Diamond anvil cells (DAC) coupled with x-ray diffraction (XRD) measurements are one of the primary techniques for investigating structural stability of materials at high pressure-temperature (P-T) conditions. DAC-XRD has been predominantly used to resolve structural information at set P-T conditions and, consequently, provides P-T phase diagram information on a broad range of materials. With advances in large scale synchrotron x-ray facilities and corresponding x-ray diagnostic capabilities, it is now becoming possible to perform sub-second time resolved measurements on micron sized DAC samples. As a result, there is an opportunity to gain valuable information about the kinetics of structural phase transformations and extend our understanding of material behavior at high P-T conditions. Using DAC-XRD time resolved measurements, we have investigated the kinetics of the α to ω transformation in zirconium. We observe a clear time and pressure dependence in the martensitic α-ω transition as a function of pressure-jump, i.e., drive pressure. The resulting data are fit using available kinetics models, which can provide further insight into transformation mechanism that influence transformation kinetics. Our results help shed light on the discrepancies observed in previous measurements of the α-ω transition pressure in zirconium.

The dependence of the Curie temperature T Curie on nearly hydrostatic pressure has been determined to 17.2 GPa for the weak itinerant ferromagnetic SrRuO 3 in both polycrystalline and single-crystalline form. T Curie is found to decrease under pressure from 162 K to 42.7 K at 17.2 GPa in nearly linear fashion at the rate dT Curie /dP ≃ −6.8 K/GPa. No superconductivity was found above 4 K in the pressure range 17 to 34 GPa. Room-temperature Xray diffraction studies to 25.2 GPa reveal no structural phase transition but indicate that the average Ru-O-Ru bond angle β passes through a minimum near 15 GPa. The bulk modulus and its pressure derivative were determined to be B o = 192(3) GPa and B ′ o = 5.0(3), respectively. Parallel ac susceptibility studies on polycrystalline CaRuO 3 at 6 and 8 GPa prsesure found no evidence for either ferromagnetism or superconductivity above 4 K.

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Tuberous sclerosis complex (TSC) is a dominantly inherited multisystem disorder resulting in the development of hamartomatous growths in many organs. Genetic heterogeneity has been demonstrated linking the familial cases to either TSC1 at 9q34.3, or TSC2 at 16p13.3. About two-thirds of the TSC cases are sporadic and appear to represent new mutations. While both genes are thought to account for all familial cases, with each representing approximately 50% of the mutations, the proportion of sporadic cases with mutations in TSC1 and TSC2 is yet to be determined. We have examined the entire coding sequence of the TSC2 gene in 20 familial and 20 sporadic cases and identified a total of twenty-one mutations representing 50% and 55% of familial and sporadic cases respectively. Our rate of mutation detection is significantly higher than other published reports. Twenty out of 21 mutations are novel and include 6 missense, 6 nonsense, 5 frameshifts, 2 splice alterations, a 34 bp deletion resulting in abnormal splicing, and an 18 bp deletion which maintains the reading frame. The mutations are distributed throughout the coding sequence with no specific hot spots. There is no apparent correlation between mutation type and clinical severity of the disease. Our results document that at least 50% of sporadic cases arise from mutations in the TSC2 gene. The location of the mutations described here, particularly the missense events, should be valuable for further functional analysis of this tumor suppressor protein.