Passive adaptation to stress in adulthood after short-term social instability stress during adolescence in mice.

This study reports that short-term social instability stress (SIS) in adolescence increases passive-coping in adulthood in male mice. Short-term SIS decreased the latency of immobility and increased the frequency and time of immobility in tail suspension test. These findings support the hypothesis that adolescent stress can induce a passive adaptation to stress in adulthood, even if it is a short period of stress.

Long-lasting monoaminergic and behavioral dysfunctions in a mice model of socio-environmental stress during adolescence.

Adolescence is one of the critical periods of development and has great importance to health for an individual as an adult. Stressors or traumatic events during this period are associated with several psychiatric disorders as related to anxiety or depression and cognitive impairments, but whether negative experiences continue to hinder individuals as they age is not as well understood. We determined how stress during adolescence affects behavior and neurochemistry in adulthood. Using an unpredictable paradigm (2 stressors per day for 10days) in Balb/c mice, behavioral, hormonal, and neurochemical changes were identified 20days after the cessation of treatment. Adolescent stress increased motor activity, emotional arousal and vigilance, together with a reduction in anxiety, and also affected recognition memory. Furthermore, decreased serotonergic activity on hippocampus, hypothalamus and cortex, decreased noradrenergic activity on hippocampus and hypothalamus, and increased the turnover of dopamine in cortex. These data suggest behavioral phenotypes associated with emotional arousal, but not depression, emerge after cessation of stress and remain in adulthood. Social-environmental stress can induce marked and long-lasting changes in HPA resulting from monoaminergic neurotransmission, mainly 5-HT activity.

Migration of transjugular intrahepatic portosystemic shunt to the right atrium: complications in the intraoperative period of liver transplantation.

This article reports the case of a patient who underwent transjugular intrahepatic portosystemic shunt, which migrated to the right atrium. During liver transplantation, the extracardiac portion was sectioned and the portion adherent inside the atrium was managed expectantly.

Altered expression of cruzipain and a cathepsin B-like target in a Trypanosoma cruzi cell line displaying resistance to synthetic inhibitors of cysteine-proteinases.

The therapeutic potential of synthetic inhibitors to the major cysteine-proteinase from Trypanosoma cruzi (cruzain or cruzipain) was recently demonstrated in animal models of Chagas' disease. A possible limitation of this strategy would be the emergence of parasite populations developing resistance to cysteine-proteinase inhibitors. Here, we describe the properties of a phenotypically stable T. cruzi cell line (R-Dm28) that displays increased resistance to Z-(SBz)Cys-Phe-CHN2, an irreversible cysteine-proteinase inhibitor which preferentially inactivates cathepsin L-like enzymes. Isolated from axenic cultures of the parental cells (IC50 1.5 microM), R-Dm28 epimastigotes exhibited 13-fold (IC50) 20 microM) higher resistance to this inhibitor and did not display cross-resistance to unrelated trypanocidal drugs, such as benznidazol and nifurtimox. Western blotting (with mAb), affinity labeling (with biotin-LVG-CHN2) and FACS analysis of R-Dm28 log-phase epimastigotes revealed that the cruzipain target was expressed at lower levels, as compared with Dm28c. Interestingly, this deficit was paralleled by increased expression of an unrelated Mr 30 000 cysteine-proteinase whose activity was somewhat refractory to inhibition by Z-(SBz)Cys-Phe-CHN,. N-terminal sequencing of the affinity-purified biotin-LVG-proteinase complex allowed its identification as a cathepsin B-like enzyme. Increased antigenic deposits of this proteinase were found in the grossly enlarged and electron dense reservosomes from R-Dm28 epimastigotes. Our data suggest that R-Dm28 resistance to toxic effects induced by the synthetic inhibitor may result from decreased availability of the most sensitive cysteine-proteinase target, cruzipain. The deficit in metabolic functions otherwise mediated by this cathepsin L-like proteinase is likely compensated by increased expression/accumulation of a cathepsin B-like target.