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 & Dementia. 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.

Parent training of toddlers in day care in low-income urban communities.

Abstract: The authors tested a 12-week parent training program with parents (n = 208) and teachers (n = 77) of 2-3-year-olds in day care centers serving low-income families of color in Chicago. Eleven centers were randomly assigned to 1 of 4 conditions: (a) parent and teacher training (PT + TT), (b) parent training (PT), (c) teacher training (TT), and (d) waiting list control (C). After controlling for parent stress, PT and PT + TT parents reported higher self-efficacy and less coercive discipline and were observed to have more positive behaviors than C and TT parents. Among toddlers in high-risk behavior problem groups, toddlers in the experimental conditions showed greater improvement than controls. Most effects were retained 1 year later. Benefits were greatest when parents directly received training.

[Formula: see text]Neuropsychologists' Validity Testing Beliefs and Practices: A Survey of North American Professionals.

Abstract: Objective: The current study investigated changes in neuropsychologists’ validity testing beliefs and practices since publication of the last North American survey targeting these issues in 2007 and explored emerging issues in validity testing that had not been previously addressed in the professional survey literature. Methods: Licensed North American neuropsychologists (n = 316), who primarily evaluate adults, were surveyed in regard to the following topics: (1) comparison of objective validity testing, qualitative data, and clinical judgment; (2) approaches to validity test administration; (3) formal communication in cases of suspected malingering; (4) reporting of validity test results; (5) suspected causes of invalidity; (6) integration of stand-alone, embedded, and symptom-report validity measures; (7) multiple performance validity test interpretation; (8) research practices; and (9) popularity of specific validity instruments. Results: Overall, findings from the current survey indicated that all bu...

TDP-43 stage, mixed pathologies, and clinical Alzheimer's-type dementia.

Abstract: Hyperphosphorylated transactive response DNA-binding protein 43 (TDP-43, encoded by TARDBP ) proteinopathy has recently been described in ageing and in association with cognitive impairment, especially in the context of Alzheimer's disease pathology. To explore the role of mixed Alzheimer's disease and TDP-43 pathologies in clinical Alzheimer's-type dementia, we performed a comprehensive investigation of TDP-43, mixed pathologies, and clinical Alzheimer's-type dementia in a large cohort of community-dwelling older subjects. We tested the hypotheses that TDP-43 with Alzheimer's disease pathology is a common mixed pathology; is related to increased likelihood of expressing clinical Alzheimer's-type dementia; and that TDP-43 pathologic stage is an important determinant of clinical Alzheimer's-type dementia. Data came from 946 older adults with ( n = 398) and without dementia ( n = 548) from the Rush Memory and Aging Project and Religious Orders Study. TDP-43 proteinopathy (cytoplasmic inclusions) was present in 496 (52%) subjects, and the pattern of deposition was classified as stage 0 (none; 48%), stage 1 (amygdala; 18%), stage 2 (extension to hippocampus/entorhinal; 21%), or stage 3 (extension to neocortex; 14%). TDP-43 pathology combined with a pathologic diagnosis of Alzheimer's disease was a common mixed pathology (37% of all participants), and the proportion of subjects with clinical Alzheimer's-type dementia formerly labelled 'pure pathologic diagnosis of Alzheimer's disease' was halved when TDP-43 was considered. In logistic regression models adjusted for age, sex, and education, TDP-43 pathology was associated with clinical Alzheimer's-type dementia (odds ratio = 1.51, 95% confidence interval = 1.11, 2.05) independent of pathological Alzheimer's disease (odds ratio = 4.30, 95% confidence interval = 3.08, 6.01) or other pathologies (infarcts, arteriolosclerosis, Lewy bodies, and hippocampal sclerosis). Mixed Alzheimer's disease and TDP-43 pathologies were associated with higher odds of clinical Alzheimer's-type dementia (odds ratio = 6.73, 95% confidence interval = 4.18, 10.85) than pathologic Alzheimer's disease alone (odds ratio = 4.62, 95% confidence interval = 2.84, 7.52). In models examining TDP-43 stage, a dose-response relationship with clinical Alzheimer's-type dementia was observed, and a significant association was observed starting at stage 2, extension beyond the amygdala. In this large sample from almost 1000 community participants, we observed that TDP-43 proteinopathy was very common, frequently mixed with pathological Alzheimer's disease, and associated with a higher likelihood of the clinical expression of clinical Alzheimer's-type dementia but only when extended beyond the amygdala.

ABT-378/ritonavir plus stavudine and lamivudine for the treatment of antiretroviral-naive adults with HIV-1 infection: 48-week results.

Abstract: Objective: To evaluate the safety and antiviral activity of different dose levels of the HIV protease inhibitor ABT-378 combined with low-dose ritonavir, plus stavudine and lamivudine in antiretroviral-naive individuals. Design: Prospective, randomized, double-blind, multicenter. Methods: Eligible patients with plasma HIV-1 RNA > 5000 copies/ml received ART378 200 or 400 mg with ritonavir 100 mg every 12 h; after 3 weeks stavudine 40 mg and lamivudine 150 mg every 12 h were added (group I, n = 32). A second group initiated treatment with ABT-378 400 mg and ritonavir 100 or 200 mg plus stavudine and lamivudine every 12 h (group II, n = 68). Results: Mean baseline HIV-1 RNA was 4.9 logic copies/ml in both groups and CD4 cell count was 398 X 10 6 /l and 310 X 10 6 /l in Groups I and II respectively, In the intent-to-treat (ITT; missing value = failure) analysis at 48 weeks, HIV-1 RNA was < 400 copies/ml for 91% (< 50 copies/ml, 75%) and 82% (<50 copies/ml, 79%) of patients in groups I and II respectively. Mean steady-state ABT-378 trough concentrations exceeded the wild-type HIV-1 EC 50 (effective concentration to inhibit 50%) by 50-100-fold. The most common adverse events were abnormal stools, diarrhea and nausea. No patient discontinued before 48 weeks because of treatment-related toxicity or virologic rebound. Conclusions: ABT-378 is a potent, well-tolerated protease inhibitor. The activity and durable suppression of HIV-1 observed in this study is probably attributable to the observed tolerability profile and the achievement of high ABT-378 plasma concentrations.