SDF2L1 Inhibits Cell Proliferation, Migration, and Invasion in Nasopharyngeal Carcinoma.

The purpose of this study was to explore the relationship between stromal cell-derived factor 2-like 1 (SDF2L1) and nasopharyngeal carcinoma (NPC). 12 NPC tissues and 12 chronic nasopharyngitis tissues were involved in our study. Quantitative real-time PCR (qRT-PCR) and Western Blot were utilized to detect the expression of SDF2L1. Besides, immunofluorescence analysis was utilized to determine the protein expression of 97 paraffin-embedded NPC tissues and 58 nasopharyngitis tissues. Biological functional experiment included Cell Counting Kit-8 (CCK-8) assay, cell clone formation assay, cell scratch migration assay, Transwell migration assay, and Transwell invasion assay. All data were analyzed by SPSS. Results showed that downexpression of SDF2L1 was prominently present in NPC tissues and cells. Furthermore, silencing the expression of SDF2L1 promoted NPC proliferation, migration, and invasion in vitro, while overexpression of SDF2L1 has the opposite effect. In conclusion, SDF2L1 may act as a cancer suppressor gene, play a crucial role in the occurrence and development of NPC, and be a new therapeutic target or prognostic indicator for NPC.

Septin 9 Methylation in Nasopharyngeal Swabs: A Potential Minimally Invasive Biomarker for the Early Detection of Nasopharyngeal Carcinoma.

Nasopharyngeal carcinoma (NPC) is highly prevalent in Southeast Asia, and an unfavorable outcome is usually attributed to advanced stage NPC. Current methods for the early diagnosis of NPC have limitations in clinical practice. The aim of this study was to investigate the diagnostic ability of Septin 9 methylation for NPC. A quantitative methylation-sensitive PCR (qMS-PCR) assay was developed to measure the methylation status and levels of Septin 9 in nasopharyngeal tissues and paired swabs from patients with NPC, chronic nasopharyngitis, and healthy donors. Methylated Septin 9 was detected in 92% (23/25) of NPC tissues and 25% (4/16) of nasopharyngitis controls (p < 0.05). High-frequency hypermethylation with decreased mRNA expression of Septin 9 in NPC was also identified. Further, Septin 9 methylation was identified in 90.5% (19/21) of NPC biopsies and 71.4% (15/21) of paired swabs, indicating a good concordance between the two sample types. In addition, methylated Septin 9 was found in 16 (72.7%) nasal swabs from 22 NPC patients, 2 of 19 (10.5%) nasopharyngitis, but not in any of the healthy controls (p < 0.01). The methylation score in nasal swabs of the NPC group was also significantly higher than that of non-NPC controls (p < 0.001). Moreover, receiver operating characteristic (ROC) curve analysis showed an area under the curve (AUC) of 0.882 of Septin 9 methylation tests to discriminate NPC from non-NPC subjects. Our study demonstrated that frequent methylation of Septin 9 was present in NPC. Its detection in nasopharyngeal swabs may provide a minimally invasive and informative method for identifying early NPC cases.

Serum- and glucocorticoid-inducible kinase 3 is a potential oncogene in nasopharyngeal carcinoma / Quinase 3 sérica induzida por glicocorticoide é um potencial oncogene no carcinoma nasofaríngeo

