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Objective: The Northern Ireland Public Access Defibrillation (NIPAD) project was established to train lay volunteers as First Responders (FRs) in the use of an automated external defibrillator (AED) at an out of hospital cardiac arrest (OHCA). We wished to establish the background and experience of the FRs. Methods: A questionnaire was distributed to FRs with a prepaid reply envelope and a follow up reminder letter was sent to non-respondents after six weeks. Results: There were 178 questionnaires returned of whom 71/178 (39.9%) were male. The mean age of the FRs was 45.9 yrs (SD 10.7). The education level of the FRs was assessed: 49/178 (27.5%) had received no school education after age 16 and 60/178 (33.7%) were educated at university. Basic medical skills prior to enrolling in the NIPAD project were assessed. 30/178 (16.9%) had no previous first aid training, 45/178 (25.3%) had participated in a basic first aid course, 81/178 (45.5%) had training in basic life support and 17/178 (9.6%) had training in advanced life support. Following training 163/178 (91.6%) felt "totally confident" or "reasonably confident" in using an AED at the scene of an OHCA. No volunteer considered the AED difficult to use. In total 34/178 (19.1%) of FRs were willing to hold an AED permanently. No FR required the use of the confidential counselling service employed by the project. Conclusion: First Responders can be recruited from a variety of backgrounds. The First Responders reported the AED to be easy to use following training. [ABSTRACT FROM AUTHOR]

Purpose of Review: This paper reviews the unique processes and treatments of post-traumatic stress in implantable cardioverter-defibrillator (ICD) patients and posits specific clinical management recommendations., Recent Findings: PTSD is a common presenting problem for a prospective ICD patient and is a common response to ICD shocks. Approximately 32% of patients with sudden cardiac arrest report significant PTSD symptoms. Following ICD shock, approximately 20% experience PTSD from the shocks. Regardless, PTSD can interrupt and undermine clinical management from a cardiologist perspective and create significant disturbance in patients and families. Few cardiology clinics are outfitted to effectively manage psychological distress, in general, and PTSD, in particular. Effective management of PTSD patients can be achieved with both direct care in the cardiac clinic, as well as indirect care via multidisciplinary consultation and expertise. The importance of emotional validation, return to physical activity, and family engagement is emphasized in current management., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Health equity means that everyone has the opportunity to be as healthy as possible, but achieving health equity requires the removal of obstacles to health such as poverty, discrimination, unsafe environments, and lack of access to health care. The pandemic has highlighted the awareness and urgency of delivering patient-centered, high-value care. Disparities in care are antithetical to health equity and have been seen throughout medicine and radiology, including neuroradiology. Health disparities result in low value and costly care that is in conflict with evidence-based medicine, quality standards, and best practices. Although the subject of health equity is often framed as a moral or social justice issue, there are compelling economic arguments that also favor health equity. Not only can waste in health care expenditures be countered but more resources can be devoted to high-value care and other vital national economic interests, including sustainable support for our health system and health providers. There are many opportunities for neuroradiologists to engage in the advancement of health equity, while also advancing the interests of the profession and patient-centered high-value care. Although there is no universal consensus on a definition of health equity, a recent report seeking clarity on the lexicon offered the following conceptual framework: "Health equity means that everyone has a fair and just opportunity to be as healthy as possible. This requires removing obstacles to health such as poverty, discrimination, and their consequences, including powerlessness and lack of access to good jobs with fair pay, quality education and housing, safe environments, and health care." 1 This definition contrasts with that of health disparities that contribute to inequitable care as a result of demographic differences among populations such as those attributable to race, sex, access, residence, socioeconomic status, insurance status, age, religion, and disability. 2,3 In effect, the greater the health disparities and negative social determinants of health, the greater the health inequities will be., (© 2022 by American Journal of Neuroradiology.)

The appropriate imaging of patients with headache presents a number of important and vexing challenges for clinicians. Despite a number of guidelines and studies demonstrating a lack of cost-effectiveness, clinicians continue to image patients with chronic nonfocal headaches, and the trend toward imaging is increasing. The reasons are complex and include the fear of missing a clinically significant lesion and litigation, habitual and standard of care practices, lack of tort reform, regulatory penalties and potential impact on one's professional reputation, patient pressures, and financial motivation. Regulatory and legislative reforms are needed to encourage best practices without fear of professional sanctions when following the guidelines. The value of negative findings on imaging tests requires better understanding because they appear to provide some measure of societal value. Clinical decision support tools and machine intelligence may offer additional guidance and improve quality and cost-efficient management of this challenging patient population., (© 2020 by American Journal of Neuroradiology.)

