To evaluate the role of neurobehavioural factors in the aetiology of recurrent automobile accidents, we administered the Revised Wechsler Adult Intelligence Scale (WAIS-R), the Eysenck Personality Questionnaire (EPQ), and choice and simple reaction time tests to 31 accident-prone automobile drivers. These drivers who had caused three or more traffic accidents during the years 1980-1984, were selected from records of 2723 traffic accidents registered by Hefei Traffic Police Department during the years 1980-1984. The same tests were administered to an equal number of sex- and age-matched control drivers who had no reported involvement in automobile accidents. None of the subjects had suffered from any neuropsychiatric illness or head injury. Comparisons between the two groups indicated that for accident-prone drivers scores on picture completion and block design subtests of the WAIS-R were significantly lowered (p less than 0.05); scores for neurosis extrovert behaviour and psychosis (EPQ) were significantly higher (p less than 0.05); and the number of errors in the choice reaction time test was significantly higher (p less than 0.01). It is suggested that accident-prone drivers have lower psychological performance, poorer judgement and a higher tendency than safe drivers to be neurotic, extrovert and psychotic.

Purpose: Spontaneous intracerebral hemorrhage (ICH) is still a major public health problem, with high mortality and disability. Ulinastatin (UTI) was purified from human urine and has been reported to be anti-inflammatory, organ protective, and antioxidative stress. However, the neuroprotection of UTI in ICH has not been confirmed, and the potential mechanism is unclear. In the present study, we aimed to investigate the neuroprotection and potential molecular mechanisms of UTI in ICH-induced early brain injury in a C57BL/6 mouse model. Methods: The neurological score, brain water content, neuroinflammatory cytokine levels, oxidative stress levels, and neuronal damage were evaluated. Results: UTI treatment markedly increased the neurological score, alleviated brain edema, decreased the levels of the inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and NF-κB, decreased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and upregulated the levels of glutathione (GSH), superoxide dismutase (SOD), and Nrf2. This finding indicated that UTI-mediated inhibition of neuroinflammation and oxidative stress alleviated neuronal damage after ICH. The neuroprotective capacity of UTI is partly dependent on the ROS/MAPK/Nrf2 signaling pathway. Conclusions: UTI improves neurological outcomes in mice and reduces neuronal death by protecting against neural neuroinflammation and oxidative stress.