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Question: Does activity coaching add value to physiotherapy from the perspective of physiotherapists and patients in neurological rehabilitation? Is the use of activity coaching to promote walking and physical activity considered feasible by these physiotherapists and patients?, Design: Qualitative study using interviews., Participants: Five pairs of physiotherapists and their patients with neurological conditions., Intervention: A research physiotherapist trained in health coaching delivered an activity coaching intervention. This was provided in addition to standard physiotherapy. The treating physiotherapists observed the activity coaching session undertaken by their patients., Results: Observing the coaching interview was valuable for the treating physiotherapists in that it provided a way to refocus, step back, gain insight, and facilitate more active involvement for their patients in the rehabilitation process. Similarly patients valued the opportunity to focus on what was important and put into action their rehabilitation goals. Contrasting perceptions were evident, which limits the practical usefulness of this intervention due to the concerns voiced by some of the physiotherapists., Conclusion: The activity coaching was perceived as providing a valuable addition to standard practice and was acceptable to patients but the mixed responses of physiotherapists limit the feasibility of this approach. Use of strategies and specific training for physiotherapists may be needed before approaches like activity coaching can be adopted successfully., (Copyright © 2013 Australian Physiotherapy Association. Published by .. All rights reserved.)

An environmental assessment of long-chain alcohols (LCOH) has recently been conducted under the OECD SIDS High Production Volume (HPV) Program via the Global International Council of Chemical Associations (ICCA) Aliphatic Alcohols Consortium. LCOH are used primarily as intermediates, as a precursor to alcohol-based surfactants and as alcohol per se in a wide variety of consumer product applications. Global production volume is approximately 1.58 million metric tonnes. The OECD HPV assessment covers linear to slightly branched LCOH ranging from 6 to 22 alkyl carbons (C). LCOH biodegrade exceptionally rapidly in the environment (half-lives on the order of minutes); however, due to continuous use and distribution to wastewater treatment systems, partitioning properties, biodegradation of alcohol-based surfactants, and natural alcohol sources, LCOH are universally detected in wastewater effluents. An environmental risk assessment of LCOH is presented here by focusing on the most prevalent and toxic members of the linear alcohols, specifically, from C(12-15). The assessment includes environmental monitoring data for these chain lengths in final effluents of representative wastewater treatment plants and covers all uses of alcohol (i.e., the use of alcohol as a substance and as an intermediate for the manufacturing of alcohol-based surfactants). The 90th percentile effluent discharge concentration of 1.979microg/L (C(12)-C(15)) was determined for wastewater treatment plants in 7 countries. Chronic aquatic toxicity studies with Daphnia magna demonstrated that between C(13) and C(15) LCOH solubility became a factor and that the structure-activity relationship was characterized by a toxicity maximum between C(13) and C(14). Above C(14) the LCOH was less toxic and become un-testable due to insolubility. Risk quotients based on a toxic units (TU) approach were determined for various scenarios of exposure and effects extrapolation. The global average TU ranged from 0.048 to 0.467 depending on the scenario employed suggesting a low risk to the environment. The fact that environmental exposure calculations include large fractions of naturally derived alcohol from animal, plant, and microbially mediated biotransformations further supports a conclusion of low risk.

Surface seawater samples were collected in the Irish Sea and Liverpool Bay area from the R.V. Prince Madog during the period of 25-31 of March 2006. VOCs were purged with nitrogen, pre-concentrated on a SPME fibre and analysed immediately on a GC-MS. Target compounds quantified were halogenated (0.2-1400 ng L(-1)), BTEXs and mono-aromatics (1.5-2900 ng L(-1)), aliphatic hydrocarbons and others (0.6-15,800 ng L(-1)). Day and night sampling was performed at a single station and suggested that factors such as sunlight and tide affect the presence of many of these compounds. Sample variability was high due to the variable weather conditions at the station. Poor correlations were found between marine phytopigments and selected VOCs. Principal component analysis (PCA) analysis showed that chlorinated compounds such as 1,2-dichloroethane, 1,1,1-trichloroethane, trichloroethene, tetrachloroethene and carbon tetrachloride, predominantly from anthropogenic sources, originated from the River Mersey. Other brominated and iodinated compounds quantified were more likely to be from biogenic sources including novel marine compounds such as 2-chloropropane, 1-bromoethane and 1-chlorobutane.

