Significance of local extradural cooling on cervical spinal cord (experimental study)

The PQ-interval was measured while resting supine before exercise testing, in the erect position on the bicycle before starting exercise, and resting supine after exercise in 68 men 6--8 weeks after acute myocardial infarction. During a 6-year follow-up period the death was non-sudden (greater than 1 hour) in 25 of these patients. In this group the PQ-time was significantly shorter (p less than 0.001) during somatomotor activation on the bicycle before exercise than resting supine. The same directional change (p less than 0.01) was seen in the sudden death (less than 1 hour) group (N = 21), but not in the patients who survived. PQ-time at supine rest before exercise testing, however, was significantly shorter (p less than 0.02) in surviving patients than in the non-sudden death group. The possible mechanisms of these, and of previously reported changes in the R-wave amplitudes and QT-times, are discussed.     

Determination of oxygenates in gasoline by FTIR

Oxygenates of the type C₁ to C₄ alcohols and MTBE have been used for improving the octane number of gasoline and helping in reduction of emissions. These oxygenates are used as substitutes for the poisonous tetraethyl lead. The ASTM D-4815 method utilizes a GC method for determining methanol, ethanol, 1-propanol, 2-propanol, 1-butanol, 2-butanol, isobutanol (2-methyl-1-propanol), tert-butanol (2-methyl-2-propanol) and methyl tert-butyl ether (MTBE) in gasoline. However, since this method requires a variety of column switching and back-flushing systems, the possibility of using a simple and fast mid-IR transmission method for accomplishing the same task was pursued. For this, an instrument manufacturer's software that utilizes a partial least square (PLS) regression analysis in the region of importance for alcohols and ethers (1300 to 810 cm⁻¹) was chosen and successfully developed. A set of fuel blend samples (32) that contained concentrations in the range of 0.7 to 4.0 (wt/vol) of the components were used for calibration purposes. Results indicated that the correlation (R²) between the actual and predicted values of 70 laboratory prepared samples of concentrations in the range 0.7 to 8.1% (wt/vol) were 0.995, 0.995, 0.991, 0.992, 0.983, 0.995, 0.989, 0.984 and 0.996 for methanol, ethanol, 1-propanol, 2-propanol, 1-butanol, 2-butanol, isobutanol, tert-butanol and MTBE respectively.     

Exacerbation of inflammation-associated colonic injury in rat through inhibition of cyclooxygenase-2

Cyclooxygenase type 1 is constitutively expressed and accounts for synthesis of prostaglandins in the normal gastrointestinal tract. Cyclooxygenase-2 is expressed at sites of inflammation. Selective inhibitors of cyclooxygenase-2 have been suggested to spare gastrointestinal prostaglandin synthesis, and therefore lack the ulcerogenic effects associated with standard nonsteroidal antiinflammatory drugs. However, the effects of cyclooxygenase-2 inhibitors on inflamed gastrointestinal mucosa have not been examined. We examined cyclooxygenase-2 mRNA and protein expression before and after induction of colitis in the rat, the contribution of cyclooxygenase-2 to colonic prostaglandin synthesis during colitis and the effects of selective inhibitors of cyclooxygenase-2 on colonic injury in this model. Cyclooxygenase-2 mRNA expression increased three to sixfold during the period 24 h to 1 wk after induction of colitis, with marked increases in cyclooxygenase-2 protein expression in the lamina propria and muscularis of the colon during colitis. Cyclooxygenase-1 expression (mRNA and protein) was not affected by the induction of colitis. The prostaglandins produced during colitis were largely derived from cyclooxygenase-2. Treatment with selective cyclooxygenase-2 inhibitors resulted in exacerbation of colitis, with perforation occurring when the compounds were administered for a week. These studies demonstrate that suppression of cyclooxygenase-2 can result in exacerbation of inflammation-associated colonic injury.     

Induction of cyclooxygenase 1 and 2 in the rat stomach during endotoxemia: role in resistance to damage

The P segments of the voltage-dependent Na+ channel line the outer mouth and selectivity filter of the pore. The residues that form the cytoplasmic mouth of the pore of the channel have not been identified. To study the structure of the inner pore mouth, the presumed selectivity filter residues (D400, E755, K1237, and A1529), and three amino acids just amino-terminal to each of these residues in the rat skeletal muscle Na+ channel, were mutated to cysteine and expressed in tsA 201 cells. These amino acids are predicted (by analogy to K+ channels) to be on the cytoplasmic side of the putative selectivity filter residues. Inward and outward Na+ currents were measured with the whole-cell configuration of the patch-clamp technique. Cysteinyl side-chain accessibility was gauged by sensitivity to Cd2+ block and by reactivity with methanethiosulfonate (MTS) reagents applied to both the inside and the outside of the cell. Outward currents through the wild-type and all of the mutant channels were unaffected by internal Cd2+ (100 microM). Similarly, 1 mM methanethiosulfonate ethylammonium (MTSEA) applied to the inside of the membrane did not affect wild-type or mutant outward currents. However, two mutants amino-terminal to the selectivity position in domain III (F1236C and T1235C) and one in domain IV (S1528C) were blocked with high affinity by external Cd2+. The Na+ current through F1236C and S1528C channels was inhibited by MTSEA applied to the outside of the cell. The accessibility of these mutants to externally applied cysteinyl ligands indicates that the side chains of the mutated residues face outward rather than inward. The K+ channel model of the P segments as protein loops that span the selectivity region is not applicable to the Na+ channel.     

Investigation of the energy distribution of stress-induced oxide traps by numerical analysis of the TAT of HEs

This paper investigates by numerical modeling the results of substrate hot electron (SHE) injection experiments in virgin and stressed devices and the corresponding increase of the contribution of HEs to the gate current due to the stress-induced oxide traps. Experimental evidence of HE trap-assisted tunneling (HE TAT) is found after Fowler-Nordheim (FN) stress and SHE stress. An accurate physically based model developed to interpret the experimental results allowed us to study the energy distribution of generated oxide traps in the two different stress regimes. It is found that degradation in HE stress conditions and FN stress conditions cannot be explained by the same trap distribution. For a given stress-induced low field leakage current, a larger concentration of traps in the top part of the oxide band gap is needed to explain HE TAT after SHE stress than after FN stress. The range of trap energy where each technique is sensitive is also identified.