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How much translational energy atoms and molecules lose in collisions at surfaces determines whether they adsorb or scatter. The fact that hydrogen (H) atoms stick to metal surfaces poses a basic question. Momentum and energy conservation demands that the light H atom cannot efficiently transfer its energy to the heavier atoms of the solid in a binary collision. How then do H atoms efficiently stick to metal surfaces? We show through experiments that H-atom collisions at an insulating surface (an adsorbed xenon layer on a gold single-crystal surface) are indeed nearly elastic, following the predictions of energy and momentum conservation. In contrast, H-atom collisions with the bare gold surface exhibit a large loss of translational energy that can be reproduced by an atomic-level simulation describing electron-hole pair excitation., (Copyright © 2015, American Association for the Advancement of Science.)

Recent evidence has suggested that miRNA is implicated in the immune response of allergic and inflammatory diseases. However, little is known about its role in the mechanism that underlies the establishment of pro-allergic DCs in allergic rhinitis is not fully understood. This study assessed whether and how microRNA (miR)-106b regulates the pro-allergic properties of DCs upon allergen stimulation in vitro. Bone marrow-derived dendritic cells (BMDCs) were generated and stimulated with ovalbumin (OVA) to identify the miRNA expression profile. After transfection with miR-106b mimics and inhibitors OVA-activated BMDCs were further evaluated for surface marker expression using flow cytometry, cytokine production using ELISA and subsequent effects on Th2 cell polarisation using flow cytometry. Moreover, the upstream controllers and potential target proteins of miR-106b were examined in a western blot analysis. Results showed that MiR-106b expression was significantly inhibited in activated BMDCs upon OVA stimulation (p<0.05). Surface marker expression (e.g., MHC class II, CD80 and CD86) was significantly upregulated after the transfection of an miR-106b inhibitor (p<0.05), and the proportion of GATA-3(+) T cells was significantly increased among CD4(+) T cells that were cocultured with miR-106b inhibitor-pretreated BMDCs (p<0.05). Conversely, IL-12 production from OVA-activated BMDCs and the proportion of T-bet(+) T cells increased significantly in a coculture of CD4(+) T cells and miR-106b mimics-transfected BMDCs (p<0.05). The early growth response (Egr)-2 was identified via luciferase reporter assays as a target gene of miR-106b, and significant Egr-2 upregulation was observed in OVA-activated BMDCs following transfection with a miR-106b inhibitor (p<0.05). In conclusion, our results suggest that miR-106b negatively regulates the pro-allergic properties of BMDCs and subsequent Th2 polarisation upon OVA stimulation and might represent a promising therapeutic target for allergic inflammation., (Copyright © 2015. Published by Elsevier B.V.)

Introduction: Genetic analyses including genome-wide association studies have reported an intronic single nucleotide polymorphism (SNP) rs1006737 in CACNA1C gene (encoded calcium channel, voltage-dependent, L type, alpha 1C subunit) as a risk factor for schizophrenia in European populations. The replications in other ethnic populations such as East Asians have also been conducted, but the results were inconsistent, either likely due to the limited sample size of single study or genetic heterogeneity between continental populations on this locus., Methods: We performed a comprehensive meta-analysis of all available samples from existing studies of East Asian populations, including a total of 9,432 cases and 10,661 controls, to further confirm whether CACNA1C rs1006737 is an authentic risk SNP for schizophrenia in East Asian populations., Results: Our results revealed a significant association between rs1006737 and schizophrenia (allelic model, P = 4.39 × 10(-6) , pooled odds ratio [OR] = 1.20), and the results were much strengthened when the European and East Asian samples were combined together (P = 2.40 × 10(-17) , pooled OR = 1.12). There is no significant heterogeneity or publication bias between individual studies, and removal of any single study still remained significant associations between rs1006737 and schizophrenia., Discussion: Our results further confirmed that rs1006737 should be categorized as an authentic risk SNP for schizophrenia in the general populations., (© 2015 Wiley Publishing Asia Pty Ltd.)

