SemOpenAlex |

SemOpenAlex

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2900549557> ?p ?o ?g. }

Showing items 1 to 100 of ±263 with 100 items per page.

W2900549557 endingPage "423" @default.
W2900549557 startingPage "379" @default.
W2900549557 abstract "This text is excerpted from the complete document, which includes the Consortium Member Organizations and Steering Committee Representatives, Acknowledgments, Reviewers, Glossary, and Appendix (Search Strategies).Administrative and financial support provided by Paralyzed Veterans of America.Reprinted with permission from the Paralyzed Veterans of America (PVA) Consortium for Spinal Cord Medicine Clinical Practice Guidelines Consumer Guide: “Cardiometabolic Risk after Spinal Cord Injury: A Clinical Practice Guideline for Health Care Providers.” Washington, DC: © 2018 Paralyzed Veterans of America. Copies of the PVA's Guidelines are available at www.pva.org.These guidelines have been prepared based on scientific and professional information available in 2018. Users should periodically review this material to ensure that the advice herein is consistent with current reasonable clinical practice. The websites noted in this document were current at the time of publication; however, because web addresses and the information contained therein change frequently the reader is encouraged to stay apprised of the most current information.Cardiometabolic disease (CMD) can be thought of as a silent killer. The clinical manifestations of this secondary complication of spinal cord injury (SCI) may not be apparent until too late to intervene. Until now, CMD has been less of a focus of the SCI community as a whole, compared to the other major secondary conditions of neurogenic bowel and bladder, autonomic dysfunction, respiratory insufficiency, depression, sexual dysfunction, pressure injuries, and venous thromboembolism, which are overt in their presentation and have been addressed in previous guidelines.The recommendations of this Clinical Practice Guideline (CPG) regarding identifying and managing CMD risks are in line with current recommendations for identifying and managing CMD risks in people without SCI, which have also been recently updated. However, these recommendations also take into consideration the differences between the body composition and physiology of those with SCI and those without SCI, and the risks of certain interventions for persons with SCI, given the presence of other secondary conditions such as neurogenic bowel, and also acknowledge the challenges to implementing the recommendations within the SCI community.We were fortunate in the development and peer review of this CPG to have representation from all the various stakeholders and subspecialties impacted by these recommendations, including a range of experts in nutrition, exercise, cardiology, endocrinology, internal medicine, and rehabilitation. This wide-ranging representation will hopefully translate into uniform, quality practice through the widespread use of this CPG to guide CMD prevention and treatment in all settings, which can only result in the best outcomes and least amount of morbidity and mortality for those who experience SCI.On behalf of the consortium steering committee, I want first to acknowledge the leadership of the guideline panel, namely the Chair, Mark Nash, and Co-Chair Suzanne Groah, in guiding this panel through the ups and downs of a development process which spanned five years. The panel members themselves, who kept to task for so long, and the many reviewers who provided valuable feedback from all areas, are to be commended. Everyone, including the panel Chair and Co-Chair, volunteered their time to help produce this superb document. In addition, I wish to acknowledge the ongoing support of Paralyzed Veterans of America (Paralyzed Veterans), especially President David Zurfluh, Executive Director Carl Blake, and Director of Research and Education Cheryl Vines, as well as the rest of the leadership team, without whose support these guidelines would not exist.Thomas N. Bryce, MDChair, Steering CommitteeConsortium for Spinal Cord MedicineThe following Guideline is the first from the Consortium for Spinal Cord Medicine to address CMD after SCI. In doing so, it reports the emergence of all-cause cardiovascular diseases (CVD) and CVD-related risks as significant health hazards for persons with SCI and establishes a foundational standard for identification and management of cardiometabolic risks. The spinal cord community was first made aware of these risks in the early 1980s. Since then, hundreds of scholarly articles have examined antecedents, causes, personal and population characteristics, co-morbidities and treatments for these hazards. These studies have confirmed that persons with SCI are frequently sedentary, overweight, dyslipidemic and at elevated risk for insulin resistance, thus placing them in jeopardy of developing CMD. None of the health hazards imposed by the five archetypical CMD risk components foretells the long, active, productive, and healthy life