Effects of Sound on Postural Stability during Quiet Standing

Loss of postural stability can increase the likelihood of slips and falls in workplaces. The present study intended to extend understanding of the effects of frequency and pressure level of sound on postural stability during standing. Eleven male subjects participated. Standing on a force platform, the subjects' center of pressures were measured under different combinations of pressure level and frequency of the sound. Variables such as the position variability of COP and the length of postural sway path in anterior-posterior (AP) and medio-lateral (ML) direction were evaluated. Subjective ratings of perceived disturbance at each experimental condition were also obtained using a 7-point rating scale. Results showed that the length of sway path and the position variability of COP increased as the frequency of sound increased in posterior-anterior axis. The effect of sound pressure level, however, was not significant on both the postural sway length and the position variability of COP. These results suggested substantial disturbance of standing balance system among subjects exposed to high frequency noise. The results implied that physical workers should be alerted that their abilities of postural balance could be degraded significantly as disturbance caused by a sound existed

Micro Sensor Node for Air Pollutant Monitoring: Hardware and Software Issues

Wireless sensor networks equipped with various gas sensors have been actively used for air quality monitoring. Previous studies have typically explored system issues that include middleware or networking performance, but most research has barely considered the details of the hardware and software of the sensor node itself. In this paper, we focus on the design and implementation of a sensor board for air pollutant monitoring applications. Several hardware and software issues are discussed to explore the possibilities of a practical WSN-based air pollution monitoring system. Through extensive experiments and evaluation, we have determined the various characteristics of the gas sensors and their practical implications for air pollutant monitoring systems

Neutrality of the canonical NF-kappaB-dependent pathway for human and murine cytomegalovirus transcription and replication in vitro

Cytomegalovirus (CMV) is known to rapidly induce activation of nuclear factor �B (NF-�B) after infection of fibroblast and macrophage cells. NF-�B response elements are present in the enhancer region of the CMV major immediate-early promoter (MIEP), and activity of the MIEP is strongly upregulated by NF-�B in transient-transfection assays. Here we investigate whether the NF-�B-dependent pathway is required for initiating or potentiating human and murine CMV replication in vitro. We show that expression of a dominant negative mutant of the inhibitor of NF-�B-alpha (I�B�M) does not alter the replication kinetics of human or mouse CMV in cultured cells. In addition, mouse embryo fibroblasts genetically deficient for p65/RelA actually showed elevated levels of MCMV replication. Mutation of all NF-�B response elements within the enhancer of the MIEP in a recombinant mouse CMV containing the human MIEP (hMCMV-ES), which we have previously shown to replicate in murine fibroblasts with kinetics equivalent to that of wild-type mouse CMV, did not negatively affect replication in fibroblasts. Taken together, these data show that, for CMV replication in cultured fibroblasts activation of the canonical NF-�B pathway and binding of NF-�B to the MIEP are dispensable, and in the case of p65 may even interfere, thus uncovering a previously unrecognized level of complexity in the host regulatory network governing MIE gene expression in the context of a viral infection

Specific remodeling of splenic architecture by cytomegalovirus.

Efficient immune defenses are facilitated by the organized microarchitecture of lymphoid organs, and this organization is regulated by the compartmentalized expression of lymphoid tissue chemokines. Mouse cytomegalovirus (MCMV) infection induces significant remodeling of splenic microarchitecture, including loss of marginal zone macrophage populations and dissolution of T and B cell compartmentalization. MCMV preferentially infected the splenic stroma, targeting endothelial cells (EC) as revealed using MCMV-expressing green fluorescent protein. MCMV infection caused a specific, but transient transcriptional suppression of secondary lymphoid chemokine (CCL21). The loss of CCL21 was associated with the failure of T lymphocytes to locate within the T cell zone, although trafficking to the spleen was unaltered. Expression of CCL21 in lymphotoxin (LT)-alpha-deficient mice is dramatically reduced, however MCMV infection further reduced CCL21 levels, suggesting that viral modulation of CCL21 was independent of LTalpha signaling. Activation of LTbeta-receptor signaling with an agonistic antibody partially restored CCL21 mRNA expression and redirected transferred T cells to the splenic T cell zone in MCMV-infected mice. These results indicate that virus-induced alterations in lymphoid tissues can occur through an LT-independent modulation of chemokine transcription, and targeting of the LT cytokine system can counteract lymphoid tissue remodeling by MCMV

