Elasticity of diopside CaMgSi(2)O(6) measured by means of the resonant sphere technique, RST

Resonant frequencies for a single crystad diopside sphere are measured accurately and rhirteen elastic moduli are reluced by the least squares calculation, A set of mduli gives theoretical resonant frequencies close enough to the observed ones

Ferroelectric property of an epitaxial lead zirconate titanate thin film deposited by a hydrothermal method

Deposition of thin films via hydrothermal method has various advantages: low deposition temperature, high purity, deposition on a three-dimensional structure,and a large thickness. Although an epitaxial lead zirconate titanate (PZT) thin-film deposition has been reported, the ferroelectric measurement has not been conducted due to the peel-off morphology of the film. The current paper investigates the improvement of an epitaxial PZT thin film deposited via a hydrothermal method. By adjusting the position at which the substrate was suspended in the solution, smooth morphology surface was successfully obtained. As a bottom electrode, a 200-nm SrRuO3 thin film was deposited on SrTiO3 single crystals, and the PZT thin film was deposited on SrRuO3. The remanent polarization 2Pr and coercive electric field for PZT on SrRuO3/SrTiO3 (001) were 17.1 μC/cm2 and 36 kV/cm, respectively, and those of PZT on SrRuO3/SrTiO3 (111) were 32.7 μC/cm2 and 59 kV/cm, respectively. The reason for large imprint electrical field, 91 kV/cm and 40 kV/cm for each film, was unclear at this stage, although it is associated with self-alignment poling direction. This self-alignment poling direction was confirmed via scanning nonlinear dielectric microscopy and is thought to have been related to the deposition mechanism

Potential role of group X secretory phospholipase A2 in cyclooxygenase-2-dependent PGE2 formation during colon tumorigenesis

AbstractAlthough the cyclooxygenase-2 (COX-2) pathway of the arachidonic acid cascade has been suggested to play an important role in colon carcinogenesis, there is little information concerning the identity of phospholipase A2 (PLA2) involved in the arachidonic acid release in colon tumors. Here, we compared the potencies of three types of secretory PLA2s (group IB, IIA and X sPLA2s) for the arachidonic acid release from cultured human colon adenocarcinoma cells, and found that group X sPLA2 has the most powerful potency in the release of arachidonic acid leading to COX-2-dependent prostaglandin E2 (PGE2) formation. Furthermore, immunohistological analysis revealed the elevated expression of group X sPLA2 in human colon adenocarcinoma neoplastic cells in concert with augmented expression of COX-2. These findings suggest a critical role of group X sPLA2 in the PGE2 biosynthesis during colon tumorigenesis

Genetic Deletion of Vasohibin-2 Exacerbates Ischemia-Reperfusion-Induced Acute Kidney Injury

Acute kidney injury (AKI) has been increasingly recognized as a risk factor for transition to chronic kidney disease. Recent evidence suggests that endothelial damage in peritubular capillaries can accelerate the progression of renal injury. Vasohibin-2 (VASH2) is a novel proangiogenic factor that promotes tumor angiogenesis. However, the pathophysiological roles of VASH2 in kidney diseases remain unknown. In the present study, we examined the effects of VASH2 deficiency on the progression of ischemia-reperfusion (I/R) injury-induced AKI. I/R injury was induced by bilaterally clamping renal pedicles for 25 min in male wild-type (WT) andVash2homozygous knockout mice. Twenty-four hours later, I/R injury-induced renal dysfunction and tubular damage were more severe in VASH2-deficient mice than in WT mice, with more prominent neutrophil infiltration and peritubular capillary loss. After induction of I/R injury, VASH2 expression was markedly increased in injured renal tubules. These results suggest that VASH2 expression in renal tubular epithelial cells might be essential for alleviating I/R injury-induced AKI, probably through protecting peritubular capillaries and preventing inflammatory infiltration

Luteal blood flow in patients undergoing GnRH agonist long protocol

<p>Abstract</p> <p>Background</p> <p>Blood flow in the corpus luteum (CL) is closely related to luteal function. It is unclear how luteal blood flow is regulated. Standardized ovarian-stimulation protocol with a gonadotropin-releasing hormone agonist (GnRHa long protocol) causes luteal phase defect because it drastically suppresses serum LH levels. Examining luteal blood flow in the patient undergoing GnRHa long protocol may be useful to know whether luteal blood flow is regulated by LH.</p> <p>Methods</p> <p>Twenty-four infertile women undergoing GnRHa long protocol were divided into 3 groups dependent on luteal supports; 9 women were given ethinylestradiol plus norgestrel (Planovar) orally throughout the luteal phase (control group); 8 women were given HCG 2,000 IU on days 2 and 4 day after ovulation induction in addition to Planovar (HCG group); 7 women were given vitamin E (600 mg/day) orally throughout the luteal phase in addition to Planovar (vitamin E group). Blood flow impedance was measured in each CL during the mid-luteal phase by transvaginal color-pulsed-Doppler-ultrasonography and was expressed as a CL-resistance index (CL-RI).</p> <p>Results</p> <p>Serum LH levels were remarkably suppressed in all the groups. CL-RI in the control group was more than the cutoff value (0.51), and only 2 out of 9 women had CL-RI values < 0.51. Treatments with HCG or vitamin E significantly improved the CL-RI to less than 0.51. Seven of the 8 women in the HCG group and all of the women in the vitamin E group had CL-RI < 0.51.</p> <p>Conclusion</p> <p>Patients undergoing GnRHa long protocol had high luteal blood flow impedance with very low serum LH levels. HCG administration improved luteal blood flow impedance. This suggests that luteal blood flow is regulated by LH.</p