Abstract Introduction: Serum- and glucocorticoid-inducible kinase 3, a serine/threonine kinase that functions downstream of the PI3K signaling pathway, plays a critical role in neoplastic processes. It is expressed by various tumors and contributes to carcinogenesis. Objective: The objective was to investigate serum- and glucocorticoid-inducible kinase 3 expression in nasopharyngeal carcinoma, to study the anti-tumor effects of serum- and glucocorticoid-inducible kinase 3 shRNA by inhibiting its expression in nasopharyngeal carcinoma cells and to discuss the potential implications of our findings. Methods: Serum- and glucocorticoid-inducible kinase 3 protein expression in nasopharyngeal carcinoma cell lines (CNE-1, CNE-2, HNE-1, HONE-1, and SUNE-1) and the human immortalized nasopharyngeal epithelium cell line NP69 were assayed by western blotting. Serum- and glucocorticoid-inducible kinase 3 expression in 42 paraffin-embedded nasopharyngeal carcinoma tissues were performed by immunohistochemistry. MTT assay, flow cytometry, and scratch tests were performed after CNE-2 cells were transfected with the best serum- and glucocorticoid-inducible kinase 3 shRNA plasmid selected by western blotting using lipofectamine to study its effect on cell proliferation, apoptosis, and migration. Results: Serum- and glucocorticoid-inducible kinase 3 was overexpressed in human nasopharyngeal carcinoma tissues and cells. Serum- and glucocorticoid-inducible kinase 3 expression decreased markedly after CNE-2 cells were transfected with the serum- and glucocorticoid-inducible kinase 3 shRNA, leading to strong inhibition of cell proliferation and migration. In addition, the apoptosis rate increased in CNE-2 cells after serum- and glucocorticoid-inducible kinase 3 knockdown. Conclusion: Serum- and glucocorticoid-inducible kinase 3 expression was more frequently observed as the nasopharyngeal epithelium progresses from normal tissue to carcinoma. This suggests that serum- and glucocorticoid-inducible kinase 3 contributes to the multistep process of NPC carcinogenesis. Serum- and glucocorticoid-inducible kinase 3 represents a target for nasopharyngeal carcinoma therapy, and a basis exists for the further investigation of this adjuvant treatment modality for nasopharyngeal carcinoma.

Resumo Introdução: A quinase 3 sérica induzida por glicocorticoide, uma serina/treonina quinase que funciona downstream da via de sinalização PI3K, desempenha um papel crítico nos processos neoplásicos. É expressa por vários tumores e contribui para a carcinogênese. Objetivo: Investigar a expressão de quinase 3 sérica induzida por glicocorticoide no carcinoma nasofaríngeo, estudar os efeitos antitumorais do shRNA da quinase 3 sérica induzida por glicocorticoide, que inibem sua expressão em células de carcinoma nasofaríngeo, e discutir as implicações potenciais de nossos achados. Método: A expressão de proteína quinase 3 sérica induzida por glicocorticoide em linhagens de células de carcinoma nasofaríngeo (CNE-1, CNE-2, HNE-1, HONE-1 e SUNE-1) e a linhagem de células humanas imortalizadas do epitélio nasofaríngeo NP69 foram avaliadas por Western blot. A expressão da quinase 3 sérica induzida por glicocorticoide em 42 tecidos de CNF embebidos em parafina foi feita por imuno-histoquímica. Testes com MTT, citometria de fluxo e testes de raspagem foram feitos após as células CNE-2 terem sido transfectadas com o melhor plasmídeo shRNA da quinase 3 sérica induzida por glicocorticoide selecionado por Western blot, com o uso de lipofectamina para estudar seu efeito na proliferação, apoptose e migração celular. Resultados: Foi observada uma sobre-expressão da quinase 3 sérica induzida por glicocorticoide em tecidos e células de carcinoma nasofaríngeo humanas. A expressão de quinase 3 sérica induzida por glicocorticoide diminuiu acentuadamente após as células CNE-2 terem sido transfectadas com o shRNA da quinase 3 sérica induzida por glicocorticoide, conduzindo a forte inibição de proliferação e migração celular. Além disso, a taxa de apoptose aumentou nas células CNE-2 após o knockdown da quinase 3 sérica induzida por glicocorticoide. Conclusão: A expressão de quinase 3 sérica induzida por glicocorticoide foi observada com maior frequência à medida que o epitélio nasofaríngeo progride de tecido normal para carcinoma. Isso sugere que a quinase 3 sérica induzida por glicocorticoide contribui para o processo multietapas da carcinogênese do carcinoma nasofaríngeo. A quinase 3 sérica induzida por glicocorticoide representa um alvo para a terapia do carcinoma nasofaríngeo e há uma base para a investigação adicional dessa modalidade de tratamento adjuvante para o carcinoma nasofaríngeo.

Role of ectodysplasin signalling in middle ear and nasal pathology in rat and mouse models of hypohidrotic ectodermal dysplasia.

