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A series of environmentalegeological problems have been caused by over-exploitation of deep groundwater (i.e., confined aquifer water) in the North China Plain. In order to better understand the status of deep groundwater over-exploitation and the resultant environmentalegeological problems on a regional scale, the over-exploitation of groundwater has been assessed by way of the groundwater exploitation potential coefficient (i.e., the ratio of exploitable amount of deep groundwater to current exploitation), cumulative land subsidence, and long-term average lowering rate of the groundwater table. There is a good correlation among the results calculated by the different methods. On a regional scale, deep groundwater has been over-exploited and there is no further exploitation potential under the current conditions. The groundwater exploitation degree index takes the exploitation in 2003 as the reference for the calculations, so the results mainly reflect the degree of current groundwater exploitation. The results of over-exploitation of deep groundwater obtained by land subsidence data and long-term average rate of depression of the water table mainly reflect environmentalegeological problems caused by exploitation of deep groundwater. ª 2011, China University of Geosciences (Beijing) and Peking University. Production and hosting by Elsevier B.V. All rights reserved.

Objective To identify rheumatoid arthritis (RA)-associated susceptibility genes and pathways through integrating genome-wide association study (GWAS) and gene expression profile data. Methods A transcriptome-wide association study (TWAS) was conducted by the FUSION software for RA considering EBV-transformed lymphocytes (EL), transformed fibroblasts (TF), peripheral blood (NBL), and whole blood (YBL). GWAS summary data was driven from a large-scale GWAS, involving 5539 autoantibody-positive RA patients and 20,169 controls. The TWAS-identified genes were further validated using the mRNA expression profiles and made a functional exploration. Results TWAS identified 692 genes with PTWAS values < 0.05 for RA. CRIPAK (PEL = 0.01293, PTF = 0.00038, PNBL = 0.02839, PYBL = 0.0978), MUT (PEL = 0.00377, PTF = 0.00076, PNBL = 0.00778, PYBL = 0.00096), FOXRED1 (PEL = 0.03834, PTF = 0.01120, PNBL = 0.01280, PYBL = 0.00583), and EBPL (PEL = 0.00806, PTF = 0.03761, PNBL = 0.03540, PYBL = 0.04254) were collectively expressed in all the four tissues/cells. Eighteen genes, including ANXA5, AP4B1, ATIC (PTWAS = 0.0113, downregulated expression), C12orf65, CMAH, PDHB, RUNX3 (PTWAS = 0.0346, downregulated expression), SBF1, SH2B3, STK38, TMEM43, XPNPEP1, KIAA1530, NUFIP2, PPP2R3C, RAB24, STX6, and TLR5 (PTWAS = 0.04665, upregulated expression), were validated with integrative analysis of TWAS and mRNA expression profiles. TWAS-identified genes functionally involved in endoplasmic reticulum organization, regulation of cytokine production, TNF signaling pathway, immune response-regulating signaling pathway, regulation of autophagy, etc. Conclusion We identified multiple candidate genes and pathways, providing novel clues for the genetic mechanism of RA.