Objective To develop a method for determination of trace organic pollutants in drinking water. Methods The organic pollutants in water were enriched and separated by a solid-phase extraction method with the big form resin of hole pattern as the enrichment of stationary phase and then were detected by GC-MS. Results The ideal test condition and the enriched method of sample were established in the present paper. Many water samples were determined by the newly established method. Over 100 organic pollutants were identified in these samples. Conclusion The newly established method is simple, fast, sensitive and easy to popularize and is suitable for determining organic chemical compounds in tap water, clean underground water and the water of source water.

Objective To investigate the association of the major histocompatibility complex class Ⅰ chain-related antigens A (MICA)-129 gene polymorphism and soluble MICA (sMICA) levels with ulcerative colitis (UC) in Hubei Han nationality. Methods The genetic polymorphism of MICA-129 was examined using a polymerase chain reaction-sequence based test (PCR-SBT) in 256 UC patients and 460 healthy controls. From the above subjects, 80 patients and 90 healthy individuals were randomly selected for determining serum sMICA concentrations by ELISA. Results The frequencies of variant allele (G) and genotype (GG) in MICA-129 gene were significantly higher in the UC patients than in the controls(76. 8%vs 72. 2%, P =0. 060; 55.9% vs 46. 3% ,P =0. 016). Serum sMICA levels were significantly elevated in the patients compared to the controls[(576. 47 ±279. 02) ng/L vs( 182. 17 ±73. 11 ) ng/L,P ＜0. 001]. In addition, the sMICA levels were higher in the patients carrying MICA-129 GG genotypes than in those carrying ( GA + AA) genotypes [( 638. 87 ± 347. 15 ) ng/L vs ( 507. 51 ± 152. 87 ) ng/L, P = 0. 035].Conclusions The genetic polymorphism of MICA-129 and sMICA levels are correlated with the UC patients in Hubei Han nationality. Our findings demonstrate that MICA-129 gene may contribute to the pathogenesis of UC.

Abnormally activated CDK9 participates in the super-enhancer mediated transcription of short-lived proteins required for cancer cell survival. Targeting CDK9 has shown potent anti-tumor activity in clinical trials among different cancers. However, the study and knowledge on drug resistance to CDK9 inhibitors are very limited. In this study, we established an AML cell line with acquired resistance to a highly selective CDK9 inhibitor BAY1251152. Through genomic sequencing, we identified in the kinase domain of CDK9 a mutation L156F, which is also a coding SNP in the CDK9 gene. By knocking in L156F into cancer cells using CRISPR/Cas9, we found that single CDK9 L156F could drive the resistance to CDK9 inhibitors, not only ATP competitive inhibitor but also PROTAC degrader. Mechanistically, CDK9 L156F disrupts the binding with inhibitors due to steric hindrance, further, the mutation affects the thermal stability and catalytic activity of CDK9 protein. To overcome the drug resistance mediated by the CDK9-L156F mutation, we discovered a compound, IHMT-CDK9-36 which showed potent inhibition activity both for CDK9 WT and L156F mutant. Together, we report a novel resistance mechanism for CDK9 inhibitors and provide a novel chemical scaffold for the future development of CDK9 inhibitors.