Curcumin-Encapsulated Chitosan-Coated Nanoformulation as an Improved Otoprotective Strategy for Ototoxic Hearing Loss.

Overexpression of apoptotic factors in the inner ear is generally proven to induce ototoxicity. This has aroused research interest in various antiapoptotic drugs, the most representative of which is curcumin (CUR). In this study, two nanoformulations of CUR were developed with sustained-release behavior to improve their protective effects against ototoxic hearing loss (HL), which were the nanoparticles of CUR-loaded poly(lactic acid-glycolic acid) (CUR-PLGA NPs) and CUR-loaded chitosan-coated PLGA NPs (CUR-CS/PLGA NPs). The obtained results revealed that both CUR-NPs provided otoprotection in vitro and in vivo, and their effective doses in guinea pigs were much less than that of dexamethasone, which was clinically used to treat HL. Moreover, relative to CUR and CUR-PLGA NPs, CUR-CS/PLGA NPs exhibited the highest accumulation in HEI-OC1 cells and guinea pigs' cochlea. In pharmacodynamic experiments, the optimal administration timing was investigated, and CUR-CS/PLGA NPs showed sustained efficacy and the best hearing improvement at all tested sound frequencies. Lastly, the protective effect of CUR nanoformulations was further validated via inhibition of Caspase-3 and Bax activation, thereby reducing the concentration of reactive oxygen species and protecting mitochondrial integrity in hair cells. Collectively, CUR-CS/PLGA NPs demonstrated potent and lasting effects against ototoxic HL, making our novel formulation a promising candidate for the alleviation of sensorineural HL.

Glycyrrhiza glabra suppresses nasopharyngeal carcinoma cell proliferation through inhibiting the expression of lncRNA, AK027294.

Glycyrrhiza glabra is considered as potential drug for nasopharyngeal carcinoma (NPC). However, whether the long noncoding RNAs' (lncRNAs) contributes to the anti-cancer function of this herb is unknown. In present study, we analyzed the differential expression of lncRNA between G. glabra-treated and untreated C666-1 cells. Out of those tumor-related lncRNAs, AK027294 had a strongest down-regulation upon G. glabra treatment. Knockdown of AK027294 suppresses the proliferation of C666-1 cells by inducing the apoptosis. Moreover, either G. glabra treatment or knockdown of AK027294 significantly increases the production of EZH1 (Enhancer of zeste 1 polycomb repressive complex 2 subunit). Collectively, we have identified a potential mechanism that the down-regulation of AK027294 contributes to the anti-cancer function of G. glabra and also provide the potential inter-relationship between AK027294 and EZH1.

CircHIPK3 promotes proliferation and invasion in nasopharyngeal carcinoma by abrogating miR-4288-induced ELF3 inhibition.

Circular RNAs (circRNAs) are reported to regulate the development and progression of multiple cancers. However, the functions of circRNAs in nasopharyngeal carcinoma (NPC) are unclear. In this study, we identified that circular homeodomain interacting protein kinase 3 (circHIPK3) was highly expressed in NPC tissues and cell lines. Moreover, we found that circHIPK3 expression levels could act as a prognostic marker in NPC patients. We showed that circHIPK3 silence repressed NPC cell proliferation, migration, and invasion in vitro. In addition, circHIPK3 depletion dramatically repressed tumor growth and metastasis in vivo. Mechanistically, we revealed circHIPK3 as a competing endogenous RNA of microRNA (miR)-4288 that targets E74-like ETS transcription factor 3 (ELF3) in NPC cells. We found that miR-4288 inhibition reversed the effects of circHIPK3 silence on NPC cells. Furthermore, rescue assays also indicated that circHIPK3 promoted the malignant behaviors of NPC cells via enhancing ELF3 expression by suppressing the miR-4288 levels. In conclusion, our findings demonstrated that circHIPK3 facilitated NPC progression through protecting ELF3 from miR-4288-mediated silencing, which suggested that the circHIPK3-miR-4288-ELF3 regulatory loop might be a potential target for NPC prevention.

