147 research outputs found

    Sustainable Municipal Operations: Independence, Oregon

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    Portland State University, Hatfield School of Government (PSU), and Northwest Energy Efficiency Alliance (NEEA), has formed a partnership to develop Sustainable Municipal Operations Plans that documents sustainability and energy management best practices. The goal of this partnership is to determine how a City/municipality can actively manage energy as a controllable expense by following a predetermined operation protocol. The PSU team developed a framework of best practices for sustainable municipal operations in different categories including facilities, fleet, purchasing, operations and the work environment. After identifying pilot jurisdictions, the team applied these best practices to the current operations of local governments in Oregon with limited capacity to do so independently. A list of criteria was used to select the jurisdictions based on the commitment to sustainability and executive level management support. Independence was selected as a pilot for these reasons following detailed conversations with City administrators and management staff on the issues the team would be investigating. The results of this project are intended to both serve as a foundation for each jurisdiction to move forward with implementing improvements, and also as a starting point in learning new and innovative approaches to sustainable operations in municipal and City governments. The PSU team, compiled of experienced practitioners, worked with Independence initially to provide clarity around the goals and deliverables of the project, solidifying the commitment of the City to provide information and relevant data for the purpose of drafting this report. We visited the City on numerous occasions to understand the current operations, state of facilities, challenges and opportunities for the City and staff. The following report provides an overview of our process working with Independence to collect and gather information, our findings and recommendations for both the immediate and long term, as well as suggested strategies for implementation

    Cilostazol for Secondary Stroke Prevention: History, Evidence, Limitations, and Possibilities

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    Cilostazol is a phosphodiesterase III inhibitor with a long track record of safety that is FDA and EMA approved for the treatment of claudication in patients with peripheral arterial disease. In addition, cilostazol has been approved for secondary stroke prevention in several Asian countries based on trials that have demonstrated a reduction in stroke recurrence among patients with non-cardioembolic stroke. The onset of benefit appears after 60–90 days of treatment, which is consistent with cilostazol’s pleiotropic effects on platelet aggregation, vascular remodeling, blood flow, and plasma lipids. Cilostazol appears safe and does not increase the risk of major bleeding when given alone or in combination with aspirin or clopidogrel. Adverse effects such as headache, gastrointestinal symptoms and palpitations, however, contributed to a 6% increase in drug discontinuation among patients randomized to cilostazol in a large secondary stroke prevention trial (CSPS.com). Due to limitations of prior trials, such as open label design, premature trial termination, large loss to follow-up, lack of functional or cognitive outcome data, and exclusive enrollment in Asia, the existing trials have not led to a change in clinical practice or guidelines in Western countries. These limitations could be addressed by a double-blind placebo-controlled randomized trial conducted in a broader population. If positive, it would increase the evidence in support of long-term treatment with cilostazol for secondary prevention in the millions of patients worldwide who have suffered a non-cardioembolic ischemic stroke

    Tracking Onslow: a community in transition. edition 5, October 2014

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    This is the fifth edition of Tracking Onslow and the first that is not the result of a visit to the town. In June 2014 we were told that the Shire would not be funding the flights, accommodation or printing for the edition and so the ECU crew looked for other ways to continue documenting the impact of Wheatstone and Macedon on Onslow. Fortunately, our previous visits in July 2012, February 2013, July 2013 and February 2014 had filled our contact books with names and numbers and clued us in to issues that needed to be followed up. After a phone around for updates it was clear that this is not the time to be letting go of the process of documenting the challenges facing the Onslow community. We are very grateful to teacher James Trimble and his students, Amber and Taylor, for helping with the In Your Words section. We’d also like to thank everyone who spoke to us by phone and sent us images. We heard that there were concerns expressed earlier in the year about an image of the Anzac Memorial on our last cover and we would like to clarify that we did nothing to encourage the children to climb on it. We saw them there and snapped the picture. The photo is a true representation of something that happens in Onslow, and as such we reported it. One of the key functions of journalism is operating as a ‘town square’, where the opinions of different members of the community are aired. In this way a publication can help facilitate debate and understanding between different groups. We know that not everyone in Onslow agrees with each other, but we seek to allow everyone a space to speak through our pages. Sometimes opinions are based on misunderstood facts and so some of the things people say may not be true. We can’t vouch for the truth of what the people we spoke to said, but we have faithfully recorded it so that this edition is a true record of what was being said in and about Onslow in mid-late 2014. We hope you enjoy reading it

    Somatosensory predictors of response to pregabalin in painful chemotherapy-induced peripheral neuropathy: A randomized, placebo-controlled, crossover study