Patients with mutations in the ectodysplasin receptor signalling pathway genes - the X-linked ligand ectodysplasin-A (EDA), the receptor EDAR or the receptor adapter EDARADD - have hypohidrotic ectodermal dysplasia (HED). In addition to having impaired development of teeth, hair, eccrine sweat glands, and salivary and mammary glands, HED patients have ear, nose and throat disease. The mouse strains Tabby (EdaTa ) and downless (Edardl-J/dl-J ) have rhinitis and otitis media due to loss of submucosal glands in the upper airway. We report that prenatal correction of EDAR signalling in EdaTa mice with the agonist anti-EDAR antibody rescues the auditory-tube submucosal glands and prevents otitis media, rhinitis and nasopharyngitis. The sparse- and wavy-haired (swh) rat strain carries a mutation in the Edaradd gene and has similar cutaneous HED phenotypes to mouse models. We report that auditory-tube submucosal glands are smaller in the homozygous mutant Edaraddswh/swh than those in unaffected heterozygous Edaraddswh/+ rats, and that this predisposes them to otitis media. Furthermore, the pathogenesis of otitis media in the rat HED model differs from that in mice, as otitis media is the primary pathology, and rhinitis is a later-onset phenotype. These findings in rodent HED models imply that hypomorphic as well as null mutations in EDAR signalling pathway genes may predispose to otitis media in humans. In addition, this work suggests that the recent successful prenatal treatment of X-linked HED (XLHED) in humans may also prevent ear, nose and throat disease, and provides diagnostic criteria that distinguish HED-associated otitis media from chronic otitis media with effusion, which is common in children.

Serum- and glucocorticoid-inducible kinase 3 is a potential oncogene in nasopharyngeal carcinoma.

INTRODUCTION: Serum- and glucocorticoid-inducible kinase 3, a serine/threonine kinase that functions downstream of the PI3K signaling pathway, plays a critical role in neoplastic processes. It is expressed by various tumors and contributes to carcinogenesis. OBJECTIVE: The objective was to investigate serum- and glucocorticoid-inducible kinase 3 expression in nasopharyngeal carcinoma, to study the anti-tumor effects of serum- and glucocorticoid-inducible kinase 3 shRNA by inhibiting its expression in nasopharyngeal carcinoma cells and to discuss the potential implications of our findings. METHODS: Serum- and glucocorticoid-inducible kinase 3 protein expression in nasopharyngeal carcinoma cell lines (CNE-1, CNE-2, HNE-1, HONE-1, and SUNE-1) and the human immortalized nasopharyngeal epithelium cell line NP69 were assayed by western blotting. Serum- and glucocorticoid-inducible kinase 3 expression in 42 paraffin-embedded nasopharyngeal carcinoma tissues were performed by immunohistochemistry. MTT assay, flow cytometry, and scratch tests were performed after CNE-2 cells were transfected with the best serum- and glucocorticoid-inducible kinase 3 shRNA plasmid selected by western blotting using lipofectamine to study its effect on cell proliferation, apoptosis, and migration. RESULTS: Serum- and glucocorticoid-inducible kinase 3 was overexpressed in human nasopharyngeal carcinoma tissues and cells. Serum- and glucocorticoid-inducible kinase 3 expression decreased markedly after CNE-2 cells were transfected with the serum- and glucocorticoid-inducible kinase 3 shRNA, leading to strong inhibition of cell proliferation and migration. In addition, the apoptosis rate increased in CNE-2 cells after serum- and glucocorticoid-inducible kinase 3 knockdown. CONCLUSION: Serum- and glucocorticoid-inducible kinase 3 expression was more frequently observed as the nasopharyngeal epithelium progresses from normal tissue to carcinoma. This suggests that serum- and glucocorticoid-inducible kinase 3 contributes to the multistep process of NPC carcinogenesis. Serum- and glucocorticoid-inducible kinase 3 represents a target for nasopharyngeal carcinoma therapy, and a basis exists for the further investigation of this adjuvant treatment modality for nasopharyngeal carcinoma.

High HLA-F Expression Is a Poor Prognosis Factor in Patients with Nasopharyngeal Carcinoma.

