Objective:To research PHA-CIK cells' phenotype and cytotoxicity. Methods: Using phytohemagglutinin(PHA)to stimulate peripheral blood mononuclear cells(PBMNCs) for 24 h,then cultured like incubating cytokine induced killers by traditional method. On 15th day examined its immunophenotype by flow cytometry and using MTT method to evaluate cytotoxicity. Results: The ratio of CD3+,CD8+, CD3+ CD8+ and CD3+ CD56+ cells were high.PHA-CK cells cytotoxicity was strong in some degree.Conclusion:PHA-CIK cells had strong cytotoxicity.The result provides an experimental basis for biotherapy.

Background and purpose: Bladder cancer is the most common urological malignancy in our country which seriously threatens human health, and its incidence increased year by year. This study aimed to investigate the effects of hinokitiol on the proliferation, apoptosis and autophagy in human bladder cancer cell lines. Methods:CCK-8 assays were performed to analyze the effects of hinokitiol on the proliferation of J82 cells. Apoptosis rate was determined by lfow cytometry. Cleaved caspase 3, LC3 and P62 protein expression was determined using Western blot. EGFP-LC3 microscopy assay was performed to assess autophagy. Results: Hinokitiol significantly inhibited the proliferation of J82 cells and induced cell apoptosis via caspase pathway. The apoptosis effect of hinokitiol could be partially antagonized by Z-VAD-FMK. Hinokitiol induced autophagy of J82 cells, increased LC3 expression and down-regulated P62 expression. 3-MA is able to rescue Tet-induced cell death. Conclusion:Hinokitiol can inhibit the proliferation of J82 cells and induce cell apoptosis via autophagy activation.

Objective To detect the relationship between tumor markers (TM) and prognosis of NSCLC.Methods The level of TM of 178 NSCLC cases,which all accord with the standard of advanced NSCLC come from Guang'an Men Hospital of China Academy of TCM from 2006 October to 2009 March.Was divided into 5 groups:group 1 (0～3 months)、group 2 (4～6 months)、group 3 (7～9 months)、group 4 ( 10～ 12 months)、group 5 ( ＞ 12 months) according to time to progression (TTP).Studied the correlation between TM,TTP and one year survival retrospectively.Results The serum level of Ca125 in TTP 1～5 group was:(227.9± 73.3)U/ml,(83.4± 127.6)U/ml,(74.8 ± 174.5)U/ml,(53.15 ± 26.3)U/ml,(24.69± 8.78)U/ml respectively which indicated that the higher the serum level of Ca125 was,the more quickly the progress of disease would be(P=0.02); The serum level of Cyfra211 [(9.8±9.4)ng/ml,(10± 6.9) ng/ml,(41.55±9.3) ng/ml,(11.98 ± 9.9) ng/ml,(4.1 ± 0.5) ng/ml) ],CEA [ (88.4± 227) ng/ml,(75.8 ± 272) ng/ml,(57.4 ±153)ng/ml,(35.4±52.5)ng/ml,(17.1± 15.4)ng/ml] and Ca153 [(42.6±52.3)ng/ml,(47.6±147.0) ng/ml,(57.4± 153)ng/ml,(19.4± 12.7)ng/ml,(33.7± 14.6)ng/ml] was associated with prognosis,the higher level they were the lower possibility of one-year survival would be (P=0.041 ).Conclusion Ca 125、Cyfra211、CEA and Ca153 had certain value for prognostic judgment and it was of great significance that measuring rational serum tumor markers on judging prognosis of NSCLC.

AIM:To investigate the possible mechanism of magnolol on the damage of PC12 cell induced by the addition of 6-OHDA placed in an incubator for 24 h with rat's pheochromocytoma cell of adrenal medulla in the absence and presence of magnolol. METHODS:Cell viability was measured by MTT method. Reactive oxygen species (ROS) and aspartate-specific cysteine proteases-3 (Caspase-3) concentration(s) were assayed by fluorescence spectrophotometer. RESULTS:Cell activity declined sharply by the addition of 6-OHDA at concentration of 100 ?mol/L,the pre-treatment of magnolol(0.1~10 ?mol/L)could significantly increase the PC12 cell activity and prevent the increased ROS and caspase-3. CONCLUSION:Magnolol may protect the cell trauma induced by 6-OHDA,and the mechanism is related to inhibiting the 6-OHDA-induced elevation in intracellular ROS levels and reducing the caspase-3 activity.