Recently, DNA aptamer-gold nanoparticle (AuNP) conjugates have emerged as novel biosensing tools. Although RNA aptamers are more advantageous than DNA aptamers, their vulnerable nature during the construction of these conjugates restricts the development of RNA aptasensors. In this study, we developed an RNA aptamer-based AuNP sensor for the detection of theophylline in serum, combining the high binding affinity and selectivity of a theophylline RNA aptamer and the fluorescence quenching ability of AuNPs. In order to prevent nuclease degradation during the experimental process, the single strand of the theophylline RNA aptamer (33-mer) was split at the end loop region into two shorter halves, which were able to reassemble to form the theophylline-binding pocket. One fragment was linked to a DNA sequence that included a 15 thymine (T15) spacer and a polyadenine (polyA, A12) tail. The chimeric RNA/DNA oligonucleotide was attached to AuNPs within a few minutes via adsorption of the polyA tail. The other fragment was labeled with a fluorophore (Cy3). The two individual fragments self-assembled in the presence of theophylline. Upon ligand binding, the fragments came into close proximity, resulting in fluorescence quenching. This sensor exhibited a low detection limit of 0.05 µM, with a linear dynamic range from 0.1 to 10 µM in serum. Moreover, the sensor did not recognize theophylline-related compounds (e.g., caffeine and theobromine), demonstrating its high selectivity. This strategy offers new possibilities for the application of RNA aptasensors in clinical settings., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Objective: Hereditary hearing loss is a clinically and genetically heterogeneous disorder associated with mutations of a large number of diverse genes. In this study we applied targeted capture and massively parallel sequencing to identify the disease-causing gene of a Chinese family segregating recessive inherited deafness., Methods: After excluding mutations in common deafness genes GJB2, SLC26A4, mitochondrial m.1555A>G, genomic DNA of the proband of family GDSW24 was subjected to targeted next-generation sequencing. Subsequently, a candidate homozygous mutation was confirmed by Sanger sequencing., Results: A novel PCDH15 c.2367&#95;2369delTGT/p.V788-homozygous mutation was detected. In this family, no obvious vestibular disorder was found. The in-frame mutation c.2367&#95;2369delTGT is located in the evolutionarily conserved EC7 domain of Protocadherin-15 and was predicted to be pathogenic., Conclusion: The novel homozygous mutation in a family segregating non-syndromic hearing loss family supports previous reported observations that PCDH15 does not only causes Usher syndrome type 1F, but also DFNB23., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Objective: This study addresses the characters of magnetic resonance imaging (MRI) and clinical features, and curative effects in the screening of SSNHL due to inner-ear hemorrhage., Methods: MRI and relevant audiometric test were given to 160 patients with SSNHL, who were hospitalized in the First Affiliated Hospital of Sun Yat-sen University from January 2011 to April 2013. The clinical features and curative effects of patients with high signals in the labyrinth on MRI were analyzed., Results: MRI abnormities were found in 22 (13.8%) of the patients. Specifically, eight cases were considered for inner-ear hemorrhage. For the eight inner-ear hemorrhage cases, clinical features included the sudden onset of complete hearing loss, which worsened within several hours. Pure tone audiometry indicated profound sensorineural deafness. The prevalence of inner-ear hemorrhage was 5% in SSNHL cases and 18.6% in cases of profound sensorineural. MRI showed high signal intensity in the cochlear, semicircular canals or vestibule on unenhanced T1-weighted and fluid-attenuated inversion recovery images. The high signal intensity in the inner ear gradually degraded in six months. There was no improvement in hearing for the patients with inner-ear hemorrhage following symptomatic therapy., Conclusion: SSNHL due to inner-ear hemorrhage is characterized by profound sensorineural deafness in all frequencies, and high signal intensity for the hemorrhagic inner ear on T1-weighted MRI, with poor prognosis.