we seek for persons with SCI. These conditions may also prohibit persons with SCI from undergoing, or ultimately benefiting from, the restorative therapies in clinical trials, or from using rehabilitation technologies that require a relatively lean and healthy body for their efficient use.Unlike some diseases and disorders addressed by other Consortium Guidelines, CMD typically develops slowly and without overt symptoms. Unless routinely surveilled in the SCI population, CMD may be irreversible once clinically detected. The panel seriously considered the possibility that CMD and its component risks, once identified, will be far more challenging to treat in persons with SCI than their non-disabled counterparts. For these reasons, this guideline will favor scheduled surveillance, early risk assessment, timely symptom recognition, and prudent interventional care. In arriving at these recommendations, the Panel asserts that an enlightened and compassionate health care system, and a caring society, will unquestionably favor early assessment and aggressive preemptive care when not doing so might result in early morbidity and uncertain mortality.The consumers of this guideline – health professionals and stakeholders with SCI– will note that its evidence and opinions may sometimes point to persons with SCI being at no greater risk for a diagnosis of CMD or its component risks than their non-disabled cohorts. It should be emphasized, however, that all-cause CVD and related conditions are among the most prevalent, life threatening, function compromising and costly of known medical hazards. In making recommendations, the Panel has also taken into consideration that our health care system is even less prepared to effectively treat CMD in those with SCI than to prevent it. Given these circumstances, we believe it is practical to embrace primary prevention as a best-practice, strategic approach. In some instances, the Panel found no evidence or clinical intuition to sidestep the adoption of several recommendations that currently exist for CMD diagnosis and management in the general population. These strategic guidelines provide an extensively vetted, evidence-based standard in cases where no such guideposts have been fashioned or applied for the benefit of the SCI population. When adopting standards used for the general population, we have also identified areas in need of investigation so that the foundational evidence for CMD identification and management can become even more representative of, and relevant for, the SCI population.In publishing the Guideline, we extend our sincerest thanks for the dedicated work and meaningful contributions of Panel Members, Drs. Trevor Dyson-Hudson, David Gater, Jesse Lieberman, Jonathan Myers, Sunil Sabharwal and Allen Taylor. We further note with appreciation the contributions of Ms. Cheryl Vines, Dr. Thomas Bryce, the Paralyzed Veterans CPG Steering Committee, and the Consortium Partners who collectively recognized the importance of this topic and unfailingly supported the Panel's activities to their completion.Mark S. Nash, PhD, FACSM, Panel ChairLeonard M. Miller School of Medicine,The University of MiamiMiami, FLSuzanne L. Groah, MD, MPH, Panel Co-ChairMedstar National Rehabilitation HospitalGeorgetown University Medical CenterWashington, DCThe overall objective of this guideline is to improve the care of patients with spinal cord injury by guiding clinicians and policymakers with its recommendations. The following recommendations use available evidence and – where evidence is limited – Panel experience and consensus. The Panel based its evidence ratings primarily on research in which the focus of the study was SCI. This information was supplemented using evidence from trials, guidelines, and expert opinions contained in the scientific literature of non-SCI populations.For individual patients, decisions are best made by considering these recommendations combined with clinical judgment, the latter based on specific knowledge about each patient's risk factors for cardiometabolic disease, the potential for adverse effects, and the availability of various options within one's center. The bracketed rating refers to the level of scientific evidence, the strength of the evidence, and the level of panel agreement with the recommendations.1Recommendations:Recommendations:Recommendations:Recommendations:Recommendations:Recommendations:Recommendation:Recommendations:Recommendations:Recommendations:Recommendations:Recommendations:The Consortium of Spinal Cord Medicine is a collaboration of professional and consumer organizations with a common interest in healthcare for individuals living with spinal cord injury. The Consortium's mission is to direct the development and dissemination of evidence-based clinical practice guidelines (CPGs) and companion consumer guides. This mission is solely directed to improving the health care and quality of life for persons with SCI.The Consortium is funded and administered by Paralyzed Veterans of America (Paralyzed Veterans). The Steering Committee, administratively