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OBJECTIVE: Kidney stone formers have a high rate of stone recurrence after kidney stone removal surgery and there is no effective medication for treatment. Hydroxycitric acid (HCA), which is the major component of Garcinia cambogia extract, can dissolve calcium oxalate crystals in vitro, suggesting that Garcinia cambogia could be used to treat calcium oxalate kidney stone. In this study, we used the Drosophila kidney disease model to evaluate the effect of Garcinia cambogia on the prevention and removal of calcium oxalate stones in vivo. MATERIALS AND METHODS: Flies were reared in fly food containing different concentrations of GCE for one week. The effect of GCE on preventing the formation of calcium oxalate stone was examined. WT and v-ATPase gene RNAi knockdown flies were reared in fly food with 0.3% NaOx for one week, then fed different concentrations of GCE for one week. The effect of GCE on the removal of calcium oxalate stone was examined. RESULTS: Garcinia cambogia extract dissolves calcium oxalate crystals from Malpighian tubules in both genetic and non-genetic Drosophila kidney stone models compared to citric acid. Hydroxycitric acid also directly dissolves calcium oxalate crystals in Drosophila Malpighian tubules ex vivo. CONCLUSIONS: Garcinia cambogia extract removes calcium oxalate kidney stones from Drosophila Malpighian tubules via directly dissolving calcium oxalate stones by HCA. Our study strongly suggests that clinical-grade Garcinia cambogia extract could be used to treat patients with nephrolithiasis in the future. [ABSTRACT FROM AUTHOR]

Single-phase Gd[sub 2]Co[sub 17-x]V[sub x] compounds (x = 0.0-1.5) crystallizing in the rhombohedral Th[sub 2]Zn[sub 17] structure have been synthesized. The lattice parameters a and c of the compounds increase linearly with increasing V content, and the rate of increase of c is about 2.5 times as large as that of a. Substitution of a small amount of V atoms (x = 0.3) for Co atoms leads to the occurrence of uniaxial magnetocrystalline anisotropy of Gd[sub 2]Co[sub 17-x]V[sub x]. The anisotropy field H[sub A] increases drastically with increasing V content. The variations of both the lattice parameters and the magnetocrystalline anisotropy with V content suggest a preferential occupation of the V atoms at the 6c dumbbell site. The Curie temperature T[sub C], saturation moment M[sub S], and average Co moment 〈μ[sub Co]〉 of the compounds decrease greatly as the V content increases. The rapid decrease of T[sub C] is essentially attributed to a serious weakening of the Co-Co interactions due to the preferential occupation of the V atoms at the 6c site. The effect of a strong hybridization between the V and Co atoms is plausibly responsible for the decreases of the Ms and 〈μ[sub Co]〉. [ABSTRACT FROM AUTHOR]

OBJECTIVE: We explored the protective effect of retigabine (RTG) on focal cerebral ischemic injury and the potential molecular mechanism. MATERIALS AND METHODS: A mouse model of middle cerebral artery occlusion (MCAO) was established to induce cerebral ischemic injury. Blood samples were collected for the measurement of malondialdehyde (MDA), superoxide dismutase (SOD) and reduced glutathione (GSH). The brain infarct volume was stained by triphenyltetrazolium chloride. The cell apoptosis was observed by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nickend labeling (TUNEL) staining. The expression of B-cell lymphoma-2 (Bcl-2), BCL2-Associated X (Bax), cleaved caspase 3, p-p38 and p-JNK, were determined by Western blot. RESULTS: RTG treatment reduced the MCAO-induced increase in brain infarct volume and neurological deficit scores. RTG treatment reduced the level of MDA and increased the activity of SOD and GSH. RTG treatment also decreased the Bax/Bcl-2 ratio and cleaved caspase 3 expression in the ischemic tissues. Further, RTG treatment decreased the phosphorylation levels of p38 and JNK in the ischemic tissues. CONCLUSIONS: RTG attenuated cerebral ischemic injury through reducing oxidative stress and mitochondria-mediated apoptosis via inhibiting p38 and JNK phosphorylation. [ABSTRACT FROM AUTHOR]

The crystal structure and superconducting properties of RuSr[sub 2-x]Ba[sub x]GdCu[sub 2]O[sub 8] (0<=x<=0.1) have been investigated. X-ray powder diffraction (XRD) patterns show that the solid solution range is 0<=x<=0.1. The superconducting transition temperature was raised up to 35 K (zero) and 62 K (onset) for x=0.07, from 16 K (zero) and 45 K (onset) for x=0.0, and then T[sub C] decreases with x when x>0.07. Rietveld refinement for XRD data of RuSr[sub 2-x]Ba[sub x]GdCu[sub 2]O[sub 8] show that the apical Cu–O(1) bond length increases with an increase of x, while the Ru–O(1) bond length decreases, This may account for the enhancement of the superconducting transition temperature. © 2004 American Institute of Physics. [ABSTRACT FROM AUTHOR]

Crystal structure and magnetic properties of the NdCo[sub 9.5-x]Fe[sub x]V[sub 2.5] compounds with x=0–3.5 have been investigated. The lattice parameters increase linearly with the Fe content and the Curie temperature increases substantially at small amount of Fe content and then gradually with the further increase of x. A domain-wall pinning phenomenon was observed in all of the compounds and becomes less obvious as x increases. At a higher field, the compounds exhibit a field-induced metamagnetic transition. The critical field for the metamagnetic transition increases first then decreases with the Fe content, whereas the difference of the magnetization between 14 and 5 T increases with x. The observation can be understood by considering an interplay of the volume expansion, enhanced exchange coupling parameter J[sub RT] and the T sublattice moment μ[sub T] due to the Fe substitution for Co. © 2004 American Institute of Physics. [ABSTRACT FROM AUTHOR]