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Search Results: 1 - 10 of 209995 matches for " Danielle L Davison "
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Neurogenic pulmonary edema
Danielle L Davison, Megan Terek, Lakhmir S Chawla
Critical Care , 2012, DOI: 10.1186/cc11226
Abstract: The syndrome of NPE has been recognized for over a century. In 1903, Harvey Williams Cushing, described the connection between CNS injury and hemodynamic dysfunction [6]; and, in 1908, W. T. Shanahan reported 11 cases of acute pulmonary edema as a complication of epileptic seizures [7]. Francois Moutier described the sudden onset of pulmonary edema among soldiers shot in the head in World War I [8]. Similar reports exist of observed alveolar edema and hemorrhage in the lungs of 17 soldiers dying after isolated bullet head wounds in the Vietnam War [1].Because much of the clinical information on NPE has been derived from case reports and autopsy series, the true incidence of NPE is unknown and is likely underreported. Any acute CNS insult, including spinal cord trauma, can result in pulmonary edema. In patients with SAH, reports of NPE incidence range from 2% to 42.9% [3,9,10]. Clinically, the likelihood of developing NPE following SAH correlates with increasing age, delay to surgery, vertebral artery origin, and the severity of clinical and radiographic presentation (e.g., Hunt-Hess and Fischer grades) [10,11]. Patients with SAH who develop NPE have a higher mortality rate, nearing 10% [3]. In patients with TBI, the incidence of NPE has been estimated to be up to 20% [12]. Rogers et al. examined a large autopsy and inpatient database on patients with acute head injury in an effort to better characterize NPE in this patient population. The authors found that the incidence of NPE in patients with TBI who died at the scene was 32%. Among the TBI patients who died within 96 hours, the incidence of NPE rose to 50% [2]. There was a direct correlation between decreasing cerebral perfusion pressure (CPP) and reduced PaO2/FiO2 ratios in the TBI patients [2]. NPE in patients who suffer seizures is rare; however, up to 80 to 100% of epileptics who die unexpectedly of seizures are also found to have NPE [13]. In other series, close to one-third of patients with status epileptic
Anatomy of Free Flap Failures: Dissection of a Series  [PDF]
Steven P. Davison, Mark W. Clemens, Andrew L. Kochuba
Modern Plastic Surgery (MPS) , 2013, DOI: 10.4236/mps.2013.33018
Abstract:

Introduction: Free flap success rates have remained stable in recent years ranging 93% to 98%. Historically, the causes of free flap failures were attributed to the surgeon’s inexperience and technique. However, there are factors beyond the surgical anastomosis that contribute to flap failure. The purpose of this study is to review each case of total flap loss in detail to develop a better understanding of complications. Methods: A retrospective study was performed over eleven years in a single surgeon’s practice, a predominantly head and neck reconstructive practice. All charts were independently reviewed. In patients who sustained total flap loss, a review was conducted of patient comorbidites, anesthesia records, perioperative and follow-up notes. Results: A total of 514 free flaps were performed. 76% (392) of these flaps were for head and neck reconstruction. There were 22 total flap losses (4%) and 26 partial flap losses (5%). Of the 22 total flap losses, four flaps were avulsed, five flaps were in patients later found to have coagulation disorders (homozygous mutations of the MTHFR gene and factor V Leiden), four patients were exposed to neosynephrine, two patients remained hypotensive perioperatively, and four delayed flap losses were attributed to pseudomonal infection. Five losses were technical or related to flap inexperience. Several representative case scenarios are illustrated. Conclusion: Careful review of free flap failures indicates that a thorough workup (particularly coagulation disorders), flap selection, surgeon to anesthesia communication, proper securing of the flap, and postoperative patient blood pressure and infection control have a greater part to play in this new era of anastomotic success.

