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Occupational stress represents a significant precipitating factor in different diseases but its role in Irritable Bowel Syndrome (IBS) needs to be clarified. The present cross-sectional study aimed at investigating the prevalence of IBS diagnosis in a sample of health workers and exploring the potential relationships between IBS, work-related stress levels and work ability.

653 health workers undergoing periodical occupational health surveillance at the Occupational and Preventive Medicine Unit of a major University Hospital in central Italy, were consecutively recruited and screened for IBS diagnosis, according to ROMA IV criteria. The rating scales IBS Severity Scoring System (IBS-SSS), Demand-Control-Support Questionnaire (DCSQ) and Work Ability Index (WAI) were used to assess respectively IBS severity, occupational stress and work ability levels.

IBS prevalence in the sample was 16.8%. Participants suffering from IBS were characterized by a higher prevalence of psychiatric diagnosis and sleep disturbances, higher levels of job strain and isostrain as well as by lower levels of work ability compared to non affected subjects. Moreover, the severity of IBS correlated positively with occupational stress and both were negatively associated with work ability.

The present results suggest the need for preventive, organizational and management strategies at workplace aimed at protecting the health and well-being but also productivity of the worker with IBS.

The present results suggest the need for preventive, organizational and management strategies at workplace aimed at protecting the health and well-being but also productivity of the worker with IBS.Guillain-Barré syndrome (GBS) is an autoimmune disease in which the peripheral nerves are affected. GBS has different subtypes, such as acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). Infections, e.g. Campylobacter jejuni, influenza, etc., can lead to GBS. Both environmental and genetic factors play a major role in the occurrence of GBS. Several studies have investigated the genetic basis of GBS. Human leukocyte antigens (HLA) genes, Cluster of Differentiation (CD) 1A, FAS, Fc gamma receptors (FcGR), Intercellular adhesion molecule-1 (ICAM1), different interleukins, Nucleotide oligomerization domain (NOD), Toll-like receptor 4 (TLR4), Tumor necrosis factor-α (TNF-α) are among the genes reported to be involved in susceptibility to the disease. Dysregulation and dysfunction of the mentioned gene products, even though their role in the pathogenesis of GBS is controversial, play a role in inflammatory pathways, regulation of immune cells and system, antigen presentation, axonal degeneration, apoptosis, and cross-reaction. This review aims to summarize associated genes with GBS to contribute to better understanding of GBS pathogenesis and discover the gene pathways that play role in GBS occurrence.

Japanese encephalitis is an acute inflammatory disease caused by Japanese encephalitis virus (JEV). In this study we aim to determine the association of IL-6 (174) and IL-12B (1188A/C) gene polymorphisms with JEV susceptibility, disease severity and outcomes in north Indian population.

This study was performed an equal number of cases and control individuals (125). Gene polymorphism has been analyzed by PCR-RFLP and expression by ELISA.

Homozygous(C/C) genotypes of IL-12B were significantly associated with protection in JE infection (p=0.008, OR=0.368) whereas IL-6 was not associated with JEV infection (p=0.269, OR=1.245). The C allele of IL-6 was associated with protection in JE disease and G/C genotype was associated with outcomes with recovered individuals.

IL-12B gene polymorphism leads to increase level of IL-12B in JE patients, which can contribute to JE susceptibility and disease severity. IL-6 polymorphism has not been associated with susceptibility of JE. Overall, this is the first information from northern India shows association of IL-6 and IL-12B polymorphisms with JE disease.

IL-12B gene polymorphism leads to increase level of IL-12B in JE patients, which can contribute to JE susceptibility and disease severity. IL-6 polymorphism has not been associated with susceptibility of JE. Overall, this is the first information from northern India shows association of IL-6 and IL-12B polymorphisms with JE disease.Response to weekly evidence-based PTSD treatments varies. Little is known about response trajectories and predictors in intensive PTSD treatments. This study sought to identify different trajectories of symptom change among veterans who completed a 3-week CPT-based intensive PTSD treatment program and examined potential predictors of trajectory group membership. Four hundred fifty-two veterans completed the program. Demographics, PTSD and depression severity, negative posttrauma cognitions, and alcohol use were assessed at intake and evaluated as possible predictors of group membership. Group based trajectory modeling was used to determine distinct groups based on PTSD symptom trajectory over the course of treatment, as well as predictors of group membership. Four distinct treatment trajectories were identified Fast responders (15.3%), steady responders (32.0%), partial responders (38.4%), and minimal responders (14.4%). Fast and steady responders reported substantial symptom reductions and dropped below the "probable PTSD" threshold, with fast responders achieving improvements after just one week of treatment. Partial responders experienced clinically significant reductions but remained above the "probable PTSD" threshold. Minimal responders reported the highest baseline PTSD symptoms and changed the least throughout treatment. Negative posttrauma cognitions as well as self-reported and clinician-rated PTSD symptom severity assessed at intake successfully predicted trajectory membership. The identified trajectories closely resemble findings in the limited existing literature on intensive PTSD treatment trajectories. Results suggest that some individuals may improve with even shorter interventions and others might benefit from additional treatment sessions. Sodiumhydroxide Overall, findings support the importance of evaluating individual- and group-level treatment responses.

