Traumatic brain injury (TBI) is a major cause of death and disability and impairs health-related quality of life (HRQOL). Psychiatric disorders have been recognized as major components of TBI morbidity, yet few studies have addressed the relationship between these outcomes. Sample size, selection bias, and retrospective design, are methodological limitations for TBI-related psychiatric studies. For this study, 33 patients with severe TBI were evaluated prospectively regarding demographic, clinical, radiological, neurosurgical, laboratory, and psychosocial characteristics, as well as psychiatric manifestations and HRQOL, 18 months after hospitalization. Psychiatric manifestations were assessed using the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I), the Hospital Anxiety and Depression Scale (HADS), the Brief Psychiatric Rating Scale (BPRS), and the Apathy Evaluation Scale (AES). HRQOL was determined using the Medical Outcomes Study's 36-item Short-Form Health Survey (SF-36). Following TBI, a significant increase in the prevalence of major depressive disorder (MDD) and generalized anxiety disorder (p=0.02), and a significant decrease in the prevalence of alcohol and cannabinoid abuse (p=0.001) were observed. The most frequent psychiatric disorders following severe TBI were found to be MDD (30.3%), and personality changes (33.3%). In comparison to patients without personality changes, patients with personality changes experienced a decline in general health and impairments in physical and social functioning. Patients with MDD showed impairment in all SF-36 domains compared to non-depressed patients. This prospective TBI-related psychiatric study is the first to demonstrate a significant association between MDD, personality changes, and HRQOL, following severe TBI in a well-defined sample of patients.

e Malaria pathology is linked to remodeling of red blood cells by eukaryotic Plasmodium parasites. Central to host cell refurbishment is the trafficking of parasite-encoded virulence factors through the Plasmodium translocon of exported proteins (PTEX). Much of our understanding of its function is based on experimental work with cultured Plasmodium falciparum, yet direct consequences of PTEX impairment during an infection remain poorly defined. Using the murine malaria model parasite Plasmodium berghei, it is shown here that efficient sequestration to the pulmonary, adipose, and brain tissue vasculature is dependent on the PTEX components thioredoxin 2 (TRX2) and PTEX88. While TRX2-deficient parasites remain virulent, PTEX88-deficient parasites no longer sequester in the brain, correlating with abolishment of cerebral complications in infected mice. However, an apparent trade-off for virulence attenuation was spleen enlargement, which correlates with a strongly reduced schizont-to-ringstage transition. Strikingly, general protein export is unaffected in PTEX88-deficient mutants that mature normally in vitro. Thus, PTEX88 is pivotal for tissue sequestration in vivo, parasite virulence, and preventing exacerbation of spleen pathology, but these functions do not correlate with general protein export to the host erythrocyte. The presented data suggest that the protein export machinery of Plasmodium parasites and their underlying mechanistic features are considerably more complex than previously anticipated and indicate challenges for targeted intervention strategies.

These results in Brazilian patients reinforce the external validation of previous findings in Canadian patients showing that presurgical depression and complete seizure control after surgery are independent predictors for meaningful improvement in QOL after ATL, and have implications for the surgical management of MTLE patients.

Plasma levels of TBARS and carbonyl increase significantly in the first 70 hours after severe TBI but are not independently associated with the hospital mortality.