The dependence of Galactic outflows on the properties and orientation of zCOSMOS galaxies at z ~ 1

We present an analysis of cool outflowing gas around galaxies, traced by MgII absorption lines in the co-added spectra of a sample of 486 zCOSMOS galaxies at 1 < z < 1.5. These galaxies span a range of stellar masses (9.45< log[M*/Msun]<10.7) and star formation rates (0.14 < log [SFR/Msun/yr] < 2.35). We identify the cool outflowing component in the MgII absorption and find that the equivalent width of the outflowing component increases with stellar mass. The outflow equivalent width also increases steadily with the increasing star formation rate of the galaxies. At similar stellar masses the blue galaxies exhibit a significantly higher outflow equivalent width as compared to red galaxies. The outflow equivalent width shows strong effect with star formation surface density ({\Sigma}SFR) of the sample. For the disk galaxies, the outflow equivalent width is higher for the face-on systems as compared to the edge-on ones, indicating that for the disk galaxies, the outflowing gas is primarily bipolar in geometry. Galaxies typically exhibit outflow velocities ranging from -200 km/s to -300 km/s and on average the face-on galaxies exhibit higher outflow velocity as compared to the edge-on ones. Galaxies with irregular morphologies exhibit outflow equivalent width as well as outflow velocities comparable to face on disk galaxies. These galaxies exhibit minimum mass outflow rates > 5-7 Msun/yr and a mass loading factor ({\eta} = dMout/dt /SFR) comparable to the star formation rates of the galaxies.Comment: 12 pages, 14 figures, ApJ submitte

Cerebral atrophy as outcome measure in short-term phase 2 clinical trials in multiple sclerosis

Cerebral atrophy is a compound measure of the neurodegenerative component of multiple sclerosis (MS) and a conceivable outcome measure for clinical trials monitoring the effect of neuroprotective agents. In this study, we evaluate the rate of cerebral atrophy in a 6-month period, investigate the predictive and explanatory value of other magnetic resonance imaging (MRI) measures in relation to cerebral atrophy, and determine sample sizes for future short-term clinical trials using cerebral atrophy as primary outcome measure

Revisiting Brain Atrophy and Its Relationship to Disability in Multiple Sclerosis

Brain atrophy is a well-accepted imaging biomarker of multiple sclerosis (MS) that partially correlates with both physical disability and cognitive impairment.Based on MRI scans of 60 MS cases and 37 healthy volunteers, we measured the volumes of white matter (WM) lesions, cortical gray matter (GM), cerebral WM, caudate nucleus, putamen, thalamus, ventricles, and brainstem using a validated and completely automated segmentation method. We correlated these volumes with the Expanded Disability Status Scale (EDSS), MS Severity Scale (MSSS), MS Functional Composite (MSFC), and quantitative measures of ankle strength and toe sensation. Normalized volumes of both cortical and subcortical GM structures were abnormally low in the MS group, whereas no abnormality was found in the volume of the cerebral WM. High physical disability was associated with low cerebral WM, thalamus, and brainstem volumes (partial correlation coefficients ~0.3-0.4) but not with low cortical GM volume. Thalamus volumes were inversely correlated with lesion load (r = -0.36, p<0.005).The GM is atrophic in MS. Although lower WM volume is associated with greater disability, as might be expected, WM volume was on average in the normal range. This paradoxical result might be explained by the presence of coexisting pathological processes, such as tissue damage and repair, that cause both atrophy and hypertrophy and that underlie the observed disability

Whole-scalp EEG mapping of somatosensory evoked potentials in macaque monkeys

High-density scalp EEG recordings are widely used to study whole-brain neuronal networks in humans non-invasively. Here, we validate EEG mapping of somatosensory evoked potentials (SSEPs) in macaque monkeys (Macaca fascicularis) for the long-term investigation of large-scale neuronal networks and their reorganisation after lesions requiring a craniotomy. SSEPs were acquired from 33 scalp electrodes in five adult anaesthetized animals after electrical median or tibial nerve stimulation. SSEP scalp potential maps were identified by cluster analysis and identified in individual recordings. A distributed, linear inverse solution was used to estimate the intracortical sources of the scalp potentials. SSEPs were characterised by a sequence of components with unique scalp topographies. Source analysis confirmed that median nerve SSEP component maps were in accordance with the somatotopic organisation of the sensorimotor cortex. Most importantly, SSEP recordings were stable both intra- and interindividually. We aim to apply this method to the study of recovery and reorganisation of large-scale neuronal networks following a focal cortical lesion requiring a craniotomy. As a prerequisite, the present study demonstrated that a 300-mm2 unilateral craniotomy over the sensorimotor cortex necessary to induce a cortical lesion, followed by bone flap repositioning, suture and gap plugging with calcium phosphate cement, did not induce major distortions of the SSEPs. In conclusion, SSEPs can be successfully and reproducibly recorded from high-density EEG caps in macaque monkeys before and after a craniotomy, opening new possibilities for the long-term follow-up of the cortical reorganisation of large-scale networks in macaque monkeys after a cortical lesion