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The validation of biomarkers has become a key goal of translational biomedical research. The purpose of this article is to discuss the role of biomarkers in the management of acute lung injury (ALI) and related research. Biomarkers should be sensitive and specific indicators of clinically important processes and should change in a relevant timeframe to affect recruitment to trials or clinical management. We do not believe that they necessarily need to reflect pathogenic processes. We critically examined current strategies used to identify biomarkers and which, owing to expedience, have been dominated by reanalysis of blood derived markers from large multicenter Phase 3 studies. Combining new and existing validated biomarkers with physiological and other data may add predictive power and facilitate the development of important aids to research and therapy.
The syndrome acute lung injury (ALI) and its more severe counterpart acute respiratory distress syndrome (ARDS) are defined by radiographic and physiological changes that characterize patients with acute lung failure (Table 1) [1]. All age groups may be affected, although the syndrome has a higher incidence and mortality in older people. Across all ages the incidence is approximately 200,000 cases per year in the United States with a mortality of around 35% [2]. Survivors face a long-term reduction in quality of life; for example, only 54% of survivors were able to return to work 12 months after hospital discharge [3].
The validation of biomarkers, for use in clinical trials and ultimately in practice, has become a central tenet of translational biomedical research [4]. The purpose of this article is to discuss the role of biomarkers in the management of ALI and related research. We shall not present a state of the art review of the field of all the biomarkers that have been investigated in this field, excellent examples of which have been produced recently [5,6]. Rather, we shall question current strategies to identify biomarkers and whether what has been achieved thus far has advanced the field.
The natural history of acute lung injury
Regardless of the wide variety of insults that cause or contribute to the development of ALI, the response of the lung is largely stereotypic. A combination of tissue injury and inflammation affecting the gas exchange surface of the lung, the alveolar-capillary membrane, causes high permeability pulmonary edema. The presence of a protein-rich inflammatory exudate in the airspace impairs surfactant function [7]. The resulting collapse and consolidation of the lung causes profound hypoxemia because inflammatory mediators induce changes in the control of vascular tone that disable hypoxic pulmonary vasoconstriction [8]. Loss of pulmonary capillary surface area associated with localized lung destruction and occlusion of the vascular bed by intravascular thrombosis, increases the anatomical dead space, itself associated with a poor outcome [9], giving rise to carbon dioxide retention. Host factors, both inherited [10,11] and acquired, influence individual susceptibility, (for example, excessive alcohol consumption predisposes, while diabetes mellitus protects) [12,13]. Precipitating causes or risk factors, which often "hunt in packs", either affect the lung directly (pneumonia, aspiration of stomach contents and thoracic trauma) or cause ALI indirectly through a systemic inflammatory response syndrome (SIRS) associated with multiple organ dysfunction, exemplified by severe sepsis and transfusion related ALI [14]. These causes, to a large part, determine the initial clinical course and outcome, but most patients subsequently require invasive mechanical ventilation in an intensive care unit to maintain adequate gas exchange and often other organ supports.
While the development of pulmonary fibrosis in a patient with ALI predicts the requirement for prolonged respiratory support and a poor outcome [15], relatively little is known about the processes that determine the resolution of inflammation, injury and subsequent lung repair [16]. The consecutive three-phase pathological model of ALI (exudative, proliferative and fibrotic) is a gross over-simplification. Fibrosis is evident histologically as early as a week after the onset of the disorder [17] and procollagen III peptide, a precursor of collagen synthesis, is elevated in the broncho-alveolar lavage (BAL) fluid of ARDS patients at the time of tracheal intubation [18]. Indeed, not only is the injured lung known to be heterogeneously affected [19], it also seems likely from the examination of lavage samples from patients that these pathological processes coincide in the same lung region [20]. Similarly, while several pro-inflammatory mediators are also pro-fibrotic, distinct patterns of gene expression are associated with acute inflammation and fibrosis in the injured lung, suggesting that fibrosis is not simply an inevitable consequence of unresolved inflammation [21]. Indeed, current thinking emphasizes the primary role of disordered epithelial repair, which may be contributed to by repeated or persistent injury and inflammation, in driving a pathological fibrotic response [22].
Despite years of concerted effort and very many clinical trials, a minority of which have been capable of producing a definitive result, there are no treatments (as opposed to modifications of organ support [23,24]) that improve the outcome of patients with ALI [25]. What has become evident, both in this field and in critical care in general, is the extent and importance of iatrogenic injury. Hence, half of ALI arises in patients who were subjected to mechanical ventilation for another reason: the four major culprits being mechanical ventilation that targets normal blood gas parameters, transfusion of blood products, excessive fluid resuscitation and hospital acquired pneumonia (Figure 1) [26-29]. Accordingly, recent epidemiological evidence suggests that targeting hospital acquired injury can halve the incidence of ARDS despite an increase in patients' severity of illness, the number of comorbidities and the prevalence of major ARDS risk factors [30].
Figure 1. Process-based pathogenesis of ALI. Traditional causes of or risk factors for ALI maybe contributed to in certain patients by hospital-acquired harm (red) and modified in their potency for causing ALI by multiple patient's susceptibility (blue). Depending on the balance of these factors the processes that determine the natural history of ALI are initiated in the lung.
Hence, studying patients with ALI is a challenge because the syndrome is the end result of an almost infinite variety of scenarios. These range from young fit patients with severe pneumonia or thoracic trauma to older patients who fail to recover from routine procedures, suffer complications, require respiratory support because of a combination of a chronic cardio-respiratory condition and hospital-acquired pneumonia, and ultimately develop ARDS on a ventilator. As a consequence, the water is muddied both by heterogeneity in the host and in the risk factors, and by the variety of other co-incident processes. Furthermore, it is often difficult to define precisely when the syndrome started, which may have a dramatic effect on measured variables in cases where the condition changes rapidly. Finally, variable management regimens may contribute to patient heterogeneity, both in the face of clear evidence (for example, poor adherence to low tidal volume ventilation) [31] and where evidence is lacking (for example, in the use of adjuncts to respiratory support like prone positioning, inhaled nitric oxide and high frequency oscillation). Conversely, critically ill patients are closely monitored, physiological data are electronically stored and their clinical condition may paradoxically render them more amenable to undergoing invasive procedures.
Why invest in biomarkers for ALI?
Biomarkers are potentially useful as guides to clinical management and as research tools. In the clinical setting there is a high premium on biomarker data being easily and safely obtained within a timeframe that is relevant to the disease process (Table 2). For example, an indicator of poor prognosis that may encourage referral to a specialist center would need to be available within hours, whereas a marker of ventilator-associated lung injury (VALI) that was being used to fine-tune ventilator settings would have to be "turned around" within minutes. No biomarkers that are currently available have penetrated routine clinical practice with the possible exception of the use of procalcitonin (PCT) to diagnose sepsis in critically ill patients and to guide their antibiotic therapy [32]. Sepsis syndromes commonly both cause and complicate ALI; ventilator associated pneumonia in particular frequently exacerbates ALI causing diagnostic difficulty. Procalcitonin levels correlated with severe sepsis and bacteraemia [33], but did not consistently differentiate survivors from non-survivors [34]. A PCT-based algorithm guiding initiation and duration of antibiotic therapy in critically ill patients with suspected bacterial infection was associated with a 23% relative reduction in antibiotic exposure with no significant increase in mortality [32]. Aside from this role in limiting antibiotic exposure, a recent review of the role of PCT in diagnosing ventilator associated pneumonia concluded that the biomarker showed good specificity but low sensitivity [35].
Table 2. Proposed characteristics of an ideal biomarker for acute lung injury
Clinical research in ALI has used biomarkers as surrogate outcomes for early Phase 2 studies and may in the future be valuable in categorizing patients into subgroups that are predicted to be most likely to benefit from particular interventions. For example, in the single-centre BALTI 1 study 40 patients with ALI were enrolled to demonstrate the ability of seven days of treatment with intravenous salbutamol to decrease extravascular lung water measured by the single indicator transpulmonary thermodilution method (PiCCO, Pulsion Medical Systems, Munich, Germany) [36]. The resolution of pulmonary edema is central to recovery from ALI as it entails defervescence of air space inflammation and restoration of a functioning alveolar-capillary membrane. Accordingly, elevated extravascular lung water measured using this technique early in the course of ALI/ARDS, particularly if indexed to predicted body weight, was associated with a poor outcome [37-39]. The initial ratio of PaO2/FiO2 was reported to be lower in non-survivors [9,40-42] and predicted mortality in univariate analyses [9,40,42]. In addition, in one large cohort study, PaO2/FiO2 ratio was an independent predictor of mortality [42]. However, this variable does not take into account the mode or even presence of mechanical ventilation and apart from measurements at the extremes of the spectrum, it is generally not considered to be a robust predictor of outcome in ALI. Hence, the use of a surrogate rather than a clinical end-point, such as ventilator-free days or intensive care unit length of stay, decreased the recruitment target to what was achievable for a single center. However, in hindsight it is arguable whether this positive result then justified the investment in two Phase 3 large multicenter trials, which failed to show a survival benefit from using both inhaled and intravenous formulations of short-acting beta agonists [25].
