OBJECTIVE:To standardize the ward rescue and essential drugs quality management in wards,and reduce the med-ication risk of patients. METHODS:Failure mode and effect analysis(FMEA)was used to analyze the inspection items and failure modes of quality management of ward rescue and essential drugs. According to scoring the possibility,severity and detectability de-gree of the failure modes and calculating the risk priority number(RPN),failure modes that should be given priority improvement were quantified and determined,improvement measures were developed and conducted,and management effects were evaluated af-ter 6 months. RESULTS:12 failure modes were determined,including the residue treatment of narcotic and the first-class psycho-tropic drugs was not recorded,drug storage temperature was not up to standard and drug expired,etc. Improving related systems, enhancing the inspection management,cold chain management,daily management and other measures were implemented and con-ducted. After 6 months,the top 3 items with the highest RPNs were dropped from 320,240,216 score to 16,16,27 scores,re-spectively,all in a relatively low risk area. Numbers of failure mode event were dropped from 1869 to 218,dropping by 88.3%. CONCLUSIONS:According to qualifying the failure modes in ward rescue and essential drugs quality management by using FMEA in our hospital,the management items with the highest risk has determined and improved,the medication risk of patients has significantly reduced.

OBJECTIVETo study the influence of selenium and fluoride on apoptosis and lipid peroxidation in human hepatocytes in vitro.

METHODSThe apoptosis, cell cycle, GSH content and lipid peroxides (LPO) level in human hepatocytes, LPO level and LDH, AST and ALT activity in cell culture supernatants were investigated after hepatocytes were incubated with selenium and/or fluoride for around 12 hours periods in vitro.

RESULTSThe percentage of hepatocyte apoptosis bodies (15.557 +/- 2.056)%, the number of cells in S phase (4.823 +/- 0.454)% and LPO level in liver tissue and supernatant [(2.884 +/- 0.589) and (3.547 +/- 0.561) nmol/L MDA/mg.prot, respectively], AST and LDH activity in supernatants (91.1 +/- 36.4 and 140.4 +/- 7.6 U/L, respectively) in the fluoride treated group was higher than the control group [(10.313 +/- 1.023)%, (3.253 +/- 0.743)%, (1.473 +/- 0.401) nmol/L MDA/mg.prot, (1.694 +/- 0.443) nmol/L MDA/mg.prot, (54.5 +/- 3.2) U/L and (126.4 +/- 2.6) U/L, respectively], The GSH content in live tissue [(4.225 +/- 0.781) microgram/mg.prot] is lower than control group [(7.595 +/- 1.042) microgram/mg.prot]. Selenium treatment reduced these kinds of toxicity of fluoride through raising GSH content, reducing LPO level, LDH and AST activity and percentage of apoptosis bodies.

CONCLUSIONSSelenium can antagonist apoptosis and lipid peroxidation of hepatocytes induced by fluoride.

Alanine Transaminase ; drug effects ; metabolism ; Apoptosis ; drug effects ; Aspartate Aminotransferases ; drug effects ; metabolism ; Cell Cycle ; drug effects ; Cells, Cultured ; Fluorides ; pharmacology ; Glutathione ; drug effects ; metabolism ; Hepatocytes ; cytology ; drug effects ; metabolism ; Humans ; L-Lactate Dehydrogenase ; drug effects ; metabolism ; Lipid Peroxidation ; drug effects ; Lipid Peroxides ; metabolism ; Selenium ; pharmacology ; Time Factors

OBJECTIVETo explore the DNA damage effects and apoptosis in brain cells of rats induced by sodium fluoride.

METHODSSD rats were divided into two groups, i.e. control group and fluoride treated group, which were injected intraperitoneally with distilled water and sodium fluoride (20 mg.kg(-1).d(-1)) respectively. On the hand, 5 mmol/L NaF were used in in vitro study. Single Cell Gel Electrophosis (SCGE or Comet Assay) was utilized to measured DNA damage and apoptosis was detected by the TUNEL method and Flow Cytometry (FCM).

RESULTSThe DNA damage in pallium neurons in rats of the fluoride group was much more serious compared with those of the control group, with the Ridit value being 0.351 and 0.639 respectively (P < 0.01) in vivo, and 0.384 4 and 0.650 1 respectively (P < 0.01) in vitro. TUNEL positive cells were found in pallium, hippocampus and cerebellar granule cells in rats of fluoride group, whereas those in the control group were rare. It was demonstrated by FCM results that the percentages of apoptotic cells both in pallium and hippocampus were significantly higher (P < 0.01) in rats of fluoride group (27.12 +/- 3.08, 34.97 +/- 5.46) than those in control group (4.63 +/- 0.98, 5.35 +/- 0.79), (P < 0.01).

CONCLUSIONSodium fluoride could induce DNA damage and apoptosis in rats brain.

Animals ; Apoptosis ; genetics ; Brain ; drug effects ; metabolism ; pathology ; Comet Assay ; DNA ; drug effects ; genetics ; metabolism ; Flow Cytometry ; In Situ Nick-End Labeling ; Male ; Rats ; Rats, Sprague-Dawley ; Sodium Fluoride ; pharmacology