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Objective: This study was designed to examine the classification accuracy of verbal fluency (VF) measures as performance validity tests (PVT). Method: Student volunteers were assigned to the control ( n  = 57) or experimental malingering ( n  = 24) condition. An archival sample of 77 patients with TBI served as a clinical comparison. Results: Among students, FAS T-score ≤29 produced a good combination of sensitivity (.40-.42) and specificity (.89-.95). Animals T-score ≤31 had superior sensitivity (.53-.71) at .86-.93 specificity. VF tests performed similarly to commonly used PVTs embedded within Digit Span: RDS ≤7 (.54-.80 sensitivity at .93-.97 specificity) and age-corrected scaled score (ACSS) ≤6 (.54-.67 sensitivity at .94-.96 specificity). In the clinical sample, specificity was lower at liberal cutoffs [animals T-score ≤31 (.89-.91), RDS ≤7 (.86-.89) and ACSS ≤6 (.86-.96)], but comparable at conservative cutoffs [animals T-score ≤29 (.94-.96), RDS ≤6 (.95-.98) and ACSS ≤5 (.92-.96)]. Conclusions: Among students, VF measures had higher signal detection performance than previously reported in clinical samples, likely due to the absence of genuine impairment. The superior classification accuracy of animal relative to letter fluency was replicated. Results suggest that existing validity cutoffs can be extended to cognitively high functioning examinees, and emphasize the importance of population-specific cutoffs.

Atherosclerosis is the narrowing of arteries due to the accumulation of macrophages overloaded with lipids resulting in foam cell formation, and these events occur preferentially at the branching points of arteries which are particularly susceptible to hyperlipidemic stress-induced inflammation and oxidative stress. The different stages of atherogenesis rely on oxidative stress, endothelial dysfunction, and inflammation, and hypertension or dyslipidemia can independently trigger these stages. Dyslipidemia and hypertension are pathological conditions that damage the endothelium, triggering cell proliferation, vascular remodeling, apoptosis, and increased cellular permeability with increased adhesion molecules that bind monocytes and T lymphocytes to create a vicious cocktail of pathophysiological factors. Correspondingly, the factors are redirected by chemo-attractants and pro-inflammatory cytokines into the intima of the vasculature, where monocytes differentiate into macrophages taking up oxidized LDL uncontrollably to form foam cells and atherosclerotic lesions. Moreover, endothelial damage also causes loss of vasomotor activity, disproportionate vascular contractility, and elevation of blood pressure in dyslipidemic patients, while in hypertensive patients, further elevation of blood pressure occurs, creating a self-perpetuating vicious cycle that aggravates the development and progression of atherosclerotic lesions. This review offers an in-depth analysis of atherosclerosis and the related interplay between dyslipidemia/hypertension and critically appraises the current diagnosis, etiology, and therapeutic options.

Aim: To observe the effects of concussion history on cognitive-motor integration in elite-level athletes., Methods: The study included 102 National Hockey League draft prospects (n = 51 concussion history [CH]; n = 51 no history [NC]). Participants completed two computer-based visuomotor tasks, one involved 'standard' visuomotor mapping and one involved 'nonstandard' mapping in which vision and action were decoupled., Results: We observed a significant effect of group on reaction time (CH slower) and accuracy (CH worse), but a group by condition interaction only for reaction time (p < 0.05). There were no other deficits found. We discussed these findings in comparison to our previous work with non-elite athletes., Conclusion: Previously concussed elite-level athletes may have lingering neurological deficits that are not detected using standard clinical assessments., Competing Interests: Financial & competing interests disclosure The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties. No writing assistance was utilized in the production of this manuscript.

Mutations in the lamin A/C gene (LMNA) cause lipodystrophy. However, little data are available on lamin A/C expression in various fat depots in women. We recruited 34 women scheduled for gynecologic surgery. Blood samples were collected on the morning of surgery to obtain a detailed lipid profile. Radiological examinations were performed to measure total body fat mass and abdominal fat accumulation. Fat samples were taken from the subcutaneous (SC) fat depot and from the greater omentum (OM) during the surgical procedure. Whole adipose tissue samples were used for total messenger RNA (mRNA) extraction and real-time polymerase chain reaction quantification of the LMNA transcript. No association was observed between lamin A/C mRNA expression, either in SC or OM fat tissue, and adiposity measures. Women with low SC lamin A/C expression, identified on the basis of the median value of SC lamin A/C mRNA expression, had a significantly altered lipid profile including lower levels of high-density lipoprotein (HDL) cholesterol and HDL(2) cholesterol and reduced HDL(2) cholesterol to HDL(3) cholesterol ratio (P < .05 for all). These women were also characterized by higher cholesterol to HDL cholesterol, low-density lipoprotein-triglycerides, very low-density lipoprotein-apolipoprotein B, and low-density lipoprotein cholesterol to HDL cholesterol (P < .05 for all). Low SC lamin A/C mRNA expression levels were also associated with significantly increased lipolysis in isolated fat cells from this fat depot. Specifically, the response to lipolytic agent isoproterenol was significantly increased at doses ranging from 10(-5) to 10(-10) mol/L (P < .05). A similar trend was observed in OM fat cells but did not reach significance. In conclusion, low lamin A/C expression in SC adipose tissue is associated with significant alterations in the lipid profile and increased fat cell lipolysis, independent of the level of total or abdominal adiposity., (Copyright 2010 Elsevier Inc. All rights reserved.)