Exploring the relationship among hikikomori tendencies, autistic traits, computer game use and eating disorder symptoms.

Objective: The hikikomori phenomenon has recently gained growing global interest, and evidences of its association with other psychopathological dimensions are slowly but steadily emerging. We aimed to evaluate the presence and correlates of hikikomori tendencies in an Italian University population, focusing on its relationships with autism spectrum, pathological computer gaming, and eating disorders. In particular, to our knowledge, no study has yet systematically evaluated the latter association, using psychometric instruments tailored to assess eating disorder symptoms.

Assessing Autistic Traits, Hikikomori Tendencies, Pathological Videogaming, and Eating Disorders in University Students: Are Pathological Videogaming and Eating Disorders Gender-Specific Manifestations of the Autism Spectrum?

In the previous literature, specific attention has been paid to investigate autism spectrum symptoms and traits in university students. In this framework, we aimed to evaluate the presence and correlates of autistic traits, hikikomori tendencies, altered eating behaviors, and pathological videogaming in a sample of Italian university students enrolled in bachelor's degree courses. A total of 1192 students were recruited via an online survey and assessed with the Hikikomori Questionnaire-25, the Adult Autism Subthreshold Spectrum Questionnaire, the Eating Attitude test-26, and the Assessment of Internet and Computer Game Addiction.

Case report: hikikomori syndrome in Italy and its link with autistic traits and internet gaming disorder.

During the last few decades, a growing field of literature is focusing on hikikomori, a phenomenon described as a form of pathological social withdrawal or social isolation that lasts for more than 6 months leading to significant functional impairment and/or distress. Despite initially considered a culture-bound syndrome, hikikomori syndrome later gained a wider recognition in different countries, ranging from an attempt to take refuge in an idealistic world, when society success' standards are not reached, to a maladaptive coping strategy complicating several psychiatric illnesses such as anxiety disorders, major depression, internet addiction, internet gaming disorder (IGD) and autism spectrum disorder (ASD). In this framework, difficulties in social interaction, in problem solving strategies and socio-emotional reciprocity, may lead to social withdrawal and hikikomori-like behaviors.

Disease-associated astrocyte epigenetic memory promotes CNS pathology.

Disease-associated astrocyte subsets contribute to the pathology of neurologic diseases, including multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), an experimental model for multiple sclerosis. However, little is known about the stability of these astrocyte subsets and their ability to integrate past stimulation events. Here we report the identification of an epigenetically controlled memory astrocyte subset that exhibits exacerbated pro-inflammatory responses upon rechallenge.

Post-traumatic Stress and Depressive Symptoms in Women With Ovarian Cancer 3-6 Months After Diagnosis.

Background/aim: The potentially traumatic role of severe life-threatening medical conditions is still debated in psychiatry and not yet recognized, particularly among post-traumatic stress disorders. However, increasing evidence suggests the psychopathological impact of severe medical conditions related to their poor prognosis, high lethality, treatments heaviness and invasiveness. Ovarian cancer (OC) is one of the malignancies with the highest mortality and the aim of this study was to investigate post-traumatic stress and depressive symptoms in women 3 to 6 months after diagnosis.

Disease-associated astrocyte epigenetic memory promotes CNS pathology.

Astrocytes play important roles in the central nervous system (CNS) physiology and pathology. Indeed, astrocyte subsets defined by specific transcriptional activation states contribute to the pathology of neurologic diseases, including multiple sclerosis (MS) and its pre-clinical model experimental autoimmune encephalomyelitis (EAE) . However, little is known about the stability of these disease-associated astrocyte subsets, their regulation, and whether they integrate past stimulation events to respond to subsequent challenges.

May Female Autism Spectrum Be Masked by Eating Disorders, Borderline Personality Disorder, or Complex PTSD Symptoms? A Case Series.

The prevalence of Autism Spectrum Disorder (ASD) is four times higher in males than females; however, females are significantly more likely to go undiagnosed due to the existence of a "female autistic phenotype", a manifestation unique to females that conflicts with conventional, masculine conceptualizations of ASD. Furthermore, subthreshold autistic traits, which exert a significantly negative impact on quality of life and represent a vulnerability factor for the development of other psychopathological conditions, may remain even more under-recognized. Subsequently, many women with ASD may never receive a diagnosis or any resulting care, with serious consequences for their health.

Rumination and altered reactivity to sensory input as vulnerability factors for developing post-traumatic stress symptoms among adults with autistic traits.

Objective: Recent literature has suggested that individuals with autism spectrum disorder (ASD) or autistic traits (ATs) would be more likely to encounter traumatic events in their lifetime and to develop post-traumatic stress disorder (PTSD). However, the nature of this relationship has not yet been fully elucidated. The aims of this study were to evaluate the relationship between AT and PTSD and to investigate which specific autistic dimension was more associated with trauma and stress-related symptoms.

Lactate limits CNS autoimmunity by stabilizing HIF-1α in dendritic cells.

Dendritic cells (DCs) have a role in the development and activation of self-reactive pathogenic T cells. Genetic variants that are associated with the function of DCs have been linked to autoimmune disorders, and DCs are therefore attractive therapeutic targets for such diseases. However, developing DC-targeted therapies for autoimmunity requires identification of the mechanisms that regulate DC function.

Autism Spectrum, Hikikomori Syndrome and Internet Gaming Disorder: Is There a Link?

