45 research outputs found

    Early Identification of HIV: Empirical Support for Jail-Based Screening

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    BACKGROUND: Although routine HIV testing is recommended for jails, little empirical data exist describing newly diagnosed individuals in this setting. METHODS: Client-level data (CLD) are available on a subset of individuals served in EnhanceLink, for the nine of the 10 sites who enrolled newly diagnosed persons in the client level evaluation. In addition to information about time of diagnosis, we analyzed data on initial CD4 count, use of antiretroviral therapy (ART), and linkage to care post discharge. Baseline data from newly diagnosed persons were compared to data from persons whose diagnoses predated jail admission. RESULTS: CLD were available for 58 newly diagnosed and 708 previously diagnosed individuals enrolled between 9/08 and 3/11. Those newly diagnosed had a significantly younger median age (34 years) when compared to those previously diagnosed (41 years). In the 30 days prior to incarceration, 11% of those newly diagnosed reported injection drug use and 29% reported unprotected anal intercourse. Median CD4 count at diagnosis was 432 cells/mL (range: 22–1,453 cells/mL). A minority (21%, N = 12) of new diagnoses started antiretroviral treatment (ART) before release; 74% have evidence of linkage to community services. CONCLUSION: Preliminary results from a cross-sectional analysis of this cohort suggest testing in jails finds individuals early on in disease progression. Most HIV(+) detainees did not start ART in jail; therefore screening may not increase pharmacy costs for jails. Detainees newly diagnosed with HIV in jails can be effectively linked to community resources. Jail-based HIV testing should be a cornerstone of “test and treat” strategies

    Handling gait impairments of persons with Parkinson\u2019s disease by means of real-time biofeedback in a daily life environment

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    A smartphone app with telemedicine capability integrating data from foot-mounted inertial measurement units (CuPiD-system) was developed to realize a portable gait analysis system and, on top of it, to provide people with Parkinson\u2019s disease (PD) remote supervision and real-time feedback on gait performance. Eleven persons with PD were recommended to perform gait training for 30 min, three times per week for six weeks. The app offered praising/corrective verbal feedback, encouraging participants to keep the spatio-temporal gait parameters within a clinically determined \u2018therapeutic window\u2019. On average, persons performed 20 training sessions of 1.8 km in 24 min and received 28 corrective and 68 praising messages. The mean walking rhythm was 58 strides/min with a stride length of 1.28 m. System\u2019s usability was determined as positive by the users. In conclusion, CuPiD resulted to be effective in promoting gait training in semi-supervised conditions, stimulating corrective actions and promoting selfefficacy to achieve optimal performance

    The nuclear effector of Wnt-signaling, Tcf1, functions as a T-cell-specific tumor suppressor for development of lymphomas

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    The HMG-box factor Tcf1 is required during T-cell development in the thymus and mediates the nuclear response to Wnt signals. Tcf1(-/-) mice have previously been characterized and show developmental blocks at the CD4-CD8- double negative (DN) to CD4+CD8+ double positive transition. Due to the blocks in T-cell development, Tcf1(-/-) mice normally have a very small thymus. Unexpectedly, a large proportion of Tcf1(-/-) mice spontaneously develop thymic lymphomas with 50% of mice developing a thymic lymphoma/leukemia at the age of 16 wk. These lymphomas are clonal, highly metastatic, and paradoxically show high Wnt signaling when crossed with Wnt reporter mice and have high expression of Wnt target genes Lef1 and Axin2. In wild-type thymocytes, Tcf1 is higher expressed than Lef1, with a predominance of Wnt inhibitory isoforms. Loss of Tcf1 as repressor of Lef1 leads to high Wnt activity and is the initiating event in lymphoma development, which is exacerbated by activating Notch1 mutations. Thus, Notch1 and loss of Tcf1 functionally act as collaborating oncogenic events. Tcf1 deficiency predisposes to the development of thymic lymphomas by ectopic up-regulation of Lef1 due to lack of Tcf1 repressive isoforms and frequently by cooperating activating mutations in Notch1. Tcf1 therefore functions as a T-cell-specific tumor suppressor gene, besides its established role as a Wnt responsive transcription factor. Thus, Tcf1 acts as a molecular switch between proliferative and repressive signals during T-lymphocyte development in the thymus.Stemcel biology/Regenerative medicine (incl. bloodtransfusion
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