Youth at risk of physical inactivity may benefit more from activity-related support than youth not at risk
Kirsten Davison, Dorothy L Schmalz
International Journal of Behavioral Nutrition and Physical Activity , 2006, DOI: 10.1186/1479-5868-3-5
Abstract: Methods:Participants included 202 middle-school-aged girls (N = 92) and boys (N = 110). Physical activity was assessed using three self-report questionnaires. Activity-related support from mothers, fathers, siblings, and peers was assessed using the Activity Support Scale. Perceived sport competence was assessed using the Physical Activity Self Description Questionnaire. Participants' height and weight were measured and used to calculate their age- and sex-adjusted Body Mass Index percentile. Participants were classified as being at high risk for physical inactivity if they fulfilled two of the following three criteria: (1) overweight; (2) female; or (3) having low perceived sport competence.Results:Activity-related support from all sources was associated with higher levels of physical activity among adolescents. A stronger association between activity support and physical activity was found for adolescents at high risk for physical inactivity in comparison to adolescents at low risk.Conclusions:Findings from this study suggest that the activity-related support from family and friends may be an effective tool in promoting physical activity among youth at risk of physical inactivity.Numerous studies point to the potential benefits of activity-related support from significant others on physical activity levels among youth. In particular, research to date has shown that children and adolescents are more likely to be physically active when their parents and friends are active [1-5], encourage them to be active [6-8] and participate in sport or physical activity with them [1,2,6,9,10]. Furthermore, children show higher levels of physical activity when their parents take them to places where they can be active, enroll them in organized activities and pay the associated fees [1,2,11,12]. This body of research suggests that activity-related support from family and friends is important to consider as a mechanism to promote physical activity among youth.Before designing and i
Critical appraisal of denosumab in the treatment and prevention of postmenopausal osteoporosis and bone loss in patients undergoing hormone ablation
David L Kendler, Kenneth Shawn Davison
Orthopedic Research and Reviews , 2010, DOI: http://dx.doi.org/10.2147/ORR.S6124
Abstract: itical appraisal of denosumab in the treatment and prevention of postmenopausal osteoporosis and bone loss in patients undergoing hormone ablation Review (2907) Total Article Views Authors: David L Kendler, Kenneth Shawn Davison Published Date September 2010 Volume 2010:2 Pages 49 - 69 DOI: http://dx.doi.org/10.2147/ORR.S6124 David L Kendler1, Kenneth Shawn Davison2 1Prohealth Clinical Research, University of British Columbia, Vancouver, British Columbia, Canada; 2Department of Medicine, Division of Immunology and Rheumatology, Laval University, Quebec, Canada Abstract: Antiresorptive therapies are the mainstay for treating patients with excessively high rates of bone resorption. The receptor activator of nuclear factor-κB (RANK) ligand (RANKL), secreted by osteoblasts, binds to the RANK receptor on the surface of preosteoclasts and osteoclasts to elicit osteoclast formation, survival, and activity. Osteoprotegerin, also secreted by the osteoblast, acts as a decoy RANK receptor reducing RANKL binding to RANK and reducing bone resorption. Denosumab, a fully human monoclonal antibody, has a high affinity and specificity for RANKL. Denosumab rapidly decreases bone resorption and increases bone mineral density (BMD) at the lumbar spine, total hip, femoral neck, and one-third radius sites. In head-to-head trials, denosumab increased BMD and decreased bone resorption to a significantly greater degree than alendronate. In postmenopausal osteoporotic women, denosumab decreased the risk of vertebral fracture (68%), nonvertebral fracture (20%), and hip fracture (40%) over 36 months, compared to placebo. In patients with iatrogenic hypogonadism, denosumab rapidly decreased markers of bone resorption and increased BMD. In men treated with GnRH agonist for prostate cancer, treatment with denosumab led to a 62% decreased risk of new vertebral fracture over 3 years, as compared to placebo. In all trials completed to date, comparable adverse events have been observed in both denosumab and placebo or treatment groups.
