymph nodes and visceral organs. Reported herein is a case of FDCS arising from cervical lymph nodes in a 16-year-old Japanese boy, who died of the disease 3 years after diagnosis. The tumor cells were pale eosinophilic and elongated with euchromatic nuclei and were positive for CD21, clusterin, and CNA-42 on immunohistochemistry, as well as desmosome-like junctions on electron microscopy. The presence of microtubuloreticular structures (MTRS) in the tumor cells and associated lymphocytes characterized this case, suggesting some viral infection, although qualitative polymerase chain reaction of genomic and complementary DNA obtained from the tumor failed to demonstrate any viral infection at the laboratory level. The stimulation of dispersed tumor cells and peripheral blood mononuclear cells with mAb to CD3 and interleukin-2 was attempted; and the cell line established by the authors (FDCS-Sa) was stimulated with iododeoxyuridine. Virus-like particles (VLP) were successfully induced from each cellular source. The VLP, 100 nm in diameter, showed an electron-dense thorny envelope and granular core. This is the first case of FDCS with MTRS accompanying VLP production in vitro.

Utility of sonography for evaluation of clinical T1 and T2 glottic carcinoma.

OBJECTIVE: The aim of this study was to evaluate the prognostic impact of sonographically determined tumor features in relation to local control of clinical T1 and T2 glottic carcinoma treated by definitive radiation therapy. METHODS: Between 1999 and 2005, 72 patients with T1 and T2 glottic carcinoma were evaluated by percutaneous sonography in terms of tumor detectability, maximum tumor dimension, involvement of the anterior commissure, presence of supraglottic, subglottic, or paraglottic spread, and thyroid cartilage invasion. Factor analyses for local control included clinical features, sonographic findings, and treatment factors. RESULTS: Forty-one lesions (57%) were detected as hypoechoic masses on sonography. For detectable T2 tumors, sonographic and laryngoscopic findings were in agreement in all cases with respect to spread to anatomic subsites. The 3-year local control rate with radiation therapy alone was 82%. Univariate analysis of the sonographic characteristics revealed that the maximum tumor dimension and thyroid cartilage invasion predicted a loss of local control, whereas none of the clinical or treatment characteristics was significant. Multivariate analysis showed that thyroid cartilage invasion was an independent negative prognostic factor for local control. CONCLUSIONS: Sonography provides information about the likely outcome of radiation therapy for patients with clinical T2 glottic carcinoma, although its utility for T1 lesions is not proven. Thyroid cartilage invasion may be an independent negative predictor of the outcome.

Spatiotemporal expression of cochlin in the inner ear of rats during postnatal development.

Cochlin (encoded by COCH) constitutes 70% of non-collagenous protein in the inner ear, and the expression of cochlin is highly specific to the inner ear. Eleven missense mutation and one in-frame deletion have been reported in the COCH gene, causing hereditary progressive sensorineural hearing loss and vestibular dysfunction, DFNA9. These data imply that cochlin should bear an essential and crucial role in the inner ear function. However, the role of cochlin has not been fully clarified. We have investigated the spatiotemporal expression of cochlin in the inner ear of rats during postnatal development to better understand the functional role of cochlin. By immunohistochemistry, cochlin expression was faint in the cochlea and vestibule on the 6th day after birth (DAB6). At DAB70, strong expression of cochlin was detected in the spiral limbus and spiral ligament within the cochlea, and in the stromata of the maculae of otolithic organs and crista ampullaris within the vestibule. Immunoreactivity for cochlin increased during the postnatal development. Western blot analysis also showed an increase in the expression of cochlin isoforms. Furthermore, the dominant isoform of cochlin expressed changed from p63s to p40s between DAB24 and DAB70. These results suggest that the expression of cochlin may be related to the maturation of inner ear function, and the change in isoforms of cochlin expressed will provide important insight into the understanding of both cochlin function and formation of cochlin isoforms. This is the first to report about the spatiotemporal expression of cochlin in the developing rat inner ear.

Adsorption of humic acid from aqueous solution onto irradiation-crosslinked carboxymethylchitosan.

