OBJECTIVE:To provide references for rational application of full-automatic tablet dispensing machine in the inpa-tient pharmacy of the hospital. METHODS:According to the work flow and use of the machine,the errors and problems arising from the use thereof by our hospital were summarized and analyzed,and corresponding improvement measures and solutions were put forward. RESULTS & CONCLUSIONS:Common errors in the use of full-automatic tablet dispensing machine included errors for the machine(including in-box drug shortage warnings accounting for 58.61% and abnormal responses to the quantity of in-box drugs accounting for 36.96%),errors caused by human factors(including errors of inputting doctor’s order and errors of pharma-cist’s adding drugs)and errors of material installation and operation. The solutions put forward are as follows as adjusting the tilt angle of the outlet mouth and controlling the quantity of the drugs added to the box to reduce the errors for the machine;two phar-macists’checking doctor’s order in the hospital information system in advance to reduce the errors caused by human factors;carry-ing out operation training for operators to reduce the errors of material installation;designating special personnel to maintain the ma-chine,etc.

Animals ; Disease Models, Animal ; Sleep Deprivation ; physiopathology ; psychology

Objective To investigate the effects of silymarin on expressions of nuclear factor kappa B(NF-?B) and intercellular adhesion molecule-1(ICAM-1) in the kidneys of rats with unilateral ureteral obstruction(UUO)-induced renal fibrosis.Methods Seventy-two male Sprague-Dawley rats were randomly divided into 3 groups: sham-operated group(n=24),operated group(n=24) and silymarin treated group(n=24).Renal tubulointerstitial fibrosis model was established via UUO.Silymarin was given by gavage with 30 mg/(kg?d) in silymarin treated group,and the same volume normal saline was given by gavage in operated group and sham-operated group.In each group,8 rats were killed at 7,14 and 21 d after operation.Histological changes were observed in tubulointerstitial injury under microscope.The expressions of NF-?B and ICAM-1 in renal tissue were determined with immunohistochemical method.Results Tubuloin-terstitial injury scores in operated group at 7,14 and 21 d were 1.168?0.108,1.776?0.064 and 2.301?0.157,respectively,and Tubulointerstitial injury scores in the treated group at 7,14 and 21 d were 1.043?0.114,1.677?0.083 and 2.084?0.201,respectively.Tubulointerstitial injury scores in silymarin treated group were significantly lower than those in operated group(Pa

Objective To analyze the assessment results of iodine deficiency disorders(IDD) External Quality Control Laboratories at all levels in Guizhou province and the network operation to further standardize and improve the laboratory, improve network performance, provide reliable laboratory quality assurance for epidemiological surveillance and control of IDD and reliable decision-making. Methods The results of different level of IDD labs in Guizhou that took part in the entire country's IDD lab exo-network quality control examination of 1999 - 2008, which organized by the nation iodine deficiency disorder reference lab were analyzed. Results In the past 10 years, except the provincial laboratory examination results of urinary iodine in 2000 was failed, the other results were all qualified in the rest 9 years;iodized salt examination results were qualified. The urinary iodine laboratory response rate of Guizhou provinces and municipalities(state, district), from 1999 to 2002, were 88.9%(8/9), 66.7%(6/9), 77.8%(7/9), 66.7%(6/9), respectively, and the rate was stable at 100% from 2003 to 2008. Qualifying rate reached 100% in 2007, the remaining 9 years were 33.0%(3/9) - 88.9%(8/9). The iodized salt laboratory response rates were 100%(9/9) in 2000 - 2008. The pass rates were 77.8%(7/9), 88.9%(8/9),77.8%(7/9) from 2001 to 2003, 88.9%(8/9) in 2007, and the remaining 5 years 100%. Response rate of iodized salt laboratory at the county level that participated in the External Quality Control were 66.7% (20/30), 90.0%(27/30), 80.0% (24/30), 96.7% (29/30) from 2000 to 2003, respectively, and 2006 was 96.7% (29/30), and the remaining four years were all 100% (30/30). The pass rates in 2000 - 2008 were between 53.3% (16/30) -93.3%(28/30). Conclusions The accuracy of test results of external quality controls and the normal operation of the network at all levels of laboratories is closely related to the IDD laboratory conditions, detection techniques, and the degree of attention of relevant departments and professional bodies.

OBJECTIVETo investigate the effect of extracellular regulating kinase (ERK) signaling pathway on the secretion of gamma-aminobutyric acid (GABA) in cultured rat hippocampal neurons induced by stromal cell derived factor-1 (SDF-1).

METHODSThe hippocampal neurons of newborn SD rats were cultured and identified in vitro; the phosphorylation level of ERK1/2 was examined by Western blot; ELISA was used to detect the effect of PD98059, a ERK1/2 specific blocker on GABA secretion of cultured hippocampal neurons and Western blot were adopted to measure the protein expression levels of glutamate decarboxylase (GAD65/67) and gamma aminobutyric acid transporter (GAT); after blocking ERK1/2 signaling pathway with PD98059; RT-PCR was used to detect the mRNA expression levels of GAT-1 and GAD65 after treated with PD98059.

