Objective To shorten the average length of stay for single disease entities and enhance the hospitals competitiveness through hospitalization process recombination while guaranteeing the quality of its medical service. Method The method of "systematic reintegration" from the theory of operation process recombination was adopted to recombine the hospitalization process for common disease entities in general surgery. Result After the recombination, the number of discharged patients with disease entities covered by the year 2000 research increased by 14.78%, the average length of stay was shortened by 3.83 days, a reduction of 21.58%, the average hospitalization fees incurred on the patients were reduced by 108 yuan, a reduction of 1.18%, and the business income increased by 13.43%, as compared with 1999, when recombination was not yet initiated. Conclusion Hospitalization process recombination can improve the quality and efficiency of a hospitals medical service and increase its business income while its medical service resources remain unchanged.

To enhance the quality and efficiency of ozagrel by investigating the differences between the ozagrel polymorphs in bioavailability. Solid ozagrel in different polymorph forms were orally administered to SD rats. An HPLC method was established to determinate plasma level of ozagrel. The bioavailabilities of two polymorph forms were calculated and compared. The pharmacokinetic parameters of ozagrel, were as follows: Cmax was 32.72 ± 17.04 and 34.01 ± 19.13 mg · L(-1), respectively; AUC0-t was 61.14 ± 14.76 and 85.56 ± 18.08 mg · L(-1) · h, respectively; t½ was 1.53 ± 0.51 and 4.73 ± 3.00 h, respectively. There was no significant difference in pharmacokinetic parameters between form I and II polymorphs of ozagrel while the t½ of form II is longer, which indicates that the use of form II polymorph as pharmaceutical product may prolong the effective action time in clinics. This would help the polymorph quality control in drug production.

Experimental studies on the myocardial ischemia and reperfusion injury in 16 anaethetized SDrats,of which,8 animals were pretreated with morphine(5 mg/kg,i.p.)for preventing of arrhyth-mias,were studied immunocytochemically with anti-muscle actin specific monoclonal antibody (HHF_(35)),8 shan-operated rats were used as control.With HHF_(35) ABC immunocytochemical method,the area of myocardial ischemia and reperfusion injury(without morphine)showed decrease or ab-sence of staining,large areas of staining loss were also seen.In the group with morphine,only smallfoci of staining absence were shown.The myocardium in control animals showed evenly positive stain-ing.No change were seen with HE staining in all groups.The results obtained with HHF_(35) stainingsupport its important value in studying on myocardic reperfusion injury,and indicated that the degreeof myocardic damage may be relative to the arrhythmias in myocardial reperfusion injury.

Salvianolic acid A (Sal A) is one of the most effective compounds isolated from the root of Salvia miltiorrhiza. Up to now, several studies regarding the pharmacokinetic profiles of Sal A have been reported, however there is no such study reported in monkeys, the species which is more similar to human. The aim of this study is to develop a LC-MS method for the determination of Sal A in monkey plasma and apply it to the pharmacokinetic studies of monkeys. After single intravenous administration of Sal A, the plasma concentration-time curves were observed and the main pharmacokinetic parameters were calculated. The plasma concentration at 2 min (C2 (min)) values were (28.343 ± 6.426), (45.679 ± 12.301) and (113.293 ± 24.360) mg x L(-1) for Rhesus monkeys treated with Sal A at 2.5, 5 and 10 mg x kg(-1). The area under the concentration-time curve (AUC(0-∞)) values were (3.316 ± 0.871), (5.754 ± 2.150) and (13.761 ± 2.825) μg x L(-1) x h, respectively. Furthermore, this method was improved and applied to the simultaneous determination of Sal A, Sal B and Sal C, which provided useful information for preclinical studies and clinical trials of Sal A, Sal B and Sal C.

Objective To study the molecular regulation mechanism of VEGF in the model of ATRA induced differentiation in HL-60 cells,and to provide new targets for leukemia anti-angiogenic therapy.Methods The morphology was observed by Wright-Gimesa staining; HL-60 cells differentiation was detected by NBT reduction experiment.VEGF,STAT3,c-myc mRNAs were measured by reverse transcription-PCR;VEGF,STAT3 and c-myc proteins were determined by Western blot.Results The proliferation of HL-60 cells was inhibited obviously by ATRA(1 μmol/L) with the induction of differentiation,NBT positive rate was 82.59％ (t =-24.157,P ＜ 0.01) ; VEGF mRNA (t =7.339,P ＜ 0.05),STAT3 mRNA (t =3.667,P ＜0.05) and c-myc mRNA (t =6.858,P ＜ 0.05) were all down-regulated.VEGF protein (t =3.386,P ＜0.05),STAT3 protein(t =4.074,P ＜ 0.05) and c-myc protein (t =3.333,P ＜ 0.05) were all down-regulated.Conclusion VEGF expression level is reduced with the procession of differentiation of HL-60 cells,which may be largely correlated with the down regulation of STAT3 and c-myc.

