Experimental and theoretical investigations of adsorption hysteresis and criticality in MCM-41: Studies with O-2, Ar, and CO2

MCM-41 materials of six different pore diameters were prepared and characterized using X-ray diffraction, transmission electron microscopy, helium pycnometry, small-angle neutron scattering, and gas adsorption (argon at 77.4 and 87.4 K, nitrogen and oxygen at 77.4 K, and carbon dioxide at 194.6 K). A recent molecular continuum model of the authors, previously used for adsorption of nitrogen at 77.4 K, was applied here for adsorption of argon, oxygen, and carbon dioxide. While model predictions of single-pore adsorption isotherms for argon and oxygen are in satisfactory agreement with experimental data, significant deviation was found for carbon dioxide, most likely due to its high quadrupole moment. Predictions of critical pore diameter, below which reversible condensation occurs: were possible by the model and found to be consistent with experimental estimates, for the adsorption of the various gases. On the other hand, existing models such as the Barrett-Joyner-Halenda (BJH), Saito-Foley, and Dubinin-Astakhov models were found to be inadequate, either predicting an incorrect pore diameter or not correlating the isotherms adequately. The wall structure of MCM-41 appears to be close to that of amorphous silica, as inferred from our skeletal density measurements.

Microsatellite instability and loss of heterozygosity at DNA mismatch repair gene loci occurs during hepatic carcinogenesis

DNA mismatch repair is an important mechanism involved in maintaining the fidelity of genomic DNA. Defective DNA mismatch repair is implicated in a variety of gastrointestinal and other turners; however, its role in hepatocellular carcinoma (HCC) has not been assessed. Formalin-fixed, paraffin-embedded archival pathology tissues from 46 primary liver tumors were studied by microdissection and microsatellite analysis of extracted DNA to assess the degree of microsatellite instability, a marker of defective mismatch repair, and to determine the extent and timing of allelic loss of two DNA mismatch repair genes, human Mut S homologue-2 (hMSH2) and human Mut L homologue-1 (hMLH1), and the tumor suppressor genes adenomatous polyposis coli gene (APC), p53, and DPC4. Microsatellite instability was detected in 16 of the tumors (34.8%). Loss of heterozygosity at microsatellites linked to the DNA mismatch repair genes, hMSH2 and/or hMLH1, was found in 9 cases (19.6%), usually in association with microsatellite instability. Importantly, the pattern of allelic loss was uniform in 8 of these 9 tumors, suggesting that clonal loss had occurred. Moreover, loss at these loci also occurred in nonmalignant tissue adjacent to 4 of these tumors, where it was associated with marked allelic heterogeneity. There was relatively infrequent loss of APC, p53, or DPC4 loci that appeared unrelated to loss of hMSH2 or hMLH1 gene loci. Loss of heterozygosity at hMSH2 and/or hMLH1 gene loci, and the associated microsatellite instability in premalignant hepatic tissues suggests a possible causal role in hepatic carcinogenesis in a subset of hepatomas.

Parallel simulation system for earthquake generation: Fault analysis modules and parallel coupling analysis

Solid earth simulations have recently been developed to address issues such as natural disasters, global environmental destruction and the conservation of natural resources. The simulation of solid earth phenomena involves the analysis of complex structures including strata, faults, and heterogeneous material properties. Simulation of the generation and cycle of earthquakes is particularly important, but such simulations require the analysis of complex fault dynamics. GeoFEM is a parallel finite-element analysis system intended for solid earth field phenomena problems. This paper describes recent development in the GeoFEM project for the simulation of earthquake generation and cycles.