This paper presents the adsorption of humic acid from aqueous solution onto crosslinked chitosan derivative (carboxymethylchitosan), formed by additionless irradiation technique. The surface charge and swelling properties of crosslinked samples were investigated. The adsorption of humic acid onto crosslinked carboxymethylchitosan was carried out by the batch method at room temperature, and it was found to be strongly pH-dependent. Maximum amount of humic acid was adsorbed under acidic conditions at the optimum pH value of 3.5. Adsorption kinetic studies indicated the adsorption process was transport-limited at the same pH. The adsorption isotherm analysis data under various initial humic acid concentrations confirms that experimental data fitted well into the Langmuir equation. X-ray photoelectron spectroscopy (XPS) revealed that the amino groups of carboxymethylated chitosan were protonated, suggesting the formation of organic complex between the protonated amino groups and humic acid. From these preliminary evaluations, it was concluded that crosslinked carboxymethylated chitosan derivatives have a great potential in water treatment for the removal of humic acid and other polarized or electrically charged species.

Expression of MCP-4 by TLR ligand-stimulated nasal polyp fibroblasts.

CONCLUSION: These results indicate that nasal polyp fibroblasts contribute to innate immunity and eosinophilic inflammation such as nasal polyposis. OBJECTIVE: It is generally accepted that type 2 T helper (Th2) cytokines and some chemoattractants play an essential role in the pathogenesis of nasal polyposis. Nasal polyposis is characterized by chronic eosinophilic inflammation. The mechanisms that cause the predominance of eosinophilic infiltration in nasal polyposis have yet to be clarified. There is growing evidence that fibroblasts could be a major source of Th2 chemokines. Because the nasal and paranasal mucosae are the first respiratory tissues that environmental agents encounter, those tissues are exposed to injurious agents, including microorganisms and their breakdown products. We investigated whether nasal polyp fibroblasts produce a C-C chemokine, MCP-4, when stimulated with the breakdown products of microorganisms and a Th2 cytokine (interleukin (IL)-4). MATERIALS AND METHODS: Fibroblast lines were established from nasal polyp tissues. The expression of MCP-4 mRNA was evaluated by real-time RT-PCR. The amount of MCP-4 in the supernatants was measured by ELISA. RESULTS: TLR2, 3, 4 and 5 ligands, but not TLR7/8 or 9 ligands, induced small amounts of MCP-4. TLR2, 3, 4 and 5 ligands synergized with IL-4 to induce the production of MCP-4.

Pathological localization of so-called posterior canal BPPV.

OBJECTIVE: Based on the hypothesis that the origin of nystagmus is from the posterior canal (PC), the nystagmus in the head hanging and sitting position should be mirror images. To clarify the anatomical origin of positioning nystagmus in BPPV patients, we analyzed the positioning nystagmus of benign paroxysmal positioning vertigo (BPPV) patients three-dimensionally. METHODS: Twenty-six patients with BPPV participated in this study. The positioning nystagmus was recorded in complete darkness from the patient's left eye by means of an infrared CCD camera. We performed three-dimensional analysis of nystagmus using video image analysis system (VIAS). Subsequently, the rotation axis of the 3D eye movements of the positioning nystagmus was calculated. RESULTS: Among the 26 patients tested, 20 patients demonstrated the axes of nystagmus in good or relatively good alignment to the PC axis. However, in 11 of these 20 patients there was poor alignment of the axis of nystagmus in the sitting position to the PC axis. In addition, six patients showed axes of nystagmus with poor alignment to the PC in the head hanging position. Among them, two patients exhibited axes of nystagmus in good alignment with the anterior canal, in spite of diagnosis of these patients as PC BPPV by experienced examiner based on the positioning nystagmus test. CONCLUSION: These results demonstrated that only one-third of patients who were diagnosed as BPPV, could be diagnosed as true BPPV which originates from a PC pathology. Besides the possibility that the pathology may originate from the AC, it is still unclear which part of the inner ear may be the candidate site of origin of the pathology of BPPV in the other 15 patients.

Three-dimensional analysis of eye movements using four times high-speed video camera.

In order to record and analyze the rapid eye movement non-invasively in human subjects, a four times high-speed video camera (4TC) with a new computer software was developed and utilized. Nine healthy volunteers and four patients with vestibular dysfunction participated in this study. Caloric stimulation was applied to the healthy subjects and the eye movements were recorded using a standard camera (SC) and a 4TC. In four patients, the positional and/or positioning nystagmus was recorded using SC and 4TC. Analysis of the eye speed of the quick phase of nystagmus was performed manually from the print out of the chart. The quick phase of the caloric nystagmus was adequately analyzed from the data using 4TC. However, using SC the sampling rate was not sufficiently enough for this purpose, as prospected. The adaptability of the 4TC in clinical examination is exactly similar to that of SC, because of the size and weight of the camera. Although the time taken to analyze eye movements using 4TC is about four times longer than that using SC, this system is quite useful and adequate for analyzing the quick eye movements in vestibular nystagmus, in an out-patient clinic set up.