Specific remodeling of splenic architecture by cytomegalovirus. PLoS Pathog 2

Efficient immune defenses are facilitated by the organized microarchitecture of lymphoid organs, and this organization is regulated by the compartmentalized expression of lymphoid tissue chemokines. Mouse cytomegalovirus (MCMV) infection induces significant remodeling of splenic microarchitecture, including loss of marginal zone macrophage populations and dissolution of T and B cell compartmentalization. MCMV preferentially infected the splenic stroma, targeting endothelial cells (EC) as revealed using MCMV-expressing green fluorescent protein. MCMV infection caused a specific, but transient transcriptional suppression of secondary lymphoid chemokine (CCL21). The loss of CCL21 was associated with the failure of T lymphocytes to locate within the T cell zone, although trafficking to the spleen was unaltered. Expression of CCL21 in lymphotoxin (LT)-a–deficient mice is dramatically reduced, however MCMV infection further reduced CCL21 levels, suggesting that viral modulation of CCL21 was independent of LTa signaling. Activation of LTb-receptor signaling with an agonistic antibody partially restored CCL21 mRNA expression and redirected transferred T cells to the splenic T cell zone in MCMV-infected mice. These results indicate that virus-induced alterations in lymphoid tissues can occur through an LT-independent modulation of chemokine transcription, and targeting of the LT cytokine system can counteract lymphoid tissue remodeling by MCMV

Reduced CCL21-ser Expression after MCMV Infection

<div><p>Spleens from B6 mice mock-infected or infected with 3.2 × 10⁵ (A,B,D) or 1.5 × 10⁵ (C) pfu of MCMV were harvested at day 3 post-infection. Gene expression was measured by quantitative PCR and was normalized to 18S RNA and presented as relative mRNA levels compared to uninfected mice (A and D) or as absolute values (C). When presented as relative values, mRNA levels from three uninfected mice (mock) were determined and averaged for comparison for each experiment.</p><p>Open symbols in (A) represent mice infected with UV-inactivated MCMV (equivalent to 3.2 × 10⁵ pfu).</p><p>(B) Immunohistochemical analysis of CCL21 expression in the spleen of a mock or MCMV-infected B6 mouse 3 d post-infection; the location of the periarteriolar lymphoid sheath “PALS” and B-cell follicles “B” is noted, and the interrupted white line indicates the outer edge of the MZ. This section is representative of three experiments (<i>n</i> = 3 mice per group).</p><p>In (C), primers used for analysis of CCL21 levels amplified either the serine (CCL21-ser), leucine (CCL21-leu), or both (CCL21u) isoforms.</p><p>The data in (D) is an average of three infected mice ± SEM (<i>p</i> < .001).</p></div

MCMV Splenic Tropism

<div><p>All analysis was performed 3 d post virus infection.</p><p>(A) Splenic stromal cells from mock or MCMV (2 × 10⁵ pfu, Smith strain) infected spleens were separated from hematopoietic cells by extrusion through a nylon mesh filter (see <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.0020016#s4" target="_blank">Materials and Methods</a>). Total cell RNA was then isolated from either the stromal cells (S) or hematopoietic cells (H) fractions, and quantitative RT-PCR was performed to detect expression of CCL21-ser, CCL19, and CXCL13 as well as expression of the MCMV immediate early-1 (IE1) transcript.</p><p>(B) Spleens from MCMV-GFP infected mice (2 × 10⁵ pfu) were examined by immunohistochemistry. Panels are color-coded with the text for the antigen examined, and field magnification is shown to the right of the panels. No background staining was seen in uninfected mouse spleen when directly detecting GFP expression or when using an anti-GFP antibody (αGFP) for signal amplification.</p><p>WP, white pulp.</p></div

MCMV-Induced Suppression of CCL21 Abolishes T Cell Localization to the White Pulp

<div><p>Mock- or MCMV-infected B6 mice (1.5 × 10⁵ pfu) were injected with CFSE labeled naive T cells, and spleens were removed for analysis 2 h later.</p><p>(A) Flow cytometry was used to assess the total number of CFSE-labeled cells in the spleen after adoptive transfer into mice 3 d post-infection.</p><p>(B) Immunohistochemical analysis of T cell localization in the spleen at 3 d post-infection using the MOMA-1 marker to identify MMM (shown in blue, magnification 10×). WP, white pulp; RP, red pulp.</p></div

MCMV Modulates Splenic Architecture

<div><p>(A) Spleens from PBS (mock) or MCMV-infected B6 mice (3.2 × 10⁵ pfu) were harvested at day 3 post-infection for immunohistochemical analysis. Spleen sections were incubated with markers specific to MMM (MOMA-1, MMM, blue), MZM (ER-TR9, MZM, red), granulocytes (Gr-1/Ly-6G, green), stromal cell populations (BP-3, blue, to identify B-cell-zone stromal cells and gp38, red, to identify T-cell-zone stromal cells, in uninfected mice), and B (B220, blue), and T lymphocytes (Thy1.2, red) (magnification 20×). These sections are representative of four independent experiments with <i>n</i> = 3 mice per group with two or more sections taken from each spleen. White pulp (WP) and red pulp (RP) and the location of the central arteriole (ca) are indicated.</p><p>(B) Similar immunohistochemical analysis performed on Balb/c mice, 3 d post-MCMV-infection (1 × 10⁵ pfu).</p></div