supported by Paralyzed Veterans's Research and Education Department, is made up of one representative from each consortium-member organization.The development of these guidelines involved the following major steps: creating a list of formal, key questions to be addressed, systematic searches of published literature related to these questions, critical appraisal of the quality of the retrieved studies, abstraction of relevant study results, creation of evidence-based recommendations, development of rationale that explain the recommendations, and review and agreement by panel members. The SCI Consortium's CPG development process also involved extensive field review and a legal review.Paralyzed Veterans contracted the literature searches and evidence reviews to an independent firm and provided administrative support for the process. Panel members received no compensation for their participation and declared all potential financial or other conflicts of interest.A medical librarian searched Ovid MEDLINE® (1980 through September, Week 2 2015), the Cochrane Central Register of Controlled Trials® (1980 through September 22, 2015), Cochrane Health Technology Assessments (searched September 22, 2015), and the Cochrane Database of Systematic Reviews® (2005 through September 2015) using search terms related to chronic spinal cord injury. We also searched Ovid MEDLINE for names of authors known to have published in this area (on September 22, 2015). See the Appendix for complete search strategies. We attempted to identify additional studies through hand searches of reference lists of included studies and reviews. All citations were imported into an electronic database (Endnote® X7, Thomson Reuters).Selection of included studies was based on the inclusion criteria created in consultation with Paralyzed Veterans. Two reviewers independently assessed titles and abstracts of citations identified through literature searches for inclusion, using the criteria below. Full-text articles of potentially relevant citations were retrieved and were assessed for inclusion by both reviewers. Disagreements were resolved by consensus. Results published only in abstract form were not included because inadequate details were available for quality assessment (risk of bias). Abstracts that had additional information available in slide sets from conference presentations, or those that provided supplemental data from published studies, were considered for inclusion.In consultation with Paralyzed Veterans, 14 key questions were formulated relating to the prevalence of CMD and risk factors for disease, screening for CMD, CMD diagnosis methods, and the comparative effectiveness of treatment for CMD in the SCI population. Key questions 13 and 14 regarding CMD guidelines were not part of the systematic review, but they provide information on relevant guideline recommendations. Key questions and inclusion criteria are below.Patients with nonacute, traumatic, or atraumatic irreversible spinal cord injury or dysfunction resulting in paralysis (excluding patients with spinal stroke)Information was abstracted on population characteristics, interventions, subject enrollment, prevalence, results for efficacy, effectiveness, and harms outcomes for trials, observational studies, and systematic reviews. When reported, intent-to-treat results were recorded. Data abstraction was performed by one reviewer and independently checked by a second reviewer. Differences were resolved by consensus.We assessed the internal validity (risk of bias) of trials, observational studies, and systematic reviews based on predefined criteria. These criteria are based on the U.S. Preventive Services Task Force and the National Health Service Centre for Reviews and Dissemination (United Kingdom) criteria7–8 and the GRADE guidelines.9 We rated the internal validity of each trial based on the methods used for randomization, allocation concealment, blinding, the similarity of compared groups at baseline, loss to follow-up, and the use of intent-to-treat analysis. Trials that had a fatal flaw were rated at a high risk of bias, trials that met all criteria were rated at a low risk of bias, and the remainder were rated at a moderate risk of bias. As the moderate risk of bias category is broad, studies with this rating vary in their strengths and weaknesses. The results of some studies rated moderate risk of bias are likely to be valid, while others are only possibly valid. A fatal flaw is reflected by failure to meet combinations of items on the risk-of-bias checklist. An example would be a study with high attrition (e.g., 60%) combined with the inadequate handling of missing data, or one where details on randomization and/or allocation concealment were lacking, and there were baseline differences in important prognostic characteristics. Observational studies were rated on non-biased selection, loss to follow-up, pre- specification of outcomes, well-described and adequate ascertainment techniques, statistical analysis of potential confounders, and adequate duration of