Objective: Consistent evidence-practice gaps in osteoarthritis (OA) care are observed in primary care settings globally. Building workforce capacity to deliver high-value care requires a contemporary understanding of barriers to care delivery. We aimed to explore barriers to OA care delivery among clinicians and students., Design: A cross-sectional, multinational study sampling clinicians (physiotherapists, primary care nurses, general practitioners (GPs), GP registrars; total possible denominator: n = 119,735) and final-year physiotherapy and medical students (denominator: n = 2,215) across Australia, New Zealand and Canada. Respondents answered a survey, aligned to contemporary implementation science domains, which measured barriers to OA care using categorical and free-text responses., Results: 1886 clinicians and 1611 students responded. Items within the domains 'health system' and 'patient-related factors' represented the most applicable barriers experienced by clinicians (25-42% and 20-36%, respectively), whereas for students, 'knowledge and skills' and 'patient-related factors' (16-24% and 19-28%, respectively) were the most applicable domains. Meta-synthesis of qualitative data highlighted skills gaps in specific components of OA care (tailoring exercise, nutritional/overweight management and supporting positive behaviour change); assessment, measurement and monitoring; tailoring care; managing case complexity; and translating knowledge to practice (especially among students). Other barriers included general infrastructure limitations (particularly related to community facilities); patient-related factors (e.g., beliefs and compliance); workforce-related factors such as inconsistent care and a general knowledge gap in high-value care; and system and service-level factors relating to financing and time pressures, respectively., Conclusions: Clinicians and students encounter barriers to delivery of high-value OA care in clinical practice/training (micro-level); within service environments (meso-level); and within the health system (macro-level)., (Copyright © 2019 Osteoarthritis Research Society International. All rights reserved.)

Clinical practice guidelines and clinical practice parameters are among the tools that clinicians and radiologists use to inform decision making in the diagnosis and treatment of patients. Radiologists have been urged to objectively establish their value and measurable contributions to patient care. Radiology's contribution to the health care value stream can be established in the development of sound clinical practice guidelines. Neuroradiologists have been quite active in developing clinical guidelines, particularly in collaboration with the American College of Radiology, but there is a need to increase the visibility and accessibility of such documents. Increasing access and visibility can contribute to improved patient outcomes and an improved overall quality of care., (© 2019 by American Journal of Neuroradiology.)

The American Society of Neuroradiology has teamed up with the American College of Radiology and the Radiological Society of North America to create a catalog of neuroradiology common data elements that addresses specific clinical use cases. Fundamentally, a common data element is a question, concept, measurement, or feature with a set of controlled responses. This could be a measurement, subjective assessment, or ordinal value. Common data elements can be both machine- and human-generated. Rather than redesigning neuroradiology reporting, the goal is to establish the minimum number of "essential" concepts that should be in a report to address a clinical question. As medicine shifts toward value-based service compensation methodologies, there will be an even greater need to benchmark quality care and allow peer-to-peer comparisons in all specialties. Many government programs are now focusing on these measures, the most recent being the Merit-Based Incentive Payment System and the Medicare Access Children's Health Insurance Program Reauthorization Act of 2015. Standardized or structured reporting is advocated as one method of assessing radiology report quality, and common data elements are a means for expressing these concepts. Incorporating common data elements into clinical practice fosters a number of very useful downstream processes including establishing benchmarks for quality-assurance programs, ensuring more accurate billing, improving communication to providers and patients, participating in public health initiatives, creating comparative effectiveness research, and providing classifiers for machine learning. Generalized adoption of the recommended common data elements in clinical practice will provide the means to collect and compare imaging report data from multiple institutions locally, regionally, and even nationally, to establish quality benchmarks., (© 2019 by American Journal of Neuroradiology.)

The growing burden of chronic disease and the current nature of healthcare systems which are structurally ill-equipped to cater to the complex needs of patients with chronic conditions has led to governments and healthcare providers seeking alternative ways to improve patients own capacity to actively self-manage their chronic condition. In Australia, there has been a focus on patient education and self-management programs within the healthcare system to achieve this. These programs aim to empower patients through providing information and teaching skills and techniques to improve self-care and doctor-patient interaction with the ultimate goal of improving quality of life. Patient education and self-management programs have been supported through several national government initiatives and implemented within the healthcare setting. This paper describes the current position of patient education and self-management within the Australian healthcare system. It further describes a new collaboration project between an Australian and a German research team which aims at translating an assessment questionnaire used in Australia for the evaluation of self-management programs, the "Health Education Impact Questionnaire" ("heiQ"); this instrument is expected to be of significant use in the German rehabilitative system.

We sought to evaluate the economic impact and diagnostic utility of magnetic resonance imaging (MRI) in the management of patients with headache and nonfocal physical examinations. Computerized medical records were retrospectively reviewed of 1,233 patients presenting for MRI of headache at our institution over a 3-year period (1992-1995). Patients with focal findings at physical examination, prior brain surgery, head trauma, or immunocompromise were excluded. A model was developed to assess the cost associated with the MR test results, and actual average institutional costs of performing an examination applied. Correlative statistical analysis of referring specialties and positive tests was also performed. Three hundred twenty-eight patients who met the above criteria were retained in the sample. One hundred sixty-three patients (50%) had negative MR test results. Of the 50% of patients with positive studies, only 5 (1.5%) had clinically significant MR results. The average cost of an MR examination was 517 dollars (1998 dollars). The cost per clinically significant managed case detected was 34,535 dollars. No statistically significant difference was found among referring specialties and clinically significant MR results. Our results indicate that MRI of nonfocal headache yields a low percentage of positive clinically significant results and has limited cost-effectiveness. Referring specialty had no significant bearing on these outcomes, regardless of specialist experience.