RESULTSThe levels of ERKl/2 phosphorylation were increased significantly by SDF1 acting on hippocampal neurons, and CX-CR4 receptor blocker AMD3100, could inhibit SDF-1 induced ERK1/2 activation; SDF-1 could inhibit the secretion of GABA in cultured hippocampal neurons, and ERK1/2 specific inhibitor PD98059, could partly reverse the inhibition of GABA secretion by SDF-1. The effects of SDF-1 on cultured hippocampal neurons was to decrease the mRNA genesis of glutamic acid decarboxylase GAD65 and GABA transporter GAT-1, besides, ERK inhibitor PD98059 could effectively flip the effect of SDF-1. The results of Western blot showed that SDF-1 could inhibit the protein expression of GAT-1 and GAD65/67 in hippocampal neurons and the inhibition of GAT-1 and GAD65/67 protein expression could be partially restored by ERK1/2 blocker.

CONCLUSIONSDF-1 acts on the CXCR4 of hippocampal neurons in vitro, and inhibits the expression of GAD by activating the ERK1/2 signaling pathway, and this may represent one possible pathway of GABA secretion inhibition.

Animals ; Blotting, Western ; Cells, Cultured ; Chemokine CXCL12 ; pharmacology ; Flavonoids ; pharmacology ; Glutamate Decarboxylase ; metabolism ; Hippocampus ; cytology ; MAP Kinase Signaling System ; Neurons ; metabolism ; Phosphorylation ; RNA, Messenger ; Rats ; Rats, Sprague-Dawley ; Receptors, CXCR4 ; metabolism ; gamma-Aminobutyric Acid ; secretion

Adult ; Cranial Fossa, Middle ; pathology ; Cranial Fossa, Posterior ; pathology ; Female ; Granuloma ; pathology ; Humans ; Mastoid ; pathology

Objective To evaluate the development of immature oocytes after freezing-thawing by conventional cryopreservation method for mature oocytes.Methods Immature oocytes were collected from stimulated ovaries of intracytoplasmic sperm injection(ICSI)cycles.Immature oocytes were in vitro matured directly or after slow freezing-fast thawing and immunostained for tubulin and chromatin and at last visualized by confocal microscopy.Results No statistical difference was found in maturity rate between freezing groups and the controls.There was a statistically significant increase in abnormalities of chromosome(23.7% vs. 50%)and spindle(28.9% vs.53.9%)in the GV freezing group compared with the GV control(P

Abnormalities, Multiple ; diagnosis ; Child ; Diabetes Mellitus, Type 2 ; complications ; Female ; Hearing Loss, Sensorineural ; complications ; Humans ; Obesity ; complications ; Prognosis ; Retinitis Pigmentosa ; complications ; Skin ; pathology ; Syndrome

Objective The purpose of this study was to investigate the expression of human mitochondrial transcription termi-nation factor-3 ( hMTERF3) in non-small cell lung cancer ( NSCLS) and to analyze its clinicopathological significance. Methods The paraffin block samples used in this study included 65 cases of NSCLC and 32 cases of normal alveolar epithelial tissues. We determined the expressions of hMTERF3 in NSCLC and normal alveolar epithelial tis-sues by immunohistochemistry, calculate the survival rate using the Kaplan-Meier method, and analyzed the risk factors affecting the prognosis of NSCLC using the Cox Proportional Hazard Model. Results In the 65 cases of NSCLC, 31 ( 47. 69%) showed positive expression of hMTERF3. The total survival time was significantly shor-ter in the patients with a high than in those with a low hMTERF3 ex-pression ([30.39±3.35] vs [57.61±7.12] mo, P<0.05). The riskfactors affecting the prognosis of NSCLC included positive expression of hMTERF3 (HR=3.302, 95% CI:1.598-6.905) and lymph node metastasis (HR=4.052, 95% CI: 1.212-12.398). Conclusion hMTERF3 is overexpressed in NSCLC. Highly expressed hMTERF3 and lymph node metastasis reduce the survival time of NSCLC patients, suggesting that hMTERF3 may be a potential bio-marker for the prognosis of NSCLC.

Objective To investigate the effects of ZMS,the active component of Zhimu,on amyloid precursor protein(APP) and ?-site APP cleaving enzyme 1(BACE1) in HEK293sw cells. Methods HEK293sw cells were pretreated with different concentrations of ZMS in routine culture medium for 24 h,and then serum-free medium with ZMS was used for further culture for 48 h.Cells were examined for expression of APP and ?-secretase BACE1 with Western blotting and RT-PCR,and were then examined for BACE1 activity with fluorescence method. Results 1 ?mol/L and 10 ?mol/L ZMS significantly decreased the expression of BACE1 mRNA and protein,while had no effect on the expression of APP mRNA and protein.It was indicated by fluorescence analysis that 10 ?mol/L ZMS significantly decreased the ?-secretase activity.Conclusion ZMS significantly decreases the activity and expression of ?-secretase BACE1,while has no effect on the expression of APP in HEK293sw cells.