BACKGROUND AND AIMS: In patients with nasopharyngeal carcinoma (NPC), local treatment failure and distant metastasis contribute largely to poor outcomes. The nasopharynx is an important lymphoid tissue, and NPC tumourigenesis and development are partly attributed to immune system disorders. Human leukocyte antigen F (HLA-F) has shown a close correlation with NPC in many genome-wide association studies (GWASs). However, clinical studies rarely explore the relationship of HLA-F expression with the clinical parameters and outcomes in patients with NPC. METHODS: In this study, we used immunohistochemistry to evaluate HLA-F expression in 74 paraffin-embedded NPC tissue sections and then analysed the association between HLA-F expression and clinical parameters and outcomes. The plasma concentration of soluble HLA-F (sHLA-F) in NPC patients and normal controls was also detected, via enzyme-linked immunosorbent assay (ELISA). RESULTS: Low, moderate, and high HLA-F expression levels were observed in 47.3% (35/74), 35.1% (26/74), and 17.6% (13/74), respectively, of the tissue samples. HLA-F expression showed a significant correlation with local recurrence (p = 0.037) and distant metastasis (p = 0.024) and was also an independent factor for local recurrence-free survival (LRFS; p = 0.016) and distant metastasis-free survival (DMFS; p = 0.004). Although the mean concentration of plasma sHLA-F in the NPC patients was higher than that in the normal controls (13.63 pg/ml vs. 10.06 pg/ml), no statistical significance was observed (p = 0.118). CONCLUSIONS: Our study provides the first evidence that high HLA-F expression is associated with NPC local recurrence and distant metastasis and may be regarded as a poor prognostic factor for NPC patients. Additional studies using larger sample sizes may be necessary to determine whether sHLA-F is a feasible NPC diagnostic indicator.

MicroRNA­342­3p suppresses proliferation and invasion of nasopharyngeal carcinoma cells by directly targeting Cdc42.

Deregulated microRNAs play an important role in the development and progression of various types of cancer. In our previous study, we observed that microRNA­342­3p (miR­342­3p) was one of the most markedly downregulated microRNAs in two nasopharyngeal carcinoma (NPC) cell lines compared to non­neoplastic cells by using whole genome small RNA sequencing. In the present study, we confirmed that the expression of miR­342­3p was significantly reduced in NPC tissues compared with normal nasopharyngeal epithelial tissues. Overexpression of miR­342­3p inhibited proliferation, epithelial­mesenchymal transition (EMT), migration and invasiveness of NPC cells. In addition, we observed that Cdc42, a Rho GTPase family member involved in cell proliferation and metastasis, is a direct target of miR­342­3p. Additionally, ML141, a small­molecule inhibitor of Cdc42, efficiently suppressed the invasion of NPC cells compared with the control cells. Finally, we analyzed NPC tissues derived from 10 NPC patients and subjected them to quantitative RT­PCR and immunohistochemistry assays for concomitant determination of the expression levels of miR­342­3p and Cdc42. Our results revealed that miR­342­3p levels were significantly inversely correlated with the protein levels of its target Cdc42. The results of the present study indicated that miR­342­3p inhibited NPC tumor growth and invasion by directly targeting the Cdc42 pathway.

Distinctive microRNA expression in early stage nasopharyngeal carcinoma patients.

The goal of this study was to investigate microRNAs (miRs) expression at different stages of nasopharyngeal carcinoma (NPC). MiR expression profiling at various stages of NPC was performed by miR array and further verified using quantitative real-time RT-PCR. Pathway enrichment analysis was carried out to identify the functional pathways regulated by the miRs. The expression of a selected group of identified miRs was verified in stage I NPC by in situ hybridization (ISH). A total of 449 miRs were identified with significantly different expressions between NPC tissues and normal pharyngeal tissues. Eighty-four miRs were dysregulated only in stage I NPC, among which 45 miRs were up-regulated and the other 39 were down-regulated. Pathway enrichment assay revleaed that three significantly down-regulated and three significantly up-regulated miRs involved in 12 pathways associating with tumour formation and progression. Quantitative RT-PCR confirmed the miR array result. In addition, the low expression levels of hsa-miR-4324, hsa-miR-203a and hsa-miR-199b-5p were further validated in stage I NPC by ISH. This present study identifed the miR signature in stage I NPC, providing the basis for early detection and treatment of NPC.