Objective: Waardenburg syndrome is clinically and genetically heterogeneous. The SOX10 mutation related with Waardenburg syndrome type II is rare in Chinese. This study aimed to uncover the genetic causes of Waardenburg syndrome type II in a three-generation family to improve genetic counseling., Methods: Complete clinical and molecular evaluations were conducted in a three-generation Han Chinese family with Waardenburg syndrome type II. Targeted genetic counseling was provided to this family., Results: We identified a rare heterozygous dominant mutation c.621C>A (p.Y207X) in SOX10 gene in this family. The premature termination codon occurs in exon 4, 27 residues downstream of the carboxyl end of the high mobility group box. Bioinformatics prediction suggested this variant to be disease-causing, probably due to nonsense-mediated mRNA decay. Useful genetic counseling was given to the family for prenatal guidance., Conclusion: Identification of a rare dominant heterozygous SOX10 mutation c.621C>A in this family provided an efficient way to understand the causes of Waardenburg syndrome type II and improved genetic counseling., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Intact spiral ganglion neurons are required for cochlear implantation or conventional hearing amplification as an intervention for sensorineural hearing loss. Treatment strategies to replace the loss of spiral ganglion neurons are needed. Recent reports have suggested that amniotic fluid-derived stem cells are capable of differentiating into neuron-like cells in response to cytokines and are not tumorigenic. Amniotic fluid stem cells represent a potential resource for cellular therapy of neural deafness due to spiral ganglion pathology. However, the directional differentiation of amniotic fluid stem cells is undetermined in the absence of cytokines and the consequence of inner ear supporting cells from the mouse cochlea organ of Corti on the differentiation of amniotic fluid stem cells remains to be defined. In an effort to circumvent these limitations, we investigated the effect of inner ear stem cells derived feeder layer on amniotic fluid stem cells differentiation in vitro. An inner ear stem cells derived feeder layer direct contact system was established to induce differentiation of amniotic fluid stem cells. Our results showed that inner ear stem cells derived feeder layer successfully promoted directional differentiation of amniotic fluid stem cells into neurons with characteristics of functionality. Furthermore, we showed that Wnt signaling may play an essential role in triggering neurogenesis. These findings indicate the potential use of inner ear stem cells derived feeder layer as a nerve-regenerative scaffold. A reliable and effective amniotic fluid stem cell differentiation support structure provided by inner ear stem cells derived feeder layer should contribute to efforts to translate cell-based strategies to the clinic., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Objective: Waardenburg syndrome is a rare genetic disorder, inherited as an autosomal dominant trait. The condition is characterized by sensorineural hearing loss and pigment disturbances of the hair, skin, and iris. The de novo mutation in the SOX10 gene, responsible for Waardenburg syndrome type II, is rarely seen. The present study aimed to identify the genetic causes of Waardenburg syndrome type II in a Chinese family., Methods: Clinical and molecular evaluations were conducted in a Chinese family with Waardenburg syndrome type II., Results: A novel SOX10 heterozygous c.259-260delCT mutation was identified. Heterozygosity was not observed in the parents and sister of the proband, indicating that the mutation has arisen de novo. The novel frameshift mutation, located in exon 3 of the SOX10 gene, disrupted normal amino acid coding from Leu87, leading to premature termination at nucleotide 396 (TGA). The high mobility group domain of SOX10 was inferred to be partially impaired., Conclusion: The novel heterozygous c.259-260delCT mutation in the SOX10 gene was considered to be the cause of Waardenburg syndrome in the proband. The clinical and genetic characterization of this family would help elucidate the genetic heterogeneity of SOX10 in Waardenburg syndrome type II. Moreover, the de novo pattern expanded the mutation data of SOX10., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Purpose: The aim of this study is to assess the value of magnetic resonance imaging in identifying the etiology of sudden sensorineural hearing loss, and to correlate the high signals in the labyrinth with clinical features to identify if inner ear hemorrhage could be implicated., Materials and Methods: In this retrospective study, inner ear magnetic resonance imaging was given to 112 patients with sudden sensorineural hearing loss in the First Affiliated Hospital of Sun Yat-sen University from 2011 to 2012. The clinical features of patients with high signals in the labyrinth on magnetic resonance imaging were analyzed., Results: Abnormal magnetic resonance images were identified in 13 (11.6%) patients. Retrocochlear pathology was found in six patients, including two cases of lacunar infarction, one case of multiple ischemias in the brainstem and bilateral centrum semiovale, two cases of acoustic neuroma, and one case of inner ear hemangioma. There were seven cases showing high signals in the labyrinth on unenhanced T1-weighted and fluid-attenuated inversion recovery images. Clinical features of these seven patients were characterized by irreversible profound hearing impairment and vestibular dysfunction. These findings were consistent with the hypothesis that their symptoms were caused by an inner ear hemorrhage., Conclusion: The results indicate the importance of magnetic resonance imaging in sudden sensorineural hearing loss in patients. Moreover, patients with vestibular dysfunction and sudden profound hearing loss may have an inner ear hemorrhage evident by interpreting clinical and magnetic resonance imaging results., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: Racial and regional factors are important for the clinical diagnosis of non-syndromic hearing impairment. Comprehensive genetic analysis of deaf patients in different regions of China must be performed to provide effective genetic counseling. To evaluate the mutational spectrum of south Chinese families, we performed genetic analysis for non-syndromic hearing impairment in this population., Methods: Complete clinical evaluations were performed on 701 unrelated patients with non-syndromic hearing impairment from six provinces in south China. Each subject was screened for common mutations, including SLC26A4 c.IVS7-2A > G, c.2168A > G; mitochondrial DNA m.1555A > G, m.1494C > T, m.7444G > A, m.7445A > G; GJB3 c.538C > T, c.547G > A; and WFS1 c.1901A > C, using pyrosequencing. GJB2 and SLC26A4 coding region mutation detection were performed using Sanger sequencing., Results: Genetic analysis revealed that among the etiology of non-syndromic hearing impairment, GJB2, SLC26A4, and mitochondrial m.1555A > G mutations accounted for 18.0%, 13.1%, and 0.9%, respectively. Common mutations included GJB2 c.235delC, c.109G > A, SLC26A4 c.IVS7-2A > G, c.1229 T > C, and mitochondrial m.1555A > G. The total mutation rate was 45.1% in all patients examined in south China. Overall, the clear contribution of GJB2, SLC26A4, and mitochondrial m.1555A > G to the etiology of the non-syndromic deafness population in south China was 32.0%., Conclusions: Our study is the first genetic analysis of non-syndromic hearing impairment in south China, and revealed that a clear genetic etiology accounted for 32.0% of non-syndromic hearing cases in patients from these regions. The mutational spectrum of non-syndromic hearing impairment in the south Chinese population provides useful and targeted information to aid in genetic counseling.

A gold nanoparticle (AuNP)-based colorimetric method was developed for the molecular weight (MW) determination of polyethylene glycol (PEG), a commonly used hydrophilic polymer. Addition of a salt solution to PEG-coated AuNP solutions helps in screening the electrostatic repulsion between nanoparticles and generating a color change of the solutions from wine red to blue in 10 min in accordance with the MW of PEG, which illustrates the different stability degrees (SDs) of the AuNPs. The SDs are calculated by the absorbance ratios of the stable to the aggregated AuNPs in the solution. The root mean square end-to-end length (〈h2〉1/2) of PEG molecules shows a linear fit to the SDs of the PEG-coated AuNPs in a range of 1.938 ± 0.156 to 10.151 ± 0.176 nm. According to the Derjaguin-Landau-Verwey-Overbeek theory, the reason for this linear relationship is that the thickness of the PEG adlayer is roughly equivalent to the 〈h2〉1/2 of the PEG molecules in solution, which determines the SDs of the AuNPs. Subsequently, the MW of the PEG can be obtained from its 〈h2〉1/2 using a mathematical relationship between 〈h2〉1/2 and MW of PEG molecule. Applying this approach, we determined the 〈h2〉1/2 and the MW of four PEG samples according to their absorbance values from the ordinary ultraviolet-visible spectrophotometric measurements. Therefore, the MW of PEG can be distinguished straightforwardly by visual inspection and determined by spectrophotometry. This novel approach is simple, rapid, and sensitive.

