OBJECTIVE To survey the antibiotic usage and its rationality in clinical.METHODS From Jan 2009 to May of 2009,950 medical records were selected to conduct a retrospective investigation.RESULTS The incidence of antibiotic usage was 88.2%,71.6% cases were intended for active treatment,28.4% for preventive regimen.72% cases in internal medicine were for active treatment whereas 94% were for surgical prophylaxis.In terms of the antibiotic use,single drug accounted for 56.2%,two-drug 38.9% and three-drug 4.9%.Inspection rate of drug treatment was 69.7% and hospital infection rates was 2.1%.CONCLUSIONS To improve antibiotic administration,systematic efforts are required to keep the medical staff updated of antibiotic principles so as to improve clinical rational use of antibiotics.

Objective To investigate the mechanism of brain injury caused by thrombin and the intervention effect of hirudin and nimodipine.Methods Different doses of thrombin or/and hirudin were injected into nucleus caudatus of SD rats,nimodipine was given intraperitoneally.Dry-wet-weighing technique,immunohistochemical method and TUNEL were used to examine brain edema,the changes of cytoskeleton,neuron apoptosis and histological changes.Results(1) High dose of thrombin resulted in severe cerebral edema as early as 4 h after injection and the maximum edema occurred at 24~48 h.The edema gradually decreased and got close to normal within 3~7 d.Cytoskeleton changes were observed at early stage(4h),reversible or irreversible injuries presented at 24~48 h,and neuron necrosis occurred within 3~7 d.Neuron apoptosis started at 4h and peaked at 24~48 h.In contrast,low dose of thrombin and normal saline did not show these effects.(2) The effects of thrombin could be inhibited by hirudin and nimodipine(a calcium-ion antagonist) could relieve or delay cell injury.Conclusions High dose of thrombin may result in severe brain edema,neuron irreversible injury and apoptosis,which all peak at 24~48 h.Early treatments could greatly reduce brain damage and improve prognosis of intracerebral hemorrhage.

BACKGROUND:In terms of the histocompatibility, immune rejection and scar formation after repair, acel ular nerve al ograft is closer to autologous nerve cel s. At present, hyaluronic acid has been applied for autologous peripheral nerve repair;however, research on the nerve al ograft is rarely reported.
OBJECTIVE:To explore the effect of hyaluronic acid on the anastomotic scar in acel ular nerve al ograft repair of rat sciatic nerve defect.
METHODS:Thirty-six Sprague-Dawley rats were randomly divided into three groups (n=12 per group). The rat model of nerve defect of 10 mm was established by cutting the sciatic nerve of the left hind leg and then given nerve al ograft combined with the injection of hyaluronic acid at anastomosis (experimental group), only nerve al ograft (control group) and autologous nerve graft (nerve autograft group), respectively. Afterwards, the healing of the proximal anastomosis was observed and scar components were assessed.
RESULTS AND CONCLUSION:Gross observations showed that the rat skin and muscle fascia had no significant differences in healing among groups, while the surrounding tissue adhesion in the experimental group was milder than that in the control group (P<0.05). Masson staining found that col agen deposition in the epinerium could be observed in each group. In the experimental group, a smal amount of col agen fibers arranged orderly in the epineurium;in the control group numerous col agen fibers accumulated and arranged irregularly;in the nerve autograft group, sparse epineurial col agen fibers appeared in an order arrangement. The gray value of col agen type I in the experimental group was higher than that in the control group (P<0.05), while the gray value of col agen type III was lower than that in the control group (P<0.05). No significant differences were found in the sum gray values of col agen type I and III among groups (P>0.05). These findings indicate that in the peripheral nerve repair, hyaluronic acid abrogates the scar formation by increasing the deposition of col agen type III and reducing the deposition of col agen type I.

