Dysfunction of glutamatergic neurotransmission may be relevant to the pathogenesis of post-traumatic stress disorder (PTSD). Preclinical and clinical evidence suggests that PTSD symptoms could be alleviated following enhancement of neurotransmission mediated at the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors. Eleven patients with chronic PTSD participated in a double-blind, placebo-controlled, cross-over trial with 50 mg/d D-cycloserine which acts as a partial agonist at the glycine regulatory site on the NMDA receptor. D-cycloserine treatment resulted in significant improvements in numbing, avoidance, and anxiety symptoms; however, similar effects were also observed during placebo treatment. In addition, D-cycloserine treatment resulted in a significant (p=0.03), reduction in the perseverative error scores as measured by the Wisconsin Card Sorting Test. This pilot study is the first to assess the efficacy of a NMDA receptor modulator for PTSD treatment and its results warrant further, larger-scale investigation.

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We present a new family of frames, which are generated by perfect reconstruction filter banks of linear phased filters. The filter banks are based on discrete interpolatory splines and are related to Butterworth filters. Each filter bank contains one interpolatory symmetric low-pass filter and two high-pass filters, one of which is also interpolatory and symmetric. The second high-pass filter is either symmetric or antisymmetric. These filter banks generate the analysis and synthesis scaling functions and pairs of framelets. We introduce the concept of semi-tight frame. All the analysis waveforms in a tight frame coincide with their synthesis counterparts. In the semi-tight frame we can trade properties of smoothness and number of vanishing moments between the synthesis and the analysis framelets. We construct dual pairs of frames, where all the waveforms are symmetric and all the framelets have the same number of vanishing moments. Although most of the designed filters are IIR, they allow fast implementation via recursive procedures. The waveforms are well localized in time domain despite their infinite support. The frequency response of the designed filters is flat.

Neglect behavior of experimental animals with unilateral posterior cortical lesions improves with the placement of a second lesion in the contralesional superior colliculus or in the intercollicular commissure. Given that the retinotectal fibers are mainly crossed, it has been speculated that ipsilesional eye patching, by depriving the contralesional superior colliculus of its main facilitatory visual input, might achieve similar results, and thus be used as a remediation maneuver in patients with neglect. From six patients with severe persistent neglect, only one showed an unequivocal beneficial effect from ipsilesional eye patching. We discuss the factors which possibly underlie success and failure with this procedure, and the place for it in neglect rehabilitation.

The calnexin/calreticulin cycle is a quality control system responsible for promoting the folding of newly synthesized glycoproteins entering the endoplasmic reticulum (ER). The association of calnexin and calreticulin with the glycoproteins is regulated by ER glucosidase II, which hydrolyzes Glc 2Man X GlcNAc 2 glycans to Glc 1Man X GlcNAc 2 and further to Glc 0Man X GlcNAc 2 ( X represents any number between 5 and 9). To gain new insights into the reaction mechanism of glucosidase II, we developed a kinetic model that describes the interactions between glucosidase II, calnexin/calreticulin, and the glycans. Our model accurately reconstructed the hydrolysis of glycans with nine mannose residues and glycans with seven mannose residues, as measured by Totani et al. [Totani, K., Ihara, Y., Matsuo, I., and Ito, Y. (2006) J. Biol. Chem. 281, 31502-31508]. Intriguingly, our model predicted that glucosidase II was inhibited by its nonglucosylated end products, where the inhibitory effect of Glc 0Man 7GlcNAc 2 was much stronger than that of Glc 0Man 9GlcNAc 2. These predictions were confirmed experimentally. Moreover, our model suggested that glycans with a different number of mannose residues can be equivalent substrates of glucosidase II, in contrast to what had been previously thought. We discuss the possibility that nonglucosylated glycans, existing in the ER, might regulate the entry of newly synthesized glycoproteins into the calnexin/calreticulin cycle. Our model also shows that glucosidase II does not interact with monoglucosylated glycans while they are bound to calnexin or calreticulin.