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Heteroepitaxy of corundum-structured α-Ga2O3 and intriguing ferroelectric κ-Ga2O3 is proven as an alternative strategy to solve current challenges in heat dissipation and large-scale productivity for Ga2O3-based power electronic devices, whereas the fundamental growth dynamics and phase control of metastable Ga2O3 are still far unexplored. In this Letter, we demonstrate the strategy of strain engineering for the in situ phase manipulation of metastable Ga2O3 by embedding α-In2O3 submicrometer dots. Phase transition is modulated by the surface coverage of α-In2O3 due to the competitive growth of κ-Ga2O3 upon α-In2O3 and the homoepitaxy of α-Ga2O3 on the exposed α-Ga2O3 seed region. Upon discrete α-In2O3 submicrometer dots with a low surface coverage, the growth undergoes a nano-scale epitaxial lateral overgrowth mode, in which the selective homoepitaxy of α-Ga2O3 is dominant, and embedded α-In2O3 serves as nano-masks to prevent the threading dislocation propagation into the lateral overgrown Ga2O3 layer. In comparison, κ-Ga2O3 is energetically favorable on the interconnected α-In2O3 submicrometer dots, which are driven by the in-plane tensile strain as probed by the geometric phase analysis of transmission electron microscopy. Phase manipulation by embedded sub micrometer dots allows us to deliver high-quality Ga2O3 with well-defined phases and to conceive advanced devices with ultra-low loss, high frequency, and memorizing functionality. [ABSTRACT FROM AUTHOR]

Epitaxial film quality is critical to the success of high-performance α-Ga2O3 vertical power devices. In this work, the origins of threading dislocation generation and annihilation in thick α-Ga2O3 films heteroepitaxially grown on sapphire by the mist-CVD technique have been examined by means of high-resolution X-ray diffraction and transmission electron microscopies. By increasing the nominal thickness, screw dislocations exhibit an independent characteristic with a low density of about 1.8 × 106 cm−2, while edge dislocations propagating along the c-axis are dominant, which decrease down to 2.1 × 109 cm−2 in density for an 8 μm-thick α-Ga2O3 layer and exhibit an inverse dependence on the thickness. In the framework of the glide analytical model, parallel edge dislocations are generated at the interface due to the misfit-induced strain relaxation, while the dislocation glide and coalescence result in the annihilation and fusion behaviors. The optimal thick α-Ga2O3 with low dislocation densities may provide a prospective alternative to fully realize α-Ga2O3 power devices. [ABSTRACT FROM AUTHOR]

Deals with a study which determined the formation of iron-silicide by ion implantation of iron into silicon. Methodology of the study; Results and discussion.

Indoor living walls are becoming increasingly popular as they can provide good aesthetic effects and other environmental benefits. This research aims to analyse the environmental performance of indoor living walls by developing analytical models using embodied energy (EE) and carbon (EC). To assess the environmental impacts, a system of accounts is constructed based on an input-output model and the total direct and indirect energy and carbon requirements for each output made by the system are estimated. It is found that indoor living walls could be more environmentally sound if recycled materials, renewable energy and sustainable design and maintenance practices are applied. For example, by adopting recycled materials (such as HDPE), the EE can be reduced by 4-49%; the EC can be reduced by 6-19%. [ABSTRACT FROM AUTHOR]

The neurotoxicity of interleukin-6 (IL-6) and sodium nitroprusside (SNP, CAS 13755-38-9) was examined using primary cultures of rat hippocampal neurons. The cell viability was significantly reduced after the cultures were co-incubated with IL-6 4, 40, 400 ng/ml or SNP 1, 10, 100 mumol/l for 24 h. In addition, N omega-nitro-L-arginine (NNA, CAS 2149-70-4) at 0.1 mmol/l, when co-added with IL-6 400 ng/ml in cultures, significantly increased IL-6 reduced viability from 78.3 +/- 6.7% to 113.3 +/- 10.0%. These results indicate that IL-6 exerts neurotoxicity on cultured hippocampal neurons probably via overformation of nitric oxide in cultures.

Bilateral infusion of interleukin-6 (IL-6) 80 ng into the hippocampus has been shown to impair retention of a step-through passive avoidance task via shortening the step-through latency in testing. This infusion with IL-6 also increased the levels of nitrite and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in rat hippocampus. In addition, intraperitoneal injection of NG-nitro-L-arginine (CAS 2149-70-4) 100 mg/kg for 5 days improved the retention impairment induced by IL-6 and meanwhile antagonized the increase in nitrite levels. Furthermore, intraperitoneal injection with indometacin (CAS 53-86-1) 10 mg/kg daily for 5 days reduced the IL-6-induced increase in 6-keto-PGF1 alpha levels. These results indicate that IL-6 impairs retention of passive avoidance probably via the overproduction of nitric oxide (NO) and suggest that IL-6 may possess an inducible effect on NO synthase and cyclo-oxygenase in the hippocampus. These findings support the hypothesis that central IL-6 participates in the pathogenesis of Alzheimer's disease, and the overproduction of nitric oxide in the brain may partially mediate the amnesic effect of IL-6.

