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Speech recognition scores in noise can be affected by measurement conditions such as the spatial configuration, room acoustic properties, or the position and head orientation of a test person. This is critical when comparing repeated measurements, e.g., during hearing aid verification. While the basic effects of these factors are known, specific effect sizes for practically relevant configurations have not previously been reported. We investigated the effects of audiological test-room acoustics with low reverberation, and of head movements on speech-in-noise tests for typical spatial configurations. Speech-recognition thresholds (SRTs) and head movements were measured in 240 normal-hearing participants in six rooms for five loudspeaker configurations (S0N0, S0N±45, S0N±90, S0N180 and S±45N∓45). Additionally, head positions were reproduced with an artificial head, and using a binaural speech intelligibility model, binaural room impulse responses were measured to estimate the influence of head movements on the SRT. The results show that the effects of room acoustic properties and head movements varies greatly between spatial configurations. Head rotations around the vertical axis can affect speech recognition scores by up to 8 dB, most critically for the configuration S0N180. For spatially separated sound sources, different room acoustic conditions caused differences in SRT of up to 5 dB.

In order to gain a better understanding of wideband acoustic immitance (WAI) measurements, in this second part of a two-part paper, the parametric electro-acoustic model of the ear canal and the middle ear of young infants proposed in the first part is extended. The extension allows predictions of the influence of the pathological middle ear conditions middle ear effusion and negative static air pressure difference between the middle ear and the ear canal. Comparisons of the acoustic input impedance of the ear predicted by the model with real ear measurements in young infants’ ears with middle ear effusion show that the effects due to the pathology can be predicted well. For the negative static air pressure, a modeling approach was proposed but could not be confirmed yet, due to a lack of available measurement data. Furthermore, comparisons between different middle ear states (healthy, middle ear effusion and static air pressure difference) predicted by the model showed characteristic differences in all relevant WAI measures. However, it is also shown that WAI measures requiring an estimate of the cross-sectional area at the measurement position, i.e., absorbance and reflectance, are highly sensitive to this estimate.

Author(s): Stephan Culemann [sup.1] [sup.2] , Anika Grüneboom [sup.1] [sup.2] , José Ángel Nicolás-Ávila [sup.3] , Daniela Weidner [sup.1] [sup.2] , Katrin Franziska Lämmle [sup.1] [sup.2] , Tobias Rothe [sup.1] [...], Macrophages are considered to contribute to chronic inflammatory diseases such as rheumatoid arthritis.sup.1. However, both the exact origin and the role of macrophages in inflammatory joint disease remain unclear. Here we use fate-mapping approaches in conjunction with three-dimensional light-sheet fluorescence microscopy and single-cell RNA sequencing to perform a comprehensive spatiotemporal analysis of the composition, origin and differentiation of subsets of macrophages within healthy and inflamed joints, and study the roles of these macrophages during arthritis. We find that dynamic membrane-like structures, consisting of a distinct population of CX.sub.3CR1.sup.+ tissue-resident macrophages, form an internal immunological barrier at the synovial lining and physically seclude the joint. These barrier-forming macrophages display features that are otherwise typical of epithelial cells, and maintain their numbers through a pool of locally proliferating CX.sub.3CR1.sup.- mononuclear cells that are embedded into the synovial tissue. Unlike recruited monocyte-derived macrophages, which actively contribute to joint inflammation, these epithelial-like CX.sub.3CR1.sup.+ lining macrophages restrict the inflammatory reaction by providing a tight-junction-mediated shield for intra-articular structures. Our data reveal an unexpected functional diversification among synovial macrophages and have important implications for the general role of macrophages in health and disease. Analysis of macrophage subsets within joints reveals a population of CX.sub.3CR1.sup.+ tissue-resident macrophages that form a tight-junction-mediated barrier at the synovial lining, protecting the joint from the invasion of inflammatory cells.

