Si amorphization by focused ion beam milling: Point defect model with dynamic BCA simulation and experimental validation.

A Ga focused ion beam (FIB) is often used in transmission electron microscopy (TEM) analysis sample preparation. In case of a crystalline Si sample, an amorphous near-surface layer is formed by the FIB process. In order to optimize the FIB recipe by minimizing the amorphization, it is important to predict the amorphous layer thickness from simulation. Molecular Dynamics (MD) simulation has been used to describe the amorphization, however, it is limited by computational power for a realistic FIB process simulation. On the other hand, Binary Collision Approximation (BCA) simulation is able and has been used to simulate ion-solid interaction process at a realistic scale. In this study, a Point Defect Density approach is introduced to a dynamic BCA simulation, considering dynamic ion-solid interactions. We used this method to predict the c-Si amorphization caused by FIB milling on Si. To validate the method, dedicated TEM studies are performed. It shows that the amorphous layer thickness predicted by the numerical simulation is consistent with the experimental data. In summary, the thickness of the near-surface Si amorphization layer caused by FIB milling can be well predicted using the Point Defect Density approach within the dynamic BCA model.

Cataract development in diabetic sand rats treated with alpha-lipoic acid and its gamma-linolenic acid conjugate.

BACKGROUND: Diabetes commonly leads to long-term complications such as cataract. This study investigated the effects of alpha-lipoic acid (LPA) and its gamma-linolenic acid (GLA) conjugate on cataract development in diabetic sand rats. METHODS: Two separate experiments were conducted. In Experiment 1, sand rats were fed a "high-energy" diet (70% starch), an acute model of Type 2 diabetes, and injected with LPA. In Experiment 2, the animals received a "medium-energy" diet (59% starch), a chronic diabetic model, and were intubated with LPA or its GLA conjugate. Throughout the experiments, blood glucose levels and cataract development were measured. At the termination of the experiments, lens aldose reductase (AR) activity and lenticular reduced glutathione (GSH) levels were analyzed. RESULTS: LPA injection significantly inhibited cataract development and reduced blood glucose levels in rats fed the "high-energy" diet. Lens AR activity tended to be lower, while lenticular GSH levels increased. In sand rats fed a "medium-energy" diet (59% starch), LPA intubation had no effect on blood glucose levels and cataract development but GSH levels were increased. In contrast, sand rats intubated with GLA conjugate showed the highest blood glucose levels and accelerated cataract development. The conjugate treatment also decreased lenticular GSH content. CONCLUSIONS: The hypoglycemic effects of LPA are beneficial in the prevention of acute symptoms of Type 2 diabetes. It remains to be shown that the antioxidant activity of LPA is responsible for prevention or inhibition of cataract progression in sand rats.

A viscoelastic model of phagosome motion within cells based on cytomagnetometric measurements.

Cytomagnetometry is a noninvasive method to investigate intracellular movements of organelles such as phagosomes by introducing magnetic particles into cells by phagocytosis, magnetizing them and measuring the field from the cells. To analyze the results of the cell-field measurement, we introduce a model for intracellular phagosome motion and investigate their behavior in terms of the cell field. The model includes an elastic body and two viscosity components which are ascribed to the filamentous structures surrounding the phagosomes. The magnetic relaxation phenomenon is assumed to derive from the rotationary Brownian motion as in our previous model. Although the model is simple, its behavior is not trivial because it contains a nonlinear term and the Brownian motion term. This model is the simplest one possible having a viscoelastic body and its behavior hence should be investigated thoroughly.

Prostanoids mediate IL-1beta-induced beta-adrenergic hyporesponsiveness in human airway smooth muscle cells.

We have previously reported that pretreatment of cultured human airway smooth muscle (HASM) cells with interleukin-1beta (IL-1beta) results in decreased beta-adrenergic responsiveness. The purpose of this study was to determine whether prostanoids released as a result of cyclooxygenase-2 (COX-2) induction by IL-1beta contribute to this effect of the cytokine. Confluent serum-deprived HASM cells were studied in passages 4-7. IL-1beta (20 ng/ml for 22 h) reduced the ability of the beta-agonist isoproterenol (Iso) to decrease stiffness of HASM cells as measured by magnetic twisting cytometry. The effect of IL-1beta on Iso-induced changes in cell stiffness was abolished by nonselective [indomethacin (Indo), 10(-6) M] and selective (NS-398, 10(-5) M) COX-2 inhibitors. Indo and NS-398 also inhibited both the increased basal cAMP and the decreases in Iso-stimulated cAMP production induced by IL-1beta. IL-1beta (20 ng/ml for 22 h) caused an increase in both basal (15-fold) and arachidonic acid (AA)-stimulated (10-fold) PGE2 release. Indo blocked basal and AA-stimulated PGE2 release in both control and IL-1beta-treated cells. NS-398 also markedly reduced basal and AA-stimulated PGE2 release in IL-1beta-treated cells but had no significant effect on AA-stimulated PGE2 release in control cells. Western blot analysis confirmed the induction of COX-2 by IL-1beta. Exogenously administered PGE2 (10(-7) M, 22 h) caused a significant reduction in the ability of Iso to decrease cell stiffness, mimicking the effects of IL-1beta. Cycloheximide (10 microg/ml for 24 h), an inhibitor of protein synthesis, also abolished the effects of IL-1beta on Iso-induced cell stiffness changes and cAMP formation. In summary, our results indicate that IL-1beta significantly increases prostanoid release by HASM cells as a result of increased COX-2 expression. The prostanoids appear to contribute to beta-adrenergic hyporesponsiveness, perhaps by heterologous desensitization of the beta2 receptor.