The risk factors for radicalization and terrorism represent a key research issue. While numerous data on the sociological, political, and criminological profiles of radicalized people and terrorists are available, knowledge about psychiatric disorders among these populations remains scarce and contradictory.

We conducted a systematic review of the literature regarding psychiatric disorders among both radicalized and terrorist populations.

We screened 2,856 records and included a total of 25 articles to generate a complete overview. The vast majority of studies were of poor methodological quality. We assessed three population groups people at risk of radicalization, radicalized populations, and terrorist populations. The results showed important variations in the prevalence rates of psychiatric disorders depending on the study population and methodology. People at risk of radicalization have been reported to have depressive disorders, but contradictory findings exist. Psychiatric disorders range from 6% to 41% in the radicalized population and from 3.4% to 48.5% among terrorists. Among terrorists, psychiatric disorders are more frequent for lone-actor terrorists than for those in groups.

We were not able to identify a significant association between radicalization, terrorism, and psychiatric disorders in our systematic review. However, some research suggests high rates of psychiatric disorders in subgroups of radicalized people and lone-actor terrorists. Further studies using standardized psychiatric assessment methods are urgently needed.

We were not able to identify a significant association between radicalization, terrorism, and psychiatric disorders in our systematic review. However, some research suggests high rates of psychiatric disorders in subgroups of radicalized people and lone-actor terrorists. Further studies using standardized psychiatric assessment methods are urgently needed.Brain-derived neurotrophic factor (BDNF) and the immune-inflammatory response system (IRS) have been implicated in the pathophysiology of schizophrenia. However, no research examined the associations between BDNF and immune activation both before and after treatment in antipsychotic-naïve first episode psychosis (AN-FEP). This study aims to examine serum BDNF levels and their association with IRS and the compensatory immune-regulatory reflex system (CIRS) in AN-FEP before and after risperidone treatment. We included 31 AN-FEP and 22 healthy controls. AN-FEP showed reduced levels of BDNF as compared to controls, and BDNF levels normalized after treatment with risperidone. BDNF levels were inversely correlated with a greater IRS response. Higher levels of IRS/CIRS biomarkers were associated with lower levels of BDNF including M1 macrophage, T-helper (Th)-1, Th-2, and Th-17, and T-regulatory (Treg) cell responses. Our findings indicate that AN-FEP is characterized by decreased levels of BDNF, which are normalized after treatment with risperidone. BDNF levels were inversely associated with activated immune-inflammatory pathways. The findings support the hypothesis that, increased IRS is linked to neurotoxicity, and that a decrease in BDNF may be part of the IRS/CIRS responses in FEP and, thus, be involved in the development of psychosis.In light of the need for objective mechanism-based diagnostic tools, the current research describes a novel diagnostic support system aimed to differentiate between anxiety and depression disorders in a clinical sample. Eighty-six psychiatric patients with clinical anxiety and/or depression were recruited from a public hospital and assigned to one of the experimental groups Depression, Anxiety, or Mixed. The control group included 25 participants with no psychiatric diagnosis. Participants performed a battery of six cognitive-behavioral tasks assessing biases of attention, expectancies, memory, interpretation and executive functions. Data were analyzed with a machine-learning (ML) random forest-based algorithm and cross-validation techniques. The model assigned participants to clinical groups based solely on their aggregated cognitive performance. By detecting each group's unique performance pattern and the specific measures contributing to the prediction, the ML algorithm predicted diagnosis classification in two models (I) anxiety/depression/mixed vs. control (76.81% specificity, 69.66% sensitivity), and (II) anxiety group vs. depression group (80.50% and 66.46% success rates in classifying anxiety and depression, respectively). The findings demonstrate that the cognitive battery can be utilized as a support system for psychiatric diagnosis alongside the clinical interview. This implicit tool, which is not based on self-report, is expected to enable the clinician to achieve increased diagnostic specificity and precision. Further, this tool may increase the confidence of both clinician and patient in the diagnosis by equipping them with an objective assessment tool. Finally, the battery provides a profile of biased cognitions that characterizes the patient, which in turn enables more fine-tuned, individually-tailored therapy.