Objective To analyze the reason of necrosis for pedunculated skin flaps repaired after floor of the mouth defect repair.Methods 56 cases of pedunclated-flaps restoring the floor of the mouth from 1996 to 2001 were reviewed, and pedunclated-flap repair was performed after operation in 11 cases suffering from malignant tumors in the floor of the mouth, and 5 kinds of pedunculated flaps were compared.Results Five kinds of pedunculated flaps were used to reconstruct the floor of the mouth defects. Its successful sequence was as following: forehead flap, pectoralis major myocutaneous flap, sternocleidomastoid flaps,trapezius myocutaneous flaps, and subhyoid flap.Conclusions Causes of those flaps necrosis might relate to furnishing blood with supplied-flaps region and structure of anatomy in received-flaps region, also it is related to operater's skill.So the reason of repair failure of skin flaps with pedicle needs comprehensive analysis.

Objective T o investigate the serum IgE w ith various postm ortem intervals (PMI) in guinea pigs due to sudden death from anaphylactic shock and to explore the effect of refrigeration of corpse on serum IgE level and its application value in forensic m edicine. Methods T he anim al death m odels of anaphylactic shock w ere established. T he corpses w ere preserved at room tem perature (20℃) for 6 h and then refrigerated at 4℃. T he serum w as sam pled at 6, 12, 24, 36 and 48 hours after death. T he IgE level of serum w as detected w ith ELISA . The control group w as also established. Results The serum IgE level had significant difference betw een the experim ental group and the control group (P<0.05). T here w as no significant difference am ong the experim ental groups at 6, 12, 24, 36 and 48 hours post-m ortem (P>0.05). Conclusion If the corpses w ere placed in 4℃ conditions 6 hours after anaphylactic death, the serum IgE still show s a good m arker w ithin 48 h for forensic investigation.

Objective To assess the long-term efficacy and safety of mid-dosage (13～15 mg?kg-1?g-1) ursodeoxycholic acid (UDCA) treatment for primary biliary cirrhosis (PBC). Methods A systematic review of all randomized controlled trials (RCT) comparing UDCA with placebo was performed. Results Seven trials including 1038 patients were assessed. UDCA could significantly improve liver biochemistry, but had no effect on pruritus and fatigue. In the patients with initial stage Ⅰ-Ⅱ, there was a significant decrease in the histologic progression after treatment with UDCA for 2 years compared with the placcebo group(P=0.03), but there was no significant difference between the two groups when considering overall patients with initial stage Ⅰ-Ⅳ (P=0.08). Meta-analysis showed no significant difference in the incidence of death (odds ratio 0.99, 95% confidence interval 0.62-1.58), liver related death (1.05, 0.53-2.05), liver trans-plantation (0.87, 0.53-1.41), death and/or liver transplantation (0.92, 0.64-1.31) and liver decompensation (0.94, 0.60-1.49) between the UDCA and placebo groups. Conclusions The analysis of RCTs of UDCA versus placebo shows improvement of liver biochemistry, but not improvement of clinical symptoms and survival. UDCA may slow down liver histologic progression in the early-stage patients with PBC.

OBJECTIVE: To investigate the serum IgE with various postmortem intervals (PMI) in guinea pigs due to sudden death from anaphylactic shock and to explore the effect of refrigeration of corpse on serum IgE level and its application value in forensic medicine. METHODS: The animal death models of anaphylactic shock were established. The corpses were preserved at room temperature (20 °C ) for 6 h and then refrigerated at 4 °C. The serum was sampled at 6, 12, 24, 36 and 48 hours after death. The IgE level of serum was detected with ELISA. The control group was also established. RESULTS: The serum IgE level had significant. difference between the experimental group and the control group (P < 0.05). There was no significant difference among the experimental groups at 6, 12, 24, 36 and 48 hours post- mortem (P > 0.05). CONCLUSION If the corpses were placed in 4 °C conditions 6 hours after anaphylactic death, the serum IgE still shows a good marker within 48 h for forensic investigation.
Anaphylaxis/blood* ; Animals ; Autopsy/veterinary* ; Death, Sudden ; Enzyme-Linked Immunosorbent Assay ; Forensic Medicine ; Guinea Pigs ; Immunoglobulin E/blood* ; Postmortem Changes ; Refrigeration ; Serum