Expression of full-length Cochlin p63s is inner ear specific.

OBJECTIVE: The COCH gene mutated in DFNA9, murine an autosomal dominant hereditary hearing impairment, encodes Cochlin. Cochlin is also suggested to be the self-antigen of autoimmune sensorineural hearing loss. We previously reported that Cochlin constitutes 70% of the inner ear proteins and is classified into three types of isoform, p63s, p44s, and p40s. To study the specificity of expression of Cochlin isoforms in various organs, here we have investigated expression of the COCH gene at both the transcriptional and translational level. METHODS: COCH gene expression was studied by RT-PCR and Southern blot analysis. Cochlin isoforms were studied by Western blot analysis using an isoform specific antibody. RESULTS: At the transcriptional level, COCH mRNA was detected only in the inner ear by RT-PCR. Southern blot analysis of RT-PCR products detected a high level of COCH mRNA in the inner ear, lower level in spleen, and very low levels in the cerebrum, cerebellum/brain stem, eye, liver and kidney. At the translational level, Western blot analysis showed that a set of isoform, p63s, p44s, and p40s was detected at high levels only in the inner ear. In contrast, multiple proteins were detected at much lower levels in other organs tested. Notably, full-length Cochlin p63s was detected only in the inner ear. CONCLUSION: Our findings demonstrate that the COCH gene is expressed preferentially in the inner ear and that expression of full-length Cochlin p63s is specific to the inner ear. These results will be central to understanding the function of Cochlin and its role in the pathophysiology of DFNA9.

[Spontaneous dislocation of the arytenoid cartilage].

Dislocation of the arytenoid cartilage occurs following medical instrumentation involving the laryngeal cavity or laryngeal injury from outside the larynx. We reported a case of spontaneously posterior dislocation of the arytenoid cartilage. A 53 year-old man suffering from suddenly recurring aphonia and its improvement many over 3 months without laryngeal injury or inducement eventually ceased to improve. Laryngoscopic findings showed that the left vocal fold was tensely prolonged and the vocal process of the arytenoid cartilage on the left side was dislocated posterolaterally. X-ray videofluorography of the larynx on repetitive phonation of /he/ showed abnormally high and diagonal displacement of the vocal fold and the upper structure of the arytenoid cartilage on the left side. Palpating the cricoarytenoid joint on the left side showed abnormal swelling with tenderness. Electomyography of the intrinsic laryngeal muscle on the left side showed normal action potential. From these findings, we diagnosed his voice disorder as spontaneously posterior dislocation of the arytenoid cartilage. We manually reduced it by pulling up a balloon inserted from the piriform sinus of the affected side to the esophagus.

Mast cell-IgE-and mast cell-structural cell interactions in allergic airway disease.

Allergic diseases like atopic rhinitis, bronchial asthma, and urticaria are prevalent and on the rise. Mast cells are known to play a central role in the immediate phase reaction of allergic diseases through the IgE-mediated release of a variety of chemical mediators like histamine, leukotrienes, and prostaglandins. On the other hand, T lymphocytes, basophils and eosinophils are thought to be responsible in inducing the late phase response. Yet, recent studies show that the mast cell cannot be simplistically assigned a role in the immediate phase allergic response, and that this cell plays a crucial role in ongoing allergic inflammation, including the development of hyper-responsiveness. In the present article, the author will try to discuss the integrated roles of mast cells in IgE-mediated allergic inflammation with specific emphasis on the roles of mast cell-IgE networking and mast cell-structural cell interactions in the late phase allergic response and chronic allergic inflammation.

Nuclear-factor kappa B (NF-kappa B)-inducible nitric oxide synthase (iNOS/NOS II) pathway damages the stria vascularis in cisplatin-treated mice.

