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Molecular ferroelectric crystals have attracted growing interest as potential alternatives to conventional leadbased ceramic ferroelectrics. We have recently discovered that a class of compounds known as plastic crystals can show multiaxial ferroelectricity, which allows ferroelectric performance even in polycrystalline forms. Here, we report new plastic/ ferroelectric ionic molecular crystals that exhibit remarkably small coercive electric fields at room temperature. The easily switchable ferroelectric polarization enables low-voltage switching operations and high-frequency performance. Such ferroelectric crystals can be readily processed into bulk polycrystalline forms with desired shapes that are characterized by unprecedentedly high pyroelectric figures of merit and large piezoelectricity. These multifunctional molecular crystals represent highly attractive prospects for device elements with a diverse range of applications, which will significantly boost the development of molecular ferroelectric crystals.

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This report describes a newly observed phenomenon: pressure-induced crystallization from amorphous calcium carbonate (ACC). Synthetic ACC samples were pressurized up to 800 MPa at room temperature. Then crystallization of vaterite and calcite was observed from X-ray diffraction patterns. The crystallization pressure depends on the H2O contents of ACCs. The ACC samples with high-H2O content (21 wt %), middle-H2O content (17 wt %), and low-H2O content (10 wt %) underwent crystallization at pressures higher than 240 MPa, 400 MPa, and 640 MPa, respectively. These results indicate that H2O in the ACC serves an important role in the crystallization process and that we should treat ACC carefully in preparation for analyses such as infrared spectroscopy to obtain the intrinsic information related to amorphous materials.

Doping large amounts of a incompatible element into calcite, a polymorph of CaCO 3 , was achieved by pressurizing amorphous calcium carbonate (ACC) containing a dopant. Strontium-doped ACC samples were prepared from supersaturated solutions. ACC was transformed to calcite at 0.8 GPa and 25 °C. The lattice volume of calcite obtained by pressurizing ACC increased monotonically up to 372.5 Å 3 (1.3% increase from a Sr-free sample) with increasing Sr content in ACC up to 0.15 in Sr/(Sr + Ca). For comparison, the lattice volumes of calcite samples precipitated from supersaturated CaCO 3 solution containing Sr were obtained, but the lattice volume of calcite precipitated from supersaturated solutions showed no noteworthy increase. Results of this study indicate that pressure-induced crystallization is an efficient pathway to dope incompatible elements into crystals.

Bezafibrate improved hepatic steatosis and potently prevented inflammation, oxidative stress, HSC activation, and fibrogenesis in the liver. Moreover, this study was the first to demonstrate that bezafibrate directly inhibits hepatic fibrogenic response induced by TGF-beta1 in vitro. Hence bezafibrate may be a new therapeutic strategy against NASH and hepatic fibrosis.

Calcite is a ubiquitous mineral in nature. Heavy alkaline-earth elements with large ionic radii such as Sr2+ and Ba2+ are highly incompatible to calcite. Our previous study clarified that incompatible Sr2+ ions can be structurally incorporated into calcite through crystallization from amorphous calcium carbonate (ACC). In this study, we synthesized Sr-doped calcite with Sr/(Sr + Ca) up to 30.7 ± 0.6 mol% and Ba-doped calcite with Ba/(Ba + Ca) up to 68.6 ± 1.8 mol%. The obtained Ba-doped calcite samples with Ba concentration higher than Ca can be interpreted as Ca-containing barium carbonates with the calcite structure which have not existed so far because barium carbonate takes the aragonite structure. X-ray diffraction (XRD) patterns of the Sr-doped and Ba-doped calcite samples obtained at room temperature showed that reflection 113 gradually weakened with increasing Sr/(Sr + Ca) or Ba/(Ba + Ca) ratios. The reflection 113 disappeared at Ba/(Ba + Ca) higher than 26.8 ± 1.6 mol%. Extinction of reflection 113 was reported for pure calcite at temperatures higher than 1240 K, which was attributed to the rotational (dynamic) disorder of CO32− in calcite. Our Molecular Dynamics (MD) simulation on Ba-doped calcite clarified that the CO32− ions in Ba-doped calcites are in the static disorder at room temperature. The CO32− ions are notable tilted and displaced from the equilibrium position of pure calcite.

regulates the expression and enzyme activity of 11␤-hydroxysteroid dehydrogenase type 1 in murine adipose tissue and 3T3-L1 adipocytes. Am J Physiol Endocrinol Metab 292: E1213-E1222, 2007. First published December 26, 2006; doi:10.1152/ajpendo.00340.2006.-A clinically employed antihyperlipidemic drug, bezafibrate, has been characterized as a PPAR(␣, -␥, and -␦) pan-agonist in vitro. Recent extended trials have highlighted its antidiabetic properties in humans. However, the underlying molecular mechanism is not fully elucidated. The present study was designed to explore potential regulatory mechanisms of intracellular glucocorticoid reactivating enzyme, 11␤-HSD1 and anti-diabetic hormone, adiponectin by bezafibrate in murine adipose tissue, and cultured adipocytes. Treatment of db/db mice with bezafibrate significantly ameliorated hyperglycemia and insulin resistance, accompanied by a marked reduction of triglyceride and nonesterified fatty acids. Despite equipotent in lipid-lowering effects, another fibrate, fenofibrate, did not show such beneficial effects on glycemic control. Treatment of bezafibrate caused a marked decrease in the mRNA level of 11␤-HSD1 preferentially in adipose tissue of db/db mice (Ϫ47%, P Ͻ 0.05), concomitant with a significant increase in plasma adiponectin level (ϩ37%, P Ͻ 0.01). Notably, treatment of bezafibrate caused a marked decrease in the mRNA level (Ϫ34%, P Ͻ 0.01) and enzyme activity (Ϫ32%, P Ͻ 0.01) of 11␤-HSD1, whereas the treatment substantially augmented the expression (ϩ71%, P Ͻ 0.01) and secretion (ϩ27%, P Ͻ 0.01) of adiponectin in 3T3-L1 adipocytes. Knockdown of 11␤-HSD1 by siRNA confirmed that 11␤-HSD1 acts as a distinct oxoreductase in adipocytes and validated the enzyme activity assays in the present study. Effects of bezafibrate on regulation of 11␤-HSD1 and adiponectin in murine adipocytes were comparable with those in thiazolidinediones. This is the first demonstration that bezafibrate directly regulates 11␤-HSD1 and adiponectin in murine adipocytes, both of which may contribute to metabolicallybeneficial effects by bezafibrate. metabolic syndrome; adiponectin FAMILY GENES of peroxisome proliferator-activated receptors (PPARs) are profoundly relevant to fuel homeostasis (14, 41). Agonists for PPAR␣ and PPAR␥ have been widely used for the treatment of dyslipidemia and type 2 diabetes (46). Recent research progress (3) has highlighted the potential usefulness of PPAR␣/␥ dual agonists or PPAR(␣, -␥, and -␦) pan-agonists for metabolic diseases. However, some of these compounds are reported to cause adverse effects, including carcinogenesis, edema, hepatotoxicity, and increase in body weight in rodent experiments (45). Bezafibrate has been widely used for the treatment of dyslipidemia in human clinics (11). Recent in vitro experiments have shown that bezafibrate serves as a pan-agonist for PPAR␣, -␥, and -␦ (9, 48). Furthermore, recent extended clinical trials (15, 43) have highlighted its antidiabetic properties. However, the underlying mechanism is not fully clarified...