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In addition, the consistent enrichment of Pseudomonadacea in male and female may be the characteristic disease-related gut microbiota of BD. Besides, the diagnostic potential of gender specific biomarker panel in male (male validation AUC 0.758-0.874, accurancy 0.693-0.792; female validation AUC 0.727-0.883, accurancy 0.678-0.781) and female (male validation AUC 0.787-0.883, accurancy 0.719-0.784; female validation AUC 0.795-0.898, accurancy 0.689-0.838) has also been identified and confirmed.

The microbiological changes in both MDD and BD are sex specific, and gender specific biomarker panel has better diagnostic performance, which provide a certain reference in sex difference for future clinical differentiation and microbial intervention.

The microbiological changes in both MDD and BD are sex specific, and gender specific biomarker panel has better diagnostic performance, which provide a certain reference in sex difference for future clinical differentiation and microbial intervention.

The present study aims to (1) follow up with 4-year changes in the efficacy outcome, defense style questionnaire (DSQ) score, and clinical features of patients with obsessive-compulsive disorder (OCD) and (2) analyze the relationship between different levels of efficacy and changes in the patients' psychological defense mechanisms.

The following data collection and 4-year follow-up were completed for 153 patients with OCD (1) the treatment process, efficacy outcome, course of disease, and clinical features of OCD were collected using a self-made general information questionnaire and (2) the control method was used to analyze the changes in clinical symptoms (Yale-Brown obsessive compulsive scale [YBOCS], Hamilton anxiety score [HAMA], and Hamilton depression scale [HAMD]) in patients with OCD. Moreover, the changes in the psychological defense mechanism (measured by DSQ) and the relation between the prognosis and DSQ score were investigated.

(1) The HAMA score (8.7 ± 4.8 points), HAMD score (12.0 ± 6.6 points) and YBOCS score (16.4 ± 8.4 points) were significantly lower during the follow-up than at the time of enrollment (p < 0.01). In the two DSQ evaluations, there were no significant differences in the factors, with the exception of a significant decrease in the use of "reaction formation" (t = 2.533, p = 0.015). The changes of mature defense factors in the significant efficacy group significantly increased (p < 0.01). Which was mainly manifested in the significant increase in the score of "sublimation" item, and the difference was extremely significant (t = -3.093, p = 0.006).

An abnormal psychological defense mechanism plays an important role in OCD, and the use of a mature defense mechanism is significantly related to the treatment efficacy.

An abnormal psychological defense mechanism plays an important role in OCD, and the use of a mature defense mechanism is significantly related to the treatment efficacy.

We assessed the effectiveness of switching from intravenous to subcutaneous infliximab in patients with inflammatory bowel diseases (IBDs) treated with or without intensified intravenous regimen.

In this multicenter observational study, IBD patients in clinical remission (partial Mayo score ≤2 or Harvey-Bradshaw index ≤4) were switched to a unique dose of subcutaneous infliximab (120 mg every other week). Pharmacological and biological data were collected at baseline, visit 1 (4-8 weeks postswitch), visit 2 (8-16 weeks postswitch), and visit 3 (16-24 weeks postswitch). Relapse was defined as clinical relapse or fecal calprotectin increase ≥150 μg/g compared with baseline.

Among 184 eligible patients, 72.3% (n= 133 of 184) agreed to switch to subcutaneous infliximab. At visit 3, a relapse occurred in 10.2% (n= 6 of 59), 7.3% (n= 3 of 38), 16.7% (n=3 of 18), and 66.7% (n= 10 of 15) (P < .001) of patients receiving 5 mg/kg every 8 weeks, 10 mg/kg every 8 weeks, 10 mg/kg every 6 weeks, and 10 mg/kg everyy 4 weeks requiring 240 mg every other week.

Switching from intravenous to subcutaneous infliximab 120 mg every other week is safe and well accepted, leading to a low risk of relapse in IBD patients except for those receiving 10 mg/kg every 4 weeks requiring 240 mg every other week.The coronavirus disease 2019 (COVID-19) pandemic has presented unprecedented challenges for youth and families dealing with remote school and work, lack of childcare, and social isolation over the course of 2 years. In response, the US Surgeon General recently published an advisory warning of a mental health crisis among youth,1 noting that youth with intellectual and developmental disabilities, racial/ethnic and sexual/gender minority youth, and youth in low-income, rural, and immigrant households were at higher risk of mental health challenges in the pandemic. The advisory arrived on the heels of an emergency declaration about child and adolescent mental health put forth by the American Academy of Pediatrics, American Academy of Child and Adolescent Psychiatry, and Children's Hospital Association in October 2021. Both emphasize that the COVID-19 pandemic exacerbated already growing youth mental health concerns and highlight the key role schools must play in preventing youth suicide. In this commentary, we make the case for why we need schools to be in the business of youth suicide prevention.

Pediatric social anxiety disorder consistently shows the poorest treatment response of all anxiety disorders. CPI-0610 The current study compared a generic cognitive-behavioral therapy (CBT) treatment for pediatric anxiety against a modified (social anxiety) treatment that incorporated specific components to target theoretically important maintaining processes.