Survivin gene functions and relationships between expression and prognosis in patients with nasopharyngeal carcinoma.

This study aimed to investigate the relationship between prognosis and protein and mRNA expression of an apoptotic inhibitor gene, survivin, in patients with nasopharyngeal carcinoma. Furthermore, functions of the survivin gene in the CNE2 nasopharyngeal carcinoma cell line were assessed. Immunohistochemistry and in situ hybridization were used in detecting the survivin protein and mRNA in 44 nasopharyngeal carcinoma specimens, and 30 chronic nasopharyngitis samples as controls. Survivin gene expression in CNE2 cell line was suppressed with an shRNA (short hairpin RNA). The positive ratios of expression for survivin protein and mRNA in nasopharyngeal carcinoma were 79.5% and 75.0% respectively, obviously higher than in the control group (p<0.01), and there is very good consistency between the two methods. The mean survival time of patients with higher survivin protein or mRNA expression was shorter than in patients with lower levelsv(p<0.01). Proliferation of the CNE2 cell line was distinctly inhibited by the shRNA . The results indicate that overexpression of the survivin gene plays an important role in onset and development of nasopharyngeal carcinoma, and it may be helpful for prognostic appraisal.

Overexpression of CSF-1R in nasopharyngeal carcinoma.

BACKGROUND: Tumor-associated macrophages play a significant role in tumor progression. CSF-1/CSF-1R is one of the most primary regulators of macrophage physiology in immune system. The expression of CSF-1/CSF-1R in nasopharyngeal carcinoma is unclear. OBJECTIVES: The aim of this study was to compare the expression of CSF-1R in nasopharyngeal carcinoma to nasopharyngitis for assessing the role CSF-1/CSF-1R in nasopharyngeal carcinoma. MATERIALS AND METHODS: Diagnostic tissues from 56 nasopharyngeal carcinoma patients and 32 nasopharyngitis patients were evaluated retrospectively by immunohistochemical analysis for the expression of CSF-1R. RESULTS: Significant differences of CSF-1R expression exists between nasopharyngeal carcinoma patients and nasopharyngitis patients (p<0.001). However, there is no relevance between CSF-1R and worse survival.

Aberrant expression levels of MTA1 and RECK in nasopharyngeal carcinoma: association with metastasis, recurrence, and prognosis.

OBJECTIVES: We investigated the expression and clinical value of MTA1 and RECK genes in patients with nasopharyngeal carcinoma (NPC). METHODS: We examined MTA1 and RECK expression in nasopharyngeal tissue from patients with chronic nasopharyngitis, lymph nodes with metastasis of NPC, and primary NPC tumor tissue by means of in situ hybridization and analyzed their correlation with the clinicopathologic features of NPC. RESULTS: The positive expression of MTA1 in the NPC tissues and metastatic lymph nodes was significantly higher than that in the chronic nasopharyngitis tissues (p < 0.05). The positive expression of RECK in the NPC tissues and metastatic lymph nodes was significantly lower than that in the chronic nasopharyngitis tissues (p < 0.05). The RECK expression level was inversely correlated with the MTA1 expression level in the NPC tissues (p < 0.05). The increased MTA1 and decreased RECK expressions in the NPC tissues had no association with gender, age, T-stage, or clinical stage (p > 0.05). However, they had a positive correlation with cervical lymph node metastasis, tumor recurrence, and 5-year overall survival rate of the patients with NPC (p < 0.05). Moreover, multivariate analysis showed that MTA1 and RECK expressions were independent prognostic factors for survival (p < 0.05). CONCLUSIONS: The conversely abnormal expression levels of MTA1 and RECK may be collectively involved in progression of malignancies and may serve as molecular predictors for metastasis, recurrence, and prognosis of NPC.

Association of adenoid hyperplasia and bacterial biofilm formation in children with adenoiditis in Taiwan.