The aim of this study is to review the available literature investigating the relationship between hikikomori, a pathological condition characterized by severe social withdrawal or isolation, autism spectrum disorder (ASD) and Internet gaming disorder (IGD). Studies on the relationship between ASD and IGD have found significant positive correlations between these two conditions. Individuals with ASD would appear to be at risk of developing a problematic use of the Internet, which, to the right extent, would represent a useful tool for social interaction and cognitive development.

Engineered probiotics limit CNS autoimmunity by stabilizing HIF-1α in dendritic cells.

Dendritic cells (DCs) control the generation of self-reactive pathogenic T cells. Thus, DCs are considered attractive therapeutic targets for autoimmune diseases. Using single-cell and bulk transcriptional and metabolic analyses in combination with cell-specific gene perturbation studies we identified a negative feedback regulatory pathway that operates in DCs to limit immunopathology.

Modulation of the Aryl Hydrocarbon Receptor Signaling Pathway Impacts on Junín Virus Replication.

Junín virus (JUNV), a member of the family , is the etiological agent of the Argentine hemorrhagic fever, an endemic disease in the rural region of Argentina lacking a specific chemotherapy. Aryl hydrocarbon receptor (AHR) is expressed in several mammalian tissues and has been indicated as a sensor of ligands from variable sources and a modulator of the cell immune response. Interestingly, recent studies have suggested that the activation or depression of the AHR signaling pathway may play a role in the outcome of diverse human viral infections.

Identification of astrocyte regulators by nucleic acid cytometry.

Multiple sclerosis is a chronic inflammatory disease of the central nervous system. Astrocytes are heterogeneous glial cells that are resident in the central nervous system and participate in the pathogenesis of multiple sclerosis and its model experimental autoimmune encephalomyelitis. However, few unique surface markers are available for the isolation of astrocyte subsets, preventing their analysis and the identification of candidate therapeutic targets; these limitations are further amplified by the rarity of pathogenic astrocytes.

Nasal administration of anti-CD3 monoclonal antibody modulates effector CD8+ T cell function and induces a regulatory response in T cells in human subjects.

Background: Parenteral anti-CD3 Mab (OKT3) has been used to treat transplant rejection and parental administration of a humanized anti-CD3 Mab (Teplizumab) showed positive effects in diabetes. Nasal administration of anti-CD3 Mab has not been carried out in humans. Nasal anti-CD3 Mab suppresses autoimmune diseases and central nervous system (CNS) inflammation in animal models.

Identification of environmental factors that promote intestinal inflammation.

Genome-wide association studies have identified risk loci linked to inflammatory bowel disease (IBD)-a complex chronic inflammatory disorder of the gastrointestinal tract. The increasing prevalence of IBD in industrialized countries and the augmented disease risk observed in migrants who move into areas of higher disease prevalence suggest that environmental factors are also important determinants of IBD susceptibility and severity. However, the identification of environmental factors relevant to IBD and the mechanisms by which they influence disease has been hampered by the lack of platforms for their systematic investigation.

Promyelocytic leukemia protein is a restriction factor for Junín virus independently of Z matrix protein.

The New World (NW) mammarenavirus Junín (JUNV) is the etiological agent of Argentine hemorrhagic fever, a human endemic disease of Argentina. Promyelocytic leukemia protein (PML) has been reported as a restriction factor for several viruses although the mechanism/s behind PML-mediated antiviral effect may be diverse and are a matter of debate. Previous studies have reported a nuclear to cytoplasm translocation of PML during the murine Old World mammarenavirus lymphocytic choriomeningitis virus (LCMV) infection.

AHR signaling is induced by infection with coronaviruses.

Coronavirus infection in humans is usually associated to respiratory tract illnesses, ranging in severity from mild to life-threatening respiratory failure. The aryl hydrocarbon receptor (AHR) was recently identified as a host factor for Zika and dengue viruses; AHR antagonists boost antiviral immunity, decrease viral titers and ameliorate Zika-induced pathology in vivo. Here we report that AHR is activated by infection with different coronaviruses, potentially impacting antiviral immunity and lung epithelial cells.

The Aryl Hydrocarbon Receptor as a Modulator of Anti-viral Immunity.

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor, which interacts with a wide range of organic molecules of endogenous and exogenous origin, including environmental pollutants, tryptophan metabolites, and microbial metabolites. The activation of AHR by these agonists drives its translocation into the nucleus where it controls the expression of a large number of target genes that include the AHR repressor (AHRR), detoxifying monooxygenases (CYP1A1 and CYP1B1), and cytokines. Recent advances reveal that AHR signaling modulates aspects of the intrinsic, innate and adaptive immune response to diverse microorganisms.

Gut-licensed IFNγ NK cells drive LAMP1TRAIL anti-inflammatory astrocytes.

Astrocytes are glial cells that are abundant in the central nervous system (CNS) and that have important homeostatic and disease-promoting functions. However, little is known about the homeostatic anti-inflammatory activities of astrocytes and their regulation. Here, using high-throughput flow cytometry screening, single-cell RNA sequencing and CRISPR-Cas9-based cell-specific in vivo genetic perturbations in mice, we identify a subset of astrocytes that expresses the lysosomal protein LAMP1 and the death receptor ligand TRAIL.

Zika virus infection of first trimester trophoblast cells affects cell migration, metabolism and immune homeostasis control.

Zika virus (ZIKV) re-emerged after circulating almost undetected for many years and the last spread in 2015 was the major outbreak reported. ZIKV infection was associated with congenital fetal growth anomalies such as microcephaly, brain calcifications, and low birth weight related to fetal growth restriction. In this study, we investigated the effect of ZIKV infection on first trimester trophoblast cell function and metabolism.