Diffusion and perfusion magnetic resonance imaging following closed head injury in rats

Diffusion-, perfusion-, T1-, and T2-weighted magnetic resonance imaging (MRI) were performed at 1–2 h, 24 h, and 1 week following closed head injury (CHI) in rats, and data was compared with hematoxylin and eosin histology. At 1–2 h, large areas of low perfusion in the damaged hemisphere overestimate the histological damage. In the first 2 h, the histological damage seems to be a superposition of abnormalities in the T1- and diffusion-weighted images. In areas with more than 10% reduction in the apparent diffusion coefficients (ADCs), reduced regional cerebral blood volume (r-CBV) was also observed. The decrease in ADCs and rCBV correlated with r = 0.78. Changes in the MRI parameters revealed the following: (a) Further reduction in ADC occurred from 83 ± 15% at 1–2 h after trauma to 69 ± 9% at 24 h, and 1 week later a marked elevation in the ADC values is observed. (b) Blood perfusion measurements performed 1–2 h posttrauma revealed a pronounced reduction in r-CBV (53 ± 18%) in the damaged hemisphere in all rats. At 24 h postimpact, areas of hyper- and hypoperfusion were observed. One week later, similar perfusion was found in both hemispheres of all rats. (c) T2 hyperintensity at 24 h overestimated the histological damage found at 1 week. At one week following the trauma, the T2 hyperintensity underestimated the histological damage. It is concluded that CHI, which is a heterogeneous insult, should be studied by a combination of MRI techniques. The superposition of the abnormalities seen on T1 and on the diffusion-weighted MR images at early time point represents best the histological damage. Both T2 and rCBV images are less informative in terms of actual histological damage

Electrostatic Properties of Adsorbed Polar Molecules: Opposite Behavior of a Single Molecule and a Molecular Monolayer

Abstract: We compare the electrostatic behavior of a single polar molecule adsorbed on a solid substrate with that of an adsorbed polar monolayer. This is accomplished by comparing first principles calculations obtained within a cluster model and a periodic slab model, using benzene derivatives on the Si(111) surface as a representative test case. We find that the two models offer diametrically opposite descriptions of the surface electrostatic phenomena. Slab electrostatics is dominated by dipole reduction due to intermolecular dipole-dipole interactions that partially depolarize the molecules, with charge migration to the substrate playing a negligible role due to electric field suppression outside the monolayer. Conversely, cluster electrostatics is dominated by dipole enhancement due to charge migration to/from the substrate, with only a small polarization of the molecule. This establishes the important role played by long-range interactions, in addition to local chemical properties, in tailoring surface chemistry via polar molecule adsorption

Blood glutamate scavenging: insight into neuroprotection.

Brain insults are characterized by a multitude of complex processes, of which glutamate release plays a major role. Deleterious excess of glutamate in the brain's extracellular fluids stimulates glutamate receptors, which in turn lead to cell swelling, apoptosis, and neuronal death. These exacerbate neurological outcome. Approaches aimed at antagonizing the astrocytic and glial glutamate receptors have failed to demonstrate clinical benefit. Alternatively, eliminating excess glutamate from brain interstitial fluids by making use of the naturally occurring brain-to-blood glutamate efflux has been shown to be effective in various animal studies. This is facilitated by gradient driven transport across brain capillary endothelial glutamate transporters. Blood glutamate scavengers enhance this naturally occurring mechanism by reducing the blood glutamate concentration, thus increasing the rate at which excess glutamate is cleared. Blood glutamate scavenging is achieved by several mechanisms including: catalyzation of the enzymatic process involved in glutamate metabolism, redistribution of glutamate into tissue, and acute stress response. Regardless of the mechanism involved, decreased blood glutamate concentration is associated with improved neurological outcome. This review focuses on the physiological, mechanistic and clinical roles of blood glutamate scavenging, particularly in the context of acute and chronic CNS injury. We discuss the details of brain-to-blood glutamate efflux, auto-regulation mechanisms of blood glutamate, natural and exogenous blood glutamate scavenging systems, and redistribution of glutamate. We then propose different applied methodologies to reduce blood and brain glutamate concentrations and discuss the neuroprotective role of blood glutamate scavenging

Hall photovoltage deep-level spectroscopy of GaN films

Spectroscopy of photoinduced changes in semiconductor Hall voltage is proposed as a method to characterize deep levels. An analytical expression for the Hall coefficient as a function of the charge trapped at grain boundaries is derived. The experimental Hall voltage is demonstrated by measuring thin films of GaN grown on sapphire and is shown to be consistent with the model. The Hall voltage spectrum is correlated to spectra from three other deep-level spectroscopies: photoluminescence, photoconductivity, and surface photovoltage, obtained under the same conditions from the same sample. Comparing spectra from the various spectroscopies shows that the yellow-luminescence-related deep states in GaN are charged in equilibrium and discharged by the exciting photons, and suggests that the blue-luminescence-related states are deep donors positioned 2.8 eV above the valence band and neutral in equilibrium