The effects of indometacin (CAS 53-86-1) on lipopolysaccharide-induced impairment of active avoidance and on interleukin-6-induced increase of prostaglandin E2 release were investigated in rats. In the experiment on acquisition and retention of one-way active avoidance in a shuttle box model, bilateral infusion of lipopolysaccharides (LPS) into the hippocampus, 1 microgram per side, resulted in a significant impairment both in acquisition and retention by prolonging the latency of avoidance in training and testing. In the meantime, intraperitoneal injection of indometacin 10 mg/kg daily for 7 days, improved the LPS-induced amnesia especially in the testing by shortening the latency from 2.3 to 1.7 s (p < 0.05). In the in vivo microdialysis study in anesthetized rats, intrahippocampal infusion of 80 ng interleukin-6 (IL-6) markedly increased prostaglandin E2 (PGE2) release into hippocampal dialysates which started at 2 h post administration. Perfusion of indometacin (0.3 mol/l) into the hippocampus for 1 h obviously suppressed the IL-6-induced PGE2 response. These findings provide experimental evidence that--assuming that central inflammation may be involved with Alzheimer's disease a non-steroidal anti-inflammatory drug may be used in the treatment of Alzheimer's disease.

Aim: To study the effect of intrahippocampal infusion of interleukin-6 (IL-6) on active avoidance in rats and the possible involvement of nitric oxide (NO)., Methods: Using a shuttle-box model, the effects of bilaterally intrahippocampal infusion of IL-6 3.2, 16, and 80 ng as well as sodium nitroprusside (SNP) 400 ng on active avoidance were studied on d 8 after administration. The levels of nitrite as an index of NO in the hippocampus were detected using a fluorometric assay 24 h after infusion of IL-6 3.2 or 80 ng., Results: IL-6 16 and 80 ng impaired the acquisition performance of active avoidance by prolonging the latency of avoidance in training, but not the retention performance in testing. IL-680 ng and SNP 400 ng also resulted in a marked impairment in acquisition performances by decreasing the rate of avoidance, but not in retention performances. IL-680 ng markedly elevated the nitrite levels from 10.6 +/- 0.7 in control rats to 13.6 +/- 2.0 (nmol/g wet wt) (P < 0.01). IL-6 3.2 ng had no effect on active avoidance nor on nitrite levels., Conclusion: Intrahippocampal infusion of IL-6 impaired learning acquisition of active avoidance in rats.

The effects of 20(S)-ginsenoside-Rg2 (GRg2, CAS 52286-74-5) and cyproheptadine (CYP, CAS 129-03-3) on acquisition, retention and retrieval were examined in male Wistar rats using a two-way active avoidance method. Learning and memory were estimated by the avoidance rate (%) and/or latency (s). Acute administration of CYP 1.0 mg/kg i.p. 30 min prior to training produced a significant impairment in acquisition of 3 d learning and 48 h memory by decreasing the rate from 87.9 +/- 2.1, 75.8 +/- 4.9 in saline rats to 55.8 +/- 9.6, 53.4 +/- 8.4, respectively (F(1,14) = 10.7, 14.8, p < 0.01). The CYP administration immediately following the end of training and 30 min before testing produced the impairments in retention of 24 h memory and in retrieval of 48 h memory by decreasing the rate from 86.7 +/- 1.7, 93.3 +/- 2.7 to 55.0 +/- 5.5, 60.0 +/- 6.8, respectively (F(1,12) = 27.2, 10.5, p < 0.01). Repeated administration of GRg2 20 mg/kg i.p. significantly improved the CYP-induced recognitional deficits by increasing the CYP-decreased rate from 55.8 +/- 9.6 to 80.8 +/- 4.2 in d 3 learning acquisition (F(1,14) = 5.6, p < 0.05), from 53.4 +/- 8.4 to 60.0 +/- 8.2 in 48 h memory acquisition (F(1,14) = 7.5, p < 0.05) and from 55.0 +/- 5.5 to 88.3 +/- 2.5 in 24 h memory retention (F(1,12) 27.5, p < 0.01) as well as from 60.0 +/- 6.8 to 85.6 +/- 6.9 in 48 h memory retrieval (F(1,12) = 5.2, p < 0.05), respectively. The results also provide the suggestive evidence that central serotonin may play a positive modulatory role in the acquisition, retention and retrieval of two-way active avoidance responding in rats.

Using a multiple-trial, training-to-criterion procedure, the effects of repeated administrations of ginseng stem-leaves saponins (GSLS) on learning and memory of one-way avoidance in rats were studied in shuttle-box. In acquisition, GSLS 10, 30, and 60 mg.kg-1 ip shortened the latency of avoidance in a bell-shaped manner from 1.0 +/- 0.2 s in saline rats to 0.8 +/- 0.5, 0.5 +/- 0.1, 0.8 +/- 0.2 s (d 3 learning) and from 0.9 +/- 0.2 s to 0.8 +/- 0.2, 0.7 +/- 0.1, and 0.8 +/- 0.2 s (10 x 24 h memory), and the best dose was 30 mg.kg-1. GSLS 30 mg.kg-1 ip shortened the latency of avoidance prolonged by scopolamine 0.8 mg.kg-1 sc from 5.2 +/- 1.3 s to 3.9 +/- 0.8 s (d 1 learning acquisition) and from 2.2 +/- 0.6 s to 0.8 +/- 0.3 s (3 x 24 h memory acquisition). In retention, GSLS 30 mg.kg-1 ip shortened the latency prolonged by cycloheximide 2.5 and 5 mg.kg-1 ip from 3.4 +/- 1.0 s to 1.4 +/- 0.5 s (4 h memory) and from 1.6 +/- 0.3 s to 0.9 +/- 0.2 s (24 h memory), and increased the avoidance number decreased by cycloheximide 5 mg.kg-1 from 38.1 +/- 8.8% to 72.4 +/- 10.8% (4 h memory). The results indicate that GSLS facilitated the acquisition of learning and memory in rats, and improved the scopolamine amnesia and cycloheximide amnesia.