114 research outputs found

    Two Weeks Notice...Aloha

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    Written and published by John L. Bove, former Dean of Admissions for St. Francis College, Two Weeks Notice...Aloha documents his struggle to come to terms with his loss following the death of his wife. From its preface: “This was originally a journal through which I sought to regain some equilibrium and understanding. The loss of Fran turned my world “topsy turvy.” I was so angry and grief stricken it threatened my health. Stress of any kind, left unchecked, attacks the immune system which inevitably leads to illness. Writing gives you a focal point for your anger and grief. Introspective writing, I have discovered, is a lot like meditation. It allows you to view your thoughts much like an outside observer would do. In my case it helped me evaluate the anger, and give thoughtful consideration to my personal environment. It allowed the grief and anger to be brought into focus, and the unforgiveness to be understood. It is a great self-counseling tool.”https://dune.une.edu/unebooks/1000/thumbnail.jp

    A Critical Evaluation Of The Trigger Point Phenomenon

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    The theory of myofascial pain syndrome (MPS) caused by trigger points (TrPs) seeks to explain the phenomena of muscle pain and tenderness in the absence of evidence for local nociception. Although it lacks external validity, many practitioners have uncritically accepted the diagnosis of MPS and its system of treatment. Furthermore, rheumatologists have implicated TrPs in the pathogenesis of chronic widespread pain (fibromyalgia syndrome). We have critically examined the evidence for the existence of myofascial TrPs as putative pathological entities and for the “vicious cycles that are said to maintain them. We find that both are inventions that have no scientific basis, whether from experimental approaches that interrogate the suspect tissue or empirical approaches that assess the outcome of treatments predicated on presumed pathology. Therefore the theory of MPS caused by TrPs has been refuted. This is not to deny the existence of the clinical phenomena themselves, for which scientifically sound and logically plausible explanations based on known neurophysiological phenomena can be advanced

    Early Surgical Morbidity and Mortality in Adults with Congenital Heart Disease: The University of Michigan Experience

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    Objectives.  To review early surgical outcomes in a contemporary series of adults with congenital heart disease (CHD) undergoing cardiac operations at the University of Michigan, and to investigate possible preoperative and intraoperative risk factors for morbidity and mortality. Methods.  A retrospective medical record review was performed for all patients ≥18 years of age who underwent open heart operations by a pediatric cardiothoracic surgeon at the University of Michigan Congenital Heart Center between January 1, 1998 and December 31, 2004. Records from a cohort of pediatric patients ages 1–17 years were matched to a subset of the adult patients by surgical procedure and date of operation. Results.  In total, 243 cardiac surgical operations were performed in 234 adult patients with CHD. Overall mortality was 4.7% (11/234). The incidence of major postoperative complications was 10% (23/234) with a 19% (45/23) minor complication rate. The most common postoperative complication was atrial arrhythmias in 10.8% (25/234). The presence of preoperative lung or liver disease, prolonged cardiopulmonary bypass and aortic cross clamp times, and postoperative elevated inotropic score and serum lactates were significant predictors of mortality in adults. There was no difference between the adult and pediatric cohorts in terms of mortality and morbidity. Conclusions.  The postoperative course in adults following surgery for CHD is generally uncomplicated and early survival should be expected. Certain risk factors for increased mortality in this patient population may include preoperative presence of chronic lung or liver dysfunction, prolonged cardiopulmonary bypass and aortic cross-clamp times, and postoperative elevated inotropic score and serum lactate levels.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75596/1/j.1747-0803.2008.00170.x.pd

    Evaluating more naturalistic outcome measures:A 1-year smartphone study in multiple sclerosis

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    Objective: In this cohort of individuals with and without multiple sclerosis (MS), we illustrate some of the novel approaches that smartphones provide to monitor patients with chronic neurologic disorders in their natural setting. Methods: Thirty-eight participant pairs (MS and cohabitant) aged 18–55 years participated in the study. Each participant received an Android HTC Sensation 4G smartphone containing a custom application suite of 19 tests capturing participant performance and patient-reported outcomes (PROs). Over 1 year, participants were prompted daily to complete one assigned test. Results: A total of 22 patients with MS and 17 cohabitants completed the entire study. Among patients with MS, low scores on PROs relating to mental and visual function were associated with dropout (p < 0.05). We illustrate several novel features of a smartphone platform. First, fluctuations in MS outcomes (e.g., fatigue) were assessed against an individual's ambient environment by linking responses to meteorological data. Second, both response accuracy and speed for the Ishihara color vision test were captured, highlighting the benefits of both active and passive data collection. Third, a new trait, a person-specific learning curve in neuropsychological testing, was identified using spline analysis. Finally, averaging repeated measures over the study yielded the most robust correlation matrix of the different outcome measures. Conclusions: We report the feasibility of, and barriers to, deploying a smartphone platform to gather useful passive and active performance data at high frequency in an unstructured manner in the field. A smartphone platform may therefore enable large-scale naturalistic studies of patients with MS or other neurologic diseases

    Suprarenal fixation of endovascular aortic stent grafts: assessment of medium-term to long-term renal function by analysis of juxtarenal stent morphology.

