Background and purpose:Ever since the use of anthracycine and /or taxanes-based regimen for the adjuvant and/or neoadjuvnat chemotherapy of breast cancer,there have few sensitive agents for advanced breast cancer(ABC)when it occurs drug resistance to anthracycine and /or taxanes.The aim of this study is to evaluate the effect of gemcitabine plus cicplatin in advanced breast cancer after the failure of treatment with anthracycines and /or taxanes.Methods:From May,2005 to Jan 2007,34 ABC cases with anthracycine and/or taxanes resistance were treated with GEM(1000 mg/m2.day1,day8)and DDP(30 mg/m2,day 1 to day 3)every 3 weeks.A median of 5 cycles(2-6 cycles)of the treatment was delivered.All cases were followed up more than 6 months.Results:3 cases(8.8%)had complete response(CR),13 cases(38.2%)had partial response(PR),while 12 cases(35.3%)had stable disease(SD)and progressive disease(PD)was 6 cases(17.7%);the overall response rate was 47.0%.The median time to progression(TTP)was 6.5 months,grade 3/4 diarrhoea and thrombocytopenia were main side effects.Conclusions:GEM plus DDP are effective in the treatment of advanced breast cancer with anthracycine and/or taxanes resistance.

BACKGROUND:Static cold storage is the main storage method of liver transplantation in the past 40 years. There are success cases in foreign countries about the use of mechanical reperfusion in liver transplantation, but there is no large-scale development in China. OBJECTIVE:To investigate and compare the inflammatory cytokines and apoptotic factors in isolated liver between static cold storage and hypothermic machine perfusion before and after liver transplantation. METHODS:There were donor group, static cold storage group and hypothermic machine perfusion group in the study, and 30 dogs were in each group. Liver specimens from donor dogs were subjected to static cold storage and then transplanted into dogs in the static cold storage group. Liver specimens from dogs in the static cold storage group were subjected to hypothermic machine perfusion and then transplanted into dogs in the hypothermic machine perfusion group. Liver specimens from dogs in the hypothermic machine perfusion were used in other experiments. Dogs in the donor group were euthanatized. After liver transplantation, 20 dogs from static cold storage group and hypothermic machine perfusion group were selected respectively for further study. RESULTS AND CONCLUSION: When the liver was separated from the dogs, inflammatory cytokines and apoptosis factors had no significant difference in the static cold storage group and hypothermic machine perfusion group (P > 0.05). P53 expression in these two groups had no significant difference before and after transplantation (P > 0.05). Interleukin-1βand interleukin-8 in these two groups had no significant difference before transplantation (P > 0.05). Compared with the static cold storage group, expressions of tumor necrosis factor-α, macrophage inflammatory protein-1α, macrophage inflammatory protein-1β, CC chemokine ligand 20 and FASR were significantly lower in the hypothermic machine perfusion group before transplantation (P< 0.01). Compared with the static cold storage, interleukin-1β, tumor necrosis factor-α, interleukin-8, macrophage inflammatory protein-1α, macrophage inflammatory protein-1β, CC chemokine ligand 20, FASR and nuclear factor-κB were reduced significantly in the hypothermic machine perfusion group at 60 minutes after transplantation (P < 0.01). Taken together, hypothermic machine perfusion can significantly reduce inflammatory cytokines and apoptosis factor, which is conducive for liver transplantation.

OBJECTIVE: To study the characteristics and regularity of adverse drug reactions (ADR) occurred in our hospital. METHODS: A total of 241 ADR cases occurred in our hospital form Jan. 2006 to Jun. 2009 were analyzed statistically in respect of patients’ status, category of drug, route of administration, organs and system involved in ADR and clinical manifestations. RESULTS: Of the total 241 ADR cases, 69.71%ADR cases were induced by antibacterials. 71.78% ADR cases were induced via intravenous administration. ADR mainly appeared as lesion of skin and appendants (50.92%). CONCLUSION: It is necessary to intervene and guide clinical use of drug, strengthen the monitoring of ADR and reduce the occurrences of ADR.

