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Magnetic and magnetocaloric effects of (Mn1-xFex)5Ge3 compounds are studied systematically. The maximum of magnetic entropy changes of 8.01 J/kg K under an external field change of 5 T is obtained for (Mn0.9Fe0.1)5Ge3, which is the largest value in Mn5Ge3-based solid solutions. Moreover, the Fe substitution increases the refrigeration capacity (RC) value greatly. The largest RC value of 237 J/kg in (Mn0.8Fe0.2)5Ge3 even compares favorably to that of many well-known magnetic refrigeration materials. Thus the Fe-containing (Mn1-xFex)5Ge3 compounds are much-improved magnetic refrigerants for the application of room-temperature magnetic refrigeration. The increase of the RC value is probably resulted from the formation of magnetic nanostructure. [ABSTRACT FROM AUTHOR]

La(Fe, Si)13 hydride is regarded as one of the most promising room-temperature refrigerants. However, to use the alloys in an active magnetic regenerator machine, it is vital to prepare thin refrigerants. In this work, a high H2 gas pressure of 50 MPa was employed to suppress the desorption of hydrogen atoms during the sintering process of plate-shaped La0.5Pr0.5Fe11.4Si1.6 hydrides. At 330K, a high-density sintered thin plate shows a large magnetic-entropy change ΔSm of 15.5 J/kgK (106mJ/cm³K) for a field change of 2T. The volumetric DSm is almost twice as large as that of bonded La(Fe,Si)13 hydrides. Favorably, hysteresis is almost absent due to the existence of micropores with a porosity of 0.69% which has been analyzed with high-resolution X-ray microtomography. [ABSTRACT FROM AUTHOR]

In Fe0.75Mn1.35As compound, a metamagnetic transition from an antiferromagnetic phase to a ferrimagnetic phase can be induced above its phase transition temperature Ts = 165 K by an external magnetic field, which leads to large magnetocaloric effects around Ts. The sign of the magnetic entropy change Δ SM in the Fe0.75Mn1.35As compound is negative, not as expected as an inverse magnetocaloric effect, and the maximum value of Δ SM is 4.2 J/kg K at 167.5 K for a magnetic field change of 5 T. Although it induces an irreversible lattice expansion, the cycling of a magnetic field does not induce an irreversible change in the magnetic transitions and magnetocaloric behaviors. The antiferromagnetism-related metamagnetic transitions with a large magnetic entropy change may provide with an opportunity in searching novel materials for magnetic refrigeration. [ABSTRACT FROM AUTHOR]

The structure and formation of nanoparticles without encapsulation of the intermetallic compound DyCo2 were investigated by using x-ray diffraction and high-resolution transmission electron microscopy. The DyCo2 nanoparticles are stable in air without any shell protection. A large magnetic-entropy change of 13.2 J kg-1 K-1 was found at 7.5 K in an applied-field change from 1 to 7 T, which is ascribed to the large magnetic moment density and the weak interaction energy in the nanoparticles. Such oxidation-resistant rare-earth transition-metal compound nanoparticles with large cryogenic magnetocaloric effect are useful for refrigeration applications at low temperatures. [ABSTRACT FROM AUTHOR]

A giant magnetocaloric effect was observed at room temperature in Mn1-xCrxAs compounds with x=0.006 and 0.01. The Cr dopant reduces (or even eliminates) the large thermal hysteresis of MnAs, while it lowers the first-order transition temperature from 313 K for MnAs to 265 K for Mn0.99Cr0.01As. Near the Curie temperature, a magnetic field induces a first-order phase transition from a ferromagnetic hexagonal phase to a paramagnetic orthorhombic phase, leading to a maximum value of ΔSM of 20.2 J/kg K at 267 K for a 5 T field change for Mn0.99Cr0.01As. The study on the Mn1-xCrxAs system may open an important field in searching proper materials for room-temperature magnetic refrigeration. [ABSTRACT FROM AUTHOR]

