110 research outputs found

    Proactive or Reactive? Optimal Management of an Invasive Forest Pest in a Spatial Framework

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    This paper offers a preliminary investigation into the conditions under which it might be optimal to engage in proactive management of a non-timber forest resource in the presence of an invasive species whose spread is unaffected by management action. Proactive management is defined as treating an uninfected area in order to encourage healthy ecosystem function, given that the arrival of the invasive is inevitable. Inspired by the problem of white pine blister rust in the Rocky Mountain west, the model was solved under varying assumptions concerning the scale of management action, benefit and costs, the discount rate, and uncertainty of spread. Results showed that proactive strategies tended to be optimal when, ceteris paribus, a) more resources are available for treatment; b) the costs of treatment are rapidly increasing in forest health, or conversely, the benefits of healthy and unhealthy stands are relatively similar; and c) the discount rate is low. The introduction of uncertainty did not significantly affect the likelihood of a proactive management strategy being optimal, but did show that the conditional probabilities of infection play important role in the decision of which uninfected stand should be treated if a choice is available to the manager.Crop Production/Industries, Resource /Energy Economics and Policy,

    Prevention of Catheter-Related Blood Stream Infection: Back to Basics?

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    Background: Central venous catheter (CVC)-related infections are a substantial problem in the intensive care unit (ICU). Our infection control team initiated the routine use of antiseptic-coated (chlorhexidine-silver sulfadiazine; Chx-SS) CVCs in our adult ICUs to reduce catheter-associated (CA) and catheter-related (CR) blood stream infection (BSI) as we implemented other educational and best practice standardization strategies. Prior randomized studies documented that the use of Chx-SS catheters reduces microbial colonization of the catheter compared with an uncoated standard (Std) CVC but does not reduce CR-BSI. We therefore implemented the routine use of uncoated Std CVCs in our surgical ICU (SICU) and examined the impact of this change. Hypothesis: The use of uncoated Std CVCs does not increase CR-BSI rate in an SICU. Methods: Prospective evaluation of universal use of uncoated Std CVCs, implemented November 2007 in the SICU. The incidences of CA-BSI and CR-BSI were compared during November 2006-October 2007 (universal use of Chx-SS CVCs) and November 2007-October 2008 (universal use of Std CVCs) by t-test. The definitions of the U.S. Centers for Disease Control and Prevention were used for CA-BSI and CR-BSI. Patient data were collected via a dedicated Acute Physiology and Chronic Health Evaluation (APACHE) III coordinator for the SICU. Results: Annual use of CVCs increased significantly in the last six years, from 3,543 (2001) to 5,799 (2006) total days. The APACHE III scores on day 1 increased from a mean of 54.4 in 2004 to 55.6 in 2008 (p = 0.0010; 95% confidence interval [CI] 1.29-5.13). The mean age of the patients was unchanged over this period, ranging from 58.2 to 59.6 years. The Chx-SS catheters were implemented in the SICU in 2002. Data regarding the specific incidence of CR-BSI were collected beginning at the end of 2005, with mandatory catheter tip cultures when CVCs were removed. Little difference was identified in the incidence of BSI between the interval with universal Chx-SS use and that with Std CVC use. (Total BSI 0.7 vs. 0.8 per 1,000 catheter days; CA-BSI 0.5 vs. 0.8 per 1,000 catheter days; CR-BSI 0.2 vs. 0 per 1,000 catheter days.) No difference was seen in the causative pathogens of CA-BSI or CR-BSI. Conclusion: Eliminating the universal use of Chx-SS-coated CVCs in an SICU with a low background incidence of CR-BSIs did not result in an increase in the rate of CR-BSIs. This study documents the greater importance of adherence to standardization of the processes of care related to CVC placement than of coated CVC use in the reduction of CR-BSI.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90456/1/sur-2E2009-2E082.pd

    Aorto-ventricular tunnel

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    Aorto-ventricular tunnel is a congenital, extracardiac channel which connects the ascending aorta above the sinutubular junction to the cavity of the left, or (less commonly) right ventricle. The exact incidence is unknown, estimates ranging from 0.5% of fetal cardiac malformations to less than 0.1% of congenitally malformed hearts in clinico-pathological series. Approximately 130 cases have been reported in the literature, about twice as many cases in males as in females. Associated defects, usually involving the proximal coronary arteries, or the aortic or pulmonary valves, are present in nearly half the cases. Occasional patients present with an asymptomatic heart murmur and cardiac enlargement, but most suffer heart failure in the first year of life. The etiology of aorto-ventricular tunnel is uncertain. It appears to result from a combination of maldevelopment of the cushions which give rise to the pulmonary and aortic roots, and abnormal separation of these structures. Echocardiography is the diagnostic investigation of choice. Antenatal diagnosis by fetal echocardiography is reliable after 18 weeks gestation. Aorto-ventricular tunnel must be distinguished from other lesions which cause rapid run-off of blood from the aorta and produce cardiac failure. Optimal management of symptomatic aorto-ventricular tunnel consists of diagnosis by echocardiography, complimented with cardiac catheterization as needed to elucidate coronary arterial origins or associated defects, and prompt surgical repair. Observation of the exceedingly rare, asymptomatic patient with a small tunnel may be justified by occasional spontaneous closure. All patients require life-long follow-up for recurrence of the tunnel, aortic valve incompetence, left ventricular function, and aneurysmal enlargement of the ascending aorta

    Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

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    Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

    Ontogeny of melanophore photosensitivity in rainbow trout (Oncorhynchus mykiss)

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    Migratory species experience morphological and physiological changes during transitions between different life stages. In particular, modification of sensory systems is critical for animals to adapt to new environments. For example, to prepare for entry into seawater, salmonids undergo smoltification with dramatic changes in ultraviolet photoreceptors and polarized vision, which are important for orientation and foraging behaviours. Extraretinal organs are also involved in photoreception; however, the ontogenetic development of extraretinal photoreceptors is not well known, especially in migratory species. Here, we investigated whether rainbow trout dermal photoreceptors, melanophores, undergo change in spectral sensitivity during smoltification and which candidate molecules may account for this ontogenetic alteration. Our results showed that, contrary to parr melanophores which are insensitive to light, smolt melanophores displayed chromatic photoresponses with the emergence of cryptochrome and melanopsin expression. We suggest that these modifications may benefit the active foraging behaviour of smolts and enable adaptation to variable environments

    Proactive or Reactive? Optimal Management of an Invasive Forest Pest in a Spatial Framework

    No full text
    This paper offers a preliminary investigation into the conditions under which it might be optimal to engage in proactive management of a non-timber forest resource in the presence of an invasive species whose spread is unaffected by management action. Proactive management is defined as treating an uninfected area in order to encourage healthy ecosystem function, given that the arrival of the invasive is inevitable. Inspired by the problem of white pine blister rust in the Rocky Mountain west, the model was solved under varying assumptions concerning the scale of management action, benefit and costs, the discount rate, and uncertainty of spread. Results showed that proactive strategies tended to be optimal when, ceteris paribus, a) more resources are available for treatment; b) the costs of treatment are rapidly increasing in forest health, or conversely, the benefits of healthy and unhealthy stands are relatively similar; and c) the discount rate is low. The introduction of uncertainty did not significantly affect the likelihood of a proactive management strategy being optimal, but did show that the conditional probabilities of infection play important role in the decision of which uninfected stand should be treated if a choice is available to the manager
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