follow-up. Systematic reviews were rated on the clarity of review questions, the specification of inclusion and exclusion criteria, use of multiple databases and search for grey literature, sufficient detail of included studies, adequate assessment of the risk of bias of included studies, and adequate summarization of primary studies.Two reviewers independently assessed the quality of each study and differences were resolved by consensus.We graded quality of evidence (QoE) based on the GRADE approach.10–14 Developed to grade the overall quality of a body of evidence, this approach incorporates four key domains: risk of bias (includes study design and aggregate risk of bias), consistency, directness, and precision of the evidence. It also considers other optional domains that may be relevant for some scenarios, such as a dose- response association, plausible confounding that would decrease the observed effect, the strength of association (magnitude of effect), and publication bias.Table 1 describes the grades of evidence that can be assigned. Grades reflect the quality of the body of evidence to answer key questions. Grades do not refer to the general efficacy or effectiveness of treatments, for example. Two reviewers independently assessed each domain for each outcome and differences were resolved by consensus.The quality of the body of evidence was evaluated for each outcome by key question.We constructed evidence tables showing the study characteristics, quality ratings, and results for all included studies. We reviewed studies using a hierarchy of evidence approach, where the best evidence is the focus of our synthesis for each question, population, intervention, and outcome addressed.The following section addresses hazards for CMD and its risk components in persons with SCI.CMD is a coalescing of interrelated cardiovascular, renal,metabolic,pro-thrombotic,andinflammatory health hazards,1 and is recognized as a disease entity by the American Society of Endocrinology, the AHA, the International Diabetes Federation (IDF), the American Diabetes Association (ADA), and the World Health Organization (WHO).2 The AHA and the National Institutes of Health (NIH) National Heart Lung Blood Institute (NHLBI) define CMD as the co-occurrence of any three of the medical hazards described in Table 2.Abdominal (central) obesity, hypertension, hyperglycemia, hypertriglyceridemia, and low high-density lipoproteinemia.3 While still lacking a fully harmonized diagnosis,2 CMD is recognized to increase the probability of developing atherosclerotic disease, heart failure, and diabetes.4–5 Prevalence in the U.S. is estimated at 34% of the non-disabled adult population6 and is increasing with population aging. The CMD diagnosis confers a health risk equivalent to either the diagnosis of diabetes mellitus or extant coronary disease.CMD is ultimately caused or worsened by a mismatch between energy consumption that is excessive in intake of kilocalories and saturated fats, and insufficient daily energy expenditure.7 These risks are typically expressed through lifestyle factors reflecting poor compliance with optimal nutrition and an active lifestyle. The primary metabolic abnormality of CMD is insulin resistance, while the unified cause ensues excessive body mass, whose clinical feature is excessive visceral and ectopic fat. Inflammatory stress and endocrinopathies are not included among the AHA guideline risks, although both are recognized as either cause or consequence of the disorder. 8–9The prevalence of CMD reported in adults with SCI ranges from 31–72%, contingent on the number of possible risk factors included in the definition.10–11 Depending on the study, this prevalence at least equals, and often exceeds, the CMD prevalence for the general population, which the Panel feels informs the SCI community about the risk that it poses.The guideline component risks for CMD include obesity, insulin resistance, dyslipidemia, and hypertension. The following section addresses the hazards imposed by these individual risk components on the SCI population.“Obesity is a chronic, relapsing, neurochemical disease produced by the interaction of environment and host.”13 Emerging data suggests adipose tissue (especially visceral adiposity) and its associated connective tissue are the primary sources of systemic proinflammatory cytokines, vasoactive hormones and non-esterified fatty acids implicated in the development of dyslipidemia, insulin resistance, hypertension, and arteriosclerosis. Initially defined by the scientific community as >22% body fat (%BF) in men or >35%BF in women, the definition of obesity was changed to BMI ≥30 kg/m2 by the WHO at the turn of the century to more easily capture large populations at risk for cardiovascular disease.14Of the five AHA component risks, obesity after SCI has been most challenging to characterize and compare to non-SCI populations. BMI grossly underestimates obesity (overfat) in persons with SCI due to profound changes in fat-free mass (FFM), reflecting obligatory sarcopenia, osteopenia and reduced total