Objective:To establish a method for the determination of residual triethylamine in tenofovir disoproxil fumarate. Methods:The residual treithylamine was determined by GC with an Agilent DB-624 capillary column(30 m × 0. 53 mm,3 μm)and an FID detector. The carrier gas was nitrogen and the flow rate was 2. 0 ml · min-1 . The oven temperature was programming in-creased. The initial column temperature was 50℃,and then raised to 220℃ at a rate of 10℃·min-1 ,and maintained 4 min. Trieth-ylamine was quantified by an external standard. Results:The calibration showed a good linearity within the range of 53. 02-742. 34 μg ·ml-1 for triethylamine. The correlation coefficient was 0. 999 8. The recoveries were within the range of 96. 52%-102. 27%. The relative standard deviation(RSD)was 2. 42%(n=9). Conclusion:The method has good specificity,repeatability and sensitivity, which can be used in determining the content of residual trietbylamine in tenofovir disoproxil fumarate.

Objective To investigate the X-ray gray scale changes of calcium sulfate and evaluate its clini-cal effect in traumatic fracture treatment. Methods 23 traumatic fracture cases were treated from September 2014 to January 2016 in our hospital. The degradation rate of calcium sulfate was evaluated by X ray assay. Results Af-ter surgery,about 69%remnants at 1 week,53%remnants at 2 weeks,26%remnants at 4 weeks,7%remnants at 6 weeks were observed,while no remnants were found at 8 weeks after surgery. The initial time window of callus appearance was 3 to 9 weeks and the mean time was(6.5 ± 1.6)weeks. The fracture union time was 8 to 24 weeks and the mean time was(15.0 ± 5.2)weeks. One patient with distal humeral comminuted fracture had non-infec-tious delayed healing wound.One case of hemolytic staphylococcus in incision was cultured. Conclusion Calcium sulfate degrades rapidly,cautions should be taken for the application in the superficial bone.

Objective :To study mutation of Ps3 gene and its relationship with histologic grade and Dukes' stage in colorectal cancer. Methods :PCR-SSCP was used to detect mutations of Ps3 in 30 colorectal cancer patients. Results: It was found that 6 mutations (20. 0%) in the coding region of P53 gene. One mutation was located in exon4; 5 mutations were located in exon 5; none of mutation was found in exon 2 and 3. According to the histologic grade of of colorectal cancer,the frequencies of P53 gene mutation were 1/8 (12. 5%) in the well differentiated and in the moderately differentiated as well,3/10 (30. 0%) in the poorly differenctiated and 1/4 (25.0%) in the undifferentiated. In clinic, the frequencies of P53 gene mutation were associated with Dukes stage: 1/10 (10. 0 % ) in B stage, 2/12 (16. 7%) in C Stage,3/8(37. 5%) in D stage. Conclusion:The mutation of P53 gene is related to Dukes＇ stage,and the P53 gene mutation hardly occurs in exon 2,3 in coloretal cancer.

To investigate the effects of oxymatrine injection (OI) combined with low-dose paclitaxel on expressions of mRNAs and proteins of vascular endothelial growth factor (VEGF) and CXC chemokine receptor 4 (CXCR4) in human gastric carcinoma SGC-7901 cells.