Efficacy of chitosan dressing on endoscopic sinus surgery: a systematic review and meta-analysis.

Chitosan dressing might be promising to promote the recovery following endoscopic sinus surgery (ESS). However, the results remain controversial. We conducted a systematic review and meta-analysis to explore the influence of chitosan dressing on ESS. PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases were systematically searched. Randomized controlled trials (RCTs) assessing the effect of chitosan dressing on endoscopic sinus surgery were included. Two investigators independently searched articles, extracted data, and assessed the quality of included studies. The primary outcomes were synechia and hemostasis. Meta-analysis was performed using random-effect model. Four RCTs involving 268 patients were included in the meta-analysis. Overall following ESS, compared with control intervention, chitosan dressing significantly reduced synechia (RR = 0.25; 95% CI 0.13-0.49; P < 0.0001) and promoted hemostasis (RR = 1.70; 95% CI 1.37-2.11; P < 0.00001), but showed no impact on granulations (RR = 1.18; 95% CI 0.72-1.95; P = 0.52), mucosal edema (RR = 0.88; 95% CI 0.60-1.29; P = 0.51), crusting (RR = 0.85; 95% CI 0.48-1.53; P = 0.60), and infection (RR = 0.88; 95% CI 0.51-1.52; P = 0.64). Compared to control intervention, chitosan dressing could significantly decrease edema and improve hemostasis, but had no effect on granulations, mucosal edema, crusting and infection.

Murine cytomegalovirus employs the mixed lineage kinases family to regulate the spiral ganglion neuron cell death and hearing loss.

Cytomegalovirus (CMV)-induced sensorineural hearing loss (SNHL) is a worldwide epidemic. Recent studies have shown that the degree of spiral ganglion neuron (SGN) loss is correlated with hearing loss after CMV infection. We aimed to better understand the pathological mechanisms of CMV-related SGN death and to search for intervention measures. We found that both apoptosis and pyroptosis are involved in CMV-induced SGN death, which may be caused by the simultaneous activation of the p53/JNK and NLRP3/caspase-1 signaling pathways, respectively. Moreover, considering that mixed lineage kinase family (MLK1/2/3) are host restriction factors against viral infection and upstream regulators of the p53/JNK and inflammatory (including NLRP3-caspase1) signaling pathways, we further demonstrated that the MLKs inhibitor URMC-099 exhibited a protective effect against CMV-induced SGN death and hearing loss. These results indicate that MLKs signaling may be a key regulator and promising novel target for preventing apoptosis and even pyroptosis during the CMV infection of SGN cells and for treating hearing loss.

Ribophorin II promotes the epithelial-mesenchymal transition and aerobic glycolysis of laryngeal squamous cell carcinoma via regulating reactive oxygen species-mediated Phosphatidylinositol-3-Kinase/Protein Kinase B activation.

Ribophorin II (RPN2), a part of an N-oligosaccharyl transferase complex, plays vital roles in the development of multiple cancers. Nevertheless, its biological role in laryngeal squamous cell carcinoma (LSCC) remains unclear. The RPN2 expression levels in LSCC tissues and cell lines (AMC-HN-8 and TU212) were measured using real-time PCR, immunohistochemistry, or Western blot. The influences of RPN2 on the proliferation, migration, epithelial-mesenchymal transition, and aerobic glycolysis of LSCC cells were investigated after upregulation or downregulation of RPN2 in vitro and in vivo. Mechanically, we assessed the impact of RPN2 on the reactive oxygen species (ROS)/Phosphatidylinositol-3-Kinase (PI3K)/Protein Kinase B (Akt) signaling pathway. We found that compared with the control, RPN2 was highly expressed in LSCC tissues and cells. Overexpression of RPN2 elevated the proliferation, migration, glucose uptake, lactate production release, and levels of Vimentin, hexokinase-2 (HK-2), pyruvate dehydrogenase kinase 1 (PDK1), lactate dehydrogenase A (LDHA), and ROS, but inhibited E-cadherin expression in AMC-HN-8 cells. Knockdown of RPN2 in TU212 cells showed opposite effects on the above indexes. Meanwhile, RPN2 upregulation increased the levels of p-PI3K/PI3K and p-Akt/Akt, which were attenuated by N-acetyl-L-cysteine (NAC), an ROS inhibitor. Both NAC and PI3K inhibitor LY294002 could reverse the effects of RPN2 overexpression on the malignant phenotypes of LSCC cells. In xenografted mice, silencing RPN2 expression reduced tumor growth, ROS production, and levels of Ki-67, Vimentin, LDHA, and p-Akt/Akt, but enhanced E-cadherin expression. In conclusion, our data suggested that RPN2 promoted the proliferation, migration, EMT, and glycolysis of LSCC via modulating ROS-mediated PI3K/Akt activation.

