Guybryan5434

The UC risk genes show enrichment in progenitors, glial cells and immune cells, and drug-target genes are differentially expressed in antigen presenting cells.

Our work identifies novel population-specific plasma cell molecular signatures of UC. The transcriptional signature of UC is shared in immune cells from both inflamed and non-inflamed tissues, whereas the transcriptional response to disease is a local effect only in inflamed epithelial/stromal cells.

Our work identifies novel population-specific plasma cell molecular signatures of UC. The transcriptional signature of UC is shared in immune cells from both inflamed and non-inflamed tissues, whereas the transcriptional response to disease is a local effect only in inflamed epithelial/stromal cells.

Previous studies have shown that BD patients exhibited impairment when performing a verbal fluency task (VFT) and abnormal prefrontal cortex activation during this task. GSK269962A However, no study has specifically examined whether patients with type II BD demonstrate difficulty in performing VFT and impairments in relevant neural correlates or whether these are related to psychotic symptoms, the present study aimed to examine these issues.

Forty-nine patients with type II BD (21 patients with psychotic symptoms [BDIIp] and 28 patients without psychotic symptoms [BDIIn]) and 45 matched healthy controls (HCs) participated the study and completed the VFTs, while their brain activity was recorded with near-infrared spectroscopy (NIRS).

Both BDIIp and BDIIn patients showed poorer performance on VFTs than HCs. In addition, BDII patients showed lower brain activation than HCs in bilateral dorsolateral prefrontal cortex and right frontal pole, these results were mainly driven by BDIIn patients. Moreover, subjective psychotic symptoms were positively significantly correlated with left dorsolateral prefrontal cortex activation in BDII patients.

Type II BD patients showed significant impairment when performing VFTs and reduced activation in the prefrontal cortex, and subjective psychotic symptoms were associated with brain activation in left dorsolateral prefrontal cortex in BDII patients.

Type II BD patients showed significant impairment when performing VFTs and reduced activation in the prefrontal cortex, and subjective psychotic symptoms were associated with brain activation in left dorsolateral prefrontal cortex in BDII patients.Accumulating data presented that tryptophan metabolic pathway (TMP) may play a role in attention-deficit/hyperactivity disorder (ADHD). However, no study have investigated potential role of TMP in disruptive behavior disorders coexisting with ADHD. This study compared serum levels of tryptophan, kynurenine, kynurenic acid, 3-hydroxykynurenine and 3-hydroxyantranilic acid in medication-free children with ADHD combined presentation (ADHD-C), with ADHD-C and oppositional defiant disorder (ODD), and with ADHD-C and conduct disorder (CD) versus healthy controls. The study also compared several ratios that are previously suggested to reflect the activities of the KP enzymes (kynurenine/tryptophan, kynurenic acid/kynurenine, 3-hydroxykynurenine/kynurenine) or neuroprotective activity (kynurenic acid/3-hydroxykynurenine) among groups. A total of 122 patients were enrolled 46 children with ADHD-C alone, 43 children with ADHD-C+ODD, 33 children with ADHD-C+CD and 50 healthy controls. Targeted biochemical molecules were assessed by liquid chromatography-mass spectrometry/mass spectrometry. Compared to control group, serum kynurenine levels were significantly higher in the ADHD-C group, serum 3-hydroxykynurenine levels were significantly lower in the ADHD-C and ADHD-C+ODD groups, the serum kynurenic acid/kynurenine ratio was significantly higher in the ADHD-C, ADHD-C+ODD and ADHD-C+CD groups, and the serum 3-hydroxykynurenine/kynurenine ratio was significantly lower in the ADHD-C group. These findings suggest that TMP may play a role in the pathophysiology of ADHD-C.Large-scale protracted population stressors, such as social unrest and the coronavirus disease 2019 (COVID-19), are associated with increased symptoms of post-traumatic stress disorder (PTSD) and depression. Cost-effective mental health screening is prerequisite for timely intervention. We developed an online tool to identify prospective predictors of PTSD and depressive symptoms in the context of co-occurring social unrest and COVID-19 in Hong Kong. 150 participants completed baseline and follow-up assessments, with a median duration of 29 days. Three logistic regression models were constructed to assess its discriminative power in predicting PTSD and depressive symptoms at one month. Receiver-operating characteristic analysis was performed for each model to determine their optimal decision thresholds. Sensitivity and specificity of the models were 87.1% and 53.8% for probable PTSD, 77.5% and 63.3% for high-risk depressive symptoms, and 44.7% and 96.4% for no significant depressive symptoms. The models performed well in discriminating outcomes (AUCs range 0.769-0.811). Probable PTSD was predicted by social unrest-related traumatic events, high rumination, and low resilience. Rumination and resilience also predicted high-risk and no significant depressive symptoms, with COVID-19-related events also predicting no significant depression risk. Accessible screening of probable mental health outcomes with good predictive capability may be important for early intervention opportunities.Depressive symptoms are common in schizophrenia and have been associated with both favourable and unfavourable outcomes. We studied the longitudinal course of depressive symptoms and explored their temporal relationships with other manifestations of the illness and its treatment. This longitudinal cohort study included 126 antipsychotic naïve or only briefly treated patients with first-episode schizophrenia spectrum disorders treated with a long-acting antipsychotic over 24 months. Depressive symptoms were assessed at three monthly intervals using the Calgary Depression Scale for Schizophrenia and changes over time were assessed using linear mixed-effect models for continuous repeated measures. Depressive symptoms were most prominent at baseline with highly significant reductions during the first three months of treatment and maintenance of improvement thereafter. Most improvement occurred with antipsychotic treatment alone, with few patients requiring additional antidepressants. We also found that depressive symptoms were associated with positive symptoms, better insight and poorer quality of life, but not with negative symptoms, extrapyramidal symptoms, substance use or cumulative antipsychotic dose.