Genomic responses in rat cerebral cortex after traumatic brain injury

Background  

Traumatic brain injury (TBI) initiates a complex sequence of destructive and neuroprotective cellular responses. The initial mechanical injury is followed by an extended time period of secondary brain damage. Due to the complicated pathological picture a better understanding of the molecular events occurring during this secondary phase of injury is needed. This study was aimed at analysing gene expression patterns following cerebral cortical contusion in rat using high throughput microarray technology with the goal of identifying genes involved in an early and in a more delayed phase of trauma, as genomic responses behind secondary mechanisms likely are time-dependent.     

In situ measurement of self-heating in intrinsic tunneling spectroscopy

Using advanced sample engineering we performed simultaneous measurements of interlayer tunneling characteristics and in situ monitoring of temperature in Bi(2)Sr(2)CaCu(2)O(8 + delta) (Bi-2212) mesas. Together with a systematic study of size dependence of interlayer tunneling, this allowed unambiguous discrimination between artifacts of self-heating and gaps in the electronic spectra of Bi-2212. Such a confident spectroscopic information, which is not affected by self-heating or surface deterioration, was obtained for the first time for a high-T(c) superconductor. We also derived general expressions and formulated main principles of self-heating valid for a large variety of materials.     

PORPHYRIN-INDUCED PHOTODAMAGE TO ISOLATED HUMAN NEUTROPHILS

Abstract— Human neutrophils were irradiated with light at 340–380 nm in the presence of low concentrations of protoporphyrin or uroporphyrin. At increasing light doses or increasing concentrations of protoporphyrin, the neutrophils rapidly lost the ability of locomotion. Also, neutrophil chemiluminescence and hexose-monophosphate shunt activity rapidly declined. An early event was leakage of endogenous K⁺ followed by lactate dehydrogenase and at a later stage leakage of particle-bound acid phosphatase. A number of cellular enzymes were inactivated, the susceptibility to inactivation decreased in the order: succinate dehydrogenase > lactate dehydrogenase > glutamate dehydrogenase > acid phosphatase. Uroporphyrin had no effect on neutrophil functions, leakage of K⁺, or cellular enzymes. The results suggest that photodamage to the plasma membrane and the mitochondria are earlier events than photodamage to lysosomes.