Objective:To provide reference for clinical pharmacist in the treatment of severe bone marrow suppression complicated with infection induced by chemotherapeutic drugs .Methods:The pharmaceutical care was performed by clinical pharmacist for a pa-tient with severe bone marrow suppression complicated with pulmonary infection caused by chemotherapy .The suggestions on the drug use in the evaluation of chemotherapy regimen and the treatment of bone marrow suppression and infection were provided .Results:The bone marrow inhibition was relieved , the pulmonary infection was improved , and no other severe adverse reactions were shown .Con-clusion:Clinical pharmacist can improve effectiveness and safety in the treatment of patients with severe bone marrow suppression by providing individualized drug treatment .

The etiology and pathogenesis of intrahepatic cholestasis are complex,and those are not still very clear in current.Studies suggest that genetic factors play an important role in the pathogenesis of the disease.Some familial cholestasis have been confirmed by gene mutation causing.Bile secretion process regulated by a number of bile relation gene at the molecular level.Farnesoid X receptor (FXR) gene is related to intrahepatic bile secretion process.Bile secretion is indirect control by FXR which formats a complex network,becoming more attention to researcher in recent years.

AIM: To study the efficacy and adverse reactions of carnitine on patients with acute cerebral infarction.　METHODS: One hundred and thirty-five patients with acute cerebral infarction diagnosed by CT or MRI were randomly divided into 2 groups, on the basis of conventional therapy. Sixty-eight patients in carnitine group (M37,F31; age 60 a± s 17 a) received carnitine 2-3g, iv, drip, qd for 28 d. The other 67 patients of control group (M39, F28; age 63 a±17 a) received compound salvia miltirrhiza 20 mL in dextran-40 glucose injection 500 mL, iv, drip, qd for 28 d.　RESULTS: The total effective rates of carnitine group and control group for acute cerebral infarction were 80％ and 55％, respectively (P<0.05). No adverse reactions were found.　CONCLUSION: Carnitine is safe and effective in the treatment of acute cerebral infarction.

0.05).Heart rate was significantly slow in bisoprolol group(after treatment:66?4 vs before treatment:74?7 beats/min,P

Objective: To explore the effect of hirudin on hyperuricemia rats and its mechanism. Methods: Male Wistar rats were randomly divided into control group, model group, allopurinol (30 mg/kg) group, hirudin low-, middle- and high-dose (0.2, 0.4, 0.8 g/kg) group. Rats were ig potassium oxonate (0.75 g/kg) to induce hyperglycemia model, once a day for five weeks. And all administration groups were respectively ig corresponding doses of drugs. The level of uric acid in serum and urine of rats were measured by biochemical method; The level of organic anion transporter 1 (OAT1) in kidney was measured by immunohistochemistry; The protein expressions of glucose transporter 9 (GLUT9), OAT1 and urate transporter 1 (URAT1) in kidney were measured by western blotting; The expression levels of GLUT9, OAT1 and URAT1 mRNA in kidney were detected by qRT-PCR. Results: Compared with control group, the level of uric acid in serum and urine of rats in model group was significantly increased (P < 0.01), the expressions of GLUT9, URAT1 mRNA and protein were significantly increased (P < 0.01), the expressions of OAT1 mRNA and protein were significantly decreased (P < 0.01). Compared with model group, the level of uric acid in serum and urine of rats in hirudin group were significantly decreased (P < 0.01), the expressions of GLUT9, URAT1 mRNA and protein were significantly reduced (P < 0.01), the expressions of OAT1 mRNA and protein were significantly increased (P < 0.01). Conclusion Hirudin can reduce the uric acid by regulating the expressions of renal urate transporters OAT1, URAT1 and GLUT9 in hyperuricemia rats.

