EFFECT OF MICROSTRUCTURE ON HYDROGEN DAMAGE OFJBK-75 PRECIPITATE-STRENGTHENED AUSTENITIC STEEL

1.IntroductionHydrogenembrittlement(HE)0rhydr0gendamage(HD)ofall0ysisnotonlyrelatedt0chemicalc0mpositionsbutals0c10selyt0microstructures.Thereweres0merep0rts0ntheeffect0fmicr0structures0nHD0fsingle-phaseausteniticsteels[1-3].Themicrostructuralreas0nsofHD0fprecipitate-strengthenedausteniticsteels(PSAS),however,havereceivedlessattenti0n.Single-phaseausteniticsteelshaveproveninseveralinstancestohaveg00dresistancet0HD,butaretypicallynostr0ngerthan450MPainyieldstrength.Thus,anausteniticmatri…     

Two Algorithms for Fast Polyhedron Ray-Tracing

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Preferential adsorption, internalization and resistance to degradation of the major isoform of the Alzheimer's amyloid peptide, A beta 1-42, in differentiated PC12 cells

A central question in Alzheimer's disease (AD) is the role of amyloid in pathogenesis. Recent discoveries implicating the longer A beta 1-42 form of amyloid in pathogenesis led us to characterize the interaction of A beta with cells to elucidate differences that might account for these observations. We characterized the adsorption, internalization and degradation of radiolabeled A beta in NGF-differentiated PC12 cells under conditions that are not acutely toxic. All A beta peptides examined absorb to the surface of PC12 cells and are internalized; however the adsorption and internalization of A beta 1-42 is significantly greater than that of A beta 1-40 and A beta 1-28. The adsorption of A beta 1-42 is decreased by treatment of the cells with neuraminidase, but not heparitinase. The fate of the internalized A beta 1-42 is also very different than shorter A beta peptides; a fraction of the internalized A beta 1-42 accumulates intracellularly and is resistant to degradation for at least 3 days while A beta 1-40 and shorter peptides are eliminated with a half life of about 1 h. A beta 1-42 does not appear to inhibit lysosomal hydrolases, since A beta 1-28 is degraded at the same rate in the presence or absence of A beta 1-42. The intracellular A beta 1-42 is located in a dense organellar compartment and colocalizes with the lysosomal markers Lucifer Yellow and horseradish peroxidase. These data indicate that there are significant differences in the cell surface adsorption, internalization and catabolism of A beta 1-42 compared to A beta 1-40 and A beta 1-28. These differences may be important for the preferential accumulation of the longer A beta 1-42 isoform and its association with AD pathogenesis.     

Antro-pyloric canal values from early prematurity to full-term gestational age: an ultrasound study

PURPOSE: To evaluate antro-pyloric canal dimensions from early prematurity to full-term gestational age. MATERIALS AND METHODS: Ninety infants with no signs of regurgitation or vomiting were studied 3-5 days after birth. Their gestational ages ranged from 26 to 41 weeks (mean 33.7 weeks) and the body weight from 670 to 4150 g (mean 2067 g). Antro-pyloric muscle thickness, canal length and canal width were measured. RESULTS: A positive correlation between gestational age, muscle thickness (R = 0.71, P < 0.001), length (R = 0.63, P < 0.001) and width (R = 0.42, P < 0.001) was found. Furthermore, a positive correlation between body weight, muscle thickness (R = 0.82, P < 0.001) length, (R = 0.67, P < 0.001) and width (R = 0.55, P < 0.001) was observed. CONCLUSIONS: This study shows that antro-pyloric canal dimensions increase with gestational age. Moreover, it provides normal values for muscle thickness, canal length and canal width from the early gestation to full term.     

Effect of beta-adrenergic agonists on paracellular width and fluid flow across outflow pathway cells

PURPOSE: To determine whether the adrenergic agonists epinephrine and isoproterenol regulate fluid flow across endothelial cells cultured from the human aqueous outflow pathway and to evaluate associated cellular mechanisms. METHODS: Confluent monolayers of human trabecular meshwork (TM) or Schlemm's canal endothelial (SCE) cells were grown on porous filter supports. The monolayers were perfused with media while fluid flow, expressed as hydraulic conductivity (HC = microl/min/mm Hg/cm2), was continuously measured in preparations treated with isoproterenol, epinephrine, or control medium. Morphometric ultrastructural methods were used to measure the area occupied by the intercellular space and by each cell. RESULTS: SCE cells and TM cells exposed to isoproterenol or epinephrine responded with an increase in transendothelial fluid flow. Dose-response curves for both adrenergic agonists showed that HC increased linearly as a function of the log of the isoproterenol and epinephrine concentration. At 10(-4) M isoproterenol, the HC increased threefold, and threshold conditions were reached at 10(-9) M. The increase in HC was apparent after isoproterenol had been applied for 1 hour, reached a peak in 3 to 4 hours, and declined gradually to return to baseline conditions in 10 to 12 hours. Morphometric analyses showed that the area occupied by the intercellular space increased fourfold when isoproterenol was used at 10(-4) M, whereas the cell area decreased as a function of the concentration of adrenergic agonist. Epinephrine's effects on HC and cell morphology were blocked by pretreatment with equimolar concentrations of the nonselective beta-blocker, timolol. CONCLUSIONS: Epinephrine and isoproterenol increase flow through the paracellular pathway of SCE and TM cells through a beta-receptor mediated response that widens the intercellular space and reduces cell area. These findings support the hypothesis that epinephrine decreases the intraocular pressure in glaucoma therapy by promoting fluid flow across the SCE and TM cells lining tissues of the major aqueous outflow pathway.