Abstract Eighty-five women with newly diagnosed breast cancer were classified on the basis of high and low levels of cancer-related intrusive thoughts and avoidance at diagnosis, and their psychological adjustment was studied prospectively at 3 and 6 months post diagnosis. Patients who initially reported high levels of both intrusive thoughts and avoidance and those who reported high levels of intrusive thoughts but low avoidance experienced the highest levels of anxiety and depression symptoms, and continued intrusive thoughts and avoidance. Patients who were high in avoidance but low in intrusive thoughts also experienced adjustment problems, including increased intrusive thoughts, when compared with patients who were low in both types of symptoms. The findings highlight the value of considering subgroup differences in patterns of intrusion and avoidance as predictors of subsequent psychological adjustment to breast cancer.

Objectives: This study tested the hypothesis that a recombinant human C5a antagonist, CGS 32359, attenuates neutrophil activation and reduces infarct size in a porcine model of surgical revascularization., Methods: CGS 32359 (0.16-16 micromol/L) dose-dependently inhibited superoxide production by human C5a-activated porcine neutrophils (18 +/- 3.7 vs 1.6 +/- 0.5 nmol/5 min/5 x 10(6) neutrophils; P <.05) and reduced neutrophil adherence to coronary endothelium from 194 +/- 9 to 43 +/- 6 neutrophils/mm(2) (P <.05). The left anterior descending coronary artery was occluded for 50 minutes, after which saline solution (n = 8), mannitol-buffer vehicle (n = 9, 102 mg/kg bolus, 102 mg. kg(-1). h(-1)), or CGS 32359 (CGS, n = 7, 60 mg/kg bolus, 60 mg. kg(-1). h(-1)) was infused. After ischemia, 1-hour arrest was achieved by means of multidose hypothermic (4 degrees C) blood cardioplegia, followed by 2.5 hours of off-bypass reperfusion. The ligature on the left anterior descending artery was released before the second infusion of cardioplegic solution., Results: Area at risk was similar in all groups (saline solution, 27% +/- 2%; mannitol-buffer vehicle, 26% +/- 2%; CGS, 26% +/- 2% left ventricular mass). Infarct size (area necrosis/area at risk) was significantly reduced by CGS (18% +/- 6%, P <.05) versus saline solution (52% +/- 3%) and mannitol-buffer vehicle (60% +/- 4%). Postischemic systolic shortening (sonomicrometry) in the area at risk was significantly improved with CGS (0.8% +/- 0.9%) compared with saline solution (-3.7% +/- 1.1%) and mannitol-buffer vehicle (-6.4% +/- 1.0%). Myeloperoxidase activity from accumulated neutrophils was less in the ischemic zone of CGS (0.014 +/- 0.002 U/100 mg tissue; P <.05) than mannitol-buffer vehicle (0.133 +/- 0.012 U/100 mg tissue)., Conclusions: We conclude that the recombinant human C5a receptor antagonist CGS 32359 inhibits surgical ischemia-reperfusion injury after coronary occlusion.

This study elicited a preliminary report that reflected the perspectives and interest of health professional academicians in regard to the need for and appropriateness of genetic technology and testing information in their curricula. Of the original attainable sample of 135 departmental chairs of allied health professional education programs nationwide, 88 responded to a mailed questionnaire, for a response rate of 65%. Of the 88, 11 (13%) saw no need for such information to be provided for allied health students at the undergraduate or graduate level or for currently practicing allied health professionals (AHPs). Consequently, the elicited results were based on the responses of the other respondents who perceived a need for genetic technology and testing information to be made available to both AHP students (86% undergraduate and 92% graduate) and currently practicing AHPs (91%). In regard to preferences for required and/or recommended student exposures to and participation in genetic technology information and coursework, their responses varied.

