Factors That Introduce Intrasubject Variability Into Ear-Canal Absorbance Measurements

Wideband immittance measures can be useful in analyzing acoustic sound flow through the ear and also have diagnostic potential for the identification of conductive hearing loss as well as causes of conductive hearing loss. To interpret individual measurements, the variability in test- retest data must be described and quantified. Contributors to variability in ear-canal absorbance-based measurements are described in this article. These include assumptions related to methodologies and issues related to the probe fit within the ear and potential acoustic leaks. Evidence suggests that variations in ear-canal cross-sectional area or measurement location are small relative to variability within a population. Data are shown to suggest that the determination of the Thévenin equivalent of the ER-10C probe introduces minimal variability and is independent of the foam ear tip itself. It is suggested that acoustic leaks in the coupling of the ear tip to the ear canal lead to substantial variations and that this issue needs further work in terms of potential criteria to identify an acoustic leak. In addition, test-retest data from the literature are reviewed

Non-Ossicular Signal Transmission in Human Middle Ears: Experimental Assessment of the Acoustic Route with Perforated Tympanic Membranes

Direct acoustic stimulation of the cochlea by the sound-pressure difference between the oval and round windows (called the acoustic route ) has been thought to contribute to hearing in some pathological conditions, along with the normally dominant ossicular route. To determine the efficacy of this acoustic route and its constituent mechanisms in human ears, sound pressures were measured at three locations in cadaveric temporal bones [with intact and perforated tympanic membranes (TMs)]: (1) in the external ear canal lateral to the TM, PTM; (2) in the tympanic cavity lateral to the oval window, POW; and (3) near the round window, PRW. Sound transmission via the acoustic route is described by two concatenated processes: (1) coupling of sound pressure from ear canal to middle-ear cavity, H PCAV ≡ PCAV PTM, where PCAV represents the middle-ear cavity pressure, and (2) sound-pressure difference between the windows, HWPD ≡ (POW - PRW) PCAV. Results show that: H PCAV depends on perforation size but not perforation location; HWPD depends on neither perforation size nor location. The results (1) provide a description of the window pressures based on measurements, (2) refute the common otological view that TM perforation location affects the relative phase of the pressures at the oval and round windows, and (3) show with an intact ossicular chain that acoustic-route transmission is substantially below ossicular-route transmission except for low frequencies with large perforations. Thus, hearing loss from TM perforations results primarily from reduction in sound coupling via the ossicular route. Some features of the frequency dependence of H PCAV and HWPD can be interpreted in terms of a structure-based lumped-element acoustic model of the perforation and middle-ear cavities

Acoustic Mechanisms that Determine the Ear-Canal Sound Pressures Generated by Earphones

In clinical measurements of hearing sensitivity, a given earphone is assumed to produce essentially the same sound-pressure level in all ears. However, recent measurements [Voss et al., Ear and Hearing (in press)] show that with some middle-ear pathologies, ear-canal sound pressures can deviate by as much as 35 dB from the normal-ear value; the deviations depend on the earphone, the middle-ear pathology, and frequency. These pressure variations cause errors in the results of hearing tests. Models developed here identify acoustic mechanisms that cause pressure variations in certain pathological conditions. The models combine measurement-based Thevenin equivalents for insert and supra-aural earphones with lumped-element models for both the normal ear and ears with pathologies that alter the ear\u27s impedance (mastoid bowl, tympanostomy tube, tympanic-membrane perforation, and a \u27high- impedance\u27 ear). Comparison of the earphones\u27 Thevenin impedances to the ear\u27s input impedance with these middle-ear conditions shows that neither class of earphone acts as an ideal pressure source; with some middle-ear pathologies, the ear\u27s input impedance deviates substantially from normal and thereby causes abnormal ear-canal pressure levels. In general, for the three conditions that make the ear\u27s impedance magnitude lower than normal, the model predicts a reduced ear-canal pressure (as much as 35 dB), with a greater pressure reduction with an insert earphone than with a supra-aural earphone. In contrast, the model predicts that ear-canal pressure levels increase only a few dB when the ear has an increased impedance magnitude; the compliance of the air-space between the tympanic membrane and the earphone determines an upper limit on the effect of the middle-ear\u27s impedance increase. Acoustic leaks at the earphone-to-ear connection can also cause uncontrolled pressure variations during hearing tests. From measurements at the supra-aural earphone-to-ear connection, we conclude that it is unusual for the connection between the earphone cushion and the pinna to seal effectively for frequencies below 250 Hz. The models developed here explain the measured pressure variations with several pathologic ears. Understanding these mechanisms should inform the design of more accurate audiometric systems which might include a microphone that monitors the ear-canal pressure and corrects deviations from normal

