White matter tracts visualized on delayed enhanced-heavily T2-weighted three-dimensional fluid-attenuated inversion recovery (DE-hT2w-3D-FLAIR) images.

<p>Axial (<b>A</b> and <b>B</b>: the thalamic and the pontine levels), coronal (<b>C</b> and <b>D</b>: the basilar part and the tegmentum of the pons levels), and sagittal (<b>E</b> and <b>F</b>: the left cerebellar hemisphere and the left side of the pons levels) delayed enhanced-heavily T2-weighted three-dimensional fluid-attenuated inversion recovery (DE-hT2w-3D-FLAIR) images of a single patient who was clinically suspected of having Ménière’s disease are presented. Images were obtained 4 h after a single-dose intravenous gadolinium injection (0.2 mL (0.1 mmol)/kg body weight). Coronal and sagittal images were reconstructed from axial based three-dimensional images (voxel size, 0.5×0.5×1.0 mm). The corticospinal tract (CST), medial lemniscus (ML), and superior cerebellar peduncle (SCP) are visualized clearly and continuously as high-intensity areas. The general parameters for these images were as follows: repetition time, 9000 ms; echo time, 544 ms; inversion time, 2250 ms; number of excitations (NEX), 4.</p

The regions of interest setting on delayed enhanced-heavily T2-weighted three-dimensional fluid-attenuated inversion recovery (DE-hT2w-3D-FLAIR) images.

<p>Axial, delayed enhanced, heavily T2-weighted three-dimensional fluid-attenuated inversion recovery (hT2w-3D-FLAIR) images from the same patient as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0091860#pone-0091860-g002" target="_blank"><b>Figure 2</b></a>. Images were obtained 4 h after intravenous gadolinium injection. Images on the left side (<b>A</b> and <b>C</b>) are at the levels of the thalamus (Th), and images on the right side (<b>B</b> and <b>D</b>) are at the level of the trigeminal nerve. The corticospinal tract (CST), medial lemniscus (ML), and superior cerebellar peduncle (SCP) are visualized as areas of high signal intensity (<b>A</b> and <b>B</b>). Images <b>C</b> and <b>D</b> are trimmed magnifications of images <b>A</b> and <b>B</b>, with regions of interest (ROI) setting. Oval 5-mm² ROI were set on the CST, ML, SCP, and circular 15-mm² ROI were set on the Th, pontine parenchyma (PP), and cerebellar parenchyma (CP) (<b>C</b> and <b>D</b>). To evaluate the signal contrast between white matter (WM)-tracts and contiguous brain parenchyma, the following signal intensity ratios between WM-tracts and contiguous brain parenchyma were calculated: the ratio of the signal intensity of the CST to the signal intensity of the Th on the same side (CThR), the ratio of the signal intensity of the ML to the signal intensity of the PP on the same side (MPPR), and the ratio of the signal intensity of the SCP to the signal intensity of the CP on the same side (SCPR).</p

The signal intensity ratios on hT2w-3D-FLAIR images for each patient.

<p><i>hT2w-3D-FLAIR:</i> heavily T2-weighted three-dimensional fluid-attenuated inversion-recovery, <i>Pt no.:</i> patient number, <i>P:</i> plain (i.e., without gadolinium injection), <i>DE:</i> delayed enhancement (4 hours after intravenous gadolinium injection), <i>CThR:</i> ratio of the signal intensity of the corticospinal tract to the signal intensity of the thalamus on the same side, <i>MPPR:</i> ratio of the signal intensity of the medial lemniscus to the signal intensity of the pontine parenchyma on the same side, <i>SCPR:</i> ratio of the signal intensity of the superior cerebellar peduncle to the signal intensity of the cerebellar parenchyma on the same side, <i>L:</i> left, <i>R:</i> right, <i>F:</i> female, <i>M:</i> male, <i>SD:</i> standard deviation.</p

The signal intensity ratios of the white matter tracts to the contiguous brain parenchyma.