Objective: To explore the clinical effect and possible mechanism of macrolides on otitis media with effusion in children., Methods: Children with otitis media with effusion were recruited and prescribed for macrolides according to a designed scheme, and followed up for 8-12 weeks. Middle ear effusion samples were collected from the participants to assess the presence of biofilm., Results: Macrolides were found to have significant effect on the therapy of early stage otitis media with effusion for 88.7-92.5% of participants compared with 50.9-60.3% in control group after 8-12 weeks. Almost 72.1% of chronic otitis media with effusion patients recovered after an 8 weeks' course low dose macrolides prescription. Biofilm occurred in 30.8% (4/13) of middle ear effusion., Conclusions: The results indicate that macrolides are effective for otitis media with effusion in children. Bacterial biofilm may play an important role in the pathogenesis of otitis media with effusion., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Objective: Pendred syndrome is one of the most common hereditary determined diseases in patients with syndromic sensorineural hearing impairment. Mutations in the SLC26A4 gene are a major cause of Pendred syndrome. However, Pendred syndrome is quite rare in China. This investigation aims to identify genetic cause of a Chinese family with Pendred syndrome., Methods: Clinical and molecular evaluations were conducted in a Chinese family with Pendred syndrome., Results: A novel SLC26A4 c.662&#95;663insG mutation was detected in compound heterozygosity with IVS7-2A>G. No FOXI1, KCNJ10 or GJB2 pathogenic mutation was found. The novel mutation c.662&#95;663insG (p.G221) locates in SLC26A4 gene exon 6, and cause frameshift mutation on pendrin protein transmembrane domain five., Conclusion: The compound heterozygosity of the novel c.662&#95;663insG and IVS7-2A>G mutations in the SLC26A4 gene was considered to be the cause of Pendred syndrome in the proband. This study also supplemented the mutation spectrum of Pendred syndrome., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Objective: Systemic sclerosis (SSc) is an autoimmune disease with a predilection for women. The interaction between CD40 and CD154 (CD40L) is known to be involved in the development of SSc. Although CD40L is overexpressed in patients with SSc, the mechanisms leading to this overexpression are not well understood. We previously demonstrated that DNA demethylation reactivates the silent X chromosome, resulting in CD40L overexpression in healthy women. We hypothesized that CD40L up-regulation by DNA demethylation and subsequent reactivation of the silent X chromosome in female patients with SSc explain the susceptibility of women to SSc. The aim of this study was to investigate the effect of DNA demethylation on CD40L expression in CD4+ T cells from female patients with SSc., Methods: CD40L expression in CD4+ T cells from patients with SSc and healthy control subjects was measured by flow cytometry and real-time reverse transcription-polymerase chain reaction. Bisulfite sequencing was performed to determine the methylation status of the CD40L regulatory region., Results: CD40L expression was significantly elevated in female patients with SSc. The methylation levels of the DNA regulatory sequences were reduced in female patients with SSc compared with healthy women, and there was a significant inverse correlation between the average methylation level and CD40L mRNA expression in female patients with SSc. In contrast, no significant difference was observed in the expression of CD40L between male patients with SSc and male control subjects. The DNA regulatory regions in both male patients and male control subjects were largely unmethylated., Conclusion: Demethylation of CD40L regulatory elements on the inactive X chromosome contributes to CD40L overexpression in CD4+ T cells from female patients with SSc., (Copyright © 2012 by the American College of Rheumatology.)

Objective: Bilateral nonsyndromic sensorineural hearing loss associated with inner ear malformation is closely related to genetics. SLC26A4 is considered to be the major involved gene. Recently, FOXI1 and KCNJ10 mutations have been linked to enlarged vestibular aqueducts and GJB2 mutations linked to temporal bone malformation. The authors aimed to investigate the mutation spectrums of these genes in Chinese patients with bilateral hearing impairment associated with inner ear malformation., Study Design: Cross-sectional study., Setting: Affiliated hospital of the university., Subjects and Methods: The authors analyzed the GJB2, SLC26A4, FOXI1, and KCNJ10 gene sequences in 43 patients presenting with bilateral hearing impairment associated with inner ear malformation using pyrosequencing and direct DNA sequencing., Results: In total, 74.4% (32/43) of patients carried at least 1 of 14 pathogenic SLC26A4 mutations, including 6 novel mutations and 4 polymorphisms. Patients with enlarged vestibular aqueducts had a higher rate of SLC26A4 mutation than Mondini dysplasia patients. No FOXI1 or KCNJ10 potential pathogenic mutation was present, and GJB2 biallelic pathogenic mutations were uncommon (2.3%; 1/43). No significant correlation was observed between the genotype and phenotype of SLC26A4 mutations., Conclusion: SLC26A4 accounts for 74.4% of inner ear malformations in our cohort, whereas FOXI1, KCNJ10, and GJB2 mutations are not common. Other possible genes or external factors may contribute to this multibranch abnormality.

Background: Nasal polyps (NPs) are characterized by eosinophilic inflammation, which is generally considered sensitive to corticosteroid treatment., Objectives: We evaluated levels of neutrophilia in NPs and investigated whether increased neutrophilia in polyp tissue affected the response to corticosteroid treatment., Methods: We studied 3 independent cross-sectional groups of patients with NPs. Levels of infiltration by different types of inflammatory cells were determined by using immunohistochemical analyses and compared with those seen in control nasal tissues from subjects without NPs. Levels of inflammatory mediators were measured by using real-time PCR, ELISA, and FlowCytomix analyses. Patients with NPs received oral corticosteroid therapy (30 mg of prednisone once daily for 7 days); clinical parameters of efficacy were associated with NP phenotypes., Results: Among patients with NPs, 76.5% had an eosinophilic phenotype, 46.0% had a neutrophilic phenotype, and 35.8% had a mixed phenotype (indicated by double staining). Overall, patients' symptoms improved after corticosteroid treatment; numbers of eosinophils and levels of their mediators (IL-4 and IL-5), but not numbers of neutrophils or levels of their mediators (IL-8 and interferon-inducible protein 10), were reduced (P< .05). After corticosteroid treatment, patients with the nonneutrophilic phenotype (neutrophil negative) had significantly greater reductions in bilateral polyp size scores, nasal congestion scores, total nasal symptom scores, and nasal resistance than patients with the neutrophilic phenotype (neutrophil positive, P< .05)., Conclusions: There are different phenotypes of NPs based on the type of immune cell infiltrate and cytokines produced (eosinophilic or neutrophilic). Patients with the neutrophilic phenotype have less response to treatment with corticosteroids based on symptom scores., (Copyright © 2012 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.)

