No abstract

Background: Borderline personality disorder is associated with subtle neuropsychological deficits. A potential impairment of response inhibition is of major interest, since it could be related to impulsivity as a clinical feature of borderline personality disorder. Sampling and Methods: Response inhibition was studied in an auditory Go/Nogo paradigm in a sample of 20 female inpatients with borderline personality disorder and 18 healthy controls. The main measures of interest were general task performance, errors and reaction times. Results: Patients with borderline personality disorder performed worse in the Nogo task but not in the Go task. In the Nogo task, when response inhibition was essential, patients made more errors of commission, revealing problems to inhibit a prepotent response. Additionally, the borderline group was characterized by significantly shorter reaction times in both tasks compared to the nonclinical control group. The results for errors of commission in the Nogo task remained significant even after controlling for reaction time. Conclusions: The present results suggest a double impairment on this response inhibition task. First, borderline personality disorder patients have inadequately fast reaction times and a speed-accuracy tradeoff. Second, they show a genuine deficit of response inhibition. These results are discussed in the context of the conflicting literature on response inhibition and executive control in borderline personality disorder.

Idiosyncratic drug-induced liver injury (IDILI) is a significant source of drug recall and acute liver failure (ALF) in the United States. While current drug development processes emphasize general toxicity and drug metabolizing enzyme- (DME-) mediated toxicity, it has been challenging to develop comprehensive models for assessing complete idiosyncratic potential. In this review, we describe the enzymes and proteins that contain polymorphisms believed to contribute to IDILI, including ones that affect phase I and phase II metabolism, antioxidant enzymes, drug transporters, inflammation, and human leukocyte antigen (HLA). We then describe the various assays that have been developed to detect individual reactions focusing on each of the mechanisms described in the background. Finally, we examine current trends in developing comprehensive models for examining these mechanisms. There is an urgent need to develop a panel of multiparametric assays for diagnosing individual toxicity potential.

Bioanalogue models of composite cell envelopes were designed by electrostatically driven self-assembly of actin shells inside giant vesicles. Viscoelastic relaxation moduli were measured between 0.03 and 20 s as a function of actin density by magnetic bead microrheometry. The shear relaxation spectra exhibited by the composite shells compare well with those of natural cell envelopes and bulk entangled actin networks. Absolute value of the shear modulus was measured for the first time by deformation field mapping. Shear and bending moduli agree well with values obtained by bead fluctuations analysis.