Sonodynamic therapy exciting the herbal nanocomposite with spider-web-like effect to combat otitis media.

Otitis media, mainly caused by bacteria, is prevalent in young children and can cause hearing loss and growth retardation. Antibiotics are the most widely utilized treatment for otitis media, however, they can cause drug resistance and harmful side effects. In this study, we reported an antibacterial nanocomposite in combination with sonodynamic therapy that consists of herbal antibacterial agents such as Curcumin (CUR) and Tanshinone IIA (TSIIA), as well as Chitosan (CS), for the treatment of acute otitis media. CUR/TSIIA/CS nanocomposite (NC) with ultrasonic irradiation demonstrated that it could eliminate Staphylococcus aureus. In vivo experiments revealed that NC-mediated sonodynamic therapy had excellent antibacterial and anti-inflammatory activity, displaying a consistent performance comparable to ofloxacin. The therapeutic efficiency was attributed to capturing bacteria through spider-web-like effect and destroying bacteria through the reactive oxygen species generated under ultrasonic irradiation. Significantly, NC did not induce bacterial resistance and showed good biocompatibility. This study provides a novel strategy to develop an ultrasound-assisted nanocomposite with an enhanced antibacterial effect. Further, it unlocks new doors for the substitute of antibiotics to combat otitis media by establishing efficient therapeutic systems.

Oridonin alleviates kanamycin-related hearing loss by inhibiting NLRP3/caspase-1/gasdermin D-induced inflammasome activation and hair cell pyroptosis.

Aminoglycoside antibiotic drugs induce hearing loss in children and adults every year; however, the pathological mechanisms remain unknown. Previous studies have shown that the accumulation of reactive oxygen species (ROS) and inflammation in the inner ear may be responsible for kanamycin (KM)-induced hair cell death and hearing loss. Nucleotide-binding oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing protein 3 (NLRP3) is a specific ROS sensor that initiates inflammasome assembly as well as activates caspase-1 and downstream inflammatory factors. Therefore, this study aimed to determine whether NLRP3 inflammasomes are involved in KM-related hearing loss in mice. Compared with the control (saline) group, increased levels of activated caspase-1, interleukin (IL)-1ß, IL-18, N-terminal fragment of gasdermin D (GSDMD-N), and NLRP3 were detected by immunofluorescence, western blot, and enzyme-linked immunosorbent assay (ELISA) in the KM-plus-furosemide (LASIX)-treated group. Moreover, we also found that the NLRP3 inhibitor oridonin (Ori) could significantly rescue KM-related hearing loss by inhibiting NLRP3-inflammasome activation and caspase-1/GSDMD-related hair cell pyroptosis. These findings demonstrate that apoptosis, as well as pyroptosis, may be involved in KM-related hearing loss and that the NLRP3/caspase-1/GSDMD pathway may be a new target for treating aminoglycoside-induced hearing loss.

Co-activation of Caspase-1 and Caspase-8 in CMV-induced SGN death by inflammasome-associated pyroptosis and apoptosis.

