Rush University Medical Center

About: Rush University Medical Center is a healthcare organization based out in Chicago, Illinois, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 13915 authors who have published 29027 publications receiving 1379216 citations. The organization is also known as: Rush Presbyterian St. Luke's Medical Center.

TrkA-Immunoreactive Profiles in the Central Nervous System: Colocalization With Neurons Containing p75 Nerve Growth Factor Receptor, Choline Acetyltransferase, and Serotonin

Abstract: The present investigation used an antibody directed against the extracellular domain of the signal transducing nerve growth factor receptor, trkA, to reveal immunoreactive perikarya or fibers within the olfactory bulb and tubercle, cingulate cortex, nucleus accumbens, striatum, endopiriform nucleus, septal/diagonal band complex, nucleus basalis, hippocampal complex, thalamic paraventricular and reuniens nuclei, periventricular hypothalamus, interpeduncular nucleus, mesencephalic nucleus of the fifth nerve, dorsal nucleus of the lateral lemniscus, prepositus hypoglossal nucleus, ventral cochlear nucleus, ventral lateral tegmentum, medial vestibular nucleus, spinal trigeminal nucleus oralis, nucleus of the solitary tract, raphe nuclei, and spinal cord. Colocalization experiments revealed that virtually all striatal trkA-immunoreactive neurons (> 99%) coexpressed choline acetyltransferase (ChAT) but not p75 nerve growth factor receptor (NGFR). Within the septal/diagonal band complex virtually all trkA neurons (> 95%) coexpressed both ChAT and p75 NGFR. More caudally, dual stained sections revealed numerous trkA/ChAT (> 80%) and trkA/p75 NGFR (> 95%) immunoreactive neurons within the nucleus basalis. In the brainstem, raphe serotonergic neurons (45%) coexpressed trkA. Sections stained with a pan-trk antibody that recognizes primarily trkA, as well as trkB and trkC, labeled neurons within all of these regions as well as within the hypothalamic arcuate, supramammilary, and supraoptic nuclei, hippocampus, inferior and superior colliculus, substantia nigra, ventral tegmental area of T'sai, and cerebellular Purkinje cells. Virtually all of these other regions with the exception of the cerebellum also expressed pan-trk immunoreactivity in the monkey. The widespread expression of trkA throughout the central neural axis suggests that this receptor may play a role in signal transduction mechanisms linked to NGF-related substances in cholinergic basal forebrain and noncholinergic systems. These findings suggest that pharmacological use of ligands for trkA could have beneficial effects on the multiple neuronal systems that are affected in such disorders as Alzheimer's disease.

Comparison of arthroscopic and open anterior shoulder stabilization. A two to six-year follow-up study.

Abstract: Background: Sixty-three consecutive patients with recurrent traumatic anterior shoulder instability underwent operative repair. The decision to select either arthroscopic Bankart repair or open capsular shift was based on the findings of an examination under anesthesia and the findings at the time of arthroscopy. Thirty-nine patients with only anterior translation on examination under anesthesia and a discrete Bankart lesion underwent arthroscopic Bankart repair with use of absorbable transfixing implants. Twenty-four patients with inferior translation in addition to anterior translation on examination under anesthesia and capsular laxity or injury on arthroscopy underwent an open capsular shift. Methods: Treatment outcomes for each group were determined according to the scoring systems of Rowe et al., the American Shoulder and Elbow Surgeons, and the Short Form-36. Failure was defined as recurrence of dislocation or subluxation or the finding of apprehension. Fifty-nine (94 percent) of the sixty-three patients were examined and filled out a questionnaire at a mean of fifty-four months (range, twenty-seven to seventy-two months) following surgery. Results: There were no significant differences between the two groups with regard to the prevalence of failure or any of the other measured parameters of outcome. An unsatisfactory outcome occurred after nine (24 percent) of thirty-seven arthroscopic repairs and after four (18 percent) of twenty-two open reconstructions. All cases of recurrent instability resulted from a reinjury in a contact sport or a fall less than two years postoperatively. The treatment groups did not differ with regard to patient age, hand dominance, mechanism of initial injury, duration of follow-up, or delay until surgery. Measured losses of motion were minimal and, with the exception of forward elevation, slightly more of which was lost after the open capsular shifts (p = 0.05), did not differ between the two forms of treatment. Approximately 75 percent of the patients in each group returned to their favorite recreational sports with no or mild limitations. As rated by the patients, the result was good or excellent after thirty-one (84 percent) of the arthroscopic procedures and after twenty (91 percent) of the open procedures. Conclusions: Arthroscopic and open repair techniques for the treatment of recurrent traumatic shoulder instability yield comparable results if the procedure is selected on the basis of the pathological findings at the time of surgery.

Exploring the scope of post-intensive care syndrome therapy and care: engagement of non-critical care providers and survivors in a second stakeholders meeting.