In Fe0.8Mn1.5As compound, an external magnetic field induces a metamagnetic transition from an antiferromagnetic phase to a ferrimagnetic phase above Ts=285 K, leading to large magnetocaloric effects around room temperature. Instead of showing inverse magnetocaloric effects, the sign of the entropy change ΔSM in the compound is unexpectedly negative, revealing a different mechanism. The maximum value of ΔSM is 6.2 J/kg K at 287.5 K for a magnetic field change of 5 T. The study on systems with antiferromagnetism-related metamagnetic transitions may open an important field in searching good materials for room-temperature magnetic refrigeration. [ABSTRACT FROM AUTHOR]

Inhibition of caspase-3-mediated apoptosis has been hypothesized to be associated with chemoresistance. Investigations of apoptosis revealed that cytosolic cytochrome c is associated with a complex of apoptotic protease activating factor-1 (Apaf-1), an adapter molecule, and caspase-9 to activate caspase-3. However, whether these apoptotic molecules are involved in acquired cisplatin resistance is not understood. The present work shows reduced activation of caspase-3 and apoptosis in a cisplatin-selected HeLa cell line. Ac-DEVD-CHO, a caspase-3 inhibitor, inhibited cisplatin-induced apoptosis about 60-70% in both cell lines. Ac-LEHD-CHO, a caspase-9 inhibitor or Ac-IETD-CHO, a caspase-8 inhibitor, inhibited cisplatin-induced caspase-3 activation and apoptosis similarly in both cell lines. In addition, cisplatin induced the activation of caspase-9, the upstream activator of caspase-3, in a dose-dependent manner, and the activation of caspase-9 was less induced in resistant cells. The accumulation of cytosolic cytochrome c, an activator of caspase-9, and the induction of the mitochondrial membrane-associated voltage-dependent anion channel were also reduced in cisplatin-resistant cells. However, the concentration of Bcl-2 family proteins in cisplatin-resistant cells was normal. The concentration of Apaf-1 was unaltered in both cell lines. Increasing the cellular concentration of Apaf-1 through the transient expression of the gene increased the induction of apoptosis in resistant cells, associated with enhanced activation of caspase-9, caspase-3 and DNA fragmentation factor. Regression analysis reveals that the modification factor, the ratio of the slope in the linear range of the dose-response curve with Apaf-1 to the slope without Apaf-1, is 1.5 and 4.75 in the HeLa and cisplatin-resistant HeLa cells, respectively. These results indicate that apoptosis and caspases are less induced in cisplatin-selected HeLa cells. They also suggest that ectopic overexpression of Apaf-1 may partially reverse the acquired cisplatin resistance.

Our previous studies [Chao (1992) Biochem. J. 282, 203-207; C.C.-K. Chao, unpublished work] has suggested a correlation between the levels of constitutive UV-damaged-DNA-recognitionproteins (UVDRP) and cellular DNA repair in different cell types. In the present study, UVDRP were induced in F9 and NIH3T3 cells by 0.1 microM retinoic acid (RA) and 1 mM dibutyryl cyclic AMP (dbcAMP), which is sufficient to induce differentiation in murine F9 stem cells. The induction of UVDRP in F9 and NIH3T3 cells was optimized after 6 and 2 days incubation with RA/dbcAMP respectively. Since NIH3T3 cells were not induced to differentiate by RA/dbcAMP, the upregulation of the UVDRP in mammalian cells would thus seem not to be mediated directly by differentiation. Using a plasmid re-activation assay to estimate DNA repair, we did not find a correlation between DNA repair and UVDRP in RA/dbcAMP-treated cells. The results suggest that UVDRP may have a function other than, or in addition to, its role in DNA repair.

We have previously hypothesized that the level of UV-damage recognition protein (UVDRP) is a potential indicator of DNA-damage-mediated sensitivity or resistance of human cells to UV radiation [Chao, C.C.-K., Biochem. J. 282, 203-207, 1992]. In this study, we detected a 2-fold increase in the UVDRP binding activity in a UV-sensitive multidrug-resistant (MDR) human colon cancer cells compared to the parental SW620 cells. However, the MDR cells did not display enhanced DNA repair. The data is consistent with the conclusion that DNA excision repair is not the sole determinant of cellular sensitivity to genotoxic agents. The results also suggest that recognition of damaged DNA may be associated with generating a signal which mediates cellular sensitivity to UV radiation.