Aim To investigate the up-regulation of miR-22 through Wnt pathway inhibits the proliferation,migration and invasion in human gastric MGC803 cells induced by diallyl disulfide(DADS).Methods The effects of proliferation,migration,and invasion of gastric cancer cells were evaluated by MTT,wound-healing and invasion assays.Online prediction software was applied to search the target gene of miR-22.Luciferase report gene assay was used to assess the target genes Wnt-1 of miR-22.The expressions of Wnt-1,β-catenin and TCF-4 were tested by qRT-PCR and Western blot,respectively.Results MTT showed that DADS and miR-22 notably decreased the proliferation compared with control group(P<0.05).Wound-healing assay showed that DADS and miR-22 could significantly inhibit the migration of MGC803 cells compared with the control group, especially in miR-22+DADS(P<0.05). Invasion assay showed that DADS and miR-22 could markedly inhibit the invasion of MGC803 cells compared with the control group, especially in miR-22+DADS(P<0.05). Online prediction software to search the target gene exhibited that Wnt-1 may be a target gene of miR-22. Luciferase report gene assay disclosed that Wnt-1 was identified as a direct target of miR-22. Qrt-PCR showed that the expression of Wnt-1 Mrna was respectively down-regulated by DADS and miR-22 compared withcontrol group, especially in miR-22+DADS(P<0.05). Western blot exhibited that DADS and miR-22 obviously suppressed the expressions of Wnt-1, β-catenin and TCF-4 proteins, especially in miR-22+DADS(P<0.05).Conclusion Up-regulation of miR-22 through Wnt pathway can remarkably suppress the proliferation, migration and invasion in MGC803 cells by DADS.

Objective To discuss the national standard method of"General Test Method in Salt IndustryDetermination of Iodine Ion"and point OUt an incorrect concentration of sodium hypochlorite(NaClO)solution which is not matched with the concentration of oxalic acid solution being used in the national standard method.Methods The iodine ion in the reference salt was determined step by step as stipulated in the method.During the test,the concentration of the NaClO solution was altered from 5.0%to 0.1%in order to screen the suitable ranges of the concentration of NaClO solution.Results 5.0%NaClO solution was used according to the national standard method,which led to a significant deviation up to 700 ms/kg.The relative errors of the standard iodized salt determination were respectively 2312.0%,185.0%,4.0%,3.3%,-0.6%,-3.0%,-3.3%with different concentration NaClO(5.0%,3.0%,2.5%,1.0%,0.3%,0.2%,0.1%).Conclusion Under the circumstance that the concentration of the oxalic acid solution remains the same.the concentration of NaClO solution must be revised into 0.3%～2.5%in the national standard method to decrease testing errors.

OBJECTIVE:To explore the work model of clinical pharmacists that tailored to the needs of clinical pharmacy in China.METHODS:The definition and the contents of pharmaceutical diagnosis were expounded.Based on the contents and clinical experience,a pharmaceutical diagnosis table was designed and its clinical application was exemplified.RESULTS & CONCLUSION:The pharmaceutical diagnosis table can help pharmacists in their clinical practice to find problems related to drug use and improve pharmacists’ job skill and pharmaceutical care quality to serve for clinical pharmaceutical practice.

OBJECTIVE:To supply the reference for benchmarking framework of unit dose dispensing(UDD).METHODS:To introduce the running module and the training mode for UDD pharmacists of the UDD management mode,and the working quality was controlled using 6? management pattern.RESULTS & CONCLUSIONS:The benchmarking framework of UDD is feasible in practice and it can help guarantee dispensing accuracy,improve the quality of pharmaceutical care.

AIM:To explore the preventing effect of citalopram on neuro-cell apoptosis caused by long-term stress in CA1 and CA3 region of hippocampus.METHODS:Forty male Sprague Dawley(SD)rats were randomly divided into five groups including blank group,control group(the control group was filled the stomade by 0.9% saline)and three experimental groups(intragastric administration of citalopram hydrobromide at doses of 8 mg?kg-1?d-1,4 mg?kg-1?d-1,1 mg?kg-1?d-1,respectively).Rat stress model was made by compulsory swimming everyday for 4 weeks.Cell apoptosis in CA1 and CA3 region of hippocampus was observed by HE staining method.Apoptotic cell numbers and integral optical density in CA1 and CA3 region were tested and analyzed by terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling(TUNEL)method and Norton Internet Security BR(NIS BR)software.t-test was applied to compare apoptosis cell numbers and integral optical density.RESULTS:Control rats showed more static time and less struggling times.Conversely,static time was shorter and rats spent more time after exhaustive exercise,and more struggling times in the experimental group.Rats in control group showed more positive cells in CA1 and CA3 regions and higher integral optical density in CA3 region than those in blank group.Rats in experimental groups showed fewer positive cells in CA1 and CA3 regions.Rats in experimental group 1 and group 3 showed higher integral optical density in CA1 and CA3 regions than that in control group.CONCLUSION:Long-term stress might cause neuro-cell apoptosis in CA1 and CA3 region of hippocampus.Citalopram might have prophylactic effect on apoptosis caused by long-term stress in CA1 and CA3 region,and the prophylactic effect might not be influenced by citalopram.Our study suggests that the treatment mechanism of citalopram in neural and mental illness by long-term stress may involve in a major role by antagonizing neuronal apoptosis in both the CA1 and CA3.