Background: Recently, in vitro and in vivo models have identified that microRNAs (miRNAs), which are extensively expressed in the inner ear, play important roles in inner ear development and function. However, the function of miRNA in vertebrate tissue is not well understood., Results: The current study used an in vitro model of embryonic mouse inner ear in a stem/progenitor cell culture to demonstrate that: 1) miR-182 is expressed during differentiation of inner ear stem/progenitor cell into a hair cell-like fate, 2) ectopic miR-182 promotes inner ear stem/progenitor cell differentiation into a hair cell-like fate, and 3) the function of miR-182 may be associated with its putative target Tbx1, a transcription factors that have been implicated in inner ear development and hair cell fate., Conclusions: Our findings suggest that miR-182 could regulate inner ear progenitor cell differentiation and that miRNAs are important regulators of hair cell differentiation, providing new targets for hair cell repair., (Copyright © 2012 Elsevier B.V. All rights reserved.)

The pathogenesis of systemic sclerosis (SSc) is still unclear. CD70, a B cell costimulatory molecule that interacts with CD27 during B-T cell contact, is overexpressed due to demethylation of its promoter regulatory elements in CD4+ T cells from patients with the following autoimmune diseases, namely systemic lupus erythematosus (SLE), subacute cutaneous lupus erythematosus (SCLE) and primary Sjögren's syndrome (pSS). However, as an autoimmune disease, it is unknown whether aberrant expression and methylation of CD70 occur in SSc CD4+ T cells. We aimed to investigate whether the aberrant expression and methylation status of CD70 occur in CD4+ T cells from patients with SSc. We found that the CD70 is overexpressed and the CD70 promoter region is demethylated in SSc CD4+ T cells. These findings suggest that demethylation of CD70 promoter region contributes to the overexpression of CD70 in CD4+ T cells and may contribute to autoimmune response in SSc., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Objective: To evaluate the effects of NasoPore after packing of the middle ear in guinea pigs., Study Design: A randomized, prospective, controlled animal study., Setting: University laboratory., Subjects and Methods: Forty-one guinea pigs were divided into 3 groups. In group 1(n=12), the middle ears of animals were unilaterally implanted with NasoPore, leaving the contralateral middle ears packed with absorbable gelatin sponge soaked in a solution containing kanamycin and furosemide as an ototoxicity-positive control; group 2 (n = 17) underwent the same experimental protocol as group 1, except the gelatin sponge was unsoaked; in group 3 (n = 12), NasoPore was inserted unilaterally and no packing material was placed into the contralateral ear. Auditory brainstem responses (ABRs) were performed preoperatively and 3 months after the procedure. The surface preparation and scanning electron microscopy (SEM) were assessed 3 months postoperatively, whereas pathology of middle ear was analyzed in 5 samples of group 2., Results: ABR thresholds of the contralateral ear significantly increased in group 1 and were slightly shifted in group 2 compared with the NasoPore-packed and nonpacked ears 3 months postoperatively. The NasoPore-packed middle ears were found to have less fibrosis and inflammation and less thickened bone and tympanic membranes than Gelfoam-packed ears. Surface preparations and SEM showed no ototoxicity in the inner ear of NasoPore-packed ears., Conclusion: NasoPore appears to be effective for use in otosurgery. It caused less fibrosis in the middle ear than conventional packing agents and no ototoxicity to the inner ear.

To explore the possible abnormal resting-state activity in patients with obsessive-compulsive disorder (OCD), the regional homogeneity (ReHo) of 22 pairs of patients and well-matched healthy controls was calculated. Compared with controls, the patients showed higher ReHo in the left anterior cingulate cortex, but lower ReHo in the left inferior temporal gyrus. These findings supported the abnormal resting-state brain activity in drug-naïve OCD patients. No significant correlations between ReHo value and four clinical characteristics were found, suggesting that abnormal ReHo might be trait-related in OCD.

Although microRNA (miRNA) is expressed extensively in the postnatal mouse inner ear, its expression in the sensory epithelium during embryogenesis has not been well characterized. We investigated miRNA expression at E13.5 and E16.5 by microarray analysis, quantitative real-time-PCR, and in-situ hybridization. MiRNA-182, miRNA-140, miRNA-200c, and others showed distinct temporal and spatial expression patterns. MiRNA-194, whose expression in zebrafish seems to play an important role in the differentiation of the intestinal epithelium, was also expressed in the spiral ganglia of the mouse inner ear, where it may play a similar role in neuronal differentiation. Our results indicate that miRNAs are widely expressed in the developing inner ear, with more species recruited as hair cells differentiate, suggesting an important developmental role.

We experimentally and theoretically study the alignment structures of the rotational wavepacket created by linear molecules and two strong femtosecond laser pulses. In the experiment, we observe that the alignment structures depend on the time delay between the two laser pulses. In the theory, we find that the alignment structures are composed of the self-coupling term and the cross-coupling term. The contributions of these two terms are separately calculated. Their coherent superposition reproduces the alignment structures observed in the experiment.

