New Frontiers in the Treatment of Perfectionism

Perfectionism can present as a clinical problem in its own right or it can interfere with the successful treatment of Axis I disorders. In the past 15 years, a cognitive behavioral analysis of “clinical perfectionism” has been proposed. This approach and the measurement of the construct of clinical perfectionism have proved controversial. Nevertheless, the approach has experimental support and clinical utility; the derived treatment has been shown to lead to significant improvement on both measures of perfectionism and Axis I disorders. The cognitive behavioral intervention for perfectionism has been evaluated in a range of formats (group, individual, face-to-face, and online) and all show promise. Further work is required to address clinically important questions such as when to treat clinical perfectionism if it occurs in the context of single and multiple Axis I disorders

Higher Order Decompositions of Ordered Operator Exponentials

We present a decomposition scheme based on Lie-Trotter-Suzuki product formulae to represent an ordered operator exponential as a product of ordinary operator exponentials. We provide a rigorous proof that does not use a time-displacement superoperator, and can be applied to non-analytic functions. Our proof provides explicit bounds on the error and includes cases where the functions are not infinitely differentiable. We show that Lie-Trotter-Suzuki product formulae can still be used for functions that are not infinitely differentiable, but that arbitrary order scaling may not be achieved.Comment: 16 pages, 1 figur

Molecular dynamics of flows in the Knudsen regime

Novel technological applications often involve fluid flows in the Knudsen regime in which the mean free path is comparable to the system size. We use molecular dynamics simulations to study the transition between the dilute gas and the dense fluid regimes as the fluid density is increased.Comment: REVTeX, 15 pages, 4 EPS figures, to appear in Physica

TREX1 is expressed by microglia in normal human brain and increases in regions affected by ischemia

BACKGROUND: Mutations in the three-prime repair exonuclease 1 (TREX1) gene have been associated with neurological diseases, including Retinal Vasculopathy with Cerebral Leukoencephalopathy (RVCL). However, the endogenous expression of TREX1 in human brain has not been studied. METHODS: We produced a rabbit polyclonal antibody (pAb) to TREX1 to characterize TREX1 by Western blotting (WB) of cell lysates from normal controls and subjects carrying an RVCL frame-shift mutation. Dual staining was performed to determine cell types expressing TREX1 in human brain tissue. TREX1 distribution in human brain was further evaluated by immunohistochemical analyses of formalin-fixed, paraffin-embedded samples from normal controls and patients with RVCL and ischemic stroke. RESULTS: After validating the specificity of our anti-TREX1 rabbit pAb, WB analysis was utilized to detect the endogenous wild-type and frame-shift mutant of TREX1 in cell lysates. Dual staining in human brain tissues from patients with RVCL and normal controls localized TREX1 to a subset of microglia and macrophages. Quantification of immunohistochemical staining of the cerebral cortex revealed that TREX1 CONCLUSIONS: TREX1 is expressed by a subset of microglia in normal human brain, often in close proximity to the microvasculature, and increases in the setting of ischemic lesions. These findings suggest a role for TREX