A total of 200 children and adolescents (mean age= 9.5 years, SD= 2.2 years; 47% boys) diagnosed with social anxiety disorder as either their principal or additional disorder were randomly allocated to either the generic or the modified treatment. Both treatments were based on a manualized, empirically validated program (Cool Kids) and comprised 10 sessions over 12 weeks. Assessments comprised structured diagnostic interview and parent and youth reports, and covered diagnoses, symptoms, life impairment, and assessment of maintaining processes at post-treatment and 6-month follow-up.

The treatments did not differ significantly on the primary outcome (remisorg.au/; 12616001065482.Building a successful culture in academic dermatology is necessary now more than ever, which is compounded by the shortage of dermatologists, especially academicians. This dearth of academic dermatologists raises questions concerning who will train future generations of physicians and who will drive innovative research to advance the field and improve patient care. Recruitment and retention of dermatologists in academia faces steep challenges posed by increasing demands within academic medicine and the draw of the private sector. It is important to address barriers to a career in academia. Efforts should be focused on modifiable aspects of dermatology residency experiences to promote a career in academic dermatology. Of equal importance is the retention of faculty already in academia because midcareer shifts from academic settings to private practice can result in a significant leadership gap.Microglia have been suggested to be involved in the underlying mechanism of conditional fear memory formation by regulating inflammatory cytokines. However, the mechanism linking microglia and neuronal activity related to fear conditioning remains unclear. This study characterized the transcription profile of microglia in a fear memory conditional mouse model. Compared with those in control mice microglia, the most significantly induced genes were synapse-related, whereas immune-related genes were reduced due to fear memory consolidation. Whilst the increased expression of synapse-related genes was reversed after fear memory extinction, that of immunological genes was not, strongly suggesting a connection between microglia, neurons, and a dysregulated immune response following contextual fear conditioning. Furthermore, in the hippocampal microglia, we found that the expression of neurotransmitter release regulators, γ-aminobutyric acid (GABA) receptor GABRB3 and synapsin 1/2, increased under fear memory consolidation and restored (decreased) after extinction. In addition, compared with the transcription profile in peripheral monocytes, few overlapping genes were not enriched in biological processes. Taken together, the identified conditional fear stress-induced changes in mouse microglial transcription profiles suggest that microglia-neuron communication mediates contextual fear conditioning.Static magnetic fields (SMF) have neuroprotective and behavioral effects in rats, however, little is known about the effects of SMF on cognition, motor function and the underlying neurochemical mechanisms. In this study, we focused on the effects of short-term (5-10d) and long-term (13-38d) SMF exposure on selective attention and motor coordination of rats, as well as associated alterations in expression level of neuroplasticity-related structural proteins and cryptochrome (CRY1) protein in the cortex, striatum and ventral midbrain. The results showed that 6d SMF exposure significantly enhanced selective attention without affecting locomotor activity in open field. All SMF exposures non-significantly enhanced motor coordination (Rotarod test). Neurochemical analysis demonstrated that 5d SMF exposure increased the expression of cortical and striatal CRY1 and synapsin-1 (SYN1), striatal total synapsins (SYN), and synaptophysin (SYP), growth associated protein-43 (GAP43) and post-synaptic density protein-95 (PSD95) in the ventral midbrain. Exposure to SMF for 14d increased PSD95 level in the ventral midbrain while longer SMF exposure elevated the levels of PSD95 in the cortex, SYN and SYN1 in all the examined brain areas. The increased expression of cortical and striatal CRY1 and SYN1 correlated with the short-lasting effect of SMF on improving selective attention. Collectively, SMF's effect on selective attention attenuated following longer exposure to SMF whereas its effects on neuroplasticity-related structural biomarkers were time- and brain area-dependent, with some protein levels increasing with longer time exposure. These findings suggest a potential use of SMF for treatment of neurological diseases in which selective attention or neuroplasticity is impaired.As a ubiquitous toxic heavy metal, lead (Pb) exposure is known to be implicated in the onset and development of neurodegenerative diseases which may cause more serious health hazards with age and the accumulation of Pb in the body. Autophagy is the main degradation route for abnormal aggregated proteins and damaged cell organelles. Here, we aimed to study the effects of adolescent Pb exposure on autophagy at different life nodes. In this study, we developed a time-series model of Pb exposure in mice and randomly divided 4-week-old male C57BL/6 mice into six groups (4 C, 13 C, 16 C, 4Pb, 13Pb and 16Pb). Mice in Pb groups was consumed deionized water containing 0.2 % Pb(Ac)2 for 3 months and then reared to anticipated life nodes, while the control group consumed deionized water. Western blot and Real-time qPCR were used to assess the effects of developmental Pb exposure on individual components of the autophagy machinery and modulation of microtubule-associated protein 1 light chain 3 (LC3) at each age stage. Our results showed that Pb exposure during adolescence reduced the p-mTOR/mTOR ratios with enhanced expression of Beclin-1, Atg12 and Atg7in both the hippocampus (HPC) and prefrontal cortex (PFC) of senescent mice while upregulation of LC3II/LC3I ratios and p62 suggested that autophagy mediates degradation was interrupted.

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