We study the rotational wave packet created by nonadiabatic rotational excitation of molecules with strong femtosecond laser pulses. The applicable condition of the Delta-Kick method is obtained by comparing the laser intensity and pulse duration dependences of the wave packet calculated with different methods. The wave packet evolution is traced analytically with the Delta-Kick method. The calculations demonstrate that the rotational populations can be controlled for the rotational wave packet created by two femtosecond laser pulses. The evolution of the rotational wave packet with controlled populations produces interference patterns with exotic spatial symmetries. These calculations are validated by comparing the theoretical calculations with our experimental measurements for the rotational wave packet created by thermal ensemble CO(2) and two strong femtosecond laser pulses. Potential applications in molecular science are also discussed for the rotational wave packet with controlled populations and spatial symmetries.

Objective: This study was designed to determine whether nasal saline irrigation improved the symptoms and signs of allergic rhinitis (AR) and whether nasal saline irrigation could be used as a complementary management of AR in children while less steroids were used., Method: 26 children with AR were divided into three groups and were given nasal saline irrigation and/or topical steroid. Symptoms and signs of AR and mucociliary clearance (MCC) were evaluated, and concentration of soluble intercellular adhesion molecule (sICAM)-1 in nasal secretion was detected., Results: In AR children treated with nasal irrigation and tapered topical steroid at week 8 and week 12, a significant improvement in symptoms and signs was observed, and a significant decrease in the mean values of MCC and the mean concentrations of sICAM-1 in nasal secretions was also detected., Conclusion: Nasal saline irrigation can be viewed as a good adjunctive treatment option for AR. It permitted the use of less topical steroids for controlling AR in children, which will contribute to fewer side effects and less economic burden., (Copyright 2008 S. Karger AG, Basel.)

Objectives: To determine whether the chloride channel protein CLC-3 is upregulated in patients with allergic rhinitis (AR) and whether topical corticosteroid treatment decreases the expression of CLC-3., Design: Histologic study., Setting: Academic research., Patients: Eighteen patients with AR were included in the study., Main Outcome Measures: Expression of CLC-3 was detected by immunohistochemistry and by reverse transcription-polymerase chain reaction before and at 4 weeks after treatment with the topical corticosteroid mometasone furoate., Results: Strong CLC-3 expression was detected in epithelium and in submucosal glands. An increased presence of CLC-3 was demonstrated in nasal mucosa compared with that in normal nasal tissue. A statistically significant difference in CLC-3 gene expression level was found in nasal tissues before vs at 4 weeks after treatment with mometasone., Conclusions: CLC-3 may have a role in modulating the pathogenesis of AR. Decreased expression of CLC-3 may be the mechanism of action of corticosteroid treatment in controlling AR.

Objective: We aimed to explore the transitional process of sinus cavity mucosa after functional endoscopic sinus surgery (FESS) and divide it into different stages., Method: The morphological characteristics of sinus cavity mucosa after FESS were continuously observed., Results: Over 90% of the nasal and sinus cavities got clean within 1-2 weeks, over 80% of the operative cavities experienced a reaction to mucosa removal or regenerative diseases within 3-10 weeks, such as mucosal edema, vesicles, granulation tissue, mini-polyps, fibrous hyperplasia and adhesion, which competed against the mucosa epithelialization process. After careful treatment, 90% of the nasal and sinus cavities finished epithelialization, and 60% of them completed epithelialization within 11-14 weeks after operation., Conclusion: The recovery process of mucosa after FESS can be divided into 3 stages: the stage of clean operative cavity, the stage of mucosal transition and the stage of complete epithelialization. Proper management at the 3 stages is very essential to the whole curable effect of FESS.

The mammalian inner ear loses its sensory cells with advancing age, accompanied by a functional decrease in balance and hearing. This study investigates oxidant stress in the cochlea of aging male CBA/J mice. Glutathione-conjugated proteins, markers of H2O2-mediated oxidation, began to increase at 12 months of age; 4-hydroxynonenal and 3-nitrotyrosine, products of hydroxyl radical and peroxynitrite action, respectively, were elevated by 18 months. Immunoreactivity to these markers was stronger in the supporting cells (Deiters and pillar cells) than the sensory cells and appeared later (23 months) in spiral ganglion cells and in the stria vascularis and spiral ligament. Conversely, antioxidant proteins (AIF) and enzymes (SOD2) decreased by 18 months in the organ of Corti (including the sensory cells) and spiral ganglion cells but not in the stria vascularis. These results suggest the presence of different reactive oxygen species and differential time courses of oxidative changes in individual tissues of the aging cochlea. An imbalance of redox status may be a component of age-related hearing loss.

Objective: To study the microanatomy by endoscope-assisted via retrolabyrinthine approach., Method: Nineteen cadaveric heads fixed with formalin were dissected in our study. The data that endoscope could be extent and the distance between the important point were measured. By simulated the retrolabyrinthine approach, endoscope was placed to observe the nerves and vessels, the distance between nerves and the central point of the anterior edge of sigmoid sinus were measured., Result: The distance from the inferior margin of petrous ridge to the upper bound of endolymphatic sac was (9.93+/-1.52)mm; and from superior margin of petrous ridge to the inferior margin common bony crus was (4.64+/-0.91)mm;and from the intersection of posterior semicircular canal to the anterior wall of sigmoid was (7.85+/-1.47)mm on the left, and (5.69+/-1.68)mm on the right. The distance from inferior margin common bony crus to the anterior wall of sigmoid was (13.9+/-1.71)mm on the left, and (11.31+/-2.03)mm on the right. The trochlear nerve and abducent nerve could be observed under endoscope. The relationship between the trigeminal nerve, acoustic nerve and the vessels could be identified clearly. The distance from the central point of the anterior edge of sigmoid to the roots of the trigeminal nerve, facial nerve, vestibulocochlear nerve and glossopharyngeal nerve were (29.88+/-2.77) mm, (32.04+/-2.04) mm, (29.17+/-1.65) mm, (35.49+/-1.53) mm respectively., Conclusion: The visual field of the cerebellopontine angle appear wider by the endoscope assisted retrolabyrinthine approach. Nerves, vessel, internal acoustic pore, jugular foramen region can be clearly seen. Some minimal invasive surgery can be done by this approach.