<p><b>A)</b> The ratio of the signal intensity of the corticospinal tract to the signal intensity of the thalamus on the same side on plain (P-CThR) and delayed enhanced (DE-CThR) heavily T2-weighted three-dimensional fluid-attenuated inversion recovery (hT2w-3D-FLAIR) images. The P-CThR mean was 3.75±0.67 and the DE-CThR mean was 3.62±0.50 (p = 0.24, n = 18). There was no significant difference between P- and DE-CThR. <b>B)</b> The ratio of the signal intensity of the medial lemniscus to the signal intensity of the pontine parenchyma on the same side on plain (P-MPPR) and delayed enhanced (DE-MPPR) hT2w-3D-FLAIR images. The P-MPPR mean was 2.19±0.59 and the DE-MPPR mean was 2.08±0.53 (p = 0.25, n = 18). There was no significant difference between P- and DE-MPPR. <b>C)</b> The ratio of the signal intensity of the superior cerebellar peduncle to the signal intensity of the cerebellar parenchyma on the same side on plain (P-SCPR) and delayed enhanced (DE-SCPR) hT2w-3D-FLAIR images. The P-SCPR mean was 4.08±0.91 and the DE-SCPR mean was 4.04±0.96 (p = 0.43, n = 18). There was no significant difference between P- and DE-SCPR.</p

The regions of interest setting on plain-heavily T2-weighted three-dimensional fluid-attenuated inversion recovery (P-hT2w-3D-FLAIR) images.

<p>Axial, plain, heavily T2-weighted three-dimensional fluid-attenuated inversion recovery (hT2w-3D-FLAIR) images obtained from a single patient without gadolinium injection. Images on the left side (<b>A</b> and <b>C</b>) are at the level of the thalamus (Th) and images on the right side (<b>B</b> and <b>D</b>) are at the level of the trigeminal nerve. The corticospinal tract (CST), medial lemniscus (ML), and superior cerebellar peduncle (SCP) are visualized as areas of high signal intensity (<b>A</b> and <b>B</b>). Images <b>C</b> and <b>D</b> are trimmed magnifications of images <b>A</b> and <b>B</b>, with regions of interest (ROI) setting. Oval 5-mm² ROI were set on the CST, ML, SCP, and circular 15-mm² ROI were set on the Th, pontine parenchyma (PP), and cerebellar parenchyma (CP) (<b>C</b> and <b>D</b>). To evaluate the signal contrast between white matter (WM)-tracts and contiguous brain parenchyma, the following signal intensity ratios between WM-tracts and contiguous brain parenchyma were calculated: the ratio of the signal intensity of the CST to the signal intensity of the Th on the same side (CThR), the ratio of the signal intensity of the ML to the signal intensity of the PP on the same side (MPPR), and the ratio of the signal intensity of the SCP to the signal intensity of the CP on the same side (SCPR).</p

The location and the size of each WM-tract on axial hT2w-3D-FLAIR images.

<p><i>WM-tract:</i> white matter tract, <i>hT2w-3D-FLAIR:</i> heavily T2-weighted three-dimensional fluid-attenuated inversion-recovery, <i>P:</i> plain (i.e., without gadolinium injection), <i>DE:</i> delayed enhancement (4 hours after intravenous gadolinium injection), <i>SD:</i> standard deviation, <i>CST:</i> corticospinal tract, <i>ML:</i> medial lemniscus, <i>SCP:</i> superior cerebellar peduncle.</p>a<p>The location of each WM-tract was calculated as follows: CST, lateral distance from the lateral margin of the third ventricle at the thalamic level; ML, anterior distance from the anterior margin of the fourth ventricle at the trigeminal nerve level; and SCP, lateral distance from the lateral margin of the fourth ventricle at the trigeminal nerve level.</p>b<p>The size of each WM-tract was calculated by surrounding the margin of high intensity area: CST, at the thalamic level; ML and SCP, at the trigeminal nerve level.</p>c<p>SCP was just lateral to the fourth ventricle at the trigeminal nerve level in all patients.</p

Histological analyses of tonsil tissues infected with B95–8 using immunostaining and <i>in situ</i> hybridization with EBER-RNA.

