Self-harm is common in prisoners. There is an association between self-harm in prisoners and subsequent suicide, both within prison and on release. The aim of this study is to develop and evaluate a prediction model to identify male prisoners at high risk of self-harm.

We developed an 11-item screening model, based on risk factors identified from the literature. This screen was administered to 542 prisoners within 7 days of arrival in two male prisons in England. Participants were followed up for 6 months to identify those who subsequently self-harmed in prison. Analysis was conducted using Cox proportional hazard regression. Discrimination and calibration were determined for the model. The model was subsequently optimized using multivariable analysis, weighting variables, and dropping poorly performing items.

Seventeen (3.1%) of the participants self-harmed during follow up (median 53 days). The strongest risk factors were previous self-harm in prison (adjusted hazard ratio [aHR] = 9.3 [95% CI: 3.3–16.6]) and current suicidal ideation (aHR = 7.6 [2.1–27.4]). As a continuous score, a one-point increase in the suicide screen was significantly associated with self-harm (HR = 1.4, 1.1–1.7). At the prespecified cut off score of 5, the screening model was associated with an area under the curve (AUC) of 0.66 (0.53–0.79), with poor calibration. The optimized model saw two items dropped from the original screening tool, weighting of risk factors based on a multivariable model, and an AUC of 0.84 (0.76–0.92).

Further work is necessary to clarify the association between risk factors and self-harm in prison. Despite good face validity, current screening tools for self-harm need validation in new prison samples.

Use of antipsychotics to treat behavioural symptoms of dementia has been associated with increased risks of mortality and stroke. Little is known about individual patient characteristics that might be associated with bad or good outcomes.

We examined the risperidone clinical trial data to look for individual patient characteristics associated with these adverse outcomes.

Data from all double-blind randomised controlled trials of risperidone in dementia patients (risperidone n = 1009, placebo n = 712) were included. Associations between characteristics and outcome were analysed based on crude incidences and exposure-adjusted incidence rates, and by time-to-event analyses using Cox proportional hazards regression. Interactions between treatment (risperidone or placebo) and characteristic were analysed with a Cox proportional hazards regression model with main effects for treatment and characteristic in addition to the interaction term.

Baseline complications of depression (treatment by risk factor interaction on cerebrovascular adverse event (CVAE) hazard ratio (HR): P = 0.025) and delusions (P = 0.043) were associated with a lower relative risk of CVAE in risperidone-treated patients (HR = 1.47 and 0.54, respectively) compared to not having the complication (HR = 5.88 and 4.16). For mortality, the only significant baseline predictor in patients treated with risperidone was depression, which was associated with a lower relative risk (P<0.001). The relative risk of mortality was increased in risperidone patients treated with anti-inflammatory medications (P = 0.021).

Only anti-inflammatory medications increased mortality risk with risperidone. The reduced risks of CVAE in patients with comorbid depression and delusions, and of mortality with depression, may have clinical implications when weighing the benefits and risks of treatment with risperidone in patients with dementia.

The objective of the present study was to examine the relationship of dietary fried fish consumption and risk of cardiovascular events and all-cause mortality.

Prospective cohort study among participants of the REasons for Geographic And Racial Differences in Stroke (REGARDS) study who resided in the USA.

The primary outcome measures included the hazard ratios (HR) of incident CVD including first incident fatal or non-fatal ischaemic stroke or myocardial infarction and all-cause mortality, based on cumulative average fish consumption ascertained at baseline.

Participants (n 16 479) were enrolled between 2003 and 2007, completed the self-administered Block98 FFQ and were free of CVD at baseline.

There were 700 cardiovascular events over a mean follow-up of 5·1 years. After adjustment for sociodemographic variables, health behaviours and other CVD risk factors, participants eating ≥2 servings fried fish/week (v. <1 serving/month) were at a significantly increased risk of cardiovascular events (HR=1·63; 95 % CI 1·11, 2·40). Intake of non-fried fish was not associated with risk of incident CVD. There was no association found with dietary fried or non-fried fish intake and cardiovascular or all-cause mortality.

Fried fish intake of two or more servings per week is associated with an increased risk of cardiovascular events. Given the increased intake of fried fish in the stroke belt and among African Americans, these data suggest that dietary fried fish intake may contribute to geographic and racial disparities in CVD.