Brain Responses to Faces and Facial Expressions in 5-Month-Olds: An fNIRS Study

Processing faces and understanding facial expressions are crucial skills for social communication. In adults, basic face processing and facial emotion processing rely on specific interacting brain networks. In infancy, however, little is known about when and how these networks develop. The current study uses functional near-infrared spectroscopy (fNIRS) to measure differences in 5-month-olds’ brain activity in response to fearful and happy facial expressions. Our results show that the right occipital region responds to faces, indicating that the face processing network is activated at 5 months. Yet sensitivity to facial emotions appears to be still immature at this age: explorative analyses suggest that if the facial emotion processing network was active this would be mainly visible in the temporal cortex. Together these results indicate that at 5 months, occipital areas already show sensitivity to face processing, while the facial emotion processing network seems not fully developed

Block of death-receptor apoptosis protects mouse cytomegalovirus from macrophages and is a determinant of virulence in immunodeficient hosts.

The inhibition of death-receptor apoptosis is a conserved viral function. The murine cytomegalovirus (MCMV) gene M36 is a sequence and functional homologue of the human cytomegalovirus gene UL36, and it encodes an inhibitor of apoptosis that binds to caspase-8, blocks downstream signaling and thus contributes to viral fitness in macrophages and in vivo. Here we show a direct link between the inability of mutants lacking the M36 gene (ΔM36) to inhibit apoptosis, poor viral growth in macrophage cell cultures and viral in vivo fitness and virulence. ΔM36 grew poorly in RAG1 knockout mice and in RAG/IL-2-receptor common gamma chain double knockout mice (RAGγC(-/-)), but the depletion of macrophages in either mouse strain rescued the growth of ΔM36 to almost wild-type levels. This was consistent with the observation that activated macrophages were sufficient to impair ΔM36 growth in vitro. Namely, spiking fibroblast cell cultures with activated macrophages had a suppressive effect on ΔM36 growth, which could be reverted by z-VAD-fmk, a chemical apoptosis inhibitor. TNFα from activated macrophages synergized with IFNγ in target cells to inhibit ΔM36 growth. Hence, our data show that poor ΔM36 growth in macrophages does not reflect a defect in tropism, but rather a defect in the suppression of antiviral mediators secreted by macrophages. To the best of our knowledge, this shows for the first time an immune evasion mechanism that protects MCMV selectively from the antiviral activity of macrophages, and thus critically contributes to viral pathogenicity in the immunocompromised host devoid of the adaptive immune system

Latent classes of sexual risk and corresponding STI and HIV positivity among MSM attending centres for sexual health in the Netherlands

Objectives: Continuing high STI positivity among men who have sex with men (MSM) attending centres for sexual health (CSH) indicates that high-risk behaviour is ongoing. The objective of this study was to gain a better insight into risk behaviours among MSM attending CSH and to explore STI and HIV positivity by subgroups. Methods: We used national data routinely collected during CSH consultations for this study. From September to December 2017, questions on group sex, substance use and sex with HIV-positive partners were asked at each CSH consultation. We analysed latent classes of client-related factors and sexual risk behaviour among MSM attending CSH in this period. We examined STI positivity and prevalence ratios by latent classes. Results: A total of six classes were identified in order of increasing risk: â € overall low-risk behaviour' (n=2974; 22.0%), â € Western origin and multiple sex partners' (MSP) (n=4182; 30.9%), â € Non-Western origin and MSP' (n=2496; 18.5%), â € living with HIV' (n=827; 6.1%), â € group sex and HIV-positive partners' (n=1798; 13.3%) and â € group sex and chemsex' (n=1239; 9.2%). The any STI positivity ranged from 14.0% in the overall low-risk behaviour class to 35.5% in the group sex and chemsex class. HIV positivity did not differ significantly between classes. The Western origin and MSP class was largest and accounted for the majority of STI and HIV infections. Conclusions: Although STI positivity increased with increased risky behaviours, considerable STI positivity was found in all six latent classes. Comparable HIV positivity between classes indicates risk reduction strategies among subgroups engaged in risky behaviours. The differences in risk behaviour and STI positivity require preventive strategies tailored to each subgroup

Macrophage TNF-α mediates parathion-induced airway hyperreactivity in guinea pigs.

Organophosphorus pesticides (OPs) are implicated in human asthma. We previously demonstrated that, at concentrations that do not inhibit acetylcholinesterase activity, the OP parathion causes airway hyperreactivity in guinea pigs as a result of functional loss of inhibitory M2 muscarinic receptors on parasympathetic nerves. Because macrophages are associated with asthma, we investigated whether macrophages mediate parathion-induced M2 receptor dysfunction and airway hyperreactivity. Airway physiology was measured in guinea pigs 24 h after a subcutaneous injection of parathion. Pretreatment with liposome-encapsulated clodronate induced alveolar macrophage apoptosis and prevented parathion-induced airway hyperreactivity in response to electrical stimulation of the vagus nerves. As determined by qPCR, TNF-α and IL-1β mRNA levels were increased in alveolar macrophages isolated from parathion-treated guinea pigs. Parathion treatment of alveolar macrophages ex vivo did not significantly increase IL-1β and TNF-α mRNA but did significantly increase TNF-α protein release. Consistent with these data, pretreatment with the TNF-α inhibitor etanercept but not the IL-1β receptor inhibitor anakinra prevented parathion-induced airway hyperreactivity and protected M2 receptor function. These data suggest a novel mechanism of OP-induced airway hyperreactivity in which low-level parathion activates macrophages to release TNF-α-causing M2 receptor dysfunction and airway hyperreactivity. These observations have important implications regarding therapeutic approaches for treating respiratory disease associated with OP exposures

Two-year-olds at elevated risk for ASD can learn novel words from their parents

Education and Child Studie

Differential detection and distribution of microglial and hematogenous macrophage populations in the injured spinal cord of lys-EGFP-ki transgenic mice

The acute inflammatory response that follows spinal cord injury (SCI) contributes to secondary injury that results in the expansion of the lesion and further loss of neurologic function. A cascade of receptor-mediated signaling events after SCI leads to activation of innate immune responses including the migration of microglia and active recruitment of circulating leukocytes. Because conventional techniques do not always distinguish macrophages derived from CNS-resident microglia from blood-derived monocytes, the role that each macrophage type performs cannot be assessed unambiguously in these processes. We demonstrate that, in the normal and spinal cord-injured lys-EGFP-ki transgenic mouse, enhanced green fluorescent protein (EGFP) is expressed only in mature hematopoietic granulomyelomonocytic cells and not in microglia. This allowed us to assess the temporal and spatial relationships between microglia-derived and hematogenous macrophages as well as neutrophils during a period of 6 weeks after clip compression SCI. Within the lesion, EGFP-positive monocyte-derived macrophages were found at the epicenter surrounded by EGFP-negative-activated microglia and microglia-derived macrophages. Neutrophils were not present when EGFP-positive monocyte-derived macrophages were depleted, indicating that neutrophil persistence in the lesion depended on the presence of these monocytes. Thus, these 2 distinct macrophage populations can be independently identified and tracked, thereby allowing their roles in acute and chronic stages of SCI-associated inflammation to be defined. Copyright © 2012 by the American Association of Neuropathologists, Inc