body water associated with somatic and autonomic disruption of the spinal cord. The standard cutoff for BMI of >30 kg/m2 grossly underestimates adiposity in persons with SCI, such that the true prevalence of CMD exceeds the 31–72% prevalence of CMD in persons with SCI reported in the literature.1115–16 Multiple studies have reported a BMI of 22–25 kg/m2 in persons with SCI translates to >30% BF,17–24 which is well above the standard cut-score for obesity of 22% BF in the non-SCI population. One study recalculated CMD prevalence with SCI-specific cutoff BMI≥22 kg/m2 and found that doing so increased the range from 27–36% to 82–85% prevalence.16For accurate obesity comparisons between persons with SCI and those without, BMI cutoffs for obesity of 22 kg/m2 and 30 kg/m2, respectively, should be used. Another option to determine overweight and obesity risk is waist circumference. However, the use of this proxy has not been validated in SCI populations and is likely inadequate as a surrogate obesity marker due to varying levels and neurological completeness of abdominal muscle paralysis.25The prevalence of diabetes in people with SCI varies with the attributes of the population being studied. Prevalence studies for diabetes in people with SCI in the U. S. have primariiily focused on U.S. veterans, so findings may not be generalizable to other populations.26–28 U.S. studies report a higher prevalence of diabetes in people with SCI (16% to 33%) than those conducted in other countries (6% to 14%).29–32 Evidence indicates that the prevalence of diabetes among U.S. veterans with SCI is not different from veterans without SCI.26–27 However, moderate quality evidence from other countries indicates that persons with SCI have a higher prevalence of diabetes than able-bodied controls.29–32 Traditional risk factors for diabetes and glucose intolerance in the general population, such as increasing age, at-risk race or ethnicity (Asian, African American, Hispanic, Native American, or Pacific Islander), and family history of diabetes,33 likely apply to the SCI population as well, though evidence specific to SCI is limited and of low quality.The prevalence of dyslipidemia among persons with SCI is high when based on established cholesterol guidelines as well as comparisons to non-disabled individuals. Studies on lipid profiles reflecting higher cardiovascular risk among persons with SCI, compared to non-disabled individuals, have included the spectrum of lipid subfractions, including HDL-C, LDL-C, ratios of total cholesterol to HDL-C and LDL-C, and HDL/Apo-1 and Apo-A1/ApoB.34–41 All these findings support the Panel's recommendations. The most consistent observation from studies assessing lipid profiles of persons with SCI is depressed HDL-C levels when compared to non-disabled individuals.15383942–44 However, many of these studies lack specifics regarding which lipid abnormalities are observed, and their potential association with the level and extent of the injury and other population characteristics. This disparity has led to variation in results between studies comparing cohorts of persons with SCI versus non-disabled controls. For example, in a large study comparing U.S. Veterans 65 years and older with subjects having SCI, ambulatory older Veterans, and ambulatory control subjects, no differences were observed in the prevalence of dyslipidemia (44%, 48, and 44%, respectively).27 Conversely, in a Swedish cohort, the prevalence of dyslipidemia was markedly higher in persons with SCI than non-disabled controls (11% vs. 2%, p<0.001).29 Studies have generally reported somewhat lower total cholesterol and HDL-C levels, but higher TG and a higher ratio of total cholesterol to HDL-C among SCI individuals compared with matched groups of non-SCI subjects.34–3943 Importantly, the overall prevalence of dyslipidemia in the general US population also tends to be high, and some research has questioned whether the prevalence of dyslipidemia is appreciably higher in persons with SCI (e.g., ≈50% of Americans have some form of lipid abnormality).45 There is a lack of consistent data regarding the effects of level of injury as well as other clinical and demographic factors on the prevalence of dyslipidemia in persons with SCI.The reported prevalence of hypertension in people with SCI varies widely, ranging from 14% to 61%.273146–50 Age, gender, ethnicity, nationality, and other attributes of the population being studied may affect the reported prevalence, as may differences in methods to ascertain the presence of hypertension. Studies on the prevalence of hypertension in SCI in the United States2746–49 have mostly been conducted in U.S. veterans; findings may not be generalizable to other populations.Injury to the spinal cord influences the regulation of blood pressure. Characteristics of the SCI, including neurological level and etiology of injury, may affect the prevalence of hypertension. Prevalence of hypertension is reported to be lower in people with tetraplegia compared with paraplegia, especially those with low paraplegia (T7 and