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Born in fire. Raised by monsters. Destined to smash! On an alien planet shattered by war, no one is stronger than Skaar -- the savage Son of Hulk! But as a warlord and a princess spread chaos through the wastelands, will Skaar save the puny survivors -- or eat them? Skaar seeks the mysterious Old Power, but can even he stop the coming of the Silver Surfer-and Galactus the Devourer? The soothsayers sing: One day, monsters will clash -- the boy will confront the man who abandoned him. When the Son of Hulk seeks vengeance on his father, will Earth be turned into Planet Skaar?

The primary goal of the Human Connectome Project (HCP) is to delineate the typical patterns of structural and functional connectivity in the healthy adult human brain. However, we know that there are important individual differences in such patterns of connectivity, with evidence that this variability is associated with alterations in important cognitive and behavioral variables that affect real world function. The HCP data will be a critical stepping-off point for future studies that will examine how variation in human structural and functional connectivity play a role in adult and pediatric neurological and psychiatric disorders that account for a huge amount of public health resources. Thus, the HCP is collecting behavioral measures of a range of motor, sensory, cognitive and emotional processes that will delineate a core set of functions relevant to understanding the relationship between brain connectivity and human behavior. In addition, the HCP is using task-fMRI (tfMRI) to help delineate the relationships between individual differences in the neurobiological substrates of mental processing and both functional and structural connectivity, as well as to help characterize and validate the connectivity analyses to be conducted on the structural and functional connectivity data. This paper describes the logic and rationale behind the development of the behavioral, individual difference, and tfMRI batteries and provides preliminary data on the patterns of activation associated with each of the fMRI tasks, at both group and individual levels. •Describes logic for the behavioral battery for the Human Connectome Project (HCP)•Describes logic and development of the task fMRI (tfMRI) battery for the HCP•Provides data on brain activation associated with each tfMRI paradigm in the HCP

Like all resting-state functional connectivity data, the data from the Human Connectome Project (HCP) are adversely affected by structured noise artifacts arising from head motion and physiological processes. Functional connectivity estimates (Pearson's correlation coefficients) were inflated for high-motion time points and for high-motion participants. This inflation occurred across the brain, suggesting the presence of globally distributed artifacts. The degree of inflation was further increased for connections between nearby regions compared with distant regions, suggesting the presence of distance-dependent spatially specific artifacts. We evaluated several denoising methods: censoring high-motion time points, motion regression, the FMRIB independent component analysis-based X-noiseifier (FIX), and mean grayordinate time series regression (MGTR; as a proxy for global signal regression). The results suggest that FIX denoising reduced both types of artifacts, but left substantial global artifacts behind. MGTR significantly reduced global artifacts, but left substantial spatially specific artifacts behind. Censoring high-motion time points resulted in a small reduction of distance-dependent and global artifacts, eliminating neither type. All denoising strategies left differences between high- and low-motion participants, but only MGTR substantially reduced those differences. Ultimately, functional connectivity estimates from HCP data showed spatially specific and globally distributed artifacts, and the most effective approach to address both types of motion-correlated artifacts was a combination of FIX and MGTR.

Objectives: Ischemia/reperfusion injury is a commonly occurring event with severe pathologic consequences. Reperfusion initiates both the local and systematic damage in part through rapid oxygen generation. The glutathione system is a major mechanism of reducing this oxidative stress. If this system can be maintained or augmented during this stress then less damage may occur. Glutamine provides the source of glutamate to this system and has been shown to preserve total glutathione levels after injury/ischemia to both hepatic and gut models. To test this effect, we looked at glutamine and its role in ischemia/reperfusion injury in a rat hind limb model. Methods: Fifty male HSD/Holtzman rats weighing 350–400 g were randomized to receive glutamine (3% sol) or normal saline via intraperitoneal injections. The groups were then subjected to 2 hours of ischemia to their hind limbs using the Tourni-Cot method. Animals were then randomized to reperfusion groups of 30 minutes, 2 hours, and 4 hours. Muscle tissue assays were performed for lipid peroxidation (LPO), total glutathione (GSH), and myeloperoxidase (MPO). Peripheral blood was analyzed for creatinephosphokinase levels (CPK). Results: Animals that received glutamine showed a general trend of less lipid peroxidation products than the normal saline groups. In animals that received glutamine and underwent 2 hours of ischemia and reperfusion times of 0 minutes, 30 minutes, and 2 hours, there were significantly less percent changes in lipid peroxidation products from controls (4.6% vs 48.2%, P <0.05), (18.9% vs 123%, P <0.05), (12.6% vs 115%, P <0.05). A general trend upward was noted in CPK levels in both groups. In animals receiving 2 hours of ischemia and 30 minutes of reperfusion, there was a significantly greater level of creatinephosphokinase (CPK) calculated as percent change from control in the normal saline group as compared with the glutamine group (209.2% vs 92.7%). Myeloperoxidase assay of muscle tissue revealed a progressive increase as the reperfusion times grew. In animals receiving 2 hours of ischemia and 30 minutes of reperfusion, the normal saline group had a significantly larger percent increase from controls than the group that received glutamine (1126.4% vs 108%, P <0.05). Also, in those animals receiving 4 hours of reperfusion, the normal saline group had a significantly higher percent increase in MPO content than the glutamine group (6245% vs 108%, P <0.05). Total glutathione levels decreased rapidly as reperfusion occurred in both the normal saline and glutamine groups. No significant difference between the groups was noted. Conclusions: Total glutathione levels during reperfusion were not significantly different in the groups receiving glutamine versus normal saline. Glutamine may provide an initial protective effect on reperfusion injury after moderate reperfusion times in the hind limb model as defined by CPK and LPO levels. Glutamine may blunt neutrophil recruitment after longer reperfusion times (4 hours) in the ischemic hind limb. Total glutathione levels decreased significantly after moderate levels of ischemia (2 hours) and reperfusion (30 minutes, 2 hours).