The use of biomarkers to refine patient populations, such that clinical trials will be most likely to provide a definitive answer requiring the fewest patients, is particularly appealing for application to research involving patients with a heterogeneous syndrome like ALI. This could be beneficial by helping to characterize either a group of patients with a high mortality where mortality is the primary outcome measure, or by identifying patients in whom a pathological process, which is targeted by an intervention, is particularly prominent.
Characteristics of ideal biomarkers for ALI
Proposed criteria for characterizing ideal biomarkers for ALI, most of which are self-explanatory are listed in Table 2. It has been argued that biomarkers should inform or, at least, relate to the disease pathogenesis [43]. We disagree for philosophical reasons. Why confuse elucidating mechanisms with the pragmatic business of identifying biomarkers? We prefer as wide a definition as possible; for example, the electrocardiograph has been one of the most useful biomarkers in medicine but not much can be learned about the pathogenesis of myocardial infarction through its study.
The current definition of ALI/ARDS is such that biomarkers of the established syndrome are largely redundant. An exception would be a biomarker that was specific to the pathological process described as diffuse alveolar damage. That is, a biomarker that could exclude patients from studies who fulfilled the diagnostic criteria but who essentially have a distinct disease, which may have a different natural history and specific treatment, for example, cardiogenic pulmonary oedema, eosinophilic pneumonia and pulmonary embolism. Most studies have attempted to correlate selected biomarkers with disease severity or death, which is potentially useful both clinically to help target resources and more expensive or invasive management strategies, and in helping to power research studies using mortality as the primary outcome.
We propose that the use of biomarkers in a complex syndrome like ALI is most likely to be effective when they are specific to an individual component or process that can be manipulated. One productive approach has been to measure plasma and BAL fluid levels of mediators as a reflection of systemic and pulmonary inflammation respectively. In samples from large multicenter trials elevated levels of mediators, like soluble tumor necrosis factor-alpha receptors (sTNFR) 1 and 2 [44], soluble intercellular adhesion molecule-1 [45], and interleukin (IL)-6 [23] were associated with adverse outcomes in patients with ALI. The limitations of this strategy are that these mediators have multiple effects, have no specificity to the lung and there is no convincing evidence that manipulating the inflammatory response benefits patients with ALI. Partly because of the realization that VALI plays a major part in the pathogenesis of ALI and, as a result, many large studies have been performed examining the effects of ventilator strategies, a lot has been learned about the responses of popular biomarkers in patients undergoing protective and standard ventilation [6]. Hence, circulating mediators of inflammation (sTNFR [45], IL-6, -8 and -10 [46]), indicators of epithelial cell injury (soluble advanced glycation end-product receptors (sRAGE)) [47] and surfactant protein-D [48]) and components of the coagulation system (protein-C and plasminogen activator inhibitor-1 [49]) have all been promoted as biomarkers of VALI. However, because the proposed mechanism, whereby VALI kills patients through the exacerbation of local injury and inflammation, the mediators of which then leak into the systemic circulation causing multiple organ dysfunction [50], it would be surprising if there was not considerable overlap between markers of VALI, tissue injury, inflammation and a poor prognosis. In other words, these biomarkers inevitably lack specificity for individual processes or outcomes.
More recently the power of combining clinical parameters with a panel of traditional biomarkers to predict mortality in patients with ALI using a variety of statistical techniques has been examined in the large datasets and sample stores resulting from ARDS Network studies [51,52]. In one of these studies [52], the six clinical predictors were: age, the underlying cause, APACHE III score, plateau pressure, number of organ failures, and alveolar-arterial difference in the partial pressure of oxygen measured at enrollment prior to randomization. Eight biomarkers were measured in baseline plasma samples from enrolled patients that reflected endothelial and epithelial injury, inflammation and coagulation. A "reduced model", including just the APACHE III score, age, SP-D, and IL-8, performed almost as well as that which included all parameters and biomarkers. However, the additional predictive value of the plasma biomarkers added to the clinical predictors alone was modest; thus, further work will be needed to test the value of these biomarkers over clinical predictors alone. Furthermore, while the inclusion of biomarker data into a model improved the accuracy of mortality prediction, the predicted risk of death for the patients who ultimately died remained lower than 50%, suggesting that important contributors to mortality may not have been accounted for by the model [51].
Model systems for biomarker development
An alternative approach to examining clinical samples is to test the validity of existing or novel candidate biomarkers using models systems, in which the signal-to-noise ratio is likely to be more favorable and the time course of the biomarker's response can be more precisely determined (Figure 2). For this purpose, we believe that human models are likely to be more useful than animal models, despite the undoubted contribution of the latter to our understanding of the syndrome's pathogenesis [53,54]. For example, at the most basic level comparative proteomic analysis between BAL fluid from a patient and a mouse model of ALI identified only 21 homologous proteins [55].
Figure 2. ALI biomarkers: Ventilator Induced Lung Injury experimental models and observational clinical studies. High tidal volume ventilation (tidal volume in excess of 10 ml/kg predicted body weight) may be used to induce lung injury in experimental models (left) but, through the overspill of inflammatory mediators into the circulation (biotrauma), multiple-organ dysfunction may follow. Biomarkers may be assayed directly from the lungs (black), from the circulation (red) or as indices of dysfunction related to other organs (green). In clinical studies (right), injured lungs are susceptible to damage even when gold standard mechanical ventilation (tidal volume 6 ml/kg predicted body weight) is used. However, in the presence of existing lung injury several processes are likely to be concurrent, both affecting the lungs directly (inflammation, tissue injury, coagulation, fibrosis) and indirectly from other affected organs (sepsis). Hence, the relationship between any biomarker and ventilator settings is likely to be obscured by multiple unknowns. BAL bronchoalveolar lavage, SIRS systemic inflammatory response syndrome, MODS multiple organ dysfunction syndrome.
For an example of a human model of ALI, one lung ventilation (OLV), a technique required to facilitate lung resection surgery, has been exploited to investigate potential biomarkers of VALI [56,57]. One-lung ventilation may be a useful model of VALI because it is associated with a smaller lung volume available for ventilation, localized lung collapse or atelectasis and impaired oxygenation, resulting in exposure of the ventilated lung to volutrauma, repeated opening of collapsed airspaces (atelectotrauma), and a high inspired oxygen concentration. High tidal volume and airway pressure during OLV correlated with the development of ALI in patients undergoing lung resection {Fernandez-Perez, 2009 #1309 [58]; Licker, 2003 #38; Jeon, 2009 #532} and the incidence of ALI after lung resection over a five-year period was lower, compared to an historical control group, after introduction of a protective OLV protocol [59]. In small prospective studies the use of low tidal volume OLV was associated with reduced biomarkers of pulmonary and systemic inflammation {Michelet, 2006 #4882; [60]} Finally, in an observational prospective study of 30 patients, exhaled breath condensate pH was reduced within minutes of starting OLV suggesting that it may represent a robust and direct means of sampling the milieu of the lung. While, in the clinical setting the effect on exhaled breath condensate pH of changing ventilator settings may be drowned by "noise" from co-incident inflammatory processes in the lung, it may hold promise as a non-invasive real-time biomarker of VALI, despite the fact that the mechanism by which exhaled breath condensate acidification is poorly understood (Figure 2).
Future directions
Despite analyzing samples from large well-designed trials, there is no biomarker in current use that positively identifies patients with the classical histopathological appearances of diffuse alveolar damage, that predicts a poor outcome or that specifically identifies a pathological process [61].