Ischemia-reperfusion results in contractile dysfunction, necrosis, and vascular injury. This postischemic injury is mediated in part by superoxide radical production, neutrophils, dysfunction to ionic pumps, and edema formation. Adenosine is an autacoid released tonically by myocytes, endothelium, and neutrophils; the release of adenosine from the myocyte compartment into the interstitium is increased during ischemia. The major effects of adenosine are mediated by specific receptors identified as A1, A2a, A2b, and A3. Each receptor subtype contributes to physiological responses that influence ischemia-reperfusion injury. Adenosine has potent cardioprotective properties exerted during three major windows of opportunity: pretreatment, ischemia, and reperfusion. The cardioprotective effects exerted during pretreatment and ischemia may involve metabolic changes and hyperpolarization via K(ATP)-channel activation, mediated through A1 receptor mechanisms. The cardioprotective mechanisms exerted during reperfusion involve inhibition of neutrophils directly (superoxide anion generation, expression of adhesion molecules), and by inhibiting activation of the endothelium through A2 receptor-mediated mechanisms, thereby preventing neutrophil-endothelial cell interactions, which initiate the inflammatory-like component of reperfusion injury. Activation of the newly identified A3 receptor has been shown to be cardioprotective partially by inhibition of neutrophil adherence to endothelium and by neutrophil-independent mechanisms. These mechanisms of cardioprotection have been suggested to play major roles in the reduction of infarction and apoptosis after myocardial ischemia, cardioplegic arrest, and subsequent reperfusion. Adenosine has been used as an adjunct to both crystalloid and blood cardioplegia, but its potential as a cardioprotective agent has not been fully explored.

This study tested the hypothesis that A(3) adenosine receptors inhibit neutrophil (PMN) function and PMN-mediated reperfusion injury. 2-Chloro-N(6)-(3-iodobenzyl)adenosine-5'-N-methyluronamide (Cl-IB-MECA), an A(3) agonist, did not attenuate superoxide production or myeloperoxidase release from stimulated PMNs. However, Cl-IB-MECA reduced platelet-activating factor-stimulated PMN adherence to coronary endothelium at low concentrations: 52 +/- 27, 45 +/- 10, and 87 +/- 23 PMNs/mm(2) at 0.1, 1.0, and 10 nM vs. 422 +/- 64 PMNs/mm(2) with platelet-activating factor alone. This inhibition was not blocked by A(1) (5 microM KW-3902) or A(2a) (5 microM KF-21326) antagonists: 44 +/- 3 and 43 +/- 2 PMNs/mm(2), respectively. Endothelial pretreatment with 1 nM Cl-IB-MECA reduced PMN adherence, which was reversed by the A(3) antagonist MRS-1220 (100 nM). PMN-mediated reperfusion injury was initiated in isolated rabbit hearts by infusion of 28 x 10(6) PMNs/min for 10 min early in reperfusion. PMNs caused a significant decrease in recovery of left ventricular developed pressure and positive and negative time derivatives of pressure (23 +/- 3, 25 +/- 3, and 23 +/- 3% of baseline, respectively) vs. buffer-perfused hearts (43 +/- 7, 44 +/- 7, and 45 +/- 6%, respectively). Cl-IB-MECA (10 nM) given at reperfusion attenuated the PMN-mediated loss of contractile recovery (40 +/- 3, 46 +/- 5, and 42 +/- 4% of baseline). Cl-IB-MECA reduced myeloperoxidase release activity (5.3 +/- 0.6 absorbance units/min) and CD18-positive cells (54 +/- 9 cells/slide) compared with the untreated PMN group (17.9 +/- 1.7 absorbance units/min and 183 +/- 68 cells/slide). We conclude that Cl-IB-MECA attenuates reperfusion injury by decreasing PMN-endothelial cell interactions. These results suggest that the A(3) adenosine receptor may be a novel therapeutic target for treatment of myocardial ischemia and reperfusion.

Reperfusion of ischemic myocardium is necessary to salvage tissue from eventual death. However, reperfusion after even brief periods of ischemia is associated with pathologic changes that represent either an acceleration of processes initiated during ischemia per se, or new pathophysiological changes that were initiated after reperfusion. This 'reperfusion injury' shares many characteristics with inflammatory responses in the myocardium. Neutrophils feature prominently in this inflammatory component of postischemic injury. Ischemia-reperfusion prompts a release of oxygen free radicals, cytokines and other proinflammatory mediators that activate both the neutrophils and the coronary vascular endothelium. Activation of these cell types promotes the expression of adhesion molecules on both the neutrophils and endothelium, which recruits neutrophils to the surface of the endothelium and initiate a specific cascade of cell-cell interactions, leading first to adherence of neutrophils to the vascular endothelium, followed later by transendothelial migration and direct interaction with myocytes. This specific series of events is a prerequisite to the phenotypic expression of reperfusion injury, including endothelial dysfunction, microvascular collapse and blood flow defects, myocardial infarction and apoptosis. Pharmacologic therapy can target the various components in this critical series of events. Effective targets for these pharmacologic agents include: (a) inhibiting the release or accumulation of proinflammatory mediators, (b) altering neutrophil or endothelial cell activation and (c) attenuating adhesion molecule expression on endothelium, neutrophils and myocytes. Monoclonal antibodies to adhesion molecules (P-selectin, L-selectin, CD11, CD18), complement fragments and receptors attenuate neutrophil-mediated injury (vascular injury, infarction), but clinical application may encounter limitations due to antigen-antibody reactions with the peptides. Humanized antibodies and non-peptide agents, such as oligosaccharide analogs to sialyl Lewis, may prove effective in this regard. Both nitric oxide and adenosine exhibit broad spectrum effects against neutrophil-mediated events and, therefore, can intervene at several critical points in the ischemic-reperfusion response, and may offer greater benefit than agents that interdict at a single point in the cascade. The understanding of the molecular processes regulating actions of neutrophils in ischemic-reperfusion injury may be applicable to other clinical situations, such as trauma, shock and organ or tissue (i.e. vascular conduits) transplantation.