below).46–4750 The odds of having hypertension were significantly lower in tetraplegic injuries, compared to matched controls without SCI in a study of U.S. veterans, while paraplegic injuries had similar odds of hypertension as controls. Veterans with non-traumatic SCI had higher odds of having hypertension compared with those with traumatic SCI after controlling for available SCI characteristics, age, demographics, and comorbidities.46The following section addresses the supplementary hazards associated with SCI that are population risk-relevant but not included among the AHA risk component hazards of CMD.Exercise is a fundamental element in maintaining physical capacity and cardiovascular and metabolic health for persons of all ages and health states. The unified American College of Sports Medicine (ACSM) and WHO guidelines51 prescribe exercise and provide physical activity guidelines for supporting health and wellness in the general population, which to the best of their abilities are also recommended for individuals with SCI.52 These guidelines are in substantial agreement with both the ACSM Guidelines for Exercise Testing and Prescription51 and also the Physical Activity Guidelines for Adults with SCI that were established for SCI Action Canada.53 They are also similar to the Physical Fitness for Special Populations (PFSP) “Physical Fitness for Individuals with Spinal Cord Injury” recommendations of the American Physical Therapy Association.54A sedentary lifestyle either imposed on or adopted by persons with SCI has long identified physical inactivity as a population health risk.55 Notwithstanding a single identified cause for a sedentary lifestyle, a 1993 study reported that 1 in 4 healthy, young persons with SCI fail to satisfy a level of fitness needed to perform many essential activities of daily living.56 More recently, it was reported that approximately 50% of patients with SCI report no leisure-time physical activity and 15% report leisure-time physical activity below the threshold required for meaningful health benefit (i.e., <1 hour/week).57 This report implies that of the estimated 558,000 individuals currently living with SCI in the U.S., approximately 279,000 are completely sedentary and another 84,000 participate in a leisure-time physical activity considered inadequate to positively impact health.58 While those with sensorimotor sparing of upper limb and trunk functions (i.e., paraplegia) have far greater capacities for physical activity and more extensive exercise options,59 they are not necessarily more fit than persons with tetraplegia.5560While physical deconditioning per se is not included among the five component risks of CMD, it is linked with and considered a major cause of obesity, insulin resistance, hypertension, and dyslipidemia. Several factors, however, point to physical deconditioning after SCI as a major contributor to a CMD diagnosis. First, the SCI population was long ago identified at the lowest end of the human fitness continuum, making physical deconditioning suspect as a cause for CMD-related risks.5561–63 Second, a common finding after SCI is a low concentration of HDL-C,3640–4164 which is known in persons without disability to be both cardioprotective and strongly linked with low levels of cardiorespiratory fitness.65–67 Third, barriers to exercise participation are altogether common after SCI and may include self-imposed obstacles to exercise participation or legitimate physical barriers to exercise, lack of adapted exercise equipment, limited professional assistance, societal moirés, and financial limitations.68–72Following an acute SCI, body composition is altered by a significant loss of sublesional skeletal muscle, an increase in visceral fat mass,1–4 and an injury-dependent decrease in sympathetic nervous system activity.5 As a result, persons with SCI have decreased energy expenditure relative to energy intake, and when compared to individuals without SCI.6–8 Subsequently, central (i.e., visceral) adiposity is common among persons with chronic SCI and is more prevalent than in persons without SCI. Importantly, the greatest increase in weight often occurs during the first year after injury.9–15While physical activity has established benefits as a countermeasure to excessive caloric intake, some persons with SCI cannot substantially increase energy expenditure with physical activity alone. Some are limited by their level of injury17 and overuse injuries18–20 as well as other documented barriers to exercise.21–24 Based on the existing evidence, and appreciating that caloric expenditure from activity rarely compensates for excessive caloric intake, dietary changes appear to be a more practical target for obesity management a" @default.
W2900549557 created "2018-11-29" @default.
W2900549557 creator A5003720682 @default.
W2900549557 creator A5009309290 @default.
W2900549557 creator A5015262154 @default.
W2900549557 creator A5052125958 @default.
W2900549557 creator A5052942895 @default.
W2900549557 creator A5053998387 @default.
W2900549557 creator A5064642533 @default.