We propose that future biomarker development be driven by novel therapies and support modalities. Biomarkers potentially combined with physiological and genomic data should be used to identify patient groups for research studies and individuals who are most likely to gain from targeted therapies. For example, novel extra-corporeal carbon dioxide removal (ECCO2R) systems that will make these techniques safer, cheaper and more readily available should stimulate the search for novel biomarkers for VALI. The demonstration that gold standard low tidal volume protective ventilation was associated with signs of over-distension on CT scanning, elevated plasma markers of inflammation and a plateau airway pressure greater than 28 cmH2O in approximately a third of patients with ARDS provided a readily identifiable population on which the effectiveness of novel ECCO2R devices could be tested [62]. In a subsequent study, a group of patients with ARDS was identified by their having a plateau airway pressure greater than 28 cmH2O and in whom low tidal volume ventilation was presumed to be causing significant VALI. For these patients a novel ECCO2R device (DeCap, Hemodec, Salerno, Italy) enabled the research team to decrease tidal volume, further targeting a plateau airway pressure of less than 25 cmH2O, which was associated with a lower radiographic index of lung injury and lower levels of lung derived inflammatory cytokines [63].
Targeting component processes of ALI other than inflammation, tissue injury and VALI should be developed and incentive for this will be greatly increased as novel therapeutics are introduced (Figure 1). We believe that advances in the understanding and treatment of pulmonary fibrosis combined with the relative chronicity of this process complicating ALI, which leads to patients with a low pulmonary compliance struggling to wean from ventilatory support, make this process suitable for targeted intervention. For example, the significance of the epithelial cell integrin alpha-v beta-6 in activating transforming growth factor beta-1 (TGFβ-1) both in the evolution of ALI and repair by fibrosis has only recently been appreciated [64,65]. Supposing an effective means of targeting this pathway existed, how could the decision to administer a novel therapy be informed using biomarkers? Patients who are susceptible to or have over-activity of this pathway may be identified using a genomic approach or by identifying a biomarker that is either specific to this process or a damaging fibrotic response. Indeed, the feasibility of this approach has been illustrated by the observation that elevated levels of procollagen peptide III in lavage fluid from patients on Day 3 of ARDS were independent risk factors for mortality [66]. This so-called personalized approach has been pioneered in other chronic lung diseases but the principles are theoretically applicable to ALI [67].
Biomarker development for patients with ALI is an essential component of progress in translational medicine in this challenging area. Potential pitfalls on the road to successfully carrying out translational medicine to help patients with ALI include:
1. the heterogeneity of cases (ALI is a syndrome resulting from any cause of acute lung failure),
2. the large iatrogenic contribution to pathogenesis, rendering standardization of care crucial,
3. the gas exchange surface of the lung is relatively inaccessible to investigation and indispensible, so that pathogenic process are not well understood, and
4. the timeframes of the condition are short, such that windows for intervention may close in the time that it takes to analyse samples and process data.
Biomarkers should be sensitive and specific indicators of clinically important processes and should change in a relevant timeframe to affect recruitment to trials or clinical management. They do not necessarily need to reflect pathogenic processes. Combining biomarkers with physiological and other data may add predictive power and stimulate the development of important aids to research and therapy. While biomarkers have not yet had a major role in the management of ALI and the development of novel therapies, it is possible and even likely that biomarkers will be developed that will help to target an increasing arsenal of disease modifying therapies in the future.
ALI: acute lung injury; ARDS: Acute Respiratory Distress Syndrome; BAL: broncho-alveolar lavage; ECCO2R: extra-corporeal carbon dioxide removal; OLV: one lung ventilation; PCT: procalcitonin; SIRS: Systemic Inflammatory Response Syndrome; sTNFR: soluble tumour necrosis factor-alpha receptors; TGFβ-1: transforming growth factor beta-1; VALI: ventilator associated lung injury.
Competing interests
MG received consultancy fees, educational grants and served on advisory boards for GlaxoSmithKline (Middlesex, UK). AP and MH have not disclosed any potential conflicts of interest.
Authors' contributions
All authors contributed equally to the inception and execution of this article and read and approved the final manuscript.
This work was funded and supported by the NIHR Respiratory Disease Biomedical Research Unit at the Royal Brompton and Harefield NHS Foundation Trust and Imperial College London. The views expressed in this publication are those of the authors and not necessarily those of the NHS, the National Institute for Health Research or the Department of Health.
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Am J Physiol Lung Cell Mol Physiol 2005, 288:L426-431. PubMed Abstract | Publisher Full Text
Calfee CS, Eisner MD, Parsons PE, Thompson BT, Conner ER Jr, Matthay MA, Ware LB: Soluble intercellular adhesion molecule-1 and clinical outcomes in patients with acute lung injury.
Intensive Care Med 2009, 35:248-257. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Parsons PE, Eisner MD, Thompson BT, Matthay MA, Ancukiewicz M, Bernard GR, Wheeler AP: Lower tidal volume ventilation and plasma cytokine markers of inflammation in patients with acute lung injury.
Crit Care Med 2005, 33:1-6.
discussion 230-232PubMed Abstract | Publisher Full Text
Calfee CS, Ware LB, Eisner MD, Parsons PE, Thompson BT, Wickersham N, Matthay MA, NHLBI ARDS Network: Plasma receptor for advanced glycation end-products and clinical outcomes in acute lung injury.
Thorax 2008, 63:1083-1089. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Eisner MD, Parsons P, Matthay MA, Ware L, Greene K: Plasma surfactant protein levels and clinical outcomes in patients with acute lung injury.
Thorax 2003, 58:983-988. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Ware LB, Matthay MA, Parsons PE, Thompson BT, Januzzi JL, Eisner MD: Pathogenetic and prognostic significance of altered coagulation and fibrinolysis in acute lung injury/acute respiratory distress syndrome.
Crit Care Med 2007, 35:1821-1828. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Tremblay LN, Slutsky AS: Ventilator-induced injury: from barotrauma to biotrauma.
Proc Assoc Am Physicians 1998, 110:482-488. PubMed Abstract
Calfee CS, Ware LB, Glidden DV, Eisner MD, Parsons PE, Thompson BT, Matthay MA, National Heart, Blood, and Lung Institute Acute Respiratory Distress Syndrome Network: Use of risk reclassification with multiple biomarkers improves mortality prediction in acute lung injury.
Crit Care Med 2011, 39:711-717. PubMed Abstract | Publisher Full Text
Ware LB, Koyama T, Billheimer DD, Wu W, Bernard GR, Thompson BT, Brower RG, Standiford TJ, Martin TR, Matthay MA: Prognostic and pathogenetic value of combining clinical and biochemical indices in patients with acute lung injury.
Chest 2010, 137:288-296. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Proudfoot AG, McAuley DF, Griffiths MJ, Hind M: Human models of acute lung injury.
Dis Model Mech 2011, 4:145-153. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Bastarache JA, Blackwell TS: Development of animal models for the acute respiratory distress syndrome.
Dis Model Mech 2009, 2:218-223. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Gharib SA, Nguyen E, Altemeier WA, Shaffer SA, Doneanu CE, Goodlett DR, Schnapp LM: Of mice and men: comparative proteomics of bronchoalveolar fluid.
Eur Respir J 2010, 35:1388-1395. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Bastin AJ, Sato H, Davidson SJ, Quinlan GJ, Griffiths MJ: Biomarkers of lung injury after one-lung ventilation for lung resection.
Respirology 2011, 16:138-145. PubMed Abstract | Publisher Full Text
Moloney ED, Griffiths MJ: Protective ventilation of patients with acute respiratory distress syndrome.
Br J Anaesth 2004, 92:261-270. PubMed Abstract | Publisher Full Text
van der Werff YD, van der Houwen HK, Heijmans PJ, Duurkens VA, Leusink HA, van Heesewijk HP, de Boer A: Postpneumonectomy pulmonary edema. A retrospective analysis of incidence and possible risk factors.
Chest 1997, 111:1278-1284. PubMed Abstract | Publisher Full Text
Licker M, Diaper J, Villiger Y, Spiliopoulos A, Licker V, Robert J, Tschopp JM: Impact of intraoperative lung-protective interventions in patients undergoing lung cancer surgery.
Crit Care 2009, 13:R41. PubMed Abstract | BioMed Central Full Text | PubMed Central Full Text
Schilling T, Kozian A, Huth C, Buhling F, Kretzschmar M, Welte T, Hachenberg T: The pulmonary immune effects of mechanical ventilation in patients undergoing thoracic surgery.
Anesth Analg 2005, 101:957-965. PubMed Abstract | Publisher Full Text
Spragg RG, Bernard GR, Checkley W, Curtis JR, Gajic O, Guyatt G, Hall J, Israel E, Jain M, Needham DM, Randolph AG, Rubenfeld GD, Schoenfeld D, Thompson BT, Ware LB, Young D, Harabin AL: Beyond mortality: future clinical research in acute lung injury.
Am J Respir Crit Care Med 2010, 181:1121-1127. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Terragni PP, Rosboch G, Tealdi A, Corno E, Menaldo E, Davini O, Gandini G, Herrmann P, Mascia L, Quintel M, Slutsky AS, Gattinoni L, Ranieri VM: Tidal hyperinflation during low tidal volume ventilation in acute respiratory distress syndrome.
Am J Respir Crit Care Med 2007, 175:160-166. PubMed Abstract | Publisher Full Text
Terragni PP, Del Sorbo L, Mascia L, Urbino R, Martin EL, Birocco A, Faggiano C, Quintel M, Gattinoni L, Ranieri VM: Tidal volume lower than 6 ml/kg enhances lung protection: role of extracorporeal carbon dioxide removal.
Anesthesiology 2009, 111:826-835. PubMed Abstract | Publisher Full Text
Munger JS, Harpel JG, Giancotti FG, Rifkin DB: Interactions between growth factors and integrins: latent forms of transforming growth factor-beta are ligands for the integrin alphavbeta1.
Mol Biol Cell 1998, 9:2627-2638. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Pittet JF, Griffiths MJ, Geiser T, Kaminski N, Dalton SL, Huang X, Brown LA, Gotwals PJ, Koteliansky VE, Matthay MA, Sheppard D: TGF-beta is a critical mediator of acute lung injury.
J Clin Invest 2001, 107:1537-1544. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Clark JG, Milberg JA, Steinberg KP, Hudson LD: Type III procollagen peptide in the adult respiratory distress syndrome. Association of increased peptide levels in bronchoalveolar lavage fluid with increased risk for death.
Ann Intern Med 1995, 122:17-23. PubMed Abstract
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N Engl J Med 2004, 350:2129-2139. PubMed Abstract | Publisher Full Text
Pre-publication history
The pre-publication history for this paper can be accessed here:


text:
1. Chop onion, mint leaves, parsley, tomatoes and green pepper, set aside.
2. Scoop the eggplant, zucchini, tomato and English green pepper set aside.
3. In a pot sauté the onions and tomatoes in olive oil for some time.
4. Add the rice, parsley, mint leaves, hot peppers, tomato paste and other spices.
5. Add water and cook the rice.
6. Fill the zucchini, eggplant, green pepper and tomato with the rice mixture and cover the opening with a small piece of tomato.
7. In a pan, put the stuffed vegetables and add water to it. Spread tomato sauce on top and cook until the vegetables are soft and cooked.
8. Serve with steamed rice of flat bread.

subset: commoncrawl


text:
As cash-strapped customers cut spending, spas and gyms are doing all they can to keep a place in people's budgets.
Beyond deep discounts, some are adopting a recession spin: touting services as stress reducers, not indulgences, and highlighting the economic benefits of "wellness."
A Gold's Gym program — deemed "Fat-O-Nomics" — centers on money people can save by shedding excess weight. One stat: Being 50 pounds overweight burns nine extra gallons of gasoline per year.
"The cost of a lot of goods has gone up," spokesman Dave Reiseman says. "We're aware that there are stories out there asking, 'Is the gym membership worth it?' "
The Westin New York in Times Square has turned layoffs into sales opportunity. A "pink slip pick-me-up" spa promotion gives 20% off a facial from 10 a.m. to 2 p.m. daily.
"If you're unemployed, you need a pick-me-up — and you need to look good on your interviews," spa director Nicole Morris says.
As spa owners "feel the pinch" of consumer cutbacks, they're also all aggressively touting good, old-fashioned discounts via e-mail blasts and website updates, says Larry Oskin, spokesman for the Day Spa Association.
Businesses listed on website SpaFinder's directory service are slashing prices, President Susie Ellis says. The number of discount deals offered on its website and in its e-mail newsletter is up 25% to 30% vs. a year ago.
Spa and health club sales for 2008 aren't in yet. But on the gym front, signs of trouble started last year. Membership dropped in 2007 for the first time in more than a decade to 41.5 million from 42.7 million in 2006, says the International Health Racquet & Sportsclub Association.
Debbie Goldman of Manhasset Hills, N.Y., is keeping up her gym routine, but saving. She was an off-and-on-again member of upscale gym chain Equinox for more than 10 years, but when she got her $1,500 yearly renewal bill in September, she decided it was "too extravagant in these times." She opted for an LA Fitness chain offer of two years for $1,200.
To cater to current clients — and lure new ones — Equinox is one of the gyms playing up "mind-body balance" in stressful times.
Equinox has run full-page newspaper ads and updated its website to promote "mind over madness." Say the promotions: "In these changing times, make a renewed commitment to yourself to lead a healthy life." Each has a list of healthy endeavors — such as meditating and eating well. Of course, exercise tops the list.
Recent ads from rival gym chain Town Sports International proclaim "Protect your most important asset. Your health." They also touted an initiation fee cut to $59 from $149.
Says Town Sports marketing chief Sean O'Hearen: "We're trying to encourage our current and potential customers to focus on things they can control. Your health is one of them."
Botox providers are also doing all they can to keep their bottom lines looking good.
To lure cash-strapped clients, plastic surgeons and dermatologists have rolled out promotions for the wrinkle-reducer, including a recent "Boootox" special for Halloween.
Botox injections typically cost about $500 per site — such as between the eyebrows — according to the American Society of Plastic Surgeons. It says demand is firm but vulnerable. Botox-maker Allergan reported third-quarter sales up 7% to $318 million, but short of analysts' expectations.