BACKGROUND: Cisplatin is reported to damage the stria vascularis of the cochlea. Free radicals, especially large amounts of nitric oxide catalyzed by inducible nitric oxide synthase, are considered to have an important role in this toxicity. The induction of inducible nitric oxide synthase is regulated by nuclear-factor kappa B (NF-kappa B). We examined the damage of the stria vascularis by immunohistochemical techniques. MATERIALS AND METHODS: Cisplatin (15 mg/kg b.w.) was injected intraperitoneally into the mice. Three days after the injection, the cochleas were immunohistochemically-stained using specific antibodies for nuclear-factor kappa B (NF-kappa B), inducible nitric oxide synthase (iNOS) or single-stranded DNA. RESULTS: NF-kappa B was expressed in the cisplatin-treated cochlea, especially in the stria vascularis and the spiral ligament. iNOS was also expressed in the stria vascularis and the spiral ligament. Fragments of DNA were observed only in the stria vascularis. CONCLUSION: The large amounts of NO catalyzed by iNOS led to inner ear dysfunction. Our results indicate that apoptosis is triggered by iNOS and that it mediates the ototoxicity induced by cisplatin.

Ultrasonographic demonstration of retropharyngeal lymph nodes: preliminary report.

The aim of this study was to describe the results of ultrasonography of upper retropharyngeal lymph node (RPN) metastasis in patients with pharyngeal carcinomas. A total of 10 patients with metastatic RPN were examined using percutaneous ultrasound (US) with 3.5-MHz probes. Primary cancer sites were the nasopharynx in two patients, the oropharynx in three and the hypopharynx in five. Metastatic RPNs lay in the level of occipital bone in five patients, C1 in nine, and C2 in five. US images were compared with previously obtained computerized tomography (CT) images based on size and depth. In all of the 10 patients, metastatic RPNs were ultrasonographically demonstrated as hypoechoic masses. Nodal sizes ranged from 1.5 cm to 3.5 cm both in CT and in US. Depths of the RPN centers were from 3.5 cm to 7.0 cm in CT, and from 3.5 cm to 6.5 cm in US. Differences of sizes and depths between CT and US were from -0.5 cm to 0.5 cm and from 0.0 cm to 1.0 cm, respectively. RPNs that are 1.5 cm or more in size can be demonstrated with percutaneous US using CT guidance. This technique should be utilized for the purpose of monitoring in a radiation therapy setting.

IL-5 and eotaxin levels in middle ear effusion and blood from asthmatics with otitis media with effusion.

OBJECTIVE: The purpose of this study was to evaluate eosinophil infiltration as well as IL-5 and eotaxin levels in middle ear effusion (MEE) and blood from otitis media with effusion (OME) patients with asthma and to compare the findings with those from OME patients without asthma (control group). MATERIAL AND METHODS: Levels of IL-5 and eotaxin in MEE and blood were measured by means of enzyme-linked immunosorbent assay. RESULTS: 5 levels in MEE were significantly higher than those in blood in both groups of patients and in OME patients with asthma than in the control group. In addition, in OME patients with asthma, there was a significant correlation between the percentage of eosinophils and IL-5 levels in MEE. Eotaxin levels in blood were significantly higher than those in MEE in both groups of patients and in OME patients with asthma than in the control group. In addition, in OME patients with asthma, the percentage of eosinophils and eotaxin levels in blood tended to correlate, but did not reach statistical significance. CONCLUSION: These data suggest that, in OME patients with asthma, eosinophilia in MEE depends more on IL-5 than on eotaxin, and that eotaxin may play an important role in the mobilization of eosinophils from the bone marrow into the blood.

Incidence and characteristics of otosclerosis in the Japanese population.

OBJECTIVE: Otosclerosis is thought to be quite an uncommon disease in Japan. However, in recent years the incidence of this disease seems to have increased. Here we report about the characteristics and incidence of this disease in the Japanese population who underwent stapes surgery in our department. METHODS: A total of 80 patients (115 ears), who underwent stapes surgery by a single surgeon in 21 years and 8 months were included in this study. RESULTS: The incidence of clinical otosclerosis was found to be 0.22% among the outpatients with ear disease. During the first half of the period, the ratio of stapes surgery/tympanoplasty was less than 0.05. While, during the second half of this period, this ratio had increased to 0.08. The average number of stapes surgery performed in the first half period was 3.7 ears/year, and that in the second half was 6.8 ears/year. In contrast to otosclerosis in Caucasians, pure tone threshold in lower frequencies was much higher than that of higher frequencies (except for 8000 Hz). However, the improvement of the threshold after surgery was not so different from that reported in Caucasians. CONCLUSIONS: Taken together, the present results clearly demonstrate that the incidence of otosclerosis in Japan has been increasing. Moreover the rise in the slope of the conduction curve at higher frequencies may be a reflection of the pathological characteristics of otosclerosis in Japanese population, which is less invasive and has limited otosclerotic foci in the temporal bone.