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The effects of different forming process on the microstructure, martensitic transformation, and mechanical properties of the Ni50Mn34In14Co2 (numbers indicate at.%) alloys were investigated in detail. The results show that the microstructure of Ni50Mn34In14Co2 alloy consists of the matrix and the second phase by powder hot forging technology under the forces in different directions and spark plasma sintering (SPS), and the prepared sample has obvious preferred orientation by applied force in the three directions. The grain and the second phase of prepared sample were obviously refined by the hot forging technology. The martensitic transformation behavior was almost unchanged by different forming process. In addition, the shape memory effect of prepared Ni50Mn34In14Co2 alloy was significantly enhanced by different forming processes. [ABSTRACT FROM AUTHOR]

The magnetic properties and structural phase transformations of Heusler alloys [Ni.sub.2+x][Mn.sub.1-x]Ga and [Ni.sub.2-x][Mn.sub.1+x/2][Ga.sub.1+x/2] were investigated. It was found that the martensitic transformation temperature increases and the Curie temperature decreases with decreasing Mn concentration in the [Ni.sub.2+x][Mn.sub.1-x]Ga system, but the magnetic properties decrease faster than those do in the [Ni.sub.2-x][Mn.sub.1+x/2][Ga.sub.1+x/2] system. It suggests that the influence of the conduction electron concentration and the distance between Mn atoms on the Curie temperature is stronger than the magnetic dilution effect. The martensitic transformation temperature shows a peak value at x = 0.06 in the [Ni.sub.2-x][Mn.sub.1+x/2][Ga.sub.1+x/2] system. A large stress-free magnetic-field-induced strain (MFIS) of 1.8% has been obtained at room temperature in a single crystal sample with the composition in the first system. Index Terms--Magnetic-field-induced strain, magnetic properties, phase transformation.

The thermal properties, crystalline structure and shape memory effects of poly( l-lactide) (PLLA) and poly( l-lactide-co-ε-caprolactone) (PCLA) copolymers are systematically investigated by differential scanning calorimetry (DSC), X-ray diffraction (XRD) and tensile tests. The effects of the deformation strain on the shape recovery rate and recovery stress are also revealed. The polymers have the PLLA crystal and the amorphous phase, which are served as the fixed phase and reversible phase, respectively. The shape recovery rate and the recovery stress are significantly affected by the compositions and the deformation strain. With the increase of the deformation strain, the shape recovery rate decrease and higher shape recovery rate can be obtained in the polymers which have higher ε-CL content. However, the variation of recovery stress with the deformation strain is quite different and the maximum recovery stress of all polymers exceeds 3 MPa. [ABSTRACT FROM AUTHOR]

A Heusler Ni50Mn29Ga16Gd5 alloy with a high transformation temperature has been obtained by substituting 5 at% Gd for Ga in a ternary Ni50Mn29Ga21 ferromagnetic shape memory alloy. The microstructure and phase transformations in the Ni50Mn29Ga16Gd5 alloy have been investigated by scanning electron microscopy, transmission electron microscopy, X-ray diffraction and differential scanning calorimetry. It is shown that the microstructure of the Ni50Mn29Ga16Gd5 alloy consists of matrix and hexagonal Gd (Ni,Mn)4Ga phase, which indicates a eutectic structure composed of these two phases. One-step thermoelastic martensitic transformation occurs in this quaternary alloy. Ni50Mn29Ga16Gd5 alloy exhibits a martensite transformation start temperature up to 524 K, approximately 200 K higher than that of Ni50Mn29Ga21 alloy. At room temperature, non-modulated martensite with twin substructure is observed in Ni50Mn29Ga16Gd5 alloy. [ABSTRACT FROM AUTHOR]

Along with the rapid growth of the national economy in China, the electric utility is faced with an ever rising demand for electricity and the problem to solve large capacity power transmission. Under the support of the High Technology Research & Development Program of China, a 1.5 kA/10.5 kV 10-m long 3-phases HTS transmission power cable and a 75-m long, 3-phase, 10.5 kV/1.5 kA HTS power cable have been developed successfully by the Institute of Electrical Engineering, Chinese Academy of Sciences. The 75-m long HTS power cable operates now at a local live distribution grid of 6.6 kV to supply electric power for Changtong's factory in Baiyin, Gansu Province. The cable operates stably and reliably over 7000 hours since December 2004. [ABSTRACT FROM AUTHOR]

Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening syndrome involving a final common pathway of hypercytokinemia, in which tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and soluble interleukin 2-receptor-alpha (sIL-2Rα) are the key cytokines. Pre-B-cell colony-enhancing factor (PBEF) is an inflammatory cytokine involved in several inflammatory diseases. However, its role in HLH is unknown. In this study, we examined the role of PBEF in HLH. Plasma was collected from 22 children with HLH and 14 healthy children. The concentrations of plasma PBEF, TNF-α, IFN-γ, and sIL-2Rα were determined using an enzyme-linked immunosorbent assay. All clinical data were derived from medical records. In the acute phase, children with HLH had much higher PBEF, TNF-α, IFN-γ, and sIL- 2Rα levels than did healthy children (P < 0.05). After treatment, 13 HLH children improved and PBEF, TNF-α, and IFN-γ levels decreased to normal levels (P < 0.05); sIL-2Rα levels also decreased (P < 0.05), but remained above the normal level (P < 0.05). Two patients were lost to follow-up, while 7 patients showed a bad response to therapy and eventually died, showing high PBEF levels above those of the survivors (P < 0.01). PBEF level was significantly positively correlated with TNF-α, IFN-γ, sIL-2Rα, serum ferritin, and triglycerides (all P < 0.05), and was negatively correlated with fibrin (P < 0.05). PBEF appears to be involved in the inflammatory process of HLH, and elevated PBEF is related to disease activity. We are currently evaluating the role of PBEF as a marker for the diagnosis and management of patients.

The effects of vanadate (Na3VO4) on pancreatic B-cell function were studied in normal mouse islets. Vanadate did not affect basal insulin release but potentiated the effect of 7-30 mM glucose at concentrations of 0.1-1 mM. This effect was progressive and slowly reversible. It was abolished by omission of extracellular Ca2+ but unaffected by blockers of adrenergic or muscarinic receptors. Comparison of the changes in membrane potential, 86Rb efflux and 45Ca efflux that vanadate and ouabain produced in B-cells made it possible to exclude the hypothesis that vanadate increases insulin release by blocking the sodium pump. Vanadate was also without effect on cAMP levels. On the other hand, it markedly changed the characteristics of the Ca(2+)-dependent electrical activity and of the oscillations of cytoplasmic Ca2+ recorded in B-cells stimulated by 15 mM glucose. In the steady state, Ca2+ influx was increased by vanadate, and this resulted in a rise in cytoplasmic Ca2+. The exact mechanisms underlying these changes could not be established but a blockade of K channels was excluded. In the presence of LiCl, vanadate markedly increased inositol phosphate levels in islet cells. This effect was attenuated but not suppressed by omission of Ca2+. A small increase in inositol bisphosphate was still produced by vanadate in the absence of LiCl. These results suggest that vanadate both stimulates phosphoinositide breakdown and inhibits inositol phosphate degradation. In conclusion, vanadate does not induce insulin release, but markedly potentiates the stimulation by glucose. This property is not due to an inhibition of the sodium pump or to a rise in cAMP concentration. It results from a complex interplay between changes in B-cell membrane potential, phosphoinositide metabolism and Ca2+ handling.

The mechanisms by which arginine-vasopressin (AVP) affects pancreatic B-cell function were studied in normal mouse islets. AVP produced a dose-dependent (0.1-1000 nM; EC50 approximately 1-2 nM) amplification of glucose-induced insulin release. This amplification was of slow onset and reversibility. AVP was ineffective when the concentration of glucose was less than 7 mM, but was still very effective in 30 mM glucose. The increase in insulin release produced by AVP was accompanied by small accelerations of 86Rb and 45Ca efflux from islet cells. Omission of extracellular Ca2+ accentuated the effect of AVP on 86Rb efflux, attenuated that on 45Ca efflux, and abolished that on release. Under no condition did AVP inhibit 86Rb efflux. AVP did not significantly affect cAMP levels, but increased inositol phosphate levels in islet cells, even in the absence of extracellular Ca2+. AVP did not affect the membrane potential in unstimulated B-cells and augmented glucose-induced electrical activity only slightly. This was not due to a direct action on ATP-sensitive K+ channels as revealed by patch-clamp recordings (whole cell and outside-out patches). In conclusion, AVP is not an initiator of insulin release, but it potently amplifies glucose-induced insulin release in normal mouse B-cells. This effect involves a stimulation of phosphoinositide metabolism, and presumably an activation of protein kinase C, rather than a change in cAMP levels or a direct control of the membrane potential.