Cell surface receptors for gibbon ape leukemia virus (Glvr-1) and marine amphotropic retrovirus (Ram-i) Ram-i (10) and human Glvr-1 (7) cDNAs were cloned into pGEM-7Z (Promega) with their 5' ends adjacent to the SP6 promoter. For mRNA synthesis, the plasmids were linearized and transcribed with SP6 polymerase in the presence of m7G(5')ppp(5')G caps according to the manufacturer's directions (Pharmacia). Xenopus laevis oocytes were injected with 50 nl of mRNA (1 ng/nl) or with an equal volume of H20 and were incubated for 4-6 days at 17'C; then two-microelectrode voltage-clamp recordings or radiolabel uptake assays were performed at room temperature as described (23).Abbreviations: GALV, gibbon ape leukemia virus; Glvr-1, cell surface receptor for GALV; Ram-i, cell surface receptor for amphotropic murine retrovirus; HIV, human immunodeficiency virus; MLV, murine leukemia virus; Mo-MLV, Moloney MLV.

Rats subjected to unilateral ablation of the motor cortex and placed on a narrow beam displayed transient contralateral paresis. An immediate and enduring acceleration of recovery was produced by a single dose of d-amphetamine given 24 hours after injury. This effect was blocked by haloperidol or by restraining the animals for 8 hours beginning immediately after amphetamine administration. A single dose of haloperidol given 24 hours after injury markedly slowed recovery. This effect was also blocked by restraining the animals.

Posttraumatic stress disorder (PTSD) and mild traumatic brain injury (mTBI) are signature illnesses of the Iraq and Afghanistan wars, but current diagnostic and therapeutic measures for these conditions are suboptimal. In our study, functional magnetic resonance imaging (fMRI) is used to try to differentiate military service members with: PTSD and mTBI, PTSD alone, mTBI alone, and neither PTSD nor mTBI. Those with PTSD are then randomized to virtual reality exposure therapy or imaginal exposure. fMRI is repeated after treatment and along with the Clinician-Administered PTSD Scale (CAPS) and Clinical Global Impression (CGI) scores to compare with baseline. Twenty subjects have completed baseline fMRI scans, including four controls and one mTBI only; of 15 treated for PTSD, eight completed posttreatment scans. Most subjects have been male (93%) and Caucasian (83%), with a mean age of 34. Significant improvements are evident on fMRI scans, and corroborated by CGI scores, but CAPS scores improvements are modest. In conclusion, CGI scores and fMRI scans indicate significant improvement in PTSD in both treatment arms, though CAPS score improvements are less robust.

We integrated five sets of proteomics data profiling the constituents of cerebrospinal fluid (CSF) derived from Huntington disease (HD)-affected and -unaffected individuals with genomics data profiling various human and mouse tissues, including the human HD brain. Based on an integrated analysis, we found that brain-specific proteins are 1.8 times more likely to be observed in CSF than in plasma, that brain-specific proteins tend to decrease in HD CSF compared with unaffected CSF, and that 81% of brainspecific proteins have quantitative changes concordant with transcriptional changes identified in different regions of HD brain. The proteins found to increase in HD CSF tend to be liver-associated. These protein changes are consistent with neurodegeneration, microgliosis, and astrocytosis known to occur in HD. We also discuss concordance between laboratories and find that ratios of individual proteins can vary greatly, but the overall trends with respect to brain or liver specificity were consistent. Concordance is highest between the two laboratories observing the largest numbers of proteins. Huntington disease (HD)1 is an inherited neurodegenerative disorder characterized by progressive cognitive decline and psychiatric and movement symptoms. The cause of the disease is the expansion of trinucleotide (CAG) repeats in the coding region of the htt gene that translates into a polyglutamine tract in the huntingtin protein (1). Currently no treatment has been shown to delay the onset of the disease or slow its progression in patients. To speed assessment of therapies in clinical trials, it is critical to identify biological markers that can accurately monitor disease progression.Several genomics and proteomics approaches to identifying biomarkers for HD have been undertaken previously. Genomics studies have determined the molecular phenotype of human HD brain (2) and different tissues of HD mouse models at the mRNA level (3-6). Proteomics approaches have been applied to brain tissues of HD mouse models and humans to identify candidate markers (7-9). Blood plasma in particular has received considerable attention recently because of its ready accessibility clinically (10, 11). The candidate protein biomarkers identified in the blood proteomics studies are largely known inflammatory markers. Because HD is regarded primarily as a neurodegenerative disease, it is not entirely clear how directly general markers of neuroinflammation relate to the pathophysiology of HD, although astrocytosis and microgliosis (12) are prominent components of HD in its mid-to late stages (13). Another concern regarding markers discovered primarily in blood is that the blood-brain barrier may restrict brain proteins from entering plasma, and so plasma candidates may not directly reflect HD progression in the brain.Cerebrospinal fluid (CSF) is a more relevant biomaterial for biomarker discovery because it is proximal to the brain; it occupies the subarachnoid space of the central nervous system and the ventricular system around and inside the b...