Background: Chronic rhinosinusitis (CRS) may cover different disease entities, and the pathogenic mechanism remains unclear., Methods: The aim of this study was to evaluate the expression of chloride channel protein CLC-2 and CLC-3 in CRS without nasal polyps (CRSsNP) and evaluate the roles of interleukin (IL)-4 and transforming growth factor (TGF) beta in the up-regulation of CLC-2 and CLC-3. We detected expression of CLC-2 and CLC-3 in 17 patients with CRSsNP by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR), and we examined the concentration of TGF-beta, IL-4, IL-5, and interferon (IFN) gamma in ethmoid sinus mucosa by enzyme-linked immunosorbent assay (ELISA)., Results: We found that CLC-2 and CLC-3 is up-regulated in CRSnNP and located in submucosal glands and epithelium of the ethmoid sinus. CLC-2 and CLC-3 mRNA correlated with IL-4 in CRSsNP (r = 0.57 and 0.65; p < 0.05). CLC-2 and CLC-3 mRNA correlated negatively with mucosal TGF-beta in CRSsNP (r = -0.49 and -0.54; p < 0.05)., Conclusion: We concluded that CLC-2 and CLC-3 is up-regulated in ethmoid mucosa and may affect the development of CRSsNP. TGF-beta and IL-4 may modulate the expression of CLC-2 and CLC-3 in CRSsNP.

Background: Allergic rhinitis (AR) is a Th2 predominant disease, and its pathogenic mechanism is still poorly understood. CD4(+)CD25(+) T cells account for approximately 5% to 10% peripheral CD4(+) T cells and has been shown to regulate the activation of effector T cells in the periphery. The activity of CD4(+)CD25(+) T cells is associated with the transcription factor Foxp3. The present study aimed to evaluate the possible role of CD4(+)CD25(+) T cells as well as Foxp3 in the pathogenesis of AR., Methods: Nasal tissues and peripheral blood mononuclear cells (PBMCs) were obtained from 17 patients with AR and 11 control subjects. Foxp3 was detected in nasal tissues by immunohistochemistry and real-time reverse transcription-polymerase chain reaction (RT-PCR). CD4(+)CD25(+) T cells and Foxp3 were evaluated in PBMCs by using flow cytometry. Concentrations of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) were measured by enzyme-linked immunosorbent assay (ELISA) in cultured PBMCs in the presence or absence of stimulation with phorbol ester (PMA) and Ionomycin., Results: The numbers of Foxp3(+) cells was 129.5 +/- 35.6 and 44.2 +/- 20.5 cells/mm(2) in nasal mucosa of two groups (P < .05). There were less Foxp3(+) lymphocytes and decreased Foxp3 mRNA in AR compared with the control (P < .05). The frequencies of the CD4(+)CD25(+) population in PBMCs of two groups were 1.99 +/- 0.95% and 3.55 +/- 1.27% (P < .05). There was significant difference in the frequencies of the Foxp3(+)CD4(+) CD25(+) population (1.81 +/- 0.77 vs 3.37 +/- 1.04, P < .05) and mean fluorescence intensity (MFI) of Foxp3 (5.93 +/- 2.64 vs 11.72 +/- 4.29, P < .05) in PBMCs of two groups. After stimulation, the concentrations of IL-2 and IFN-gamma were 182.72 +/- 85.11 pg/mL and 348.94 +/- 151.88 pg/mL in PBMCs with AR, while those were 90.6 +/- 61.5 pg/mL and 155.64 +/- 68.33 pg/mL in controls (P < .05)., Conclusion: Our results indicate that CD4(+) CD25(+) regulatory T cells as well as Foxp3 may play a crucial role in immunological imbalance of AR. These findings suggest that increasing Foxp3 and CD4(+)CD25(+) T cells have the potential to be new therapeutic targets for the treatment of AR.

Aminoglycoside antibiotics strongly bind to phosphoinositides and affect their membrane distribution and metabolism. Kanamycin treatment also disrupts Rac/Rho signaling pathways to the actin cytoskeleton in the mouse inner ear in vivo. Here, we investigate the influence of kanamycin on phosphoinositide signaling in sensory cells (hair cells) of the mouse cochlea. Immunoreactivity to phosphatidylinositol-3,4,5-trisphosphate (PIP3) decreased in the organ of Corti, especially in outer hair cells, after 3-7 days of drug treatment, whereas imunoreactivity to phosphatidylinositol-4,5-bisphosphate (PIP2) increased. Immunoreactivity to PIP2 was present at the apical poles of outer hair cells, but appeared in their nuclei only after drug treatment. Furthermore, nuclear PIP2 formed a complex with histone H3 and attenuated its acetylation in outer hair cells. In agreement with reduced PIP3 signaling, phosphorylated Akt decreased in both the cytoplasm and nuclei of outer hair cells after kanamycin treatment. This study suggests that kanamycin disturbs the balance between PIP2 and PIP3, modifies gene transcription via histone acetylation and diminishes the PI3K/Akt survival pathway. These actions may contribute to the death of outer hair cells, which is a consequence of chronic kanamycin treatment.