Objective:To investigate the key mechanism of transforming growth factor-β (TGF-β) inducing the expression of interleukin-17D (IL-17D) in lung cancer-associated fibroblast (CAF) and promoting the recruitment of myeloid-derived suppressor cells (MDSCs).Methods:C57BL/6 mice were established for B16 lung melanoma metastasis model (tumor model group), and control group was set up, 6 mice in each group. Flow cytometry (FACS) was used to detect the lung CAF and the changes of its ability to secrete IL-17D and the proportion of MDSCs in tumor mice. The changes of TGF-β level in lung tumor were examined by ELISA and quantitative real-time PCR (RT-qPCR). Lung fibroblasts were screened by FACS, and the effects of TGF-β on the secretion of IL-17D, C-C motif chemokine ligand (CCL)2 and CCL7 in fibroblasts were detected by RT-PCR. The migration of MDSCs under the condition of TGF-β stimulating fibroblasts was detected by Transwell.Results:The proportion of CAF (CD45 -CD326 -CD31 -) in the tumor model group was higher than that in the control group [(28.02±2.23)% vs. (7.35±2.14)%, t=9.956, P<0.001]. The ability of CAF to secrete IL-17D in the tumor model group was significantly higher than that in the control group [(38.27±2.93)% vs. (19.04±3.16)%, t=5.995, P=0.001]. The proportion of MDSCs in the tumor model group was significantly higher than that in the control group [(12.93±1.27)% vs. (8.21±1.40)%, t=4.804, P=0.009]. Compared with the control group, the protein and transcription levels of TGF-β in lung of the tumor model group were significantly increased [(1 685.07±135.61) ng/L vs. (1 047.98±68.50) ng/L, t=5.051, P=0.002; 2.17±0.03 vs. 1.00±0.05, t=51.237, P<0.001]. In vitro, lung fibroblasts were stimulated with different concentrations of TGF-β (0, 5 and 10 μg/L) for 24 hours, the relative expressions of IL-17D mRNA secreted by stimulated fibroblasts were 0.42±0.01, 0.67±0.01 and 0.84±0.04 respectively, the relative expressions of CCL2 mRNA in each group were 0.89±0.08, 1.08±0.04, 1.19±0.01 and CCL7 were 0.53±0.05, 0.65±0.04, 0.74±0.03 respectively. With the increase of TGF-β concentration, the expression levels of IL-17D, CCL2 and CCL7 in fibroblasts were significantly increased ( F=57.384, P<0.001; F=15.802, P=0.004; F=14.544, P=0.005). In addition, compared with the control group (0 μg/L TGF-β), fibroblasts treated with 10 μg/L TGF-β for 24 hours could promote the migration of MDSCs in spleen of tumor mice [(9.59±0.21)% vs. (2.14±0.24)%, t=6.585, P<0.001]. Conclusion:TGF-β can induce high expression of IL-17D in lung CAF, which is an important factor in promoting the expressions of CCL2 and CCL7 and the migration of MDSCs in tumor microenvironment.

Aim To investigate the effects of diterpene ginkgolides meglumine injection (DGMI ) on amino acids and monoamine neurotransmitters in rats with cerebral ischemia/reperfusion injury.Methods In-traluminal suture was applied to establish middle cere-bral artery occlusion (MCAO/R)model with ischemia for 1.5 h and reperfusion for 24 h.After the adminis-tration of DGMI (i.v.),the levels of amino acid and monoamine neurotransmitters in brain tissue were de-tected through HPLC-ECD.Results DGMI down-reg-ulated the concentrations of aspartic acid, glutamic acid,glycine and γ-aminobutyric acid which were in-creased in MCAO/R group.DGMI also reduced the levels of norepinephrine epinephrine,glyoxylic acid, serotonin and 5-HIAA in cortex and hippocampus,and increased adrenaline content compared to the model group.Conclusion DGMI exhibits a protective role in rats with cerebral ischemia /reperfusion injury through regulating amino acids and monoamine neuro-transmitters.