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A look at the Prison Awareness Program at the Gwinnett County Comprehensive Correctional Complex in Lawrenceville. **WARNING** This video contains subject matter and language that may be disturbing to some viewers.**
As of Monday, June 25, 2012
© Copyright 2015 Gwinnett Daily Post
LAWRENCEVILLE -- It's 5:50 p.m. in the prison lobby. One kid has shown up with his pants sagging, exposing a crumbled bouquet of boxer shorts. In the eyes of Officer Eugene Hollis, a towering stack of discipline in paramilitary garb and elbow pads, the kid has committed a faux pas that inmates will misconstrue as an invitation. "Pull your pants up," Hollis says in an imposing baritone. "I shouldn't be looking at your drawers."
Hollis orders the kid, 15-year-old probationer Miles Holt of Lawrenceville, outside the lobby of the Gwinnett County Comprehensive Correctional Complex, where he files in with nine other youths. Each has run afoul of the law or their parents' patience. Another kid, an accused marijuana dealer in a black T-shirt, smirks. Bad idea. Hollis loathes smirking.
"You hard-headed?" Hollis says. At nearly 6 feet, 5 inches and 310 pounds, he played offensive line at Albany State University before a bum ankle sidetracked his NFL ambitions. Beside him, the teen is miniscule. The smirking ceases.
"This right here is prison, man," Hollis says, frisking their pockets with gloved hands, breaking a sweat. "There's cats in here that like little boys -- you know that?"
Thus begins a typical evening at Gwinnett's Prison Awareness Program, an unflinching glimpse at prison life for miscreants under age 18 that leaders say is unique in metro Atlanta. Held the first three Wednesdays of each month -- and every three months for girls -- the two-hour program is intense and intimidating, and while the participants' safety is never jeopardized, volunteers like Hollis are adept at making them think it is. Since the early 1990s, the program has been a crash course in things like shower shankings, weapons made of socks and rocks and brutal fights over $1 Honey Buns.
For his volunteer efforts, Hollis, the program's coordinator since 2008, was awarded the Medal of Merit earlier this year, a Gwinnett Chamber of Commerce honor for law enforcement officers who show commitment outside the regular scope of duty.
Last year, 314 boys and 89 girls endured the program as part of the disposition of their cases, said Jesse Lawler, Gwinnett Juvenile Court administrator. Local recidivism data is hard to come by, but Lawler said juvenile probation officers report "positive results" from most participants.
"This program gets (their) attention," Lawler said. "(It) gives them insight into the consequences of their actions, and the reality of the path they may be headed down."
At the state level, the Georgia Department of Corrections offers no formal programs like Gwinnett's for troubled youths at its 34 facilities, though some prisons provide tours and a program called Choose Freedom for youths in areas with high rates of convicts, said spokeswoman Gwendolyn Hogan.
Hollis estimates 80 percent of participants are on probation, while others are troublemakers at Boys and Girls Clubs or hellions at home. One recent evening, a couple from Duluth brings in their diminutive 13-year-old son -- who, on the inside, will quickly earn the nickname "Pip Squeak" -- because he'd been rebelling.
"To put it succinctly," says the teen's father, "he's been grounded for the last year straight."
Pip Squeak falls in line with a motley bunch that includes Holt, the smirker, a repeat runaway and a shaggy haired kid facing battery charges for beating up "random people" at Norcross High School. After another verbal lashing -- "The streets don't give a (expletive) about you!" -- from Hollis' counterpart, Sgt. C. George, all the kids go to prison.
Education vs. trauma
Deeper into the 800-bed compound, three inmates in white jumpsuits -- a burglar, thief and brawler -- berate the teens in a classroom. Without parents around, the language gets more raw, and the decibels rise into a cacophony of interrogatory threats. "You like to fight?" an Atlanta man convicted of aggravated assault asks the battery suspect. "I know how to fight good."
One kid winces, head down.
"Ain't no crying in here," Hollis says. "Crying ain't gonna fix it."
For all the fear-mongering, program leaders say their emphasis remains on education and steering the teens toward law-abiding positivity, not breaking them down and spitting them out.
"The 'Scared Straight' method doesn't work in my mind," said Deputy Warden Darrell Johnson, referring to the 1978 Oscar-winning documentary whose title was adopted for reality television. He isn't the only one critical of the more hard-line approach.
Joe Vignati, a program leader at the Governor's Office for Children and Families in Georgia, acknowledges that programs meant to traumatize youths succeed in getting their attention, but he argues those results are fleeting.
"The research is clear," Vignati wrote last year, "once the trauma of 'Scared Straight' has worn off, meta-analysis shows that this intervention actually increases the odds of offending."
A father of three, Hollis, 37, says he's a teacher at heart. He coaches youth softball and football when he's not fishing for crappie or taking his kids to the movies. He expanded the program's reach beyond the Gwinnett courts system in 2011 to include the Lawrenceville Boys and Girls Club and courts in DeKalb County. He volunteered for more than 300 hours.
"This is serious business right here," he says. "They're getting younger and younger by the day."
In winning the Medal of Merit, Hollis bested a seasoned Snellville detective who directs a citizens police academy and a Gwinnett police officer responsible for the C.O.P.S. Festival at Coolray Field last year. Jim Maran, Gwinnett Chamber president and CEO, said Hollis' "valiant efforts and service to the community" distinguished him.
Johnson, the deputy warden, links Hollis' effectiveness to his bulk -- and heart.
"His eyes light up when he sees a kid headed down the wrong path," Johnson said. "It's just something about his demeanor, he seems to connect with kids."
Impacting finale
Hollis herds the teens into the "max unit," a stark, two-story wall of isolation cells. Inmates' shouts rain down. Pip Squeak tells a man through a meal slot in his door that he's in prison for "lying to my mom," which earns him the antithesis of tough-guy cred.
The Atlanta inmate, a natural and nasty drill sergeant, screams orders for the teens to lay on a steel bed, their heads near the toilet. He nicknames another high-school pugilist "Thumper."
In G-dorm, the teens are lined against the wall of the showers. Hollis and company make clear that a guard won't always be watching, and that sneak attacks from behind are possible.
As the tour wraps, Pip Squeak is led alone into a dorm teaming with inmates, who scream "Fresh meat!" and "Let me take him to the showers!" A look of deer-in-headlights terror overtakes the boy.
Back in the lobby, parents swarm Hollis and ask how their kids performed. Holt, whose pants are decidedly over his hips, says the experience was impacting.
"The fighting, the killing in there ... that one guy scared me to death," he says.
Hearing this, Holt's mother says she's making a return trip the next week, with his 12-year-old brother.
"It's going to be a field trip," she says.
Hollis, surveying the crew, feels the evening was a success.
"I hope they all leave changed," he says. "That one in the black T-shirt ... I don't know."
More like this story
- Police: Inmate coordinated robberies from prison ( August 16, 2012 )
- Police: Jewelry heists were ordered from prison ( October 14, 2011 )
- Jail program to give dogs second life ( January 1, 2010 )
- Decades an inmate, a Lawrenceville man makes a play for freedom — and love ( May 6, 2015 )
- DA: Murder charges forthcoming in Phillips State Prison inmate death ( January 22, 2015 )
Mack711 3 years ago
Spartunburgh South Carolina has a similiar program for troubled kids. With one exception, They do not tell the kids when they will be released. Some have stayed for a couple of days. Parents knew how long, but kids did not. Really an eye opener, ask my granddaughter, she has not been in trouble since not even a speeding ticket. Let them stay a couple of days inside and not know when they are going home.
Wyoming1 3 years ago
Mr. Hollis and the other officers are doing a great work with the program!! Too bad not everyone shares their proper law enforcement views when it comes to this important social issue! Very nicely done story Josh Green!!


text:
Perry Mountain Fire Tower 150 Dual Sport ride
View Single Post
6Sigma Knuckle Shflr
Joined: Nov 2006
Location: Central FL
Oddometer: 10,445
Originally Posted by
I told Brian that the single track was a little rough for a dual sport and most would not like it.
I was wrong! Very wrong!
There were those who new their limits and stayed away from the first section, and then there were the fastburners who I knew would love this section, but the rest of the pack fooled me. It seems everyone was craving just a tad more of the tighter rougher trails. Good for you guys. Up for a challenge and all that. So remember next year! Be careful what you ask for, cause PM can certainly give it to you.
That was some sweet singletrack!
There were a few sections and a couple of hill climbs I did with Hatch Saturday afternoon. On Sunday, I think we rode the 11 mile loop 3 times. The first 2 times at a brisk pace. The last time at a more than brisk pace.
We also did the marked singletrack at the end of the 11 mile loop. And then... and then... and then... well... you get the point. We probably rode quite a few of the trails in the area. Lots of mud, lots of ruts, lots of barkbuster tree banging... woohoo! I suggested to Brian that maybe at the next event, there should be a small bike singletrack loop or maybe even run the same track as the enduro for those idiots, such as myself, who enjoy the punishment.
, my friends.
Mike West
He's got some of the basics down, but, in the end, that just has to create a bigger clusterfuck in that chinese fire drill of a cognitive thought he brought to the dog and pony show of his new found awareness. -
Jack Goff
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text:
Sephora 15% off Sale — Spring Makeup Madness!
Sephora 15% off Sale — Spring Makeup Madness!
According to readers, THE CODE IS WORKING EARLY! USE CODE BI15– HAPPY HAULING!
V.I.B.s (Beauty Insiders who spend over $350 in a calendar year) can save 15% off their entire purchase from April 8th through the 19th with online code V48ML6. In order to save 15% in-store, you do need to have the coupon. I received mine via snail mail last weekend, and I don't know if they'll be sending one out via email as well.
Fine Print (for VIB): Select stores will have different event hours; check your local store for exact times. Online use promo code V48ML6. Valid April 8th through April 19th, 2010 at 11:59PM PST and may be used in Sephora stores and Sephora inside JCPenney stores during regular store hours and on sephora.com (excluding Canadian checkout on sephora.com). Offer limited to Sephora V.I.B.'s only. Voucher must be presented at time of redemption when used in store. No minimum purchase required. May not be combined with any other offers. Not valid on prior purchases. May not be sold or otherwise transferred. Return of discounted merchandise will be for the price actually paid. Not valid for cash or cash equivalent. Not responsible for lost or stolen vouchers. Sephora reserves the right to change or rescind this offer at any time. Not valid for Sephora employees. Learn more about the V.I.B. program at any Sephora store or online at sephora.com/go/VIB.
B.I.s (Beauty Insiders–anyone is free to sign-up, it doesn't cost anything!) save 15% off their entire purchase from April 12th through the 19th with online code BI15. As you can see, the image I have is quite small, so I can't make out much of the fine print. Hopefully, I will have those details for you soon…
Are you shopping the sale? What's on your list?
Discussion and debate are highly encouraged, and we expect community members to participate respectfully. When asking a question, please check the FAQ section (above) for information about purchasing, price, dupes, and the like. If you have general feedback or need technical support, please contact us.
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Careers & Money Links
Interest Quizzes
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The Science Spot was developed in March 1999 by
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8th Grade Science Teacher @ Havana Junior High, Havana, IL
Activities, lessons, & worksheets available on any page of this web site are intended for use by a single teacher in his/her classroom or to share at educational conferences. Reproduction for commercial use or profit is not permitted without the consent of Tracy (Trimpe) Tomm. Visit my Frequently Asked Questions page for more details.
Note: The links on this page are not a part of this site and their
content is not the responsibility of this site.
Parent reminder: Use caution when allowing your child to view any sites on the web - this page or other links found on these sites.