Objective To establish a rabbit posttraumatic acute diffuse brain swelling (PADBS) model and investigate the mechanism of action.Methods Fifty New Zealand rabbits were assigned to control group (n =10) and model group (n =40) according to random number table.The animal model of sinus balloon compression was established under intracranial pressure monitoring by using intracranial pressure probe.The model group was subdivided equally at 1.5 hours after compression,1.5 hours after decompression,3 hours after decompression and 4.5 hours after decompression,for which intracranial pressure,brain water content,pathological mechanism and ultrastructure were measured dynamically.Results The success rate of modeling was 83％ (33/40).Intracranial pressure was (4.9 ± 0.8)mmHg in control group,(50.1 ± 4.3) mmHg in 1.5 hours after compression group,(45.2 ± 1.7) mmHg in 1.5 hours after decompression group,(48.6 ± 2.2) mmHg in 3 hours after decompression group,and (59.1 ±2.5)mmHg in 4.5 hours after decompression group (P ＜0.05).Brain water content was (75.0 ± 0.6) ％ in control gorup,(76.7 ± 0.8) ％ in 1.5 hours after compression group,(77.3 ± 0.5) ％ in 1.5 hours after decompression group,(78.5 ± 0.6) ％ in 3 hours after decompression group,and (79.4 ± 0.7) ％ in 4.5 hours after decompression group (P ＜ 0.05).Vasogenic brain oedema was seen 1.5 hours after decompression.Cytotoxicity brain swelling generated with brain tissue destroyed 3 hours after decompression.The vicious cycle of high intracranial pressure and brain tissue destruction occurred 4.5 hours after decompression.Conclusion Under intracranial pressure probe monitoring,the rabbit model of PADBS by sinus balloon compression has stable pressure of the sinus balloon and has good reliability and repeatability,which provides a reliable evidence for further study on the possible mechanism and treatment methods of PADBS.

AIM:To observe the protective effect of Nano-Se on myocardium of experimental diabetes mice.METHODS:Sixty healthy male KM mice were chosen,ten of which were selected randomly as the normal control group.After fasted for 24 h,the rest 50 mice were injected with streptozotocin(STZ,50 mg/kg)intraperitoneally for 5 d.At 7th d,the blood-sugar was measured from vena caudalis,40 mice,of which blood-sugar exceeded 16.65mmol/L,were selected and randomized into 4 groups:the positive control group,low dose(25 ?g/kg)Nano-Se group,mid dose(50 ?g/kg)Nano-Se group,high dose(50 ?g/kg)Nano-Se group.All mice were given intragastric administration of 0.2 mL normal saline and corresponding dose of Nano-Se.The body weights were measured every week,and the dose of which was adjusted according to the change of the body weights.8 weeks later,the mice were killed and cardiac muscle of the left ventricle was taken.The myocardium was prepared to 10% homogenate for measuring SOD,GSH-Px activity and MDA content.The myocardial cell apoptosis was measured by TUNEL.The expressions of Bc1-2 and Bax proteins were determined by immunohistochemistry.RESULTS:Compared to normal group,the SOD and GSH-Px activities in positive control group decreased,MDA level increased,the rate of myocardial cell apoptosis increased significantly,Bc1-2 protein expression deceased and Bax protein expression increased.Compared to positive control group,the SOD and GSH-Px activities in low and mid dose Nano-Se groups expression increased,MDA level decreased,myocardial cell apoptosis rate decreased,Bc1-2 protein expression increased and Bax protein expression decreased.Moreover,the SOD and GSH-Px activities in high dose Nano-Se group decreased obviously compared to those in mid dose Nano-Se group.MDA level and myocardial cell apoptosis rate increased,Bc1-2 protein expression decreased and Bax protein expression increased,no significant difference in SOD,GSH-Px activity,MDA level and myocardial cell apoptosis rate was observed compared with positive control group.CONCLUSION:The damage of cardiac muscle is alleviated when a certain dose of Nano-Se is supplied to diabetes mice.The protective mechanism may be related to antioxidation,blood-sugar adjustment and the increase of Bc1-2 expressing.

