Fresnel zone plate with apodized aperture for hard X-ray Gaussian beam optics.

Fresnel zone plates with apodized apertures [apodization FZPs (A-FZPs)] have been developed to realise Gaussian beam optics in the hard X-ray region. The designed zone depth of A-FZPs gradually decreases from the center to peripheral regions. Such a zone structure forms a Gaussian-like smooth-shouldered aperture function which optically behaves as an apodization filter and produces a Gaussian-like focusing spot profile. Optical properties of two types of A-FZP, i.e. a circular type and a one-dimensional type, have been evaluated by using a microbeam knife-edge scan test, and have been carefully compared with those of normal FZP optics. Advantages of using A-FZPs are introduced.

Autocrine and paracrine up-regulation of blood-brain barrier function by plasminogen activator inhibitor-1.

The blood-brain barrier (BBB) is the interface that separates the central nervous system (CNS) from the peripheral circulation. An increase in blood-borne substances including cytokines in plasma and brain affects BBB function, and this is associated with the development of pathogenesis of a number of diseases. Plasminogen activator inhibitor (PAI)-1 regulates the plasminogen activator/plasmin system as a serpin in the periphery and the CNS. We investigated whether PAI-1 alters BBB function using in vitro models of the BBB consisting of rat primary brain endothelial cells (RBECs) alone and co-cultured with pericytes. We found that PAI-1 increased the tightness of the brain endothelial barrier in a time- and dose-dependent manner, as shown by an increase in the transendothelial electrical resistance (TEER) and a decrease in the permeability to sodium fluorescein (Na-F). RBECs responded equally to PAI-1 in the blood-facing and brain-facing sides of the brain, leading to a decrease in Na-F permeability. In addition, RBECs constitutively released PAI-1 into the blood-facing (luminal) and brain-facing (abluminal) sides. This release was polarized in favor of the luminal side and facilitated by serum. The neutralization of PAI-1 by an antibody to PAI-1 in RBEC/pericyte co-culture more robustly reduced TEER of RBECs than in RBEC monolayers. These findings suggest that PAI-1 derived from the neurovascular unit and peripheral vascular system participates as a positive regulator of the BBB in facilitating the barrier function of the endothelial tight junctions.

Anti-apoptotic roles of plasminogen activator inhibitor-1 as a neurotrophic factor in the central nervous system.

Plasminogen activator inhibitor-1 (PAI-1), a member of the serpin gene family, is the primary inhibitor of urokinase-type and tissue-type PAs. PAI-1 plays an important role in the process of peripheral tissue remodeling and fibrinolysis through the regulation of PA activity. This serpin is also produced in brain tissues and may regulate the neural protease sequence in the central nervous system (CNS), as it does in peripheral tissues. In fact, PAI-1 mRNA is up-regulated in mouse brain after stroke. The serpin activity of PAI-1 helps to prevent tissue-type PA-induced neuron death. However, we have previously found that PAI-1 has a novel biological function in the CNS: the contribution to survival of neurites on neurons. In neuronally differentiated rat pheochromocytoma (PC-12) cells, a deficiency of PAI-1 in vitro caused a significant reduction in Bcl-2 and Bcl-X(L) mRNAs and an increase in Bcl-X(S) and Bax mRNAs. The change in the balance between mRNA expressions of the anti- and pro-apoptotic Bcl-2 family proteins promoted the apoptotic sequence: caspase-3 activation, cytochrome c release from mitochondria and DNA fragmentation. Our results indicate that PAI-1 has an anti-apoptotic role in neurons. PAI-1 prevented the disintegration of the formed neuronal networks by maintaining or promoting neuroprotective signaling through the MAPK/ERK pathway, suggesting that the neuroprotective effect of PAI-1 is independent of its action as a protease inhibitor. This review discusses the neuroprotective effects of PAI-1 in vitro, together with the relevant data from other laboratories. Special emphasis is placed on its action on PC-12 cells.

Differences in penetration force of intravenous catheters: effect of grinding methods on inner needles of intravenous catheters.

OBJECTIVES: To compare penetration forces of intravenous catheters based on two grinding methods used for the inner needle tip. METHOD: Forty intravenous catheters were divided into two groups according to two inner needle grinding methods: Lancet and Backcut. To compare the characteristics of inner needles, 18 gauge Surflo outer catheters, were attached to all inner needles. We measured penetration forces by attaching a "Push-Pull-Gauge" to the chamber of intravenous catheters, then we penetrated intravenous catheters through a 0.04-mm thick polyethylene film. The penetration velocity was 3.3 mm/sec. we measured penetration forces at 30- and 45-degree penetration angles. RESULTS: There was no significant difference in the penetration forces of inner needle and outer catheter between the two groups at the 45-degree penetration angle. Penetration forces of the inner needle and the outer catheter in the Backcut group was significantly lower than those of the Lancet group at the 30-degree penetration angle. The penetration force of the outer catheter was reduced from 0.3 N to 0.18 N, a 40 % reduction at 30-degree penetration angle. Computerized measurements of penetration holes indicate that the Y-shaped incision mark of the Backcut leaves larger incision hole than the actual puncture size. We hypothesize that the Y-shaped incision mark creates more efficient path for the outer catheter to advance. Therefore, lower penetration force was indicated compared to the other group. CONCLUSION: Backcut shows less penetration force of inner needles of peripheral intravenous catheters than lancet.