Abstract: Background Increasing numbers of survivors of critical illness are at risk for physical, cognitive, and/or mental health impairments that may persist for months or years after hospital discharge. The post-intensive care syndrome framework encompassing these multidimensional morbidities was developed at the 2010 Society of Critical Care Medicine conference on improving long-term outcomes after critical illness for survivors and their families. Objectives To report on engagement with non-critical care providers and survivors during the 2012 Society of Critical Care Medicine post-intensive care syndrome stakeholder conference. Task groups developed strategies and resources required for raising awareness and education, understanding and addressing barriers to clinical practice, and identifying research gaps and resources, aimed at improving patient and family outcomes. Participants Representatives from 21 professional associations or health systems involved in the provision of both critical care and rehabilitation of ICU survivors in the United States and ICU survivors and family members. Design Stakeholder consensus meeting. Researchers presented summaries on morbidities for survivors and their families, whereas survivors presented their own experiences. Meeting outcomes Future steps were planned regarding 1) recognizing, preventing, and treating post-intensive care syndrome, 2) building strategies for institutional capacity to support and partner with survivors and families, and 3) understanding and addressing barriers to practice. There was recognition of the need for systematic and frequent assessment for post-intensive care syndrome across the continuum of care, including explicit "functional reconciliation" (assessing gaps between a patient's pre-ICU and current functional ability at all intra- and interinstitutional transitions of care). Future post-intensive care syndrome research topic areas were identified across the continuum of recovery: characterization of at-risk patients (including recognizing risk factors, mechanisms of injury, and optimal screening instruments), prevention and treatment interventions, and outcomes research for patients and families. Conclusions Raising awareness of post-intensive care syndrome for the public and both critical care and non-critical care clinicians will inform a more coordinated approach to treatment and support during recovery after critical illness. Continued conceptual development and engagement with additional stakeholders is required.

Association of Traumatic Brain Injury With Late-Life Neurodegenerative Conditions and Neuropathologic Findings

Abstract: Importance The late effects of traumatic brain injury (TBI) are of great interest, but studies characterizing these effects are limited. Objective To determine whether TBI with loss of consciousness (LOC) is associated with an increased risk for clinical and neuropathologic findings of Alzheimer disease (AD), Parkinson disease (PD), and other dementias. Design, Setting, and Participants This study analyzed data from the Religious Orders Study (ROS), Memory and Aging Project (MAP), and Adult Changes in Thought study (ACT). All ROS and MAP participants and a subset of ACT participants consent to autopsy. Studies performed annual (ROS and MAP) or biennial (ACT) cognitive and clinical testing to identify incident cases of dementia and AD. The 7130 participants included members of a Seattle-area health care delivery system (ACT), priests and nuns living in orders across the United States (ROS), and Chicago-area adults in retirement communities (MAP). Of these, 1589 underwent autopsy. Primary hypothesis was that TBI with LOC would be associated with increased risk for AD and neurofibrillary tangles. Data were accrued from 1994 to April 1, 2014. Exposures Self-reported TBI when the participant was free of dementia, categorized as no more than 1 vs more than 1 hour of LOC. Main Outcomes and Measures Clinical outcomes included incident all-cause dementia, AD, and PD in all studies and incident mild cognitive impairment and progression of parkinsonian signs in ROS and MAP. Neuropathologic outcomes included neurofibrillary tangles, neuritic plaques, microinfarcts, cystic infarcts, Lewy bodies, and hippocampal sclerosis in all studies. Results Of 7130 participants (2879 [40.4%] men; overall mean [SD] age, 79.9 [6.9] years), 865 reported a history of TBI with LOC. In 45 190 person-years of follow-up, 1537 incident cases of dementia and 117 of PD were identified. No association was found between TBI with LOC and incident dementia (ACT: HR for TBI with LOC ≤1 hour, 1.03; 95% CI, 0.83-1.27; HR for TBI with LOC >1 hour, 1.18; 95% CI, 0.77-1.78; ROS and MAP: HR for TBI with LOC ≤1 hour, 0.87; 95% CI, 0.58-1.29; HR for TBI with LOC >1 hour, 0.84; 95% CI, 0.44-1.57) or AD (findings similar to those for dementia). Associations were found for TBI with LOC and incident PD in ACT (HR for TBI with LOC >1 hour, 3.56; 95% CI, 1.52-8.28) and progression of parkinsonian signs in ROS and MAP (odds ratio [OR] for TBI with LOC ≤1 hour, 1.65; 95% CI, 1.23-2.21; OR for TBI with LOC >1 hour, 2.23; 95% CI, 1.16-4.29). Traumatic brain injury with LOC was associated with Lewy bodies (any Lewy body in ACT: RR for TBI with LOC >1 hour, 2.64; 95% CI, 1.40-4.99; Lewy bodies in substantia nigra and/or locus ceruleus in ACT: RR for TBI with LOC >1 hour, 3.30; 95% CI, 1.71-6.38; Lewy bodies in frontal or temporal cortex in ACT: RR for TBI with LOC >1 hour, 5.73; 95% CI, 2.18-15.0; ROS and MAP: RR for TBI with LOC ≤1 hour, 1.64; 95% CI, 1.00-2.70; pooled RR for TBI with LOC ≤1 hour, 1.59; 95% CI, 1.06-2.39) and microinfarcts (any cortical microinfarct in ROS and MAP: RR for TBI with LOC >1 hour, 2.12; 95% CI, 1.12-4.01; pooled RR for TBI with LOC >1 hour, 1.58; 95% CI, 1.06-2.35). Conclusions and Relevance Pooled clinical and neuropathologic data from 3 prospective cohort studies indicate that TBI with LOC is associated with risk for Lewy body accumulation, progression of parkinsonism, and PD, but not dementia, AD, neuritic plaques, or neurofibrillary tangles.