OBJECTIVE:To establish a method for simultaneous determination the contents determination of hydroxysafflor yel-low A and salvianolic acid B in Compound danshen oral solution. METHODS:HPLC was performed on the column of SHIMADZU ODS-C18 with mobile phase of methanol-0.5% phosphoric acid (35:65,V/V) at flow rate of 1.0 ml/min,dection wavelength was 403 nm for hydroxysafflor yellow A and 286 nm for salvianolic acid B and column temperature was 35 ℃, the volume injection was 20μl. RESULTS:The linear range was 2.01-20.10μg/ml for hydroxysafflor yellow A(r=0.999 9)and 39.80-398.00μg/ml(r=0.999 9) for salvianolic acid B. RSDs of precision,stability and reproducibility tests were lower than 2%;recoveries were 98.26%-101.25%(RSD=0.94%,n=9)and 98.70%-101.35%(RSD=0.71%,n=9),respectively. CONCLUSIONS:The method is feasible and reproducible,and can be used for the contents determination of hydroxysafflor yellow A and salvianolic acid B in Com-pound danshen oral solution.

Linezolid is an antibacterial agent for the treatment of multi-resistant Gram-positive bacterial infections， which is widely used in clinical practice. However， there are large individual differences in the pharmacokinetic characteristics of the drug in patients， and it is difficult to obtain the optimal therapeutic effect when the drug is administered according to the conventional dose in the instructions. Therefore， it is necessary to carry out therapeutic drug monitoring （TDM） for linezolid， and guide and optimize its antibacterial treatment plan by using population pharmacokinetics （PPK） and pharmacodynamics principles. This paper summarizes the PPK changes and the research progress of individualized administration of linezolid in various populations， and recommends that the patient’s steady-state blood concentration is kept at 2-8 mg/mL through TDM when using linezolid clinically. It is recommended to appropriately reduce the dosage for patients with liver and kidney dysfunction， appropriately increase the dosage for obese， burned and children patients， and provide pharmaceutical monitoring during the medication process to promote rational drug use.

OBJECTIVE: To investigate the expression of LINC01106 in colorectal cancer and its role in regulating the proliferation and apoptosis of colorectal cancer cells. METHODS: We analyzed the data of LINC01106 expression levels in tumor tissues and normal tissues of patients with colorectal cancer in TCGA database and explored the association of LINC01106 expression level with the prognosis of the patients. Colorectal cancer SW480 cell lines with LINC01106 knockdown or overexpression were established, and their proliferation and apoptosis relative to the parental cells were evaluated using CCK-8 assay and flow cytometry, respectively. The expressions of p-STAT3, STAT3, and Bcl-2 in the cells were detected by immunoblotting. Nude mouse models bearing xenografts of SW480 cells with LINC01106 knockdown or na?ve SW480 cells were established to observe the effect of LINC01106 knockdown on the growth of SW480 cells . RESULTS: Analysis of the data from TCGA database showed that the expression level of LINC01106 was significantly higher in colorectal cancer tissues than in normal tissues, and LINC01106 expression level was significantly related to the prognosis of the patients ( < 0.05). Knockdown of LINC01106 significantly inhibited the proliferation and promoted apoptosis of SW480 cells ( < 0.05), while LINC01106 overexpression significantly promoted proliferation of the cells. LINC01106 knockdown in SW-480 cells obviously lowered the expressions of p- STAT3 and Bcl-2 and suppressed the growth of the xenograft in nude mice. CONCLUSIONS LINC01106 is significantly up-regulated in colorectal cancer tissue and is related to the prognosis of the patients. LINC01106 can regulate the proliferation and apoptosis of SW480 cells through STAT3/Bcl-2 signaling and may serve as a potential marker for the diagnosis and prognostic evaluation of colorectal cancer.

OBJECTIVE: To assess the clinical value of individualized pharmaceutical services for patients receiving vancomycin for severe infections and establish clinical monitoring procedures during vancomycin treatment. METHODS: Data were collected from patients with severe infections who received vancomycin treatment with individualized pharmacy services (test group, 144 cases) or without such services (control group, 884 cases) between January, 2017 and December, 2018. Using propensity score matching, the patients in the two groups with comparable baseline data were selected for inclusion in the study (62 in each group), and the efficacy, safety and economic indicators were compared between the two groups. RESULTS: The curative effects of the treatment did not differ significantly between the two groups, with the overall response rates of 95.16% in the test group and 91.94% in the control group ( CONCLUSIONS The participation of clinical pharmacists during the treatment can improve the clinical benefits of vancomycin in patients with severe infections.
Anti-Bacterial Agents/therapeutic use* ; Humans ; Infections/drug therapy* ; Pharmaceutical Services ; Retrospective Studies ; Vancomycin/therapeutic use*

Linezolid is an oxazolidinone antibacterial agent used in infections caused by gram-positive cocci such as methicillin-resistant staphylococcus aureus, penicillin-resistant pneumococcus and vancomycin-resistant enterococcus. Lactic acidosis is one of the adverse reactions of linezolid. The risk factors of lactic acidosis caused by linezolid are long-term exposure, liver dysfunction, renal dysfunction, mitochondrial DNA A2706G polymorphism, combined use of drugs affecting mitochondrial function, etc. The symptoms of lactic acidosis caused by linezolid are nausea, vomiting, drowsiness, shortness of breath, tachycardia, and hypotension, etc., which can be identified early by close monitoring of laboratory indicators such as blood lactic acid, pH, and blood drug concentration. The mechanism of lactic acidosis induced by linezolid may be related to mitochondrial toxicity. The lactic acidosis of linezolid can be caused by reducing drug dose, stopping drug or even in vitro renal replacement therapy, and strengthening symptomatic support therapy if necessary. This review is intended to provide ideas for the clinical prevention and treatment of lactate acidosis caused by linezolid.