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    Painful chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating and treatment-resistant sequela of many chemotherapeutic medications. Ligands of a2d subunits of voltage-gated Ca21 channels, such as pregabalin, have shown efficacy in reducing mechanical sensitivity in animal models of neuropathic pain. In addition, some data suggest that pregabalin may be more efficacious in relieving neuropathic pain in subjects with increased sensitivity to pinprick. We hypothesized that greater mechanical sensitivity, as quantified by decreased mechanical pain threshold at the feet, would be predictive of a greater reduction in average daily pain in response to pregabalin vs placebo. In a prospective, randomized, double-blinded study, 26 patients with painful CIPN from oxaliplatin, docetaxel, or paclitaxel received 28-day treatment with pregabalin (titrated to maximum dose 600 mg per day) and placebo in crossover design. Twenty-three participants were eligible for efficacy analysis. Mechanical pain threshold was not significantly correlated with reduction in average pain (P 5 0.97) or worst pain (P 5 0.60) in response to pregabalin. There was no significant difference between pregabalin and placebo in reducing average daily pain (22.5% vs 10.7%, P 5 0.23) or worst pain (29.2% vs 16.0%, P 5 0.13) from baseline. Post hoc analysis of patients with CIPN caused by oxaliplatin (n 5 18) demonstrated a larger reduction in worst pain with pregabalin than with placebo (35.4% vs 14.6%, P 5 0.04). In summary, baseline mechanical pain threshold tested on dorsal feet did not meaningfully predict the analgesic response to pregabalin in painful CIPN

    Evaluation of Treatment-Related Mortality Among Paediatric Cancer Deaths: a population based analysis.

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    BACKGROUND: Objectives were to describe the proportion of deaths due to treatment-related mortality (TRM) and to identify risk factors and probable causes of TRM among paediatric cancer deaths in a population-based cohort. METHODS: We included children with cancer ⩽18 years diagnosed and treated in Ontario who died between January 2003 and December 2012. Deaths were identified using a provincial registry, the Pediatric Oncology Group of Ontario Networked Information System. Probable causes of TRM were described. RESULTS: Among the 964 deaths identified, 821 were included. The median age at diagnosis was 6.6 years (range 0-18.8) and 51.8% had at least one relapse. Of the deaths examined, TRM occurred in 217/821 (26.4%) while 604/821 (73.6%) were due to progressive cancer. Deaths from TRM did not change over time. Using multiple regression, younger age, leukaemia diagnosis and absence of relapse were independently positively associated with TRM. The most common probable causes of TRM were respiratory, infection and haemorrhage. CONCLUSIONS: TRM was responsible for 26.4% of deaths in paediatric cancer. Underlying diagnosis, younger age and absence of relapse were associated with TRM and causes of TRM differed by diagnosis group. Future work should evaluate TRM rate and risk factors among newly diagnosed cancer patients

    Acetylcysteine has No Mechanistic Effect in Patients at Risk of Contrast-Induced Nephropathy - A Failure of Academic Clinical Science