Cytomegalovirus (CMV) infection causes newborn deafness, and the death of the spiral ganglion neurons (SGNs) is crucial in determining the degree of CMV-related hearing loss. Therefore, understanding the psychopathology of CMV-related SGN loss is important for identifying targets and exploring treatment strategies. In this study, we found that pyroptosis and apoptosis, two inflammasome-related programmed cell death pathways, are involved in CMV-induced SGN death and are mainly regulated by activated caspase-1 and caspase-8. Moreover, suppressing inflammasome assembly by blocking apoptosis-associated speck-like protein containing a CARD (ASC) interaction inhibited the activation of both caspase-1 and caspase-8, rescued SGN death, and improved hearing loss in CMV-infected newborn mice. Therefore, we propose that ASC inflammasome might be a promising target for treating CMV-related SGN death and newborn hearing loss by inhibiting caspase-1 and caspase-8 activated pyroptosis and apoptosis.

Oridonin ameliorates noise-induced hearing loss by blocking NLRP3 - NEK7 mediated inflammasome activation.

Inflammation is involved in noise-induced hearing loss (NIHL), but the mechanism is still unknown. The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, which triggers the inflammatory cascade, has been implicated in several inflammatory diseases in response to oxidative stress. However, whether the NLRP3 inflammasome is a key factor for permanent NIHL is still unknown. In this study, quantitative real-time polymerase chain reaction (qPCR), western blot, and enzyme-linked immunosorbent assays (ELISAs) demonstrated that the expression levels of activated caspase-1, interleukin (IL)-1ß, IL-18, and NLRP3 were significantly increased in the cochleae of mice exposed to broadband noise (120 dB) for 4 h, compared with the control group. These results indicate that the activation of inflammasomes in the cochleae of mice during the pathological process of NIHL as well as NLRP3, a sensor protein of reactive oxygen species (ROS), may be key factors for inflammasome assembly and subsequent inflammation in cochleae. Moreover, many recent studies have revealed that NEK7 is an important component and regulator of NLRP3 inflammasomes by interacting with NLRP3 directly and that these interactions can be interrupted by oridonin. Here, we further determined that treatment with oridonin could indeed interrupt the interaction between NLRP3 and NEK7 as well as inhibit the downstream inflammasome activation in mouse cochleae after noise exposure. Furthermore, we tested anakinra, another inflammatory inhibitor, and it was shown to partially alleviate the degree of hearing impairment in some frequencies in an NIHL mouse model. These discoveries suggest that inhibiting NLRP3 inflammasomes and the downstream signaling pathway may provide a new strategy for the clinical treatment of NIHL.

Intratympanic dexamethasone injection for sudden sensorineural hearing loss in pregnancy.

BACKGROUND: As sudden sensorineural hearing loss (SSNHL) rarely occurs in pregnant women, there is a lack of knowledge and relevant research on its management. AIM: To investigate the effect of intratympanic dexamethasone injection in the treatment of pregnant patients with SSNHL. METHODS: A retrospective chart review was made for the period between June 2017 and August 2019 at our Department of Otorhinolaryngology-Head and Neck Surgery. Pregnant women who met the criteria for SSNHL were included and grouped based on the therapeutic modalities. The treatment group received intratympanic dexamethasone (2.5 mg) q.o.d. for a total of four times, while the control group received no medication other than bed rest and medical observations. All the patients were under close care of obstetricians. Pure-tone audiograms were performed before and after treatment. RESULTS: Eleven patients who met the inclusion criteria were assigned to the treatment group (n = 7) and the control group (n = 4). The mean age of patients was 31.2 ± 3.8 years; the right ear was affected in seven (63.64%) cases. Two patients (18.2%) suffered from vertigo, 10 (90.9%) suffered from tinnitus and 6 (54.5%) suffered from aural fullness. The time from onset to clinic visit was relatively short, with a mean time of 1.3 ± 0.9 d. All the women were within the second or third trimester; the average gestation period was 26.0 ± 6.2 wk. The pure-tone averages at onset between the two groups were similar. After one wk of therapy, the treatment group had a curative rate of 57.1% and a significantly better hearing threshold and greater improvement compared to the control group (all P < 0.05). Some patients experienced transient discomfort from intratympanic injections that disappeared after getting rest, while none had permanent complications. All patients delivered healthy full-term neonates with an average Apgar score of 9.7 ± 0.5. CONCLUSION: Intratympanic dexamethasone injections can be used as a first-line therapy in pregnant women with SSNHL.

