Monitoring the gasification area and its behavior in underground coal gasification by acoustic emission technique instead of temperature measurement.

Underground Coal Gasification (UCG) requires monitoring of the gasification area because the gasification process is invisible and the reaction temperature exceeds 1000 °C. Many fracturing events that occurred due to coal heating can be captured with Acoustic Emission (AE) monitoring technique during UCG. However, the temperature conditions to generate fracturing events during UCG have not yet been clarified. Therefore, the coal heating experiment and small-scale UCG experiment are conducted by measuring the temperature and AE activities in this research to examine the applicability of the AE technique instead of temperature measurement as a monitoring method during UCG. As a result, many fracturing events are generated when the temperature of coal is changed drastically, especially during coal gasification. Besides, AE events increase in the sensor near the heat source and AE sources are expanded widely with the expansion of the high-temperature region. AE monitoring is an effective technique for the estimation of the gasification area during UCG instead of temperature monitoring.

Identification and targeted disruption of the mouse gene encoding ESG1 (PH34/ECAT2/DPPA5).

BACKGROUND: Embryonic stem cell-specific gene (ESG) 1, which encodes a KH-domain containing protein, is specifically expressed in early embryos, germ cells, and embryonic stem (ES) cells. Previous studies identified genomic clones containing the mouse ESG1 gene and five pseudogenes. However, their chromosomal localizations or physiological functions have not been determined. RESULTS: A Blast search of mouse genomic databases failed to locate the ESG1 gene. We identified several bacterial artificial clones containing the mouse ESG1 gene and an additional ESG1-like sequence with a similar gene structure from chromosome 9. The ESG1-like sequence contained a multiple critical mutations, indicating that it was a duplicated pseudogene. The 5' flanking region of the ESG1 gene, but not that of the pseudogene, exhibited strong enhancer and promoter activity in undifferentiated ES cells by luciferase reporter assay. To study the physiological functions of the ESG1 gene, we replaced this sequence in ES cells with a beta-geo cassette by homologous recombination. Despite specific expression in early embryos and germ cells, ESG1-/- mice developed normally and were fertile. We also generated ESG1-/- ES cells both by a second independent homologous recombination and directly from blastocysts derived from heterozygous intercrosses. Northern blot and western blot analyses confirmed the absence of ESG1 in these cells. These ES cells demonstrated normal morphology, proliferation, and differentiation. CONCLUSION: The mouse ESG1 gene, together with a duplicated pseudogene, is located on chromosome 9. Despite its specific expression in pluripotent cells and germ cells, ESG1 is dispensable for self-renewal of ES cells and establishment of germcells.