It is clear that complement plays an important role in the inflammatory process following oxidative stress in cellular and animal models. Clinical trials underway with novel complement inhibitors will establish the potential therapeutic benefit of complement inhibition in human disease. For as much as we understand about the role of complement in disease states, many questions remain. How is complement activated on endothelial cells following oxidative stress? What is the ligand for MBL on endothelial cells following oxidative stress? Will inhibition of MBL provide tissue protection to the extent observed with other complement inhibitors such as sCR1 or anti-C5 mAbs? These questions and more will undoubtedly be answered in the next millennium.

We tested the hypothesis that selective adenosine A(3)-receptor stimulation reduces postischemic contractile dysfunction through activation of ATP-sensitive potassium (K(ATP)) channels. Isolated, buffer-perfused rat hearts (n = 8/group) were not drug pretreated (control) or were pretreated with adenosine (20 microM), 2-chloro-N(6)-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IB-MECA; A(3) agonist, 100 nM), Cl-IB-MECA + 8-(3-noradamantyl)-1,3-dipropylxanthine (KW-3902; A(1) antagonist, 5 microM), Cl-IB-MECA + glibenclamide (Glib; K(ATP)-channel blocker, 0. 3 microM), or Glib alone for 12 min before 30 min of global normothermic ischemia followed by 2 h of reperfusion. After 2 h of reperfusion, left ventricular developed pressure (LVDP, %baseline) in control hearts was depressed to 34 +/- 2%. In hearts pretreated with Cl-IB-MECA, there was a statistically significant increase in LVDP (50 +/- 6%), which was reversed with coadministration of Glib (37 +/- 1%). Control hearts also showed similar decreases in left ventricular peak positive rate of change in pressure (dP/dt). Therefore, the A(3) agonist significantly attenuated postischemic cardiodynamic injury compared with the control, which was reversed by Glib. Cumulative creatine kinase (CK in U/min) activity was most pronounced in the control group (10.4 +/- 0.6) and was significantly decreased by Cl-IB-MECA (7.5 +/- 0.4), which was reversed by coadministration of Glib (9.4 +/- 0.2). Coronary flow was increased during adenosine infusion (160% of baseline) but not during Cl-IB-MECA infusion. Effects of Cl-IB-MECA were not reversed by the specific A(1) antagonist KW-3902. We conclude that cardioprotection afforded by A(3)-receptor stimulation may be mediated in part by K(ATP) channels. Cl-IB-MECA may be an effective pretreatment agent that attenuates postischemic cardiodynamic dysfunction and CK release without the vasodilator liability of other adenosine agonists.

The process of psychological adjustment to breast cancer was examined at diagnosis and at 3- and 6-month follow-ups in a sample of 80 women with Stage I-Stage IV breast cancer. At diagnosis, symptoms of anxiety/depression were predicted by low dispositional optimism, and this path was partially mediated by use of emotion-focused disengagement coping. Younger age also was predictive of anxiety/depression symptoms at time of diagnosis, and this relationship was fully mediated by magnitude of intrusive thoughts. At 3 months, changes in anxiety/depression symptoms were predicted only by intrusive thoughts. At 6 months, low dispositional optimism reemerged as a significant predictor of changes in anxiety/depression and again was partially mediated by the use of emotion-focused disengagement coping. Independent effects for problem-focused engagement and disengagement and emotion-focused engagement coping were also found at 6 months. Implications of these data for psychosocial interventions with breast cancer patients are highlighted.

The normal coronary vascular endothelium (VE) tonically releases nitric oxide (NO) by converting L-arginine to citrulline by a constitutive NO synthase. Reperfusion after myocardial ischemia reduces basal and stimulated release of NO. This "vascular reperfusion injury" is mediated largely by neutrophils (PMN) through specific interactions between adhesion molecules on the endothelium and the PMN, an interaction that precedes myocyte injury. NO inhibits the PMN-mediated reperfusion injury by direct effects on both the PMN and the vascular endothelium. Cardioprotective strategies include augmentation of endogenous NO by the precursor L-arginine and the administration of exogenous NO donors at the time of perfusion, which (1) attenuates PMN adherence to the coronary artery and venous endothelium, (2) reduces PMN-mediated endothelial dysfunction, (3) reduces PMN accumulation in the area at risk, and (4) reduces infarct size. Hence, NO represents a powerful therapeutic tool with which to attenuate the consequences of ischemia-reperfusion injury on vascular injury and infarction.