Stress stimuli can lead to remodeling of the actin cytoskeleton and subsequent alteration of cell adhesion and permeation as well as cell functions and cell fate. We investigated redox-dependent Rho GTPase-linked pathways controlling the actin cytoskeleton in the inner ear of the CBA mouse, by using aminoglycoside antibiotics as a noxious stimulus that causes loss of sensory cells via the formation of reactive oxygen species. Kanamycin treatment in vivo interfered with the formation of F-actin, disturbed the arrangement of beta-actin in the stereocilia of outer hair cells, and altered the intermittent adherens junction/tight junction complexes between outer hair cells and supporting cells. The drug treatment also activated Rac1 and promoted the formation of the complex of Rac1 and p67phox while decreasing the activity of RhoA and reducing the formation of the RhoA/p140mDia complex. In inner-ear-derived cell lines, expression of mutated Rac1 changed the structural arrangement of F-actin and diminished the immunoreactivity of p140mDia. These findings suggest that actin depolymerization induced by kanamycin is mediated by Rac1 activation, followed by the formation of superoxide by NADPH oxidase. These changes will ultimately contribute to aminoglycoside-induced loss of hair cells., ((c) 2006 Wiley-Liss, Inc.)

Materials are said to show a shape-memory effect if they can be deformed and fixed into a temporary shape, and recover their original, permanent shape only on exposure to an external stimulus. Shape-memory polymers have received increasing attention because of their scientific and technological significance. In principle, a thermally induced shape-memory effect can be activated by an increase in temperature (also obtained by heating on exposure to an electrical current or light illumination). Several papers have described light-induced changes in the shape of polymers and gels, such as contraction, bending or volume changes. Here we report that polymers containing cinnamic groups can be deformed and fixed into pre-determined shapes--such as (but not exclusively) elongated films and tubes, arches or spirals--by ultraviolet light illumination. These new shapes are stable for long time periods, even when heated to 50 degrees C, and they can recover their original shape at ambient temperatures when exposed to ultraviolet light of a different wavelength. The ability of polymers to form different pre-determined temporary shapes and subsequently recover their original shape at ambient temperatures by remote light activation could lead to a variety of potential medical and other applications.

Cell death in outer hair cells of the mammalian inner ear induced by aminoglycoside antibiotics is mediated by reactive oxygen species (ROS) and can be prevented by antioxidants. The current study investigates the role of the nuclear factor (NF)-kappaB pathway in cell death or survival in adult CBA mice. Kanamycin (700 mg/kg subcutaneously, twice per day) progressively destroys hair cells but after 7 days of treatment auditory function and morphology are not yet affected significantly, permitting investigations of early events in drug-induced cell death. Immunostaining for 4-hydroxynonenal, indicative of lipid peroxidation, was elevated in the cochlea, but there was no effect on nitrotyrosine, a marker for peroxynitrite. NF-kappaB was increased at 3 hr, 3 days, and 7 days of treatment, with p50 and p65 proteins as its most abundant subunits. Immunoreactivity for p50 was present in nuclei of inner hair cells and supporting cells that survive the drug treatment. In contrast, nuclei of outer hair cells were devoid of label. Concomitant injections of antioxidants, however, such as 2,3-dihydroxybenzoic acid or salicylate (which prevent cell death induced by kanamycin), promoted the translocation of NF-kappaB into the nuclei of outer hair cells. In addition, kanamycin treatment decreased tyrosine phosphorylation of the inhibitory IkappaBalpha protein, leading to increased IkappaBalpha levels in the cochlea; the effect was reversed by cotreatment with antioxidants. These results suggest that changes in the redox state of the cochlea stimulate the activation of NF-kappaB and that this activation is cell protective., (Copyright (c) 2005 Wiley-Liss, Inc.)

Objective: To study the expression of transforming growth factor alpha, beta 1 in hyperplastic tissue after endoscopic polypectomy and the effect of corticosteroid., Method: Forty patients with nasal polyps were divided into two groups randomly: corticosteroid group (n = 20) with topical application of Budesonide (BUD, 400 micrograms/d) after endoscopic polypectomy and control group (n = 20) without corticosteroid after surgery. The hyperplastic tissues in operative cavity obtained in the 1st and 8th weeks after operation were studied with HE staining and immunohistochemistry technique respectively., Result: Morphological changes of hyperplastic tissue after endoscopic polypectomy included pseudostratified epithelium, highly edematous lamina proper and inflammatory cells infiltration, in which the main infiltrative cells were eosinophils (67.5%). Transforming growth factor alpha(TGF alpha) protein was highly expressed in epithelial cells, grand cells and inflammatory cells in the hyperplastic tissue. Transforming growth factor beta 1 (TGF beta 1) protein was highly expressed in inflammatory cells in the hyperplastic tissue. The expression of TGF alpha and beta 1 was significantly decreased after topical BUD spray (P < 0.01, 0.05)., Conclusion: Transforming growth factor alpha and beta 1 may play an important role in the formation and recurrence of nasal polyps.

Objective: To discuss the estimation and treatment of adult acute epiglottitis dyspnea., Method: 126 adult with acute epiglottitis patients were analyzed., Result: None of 30 patients undergone epiglotiotomy had asphyxia, inflammation diffuse or serious hemorrhage. 8 patients undergone tracheotomy, one patient undergone thyroericotomy but died. One of 87 patients with conservative treatment died., Conclusion: Gaspping, salivating and dyslogia are symbols of severe larynx obstruction. Fibrous laryngoscope is the best way of examine. Keeping respiratory path open and eliminating epiglottis swelling is the key of treatment.