Acute respiratory distress syndrome (ARDS) is a severe inflammatory lung injury caused by various factors, including infection, trauma and shock. The predominant pathological alteration in its late stages is pulmonary fibrosis (PF), characterised by progressive extracellular matrix deposition, architectural destruction and functional impairment. Particularly in COVID-19-induced ARDS, PF incidence has markedly increased, making it a major sequela impacting patients’ long-term quality of life.

This review systematically examines post-acute lung injury (ALI)/ARDS PF through three perspectives: pathogenesis, prediction and treatment.

Mechanistically, the fibrotic process involves epithelial injury and mesenchymal transition, fibroblast activation with aberrant extracellular matrix remodelling, dysregulated inflammation with immune cell involvement and clinical management-related factors. For prediction, various biomarkers (including growth factors, matrix proteins and inflammatory markers) and imaging features (particularly high-resolution computed tomography (HRCT) and magnetic resonance imaging (MRI) characteristics) demonstrate clinical value. Integrated multiparameter models incorporating artificial intelligence show promise for early identification and risk stratification of high-risk patients. Therapeutic strategies encompass anti-inflammatory approaches (e.g., corticosteroids and antioxidants), antifibrotic agents (pirfenidone and nintedanib), cell-based therapies (mesenchymal stem cells and exosomes) and emerging genetic/RNA interventions. However, specific preventive and therapeutic approaches tailored to the post-ALI/ARDS PF population remain inadequate in clinical practice.

Future research should focus on elucidating underlying mechanisms, refining early-warning systems, exploring personalised treatments and facilitating clinical translation. The ultimate goal is to transition from traditional supportive care to proactive prevention through enhanced clinical surveillance, early prediction and rational intervention, thereby preventing fibrosis progression and improving outcomes in ARDS survivors.

Gambling disorder frequently co-occurs with other psychiatric conditions, yet its relationship with obsessive-compulsive disorder (OCD) remains unclear. Emerging evidence suggests impulsivity and compulsivity may be inter-related rather than diametrically opposed constructs, warranting investigation of their clinical overlap. The aim of this study is to examine the rate of gambling disorder in adults with OCD and to explore associated clinical, behavioral, and treatment-related characteristics.

Adults with probable OCD were recruited via online Reddit groups for OCD, OCD clinics, and support groups and completed a cross-sectional survey. OCD symptom types were assessed using the Obsessive-Compulsive Inventory-Revised, and gambling disorder was identified using the Minnesota Impulsive Disorders Interview. Additional measures included gambling severity, impulsivity, and problematic internet use. Group comparisons were conducted between participants with and without gambling disorder.

Among 186 adults with OCD, 34 (18.8%) met criteria for gambling disorder. Individuals with comorbid gambling disorder demonstrated significantly greater OCD severity, particularly in ordering, checking, and neutralizing symptoms, and reported later onset of OCD. The comorbid group showed higher impulsivity, greater problematic internet use, and distinct gambling behaviors, including higher rates of online gambling, esports betting, and use of artificial intelligence tools for gambling. They were also less likely to have received pharmacological treatment for OCD.

Gambling disorder in adults with OCD is associated with distinct clinical characteristics, greater impulsivity, problematic internet use, and concerning treatment gaps. These findings highlight the importance of screening for gambling in OCD, and vice versa, and suggest a need for integrated treatment approaches.

There has been growing interest in developing a clinical staging model for eating disorders (EDs). The aim of this scoping review is to investigate the extent, range, and nature of research that can inform clinical staging approaches for EDs.

This review was conducted following the Joanna Briggs Institute methodology for scoping reviews and the PRISMA extension for Scoping Reviews. A search of PubMed, PsycINFO, MEDLINE and Web of Science databases was conducted. Sixty studies were included for review, and data were extracted according to revised pre-published criteria. Studies were summarized using narrative synthesis.

Thirty-six of the included manuscripts were quantitative, 18 were qualitative, and six were conceptual/review papers. The included studies primarily focused on anorexia nervosa in white, female samples and compared only two stages of illness, equating to “early” and “longstanding” or “severe and enduring” EDs. “Middle” stages or transitions between stages were not well-defined. Stages have mostly been conceptualized using duration of illness or other behavioral or clinical parameters, with few (neuro) biological studies identified. Factors that may modify illness stage have not yet been integrated into ED staging literature.