Silica material variation for the Mn_xO_y-Na₂WO₄/SiO₂

The oxidative coupling of methane (OCM) is one of the best methods for the direct conversion of methane.Among the known OCM catalysts, MnxOy-Na2WO4/SiO2 is a promising candidate for an industrial appli-cation, showing a high methane conversion and C2 selectivity, with a good stability during long-termcatalytic activity tests. In the present study, some results have been already published and discussedbriefly in our previous short communication. However, we herein investigated comprehensively theinfluence of various silica support materials on the performance of the MnxOy-Na2WO4/SiO2 systemin the OCM by means of ex situ and in situ XRD, BET, SEM and TEM characterization methods andshowed new results to reveal possible support effects on the catalyst. The catalytic performance of most MnxOy-Na2WO4/SiO2 catalysts supported by different silica support materials did not differ substan-tially. However, the performance of the SBA-15 supported catalyst was outstanding and the methaneconversion was nearly twofold higher in comparison to the other silica supported catalysts at similar C2 selectivity as shown before in the communication. The reason of this substantial increase in performancecould be the ordered mesoporous structure of the SBA-15 support material, homogeneous dispersion ofactive components and high number of active sites responsible for the OCM

Strain-dependent host transcriptional responses to toxoplasma infection are largely conserved in mammalian and avian hosts

Toxoplasma gondii has a remarkable ability to infect an enormous variety of mammalian and avian species. Given this, it is surprising that three strains (Types I/II/III) account for the majority of isolates from Europe/North America. The selective pressures that have driven the emergence of these particular strains, however, remain enigmatic. We hypothesized that strain selection might be partially driven by adaptation of strains for mammalian versus avian hosts. To test this, we examine in vitro, strain-dependent host responses in fibroblasts of a representative avian host, the chicken (Gallus gallus). Using gene expression profiling of infected chicken embryonic fibroblasts and pathway analysis to assess host response, we show here that chicken cells respond with distinct transcriptional profiles upon infection with Type II versus III strains that are reminiscent of profiles observed in mammalian cells. To identify the parasite drivers of these differences, chicken fibroblasts were infected with individual F1 progeny of a Type II x III cross and host gene expression was assessed for each by microarray. QTL mapping of transcriptional differences suggested, and deletion strains confirmed, that, as in mammalian cells, the polymorphic rhoptry kinase ROP16 is the major driver of strain-specific responses. We originally hypothesized that comparing avian versus mammalian host response might reveal an inversion in parasite strain-dependent phenotypes; specifically, for polymorphic effectors like ROP16, we hypothesized that the allele with most activity in mammalian cells might be less active in avian cells. Instead, we found that activity of ROP16 alleles appears to be conserved across host species; moreover, additional parasite loci that were previously mapped for strain-specific effects on mammalian response showed similar strain-specific effects in chicken cells. These results indicate that if different hosts select for different parasite genotypes, the selection operates downstream of the signaling occurring during the beginning of the host's immune response. © 2011 Ong et al

Superorganisms of the protist kingdom : a new level of biological organization

The concept of superorganism has a mixed reputation in biology-for some it is a convenient way of discussing supra-organismal levels of organization, and for others, little more than a poetic metaphor. Here, I show that a considerable step forward in the understanding of superorganisms results from a thorough review of the supra-organismal levels of organization now known to exist among the “unicellular” protists. Limiting the discussion to protists has enormous advantages: their bodies are very well studied and relatively simple (as compared to humans or termites, two standard examples in most discussions about superorganisms), and they exhibit an enormous diversity of anatomies and lifestyles. This allows for unprecedented resolution in describing forms of supra-organismal organization. Here, four criteria are used to differentiate loose, incidental associations of hosts with their microbiota from “actual” superorganisms: (1) obligatory character, (2) specific spatial localization of microbiota, (3) presence of attachment structures and (4) signs of co-evolution in phylogenetic analyses. Three groups-that have never before been described in the philosophical literature-merit special attention: Symbiontida (also called Postgaardea), Oxymonadida and Parabasalia. Specifically, it is argued that in certain cases-for Bihospites bacati and Calkinsia aureus (symbiontids), Streblomastix strix (an oxymonad), Joenia annectens and Mixotricha paradoxa (parabasalids) and Kentrophoros (a ciliate)-it is fully appropriate to describe the whole protist-microbiota assocation as a single organism (“superorganism”) and its elements as “tissues” or, arguably, even “organs”. To account for this level of biological complexity, I propose the term “structured superorganism”