The adenoid is a bacterial reservoir that contributes to chronic otolaryngologic infections. Staphylococcus aureus (S. aureus) is a common pathogen in the adenoid. The increase of antibiotic resistance in S. aureus has become an important issue in public health. The aim of this study was to compare adenoid hyperplasia and biofilm formation in children with S. aureus adenoiditis in Taiwan. The patients were divided into methicillin-resistant and methicillin-sensitive S. aureus groups according to the S. aureus obtained from adenoid tissue after antibiotic susceptibility testing. Adenoid hyperplasia was assessed by lateral cephalometry, and the severity of sinusitis was evaluated by Water's view. Microbiological investigation of available S. aureus isolates was performed by in vivo morphological observation and an in vitro bacterial biofilm assay. Sixty isolates of S. aureus were identified in 283 children (21.2%) after adenoidectomy, of which 21 (35%) were methicillin-resistant S. aureus (MRSA). The severity of adenoid hyperplasia and extensive biofilm formation were more prominent in patients infected with methicillin-resistant S. aureus than in those infected with methicillin-sensitive S. aureus (MSSA). The primary outcome of this study was to provide evidence that S. aureus constituted a significant portion of the adenoidal pathogens. The secondary outcome of this study was that MRSA adenoiditis may be associated with adenoid hyperplasia and biofilm formation.

[Immunomodulators for topical application to prevent and manage chronic adenoiditis in children].

The authors report the results of a study on the efficacy of topical application of the immunomodulator IRS 19 in children presenting with chronic adenoiditis and grade I-III hypertrophy of adenoid vegetation. The use of this preparation is shown to faster and more efficaciously normalize the volume of the lymphoid tissue than irrigation of the nasopharynx with saline solutions. Moreover, the treatment of chronic adenoiditis with IRS 19 promoted normalization of biocenosis of the nasopharyngeal secretion and significantly decreased the abundance of pathogenic microflora. Specifically, the overall frequency of exacerbations and the frequency of exacerbations of adenoiditis decreased three- and two-fold respectively while the duration of the disease shortened. It is recommended that the topical immunomodulator IRS 19 should be included in the programs of planned seasonal treatment of children suffering chronic adenoiditis (to be applied at least 2-3 times annually).

[Expression and Significance of Notch1, P21WAF1 and involucrin in nasopharyngeal carcinoma].

BACKGROUND & OBJECTIVE: Abnormal expression of Notch1 protein was often found in many kinds of primary tumors, but its correlation with nasopharyngeal carcinoma (NPC) is still unclear. This study was designed to investigate the expression of Notch1 and its downstream proteins P21(WAF1) and Involucrin in NPC, and analyze their correlations with the differentiation of NPC cells. METHODS: The expression of Notch1, P21(WAF1), and Involucrin in 101 specimens of NPC and 20 specimens of chronic inflammatory nasopharyngeal mucosa were detected by SP immunohistochemistry. RESULTS: The positive rates of Notch1, P21(WAF1), and Involucrin were 100%, 90.0%, and 100% in chronic inflammatory nasopharyngeal mucosa, and were 77.2%, 89.1%, and 80.1% in NPC, respectively. The expression of Notch1, P21(WAF1), and Involucrin were significantly suppressed along with descending differentiation of NPC (P=0.000, P=0.026, and P=0.000). The positive rates of Notch1, P21(WAF1), and Involucrin were significantly higher in keratinizing squamous cell carcinoma (KSCC) than in differentiated nonkeratinizing carcinoma (DNKC) and undifferentiated carcinoma (UDC) (P<0.05), and were significantly higher in DNKC than in UDC (P<0.05). The expression of Notch1 in NPC was positively correlated with the expression of P21(WAF1) (r=0.306, P=0.002) and Involucrin (r=0.325, P=0.001). No significant correlation was found between the expression of P21(WAF1) and Involucin. CONCLUSION: The expression of Notch1, P21(WAF1), and Involucrin are closely correlated to the differentiation of NPC cells.

In vitro effects of some differentiation inductors in metaplastic epithelium of the human nasal cavity.