text:
76ers @ Celtics Game 7 NBA Betting Odds & Predictions
- Updated: May 25, 2012
NBA Picks
Philadelphia 76ers
Boston Celtics
Date/Time: May 26, 8:00 PM EST
Television: ABC
NBA Betting Odds from BetDSI
ATS: Boston -5.5
Total: 170
NBA Betting Game Trends
Philadelphia 76ers
- The total has gone OVER in 4 of Philadelphia's last 6 games
- The total has gone OVER in 9 of Philadelphia's last 12 games on the road
- Philadelphia is 2-5 SU in its last 7 games on the road
- Philadelphia is 8-17 SU in its last 25 games when playing Boston
- The total has gone OVER in 6 of Philadelphia's last 8 games when playing Boston
Boston Celtics
- Boston is 2-5 ATS in its last 7 games
- The total has gone OVER in 4 of Boston's last 6 games
- Boston is 16-8 SU in its last 24 games
- Boston is 2-4 ATS in its last 6 games at home
- The total has gone OVER in 4 of Boston's last 6 games at home
The 2012 Eastern Conference Finals will be set on Saturday night in Beantown with NBA betting action between the Philadelphia 76ers and the Boston Celtics. The winner of this game will take on the Miami Heat starting on Sunday after this nervy Game 7 at the TD Garden.
We really give the 76ers all of the credit in the world for coming up with such a great run here in the postseason. The No. 8 seed in the East has done it all right. We tend to forget that the Chicago Bulls, even after Derrick Rose got hurt, were still one of the best teams in the league this year, and if anyone thought that Philly wasn't legit, that has been disproven here against Boston. Home court advantage did play a huge role, and Boston Head Coach Doc Rivers admitted as much after the Sixers took Game 6 to send this series back to Beantown for a do-or-die game. Andre Iguodala might not be the true statistical leader of the team, but he is doing just about everything that he needs to do to make sure that he puts the team on his back, coming up with some flat out awesome plays on both ends of the court. Watch out for Jrue Holiday, who has rebounded from a slow start to this series to log 20 points in Game 6. He is the team's leading scorer at 15.9 points per game here in the postseason.
The hallowed court at the TD Garden is usually a place where opponents go to die, especially in big time games like this one. That being said, we have seen Rajon Rondo, Paul Pierce, Ray Allen, and Kevin Garnett get beaten in this very spot in a Game 7 against the Orlando Magic a few years back, and that could be the case again in this one. Garnett has once again been stirring with his mouth, and that might have been part of the reason that the Philly fans were on his case every step of the way on Wednesday night. Still, he is the best big man on the court on either side, and his move to the center position this year really did spark the major change for the C's. Rondo is the man that the Sixers are having all sorts of trouble keeping up with, but this is nothing new against a player that is already one of the top triple-double producers in postseason history in the NBA.
We really love what Philadelphia has done this year, but we still look back at these Celtics and think that they are a touched team. They got the benefit of not having to play the Bulls, and they might draw the Heat without Chris Bosh as well. Even without Avery Bradley in the fold, we still think that the veteran savvy will rule the day over youth and exuberance.
Philadelphia 76ers @ Boston Celtics Game 7 Pick: Boston Celtics -5.5
Adam Markowitz
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FIG. 1 is a perspective view showing my new design;
FIG. 2 is a front view thereof;
FIG. 3 is a back view thereof;
FIG. 4 is a right side view thereof;
FIG. 5 is a left side view thereof;
FIG. 6 is a top view thereof; and,
FIG. 7 is a bottom view thereof.
The broken lines shown in FIGS. 1–7 form no part of the claimed design. For the sake of clarity, the lower strap contains a break, which represents the strap as having no particular length.


text:
It all took place more than a half-century ago, but the images have an eerie similarity to Sept. 11, 2001, as does the shock of those who witnessed the attacks.
"One-third of the men on the ship were lost," retired U.S. Navy Rear Adm. Robert H. Spiro Jr. recalled of one attack. "So, it was personally devastating. It was heartrending. At the same end, for a few hours we saw blood. The ship was on fire. We thought the bow was going to break off."
The similarities don't end with the images and emotions. Looking back at Japan's infamous kamikaze, they seem more related to the pilots of al Qaeda than most Japanese today would like to admit.
They were fanatically devoted to their emperor, who was considered a god at the time. They were motivated by self-righteous anger against the West.
"Many Japanese do believe that they fought a just war," said Gregory Clark, president of Tama University in Japan. "[They believe] that they were fighting under extreme odds. And that anything was justified in the attempt to win this war, in which they were clearly the weaker power. And that included using kamikaze."
More than 5,000 kamikaze died before the end of the war, and 20,000 were still awaiting missions. But a handful who did take off on suicide missions are still alive today.
"We had no other way to fight back," said Kenichiro Onuki, a volunteer who crash-landed before reaching his target. "This was the only way to prevent the U.S. military from advancing into our homeland."
Another survivor, Kensuke Kunuki, said through a translator: "I had no fear. I wanted to sacrifice my life."
Kunuki suffered terrible burns when his plane was forced down by mechanical problems. He said his first thought at the time was that he wanted to try again because he hadn't killed any Americans.
In a new book on the kamikaze, Hideaki Kase, an outspoken Japanese nationalist, said there was no truth to the wartime propaganda that portrayed the kamikaze as a fanatical cult. He says they were no different than American youths who gave their lives in desperate military campaigns.
"They were not fanatics," Kase said. "They were not brainwashed. They were ordinary, young kids."
Even today, he says, the West has difficulty grasping the notion that suicide is a noble act in some cultures.
"Suicide can be honorable, positive, if that act was committed for the family or for the community or for the motherland," Kase said, adding that "patriotism — yes, patriotism" drove the kamikaze pilots.
Patriots? Immediately after the war, a demoralized Japan saw the kamikaze as symbols of military madness. The very word "kamikaze" became a synonym for crazy, reckless behavior.
Yet few Japanese could ignore the fact that the kamikaze spirit was deeply ingrained in the Japanese psyche — duty, loyalty, sacrifice for the good of the group. Half a century later, the kamikaze are no longer viewed in such black-and-white terms.
Rare color images of the suicide attacks from American archives are now included on popular videos in Japan. They are among a flood of retrospective books, documentaries and commercial films that portray the kamikaze more heroically.
Most of the kamikaze took off on their one-way missions from bases on Japan's southernmost island of Kyushu, and the largest base was in the town of Chiran.


text:
NASHVILLE, Tennessee — Nashville police say there was evidence of alcohol in a car that struck an SUV head-on, killing a passenger and injuring four children.
Killed in the crash Saturday night was 29-year-old Stacy Thornton. She was the girlfriend of the SUV's driver, 29-year-old Lawrence D. Belt, who was taken to Vanderbilt University Medical Center with serious injuries.
Belt's 10-month-old daughter is listed in very critical condition at Vanderbilt Children's Hospital. His other children — ages 7, 5 and 2 — are all in stable condition.
The driver of the other vehicle, 20-year-old Carl Dollarhide, is in critical but stable condition at Vanderbilt.
Investigators say Dollarhide was speeding when he crossed over into the path of the SUV.
Authorities didn't elaborate, but say there was evidence of alcohol in Dollarhide's vehicle. No charges have been filed.


text:
Karen L. Terry, 63, of Lakeside-Marblehead, died Monday, Jan. 20, 2014, in her residence with her family by her side.
She was born Feb. 23, 1950, in Berea, Ohio, the daughter of Edward and Jeanetta (Crooks) Bird. She was a 1968 graduate of John Marshall High School in Cleveland, Ohio, and then went to Lorain Community College where she received her Associate of Arts degree in Elementary Education.
Karen worked as a manager at the National City Bank Headquarters in Cleveland and later as a letter carrier and supervisor for the U.S. Postal Service in the Cleveland area. She was a member of Lakewood United Methodist Church in Lakewood, Ohio, life member of VFW in Valley City, Ohio, member of the American Legion in Marathon, Fla., and member of the Moose Lodge in Big Pine Key, Fla. She enjoyed traveling between their homes in the Florida Keys, Kelleys Island and Marblehead, going for long walks with her dog, Tia, but most importantly, she loved spending time with her grandchildren.
Survivors include her husband, John "Jack" Terry, whom she married Nov. 27, 1987; daughter, Kathleen (Walter) Krzynowek of Litchfield, Ohio; son, Michael Rancour of Louisville, Ky.; grandchildren, Ryan, Sean, and Alexa Krzynowek; brothers, Michael (Josie) Bird of Lakewood, Ohio, Jack (Virginia) Bird of Adairsville, Ga., Robert Bird of Clyde, Edward (Linda) Bird of Medina, Ohio; nieces and nephews; and her ex-husband,Thomas Rancour.
She was preceded in death by her parents.
Funeral services will be 11 a.m. Saturday, Jan. 25, at Medina United Methodist Church, 4747 Foote Road, Medina.
Memorial contributions may be made to Stein Hospice, 1200 Sycamore Line, Sandusky, OH 44870.
Condolences may be expressed at neideckerleveckcrosser.com.
The Neidecker, LeVeck & Crosser Funeral Home, Peninsula Chapel, Lakeside-Marblehead, is assisting the family with arrangements.