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    Contrast‐induced nephropathy (CIN) is a major complication of imaging in patients with chronic kidney disease (CKD). The publication of an academic randomized controlled trial (RCT; n = 83) reporting oral (N)‐acetylcysteine (NAC) to reduce CIN led to > 70 clinical trials, 23 systematic reviews, and 2 large RCTs showing no benefit. However, no mechanistic studies were conducted to determine how NAC might work; proposed mechanisms included renal artery vasodilatation and antioxidant boosting. We evaluated the proposed mechanisms of NAC action in participants with healthy and diseased kidneys. Four substudies were performed. Two randomized, double‐blind, placebo‐controlled, three‐period crossover studies (n = 8) assessed the effect of oral and intravenous (i.v.) NAC in healthy kidneys in the presence/absence of iso‐osmolar contrast (iodixanol). A third crossover study in patients with CKD stage III (CKD3) (n = 8) assessed the effect of oral and i.v. NAC without contrast. A three‐arm randomized, double‐blind, placebo‐controlled parallel‐group study, recruiting patients with CKD3 (n = 66) undergoing coronary angiography, assessed the effect of oral and i.v. NAC in the presence of contrast. We recorded systemic (blood pressure and heart rate) and renal (renal blood flow (RBF) and glomerular filtration rate (GFR)) hemodynamics, and antioxidant status, plus biomarkers of renal injury in patients with CKD3 undergoing angiography. Primary outcome for all studies was RBF over 8 hours after the start of i.v. NAC/placebo. NAC at doses used in previous trials of renal prophylaxis was essentially undetectable in plasma after oral administration. In healthy volunteers, i.v. NAC, but not oral NAC, increased blood pressure (mean area under the curve (AUC) mean arterial pressure (MAP): mean difference 29 h⋅mmHg, P = 0.019 vs. placebo), heart rate (28 h⋅bpm, P < 0.001), and RBF (714 h⋅mL/min, 8.0% increase, P = 0.006). Renal vasodilatation also occurred in the presence of contrast (RBF 917 h⋅mL/min, 12% increase, P = 0.005). In patients with CKD3 without contrast, only a rise in heart rate (34 h⋅bpm, P = 0.010) and RBF (288 h⋅mL/min, 6.0% increase, P = 0.001) occurred with i.v. NAC, with no significant effect on blood pressure (MAP rise 26 h⋅mmHg, P = 0.156). Oral NAC showed no effect. In patients with CKD3 receiving contrast, i.v. NAC increased blood pressure (MAP rise 52 h⋅mmHg, P = 0.008) but had no effect on RBF (151 h⋅mL/min, 3.0% increase, P = 0.470), GFR (29 h⋅mL/min/1.73m², P = 0.122), or markers of renal injury. Neither i.v. nor oral NAC affected plasma antioxidant status. We found oral NAC to be poorly absorbed and have no reno‐protective effects. Intravenous, not oral, NAC caused renal artery vasodilatation in healthy volunteers but offered no protection to patients with CKD3 at risk of CIN. These findings emphasize the importance of mechanistic clinical studies before progressing to RCTs for novel interventions. Thousands were recruited to academic clinical trials without the necessary mechanistic studies being performed to confirm the approach had any chance of working

    Association of a de novo 16q copy number variant with a phenotype that overlaps with Lenz microphthalmia and Townes-Brocks syndromes

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    <p>Abstract</p> <p>Background</p> <p>Anophthalmia and microphthalmia are etiologically and clinically heterogeneous. Lenz microphthalmia is a syndromic form that is typically inherited in an X-linked pattern, though the causative gene mutation is unknown. Townes-Brocks syndrome manifests thumb anomalies, imperforate anus, and ear anomalies. We present a 13-year-old boy with a syndromic microphthalmia phenotype and a clinical diagnosis of Lenz microphthalmia syndrome.</p> <p>Case Presentation</p> <p>The patient was subjected to clinical and molecular evaluation, including array CGH analysis. The clinical features included left clinical anophthalmia, right microphthalmia, anteriorly placed anus with fistula, chordee, ventriculoseptal defect, patent ductus arteriosus, posteriorly rotated ears, hypotonia, growth retardation with delayed bone age, and mental retardation. The patient was found to have an approximately 5.6 Mb deletion of 16q11.2q12.1 by microarray based-comparative genomic hybridization, which includes the <it>SALL1 </it>gene, which causes Townes-Brocks syndrome.</p> <p>Conclusions</p> <p>Deletions of 16q11.2q12.2 have been reported in several individuals, although those prior reports did not note microphthalmia or anophthalmia. This region includes <it>SALL1</it>, which causes Townes-Brocks syndrome. In retrospect, this child has a number of features that can be explained by the <it>SALL1 </it>deletion, although it is not clear if the microphthalmia is a rare feature of Townes-Brocks syndrome or caused by other mechanisms. These data suggest that rare copy number changes may be a cause of syndromic microphthalmia allowing a personalized genomic medicine approach to the care of patients with these aberrations.</p

    The effect of chronic disease warning statements on alcohol-related health beliefs and consumption intentions among at-risk drinkers

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    Informing drinkers of the health risks associated with alcohol consumption via warning statements located on alcohol products can increase their capacity to make healthier choices. This study assessed whether exposing at-risk drinkers to warning statements relating to specific chronic diseases increases the extent to which alcohol is believed to be a risk factor for those diseases and influences consumption intentions. Australians drinking at levels associated with long-term risk of harm (n = 364; 72% male) completed an online survey assessing their drinking habits, beliefs in the link between alcohol and various diseases and drinking intentions. Respondents were then exposed to one of five statements advising of the potential risks associated with alcohol consumption (either cancer, liver damage, diabetes, mental illness or heart disease). Beliefs and drinking intentions were reassessed. Significant increases in the extent to which alcohol was believed to be a risk factor for diabetes, heart disease, mental illness and cancer were found. With the exception of the liver damage and heart disease statements, exposure to each statement was associated with a significant reduction in consumption intentions. Warning statements advising of the specific chronic diseases associated with alcohol consumption can produce favourable changes in drinking intentions among at-risk drinkers
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