Library

Notes: A translational inhibitor that is activated by N-ethylmaleimide treatment can be found in the postmicrosomal fraction prepared from the brain of adult rats, but it is almost undetectable in the same fraction prepared from suckling animals. The inhibitor is thermolabile and remains in the supernatant fraction after precipitation at pH 5. During the purification procedure, the inhibitor in its unactivated state binds to the anion exchanger (diethylaminoethyl-cellulose) but not to the cation exchanger (phosphocellulose). Treatment with N-ethylmaleimide increases inhibitor affinity for the cation exchanger, and this chromatographic step purifies the inhibitor by 143-fold. Both the thermolabile nature and the behavior of the inhibitory activity during the different steps of the purification procedure suggest that this activity is most probably due to a protein. Although the addition of initiation factor 2 reverses the inhibition of protein synthesis in the presence of ATP and Mg2+, the inhibitor does not phosphorylate any of the initiation factor subunits “in vitro,” which indicates that it does not contain any intrinsic protein kinase activity. However, its presence in both a crude and a purified preparation of a kinase of the α subunit of a brain eukaryotic initiation factor increases the phosphorylation of the α subunit of the initiation factor. The mechanism of action of this inhibitor is discussed.

Notes: Abstract: An in vitro model of ischemia was obtained by subjectingPC12 cells differentiated with nerve growth factor to a combination of glucosedeprivation plus anoxia. Immediately after the ischemic period, the proteinsynthesis rate was significantly inhibited (80%) and western blots of cellextracts revealed a significant accumulation of phosphorylated eukaryoticinitiation factor 2, α subunit, eIF2(αP) (42%). Upon recovery,eIF2(αP) levels returned to control values after 30 min, whereas proteinsynthesis was still partially inhibited (33%) and reached almost controlvalues within 2 h. The activities of the mammalian eIF2α kinases,double-stranded RNA-activated protein kinase, mammalian GCN2 homologue, andendoplasmic reticulum-resident kinase, were determined. None of theeIF2α kinases studied showed increased activity in ischemic cells ascompared with controls. Exposure of cells to cell-permeable inhibitors ofprotein phosphatases 1 and 2A, calyculin A or tautomycin, induced dose- andtime-dependent accumulation of eIF2(αP), mimicking an ischemic effect.Protein phosphatase activity, as measured with [32P]phosphorylasea as a substrate, diminished during ischemia and returned to controllevels upon 30-min recovery. In addition, the rate of eIF2(αP)dephosphorylation was significantly lower in ischemic cells, paralleling boththe greatest translational inhibition and the highest eIF2(αP) levels.The endogenous phosphatase activity from control and ischemic extracts showeddifferent sensitivity to inhibitor 2 and fostriecin in in vitro assays,inhibitor-2 effect in ischemic cells being lower than in control cells.Together these results indicate that an eIF2α phosphatase, probablyprotein phosphatase 1, is implicated in the ischemia-induced eIF2(αP)accumulation in PC12 cells.

Notes: KTiOPO4 (KTP) samples heated in vacuum at temperatures in the 400–650 °C range show a broad optical absorption similar to that observed by H2 reduction. The position of the maximum depends on the reduction degree. The transparency of the sample is recovered by heating in air at high temperature (600 °C). Vacuum annealing leads to the reduction of Ti4+ to Ti3+ and also to the reduction of Fe, W, and Rh impurities present in the samples, as inferred from electron paramagnetic resonance measurements. X-ray irradiation at 15 K induces an optical absorption peaking at 585 nm. This absorption has been ascribed to the superposition of the 2T2→2E transition of Ti3+ in the two different Ti sites of the lattice. It is suggested that the absorption observed in vacuum-reduced samples consists of the overlapping of the latter contribution and a charge transfer band of Fe-Ti pairs. A loss of K and P ions has been observed after the annealing of KTP in vacuum at 800 °C forming a surface layer that scatters light. Moreover, the K and P loss decreases the optical absorption induced at lower temperature (T〈650 °C). © 1994 American Institute of Physics.

Notes: The current gain cutoff frequency of very high frequency AlGaAs/GaAs heterojunction bipolar transistors has been measured at 300 and at 20 K using the picosecond optoelectronic technique. These devices showed cutoff frequencies of 72 and 84 GHz at room temperature and at a fixture temperature of 20 K, respectively. Optical response measurements were also obtained at visible and infrared wavelengths. The visible optical response shows a FWHM of 14 and 9.5 ps at 300 and 20 K, respectively. The infrared (λ=850 nm) optical response, corresponding to deeper penetration, showed a FWHM significantly larger ((approximately-greater-than)50 ps) than the visible optical response.