Women who are diagnosed with breast cancer are at high risk for experiencing affective distress; however, previous research suggests that older women may be less likely than younger women to experience extreme distress. Two issues remain unclear regarding age and affective distress: (a) the psychological processes that account for the association of age and distress, and (b) whether this association remains stable over the course of treatment and recovery from breast cancer. This study investigated symptoms of anxiety and depression in 80 women ages 36-80 years old with newly diagnosed breast cancer near the time of their diagnosis and at 3 and 6 months post-diagnosis. Disease severity and coping style were also examined. Symptoms of anxiety/depression and age were negatively correlated near the time of diagnosis. Path analysis controlling for disease severity revealed that coping involving the ventilation of emotion fully mediated the effect of age on symptoms of anxiety and depression. However, the association of age with symptoms of anxiety/depression was no longer significant at 3 and 6 months post-diagnosis, although emotional ventilation still predicted greater emotional distress at 6 months. These findings suggest that age is a salient factor to consider in the psychological adjustment of women with breast cancer near the time of initial diagnosis, with younger women exhibiting greater affective distress and a tendency to engage in less adaptive ways of coping. However, younger and older women do not differ in their adjustment over the subsequent course of their treatment and initial recovery. The use of emotional ventilation coping remains associated with poorer adjustment, independent of patients' age.

Objective: Unmodified reperfusion without cardioplegia in minimally invasive direct coronary artery bypass grafting procedures causes endothelial dysfunction that may predispose to polymorphonuclear neutrophil-mediated myocardial injury. This study tested the hypothesis that ischemic preconditioning in a minimally invasive direct coronary artery bypass grafting model attenuates postischemic endothelial dysfunction in coronary vessels., Methods: In anesthetized dogs, the left anterior descending coronary artery was occluded for 30 minutes and reperfused for 3 hours without ischemic preconditioning (no-ischemic preconditioning; n = 7); in 7 dogs, the left anterior descending occlusion was preceded by 5 minutes occlusion followed by 5 minutes of reperfusion. Relaxation responses to stimulators of nitric oxide synthase were used to evaluate endothelial function in arteries from the ischemic-reperfused (left anterior descending) and nonischemic (left circumflex coronary artery) zones., Results: Stimulated endothelial-dependent relaxation of epicardial left anterior descending artery to incremental concentrations of acetylcholine in the no-ischemic preconditioning animals was shifted to the right, and maximal relaxation was attenuated compared with the nonischemic left circumflex coronary artery (117% +/- 4% vs 138% +/- 5%). In contrast, acetylcholine-induced maximal relaxation was comparable in the left anterior descending artery versus left circumflex coronary artery in the ischemic preconditioning group (130% +/- 6% vs 135% +/- 5%). In 150- to 200- microm left anterior descending microvessels, 50% relaxation occurred with a lower concentration (log[M]) of acetylcholine in ischemic preconditioning versus no-ischemic preconditioning (-8.0 +/- 0.4 vs -7.0 +/- 0.1) with no group differences in smooth muscle relaxation to sodium nitroprusside, suggesting endothelial-specific damage. Adherence of fluorescent labeled polymorphonuclear neutrophils to epicardial coronary artery endothelium, used as an index of basal (unstimulated) anti-polymorphonuclear neutrophil function, was significantly attenuated by ischemic preconditioning versus no-ischemic preconditioning (293 +/- 25 polymorphonuclear neutrophils/mm2 vs 528 +/- 29 polymorphonuclear neutrophils/mm2)., Conclusion: In this minimally invasive direct coronary artery bypass grafting model, both agonist-stimulated and basal postischemic endothelial dysfunction were attenuated by ischemic preconditioning.

Pain intensity, disability, and depressive symptoms are hallmarks of chronic pain conditions, but little is known about the relationships among these symptoms in the transition from acute to chronic pain. In this study, an inception cohort of men with low back pain (N = 78) was assessed at 2, 6, and 12 months after pain onset. At 6 months, pain intensity, disability, and depressive symptoms were predicted only by their respective levels at 2 months after pain onset. At 12 months, pain intensity and depressive symptoms were predicted by heightened disability at 6 months after pain onset; 12-month depressive symptoms also were predicted by 2-month disability. Pain intensity was not predictive of changes in disability or depressive symptoms. These findings suggest that functional disability plays a more prominent role than pain intensity in the transition from acute to chronic pain. A "failure to adapt" conceptual model is presented to account for these results.