text: Holographic Television Coming Soon Lauren Davis and 18 othersEditDelete Invite manuallyPromoteXDismissXUndismissBlock for io9Hide We use high-definition television, dark rooms, and surround sound to create an immersive media experience. But for those who want television that more closely resembles the holodeck, there's good news. A University of Arizona research team has made a significant breakthrough in 3-D displays that could put holographic… » 10/07/08 8:40am 10/07/08 8:40am


text:
Translation Changes Everything
Theory and Practice
In Translation Changes Everything leading theorist Lawrence Venuti gathers fourteen of his incisive essays since 2000.
The selection sketches the trajectory of his thinking about translation while engaging with the main trends in research and commentary. The issues covered include basic concepts like equivalence, retranslation, and reader reception; sociological topics like the impact of translations in the academy and the global cultural economy; and philosophical problems such as the translator's unconscious and translation ethics.
Every essay presents case studies that include Venuti's own translation projects, illuminating the connections between theoretical concepts and verbal choices. The texts, drawn from a broad variety of languages, are both humanistic and pragmatic, encompassing such forms as poems and novels, religious and philosophical works, travel guidebooks and advertisements. The discussions all explore practical applications, whether writing, publishing, reviewing, teaching or studying translations.
Venuti's aim is to conceive of translation as an interpretive act with far-reaching social effects, at once enabled and constrained by specific cultural situations.
This latest chapter in his developing work is essential reading for translators and students of translation alike.less
288 pages; ISBN 9781135107956
Read online, or download in secure EPUB or secure PDF format
Title: Translation Changes Everything
Author: Lawrence Venuti
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- Academic > Languages and Linguistics > Philology. Linguistics > Language. Linguistic theory. Comparative grammar > Translating and interpreting
- Academic > Languages and Linguistics > Philology. Linguistics > General
- Language Arts & Disciplines > Linguistics
- Language Arts & Disciplines > Translating & Interpreting


text: http://ubuntuforums.org – Hello! Here's my situation: I run a webserver Apache2, php5, and MySQL. They are all set up correctly and I can access my website at http://localhost I have, also installed, noip2 to update my IP address to no-ip.com for my domain name. Here's the problem: I can access my website through that domain name on other computers, both on internet and on the same network. But I cannot access it from my own computer (using the domain name instead of localhost). I need to be able to access the domain name on my computer because some pages on my website have been defined as the address to my domain (HowTos)


text:
Trying to find all the photos you've shared in a conversation on Facebook? These steps will show you how to access them on the Web and through your mobile app.
This high-end 13-inch laptop adds better battery life and faster performance, but doesn't upgrade its design.
In Windows 10, the Snipping tool lets you delay your shutter speed when you capture screenshots.
Microsoft Edge's new inking feature lets you take notes directly on Web pages -- and then share them with your friends.
The e-tail giant will be separating its online payment and commerce companies in mid July. Shares will be split, tax-free, right down the middle for current shareholders.
With better battery life and performance than the Yoga 3 Pro (not to mention a lower price), the Yoga 3 14 is one of the best hybrid deals around.
It lacks the design punch of the Yoga 3 Pro, but makes up for it with better battery life and performance at a lower price.
A new custom Windows 8 overlay called HiveMind makes this unique gaming PC more useful and easier to navigate.
With a Terminal command, you can add a two-finger scroll gesture to see which windows you have open for an app or folder in your Mac's Dock.
Young Minecraft architects can now start getting an education in programming while they play the popular 3D video game.
Are you ready for an upgrade?
They're hot, they're new, and they're all vying to make you want to upgrade your current TV.


text:
"Though this case has a different plaintiff, the suit is essentially based on the same claims around the tragic events of 9/11. However the court has dismissed most of the defendants," Lynne Bernabei of the law firm Bernabei & Wachtel, representing the Saudi Red Crescent Society, told ABC News.
Bernabei said the lawsuit is another attempt to get around the rulings which have been mostly adverse to the plaintiffs. Her client was in part dismissed because it was not shown to have any involvement and because it is a sovereign defendant, or state entity, for which the requirements to sue were not met.
Mark Hansen, whose law firm, Kelloff, Huber, Hansen, Todd, Evans & Figel, represented the Kingdom of Saudi Arabia in the previous 9/11 suits, said the firm does not comment on pending litigation.
While 2,983 families of 9/11 victims and 2,300 physically injured have received over $7 billion from the September 11th Victim Compensation Fund of 2001, 94 families decided not to participate in the fund. Those families received on average an estimated $5 million each, using figures from the report of Sheila Birnbaum, the 9/11 mediator. However, that information is confidential.
Only one victim's family is still pursuing litigation against United Airlines and security company Huntleigh under the plaintiff's arguments they were negligent in failing to prevent the attacks. A hearing will take place Monday in New York with a trial date scheduled for November.


