2,457 research outputs found

    Noise Pollution? What\u27s the solution?: Understanding Traffic Noise Pollution in Gettysburg, Pennsylvania

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    Noise pollution can be damaging to a community by impacting its atmosphere as well as the health of its residents, local quality of life, and local economy. Our study sought to gain insight into the level of noise pollution in Gettysburg, both in-town and on the Gettysburg College campus, and how noise pollution may be affecting the local residents and students. We selected 9 sampling sites, 6 in-town and 3 on the college campus, and measured the noise pollution in dBA with portable sound meters three days a week and three times a day over a three week period. Our data showed no major trends in terms of time of day or day of the week, but there were clear differences in noise pollution levels between the different sites in that town sites were generally louder than on campus sites. Noise pollution in town was often louder than 70 dBA, the noise threshold that indicates possible hearing damage overtime set by the World Health Organization. Gettysburg has recently enacted a noise ordinance; our study suggests the Borough possibly could do more to mitigate traffic noise by repairing roads and manipulating road design

    The respiratory chain inhibitor rotenone affects peroxisomal dynamics via its microtubule-destabilizing activity

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    This is the author accepted manuscript. The final version is available from Springer Verlag via the DOI in this record.Peroxisomes and mitochondria in mammalian cells are closely linked subcellular organelles, which maintain a redox-sensitive relationship. Their interplay and role in ROS signalling is supposed to impact on age-related and degenerative disorders. Whereas the generation of peroxisome-derived oxidative stress can affect mitochondrial morphology and function, little is known about the impact of mitochondria-derived oxidative stress on peroxisomes. Here, we investigated the effect of the mitochondrial complex I inhibitor rotenone on peroxisomal and mitochondrial membrane dynamics. We show that rotenone treatment of COS-7 cells alters peroxisome morphology and distribution. However, this effect is related to its microtubule-destabilising activity rather than to the generation of oxidative stress. Rotenone also induced alterations in mitochondrial morphology, which – in contrast to its effect on peroxisomes - were dependent on the generation of ROS but independent of its microtubule-active properties. The importance of our findings for the peroxisome-mitochondria redox relationship and the interpretation of in cellulo and in vivo studies with rotenone, which is widely used to study Parkinson’s disease, are discussed.We would like to acknowledge the support of T. A. Schrader, N. A. Bonekamp and J. Jordan (University of Castilla-La Mancha, Albacete, Spain). This work was supported by the Biotechnology and Biological Sciences Research Council (BB/K006231/1, BB/N01541X/1 to M.S.), the Portuguese Foundation for Science and Technology and FEDER/COMPETE (SFRH/BPD/37725/2007 to M.G.L), the University of Aveiro, PT and CLES, University of Exeter, UK. M.S. is supported by a Marie Curie Initial Training Network (ITN) action PerFuMe (316723)

    The respiratory chain inhibitor rotenone affects peroxisomal dynamics via its microtubule-destabilizing activity

    Get PDF
    This is the author accepted manuscript. The final version is available from Springer Verlag via the DOI in this record.Peroxisomes and mitochondria in mammalian cells are closely linked subcellular organelles, which maintain a redox-sensitive relationship. Their interplay and role in ROS signalling is supposed to impact on age-related and degenerative disorders. Whereas the generation of peroxisome-derived oxidative stress can affect mitochondrial morphology and function, little is known about the impact of mitochondria-derived oxidative stress on peroxisomes. Here, we investigated the effect of the mitochondrial complex I inhibitor rotenone on peroxisomal and mitochondrial membrane dynamics. We show that rotenone treatment of COS-7 cells alters peroxisome morphology and distribution. However, this effect is related to its microtubule-destabilising activity rather than to the generation of oxidative stress. Rotenone also induced alterations in mitochondrial morphology, which – in contrast to its effect on peroxisomes - were dependent on the generation of ROS but independent of its microtubule-active properties. The importance of our findings for the peroxisome-mitochondria redox relationship and the interpretation of in cellulo and in vivo studies with rotenone, which is widely used to study Parkinson’s disease, are discussed.We would like to acknowledge the support of T. A. Schrader, N. A. Bonekamp and J. Jordan (University of Castilla-La Mancha, Albacete, Spain). This work was supported by the Biotechnology and Biological Sciences Research Council (BB/K006231/1, BB/N01541X/1 to M.S.), the Portuguese Foundation for Science and Technology and FEDER/COMPETE (SFRH/BPD/37725/2007 to M.G.L), the University of Aveiro, PT and CLES, University of Exeter, UK. M.S. is supported by a Marie Curie Initial Training Network (ITN) action PerFuMe (316723)

    KCNQ/M currents in sensory neurons: Significance for pain therapy

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    Neuronal hyperexcitability is a feature of epilepsy and both inflammatory and neuropathic pain. M currents [I-K(M)] play a key role in regulating neuronal excitability, and mutations in neuronal KCNQ2/3 subunits, the molecular correlates of I-K(M), have previously been linked to benign familial neonatal epilepsy. Here, we demonstrate that KCNQ/M channels are also present in nociceptive sensory systems. I-K(M) was identified, on the basis of biophysical and pharmacological properties, in cultured neurons isolated from dorsal root ganglia (DRGs) from 17-d-old rats. Currents were inhibited by the M-channel blockers linopirdine (IC50, 2.1 muM) and XE991 (IC50, 0.26 muM) and enhanced by retigabine (10 muM). The expression of neuronal KCNQ subunits in DRG neurons was confirmed using reverse transcription-PCR and single-cell PCR analysis and by immunofluorescence. Retigabine, applied to the dorsal spinal cord, inhibited C and Adelta fiber-mediated responses of dorsal horn neurons evoked by natural or electrical afferent stimulation and the progressive "windup" discharge with repetitive stimulation in normal rats and in rats subjected to spinal nerve ligation. Retigabine also inhibited responses to intrapaw application of carrageenan in a rat model of chronic pain; this was reversed by XE991. It is suggested that I-K(M) plays a key role in controlling the excitability of nociceptors and may represent a novel analgesic target

    Nurses\u27 Alumnae Association Bulletin - Volume 2 Number 3

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    The Jefferson Nurse Letter from the President Delegates to Biennial Convention Attention Blood Transfusion - Plasma Unit Life in the Army Nurse Corps Secretary\u27s Report Elected to New Office 1892-1942 Progress or Alumnae Association 1892-1942 Report of the School of Nursing Staff News Please Change My Address Air Cooled Red Cross Report Fingerprinting Graduates in the U.S. Army and Navy Degrees Received Promotions Jubilee Report Engagements Marriages Births New Positions - 1941-1942 New Positions on the Nursing Staff of the Hospita
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