Background: The present study examined whether activation of nuclear factor-kappa B (NF-kappa B) occurs within podocytes in passive Heymann nephritis (PHN) and contributes to the pathogenesis of proteinuria., Methods: Electrophoretic mobility shift assays (EMSAs) were used to detect NF-kappa B activation, and supershift assays were used to determine the subunits involved. Localization of the activated NF-kappa B subunit p50 was performed by immunohistochemistry. Expression of the NF-kappa B-dependent genes interleukin-1 beta (IL-1 beta) and matrix metalloproteinase-9 (MMP-9) were determined by reverse transcription-polymerase chain reaction and, for IL-1 beta, immunohistochemistry. To inhibit activation of NF-kappa B in vivo, pyrrolidone dithiocarbamate (PDTC) was administered for 10 days following induction of PHN., Results: Glomerular nuclear extracts from rats with PHN showed increased NF-kappa B binding activity in comparison to normal rats. The major Rel/NF-kappa B proteins in these activated complexes were p65 and p50. Immunohistochemistry showed that nuclear translocation of p50 occurred predominantly within podocytes. IL-1 beta mRNA was increased in the PHN rats, and increased IL-1 beta protein was localized predominantly to podocytes by immunohistochemistry. To investigate whether activation of NF-kappa B is involved in the pathogenesis of proteinuria, PDTC was administered to rats with PHN. Electrophoretic mobility shift assays of glomerular nuclear extracts showed a significant reduction in NF-kappa B binding activity in the PDTC-treated rats with a striking reduction in MMP-9 mRNA. Compared with control rats, there was a significant reduction in albuminuria at days 15 (P < 0.001) and 20 (P < 0.001) when PHN was induced with a suboptimal dose of anti-Fx1A antiserum. There was no detectable difference in the systemic immune response to sheep Ig in the treated rats., Conclusions: These data show that NF-kappa B is activated within podocytes in PHN and suggest that it contributes to autologous phase proteinuria. The critical genes regulated by NF-kappa B in the podocyte have not yet been determined, but may include MMP-9.

Background: Vascular endothelial growth factor (VEGF) mRNA and protein expression are increased by hypoxia in a variety of cell types and organs. In the kidney, however, chronic hypoxia does not up-regulate VEGF mRNA. This suggests that VEGF may be regulated by unique mechanisms in the kidney., Methods: Unilateral ischemia was induced in rats by vascular cross-clamping (40 min) followed by reperfusion (0, 20, 40, and 80 min). The distribution of VEGF protein was determined by immunohistochemical staining and Western blotting. mRNA was detected by Northern blotting and semiquantitative reverse transcription-polymerase chain reaction (RT-PCR). Immunohistochemical staining for VEGF was verified using two VEGF antibodies. To further substantiate the immunohistochemical findings, laser scanning confocal fluorescence microscopy was used to demonstrate the distribution of VEGF protein in rat renal tubular epithelial cells (NRK52-E) subjected to hypoxia (40 min) and re-oxygenation (0, 5, 20, 40 and 80 min)., Results: Normal kidneys showed diffuse immunohistochemical staining for VEGF in all tubules of the renal cortex and medulla. Following ischemia, staining demonstrated a prominent shift of cytoplasmic VEGF to the basolateral aspect of tubular cells with both VEGF antibodies. The distribution of cytoplasmic VEGF returned to normal following 40 and 80 minutes of reperfusion. Western blots of cytoplasmic samples from ischemic kidneys reperfused for 0 and 20 minutes showed decreased levels of VEGF164 compared with normal (P < 0.01). VEGF164 and VEGF188 levels in the membrane fraction showed no change. Northern blots and semiquantitative RT-PCR showed no significant up-regulation of VEGF mRNA or change in the splice pattern. NRK52-E cells subjected to hypoxia and re-oxygenation for 0 and 5 minutes showed increased staining for VEGF compared with normal, with prominent VEGF staining at the periphery of the cell, similar to the appearance in ischemic kidneys. VEGF staining became more diffuse with further re-oxygenation., Conclusion: Although synthesis of VEGF mRNA and protein is not increased during ischemia reperfusion injury, pre-existing VEGF in the tubular cell cytoplasm redistributes to the basolateral aspect of the cells. These data suggest that the kidney may have evolved unique patterns of VEGF regulation to cope with acute hypoxia.