High SRC-1 and Twist1 expression predicts poor prognosis and promotes migration and invasion by inducing epithelial-mesenchymal transition in human nasopharyngeal carcinoma.

Steroid receptor coactivator 1 (Src-1) and Twist1 are aberrantly upregulated in a variety of tumors and play an important role in tumor progression. However, the exact role of Src-1 and Twist1 in nasopharyngeal carcinoma (NPC) is uncertain. In this study, we investigated the possible prognostic value and biological effect of Src-1 and Twist1 in NPC. Src-1 and Twist1 expression was detected in a cohort of NPC patients (n = 134) by qRT-PCR. Kaplan-Meier survival analysis was used comparing overall survival (OS) and progression-free survival (PFS). Multivariate analysis was performed using the Cox proportional hazard regression model. Biologic effect of Src-1 and Twist1 in NPC cell lines was evaluated by western blot, colony formation assay, soft agar assay, scratch wound healing assay, transwell invasion assay and tumor xenografts growth. We have found that Src-1 and Twist1 were aberrantly upregulated in human NPC tissues, and associated with advanced tumor stage, distant metastasis and unfavorable prognosis. Knockdown of Src-1 or Twist1 in human NPC cell line CNE-1 suppressed colony formation, anchorage-independent growth, cell migration, invasion and tumor xenografts growth, while enforced expression of Src-1 or Twist1 in human NPC cell line HNE-2 promotes anchorage-independent growth, cell migration and invasion. In addition, Src-1 and Twist1 could suppress E-cadherin expression and increase Vimentin expression, thus suggested that Src-1 and Twist1 enhanced the malignant behaviors of NPC cells via inducing epithelial-mesenchymal transition (EMT). Our data indicated that Src-1 and Twist1 could be possible prognostic biomarkers and potential therapy targets for patients with NPC.

CircRNA hsa_circ_100395 regulates miR-1228/TCF21 pathway to inhibit lung cancer progression.

Circular RNA (circRNA) is shown to participate in various tumors, including lung cancer. Although a few circRNAs involved in lung cancer are reported, whether circRNA negatively regulates lung cancer development remains elusive. In this study, we showed hsa_circ_100395 expression was decreased in lung cancer tissues. Besides, hsa_circ_100395 level was inversely correlated with TNM stage and metastases in lung cancer and low hsa_circ_100395 expression in patients predicted poor prognosis. Overexpression of hsa_circ_100395 dramatically inhibited lung cancer cell proliferation, arrested cell-cycle progression and reduced cell migration and invasion in vitro. Xenograft experiments showed that hsa_circ_100395 overexpression delayed tumor growth in vivo. Mechanistically, we showed hsa_circ_100395 serves as a sponge for miR-1228 targeting TCF21 in lung cancer. Rescue assays indicated that hsa_circ_100395 regulates lung cancer cell proliferation, migration and invasion through modulating miR-1228/TCF21 pathway. Altogether, our study reveals a novel regulatory loop that hsa_circ_100395/miR-1228/TCF21 axis modulates lung cancer development. ABBREVIATIONS: circRNA: circular RNA; miRNA: microRNA; RNA-FISH: RNA fluorescence in situy bridization; qRT-PCR: Reverse transcription and quantitative real-time PCR.

Anti-tumor effect of HOTAIR-miR-613-SNAI2 axis through suppressing EMT and drug resistance in laryngeal squamous cell carcinoma.

