Numerical Simulation and Analysis on the Phoenix Typhoon Rainstorm Using WRF
Rainstorm caused by the Typhoon Phoenix, between July 28th and 31st 2008, is studied by using the meso-scale numerical simulation model WRF and some NCEP reanalysis data of 1¡ã¡Á1¡ãwith 6h interval. Results show that, the distribution of the SLP, wind and rain belt was simulated successfully by the WRF model. The research shows that the strong upward motion at the 600 -700hPa and 100 -200hPa of 24¡ãN and two closure centers of near 21¡ãN-22¡ãN and 31¡ãN-33¡ãN at the high troposphere induced convective cloud cluster to develop.
Numerical study of the genesis and development of typhoon WUKONG (2000) over South China Sea
The Fifth generation NCAR/PSU mesoscale nonhydrostatic model(MM5) was used to simulate the process that a tropical disturbance developed into a strong typhoon WUKONG over the South China Sea in September 2000. The MM5 model could forecast the maximum wind and intensity of the typhoon with considerable accuracy. The natural developing characteristics of South China Sea Typhoon which involved step-by-step deepening and drastic strengthening were also well simulated. Based on some diagnostic variable analysis, the potential factors on typhoon structure as well as the genesis of typhoon eye were briefly analyzed. Sensitivity experiments on sea surface temperature (SST) effect indicate that the SST is of vital importance to the genesis and development of typhoon over South China Sea. If SST is degraded by 1 degree, the simulated typhoon would have a decrease of 10?m/s on maximum wind and a nearly seven-hour delay to reach typhoon level intensity (surpass 32.8?m/s). If SST is degraded by 2 degree (with SST still being between 26 and 27 degree), the initial tropical disturbance could hardly develop into typhoon.
Cytoplsmic uridine phosphorylase of rat liver. Characterization and kinetics.
Abstract Uridine phosphorylase (uridine:orthophosphate ribosyltransferase, EC 2.4.2.3) of rat liver cytoplasm has been purified 1900-fold. Initial velocity patterns of the phosphorolysis of uridine or deoxyuridine and of the synthesis of uridine indicated a sequential mechanism. Product inhibition patterns with uracil or ribose 1-phosphate as inhibitors were consistent with an "ordered Bi Bi" reaction in which inorganic phosphate is the first substrate to bind to the enzyme and ribose 1-phosphate the last product to leave the enzyme. The most highly purified enzyme fractions still retained uridine-, deoxyuridine-, and thymidine-cleaving activities in the ratio of 10:7:1 at pH 7.4. The fractions separated into a major and a minor band of protein on electrophoresis in phosphate buffer. Aging of the enzyme with loss of activity resulted in an increase in the proportion of the minor band. The pH optimum of the enzyme for uridine cleavage was 8.2, for deoxyuridine cleavage, 6.5, and for uridine synthesis, 8.5. Uridine or deoxyuridine synthesis was inhibited 50% in the presence of 1 mm uracil. The enzyme did not catalyze the direct transfer of ribose from uridine to uracil in the absence of phosphate. Uridine protected the enzyme to a greater degree than phosphate against inhibition by o-iodosobenzoate. Thus, at least one sulfhydryl group and possibly three are present at or near the active site. Uridine cleavage, uridine synthesis, and deoxyuridine cleavage were inhibited by deoxyglucosylthymine. The phosphorolysis of deoxyuridine and thymidine by thymidine phosphorylase, also purified from rat liver cytoplasm, was not inhibited by deoxyglucosylthymine. The molecular weights of both uridine and thymidine phosphorylases were estimated to be 110,000.