Aim To establish a gefitinib-resistant NSCLC cell line, and observe its pharmacological properties. Methods HCC827 cells were treated with hepatocyte growth factor( HGF) and increasing concen-tration of gefitinib to induce cell resistance. MTT assay was used to test cell viability and chemosensitivity. Clone formation and Edu staining were used to verify the inhibitory effect of gefitinib on cell growth. qRT-PCR and Western blot were used to assay the expres-sion of c-Met. Results The use of HGF greatly short-ened the induction time of HCC827GR resistant cells. gefitinib could significantly suppress cell viability, col-ony formation and cell proliferation of HCC827 , but had a weaker inhibitory effect on HCC827GR cells. HCC827GR overexpressed c-Met protein, and was highly sensitive to c-Met inhibitors. Conclusion The gefitinib-resistant HCC827 GR cells were induced suc-cessfully and efficiently. The growth of HCC827GR is dependent on the activity of c-Met protein, and it can be used as a phenotypic screening model of c-Met in-hibitors.

OBJECTIVE:To study the affinity of penehyclidine optical isomers to muscarinic(M)receptor subtypes,and pro-vide reference for revealing the action targets and efficacy selectivity of penehyclidine. METHODS:Homology modeling,molecu-lar docking and other molecular simulation technologies were used to analyze and predict the binding energy of 4 optical isomers to M receptor subtypes and judge its affinity by comparing the binding energy of different optical isomers R1 (3R,2′R),R2 (3R, 2′S),S1(3S,2′R),S2(3S,2′S)with M receptor subtypes M1-M5. RESULTS:All the 4 optical isomers can dock into the ac-tive sites of M receptor subtypes,and different optical isomers showed great differences in the molecular docking with different M receptor subtypes. Penehyclidine isomers showed larger binding energy to M3,the binding energy of 4 optical isomers ranged in 5736.519-5907.143 kcal/mol. The binding energy of R1 to M1 was 1190.041 kcal/mol;while those of other optical isomers to each receptor subtype were lower or negative. CONCLUSIONS:R1 shows the affinity to M1 receptor. And all the 4 optical isomer show the affinity to M3.

Aim To study the pharmacodynamics of antianxietic compound prescription capsule ( ACPC ) on acute stress in rats and the influence upon the ex-pression of ERK/CREB signal pathway and brain-de-rived neurotrophic factor ( BDNF) in the cerebral cor-tex and hippocampus of rats. Methods The elevated plus maze ( EPM ) test was applied to observe the effects of ACPC on acute stress rats administered 7 d low-, medium- and high-dose ( 0. 75 , 1. 5 , 3 g · kg-1 ) . The expression of ERK/CREB signal pathway and BDNF in the cerebral cortex and hippocampus of rats were studied by using Western blot method. Re-sults In EPM, high-dose of ACPC increased signifi-cantly the rat open arm time ( OT%) ( P<0 . 05 ) and the percentage of open arm entries ( OE%) ( P <0. 05). In Western blot, the medium-dose of ACPC reduced significantly p-ERK1/2 expression in hippo-campus ( P <0. 05 ) , and high-dose group decreased significantly the expression of p-ERK1/2 and p-CREB in the cortex and hippocampus of rats ( P <0. 05 ) . High-dose group increased significantly the expression of BDNF in the cortex and hippocampus of rats ( P<0. 05 , P<0. 01 ) . Conclusion ACPC has anti-anxie-ty effect in the model of EPM, and its mechanism may be related to the ERK/CREB signal pathway and in-creased BDNF expression.

OBJECTIVETo determine the genetic cause of an infant with multiple congenital anomalies.

METHODSRoutine karyotype analysis and chromosome microarray analysis (CMA) were carried out for the infant and her parents.

RESULTSCMA has detected a 9.3 Mb duplication at 9q34.11-q34.3. G-banding analysis suggested that the infant has a 46,XX,der(1)add(1)(p34.1) karyotype, while her father was 46, XY, t(1,9)(p36.3;q34.1). Fluorescence in situ hybridization (FISH) analysis confirmed that the 9q34 duplication has derived from the balanced translocation carried by the father.

CONCLUSIONA 9.3 Mb duplication was detected within the 9q34 region in an infant featuring multiple congenital anomalies. CMA and FISH have enabled detection of this duplication and facilitated genetic counseling and prevention of birth of further affected offspring.