W2900549557 creator A5070596081 @default.
W2900549557 date "2018-09-01" @default.
W2900549557 modified "2023-10-11" @default.
W2900549557 title "Identification and Management of Cardiometabolic Risk after Spinal Cord Injury: Clinical Practice Guideline for Health Care Providers" @default.
W2900549557 cites W1458217 @default.
W2900549557 cites W1537549309 @default.
W2900549557 cites W1540139486 @default.
W2900549557 cites W154048617 @default.
W2900549557 cites W1568353255 @default.
W2900549557 cites W1570003363 @default.
W2900549557 cites W1607111685 @default.
W2900549557 cites W1680205247 @default.
W2900549557 cites W174940535 @default.
W2900549557 cites W1750705727 @default.
W2900549557 cites W1875201314 @default.
W2900549557 cites W1964703381 @default.
W2900549557 cites W1964898634 @default.
W2900549557 cites W1965991605 @default.
W2900549557 cites W1967356882 @default.
W2900549557 cites W1969705877 @default.
W2900549557 cites W1974846915 @default.
W2900549557 cites W1975707660 @default.
W2900549557 cites W1978245267 @default.
W2900549557 cites W1980641839 @default.
W2900549557 cites W1980680910 @default.
W2900549557 cites W1983556022 @default.
W2900549557 cites W1987282451 @default.
W2900549557 cites W1988538525 @default.
W2900549557 cites W1988608522 @default.
W2900549557 cites W1989030328 @default.
W2900549557 cites W1990474431 @default.
W2900549557 cites W1992162034 @default.
W2900549557 cites W1992601446 @default.
W2900549557 cites W1997115741 @default.
W2900549557 cites W1998631080 @default.
W2900549557 cites W1998736289 @default.
W2900549557 cites W2000717800 @default.
W2900549557 cites W2002300254 @default.
W2900549557 cites W2004365762 @default.
W2900549557 cites W2004551769 @default.
W2900549557 cites W2005136472 @default.
W2900549557 cites W2005348121 @default.
W2900549557 cites W2005834159 @default.
W2900549557 cites W2006771048 @default.
W2900549557 cites W2006980165 @default.
W2900549557 cites W2008546612 @default.
W2900549557 cites W2011037209 @default.
W2900549557 cites W2014533960 @default.
W2900549557 cites W2015371669 @default.
W2900549557 cites W2017602185 @default.
W2900549557 cites W2019972220 @default.
W2900549557 cites W2020565601 @default.
W2900549557 cites W2021158673 @default.
W2900549557 cites W2024061669 @default.
W2900549557 cites W2024793465 @default.
W2900549557 cites W2025277791 @default.
W2900549557 cites W2025494397 @default.
W2900549557 cites W2026317679 @default.
W2900549557 cites W2029591368 @default.
W2900549557 cites W2030041587 @default.
W2900549557 cites W2030157468 @default.
W2900549557 cites W2030276358 @default.
W2900549557 cites W2030462853 @default.
W2900549557 cites W2031373897 @default.
W2900549557 cites W2037530550 @default.
W2900549557 cites W2037724515 @default.
W2900549557 cites W2038930474 @default.
W2900549557 cites W2042338495 @default.
W2900549557 cites W2043661819 @default.
W2900549557 cites W2045808465 @default.
W2900549557 cites W2045977346 @default.
W2900549557 cites W2049066158 @default.
W2900549557 cites W2051216268 @default.
W2900549557 cites W2053447636 @default.
W2900549557 cites W2054936668 @default.
W2900549557 cites W2056741003 @default.
W2900549557 cites W2057338072 @default.
W2900549557 cites W2058610272 @default.
W2900549557 cites W2060751297 @default.
W2900549557 cites W2062608554 @default.
W2900549557 cites W2062882596 @default.
W2900549557 cites W2065031884 @default.
W2900549557 cites W2068664171 @default.
W2900549557 cites W2070345301 @default.
W2900549557 cites W2070415982 @default.
W2900549557 cites W2071138904 @default.
W2900549557 cites W2072898081 @default.
W2900549557 cites W2073046772 @default.
W2900549557 cites W2073505261 @default.