Notes: A Monte Carlo analysis of bipolar transport and voltage fluctuations in a p+-Si/n-Si0.7Ge0.3 heterojunction and in a p+n Si homojunction under different operation regimes is presented. Comparison of the spectral density of voltage fluctuations at low frequency, SV(x,0), between both structures reveals the strong effect of the SiGe layer on the noise behavior in the heterojunction. Alloy scattering hinders the electron mobility enhancement expected from the removal of valley degeneracy in the SiGe layer. Despite this mobility reduction, the greater accumulation of carriers in the low-doped region supported by the valence band discontinuity reduce SV(x,0) in the heterojunction for a given average voltage. This study also reveals the impact of hot carriers on noise performance in the quasisaturation regime of both diodes. © 2000 American Institute of Physics.

Notes: Translational repression induced during reperfusion of the ischaemic brain is significantly attenuated by ischaemic preconditioning. The present work was undertaken to identify the components of the translational machinery involved and to determine whether translational attenuation selectively modifies protein expression patterns during reperfusion. Wistar rats were preconditioned by 5-min sublethal ischaemia and 2 days later, 30-min lethal ischaemia was induced. Several parameters were studied after lethal ischaemia and reperfusion in rats with and without acquired ischaemic tolerance (IT). The phosphorylation pattern of the α subunit of eukaryotic initiation factor 2 (eIF2) in rats with IT was exactly the same as in rats without IT, reaching a peak after 30 min reperfusion and returning to control values within 4 h in both the cortex and hippocampus. The levels of phosphorylated eIF4E-binding protein after lethal ischaemia and eIF4E at 30 min reperfusion were higher in rats with IT, notably in the hippocampus. eIF4G levels diminished slightly after ischaemia and reperfusion, paralleling calpain-mediated α-spectrin proteolysis in rats with and without IT, but they did not show any further decrease after 30 min reperfusion in rats with IT. The phosphorylated levels of eIF4G, phosphatidylinositol 3-kinase-protein B (Akt) and extracellular signal-regulated kinases (ERKs) were very low after lethal ischaemia and increased following reperfusion. Ischaemic preconditioning did not modify the observed changes in eIF4G phosphorylation. All these results support that translation attenuation may occur through multiple targets. The levels of the glucose-regulated protein (78 kDa) remained unchanged in rats with and without IT. Conversely, our data establish a novel finding that ischaemia induces strong translation of growth arrest and DNA damage protein 34 (GADD34) after 4 h of reperfusion. GADD34 protein was slightly up-regulated after preconditioning, besides, as in rats without IT, GADD34 levels underwent a further clear-cut increase during reperfusion, this time as earlier as 30 min and coincident with translation attenuation.

Notes: Objective  To assess whether infectious morbidity after total abdominal hysterectomy is decreased by the addition of 20 cc povidone–iodine gel at the vaginal apex after the usual vaginal preparation with povidone–iodine solution.Study design  Randomised controlled trial.Setting  Fifteen secondary and tertiary hospitals in Canada.Sample  A total of 1570 women undergoing planned total abdominal hysterectomy.Methods  Computer-generated randomisation using a centralised telephone service was stratified by study centre with variable block size. In the operating room, a swab for bacterial vaginosis was taken before vaginal antisepsis. Study group remained concealed until the standard surgical preparation in the operating room was complete. Then povidone-iodine gel 20 cc was placed at the vaginal apex in the intervention group only. Participants were followed for one month post-operative.Main outcome measures  The primary outcome was post-operative infectious morbidity during the 30 days after surgery, defined as: febrile morbidity with hospital stay greater than five days or antibiotic treatment, or infection requiring readmission to hospital or additional visit. Other outcomes included abdominal wound infection, pelvic abscess and other pelvic infections.Results  Post-operative infectious morbidity within 30 days occurred in 128/780 (16%) women receiving povidone–iodine gel preparation and 142/790 (18%) women not receiving gel (RR 0.9, 95% CI 0.7 to 1.1). Pelvic abscess was diagnosed in 0 patients in the gel group and in seven patients in the control group (P 〈 0.01). No significant difference was found in pelvic cellulitis (eight in each group) or abdominal wound infection (51 in the gel group and 58 in the control group, P= 0.5).Conclusion  Povidone–iodine vaginal gel antisepsis led to a 9% relative decrease in overall infectious morbidity after abdominal hysterectomy, which was not statistically significant. Povidone–iodine vaginal gel decreased the risk of pelvic abscess after total abdominal hysterectomy.

Notes: PG is a rare autoimmune bullous dermatosis of pregnancy that is characterised by linear deposition of C3, and occasionally IgG1 along the BMZ of lesional, perilesional and clinically normal skin when examined by direct immunofluorescence. Frequently there is a circulating IgG1 autoantibody (PG factor) directed against a BMZ antigen that avidly binds complement.The aberrant expression of MHC class II molecules in the placenta is important in triggering the immune response against a glycoprotein of 180 kDa found in the lamina lucida of the basement membrane of the amnion which cross reacts with that in the skin. The deposition of immune reagents in the placentae in PG has been implicated in the placental dysfunction and impaired foetal outcome which has been shown to occur in PG, Al present immunofluorescence is the key to differentiating PG from other clinically similar diseases.