AIM:To observe the effect of rosiglitazone (RGZ) pretreatment on the expression of peroxisome proliferator-activated receptor γ( PPARγ) , nuclear factor E2-related factor 2 ( Nrf2 ) and heme oxygenase-1 ( HO-1 ) in the microglia cells activated by thrombin.METHODS:Microglia cells were obtained from the brain tissues of the newborn rats and were primarily cultured in vitro.After cultured for 14 d, the microglia cells were used in the experiment.The iso-lated microglia cells were randomly divided into normal control group, thrombin stimulation group ( TH group) , rosiglita-zone intervention group ( RGZ +TH group ) and retinoic acid intervention group ( RA +TH group ) .The expression of PPARγ, Nrf2 and HO-1 was observed by immunocytochemistry, real-time PCR and Western blot.RESULTS:The number of positive staining cells of PPARγ, Nrf2 and HO-1 in TH group, RGZ+TH group and RA+TH group were increased re-markably as compared with control group.The significant increases in PPARγ, Nrf2 and HO-1 were observed in RGZ+TH group compared with other groups.The mRNA expression of PPARγ, Nrf2 and HO-1 in RGZ+TH group was increased significantly as compared with TH group, control group or RA+TH group (P<0.01), Besides, the mRNA expression of Nrf2 and HO-1 in RA+TH group was decreased as compared with TH group or RGZ+TH group (P<0.01).The protein levels of PPARγ, Nrf2 and HO-1 in RGZ+TH group were significantly increased as compared with TH group, control group or RA+TH group (P<0.01).The protein expression of Nrf2 and HO-1 in RA+TH group was decreased as com-pared with TH group or RGZ+TH group (P<0.01).CONCLUSION:Rosiglitazone pretreatment might increase the ex-pression of PPARγ, Nrf2 and HO-1 in the microglia cells activated by thrombin.By inhibiting the expression of Nrf2 after RA pretreatment, the expression of the downstream gene HO-1 is also influenced.The anti-oxidative stress effects of rosigli-tazone might be achieved partly by modulating Nrf2 to control the downstream gene HO-1.

Objective To study the development of visual function in blepharophimosis-ptosis-epianthusinversm syndrome(BPES) and evaluate the clinical effect of Multistage Correction.Design Retrospective case series.Participants 51 cases of BEPS in Beijing Tongren Hospital from June 2005 to May 2009.Methods Refraction and general ophthalmology were performed for each patient. Family history was inquired and corrected surgery were performed for every one.Main Outcome Measures Refraction,the length, width of palpebral fissure,and inner canthal distance were measured both preoperatively and postoperatively.Results 13 of the 51 cases had family history,27 cases had amblyopia and 12 cases had refractive error.4 cases combined with strabismus.Conclusions The risk of refractive error and amblyopia in patients with BPES is much higher than that of normal population,so careful regular visual follow -up and early surgery are necessary.BPES patients tend to have much more chance to get amblyopia,which will impact on the development of visual function,therefore surgery correction at early age is highly suggested.

Mesenchymal stem cell is a kind of multipotent hematopoietic stem cell.In the case of acute lung injury,it can differentiate into TypeⅠand TypeⅡepithelial cell,and to repair impaired tissues.In addition,mesenchymal stem cells have benefit effects in the treatment of lung injury by reducing proinflammatory factors IL-1,MIP-2,INF-?,TNF-?,increasing antiinflammatory factors IL-10,IL-1ra,IL-13 and alleviating inflammatory response to the acute lung injury.

Objective To activate the microglia cells by using thrombin,and then to observe the effect of precondition of rosiglitazone (RGZ)-pretreated on the expression change of peroxisome proliferator-activated receptor-γ (PPARγ),nicotinamide adenine dinucleotide phosphate:quinone oxidoreductase (NQO1) and γ-glutamylcysteine synthetase (γ-GCS).Methods Microglia cells were obtained from the brain tissues of the newborn rats and were primary cultured in vitro.The microglia cells were isolated in 14 days.The isolated microglia cells were randomly devided into normal control group (control group),thrombin stimulation group (stimulation group) and rosiglitazone intervention group (RGZ + TH group).The PPARγ,NQO1 and γ-GCS were observed by immunocytochemistry and real-time polymerase chain reaction (RT-PCR) methods.Results The immunocytochemistry showed that the number of stained cells of PPARγ,NQO1 and γ-GCS in stimulation group and RGZ + TH group were increased remarkably as compared with the control group.A significant increase of the PPARγ,NQO1 and γ-GCS was observed in the RGZ + TH group compared to the others.The RT-PCR method demonstrated that the expressions of PPARγ mRNA(211.88 ± 58.75),NQO1 mRNA(182.67 ± 62.09) and γ-GCS mRNA (188.17 ± 57.06) in RGZ + TH group were increased significantly as compared with the stimulation group (119.19 ± 44.58,101.73±32.19,108.81 ±19.71) or the control group (0.34±0.21,0.73±0.46,0.30±0.13;F=181.50,286.63,614.43,all P ＜ 0.01).Conclusion Medium-dose rosiglitazone-pretreated might increase the expression of PPARγ,NQO1 and γ-GCS in microglia cells activated by thrombin.Rosiglitazone might activate the PPARγso that increase its downstream gene to achieve its anti-oxidative stress effects.