Objective: To determine the extent to which job satisfaction predicts pain, psychological distress, and disability 6 months after an initial episode of low back pain (LBP)., Design: A longitudinal design was used to follow an inception cohort experiencing first-episode low back pain with assessment at 2 and 6 months after pain onset., Setting: Urban medical center outpatient orthopedic clinic., Patients: The consecutive sample was comprised of 82 men with initial-onset acute LBP (T6 or below, daily pain for 6 to 10 weeks)., Intervention: Usual orthopedic care., Main Outcome Measures: The primary study outcomes were pain (Descriptor Differential Scale, Visual Analog Scales); disability (Sickness Impact Profile, Quality of Well-Being); and psychological distress (Beck Depression Inventory, Hamilton Rating Scale for Depression, Automatic Thoughts Questionnaire); predictor variables were orthopedic impairment (Waddell Physical Impairment Index) and job satisfaction (Job Descriptive Index, Work APGAR)., Results: Measures of job satisfaction, pain, disability, and psychological distress at baseline and 6 months after pain onset were separately reduced into factors using principle components factor analysis. In hierarchical multiple regression analyses, baseline job satisfaction significantly predicted variance in outcome scores at 6 months after pain onset, beyond the variance explained by control factors (demographics; baseline pain, mood, and disability; orthopedic impairment). Zero-order correlations between job satisfaction and orthopedic impairment were small and nonsignificant, suggesting that these two variables act independently in predicting outcome. Although type of work performed (desk work or work requiring light, moderate, or heavy lifting) and social position were correlated with job satisfaction at baseline, neither contributed to the prediction of outcome at 6 months., Conclusions: Satisfaction with one's job may protect against development of chronic pain and disability after acute onset back pain and, alternatively, dissatisfaction may heighten risk of chronicity. Vocational factors should be considered in the rehabilitation of acute back injury.

Background: Reperfusion causes injury to the coronary artery endothelium primarily by neutrophil-mediated mechanisms. However, factors other than neutrophils may govern the extent of myocardial necrosis. This study tests the hypothesis that gradual initiation of reflow will reduce reperfusion injury and preserve postischemic endothelial function., Methods: In 16 anesthetized dogs, the left anterior descending artery was ligated for 60 minutes. In one group, reperfusion was initiated abruptly (abrupt, n = 8), whereas in the gradual reperfusion group (ramp, n = 8), flow was slowly initiated during the first 30 minutes of reperfusion. After reperfusion, coronary artery segments were isolated to assess postischemic endothelial function., Results: Infarct size (area of necrosis/area at risk) was significantly reduced in the ramp group (28.2% +/- 2.0%) compared with abrupt (41.6% +/- 1.4%). Neutrophil accumulation (myeloperoxidase) in the area at risk was significantly greater in the ramp group compared with abrupt (8.0 +/- 1.3 versus 3.5 +/- 0.8 U/g tissue). In isolated postischemic left anterior descending arterial rings, the concentration of acetylcholine that elicited a response 50% of the maximum possible response was significantly greater in abrupt (-6.88 +/- 0.04 log [mol/L]) than ramp (-7.62 +/- 0.04 log [mol/L]) and control (-7.68 +/- 0.003 log [mol/L]), suggesting endothelial dysfunction. The concentration of A23187 that elicited a response 50% of the maximum possible response was similarly greater in abrupt (-7.24 +/- 0.03 log [mol/L]) versus ramp (-7.62 +/- 0.03 log [mol/L]) and control (-7.8 +/- 0.04 log [mol/L]). Smooth muscle dysfunction (response to sodium nitrite) also occurred in the abrupt rings., Conclusions: Gradual reperfusion of an ischemic area reduces infarct size and preserves endothelial function but paradoxically increases neutrophil accumulation within the area at risk.

Diabetes exerts a major economic impact on healthcare in the United States both in terms of direct and indirect costs. Diabetes management and education programs designed to assist patients in achieving more optimal glycemic control represent a potential mechanism for reducing the morbidity and costs associated with diabetes. The relationship between HbA1c and patient hospitalizations and between HbA1c and days lost from work or school related to diabetes within the past year were evaluated. A cohort of 2359 patients with diabetes (188 type I, 2171 type II) referred to a comprehensive diabetes self-management training program was included in the analyses. Overall, 350 (14.8%) patients reported hospitalization, and 212 (9.0%) reported days lost from work or school. Patients with type I diabetes reported more hospitalizations (26.1% vs 13.9% and days lost (19.2% vs 8.1%) than type II patients. For the hospitalization outcome, the multivariate analyses indicated that younger age, the number of co-morbidities, and the duration of diabetes exerted a greater influence on the reported numbers of hospitalization than glycemic control. For the days lost outcome, the multivariate analyses indicated that there was a marginally significant association between patients with poor glycemic control and reported work or school loss related to diabetes (odds ratio = 1.5; 95% confidence interval, 1.0-2.2). These data suggest that interventions that improve glycemic control may decrease indirect costs related to diabetes.

