180 research outputs found
Evaluation of emotion processing in HIV-infected patients and correlation with cognitive performance
Background: Facial emotion recognition depends on cortical and subcortical networks. HIV infection of the central
nervous system can damage these networks, leading to impaired facial emotion recognition.
Methods: We performed a cross-sectional single cohort study consecutively enrolling HIV + subjects during routine
outpatient visits. Age, gender and education-matched HIV-negative healthy individuals were also selected. Subjects
were submitted to a Facial Emotion Recognition Test, which assesses the ability to recognize six basic emotions
(disgust, anger, fear, happiness, surprise, sadness). The score for each emotion and a global score (obtained by
summing scores for each emotion) were analyzed. General cognitive status of patients was also assessed.
Results: A total of 49 HIV + and 20 HIVâsubjects were enrolled. On the Facial Emotion Recognition Test, ANOVA
revealed a significantly lower performance of HIV + subjects than healthy controls in recognizing fear. Moreover,
fear facial emotion recognition was directly correlated with Immediate Recall of Rey Words. The lower the patientsâ
neurocognitive performance the less accurate they were in recognizing happiness. AIDS-defining events were
negatively related to the correct recognition of happiness.
Conclusions: Fear recognition deficit in HIV + patients might be related to the impaired function of neural
networks in the frontostriatal system. AIDS events, including non-neurological ones, may have a negative effect on
this system. Inclusion of an emotion recognition test in the neuropsychological test battery could help clinicians
during the long term management of HIV-infected patients, to better understand the cognitive mechanisms
involved in the reduction of emotion recognition ability and the impact of this impairment on daily lif
Formation of Zn- and Fe-sulfides near hydrothermal vents at the Eastern Lau Spreading Center: implications for sulfide bioavailability to chemoautotrophs
This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens
Bacillus anthracis TIR Domain-Containing Protein Localises to Cellular Microtubule Structures and Induces Autophagy
Toll-like receptors (TLRs) recognise invading pathogens and mediate downstream immune signalling via Toll/IL-1 receptor (TIR) domains. TIR domain proteins (Tdps) have been identified in multiple pathogenic bacteria and have recently been implicated as negative regulators of host innate immune activation. A Tdp has been identified in Bacillus anthracis, the causative agent of anthrax. Here we present the first study of this protein, designated BaTdp. Recombinantly expressed and purified BaTdp TIR domain interacted with several human TIR domains, including that of the key TLR adaptor MyD88, although BaTdp expression in cultured HEK293 cells had no effect on TLR4- or TLR2- mediated immune activation. During expression in mammalian cells, BaTdp localised to microtubular networks and caused an increase in lipidated cytosolic microtubule-associated protein 1A/1B-light chain 3 (LC3), indicative of autophagosome formation. In vivo intra-nasal infection experiments in mice showed that a BaTdp knockout strain colonised host tissue faster with higher bacterial load within 4 days post-infection compared to the wild type B. anthracis. Taken together, these findings indicate that BaTdp does not play an immune suppressive role, but rather, its absence increases virulence. BaTdp present in wild type B. anthracis plausibly interact with the infected host cell, which undergoes autophagy in self-defence
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