Laryngeal squamous cell carcinoma (LSCC) is the main pathological type of laryngeal cancer, which attacks the head and neck. Our present study aims to investigate the effect of long non-coding RNA (LncRNA) HOX transcript antisense RNA (HOTAIR) on epithelial mesenchymal transition (EMT) and drug resistance in LSCC. Firstly, the level of HOTAIR was found to be overexpressed in LSCC tissues compared with normal healthy tissues. Then, increased EMT and drug resistance were suppressed by specific HOTAIR shRNA effectively in LSCC cell lines. Besides, miR-613 was predicted to be a target of HOTAIR through bioinformatics analysis. Meanwhile, we found that a down-regulated level of miR-613 could be increased by HOTAIR shRNA and suppressed by LncRNA HOTAIR transfection in LSCC cells. The targeting relationship between miR-613 and HOTAIR was further demonstrated by a luciferase report assay. What is more, the inhibiting effect of HOTAIR shRNA on EMT and drug resistance was obviously abolished by the miR-613 inhibitor. Moreover, SNAI2, a critical regulator of EMT, was predicted as a target of miR-613 through bioinformatics analysis and luciferase report assays. As expected, the level of SNAI2 could be suppressed by HOTAIR shRNA and increased by the miR-613 inhibitor. Additionally, we discovered that SANI2 shRNA had similar inhibiting effect on EMT and drug resistance with HOTAIR shRNA in LSCC cells. Finally, the in vivo experiment further demonstrated that HOTAIR shRNA restricted tumor growth, EMT and drug resistance. Additionally, HOTAIR shRNA transfection could also increase the level of miR-613 and decrease the level of SNAI2 in vivo. Taken together, our research for the first time revealed the effect of the HOTAIR-miR-613-SNAI2 axis on EMT and drug resistance in LSCC, providing new targets for LSCC diagnosis and treatment.

Downregulation of miR-204 is associated with poor prognosis and promotes cell proliferation in hypopharyngeal squamous cell carcinoma (HSCC).

MircroRNAs (miRNAs) were identified to be involved in tumor progression and prognosis. However, the clinical significance and biological function of miR-204 in hypopharyngeal squamous cell carcinoma (HSCC) are not well appreciated. Therefore, the aim of this study is to explore the role of miR-204 in HSCC. The miR-204 expression was determined in 56 pairs of HSCC tumor and adjacent non-tumor tissues by quantitative real-time reverse transcriptive-PCR (qRT-PCR). Kaplan-Meier survival curve analysis and log-rank test were used to analyze the association between miR-204 expression and clinicopathological parameters and the over survival (OS) time in HSCC patients. Univariate and multivariate Cox analysis was applied to investigate the predicted risk factors for OS. Moreover, CCK8 cell proliferation assays, flow cytometry analysis and western-blot analysis were performed to examine the cell growth and cell cycle related protein expression in FaDu cells. In the study, our results reported that miR-204 was down-regulated in HSCC tissues. The patients with lower miR-204 expression had significantly poor OS time. Multivariable Cox analysis demonstrated that lower miR-204 expression was an independent risk factor in HSCC patients. Furthermore, CCK8 cells assays and cell cycle analysis showed that over-expression of miR-204 significantly inhibited cell proliferation, S phase cell number and inhibited the cell cycle related protein expression of CyclinD1, CDK4 and CDK6, but up-regulated the p21 expression in FaDu cells. Thus, our study demonstrated that miR-204 was downregulated in HSCC and upregulation of miR-204 suppressed cell proliferation, which highlighted that miR-204 could have potential therapeutic applications in HSCC.

[Feature and significance of bacterial biofilm formation in middle-ear mucosa in the rat model of acute otitis media].