Objective To observe the effect of astragalus polysaccharides ( APS) on glucose homeostasis regulation and focus on glycogen synthase kinase 3 beta (GSK3 beta) activity and subcellular localization (nuclear translocation).Methods HepG2 human hepatoma cells were cultured in vitro and treated with high glucose of different concentrations (30, 40 mM) to induce hepatocyte endoplasmic reticulum stress model, then acquire optimum operating concentration.The HepG2 cells were treated with APS of different concentrations (50, 100, 200, 400 μg/mL) to select the most effective concentration.The HepG2 cells were divided into seven groups with different treatment: negative control group (C), positive control group (Tm), 30 mM high glucose-induced group (G30), 45 mM high glucose-induced group (G45), negative control+APS group (CA), positive control+APS group ( TA) and high glucose-induced+APS group ( GA).Effect of APS at different concentrations on proliferation activity of HepG2 cells were detected by MTT assay, transcription and shear levels of XBPlmRNA in HepG2 cells by quantitative real-time PCR, and phosphorylation levels of GSK3βin cytoplasm and nucleus by immunoblotting techniques.Results The optimum operating glucose concentration was 30 mM.The most effective APS concentration was 200μg/mL.The transcription and shear levels of XBPlmRNA in HepG2 cells of GA group were lower than those of G30 group ( P<0.05), respectively, but there were no significant differences between TA and Tm group.The phosphorylation levels of GSK3βin cytoplasm and nucleus of GA group were higher than those of G group(P<0.05), respectively, but there were no significant differences between TA and Tm group. Conclusion APS could improve hepatic steatosis, and its mechanism might be that APS inhibits the activity and nuclear localization of GSK3β, then alleviate endoplasmic reticulum stress.

OBJECTIVE:To investigate the effects of TanshinoneⅡA sodium sulfonate injection on levels of P-selectin,glial fi-brillary acidic protein (GFAP),vascular endothelial growth factor (VEGF) and neurological function in patients with acute cere-bral infarction. METHODS:A total of 114 patients with acute cerebral infarction selected from Lianyungang First People's Hospi-tal during Apr. 2013-Apr. 2016 were divided into control group and observation group according to random number table,with 57 cases in each group. Control group was given routine treatment. Observation group was additionally given Tanshinone ⅡA sodium sulfonate injection 40 mg 0.9％ sodium chlonride injection 250 mL,ivgtt,qd. A treatment course lasted for 7 d,and both received 2 courses of treatment. NIHSS scores,the levels of serum P-selectin,GFAP and VEGF were compared between 2 groups before treatment and after 7,14 d of treatment. The occurrence of ADR was also compared. RESULTS:Before treatment,there was no statistical significance in above indexes between 2 groups(P>0.05). Compared to before treatment,NIHSS score,the levels of se-rum P-selectin and GFAP in 2 groups were decreased significantly after 7,14 d of treatment,while the serum level of VEGF was increased significantly. These indexes of 2 groups after 14 d of treatment were significantly better than 7 d of treatment,except for NIHSS score. Above indexes of observation group was significantly better than those of control group during corresponding period, with statistical significance (P<0.05). No obvious ADR was found in 2 groups. CONCLUSIONS:For acute cerebral infarction, Tanshinone ⅡA sodium sulfonate injection can significantly reduce the levels of serum P-selectin and GFAP,improve VEGF level and promote the recovery of neurological damage with good safety.

Objective To evaluate the effect of different preparation processes on preparation of the glial cell line-derived neurotrophic factor(GDNF)loaded microspheres and observe the biological activity of GDNF.Methods With polylactide-co-glycolide(PLGA)as the coating material,the GDNF-loaded microspheres were prepared by using double emulsion(W1/O/W2).Two-factor factorial design variance analysis was done to analyze the effects of the composition proportion of lactic acid(LA)and glycolic acid(GA)in PLGA and the stirring speed of multiple emulsion on particle size,entrapment efficiency,burst release and in vitro release characteristics of the GDNF-loaded microspheres.PC-12 bioassay was employed to detect the biological activity of the released GDNF so as to determine the optimal preparation process.Results The composition proportion of PLGA could affect the microspheres'burst release(P ＜ 0.05),with no effect on particle size and entrapment efficiency.with the higher.With higher proportion of GA,the release speed of GDNF in the microspheres was increased.When the stirring speed of multiple emulsion was increased from 1 000 r/min to 3 000 r/min,the particle size of the microspheres was decrease significantly(P ＜ 0.01),the burst release was increased markedly(P ＜ 0.01)and the in vitro release rate was accelerated.The activity of GDNF in the microspheres could last for about 20 days at 37℃,which was 10 days longer than that of single GDNF.Conclusions Double emulsioncan prepare the GDNF-loaded microspheres with high entrapment efficiency and suitable in vitro release time.In the meantime,the microspheres can extend the validity of GDNF.

Objective To develop an online organ doses reporting software VirtualDose-IR, which can compute the radiation doses and provide an easy access to evaluation and control of patients ′radiation doses.Methods Monte Carlo method was applied to simulating various interventional radiology ( IR) processes , which included various parameters such as different patient models at different ages and with different weights , different projection angles and regions of interest , and other parameters .All of the dose data was acquired and then integrated into a database , and displayed with hyper text markup language (HTML), so only a web browser was necessary for users .Results A web-based software that reports organ doses for patients under IR progress was developed .The organ doses assessed with VirtualDose-IR were compared with other experiment and simulation data , and the results were basically consistent with each other .Conclusions VirtualDose-IR is a easy and efficient method to assess patients′radiation doses of IR.