Objective To investigate the function of tripartite motif protein 22 (TRIM22) and the interaction with eukaryotic translation initiation factor-4E (eIF4E) in the differentiation of NB4 cells, one kind of acute promyelocytic leukemia cells, which elucidates the mechanism of TRIM22 targeting to regulate eIF4E.Methods The model of NB4 cells inducing differentiation was established in vitro.The expression changes of gene and protein of TRIM22 and eIF4E were detected by using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting.In addition, the effect on cell function and protein expression level of eIF4E after adopting electroporation technology to depress or over-express TRIM22 was detected by CCK-8 and flow cytometry.Finally, the interaction of TRIM22 and eIF4E was verified by using co-immunoprecipitation (CO-IP).Results The mRNA relative expression level of TRIM22 was gradually increasing from 1.01±0.15 to 30.98±2.79 (F=280.700, P=0.000), and the protein relative expression level was gradually increasing from 0.22±0.03 to 0.51±0.05 (F=51.430, P=0.000) after the all-trans-retinoic acid (ATRA) induction for NB4 cell.However, the mRNA relative expression level of eIF4E was gradually decreasing from 1.01±0.09 to 0.47±0.06 (F=20.520, P=0.000), with the same trend, the protein relative expression level was gradually decreasing from 0.97±0.02 to 0.64±0.09 (F=14.700, P=0.001).The expression level of PE-CD11b in the TRIM22 over-expression group with ATRA detected by flow cytometry [(78.80±2.00)%] was higher than that in the transfection group of empty vetor with ATRA [(58.70±2.70)%] (t=9.535, P=0.000) and the cotransfection group with ATRA [(61.60±3.80)%] (t=8.187, P=0.000).Meanwhile, the protein level of eIF4E changed reversely after over-expressing the gene level of TRIM22 (t=4.985, P=0.007).The CO-IP experiment was used to verify the interaction of TRIM22 and eIF4E.ConclusionTRIM22 is able to promote the cell differentiation during the process of NB4 cells differentiation.Furthermore, eIF4E is a target of TRIM22 for binding with, which plays an important role in depressing the expression of eIF4E.

OBJECTIVETo study the clinical diagnosis and treatment of the chronic pelvic pain syndrome (CPPS).

METHODSAccording to National Institute Health (NIH) classification, 165 cases of chronic prostatitis were surveyed by analysis of their laboratory results and clinical history. In addition, the chronic prostatitis symptom index (CPSI) of each patient was evaluated. All patients were treated for 6 to 8 weeks, type III A with antibiotics and alpha1 receptor inhibitor, type III B with alpha1 receptor inhibitor, diazepam diclogenatis and other narcotics. All cases were additionally treated by psychological and physical therapies. Traditional Chinese Medicine was also used in some cases.

RESULTSBased on the results of CPSI after 6 weeks treatment, 121 (73.3%) significantly improved, 26 (15.8%) slightly improved and only 18(10.9%) did not respond to the therapy.

CONCLUSIONCombined therapy can be an effective treatment for the chronic pelvic pain syndrome.

Adolescent ; Adrenergic alpha-Antagonists ; administration & dosage ; Adult ; Anti-Bacterial Agents ; administration & dosage ; Chronic Disease ; Diazepam ; administration & dosage ; Drug Therapy, Combination ; Humans ; Male ; Middle Aged ; Pelvic Pain ; drug therapy ; Prostatitis ; drug therapy

Objective To investigate the effects of duration of surgery on flash-induced visual evoked potentials (VEP) in patients undergoing spinal surgery in prone position.Methods Eighty-two ASA Ⅰ or Ⅱ patients of both sexes aged 20-76 yr weighing 43-96 kg undergoing spinal surgery in prone position were divided into 3 groups according to the duration of surgery:group S≤2 h ( n =34) ; group M 2-4 h ( n =38) and group L≥4 h ( n =10).VEP was monitored using protektor VEP monitoring device (Xltek Co.,Canada).The latency,amplitude and recovery time of wave P100 were recorded before and 10 min after induction of anesthesia and at the end of surgery.Results Compared with group S,the amplitude of wave P1000 was significantly decreased at the end of surgery in group M,the lantency of wave P100 was significantly prolonged,while the amplitude of wave P100 was decreased at the end of surgery in group L ( P ＜ 0.05).Compared with group M,the lantency of wave P100 was significantly prolonged,while the amplitude of wave P100 was decreased at the end of surgery in group L ( P ＜ 0.05).Compared with groups S and M,the recovery time of wave P100 was significantly prolonged in group L ( P ＜0.05).There was no significant difference in the recovery time of wave P100 between groups S and M ( P ＞ 0.05).Conclusion Duration of surgery (≥4 h) can affect flash-induced VEP,the longer the duration,the stronger the effects.