1ug/ml),chromatographing ona 300?3.9mm 1.D.colomn packcd with u Bondapak C_(18)(10um),and detecting at UV254nm.The mobile phase was MeOH-H_2O-TEMED-HAC(65:35:0.3:0.52)The average recovery of the whole procedure were 99.9?4.1(SD)%.CV=4.1%for clozapine)98.5?4.0(SD)%,CV=4.2% for chlopromazine.The Minimum detetionlimit was 10ng/ml serum.The developed method was applied to clinical monitoring of serum levels from11 patients who wereco administered with multiple oral doses of clozapine and chlor-promazine.The serum concentrations of 0.150-0.445?g/ml and 0.014-0.086?g/ml werefound.Futhermore,one case of suicide was encountered.

Objective:To retrospectively evaluate the prognostic risk factors of T1-2 stage breast cancer patients with one to three positive node(s) and their effects on the benefits of post-mastectomy radiation therapy (PMRT). Methods:We retrospectively analyzed 457 breast cancer patients with T1-2 stage and one to three positive axillary lymph nodes treated in our hospital between 2000 and 2002. The independent prognostic factors of the patients were calculated by the Cox proportional hazards model. The patients were fur-ther classified into high-risk and low-risk subgroups according to the risk factors to explore the benefit of PMRT on the prognosis of dif-ferent subgroups using survival analysis. Results:PMRT was not an independent beneficial factor of overall survival (OS) (HR=0.949;CI:0.435-2.074;P=0.896) or loco-regional recurrent free survival (LRRFS) (HR=0.611;CI:0.231-1.614;P=0.320) in all patients. Ex-tracapsular extension (ECE) and pathological grades were independent prognostic risk factors, and the benefits of PMRT were signifi-cantly different on the prognosis of high-risk subgroup patients (group ECE+OS:P=0.020, LRRFS:P=0.014;group GradeⅢOS:P=0.002, LRRFS:P<0.001). Meanwhile, PMRT failed to prolong the OS and LRRFS of low-risk subgroup patients (group ECE+OS:P=0.353, LRRFS:P=0.796;group GradeⅠtoⅡOS:P=0.267, LRRFS:P=0.589). Conclusion:ECE and gradeⅢwere the independent risk factors of death and loco-regional recurrence in the T1-2 breast cancer patients with one to three positive lymph node(s). PMRT was an effective adjuvant therapy to improve the prognosis of patients with high-risk factors. However, the benefit of PMRT had no sig-nificance in patients with ECE-or gradeⅠ-Ⅱ.

Objective To explore the influencing factors of coal workers''''cognitive function. Meth-ods There was a physical examination on 3205 workers in the coal mine enterprise.The physical examina-tion included height,weight,blood pressure,blood routine examination and routine urine test,and Mini Men-tal State Examination (MMSE) was used to evaluate the cognitive function.The coal workers were divided in-to cognitive dysfunction group (84 cases) and cognitive function normal group (3121 cases) according to MMSE scores.Logistic regression analysis was used to explore the influencing factors of cognitive function. Results The prevalence of cognitive dysfunction was 2. 62％ in coal workers. The age of the cognitive dys-function group(47.27±8.24) was significantly higher than that in the cognitive function normal group (41.39 ±8.65)(P<0.05),and the degree of culture in cognitive dysfunction group was significantly lower than those in the cognitive function normal group (χ2= 46. 610, P<0. 01 ) . The low density lipoprotein cholesterol ((2.72±0.65)mmol/L),urine pH(5.54±1.51) in the cognitive dysfunction group were significantly lower than those in the cognitive function normal group((2.89±0.73)mmol/L,(5.92±1.28))(P<0.05). The lo-gistic regression analysis showed that age, culture level, BMI, low density lipoprotein cholesterol, urine pH were the impacting factors of cognitive dysfunction. Conclusion Cognitive dysfunction is influenced by age, culture level,BMI and low density lipoprotein cholesterol. The higher of the age and the lower of the culture level,BMI,low density lipoprotein cholesterol,urine pH,the more vulnerable to cognitive dysfunction.

Lamin B1 (LMNB1) is highly expressed in liver cancer tissues, and its influence and mechanism on the proliferation of hepatocellular carcinoma cells were explored by knocking down the expression of the protein. In liver cancer cells, siRNAs were used to knock down LMNB1. Knockdown effects were detected by Western blotting. Changes in telomerase activity were detected by telomeric repeat amplification protocol assay (TRAP) experiments. Telomere length changes were detected by quantitative real-time polymerase chain reaction (qPCR). CCK8, cloning formation, transwell and wound healing were performed to detect changes in its growth, invasion and migration capabilities. The lentiviral system was used to construct HepG2 cells that steadily knocked down LMNB1. Then the changes of telomere length and telomerase activity were detected, and the cell aging status was detected by SA-β-gal senescence staining. The effects of tumorigenesis were detected by nude mouse subcutaneous tumorigenesis experiments, subsequent histification staining of tumors, SA-β-gal senescence staining, fluorescence in situ hybridization (FISH) for telomere analysis and other experiments. Finally, the method of biogenesis analysis was used to find the expression of LMNB1 in clinical liver cancer tissues, and its relationship with clinical stages and patient survival. Knockdown of LMNB1 in HepG2 and Hep3B cells significantly reduced telomerase activity, cell proliferation, migration and invasion abilities. Experiments in cells and tumor formation in nude mice had demonstrated that stable knockdown of LMNB1 reduced telomerase activity, shortened telomere length, senesced cells, reduced cell tumorigenicity and KI-67 expression. Bioinformatics analysis showed that LMNB1 was highly expressed in liver cancer tissues and correlated with tumor stage and patient survival. In conclusion, LMNB1 is overexpressed in liver cancer cells, and it is expected to become an indicator for evaluating the clinical prognosis of liver cancer patients and a target for precise treatment.
Animals ; Mice ; Telomerase/metabolism* ; Carcinoma, Hepatocellular/genetics* ; Liver Neoplasms/genetics* ; Telomere Shortening ; In Situ Hybridization, Fluorescence ; Mice, Nude ; Telomere/pathology* ; Carcinogenesis