AIM: To investigate the expression of FIZZ1/RELM? in lung tissue of chronic cigarette smoking rat,and to determine the relationship between airway inflammation and airway hyperresponsiveness.METHODS: Made rat model of chronic cigarette smoking was used.The expression of FIZZ1/RELM? in lung tissue was determined by immuno-histochemistry and in situ hybridization.RESULTS: In control rats,FIZZ1/RELM? protein and mRNA expressions were observed at low levels.In cigarette smoking rats,FIZZ1/RELM? expression increased in all the cells especially in bronchial smooth muscle cells,vascular wall cells and alveolar epithelial cells.CONCLUSION: FIZZ1/RELM? is a secreted peptide specifically expressed in lung.Cigarette smoking induces its upregulation,which possibly contributes to cigarette smoking-induced airway hyperresponsiveness.

Objective To investigate the value of ABCD3-I score in predicting the outcome of acute minor ischemic stroke. Methods Totally 255 patients were valued by ABCD, ABCD2, ABCD3, ABCD3-I and ESSEN score then the clinical characters, outcome and early progression of these patients were investigated. Results Forty-eight patients had poor outcome after 90 days. Univariate logistic regression indicated that the differences of hypertension, diabetes, cardiovascular disease, stenosis of criminal artery, abnormal signal in diffusion weighted imaging (DWI) and other clinical symptoms between poor outcome group and good outcome group were statistically significant (P<0.05). The AUC of ABCD, ABCD2, ABCD3, ABCD3-I and ESSEN score in predicting outcome of acute minor stroke was 0.791 0, 0.798 3, 0.827 9, 0.930 0 and 0.735 9 respectively. There was difference among patients with different ABCD3-I scores both in outcome and early progression. Conclusion ABCD3-I score can predict the outcome of acute minor stroke and supply a new method for personalized treatment.

We studied the regulatory effects of the estragen receptorbeta (ERbeta) gene on the downstream estrogen signal transfection pathway in colon cancer cells and the possible mechanisms involved. A human ERbeta gene recombinant expression plasmid, pEGFP-C1-ERbeta, was constructed and transfected into the Caco-2 colon cancer cell line, a line with low ERbeta gene expression. The expression of ERbeta mRNA and protein was detected 72 h after transfection. RT-PCR was used to examine the expression levels of the progesterone recepror (PR) gene containing the classic estrogen response element (ERE), the C-fos oncogene containing the AP-1 site (a non-classical ER binding site), the epigenetic modifying genes, such as Dnmt1, Dnmt3a, Dnmt3b, and histone methyltransferase (HMT), and the human mismatch repair gene hMLH1. Methylation-specific PCR was used to detect the changes in the methylated sites of the CpG islands in the promoters of the ERbeta, PR, and C-fos genes. The results indicated that the human ERbeta gene recombinant expression plasmid pEGFP-C1-ERbeta was successfully constructed and transfected into Caco-2 cells. As compared with the control group, the mRNA and protein expression of ERbeta gene was increased significantly 72 h after the transfection of pEGFP-C1-ERbeta into the Caco-2 cells. As compared with the control group, the mRNA expression of the PR, C-fos, Dnmt3a and Dnmt3b genes was increased significantly 72 h after the transfection of pEGFP-C1-ERbeta into the Caco-2 cells, but the mRNA expression of the Dnmt1, HMT, and hMLH1 genes decreased significantly (P<0.05). As compared with the control group, different degrees of demethylation occurred in the promoters of the ERbeta, progesterone receptor (PR), and C-fos oncogene 72 h after the transfection of pEGFP-C1-ERbeta into the Caco-2 cells. The methylation index of the estrogen signal transfection pathway in Caco-2 cells was decreased significantly following the expression restoration of ERbeta gene (P<0.05). It is concluded that the restoration or up-regulation of the ERbeta gene in Caco-2 cells may significantly activate the expression of the related target genes in the downstream estrogen signal transfection pathway and may result in the demethylation changes of the pathway. During the process, the expression level and activity of the epigenetic modifying genes and the human mismatch repair gene have changed simultaneously. The regulatory effect of the ERbeta gene on the estrogen signal transfection pathway to a certain extent partly involves demethylation.