Polyimide polymer glass-free capillary columns for gas chromatography.

Polymeric polyimide capillary tubing, both uncoated and coated with stationary phases of two polarities, is explored for use as capillary columns for gas chromatography (GC). These glass-free polyimide columns are flexible and their small winding diameter of less than a cm around a solid support makes them compatible for potential use in portable GC instruments. Polyimide columns with dimensions of 0.32 mm i.d. × 3 m are cleaned, annealed at 300°C, and coated using the static method with phenylmethylsilicone (PMS). Separations of volatile organics are investigated isothermally on duplicate sets of polyimide columns by GC with a flame ionization detector using split injection. Unlike the uncoated ones, the coated polyimide columns successfully separate Grob test mix classes of alkanes, amines, and fatty acid methyl esters. The relative standard deviations for retention time and peak area are 0.5 and 2.5 , respectively. With the 3 m PMS-coated column connected to a retention gap to permit operation at its optimum flow rate of 30 cm/s, a plate count of 3200 or plate height of 1 mm is possible. Lack of retention and tailing peaks are evident for the polyimide polymer capillary columns as compared to that of a 3 m commercial cross-linked PMS fused silica capillary. However, headspace analyses of an aromatic hydrocarbon mix and a Clearcoat automotive paint sample are viable applications on the PMS polyimide polymer column.

Absence of the transcription factor E2F1 attenuates brain injury and improves behavior after focal ischemia in mice.

Because of observations that cultured neurons from mice deficient in the transcription factor E2F1 exhibit resistance after treatment with a wide variety of cell-death inducers, the authors investigated whether resistance extended to a cerebral ischemic insult. No differences in cerebral blood flow or physiologic parameters were observed in the mutant E2F1 littermates after the focal ligation. After 2 hours of left middle cerebral artery occlusion and 1 day of reperfusion, a 33% smaller infarct (P < 0.05) was observed by 2,3,5-triphenyltetrazolium staining in the brains of E2F1-null mice compared with their E2F1+/+ and +/- littermates. A milder ischemic insult produced by 20 minutes of middle cerebral artery occlusion and 7 days of reperfusion produced a greater difference in the E2F1-null animals with a 71% smaller infarct (P < 0.001) compared to littermate controls. A decrease in neuronal damage after mild ischemia in E2F1-null mice was observed by immunohistochemical monitoring of the loss in neuronal-specific microtubule-associated protein 2 cytoskeletal protein and the appearance of nuclear DNA fragmentation by terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick end labeling. This decreased brain damage was evidenced by improved behavior in motor function of E2F1 -/- mice compared with their E2F1 +/+ littermates by 7 days of reperfusion. In an effort to address the underlying molecular mechanism of the resistance of E2F1-null mice, the expression of several downstream proapoptotic target genes (p73, Apaf1, Arf) of the E2F1 transcription factor was measured by quantitative polymerase chain reaction. Although an attenuated increase in Hsp68 mRNA was found in E2F1 -/- mice, no changes in the proapoptotic transcripts were found after ischemia, and a mechanistic inference was not possible. The authors conclude that the transcription factor E2F1 does modulate neuronal viability in brain after cerebral ischemia and corroborates the findings with cultured neurons.