Induced seismicity in the Castarthao reservoir, NE Brazil - Preliminary results

The Castanhao reservoir was built in the state of Ceara, a dry region in Northeastern Brazil, to regulate the flow of the Jaguaribe River, for irrigation, and for power generation. It is an earth-filled dam, 60 m high, with a water capacity of 4.5 x 10(9) m(3). The seismicity in the area has been monitored since 1998, with a few interruptions, using one analog or one digital station and, during a few periods, a three-station network. The first earthquakes likely to be induced events were detected in 2003, when the water level was about 20 in high. In early 2004 a very heavy rainfall season quickly filled the reservoir. Shortly after, an increase in the seismic activity occurred and many micro-earthquakes were recorded. We suggest that this activity resulted from an increase in pore pressure due to undrained response. Therefore, we may classify this cluster of microearthquakes as ""initial seismicity."" We deployed a network with four analog stations in the area, following this activity, to determine the epicentral zone. At least three epicentral areas under the reservoir were detected. The spatio-temporal analysis of the available data revealed that the seismicity occurs in clusters and that these were activated at different periods. We identified four sets of faults (N-S-, E-W-, NW-SE-, and NE-SW-oriented), some of which moved in shallow crustal levels and as recently as the Quaternary (1.8 Ma). Under the present-day stress regime, the last two sets moved as strike-slip structures. We suggest a possible correlation between dormant faults and the observed induced seismicity. (c) 2008 Elsevier B.V. All rights reserved.

Clinical and molecular delineation of the 17q21.31 microdeletion syndrome

Background: The chromosome 17q21.31 microdeletion syndrome is a novel genomic disorder that has originally been identified using high resolution genome analyses in patients with unexplained mental retardation. Aim: We report the molecular and/or clinical characterisation of 22 individuals with the 17q21.31 microdeletion syndrome. Results: We estimate the prevalence of the syndrome to be 1 in 16 000 and show that it is highly underdiagnosed. Extensive clinical examination reveals that developmental delay, hypotonia, facial dysmorphisms including a long face, a tubular or pear-shaped nose and a bulbous nasal tip, and a friendly/amiable behaviour are the most characteristic features. Other clinically important features include epilepsy, heart defects and kidney/urologic anomalies. Using high resolution oligonucleotide arrays we narrow the 17q21.31 critical region to a 424 kb genomic segment (chr17: 41046729-41470954, hg17) encompassing at least six genes, among which is the gene encoding microtubule associated protein tau (MAPT). Mutation screening of MAPT in 122 individuals with a phenotype suggestive of 17q21.31 deletion carriers, but who do not carry the recurrent deletion, failed to identify any disease associated variants. In five deletion carriers we identify a <500 bp rearrangement hotspot at the proximal breakpoint contained within an L2 LINE motif and show that in every case examined the parent originating the deletion carries a common 900 kb 17q21.31 inversion polymorphism, indicating that this inversion is a necessary factor for deletion to occur (p< 10(25)). Conclusion: Our data establish the 17q21.31 microdeletion syndrome as a clinically and molecularly well recognisable genomic disorder.