The alterations in the mucociliary unit in the course of chronic inflammation of the upper respiratory tract correspond to morphologic anomalies of the respiratory epithelium and induce cuboidal and squamous metaplasia. While the squamous pattern is most probably irreversible, it is still not clear whether it is possible to restore ciliogenesis in cuboidal metaplasia. In the present study, the action of different inductors of differentiation was evaluated in vitro in isolated cells and explants from human nasal metaplastic epithelium. Polar/apolar compounds induced secretory activity, whereas retinoic acid was able to induce ciliogenesis in some cases. Therefore, the cuboidal metaplastic condition appears to be reversible, and two distinct pathways of differentiation, secretory and ciliogenetic, are identifiable.

Mucosa-associated lymphoid tissue in middle ear and Eustachian tube in children.

The presence of mucosal lymphoid follicles with germinal centers, so called mucosa-associated lymphoid tissue (MALT), in the Eustachian tube (ET) and middle ear (ME) was investigated in 23 human temporal bones containing the entire ET obtained from 23 children, 3 months to 10 years old at death. Greater numbers of MALTs were found in specimens from children with otitis media (OM) than from those without OM. MALT showed a wedge-shaped distribution through the ME and ET: in all 3 specimens that had MALTs in the ME, these tissues were seen throughout the ET; in all 4 specimens with MALTs in the bony portion of the ET, these tissues were present both in the tympanic and pharyngeal portions of the cartilagines ET; all 7 specimens that had MALTs in the tympanic half of the cartilagines ET had MALTs in the pharyngeal portion of the cartilagines ET as well. Furthermore, MALTs were noted in the pharyngeal portion of the ET in more than half of the specimens without OM but in none of the MEs of specimens without OM. These results support the hypothesis that persistent and recurrent inflammation in the nasopharynx spreads through the ET to play a role in the pathogenesis of chronic OM in children.

The human nasal mucous membrane during chronic inflammation, before and after muco-active therapy: a study using scanning electron microscopy.

Chronic inflammation seems to induce alterations in nasal mucosa morphology. The type and extent of these alterations seem to be directly correlated with the duration of the inflammation. This study was carried out to ascertain whether the administration of muco-active drugs could modify these alterations by inducing their total or partial regression. Ten healthy control subjects, and thirty patients affected with chronic rhinopharyngitis, at various levels of severity, were studied. All the forty subjects underwent biopsy of the posterior region of the medium turbinate. The bioptic samples were examined using Scanning Electron Microscopy (SEM). Patients with phlogosis underwent treatment which consisted of a single day administration of carbocysteine-sobrerol (1125 mg carbocysteine and 180 mg sobrerol day 20 days). This group underwent biopsy again and the fragments obtained were studied using the same method. Chronic inflammation, in the nasal epithelium, causes progressive degenerative phenomena, which are related to the duration and to the severity of the pathology. The response of the nasal mucosa principally results in damage to the muco- ciliary unit, loss of cilia and consistent modifications in the mucous secretion. In cases of persistent inflammation, the nasal epithelium becomes squamous. The therapy employed was able to alter the morphological signs of degeneration in the less severe cases, and to improve the overall pattern of the most severe and irreversible pathologies.

Condrosarcoma de rinofaringe: a porpósito de un caso / Rhinopharynx chondrosarcoma: a purpose of a case

El presente trabajo se basa en el estudio de tumoración nasofaríngea que presentó paciente femenina de 37 años en enero de 1990, la misma paciente había sido tratada sintomáticamente por varios especialistas. La tumoración resultó ser un Condrosarcoma de Rinofaringe, el presente diagnóstico debió ser corroborado por microscopía electrónica, ya que hubo incongruencia entre los patólogos que evaluaron las láminas. El tratamiento aplicado fue exéresis por vía transpalatina, y posteriormente radioterapia, la evolución fue satisfactoria y actualmente permanece asintomática

Chronic idiopathic inflammation of the retropharyngeal space presenting with sequential abducens palsies.

We describe a patient who presented with sequential, bilateral abducens palsies associated with a mass of the nasopharynx. Biopsy of the mass showed chronic non-specific inflammation and fibrosis. The diagnosis of idiopathic inflammatory pseudotumor was arrived at by exclusion of other known causes of inflammation of the retropharyngeal space. Magnetic resonance imaging suggested that injury to the sixth cranial nerves probably occurred as they traversed the dura and subarachnoid space overlying the clivus.