Wideband acoustic immitance (WAI) measurements provide an objective means to detect pathological middle ear conditions. However, for ears of young infants, it is still difficult to make clear statements about the middle ear status based on WAI measurements. In order to gain a better understanding of WAI data obtained in young infants’ ears, a parametric electro-acoustic model of the ear canal and the middle ear of young infants is proposed. In this first part of the two-part paper, the development of the model for the healthy ear is presented. Based on an existing model for adult ears, the presented model is adapted to young infants’ ears, uses parameters suited to represent physiological properties, and uses a smaller number of parameters in order to reduce model complexity. A comparison of the acoustic input impedance of the ear predicted by the model with real ear measurements in young infants’ ears showed a good agreement in the main characteristics. Model predictions show that the medium frequency range (about 1–3 kHz) of the acoustic input impedance of the ear is dominated by the properties of the eardrum and the middle ear, indicating that pathological middle ear conditions can preferably be detected in this frequency range.

Introduction DCs comprise a heterogenic group of antigen-presenting cells, which share the ability to prime naive T cells (1). Upon exposure to pathogen-associated molecular patterns and endogenous danger signals, DCs [...], DCs are able to undergo rapid maturation, which subsequently allows them to initiate and orchestrate T cell-driven immune responses. DC maturation must be tightly controlled in order to avoid random T cell activation and development of autoimmunity. Here, we determined that 12/15-lipoxygenase-meditated (12/15-LO-mediated) enzymatic lipid oxidation regulates DC activation and fine-tunes consecutive T cell responses. Specifically, 12/15-LO activity determined the DC activation threshold via generation of phospholipid oxidation products that induced an antioxidative response dependent on the transcription factor NRF2. Deletion of the 12/15-LO-encoding gene or pharmacologic inhibition of 12/15-LO in murine or human DCs accelerated maturation and shifted the cytokine profile, thereby favoring the differentiation of Th17 cells. Exposure of 12/15-LO-deficient DCs to 12/15-LO-derived oxidized phospholipids attenuated both DC activation and the development of Th17 cells. Analysis of lymphatic tissues from 12/15-LO-deficient mice confirmed enhanced maturation of DCs as well as an increased differentiation of Th17 cells. Moreover, experimental autoimmune encephalomyelitis in mice lacking 12/15-LO resulted in an exacerbated Th17-driven autoimmune disease. Together, our data reveal that 12/15-LO controls maturation of DCs and implicate enzymatic lipid oxidation in shaping the adaptive immune response.

AbstractObjectiveDesignStudy sampleResultsConclusionsMeasurement of reference speech-recognition curves for a specific speech test in typical clinical testing environments and for different loudspeaker configurations.Speech-recognition scores were measured at four signal-to-noise ratios for five loudspeaker configurations in two anechoic rooms, and in four audiometric test rooms with low reverberation times.240 young participants (aged 18–25 years) without hearing impairment participated in the measurements.Reference speech-recognition curves for speech and noise from the front (S0N0) were similar across rooms. Compared to S0N0, lower speech-recognition thresholds (SRTs) were observed for all other loudspeaker configurations in which speech and noise were spatially separated. This spatial release from masking was significantly reduced for the audiometric test rooms compared to the anechoic rooms. A binaural speech-intelligibility model was used to verify the influence of room acoustic properties and loudspeaker configuration on SRT.Speech-recognition curves for spatially separated loudspeaker configurations depend on the room acoustic properties, even in audiometric test rooms with low reverberation times. This makes it more difficult to compare clinical measurements with reference speech-recognition curves, or even with data measured in a different test room. It is thus recommended to document the loudspeaker configuration and test room for each clinical measurement. [ABSTRACT FROM AUTHOR]

The checkpoints and mechanisms that contribute to autoantibody-driven disease are as yet incompletely understood. Here we identified the axis of interleukin 23 (IL-23) and the T H 17 subset of helper T cells as a decisive factor that controlled the intrinsic inflammatory activity of autoantibodies and triggered the clinical onset of autoimmune arthritis. By instructing B cells in an IL-22- and IL-21-dependent manner, T H 17 cells regulated the expression of β-galactoside α2,6-sialyltransferase 1 in newly differentiating antibody-producing cells and determined the glycosylation profile and activity of immunoglobulin G (IgG) produced by the plasma cells that subsequently emerged. Asymptomatic humans with rheumatoid arthritis (RA)-specific autoantibodies showed identical changes in the activity and glycosylation of autoreactive IgG antibodies before shifting to the inflammatory phase of RA; thus, our results identify an IL-23-T H 17 cell-dependent pathway that controls autoantibody activity and unmasks a preexisting breach in immunotolerance., Competing Interests: The authors declare no competing financial interests.