[WITHDRAWN] Spatial enrichment of the type 1 interferon signature in the brain of a neuropsychiatric lupus murine model.

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Neuropsychiatric disorders: An immunological perspective.

Neuropsychiatric diseases have traditionally been studied from brain, and mind-centric perspectives. However, mounting epidemiological and clinical evidence shows a strong correlation of neuropsychiatric manifestations with immune system activation, suggesting a likely mechanistic interaction between the immune and nervous systems in mediating neuropsychiatric disease. Indeed, immune mediators such as cytokines, antibodies, and complement proteins have been shown to affect various cellular members of the central nervous system in multitudinous ways, such as by modulating neuronal firing rates, inducing cellular apoptosis, or triggering synaptic pruning.

Overexpression of schizophrenia susceptibility factor human complement C4A promotes excessive synaptic loss and behavioral changes in mice.

The complement component 4 (C4) gene is linked to schizophrenia and synaptic refinement. In humans, greater expression of C4A in the brain is associated with an increased risk of schizophrenia. To investigate this genetic finding and address how C4A shapes brain circuits in vivo, here, we generated a mouse model with primate-lineage-specific isoforms of C4, human C4A and/or C4B.

Microglial responses to peripheral type 1 interferon.

Background: Interferon α (IFNα) is a cytokine whose production is increased endogenously in response to viral infection and in autoimmune diseases such as systemic lupus erythematosus (SLE). An elevated IFNα signature has been associated with clinically observed neuro-behavioural deficits such as mild cognitive impairment, fatigue, depression and psychosis in these diseases. However, the mechanisms underlying these neuropsychiatric symptoms remain largely unknown, and it is as yet unclear how IFNα signalling might influence central nervous system (CNS) function.

How does mutation affect the distribution of phenotypes?

The potential for mutational processes to influence patterns of neutral or adaptive phenotypic evolution is not well understood. If mutations are directionally biased, shifting trait means in a particular direction, or if mutation generates more variance in some directions of multivariate trait space than others, mutation itself might be a source of bias in phenotypic evolution. Here, we use mutagenesis to investigate the affect of mutation on trait mean and (co)variances in zebrafish, Danio rerio.

Validation of the University of Washington quality of life questionnaires for head and neck cancer patients in India.

Unlabelled: Quality of life (QOL) is a multidimensional construct capturing the subjective wellbeing of patients in physical, emotional, functional and social domains. Available work on post treatment QOL have only been made in western literature and less in Indian literature.

Aims: To translate the UW-QOL into both Hindi and Marathi and psychometrically validate the translation in HandN cancer patients in Indian population.