EXPLORING ACCESSIBILITY VERSUS OPPORTUNITY CRIME FACTORS
Elizabeth L. Davison,William R. Smith
Sociation Today , 2003,
Abstract: People often wonder why urban crime rates are higher than those in rural areas or small towns. Davison and Smith look at opportunity and accessibility as factors which make people more likely to be victims in urban areas. Under 'further reading' below you will see that crime patterns are NOT random and can be predicted by urban design.
Critical appraisal of denosumab in the treatment and prevention of postmenopausal osteoporosis and bone loss in patients undergoing hormone ablation
David L Kendler,Kenneth Shawn Davison
Orthopedic Research and Reviews , 2010,
Abstract: David L Kendler1, Kenneth Shawn Davison21Prohealth Clinical Research, University of British Columbia, Vancouver, British Columbia, Canada; 2Department of Medicine, Division of Immunology and Rheumatology, Laval University, Quebec, CanadaAbstract: Antiresorptive therapies are the mainstay for treating patients with excessively high rates of bone resorption. The receptor activator of nuclear factor-κB (RANK) ligand (RANKL), secreted by osteoblasts, binds to the RANK receptor on the surface of preosteoclasts and osteoclasts to elicit osteoclast formation, survival, and activity. Osteoprotegerin, also secreted by the osteoblast, acts as a decoy RANK receptor reducing RANKL binding to RANK and reducing bone resorption. Denosumab, a fully human monoclonal antibody, has a high affinity and specificity for RANKL. Denosumab rapidly decreases bone resorption and increases bone mineral density (BMD) at the lumbar spine, total hip, femoral neck, and one-third radius sites. In head-to-head trials, denosumab increased BMD and decreased bone resorption to a significantly greater degree than alendronate. In postmenopausal osteoporotic women, denosumab decreased the risk of vertebral fracture (68%), nonvertebral fracture (20%), and hip fracture (40%) over 36 months, compared to placebo. In patients with iatrogenic hypogonadism, denosumab rapidly decreased markers of bone resorption and increased BMD. In men treated with GnRH agonist for prostate cancer, treatment with denosumab led to a 62% decreased risk of new vertebral fracture over 3 years, as compared to placebo. In all trials completed to date, comparable adverse events have been observed in both denosumab and placebo or treatment groups.Keywords: medication adherence, fracture, bone mineral density, bone turnover markers
Time Required For a Drowning Victim to Reach Bottom
John L. Hunsucker,Scott J. Davison
Journal of Search and Rescue , 2013,
Abstract: This paper describes a mathematical model that can be used to provide an estimate for the amount of time a drowning victim takes to sink through the water and hit bottom, including a table for drift during the descent. A victim may be on the surface and then be on the bottom less than 10 seconds later. Search and rescue professionals need to be trained to understand the short time during which a victim can sink and drown and the need for immediate search and rescue from the bottom starting at the last point the victim was seen.
Space-time modelling of extreme events
Rapha?l Huser,A. C. Davison
Statistics , 2012, DOI: 10.1111/rssb.12035
Abstract: Max-stable processes are the natural analogues of the generalized extreme-value distribution for the modelling of extreme events in space and time. Under suitable conditions, these processes are asymptotically justified models for maxima of independent replications of random fields, and they are also suitable for the modelling of joint individual extreme measurements over high thresholds. This paper extends a model of Schlather (2001) to the space-time framework, and shows how a pairwise censored likelihood can be used for consistent estimation under mild mixing conditions. Estimator efficiency is also assessed and the choice of pairs to be included in the pairwise likelihood is discussed based on computations for simple time series models. The ideas are illustrated by an application to hourly precipitation data over Switzerland.