<p>Samples were obtained from EBV-infected tissues at 24 days post-infection. Pictures are representative of results from four experiments. <b>A</b>) Low-power view of tonsillar lymphoid tissue (HE stain). Magnification, ×100. <b>B</b>) Low-power view of CD3⁺ lymphocytes in an interfollicular area (CD3 stain). Magnification, ×100. <b>C</b>) Low-power view of CD20⁺ lymphocytes in a follicular area (CD20 stain). Magnification, ×100. <b>D</b>) High-power view of anti-follicular dendritic cell (FDC)⁺ in a follicular area (anti-FDC stain). Magnification, ×400. <b>E</b>) Low-power view of EBER⁺ lymphocytes (EBER ISH stain). Magnification, ×100. <b>F</b>) High-power view of EBER⁺ lymphocytes in an interfollicular area (EBER ISH stain). Magnification, ×400. <b>G</b>) High-power view of BZLF1⁺ lymphocytes (arrows) in an interfollicular area (BZLF1 stain). Magnification, ×400.</p

Kinetics of EBV DNA and expression patterns of EBV-related genes in human tonsil tissue explants infected with B95–8.

<p>Culture medium was changed every 3 days, and collected medium was centrifuged. Cell-free supernatants and cells collected from culture medium were used for quantification of EBV DNA by real-time PCR assay and quantification of viral mRNA by real-time RT-PCR assay. Data are presented as mean ± standard error of the mean. <b>A</b>) Tissue blocks on top of collagen sponge gels in a six-well plate. <b>B</b>) Kinetics of EBV DNA in cell-free supernatants. Average data were obtained from tissues derived from 12 donors. <b>C</b>) Plots of accumulated EBV DNA in cell-free culture medium after day 12 post-infection (<i>n</i> = 12). <b>D</b>) Kinetics of EBV DNA in cells from medium (<i>n</i> = 12). <b>E</b>) Levels of EBV-related gene expressions in cells at 3, 12, and 24 days post-infection (<i>n</i> = 4).</p

Inhibition by acyclovir (ACV) of EBV replication in human tonsillar tissues explants.

<p>Human tonsillar tissues were infected with B95–8 and treated with ACV at various concentrations. Antiviral activity of ACV was evaluated by comparing viral replication in ACV-treated tissues with that in untreated donor-matched control tissues. Data are presented as means ± standard errors of mean. <b>A</b>) Kinetics of EBV replication were measured by real-time PCR assay for viral DNA in culture medium (<i>n</i> = 3). <b>B</b>) EBV DNA was quantified in cells at 24 days post-infection (<i>n</i> = 3). <b>C</b>) Comparison of the number of EBV-infected cells in the presence or absence of ACV at 24 days post-infection using FISH assay (<i>n</i> = 1).</p

Data_Sheet_1_Relationship between tinnitus and olfactory dysfunction: audiovisual, olfactory, and medical examinations.xlsx

IntroductionSensory dysfunctions and cognitive impairments are related to each other. Although a relationship between tinnitus and subjective olfactory dysfunction has been reported, there have been no reports investigating the relationship between tinnitus and olfactory test results.MethodsTo investigate the relationship between tinnitus and olfactory test results, we conducted sensory tests, including hearing and visual examinations. The subjects included 510 community-dwelling individuals (295 women and 215 men) who attended a health checkup in Yakumo, Japan. The age of the subjects ranged from 40 to 91 years (mean ± standard deviation, 63.8 ± 9.9 years). The participants completed a self-reported questionnaire on subjective tinnitus, olfactory function, and hearing function, as well as their lifestyle. The health checkup included smell, hearing, vision, and blood examinations.ResultsAfter adjusting for age and sex, the presence of tinnitus was significantly associated with subjective olfactory dysfunction, poor olfactory test results, hearing deterioration, vertigo, and headache. Additionally, high serum calcium levels and a low albumin/globulin ratio were significantly associated with low physical activity and nutrition. Women scored higher than men in olfactory and hearing examinations, but there was no gender difference in vision examinations.ConclusionSubjective smell dysfunction and poor smell test results were significantly associated with tinnitus complaints. Hearing and vision were associated even after adjusting for age and sex. These findings suggest that evaluating the mutual relationships among sensory organs is important when evaluating the influence of sensory dysfunctions on cognitive function.</p