Electrical anisotropy of gas hydrate-bearing sand reservoirs in the Gulf of Mexico

We present new results and interpretations of the electrical anisotropy and reservoir architecture in gas hydrate-bearing sands using logging data collected during the Gulf of Mexico Gas Hydrate Joint Industry Project Leg II. We focus specifically on sand reservoirs in Hole Alaminos Canyon 21 A (AC21-A), Hole Green Canyon 955 H (GC955-H) and Hole Walker Ridge 313 H (WR313-H). Using a new logging-while-drilling directional resistivity tool and a one-dimensional inversion developed by Schlumberger, we resolve the resistivity of the current flowing parallel to the bedding, R‖ and the resistivity of the current flowing perpendicular to the bedding, R⊥. We find the sand reservoir in Hole AC21-A to be relatively isotropic, with R‖ and R⊥ values close to 2 Ω m. In contrast, the gas hydrate-bearing sand reservoirs in Holes GC955-H and WR313-H are highly anisotropic. In these reservoirs, R‖ is between 2 and 30 Ω m, and R⊥ is generally an order of magnitude higher. Using Schlumberger’s WebMI models, we were able to replicate multiple resistivity measurements and determine the formation resistivity the gas hydrate-bearing sand reservoir in Hole WR313-H. The results showed that gas hydrate saturations within a single reservoir unit are highly variable. For example, the sand units in Hole WR313-H contain thin layers (on the order of 10–100 cm) with varying gas hydrate saturations between 15 and 95%. Our combined modeling results clearly indicate that the gas hydrate-bearing sand reservoirs in Holes GC955-H and WR313-H are highly anisotropic due to varying saturations of gas hydrate forming in thin layers within larger sand units

Endurance exercise accelerates myocardial tissue oxygenation recovery and reduces ischemia reperfusion injury in mice

Exercise training offers cardioprotection against ischemia and reperfusion (I/R) injury. However, few essential signals have been identified to underscore the protection from injury. In the present study, we hypothesized that exercise-induced acceleration of myocardial tissue oxygenation recovery contributes to this protection. C57BL/6 mice (4 weeks old) were trained on treadmills for 45 min/day at a treading rate of 15 m/min for 8 weeks. At the end of 8-week exercise training, mice underwent 30-min left anterior descending coronary artery occlusion followed by 60-min or 24-h reperfusion. Electron paramagnetic resonance oximetry was performed to measure myocardial tissue oxygenation. Western immunoblotting analyses, gene transfection, and myography were examined. The oximetry study demonstrated that exercise markedly shortened myocardial tissue oxygenation recovery time following reperfusion. Exercise training up-regulated Kir6.1 protein expression (a subunit of ATP-sensitive K(+)channel on vascular smooth muscle cells, VSMC sarc-K(ATP)) and protected the heart from I/R injury. In vivo gene transfer of dominant negative Kir6.1AAA prolonged the recovery time and enlarged infarct size. In addition, transfection of Kir6.1AAA increased the stiffness and reduced the relaxation capacity in the vasculature. Together, our study demonstrated that exercise training up-regulated Kir6.1, improved tissue oxygenation recovery, and protected the heart against I/R injury. This exercise-induced cardioprotective mechanism may provide a potential therapeutic intervention targeting VSMC sarc-K(ATP) channels and reperfusion recovery

PDU with Integrated Cable Management Support

Cable management within a datacenter rack has become critical as rack densities continue to increase, and additional quantities of Power Distribution Units (PDU) are being installed in a rack thus resulting in less area to route and secure cables. A standard 1075mm deep rack has one PDU mounting bracket per side to mount vertical PDUs which often also gets utilized for cable management, and in some circumstances cables are even secured to the rack frame members

Little White Houses: How the Postwar Home Constructed Race in America

Book Review of Little White Houses: How the Postwar Home Constructed Race in America by Dianne Harris. Reviewed by Keli E. Rylance

Architecture Depends

Book Review of Architecture Depends / Jeremy Till.--ISBN: 978-0-262-01253-9. Reviewed by Keli E. Rylance

Precise Measurements of Branching Fractions for Ds+D_s^+ Meson Decays to Two Pseudoscalar Mesons

We measure the branching fractions for seven $D_{s}^{+}$ two-body decays to pseudo-scalar mesons, by analyzing data collected at $\sqrt{s}=4.178\sim4.226$ GeV with the BESIII detector at the BEPCII collider. The branching fractions are determined to be $\mathcal{B}(D_s^+\to K^+\eta^{\prime})=(2.68\pm0.17\pm0.17\pm0.08)\times10^{-3}$, $\mathcal{B}(D_s^+\to\eta^{\prime}\pi^+)=(37.8\pm0.4\pm2.1\pm1.2)\times10^{-3}$, $\mathcal{B}(D_s^+\to K^+\eta)=(1.62\pm0.10\pm0.03\pm0.05)\times10^{-3}$, $\mathcal{B}(D_s^+\to\eta\pi^+)=(17.41\pm0.18\pm0.27\pm0.54)\times10^{-3}$, $\mathcal{B}(D_s^+\to K^+K_S^0)=(15.02\pm0.10\pm0.27\pm0.47)\times10^{-3}$, $\mathcal{B}(D_s^+\to K_S^0\pi^+)=(1.109\pm0.034\pm0.023\pm0.035)\times10^{-3}$, $\mathcal{B}(D_s^+\to K^+\pi^0)=(0.748\pm0.049\pm0.018\pm0.023)\times10^{-3}$, where the first uncertainties are statistical, the second are systematic, and the third are from external input branching fraction of the normalization mode $D_s^+\to K^+K^-\pi^+$. Precision of our measurements is significantly improved compared with that of the current world average values

Notch3 Is Dispensable for Thymocyte β-Selection and Notch1-Induced T Cell Leukemogenesis

Notch1 (N1) signaling induced by intrathymic Delta-like (DL) ligands is required for T cell lineage commitment as well as self-renewal during “β-selection” of TCRβ+ CD4−CD8− double negative 3 (DN3) T cell progenitors. However, over-expression of the N1 intracellular domain (ICN1) renders N1 activation ligand-independent and drives leukemic transformation during β-selection. DN3 progenitors also express Notch3 (N3) mRNA, and over-expression of ligand-independent mutant N3 (ICN3) influences β-selection and drives T cell leukemogenesis. However, the importance of ligand-activated N3 in promoting β-selection and ICN1-induced T cell leukemogenesis has not been examined. To address these questions we generated mice lacking functional N3. We confirmed that DN3 progenitors express N3 protein using a N3-specific antibody. Surprisingly however, N3-deficient DN3 thymocytes were not defective in generating DP thymocytes under steady state conditions or in more stringent competition assays. To determine if N3 co-operates with N1 to regulate β-selection, we generated N1;N3 compound mutants. However, N3 deficiency did not exacerbate the competitive defect of N1+/− DN3 progenitors, demonstrating that N3 does not compensate for limiting N1 during T cell development. Finally, N3 deficiency did not attenuate T cell leukemogenesis induced by conditional expression of ICN1 in DN3 thymocytes. Importantly, we showed that in contrast to N1, N3 has a low binding affinity for DL4, the most abundant intrathymic DL ligand. Thus, despite the profound effects of ectopic ligand-independent N3 activation on T cell development and leukemogenesis, physiologically activated N3 is dispensable for both processes, likely because N3 interacts poorly with intrathymic DL4