Anion gap, anion gap corrected for albumin, base deficit and unmeasured anions in critically ill patients: implications on the assessment of metabolic acidosis and the diagnosis of hyperlactatemia
Lakhmir S Chawla, Shirley Shih, Danielle Davison, Christopher Junker, Michael G Seneff
BMC Emergency Medicine , 2008, DOI: 10.1186/1471-227x-8-18
Abstract: We conducted a chart review of ICU patients who had cotemporaneous arterial blood gas, serum chemistry, serum albumin (Alb) and lactate(Lac) levels measured from the same sample. We assessed the capacity of AG, BD, and ACAG to diagnose HL and severe hyperlactatemia (SHL). HL was defined as Lac > 2.5 mmol/L. SHL was defined as a Lac of > 4.0 mmol/L.From 143 patients we identified 497 series of lab values that met our study criteria. Mean age was 62.2 ± 15.7 years. Mean Lac was 2.11 ± 2.6 mmol/L, mean AG was 9.0 ± 5.1, mean ACAG was 14.1 ± 3.8, mean BD was 1.50 ± 5.4. The area under the curve for the ROC for BD, AG, and ACAG to diagnose HL were 0.79, 0.70, and 0.72, respectively.AG and BD failed to reliably detect the presence of clinically significant hyperlactatemia. Under idealized conditions, ACAG has the capacity to rule out the presence of hyperlactatemia. Lac levels should be obtained routinely in all patients admitted to the ICU in whom the possibility of shock/hypoperfusion is being considered. If an AG assessment is required in the ICU, it must be corrected for albumin for there to be sufficient diagnostic utility.The use of anion gap assessment to interpret and diagnose the etiology of metabolic acidosis was originally described by Emmet and Narins in 1977.[1] Lactic acid, a "gap" acid, is one cause of elevated anion gap metabolic acidosis, and an elevated serum lactate level has emerged as an important tool to screen for patients in shock. Elevated serum lactate can be caused by inadequate perfusion, but may also be a product of inflammation, cytopathic hypoxia, and increased rates of glycolysis. [2-4] In critically ill patients, an elevated lactate level is indicative of increased severity of illness and subsequent serum lactate clearance predicts an improved outcome.[5,6] Rivers et al, utilized hypotension and elevated serum lactate levels to identify patients in shock and demonstrated that emergency department patients with presumed sepsis and a serum l
Fanconi-like crosslink repair in yeast
Danielle L Daee, Kyungjae Myung
Genome Integrity , 2012, DOI: 10.1186/2041-9414-3-7
Abstract: DNA damaging agents such as nitrogen mustard [1,2], formaldehyde [3], and cisplatin [4] generate many lesions that inhibit proper DNA replication and transcription. One such lesion, the interstrand crosslink (ICL), covalently links two complementary DNA strands and prevents their separation. Importantly, since both strands are damaged, an undamaged template strand is not available for repair. Due to these blocks and repair challenges, ICLs are considered one of the most toxic DNA lesions. It is estimated that the presence of just one unrepaired ICL is sufficient to kill yeast or bacteria [5] and approximately 40 unrepaired ICLs can kill mammalian cells [6]. As a result of this high cytotoxicity, crosslinking agents are common anticancer agents [7]. Outside of chemotherapies, ICLs can be induced by exposures in the environment [8] and byproducts of normal metabolic processes [9,10]. Thus, a clearer understanding of the mechanisms of ICL repair will inform our knowledge of both normal and cancer cells. This article and another recent review [11] describe novel findings in yeast that provide insight into the mechanisms of eukaryotic ICL repair.Cells have the capacity to repair ICLs through highly complex DNA repair mechanisms. ICL repair in the prokaryotic system is relatively well defined. In Escherichia coli, nucleotide excision repair (NER) creates incisions on each side of the ICL. The resulting short oligonucleotide is attached through the ICL, but is displaced from the helix, revealing a gap. The gap is filled in by homologous recombination (HR) or translesion bypass synthesis (TLS), and the displaced oligonucleotide/ICL adduct is removed by NER [12].In lower eukaryotes, defects in most known DNA repair pathways result in ICL sensitivity suggesting that eukaryotic mechanisms are much more complex, involve multiple repair pathways, and can occur in multiple phases of the cell cycle. Several recent reviews address this complexity in detail [13-23]. In the budding y
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