OBJECTIVE:To improve the rational and scientific drug purchase quantity planned by hospital pharmacy. METH-ODS:The deficiency in present drug purchase module of hospital information system(HIS)was analyzed;the formula of planned purchase quantity was improved by incremental coefficient method,ABC analysis method and VEN analysis method. The high and low stored values and packaging volume were set to adjust planned drug purchase quantity. Based on the computer program,a one-key-getting procedure was quasi established,and five typical drugs were selected for simulation. RESULTS:Based on previous formula,the parameters representing change trend,incremental coefficient k1 and inventory coefficient k2 were added in new formu-la. The one-key-getting procedure could calculate the quantity of all drugs by simply entering the planning cycle N1 and the safe peri-od N2 of the some category drugs into the system. After simulated operation practice,compared with pre-improvement,the occupa-tion of funds was significantly decreased and the quantity of drug was rounded off according to package in post-improvement. CON-CLUSIONS:Through function improvement of drug purchase module in HIS and the quasi establishment of one-key-getting pur-chase mode,planned drug purchase quantity is more reasonable,scientific and accurate. It ensures the clinical drug supply in time without causing a backlog,and effectively reduces the cost of manpower,material and capital.

Objective To investigate the effect of Cimetidine on the adhesion between colorectal cancer LOVO cells and endothelial ECV304 cells;and study whether Cimetidine can inhibit the expression of E-selectin in ECV304 cells. Methods Cellular uptake of rose Bengal stain was used to measure the adhesion between LOVO cells and ECV304 cells. Enzyme-linked immunosorbent assay(ELISA)and flow cytometry (FCM, indirect fluorescence staining and labeling)were used to detect the expression of E-selectin. Results ECV304 cells were exposed to different concentrations of Cimetidine. Both the adhesion between LOVO cells and ECV304 cells and the levels of E-selectin significantly decreased with increasing concentration of Cimetidine(P =0. 001 and 0. 001 respectively). Conclusion Cimetidine can inhibit the adhesion of human colorectal cancer LOVO cells on endothelial ECV304 cells by blocking E-selectin expression. Our observations indicated a potential of anti-adhesion therapy using Cimetidine in cancer treatment.

PurposeTo explore the value of gemstone spectral imaging (GSI) in diagnosis of thyroid nodule hemorrhage.Materials and Methods Seventeen patients with surgery and pathology confirmed thyroid nodule hemorrhage underwent thyroid spectrum CT scan. The CT value, iodine concentration value, water concentration value and the effective atomic ordinal value as well as spectral curve slope of hemorrhagic nodules and surrounding normal thyroid tissue were measured respectively.Results Hemorrhagic thyroid nodules showed equal or high CT value, low concentration of iodine, high concentration of water, low spectral curve slope, and low effective atomic ordinal value on spectral CT imaging. There were statistically significant differences in concentration of iodine value, concentration of water value, and spectral curve slope between hemorrhagic nodules and surrounding normal thyroid tissue (Z=-5.438,-4.679 and-5.317,P<0.01), and there were statistically significant differences in CT value and effective atomic ordinal value (Z=-2.097 and-2.230,P<0.05).Conclusion Energy spectrum CT scan is important in detection and accurate diagnosis of thyroid nodule hemorrhage.

Enzalutamide (ENZ) is a second-generation androgen receptor (AR) antagonist used for the treatment of castration-resistant prostate cancer (CRPC) and reportedly prolongs survival time within a year of starting therapy. However, CRPC patients can develop ENZ resistance (ENZR), mainly driven by abnormal reactivation of AR signaling, involving increased expression of the full-length AR (ARfl) or dominantly active androgen receptor splice variant 7 (ARv7) and ARfl/ARv7 heterodimers. There is currently no efficient treatment for ENZR in CRPC. Herein, a small molecule LLU-206 was rationally designed based on the ENZ structure and exhibited potent inhibition of both ARfl and constitutively active ARv7 to inhibit PCa proliferation and suppress ENZR in CRPC. Mechanically, LLU-206 promoted ARfl/ARv7 protein degradation and decreased ARfl/ARv7 heterodimers through mouse double minute 2-mediated ubiquitination. Finally, LLU-206 exhibited favorable pharmacokinetic properties with poor permeability across the blood-brain barrier, leading to a lower prevalence of adverse effects, including seizure and neurotoxicity, than ENZ-based therapies. In a nutshell, our findings demonstrated that LLU-206 could effectively inhibit ARfl/ARv7-driven CRPC by dual-targeting of ARfl/ARv7 heterodimers and protein degradation, providing new insights for the design of new-generation AR inhibitors to overcome ARfl/ARv7-driven CRPC.