A bovine lymphosarcoma cell line infected with theileria annulata exhibits an irreversible reconfiguration of host cell gene expression

Theileria annulata, an intracellular parasite of bovine lymphoid cells, induces substantial phenotypic alterations to its host cell including continuous proliferation, cytoskeletal changes and resistance to apoptosis. While parasite induced modulation of host cell signal transduction pathways and NFκB activation are established, there remains considerable speculation on the complexities of the parasite directed control mechanisms that govern these radical changes to the host cell. Our objectives in this study were to provide a comprehensive analysis of the global changes to host cell gene expression with emphasis on those that result from direct intervention by the parasite. By using comparative microarray analysis of an uninfected bovine cell line and its Theileria infected counterpart, in conjunction with use of the specific parasitacidal agent, buparvaquone, we have identified a large number of host cell gene expression changes that result from parasite infection. Our results indicate that the viable parasite can irreversibly modify the transformed phenotype of a bovine cell line. Fifty percent of genes with altered expression failed to show a reversible response to parasite death, a possible contributing factor to initiation of host cell apoptosis. The genes that did show an early predicted response to loss of parasite viability highlighted a sub-group of genes that are likely to be under direct control by parasite infection. Network and pathway analysis demonstrated that this sub-group is significantly enriched for genes involved in regulation of chromatin modification and gene expression. The results provide evidence that the Theileria parasite has the regulatory capacity to generate widespread change to host cell gene expression in a complex and largely irreversible manner

Toxoplasma gondii Clonal Strains All Inhibit STAT1 Transcriptional Activity but Polymorphic Effectors Differentially Modulate IFN gamma Induced Gene Expression and STAT1 Phosphorylation

Host defense against the parasite Toxoplasma gondii requires the cytokine interferon-gamma (IFNγ). However, Toxoplasma inhibits the host cell transcriptional response to IFNγ, which is thought to allow the parasite to establish a chronic infection. It is not known whether all strains of Toxoplasma block IFNγ-responsive transcription equally and whether this inhibition occurs solely through the modulation of STAT1 activity or whether other transcription factors are involved. We find that strains from three North American/European clonal lineages of Toxoplasma, types I, II, and III, can differentially modulate specific aspects of IFNγ signaling through the polymorphic effector proteins ROP16 and GRA15. STAT1 tyrosine phosphorylation is activated in the absence of IFNγ by the Toxoplasma kinase ROP16, but this ROP16-activated STAT1 is not transcriptionally active. Many genes induced by STAT1 can also be controlled by other transcription factors and therefore using these genes as specific readouts to determine Toxoplasma inhibition of STAT1 activity might be inappropriate. Indeed, GRA15 and ROP16 modulate the expression of subsets of IFNγ responsive genes through activation of the NF-κB/IRF1 and STAT3/6 transcription factors, respectively. However, using a stable STAT1-specific reporter cell line we show that strains from the type I, II, and III clonal lineages equally inhibit STAT1 transcriptional activity. Furthermore, all three of the clonal lineages significantly inhibit global IFNγ induced gene expression

Signal Transmission in the Auditory System

Contains table of contents for Section 3, an introduction, and reports on seven research projects.National Institutes of Health Grant 5 R01 DC00194National Institutes of Health Grant P01 DC00119National Institutes of Health Grant F32 DC00073National Institutes of Health Grant 5 R01 DC00473National Institutes of Health Grant 2 R01 DC00238National Institutes of Health Grant 2 R01 DC00235National Institutes of Health Grant 5 P01 DC00361National Institutes of Health Grant T32 DC00006Whitaker Health Sciences Fun