Ischemia-reperfusion damages endothelium and impairs basal production of nitric oxide. Basally released nitric oxide is cardioprotective by its inhibition of neutrophil activities. Loss of endogenous nitric oxide with endothelial injury may occur during two phases: cardioplegic ischemia and reperfusion (aortic declamping). This study tested the hypothesis that inhibition of endogenously released nitric oxide in hearts subjected to regional ischemia, cardioplegic arrest, and reperfusion (1) restricts endogenous cardioprotection and permits neutrophil-mediated damage and (2) expresses damage during the reperfusion phase. L-Nitro-arginine was used to block basal nitric oxide production. In 22 anesthetized dogs, the left anterior descending artery was ligated for 90 minutes followed by 1 hour of arrest with cold multidose (every 20 minutes) blood cardioplegia. Dogs were divided into three groups: the first group received standard unsupplemented blood cardioplegia (group 1, n = 8), in the second group L-nitro-arginine was administered as an additive to blood cardioplegic solution (1 mmol) and as an infusion during reperfusion (34 mg/kg) (group 2, n = 7), and in the third group L-nitro-arginine was administered only at reperfusion (group 3, n = 7). The ligature was released during the second infusion of cardioplegic solution. Infarct size (triphenyltetrazolium chloride) was increased in group 3 (L-nitro-arginine only at reperfusion) compared with that in group 1 (standard blood cardioplegia) (49% +/- 6% vs 34% +/- 2%, respectively), but was not further extended in group 2 (L-nitro-arginine as an additive to blood cardioplegic solution and at reperfusion) (56% +/- 3%, p > 0.05 vs group 3), which suggests primarily a reperfusion process. Polymorphonuclear neutrophil-specific myeloperoxidase activity in the area at risk was elevated comparably in groups 2 and 3 (group 2: 2.9 +/- 0.5 units/gm tissue, p = 0.06 vs group 1; group 3: 3.9 +/- 1.0 units/gm tissue, p < 0.05 vs group 1) compared with that in the standard blood cardioplegia group (1.7 +/- 0.3 units/gm tissue), suggesting polymorphonuclear neutrophil accumulation occurs primarily during reperfusion. Polymorphonuclear neutrophil adherence in ischemic-reperfused left anterior descending artery segments was comparably greater in group 2 (L-nitro-arginine as an additive to blood cardioplegic solution and at reperfusion: 195 +/- 21 polymorphonuclear neutrophils/mm2 of artery, p < 0.05 vs group 1) and group 3 (L-nitro-arginine only at reperfusion: 224 +/- 20 polymorphonuclear neutrophils/mm2 of artery, p < 0.05 vs group 1) relative to that in group 1 (108 +/- 19 polymorphonuclear neutrophils/mm2 of artery). There was no significant adherence to nonischemic circumflex arteries. We conclude that blockade of endogenous nitric oxide augments postischemic injury mediated by polymorphonuclear neutrophils, and this damage is expressed primarily during the reperfusion phase.

This study tests the hypothesis that adenosine A2 receptor activation reduces reperfusion injury by inhibiting neutrophils in a canine model of ischemia and reperfusion. In 16 anesthetized, open-chest dogs, the left anterior descending coronary artery was ligated for 60 min and reperfused for 3 hr. An intracoronary infusion of either the selective adenosine A2 agonist CGS-21680 at 0.2 microgram/kg/min (n = 8) or vehicle (n = 8) was started 5 min before reperfusion and discontinued after 60 min. The area at risk was comparable between vehicle-treated and CGS-21680-treated groups (39.6 +/- 4.1 vs. 37.1 +/- 2.5% of left ventricle). Infarction size, determined with triphenyltetrazolium chloride, was smaller in the CGS-21680-treated group than in the vehicle-treated group (15.4 +/- 2.9 vs. 29.8 +/- 2.3% of area at risk, P < .05 vs. vehicle-treated group). CGS-21680 significantly reduced neutrophil accumulation (myeloperoxidase activity) in the nonnecrotic area at risk tissue, compared with the vehicle-treated group (2.12 +/- 0.5 vs. 6.47 +/- 0.6 U/g of tissue, P < .05 vs. vehicle-treated group). In in vitro studies, CGS-21680 reduced platelet-activating factor (PAF)-activated canine neutrophil adherence to the endothelial surface of normal homologous coronary artery segments. Compared with PAF-stimulated neutrophils (188.4 +/- 9.4 adhered neutrophils/mm2), CGS-21680 reduced adherence close to base-line levels (46.6 +/- 5.8 adhered neutrophils/mm2) at concentrations of 10 microM (65.6 +/- 8.2 adhered neutrophils/mm2, P < .05 vs. PAF-stimulated group) and 50 microM (56.6 +/- 4.6 adhered neutrophils/mm2, P < .05 vs. PAF-stimulated group). Superoxide anion production (cytochrome c reduction) by activated neutrophils was reduced by CGS-21680 from 33.8 +/- 5.0 to 8.9 +/- 3.6 nmol/5 min/5 x 10(5) cells (P < .05 vs. PAF-stimulated group). We conclude that specific A2 receptor stimulation with CGS-21680 at reflow reduces reperfusion injury by inhibiting neutrophil-related processes.