Hepatocellular carcinoma (HCC) is a serious threat for human health, the incidence of HCC in China accounts for more than 50% worldwide. There is an urgent need to develop novel anticancer agents for the treatment of HCC patients. Here we characterized the inhibitory effect and the molecular mechanism of protopine on HCC cancer cells. The results of a CCK-8 assay indicated that protopine displays anticancer activities on HCC cells. Flow cytometry and JC-1 staining confirmed that treatment with protopine decreased the mitochondrial membrane potential and induced apoptosis in HCC cells. Western blot analysis showed that protopine was able to increase protein expression in the mitochondrial apoptotic pathway; the level of cytochrome C, apoptotic protease activating factor-1 (Apaf-1), Bax, cleaved-poly ADP-ribose polymerase (cleaved-PARP), cleaved-caspase-3, and cleaved-caspase-9 were increased while the expression of Bcl-2 was suppressed significantly. An in vivo study revealed that protopine significantly suppressed the growth of tumors in nude mice bearing HepG2 cells. Administration of protopine intraperitoneally at a concentration of 50 mg·kg^-1 inhibited tumor growth by 72.46%. Animal experiments were carried out according to the Regulation of the Animal Ethics Committee of Southwest Medical University. This study provides preliminary evidence that there is potential to develop protopine as a lead compound for the treatment of HCC.

Dental Implants, Single-Tooth ; Dental Prosthesis, Implant-Supported ; Esthetics ; Humans ; Maxilla

Career Mobility ; China ; Humans ; Occupational Health Services ; statistics & numerical data ; Sampling Studies

OBJECTIVETo study the protective effect of puerarin on MPP(+) -induced SH-SY5Y cells by chaperone-mediated autophagy (CMA).

METHODThe Parkinson's disease cell model was established by injuring SH-SY5Y cells with 1 mmol x L(-1) MPP+. The CCK-8 staining was adopted to detect the effect the puerarin of different concentrations on the survival rate of MPP(+)-induced SH-SYSY cells. The autophagosome formation was observed under transmission electron microscope. The AO staining showed the changes in the lysosome activity. RT-PCR was used to detect the changes in Lamp2a and Hsc70 mRNA expressions. The western blotting was adopted to test the expressions of Lamp2a, Hsc70 and alpha-synuclein protein in cells.

RESULTWithin the concentration range of 12. 5-50.0 micromol x L(-1), the pretreatment with puerain for 30 minutes could protect the injury of MPP+ in SH-SY5Y cells, and showed a certain dose-effect relationship. The AO staining and electron microscope showed the effect of puerain within the concentration range of 12.5-50.0 micromol x L(-1) on 1 mmol x L(-1) MPP(+)-induced SH-SY5Y cells; autophagosomes emerged in cells, and increased along with the rise in the puerarin dose. The results of the flow cytometry revealed that 50.0 micromol x L(-1) of puerarin could protect against the increase of the ROS level in 1 mmol x L(-1) MPP(+) -induced SH-SY5Y cells and prevent the oxidative injury. The results of RT-PCR and western blotting indicated that puerain within the concentration range of 12.5-50.0 micromol x L(-1) alleviated the MPP(+)-induced SH-SY5Y cell injury, and inhibited the accumulation of alpha-synuclein proteins in MPP(+) -induced SH-SY5Y cells by up-regulating Hsc70, Lamp2a mRNA and protein level.

CONCLUSIONPuerarin could protect against the MPP(+) -induced cell injury, whose protective mechanism may be related to the chaperone-mediated autophagy pathway of interventional molecules.

Autophagy ; drug effects ; genetics ; HSC70 Heat-Shock Proteins ; genetics ; Humans ; Isoflavones ; pharmacology ; Lysosomal-Associated Membrane Protein 2 ; genetics ; Molecular Chaperones ; genetics ; Parkinson Disease ; drug therapy ; genetics ; Phagosomes ; drug effects ; genetics ; Piperidines ; pharmacology ; Pyrazoles ; pharmacology ; Tumor Cells, Cultured ; Up-Regulation ; drug effects ; genetics

Bibliometrics ; Biochemistry ; Biotechnology ; China ; Journal Impact Factor ; Periodicals as Topic ; statistics & numerical data ; Science