The Effect of arsenic trioxide (As(2)O(3)) on myelomonocytic progenitor cells of patients with myelodysplastic syndrome was studied. Bone marrow CFU-GM was assayed in the agar semi-solid culture, and the bone marrow cells were incubated in liquid culture and the expressions of CD33, CD15 and bcl-2 on the marrow cells were detected by APAAP method in 24 patients. The suppressive effects of As(2)O(3) to CFU-GM were increased with the rise of As(2)O(3) concentrations. The suppression of As(2)O(3) (0.388 micro mol/L) to cluster formation was stronger than to colony formation, the suppressive rates were 70.78% vs 34.05% in low-risk group, and 86.76% vs 65.86% in high-risk group (P < 0.01), respectively. 0.194 micro mol/L of As(2)O(3) decreased clusters and increased colonies in low-risk group, but decreased clusters and did not change colonies in high-risk group. High concentration (1.94 micro mol/L) of As(2)O(3) downregulated the expression rate of CD33 and CD15 in both groups, and low concentration (0.194 micro mol/L) downregulated the expression rate of CD33 and upregulated the expression rate of CD15 in low-risk group, but decreased expression of CD33 and did not alter CD15 in high-risk group. At the same time, the high concentration of As(2)O(3) downregulated expression of bcl-2 and resulted in karyopyknosis and cytoplasm condensation; low concentration generated similar effect on expression of bcl-2 and cell morphology in high-risk group, but did not affect in low-risk. It is concluded that As(2)O(3) suppressed myelopoiesis and impelled myelomonocytic cells to apoptosis, low concentration of As(2)O(3) induced the proliferation and differentiation of myelomonocytic cells in low-risk group, however, suppressed the growth of myelomonocytic cells and accelerated the cells apoptosis in high-risk group.

OBJECTIVE: To explore the correlation between diabetic nephropathy (DN) and cognitive impairment through examining the cognitive function and the metabolism of the cerebrum in Type 2 diabetes mellitus patients at different stages of renal function.
 METHODS: Eighty six patients with Type 2 diabetes mellitus (T2DM) were enrolled for this study. According to the urinary albumin excretion rate (UAER), the patients were divided into a T2DM without DN group (DM group, n=33), an early DN group (DN-III group, n=26) and a clinical stage group (DN-IV group, n=27). Thirty healthy adults were selected as a control group (NC group). Biochemical indexes and UAER were measured, and glomerular filtration rate (GFR) was detected by single-photon emission computed tomography (SPECT). The cognitive function was measured by Montreal Cognitive Assessment (MoCA, Beijing version) and mini-mental state examination (MMSE). The peak areas of N-acetylasparte (NAA), creatine (Cr), choline-containing compounds (Cho) were detected by proton magnetic resonance spectroscopy (1H-MRS).
 RESULTS: 1) There was no statistical difference in MMSE scores between the DM group and the control group. The scores of MoCA in the DN-III group or in the DN-IV group were significant less than that in the NC group (F=3.66, P<0.05); 2) There was significant difference in left N-acetylaspartate (LNAA), left choline (LCho) among the diabetes groups. Compared with the DM group, the level of LNAA was decreased significantly (t=3.826, P<0.05) while the LCho was increased significantly (t=4.373, P<0.05) in the DN groups, with statistic difference between the 2 groups (t=3.693, P<0.05); 3) The MoCA scores of T2DM patients were negatively correlated with UAER (r=-0.285, P<0.05), while positively correlated with GFR (r=0.379, P<0.05); 4) Logistic regression analysis indicated that UAER and GFR were the major risky factors for diabetic cognitive impairment.
 CONCLUSION Diabetic cognitive impairment is closely correlated with the nephropathy in patients with Type 2 diabetes. With the decline in glomerular filtration function, the cognitive disorder tends to be aggravated. The hippocampal brain metabolism may have some changes in left side of Cho/Cr in patients with diabetic nephropathy.
Adult ; Aspartic Acid ; analogs & derivatives ; metabolism ; Case-Control Studies ; Cerebrum ; metabolism ; Choline ; metabolism ; Cognition ; Cognition Disorders ; epidemiology ; Creatine ; metabolism ; Diabetes Mellitus, Type 2 ; physiopathology ; Diabetic Nephropathies ; epidemiology ; Glomerular Filtration Rate ; Humans ; Neuropsychological Tests