text:
Packing List
Clothing/Shoes/Weather Gear: Where good walking shoes. Dress in layers. Gets cool in the evenings.
[ View My Guestbook ]
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- Seniors
- Family Travel
- Historical Travel
Packing List
Luggage and bags: We use our regular suitcases with wheels. And our boys use thier duffel bags.
Clothing/Shoes/Weather Gear: Clothes can be pretty casual. There are some nice reseraunts, so something a little more dressy might be handy, but not super fancy.
Shoes, I would suggest some comfy walking shoes. Deadwood's main street is no parking, so you'll be walking to the casinos. For the mine tours and cave tours, take sneakers or hiking boots. I always bring my sandals and hiking boots with lightweight socks.
Weather gear, usually a light jacket or sweater is needed in the evening. Normal casual wear is okay. If you chill easy, take a light coat and sweatshirt or jacket to layer on. Lot's of people use fanny packs to carry their gambling money/winnings. Be sure to take a fanny pack or purse that won't get in your way, but can hold your things.
Toiletries and Medical Supplies: Toiletries, just what you usually take on trips.
Meds, I always take asprin and band-aids. Pretty much a basic first-aid kit works fine. Since there may be mosquitoes and insects like them, take some anti-itch cream.
Photo Equipment: I can't talk about digital cameras, but we take our regular 35 mm and sometimes those re-uesable cameras and are happy with those.
Camping/Beach/Outdoor Gear: There are campgrounds in Deadwood, but I've not stayed at them so I ccan't really answer this one.
Miscellaneous: Bring your sunscreen and maybe a small folding umbrella. Or a rain hat, for those quick showers. Something that is small and easy to use.
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text:
nvidia 6150 twinview
I have conected two monitors (19" lcd and 32"lcd) to my m2npv-vm motherboard witch has integrated nvidia 6150.
When i use nvidia drivers only 19" monitor works.
I have tryed many different settings but nothing seems to work for me.
Here is part of xorg.conf file:
Section "Monitor"
Identifier "Monitor0"
VendorName "Unknown"
ModelName "Unknown"
HorizSync 30.0 - 110.0
VertRefresh 50.0 - 150.0
Option "DPMS"
Section "Device"
Identifier "Device0"
Driver "nvidia"
VendorName "NVIDIA Corporation"
Option "TwinView" "true"
Option "TwinViewOrientation" "Clone"
Option "metamodes" "1280x1024,1280x1024; 1024x768,1024x768"
Option "HorizSync" "30.0 - 80.0"
Option "VertRefresh" "60.0 - 75.0"
Option "ConnectedMonitor" "CRT, DFP"
Section "Screen"
Identifier "Screen0"
Device "Device0"
Monitor "Monitor0"
DefaultDepth 24
SubSection "Display"
Depth 24
Modes "1600x1200" "1280x1024" "1024x768" "800x600" "640x480"
Section "Extensions"
Option "Composite" "Enable"
Re: nvidia 6150 twinview
Re: nvidia 6150 twinview
2 Attachment(s)
nvidia-bug-report.log attached
Re: nvidia 6150 twinview
Why are you using the ConnectedMonitor option? Does this problem persist if you're not using it?
Re: nvidia 6150 twinview
nvidia settings only shows my other monitor witch is connected via vga thats why i tryed connectemonitor option. Removing the option doesn't help.
Re: nvidia 6150 twinview
According to your last bug report the DFP wasn't even being detected. Is it connected directly to the graphics card with no intermediary devices (KVM, etc)?
I'd like to see an updated bug report as well.
Re: nvidia 6150 twinview
The DFP i connected with hdmi-dvi-adabter.
in nv driver mode the lcd tv works so it should be connected right.
If the dfp would be detected, I dont think there would be any problem.
Re: nvidia 6150 twinview
2 Attachment(s)
New Bug repot attached.
philips 32" lcd tv is now connected via component and dvi-> hdmi.
Re: nvidia 6150 twinview
I don't understand what you mean by "connected via component and dvi-> hdmi". How are you connecting 1 TV via two different mechanisms, and what is your goal in this setup?
The new bug report is still not detecting anything other than a single TV. Have you verified that you're using the latest motherboard BIOS?
Re: nvidia 6150 twinview
I have new htpc witch has vga and dvi-d connection. My 32" lcd tv has 2 x hdmi(no vga or dvi).
I connected those two with dvi-hdmi adabter and hdmi cabel. The problem is that when using nvidia driver tv doesn't work.
19" monitor is my other pc's main monitor witch i had to move and connect to htpc because tv wasn't working.
I connected htpc and tv with component connection so i wouldn't have to move 19" monitor all the time.
In windows it is not possible to force connection and that why I chose ubuntu.
So how do I force dvi connection on?
I thought this would have done it:
Section "Device"
Identifier "Device0"
Driver "nvidia"
VendorName "NVIDIA Corporation"
Option "TwinView" "true"
Option "TwinViewOrientation" "Clone"
Option "metamodes" "1280x1024,1280x1024; 1024x768,1024x768"
Option "HorizSync" "30.0 - 80.0"
Option "VertRefresh" "60.0 - 75.0"
Option "ConnectedMonitor" "CRT, DFP"
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text:
12 Years Later, Hundreds Of Marylanders Pay Tribute To 9/11 Victims
It's hard to believe it has been 12 years since terror attacks in New York, Washington and Pennsylvania killed thousands of people.
Gov. O'Malley: Remember 9/11 Through Service
Gov. Martin O'Malley is encouraging people to volunteer on a national day of service to mark the anniversary of the Sept. 11 attacks.
Eisenhower Memorial Faces Further Delay On Design
After more than 18 months of delays, the planned Eisenhower Memorial project near the National Mall faces further setbacks.
National Park Service Selects Superintendent For Tubman Monument
The National Park Service has chosen a superintendent for the Harriet Tubman Underground Railroad National monument.
MLK Memorial Work To Be Finished For Anniversary
Refinishing work on the Martin Luther King Jr. Memorial should be complete by the upcoming 50th anniversary of the March on Washington, officials said Thursday, allaying earlier concerns that work wouldn't be done in time.
Ex-Gay Gospel Singer Removed From MLK Concert
A gospel singer who says God delivered him from being gay was removed from a concert lineup at the Martin Luther King Jr. Memorial after a request from Washington's mayor.
Lincoln Memorial Reopens After Vandals Splatter Paint On Statue
The Lincoln Memorial reopens after vandals splatter paint on the statue.
Redesigning Eisenhower Memorial Could Cost $17M
Scrapping a disputed design for a planned Dwight D. Eisenhower Memorial near the National Mall and developing an alternate concept over the next five years would cost about $17 million, analysts have found.
Vietnam Memorial Seeks Pictures Of D.C. Veterans
The Vietnam Veterans Memorial is collecting photographs of veterans named on the memorial wall, but organizers say they are coming up short on pictures of District of Columbia veterans.
Gehry Refines Design For Eisenhower Memorial In D.C.
A federal commission charged with building a national memorial honoring President Dwight D. Eisenhower voted unanimously Wednesday to approve architect Frank Gehry's design for a park near the National Mall, allowing the project to move forward over the objections of Eisenhower's family.
Eisenhower Memorial Group Makes D-Day Film On Ike
Officials working to build a memorial honoring President Dwight D. Eisenhower in Washington are launching a new short film online to mark the 69th anniversary of the D-Day invasion of Europe during World War II.
Scholars Back Quotes At Future Eisenhower Memorial
Three historians are recommending the use of passages from key speeches by President Dwight D. Eisenhower — including his message to troops during the D-Day invasion — to help represent the 34th president in a planned memorial in the nation's capital.


text:
PLATINUM NUGGET. Kondyor Massif, Khabarovsk Krai, Far Eastern Federal District, Russian Federation. ...
2013 June 2 Nature & Science Signature Auction, featuring The Hoppel Collection of Fine Minerals - Dallas #5110
|Sold for:
|Not Sold
|Auction Ended On:
|Jun 2, 2013
|Item Activity:
0 Internet/mail/phone bidders
1,251 page views
Heritage Auctions - Design District Annex
1518 Slocum Street
Dallas, TX
|Printable auction results for all items in the 2013 June 2 Nature & Science Signature Auction, featuring The Hoppel Collection of Fine Minerals - Dallas.
Kondyor Massif, Khabarovsk Krai, Far Eastern Federal District, Russian Federation
In the remote wilderness of Far Eastern Russia, inland from the Sea of Okhotsk, is a circular feature some six kilometers across that looks exactly like a meteorite impact crater: It isn't. Although the towering walls of the structure, some 2000 feet high, look very much like the crater rim of a volcano: They're not. The structure, called the Kondyor Massif, represents the remains of an Dunite intrusion: a mass of magma with origins deep in the mantle, that carried valuable amounts of the rare metals: Platinum, Rhodium, Gold and others to the surface of the planet. Weathering allowed the rare metals to migrate downstream, forming placer deposits. Analysis of Zircon grains in the Dunite shows that the Platinum Group Elements (PGE's) formed deep in the mantle some 2.4-1.8 billion years ago. Much later, they were injected into the surface crust some 176 -143 million years ago. Being rich in PGE's, the massif was responsible for approximately 4 tons of Platinum being produced in one year. Compared to the production of most Gold mines, this is nothing. Nuggets of Platinum the size of this one, are as rare as the proverbial hen's teeth. Deceptively heavy for its size this rounded, silvery nugget weighs 7.368 ounces troy or 229.2 grams - over half a pound!
It measures a 1.63 x 1 inch (4.22 x 2.55 cm).
[Scale: 1 inch, with mark at 1 cm]
Condition Report*:Condition report available upon request.
*Heritage Auctions strives to provide as much information as possible but encourages in-person inspection by bidders. Statements regarding the condition of objects are only for general guidance and should not be relied upon as complete statements of fact, and do not constitute a representation, warranty or assumption of liability by Heritage. Please note that we do not de-frame lots estimated at $1,000 or less and may not be able to provide additional details for lots valued under $500. All lots are sold "AS IS" under the Terms & Conditions of Auction.
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text:
24 Polymer Clay Tutorials: Polymer Clay Jewelry, Home Decor, and More
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Easy Pot Holder Towel
By: Fawnda Norman for Fireflies and Jellybeans
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Easy sewing projects like this are perfect for the kitchen. When you're not using Fawnda Norman's Easy Pot Holder Towel during baking, simply hang it up by the oven to use as a towel or for decoration.
- Coordinating Dish Towel
- Pot holder
- Button
- Thread
- Sewing machine
- Needle (to hand sew the button on)
- Iron your dish towel if needed.
- Turn the towel right side down and fold the side in so that it is the width of the pot holder. Iron the folds.
- Fold in half lengthwise and iron on that fold.
- Line up your fold on to your pot holder where you are going to sew it.
- Flip the towel open so that the wrong side is facing up (with the folds showing) and pin to your pot holder.
This is what it should look like on the other side.
- Sew your towel and pot holder together, using the crease as a guide. I sew it two times to give it extra strength.
- Fold your pot holder up and mark where the loop crosses over the other side and mark for where you are going to sew your button.
- Hand sew your button on.
Hang on your towel holder, refrigerator handle, or oven handle, where ever you see fit!
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text:
Ziyi Zhang attends the Costume Institute Gala for the "PUNK: Chaos to Couture" exhibition at the Metropolitan Museum of Art on May 6, 2013 in New York City.
She's ready for the summer!
Work it, girl.
Mariah Carey, her boobs and her new beau James Packer, aka the fourth richest man in Australia, took their love to Ibiza, Spain where they gallivanted on a yacht with her kids.
Bad Girl RiRi? More like Braless RiRi.


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