OBJECTIVE: To investigate the relationship between bacterial biofilm and acute otitis media by observing the feature of bacterial biofilm formation in middle-ear mucosa in the rat model of acute otitis media and to study the possibility of application this rat model in bacterial biofilm research. METHODS: A total of 30 healthy, male SD rats were studied, 24 animals served as experimental group were bilaterally injected with 50 µl of Streptococcus pneumoniae suspension (1 × 10(8) CFU/ml) via a transbullar approach into the middle ear cavity after anesthesia and six animals were bilaterally inoculated equivalent saline account for control group. At day 1, 3, 5, 7, 10 and 14 after inoculation, bilateral middle-ear mucosal specimens were collected from three infected animals and one control animal for scanning electron microscopy (SME). Membranoid substance attached the bilateral middle ear mucosa were collected under the microscope from the other one infected animals, which were prepared for confocal laser scanning microscope (CLSM) with immunofluorescence in situ labeling technique and light microscopy using Gram staining. RESULTS: At the early stage of infection (1 day, 3 days), lots of bacterial adhesion, permanent planting in the local regions of the middle ear cavity and microcolonies formation were found, with mixed phagocytic cells, showing a primary bacterial biofilms formation. In the middle term of infection (5 days, 7 days), mature bacterial biofilm scattered on the mucosal surface, formed characteristic three-dimensional structure of "mushroom-shaped" towers. At the late inflammatory period (10 days, 14 days), the bacterial biofilms presented signs of recession. CLSM with FITC-ConA and PI double staining in situ labeling and light microscopy using Gram staining indicated that bacteria and polysaccharide matrix within the biofilms were viable. CONCLUSIONS: These preliminary findings provide evidence that bacterial biofilms form at the early phase of acute middle ear infection and it may be an important factor in the development of recurrent or persistent otitis media. The rat model of AOM established in this study may be an ideal animal model facilitating the bacterial biofilms research.

[A clinical and pathological analysis on laryngeal contact granuloma among 18 cases].

OBJECTIVE: To summarize the clinicopathologic feature and diagnostic and therapeutic experience of laryngeal contact granuloma. METHOD: A retrospective study was carried out among 18 cases with this disease through careful analysis on their clinical and pathological data. RESULT: All of 18 cases were male, aged 34 to 78 years,The most common symptoms were hoarseness. In general the granuloma located on the posterior of the larynx unilaterally. The histological appearances of the lesions were typical inflammatory granuloma. Little allotype cell were found in one histologic sample. Fifteen cases received surgical excision and the recurrence rate was 60% after operation. Recidivist received operation again,4 cases among these cases received antireflux therapy after operation but 3 cases recurrences again. Among those follow-up cases(3 cases), 1 case was self-cure and other 2 cases appeared no marked change during observation period. CONCLUSION: Laryngeal contact granuloma predilected the middle-aged male. The localization and appearance of the granuloma is very characteristic. The correct diagnosis can be established by clinical examination alone, but the histological examination is necessary in order to avoid missed diagnosis. There is a high recurrence rate after operation and the effect of antireflux therapy need further research.

[Diagnostic value of 18F-fDG Pet/CT in the detection of the cervical lymph nodes metastasis].

OBJECTIVE: To explore the diagnostic value of 18F-FDG PET/CT in the detection of the cervical lymph nodes metastasis. METHOD: According to the pathological result, the data of neck PET, CT, PET/CT of 20 patients with head and neck tumors were analyzed retrospectively. RESULT: The sensitivity, specificity and accuracy of PET, CT and PET/CT in detection cervical lymph nodes metastasis were (92.3%, 85.7%, 90.0%), (77.0%, 57.1%, 70.0%), (92.3%, 100.0%, 95.0%) respectively, the accuracy of PET/CT was better than that of CT alone (P < 0.05) and a little better than that of PET alone. Among 13 cases after irradiation,the correct diagnose was found in seven cases by CT and in 12 cases by PET/CT. Four cases were found with cervical lymph node metastasis in the seven clinical N0 (cN0) patients after functional neck dissection (FND). The preoperative diagnose of PET/CT was completely consistent with the postoperative pathological result. CONCLUSION: 18F-FDG PET/CT is better than CT alone and PET alone for the detection of cervical lymph nodes metastasis, especially for the recurrent tumors. It may be served as the indication of neck dissection in the head and neck cancers.