There is growing consensus that early- and later-stage EDs have distinct characteristics and treatment requirements; however, these distinctions require clearer definition. Recommendations for future research are outlined, emphasizing integration of psychosocial and biological research, focused investigation of illness phases outside of early and longstanding phases, and evaluation of personalized, stage-based treatments. A tentative staging model for EDs is proposed.

1. (1) To become familiar with the concept of misophonia; i.e. hatred of sounds.

2. (2) To evaluate the potential effectiveness of existing interventions for the treatment of misophonia.

3. (3) To gain insight into adapting established therapy methods to novel settings.

Vasovagal syncope is the most common cause of syncope in children, and there is no satisfactory treatment currently. We evaluated the response to midodrine treatment in patients with vasovagal syncope who failed to benefit from conventional, non-pharmacologic treatments.

The study was a single-centre retrospective study. The data of 44 children between the ages of 6 and 18 years, who were diagnosed with recurrent vasovagal syncope, did not benefit from non- pharmacological treatments, and received midodrine treatment from 2015 to 2022 were enrolled in the study.

In total, 44 patients, 38 (86.4%) were girls, and 6 (13.6%) were boys. The primary outcome measure was the change in frequency of vasovagal syncope episodes from baseline to 6 months after treatment with midodrine. Patients received a midodrine treatment at an average of 2.5–5 mg/day and were followed for a median of 23.07 (8–72) months. The median number of syncope was 4.2 (3–9.8)/year prior to treatment and 1.2 (1–5)/year (p = 0.01) following the treatment. There was a significant improvement in syncope episodes in all patients.

Vasovagal syncope is the common cause of syncope in children, and its treatment has not yet been found satisfactory. Midodrine treatment was found to be effective and safe in paediatric patients with recurrent vasovagal syncope. However, further research is needed to determine the most effective treatment for this condition.

Parenting is related to the development of callous-unemotional (CU) traits (i.e. low empathy and restricted guilt), making it an important target of interventions for childhood conduct problems (CPs). However, the relative importance of different parenting features in relation to the development of CU traits remains unclear. This study used machine learning to examine multiple parenting features assessed across infancy and early childhood as predictors of CU traits and CPs in early adolescence.

Data were from the Family Life Project (N = 1,292; 49% female, 41% Black, and 28% below the poverty line). Seventy-four parenting predictors were assessed at eight time points between children aged 6–90 months using parent-reported questionnaires and observer ratings of videotaped interactions and home visits. CU traits and CPs were assessed via parent-reported questionnaires in preadolescence (12–14 years).

Parenting features explained 8.2% of CU traits variability in preadolescence, with top predictors including early sensitive parenting and later behavior management and scaffolding practices. Prediction of CPs was weaker, with parenting explaining 4.5% of the variability.

Results highlight that disruption in close and sensitive early parent–child relationships is relevant to the development of CU traits. Results from the prediction of CPs indicate a more heterogeneous etiology. Findings support targeting parental sensitivity and behavior management within preventative interventions for CU traits and CPs.

Lactate, generated through glycolysis, plays a dual role as both a metabolic substrate and a signalling molecule, influencing cellular functions in pathophysiological scenarios. Protein lactylation, a recently identified form of post-translational modification mediated by lactate, has garnered significant and increasing attention. Globally, hepatic disorders pose a significant public health burden, frequently involving disruptions in glucose metabolism and consequent lactate buildup.

This comprehensive review examines the discovery, regulatory mechanisms and pathogenic roles of lactylation in diverse liver disorders, while critically evaluating emerging lactylation-targeted therapeutics to guide future translational research.

Lactylation modifications play a pivotal role in various pathophysiological processes, including hepatic inflammation, liver fibrosis, ischaemic injury, tumour growth and metastasis.

Modulation of lactylation pathways, coupled with pharmacological control of lactate synthesis and shuttling, emerges as a strategic approach to liver disease therapeutics.