Distinct impulsivity profiles in subtypes of violence among community-dwelling patients with severe mental disorders: a longitudinal study.

BACKGROUND: Although only a few patients with severe mental disorders (SMD) can commit violent behaviour in the community, violent behaviour aggravates the stigma towards patients with SMD. Understanding the subtypes of violent behaviour may be beneficial for preventing violent behaviour among patients with SMD, but it has rarely been studied. METHODS: This longitudinal study investigated 1914 patients with SMD in the community at baseline, and the follow-up period ranged from February 2021 to August 2021. The Barratt Impulsiveness Scale Version-11, the Buss-Perry Aggression Questionnaire, the Impulsive/Premeditated Aggression Scale, the Personality Diagnostic Questionnaire and the MacArthur Community Violence Instrument were used at baseline. The Modified Overt Aggression Scale was used to assess the occurrence of violent behaviour (outcome) during the follow-up period. Cox regression models were used to calculate hazard ratios (HRs) with 95% confidence intervals (CIs). Latent class analysis was used to characterise the subtypes of patients with SMD who engaged in violent behaviour at follow-up. RESULTS: We found that 7.2% of patients with SMD presented violent behaviour within six months in the community. Younger age (OR = 0.98, 95% CI = 0.96-1.00, p = 0.016) and no economic source (OR = 1.60, 95% CI = 1.10-2.33, p = 0.014) were risk factors for violent behaviour. Patients with SMD who engaged in violent behaviour could be classified into three subtypes: one class characterised by a history of violence and impulsivity, another class characterised by high levels of aggression and motor impulsivity, and the last class characterised by median cognitive impulsivity. CONCLUSIONS: Socio-demographic factors were risk factors for violent behaviour among patients with SMD, which could eliminate the discrimination toward this group. Impulsivity played a vital role in identifying the three subtypes of patients with SMD who engaged in violent behaviour. These findings may be helpful for the development of a personalised violence risk management plan for patients with SMD who commit violent behaviour in the community.

Stir-fried Semen Armeniacae Amarum Suppresses Aristolochic Acid I-Induced Nephrotoxicity and DNA Adducts.

OBJECTIVE: To investigate the protective effects of stir-fried Semen Armeniacae Amarum (SAA) against aristolochic acid I (AAI)-induced nephrotoxicity and DNA adducts and elucidate the underlying mechanism involved for ensuring the safe use of Asari Radix et Rhizoma. METHODS: In vitro, HEK293T cells overexpressing Flag-tagged multidrug resistance-associated protein 3 (MRP3) were constructed by Lentiviral transduction, and inhibitory effect of top 10 common pairs of medicinal herbs with Asari Radix et Rhizoma in clinic on MRP3 activity was verified using a self-constructed fluorescence screening system. The mRNA, protein expressions, and enzyme activity levels of NAD(P)H quinone dehydrogenase 1 (NQO1) and cytochrome P450 1A2 (CYP1A2) were measured in differentiated HepaRG cells. Hepatocyte toxicity after inhibition of AAI metabolite transport was detected using cell counting kit-8 assay. In vivo, C57BL/6 mice were randomly divided into 5 groups according to a random number table, including: control (1% sodium bicarbonate), AAI (10 mg/kg), stir-fried SAA (1.75 g/kg) and AAI + stir-fried SAA (1.75 and 8.75 g/kg) groups, 6 mice in each group. After 7 days of continuous gavage administration, liver and kidney damages were assessed, and the protein expressions and enzyme activity of liver metabolic enzymes NQO1 and CYP1A2 were determined simultaneously. RESULTS: In vivo, combination of 1.75 g/kg SAA and 10 mg/kg AAI suppressed AAI-induced nephrotoxicity and reduced dA-ALI formation by 26.7%, and these detoxification effects in a dose-dependent manner (P<0.01). Mechanistically, SAA inhibited MRP3 transport in vitro, downregulated NQO1 expression in vivo, increased CYP1A2 expression and enzymatic activity in vitro and in vivo, respectively (P<0.05 or P<0.01). Notably, SAA also reduced AAI-induced hepatotoxicity throughout the detoxification process, as indicated by a 41.3% reduction in the number of liver adducts (P<0.01). CONCLUSIONS: Stir-fried SAA is a novel drug candidate for the suppression of AAI-induced liver and kidney damages. The protective mechanism may be closely related to the regulation of transporters and metabolic enzymes.