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    Objective: The effect of supra-renal stent fixation during endovascular aortic aneurysm repair (EVAR) on renal function remains unclear. Using a unique validated 3D intraluminal imaging technique, we analysed the effect of suprarenal stent position relative to renal artery orifices and its medium to long term effects on renal function.Methods: Thirty-four consecutive patients from a single institution were studied following EVAR using the Zenith endograft system from September 1999 to March 2002. The precise locations of the uncovered supra-renal stent struts were assessed by a virtual endoscopic imaging technique. Anatomical and quantitative categorisation of patients was made according to the configuration of uncovered stent struts across the renal artery ostia (RAO). The anatomical subgroups were defined as struts located centrally or peripherally across both RAO. The quantitative subgroups were defined as RAO crossed by multiple struts, a solitary strut or no struts. The subgroups were compared for their renal function as assessed by temporal measurements of serum creatinine concentration and creatinine clearance, and renal parenchymal perfusion defects as assessed using contrast-enhanced computerised tomography (CT).Results: Mean follow-up was 52.7 months. Separate subgroup analysis for both anatomical and quantitative configurations did not demonstrate any significant difference in renal function between the different strut permutations (p&gt;0.05). Follow-up imaging confirmed one case of renal infarction secondary to an occluded accessory renal artery, although, this patient had normal creatinine levels.Conclusion: RAO coverage by supra-renal uncovered stents does not appear to have a significant effect on renal function as evaluated by creatinine measurements in patients with normal pre-operative renal function

    The Ubiquitin-Proteasome Reporter GFPu Does Not Accumulate in Neurons of the R6/2 Transgenic Mouse Model of Huntington's Disease

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    Impairment of the ubiquitin-proteasome system (UPS) has long been considered an attractive hypothesis to explain the selective dysfunction and death of neurons in polyglutamine disorders such as Huntington's disease (HD). The fact that inclusion bodies in HD mouse models and patient brains are rich in ubiquitin and proteasome components suggests that the UPS may be hindered directly or indirectly by inclusion bodies or their misfolded monomeric or oligomeric precursors. However, studies into UPS function in various polyglutamine disease models have yielded conflicting results, suggesting mutant polyglutamine tracts may exert different effects on the UPS depending on protein context, expression level, subcellular localisation and cell-type. To investigate UPS function in a well-characterised mouse model of HD, we have crossed R6/2 HD mice with transgenic UPS reporter mice expressing the GFPu construct. The GFPu construct comprises GFP fused to a constitutive degradation signal (CL-1) that promotes its rapid degradation under conditions of a healthy UPS. Using a combination of immunoblot analysis, fluorescence and immunofluorescence microscopy studies, we found that steady-state GFPu levels were not detectably different between R6/2 and non-R6/2 brain. We observed no correlation between inclusion body formation and GFPu accumulation, suggesting no direct relationship between protein aggregation and global UPS inhibition in R6/2 mice. These findings suggest that while certain branches of the UPS can be impaired by mutant polyglutamine proteins, such proteins do not necessarily cause total blockade of UPS-dependent degradation. It is therefore likely that the relationship between mutant polyglutamine proteins and the UPS is more complex than originally anticipated

    Fenoldopam use in a burn intensive care unit: a retrospective study

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    <p>Abstract</p> <p>Background</p> <p>Fenoldopam mesylate is a highly selective dopamine-1 receptor agonist approved for the treatment of hypertensive emergencies that may have a role at low doses in preserving renal function in those at high risk for or with acute kidney injury (AKI). There is no data on low-dose fenoldopam in the burn population. The purpose of our study was to describe our use of low-dose fenoldopam (0.03-0.09 ÎĽg/kg/min) infusion in critically ill burn patients with AKI.</p> <p>Methods</p> <p>We performed a retrospective analysis of consecutive patients admitted to our burn intensive care unit (BICU) with severe burns from November 2005 through September 2008 who received low-dose fenoldopam. Data obtained included systolic blood pressure, serum creatinine, vasoactive medication use, urine output, and intravenous fluid. Patients on concomitant continuous renal replacement therapy were excluded. Modified inotrope score and vasopressor dependency index were calculated. One-way analysis of variance with repeated measures, Wilcoxson signed rank, and chi-square tests were used. Differences were deemed significant at p < 0.05.</p> <p>Results</p> <p>Seventy-seven patients were treated with low-dose fenoldopam out of 758 BICU admissions (10%). Twenty (26%) were AKI network (AKIN) stage 1, 14 (18%) were AKIN stage 2, 42 (55%) were AKIN stage 3, and 1 (1%) was AKIN stage 0. Serum creatinine improved over the first 24 hours and continued to improve through 48 hours (<it>p </it>< 0.05). There was an increase in systolic blood pressure in the first 24 hours that was sustained through 48 hours after initiation of fenoldopam (<it>p </it>< 0.05). Urine output increased after initiation of fenoldopam without an increase in intravenous fluid requirement (<it>p </it>< 0.05; <it>p </it>= NS). Modified inotrope score and vasopressor dependency index both decreased over 48 hours (<it>p </it>< 0.0001; <it>p </it>= 0.0012).</p> <p>Conclusions</p> <p>These findings suggest that renal function was preserved and that urine output improved without a decrease in systolic blood pressure, increase in vasoactive medication use, or an increase in resuscitation requirement in patients treated with low-dose fenoldopam. A randomized controlled trial is required to establish the efficacy of low-dose fenoldopam in critically ill burn patients with AKI.</p
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