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Molecules including major histocompatibility complex (MHC) II and CD40 [15]. Microglia expressing MHC II induce CD4+ T cells to generate IFN-g and TNF-a [16]. In the case of both HAD and AD, this response is considered harmful to the brain and in both diseases TNFa is elevated to neurotoxic levels while only in HAD is IFN-g is prominently elevated [14]. In HIV associated dementia (HAD; also known

Fraction of responding proteins is depleted from DRM in both m cd treatment and smt1. Numbers of significant proteins are similar in both experiments even though number of proteins analyzed in total was lower in m cd experiment. Count of copurifiying proteins being enriched in smt1 DRM was twofold higher in comparison to m cd treatment. Blue triangles indicate proteins significantly depleted in DR

Infection in vitro, this protein was tested for clinical efficacy in HIV-1-infected individuals; however, no effect on plasma viral loads was observed [13]. Further examination revealed that doses of sCD4 that were significantly higher than those achieved in the clinical trial were required to neutralize primary clinical isolates of HIV-1, in contrast to the relatively sensitive, laboratory-adapte

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Ator of nuclear receptors, we explored its prognostic value in relation to estrogen-receptor-a (ESR1) and -b (ESR2) and evaluated its predictive value for response to tamoxifen treatment. Methods: DC-SCRIPT mRNA levels were measured by real-time PCR in 1,505 primary invasive breast cancers and associated with outcome (disease-free survival (DFS), metastasis-free survival (MFS) and overall survival

Ator of nuclear receptors, we explored its prognostic value in relation to estrogen-receptor-a (ESR1) and -b (ESR2) and evaluated its predictive value for response to tamoxifen treatment. Methods: DC-SCRIPT mRNA levels were measured by real-time PCR in 1,505 primary invasive breast cancers and associated with outcome (disease-free survival (DFS), metastasis-free survival (MFS) and overall survival