Objective To set up traumatic brain injury(TBI)in rats by the improved device of FEENEY ’s weight dropping model and to ex?plore the spirit behavioral changes of mental disorders caused by TBI. Methods SD rats were randomly divided into normal control group(normal group,n=10),traumatic brain injury group(TBI group,n=10)and sham group(n=10). The improved device of FEENEY’s method was ad?opted to establish rat TBI model. For the following 15 days after TBI,open?field(OF)and forced swimming(FS)tests were carried out and the be?havior of the TBI rats within 5 minutes were recorded,the behavioral indexes,such as distance moved total(DMT),velocity mean(VM)and immo?bility time total(ITT),were analyzed. With above experiments,rats' fear response to environment,high alertness and anxiety and depression be?havior were evaluated. Results DMT and VM of TBI group rats(1 228.10±204.97 cm,4.09±0.68 cm/s)were significantly lower than those of the normal group(2 022.32±280.92 cm,7.28±1.80 cm/s)or sham group(1 660.01±332.09 cm,5.53±1.10 cm/s)(P<0.05).The ITT of TBI group (149.88±27.36 s,P<0.05)was longer than that of the normal group(106.10±29.03 s)or sham group(120.55±22.31 s)significantly(P<0.05). Conclusion TBI leads to rats' abnormal emotional and behavioral response.

Objective To Evaluate the performance of serum adenosine deaminase assays of different manufacturers and explore the approach for harmonization of test results.Methods It was evaluated the indice including the limit of blank ,precision,linearity range and reference interval of 10 test systems.It was as the reference system by Mindray test system to evaluate the comparability and the difference of ADA results among 10 different systems.The evaluation was performed before and after calibration by a selected fresh serum assigned by the reference system.A commercial calibrator of the minimum matrix effect was selected from 8 different calibrators as the long-term calibrator to harmonize the ADA results of 10 systems.Results The results of LoB were 0.1-6.3 U/L,respectively.The within-run CVs and total CVs of 10 systems were all less than 5%and actual linearity ranges were conformed to claims of manufacturers.After calibration with fresh serum calibrator ,the averaged difference of 10 test systems was reduced from 14% to 3.0%, and the average difference was 1.8% after calibration with long-term calibrator.The common reference interval of all test systems was 5-24 U/L identically.Conclusions The comparability of ADA measurements can be improved by using a common human serum calibrator and the commutable commercial calibrator.And it is necessary and feasible to develop the standardzation of ADA.

Objective To establish a method for quality control of xinshuaining mixture. Methods The herbal contents including red ginseng,milk veteh,root of red rooted salvia were identified by thin layer chromatography ( TLC) and the content of ginsenoside Rb1 in xinshuaining mixture was determined by high performance liquid chromatography ( HPLC ) . Results The herbs can be overtly identified by TLC. Ginsenoside Rb1 had a linear relationship in the range of 1. 095-5. 475μg, and the average recovery was 97. 3%(RSD 1. 98%). Conclusion The method is simple and rapid,and can be used for the quality control of xinshuaining mixture.

This study examined the effect of subcellular localization of P21 on the proliferation and apoptosis of HepG2 cells. The coding genes of the wild and the mutant P21 were amplified by mega primer PCR from the plasmid pCEP-WAF1 which contains human P21 cDNA in the nuclear localizational signal (NLS) sequence, and then inserted into the eukaryotic expression vector pDsRed1-C1. The recombinants were transfected into HepG2 cells. The transcription and expression of P21 were determined by RT-PCR and fluorescence microscopy. The cell proliferation was measured by MTT, and the cell cycle and apoptosis of HepG2 cells by flow cytometry. The results of restriction analysis, DNA sequencing and fluorescence microscopy confirmed the construction of the wild and the mutant P21 in the eukaryotic expression plasmid. The plasmid containing the mutant P21 was found to accelerate cell proliferation and the wild P21 plasmid to inhibit cell proliferation. Cell cycle analysis showed that the cell ratio of G(0)/G(1) in the wild type group was significantly increased as compared with that in the mutant type group, and cell apoptosis analysis revealed that the apoptosis rate in the wild type group was much higher than that in the mutant type group. It was concluded that the subcellular localization of P21 may contribute to the development of hepatic cancer.

Objective:To investigate the relationship between double mutations of myosin heavy chain gene (MYH6) p.Gly743Arg and p.Glu1389Lys and the cardiac phenotype.Methods:Patients carrying double mutations in the MYH6 gene p.Gly743Arg and p.Glu1389Lys were screened from 52 unrelated left ventricular hypertrophy (LVH) who were admitted to the Second Hospital of Chongqing Medical University from 2015 to 2020, and the genetic testing of peripheral blood of patients by second-generation whole-exome sequencing assay technology and genomic DNA of their family members Sanger sequencing was performed to validate the genomic DNA of the family members. The cardiac phenotype was evaluated by electrocardiogram, coronary computed tomography angiography (CTA), echocardiography, and cardiac magnetic resonance imaging (MRI) as adjuncts.Results:All whole-exome gene were detected in 52 unrelated patients with LVH, of which 1 patient (1.9%) had double mutations in MYH6 gene p.Gly743Arg and p.Glu1389Lys (proband). Two members of the maternal line of this patient carried p.Glu1389Lys mutation, but there was no obvious clinical phenotype. Two members of the paternal line carried p.Gly743Arg mutation and had obvious clinical phenotype of bradycardia, but there was no LVH. The male proband, aged 21 years old, presented with LVH and sinus bradycardia but no coronary artery stenosis on CTA before treatment, MRI showed that the left ventricular end diastolic diameter was 58 mm. After treatment with angiotensin receptor-enkephalinase inhibitor (ARNI), electrocardiogram showed that the heart rate increased significantly (from 43 bpm to 72 bpm). Echocardiography showed that the left ventricular end diastolic diameter decreased significantly (from 60 mm to 49 mm).Conclusions:The p.Glu1389Lys mutation of the MYH6 gene may not manifest the phenotype of heart disease. MYH6 gene p.Gly743Arg mutation may be manifested asymptomatic sinus bradycardia, but there is no LVH phenotype. The cardiac disease phenotype caused by the double mutations of p.Gly743Arg and p.Glu1389Lys in the MYH6 gene is more obvious. Asymptomatic LVH and sinus bradycardia can appear in adolescence, but the LVH phenotype can be reversed in a short period of time after ARNI treatment.

This study examined the effect of subcellular localization of P21 on the proliferation and apoptosis of HepG2 cells.The coding genes of the wild and the mutant P21 were amplified by mega primer PCR from the plasmid pCEP-WAF1 which contains human P21 cDNA in the nuclear localizational signal (NLS) sequence,and then inserted into the eukaryotic expression vector pDsRed1-C1.The recombinants were transfected into HepG2 cells.The transcription and expression of P21 were determined by RT-PCR and fluorescence microscopy.The cell proliferation was measured by MTT,and the cell cycle and apoptosis of HepG2 cells by flow cytometry.The results of restriction analysis,DNA sequencing and fluorescence microscopy confirmed the construction of the wild and the mutant P21 in the eukaryotic expression plasmid.The plasmid containing the mutant P21 was found to accelerate cell proliferation and the wild P21 plasmid to inhibit cell proliferation.Cell cycle analysis showed that the cell ratio of G0/G1 in the wild type group was significantly increased as compared with that in the mutant type group,and cell apoptosis analysis revealed that the apoptosis rate in the wild type group was much higher than that in the mutant type group.It was concluded that the subcellular localization of P21 may contribute to the development of hepatic cancer.