BACKGROUND: Resin-modified glass ionomer (RMGI) cements have higher bond strength, especially can release fluoride. But there are fewer reports of the clinical application for the prevention of decalcification.OBJECTIVE: To test the benefit from using RMGI cement instead of a conventional composite resin in bracket bonding for patients with malocclusion, and observe bracket-failure rates and decalcification on enamel surfaces at pretreatment and at debonding.DESIGN: Observational and comparative trial.SETTING: The Second Hospital Affiliated to Hebei Medical University.PARTICIPANTS: Forty successive patients (358 teeth) with malocclusion admitted to the Department of Orthodontics in the Second Hospital Affiliated to Hebei Medical University, were selected for the study from July to August in 2002. All the patients (21 females and 19 males, mean age 16 years) had normal and complete anterior teeth, good oral hygiene. There were no obvious differences in bilateral teeth. Informed consents were obtained from all the subjects. The experiment was also approved by the ethical committee of the hospital. Experimental materials were RMGI adhesive (Fuji, GC, Japan, Lot 0005111) and composite resin cement (enamel adhesive of Beijing and Tianjin, Tianjin product, Lot 020402). Brackets produced from Hangzhou 3B and 37% phosphoric acid were used.METHODS: ①Bonding brackets: Subjects selected according to random procedure were divided into two groups, each with 20. GroupⅠ: The left buccal surfaces bonded with light-cure RMGI were etching for 30 seconds with 37% phosphoric acid, rinsed with water; the right buccal surfaces bonded with composite resin cement were etching for 60 seconds with 37% phosphoric acid, rinsed with water and dried; Group Ⅱ: After etching for 30 seconds with 37% phosphoric acid, the right buccal surfaces were rinsed with water and bonded brackets with light-cure RMGI. The left buccal surfaces were bonded brackets with composite resin cement after etching for 60 seconds with 37% phosphoric acid, rinsing with water and drying; Attachment of 0.036-cm NiTi wires with ligature to the brackets was conducted 10 minutes after light-curing. The information about differences in bilateral bonding materials was not told to patients. To ensure an equal bonding materials containing fluoride and minimize the error, all the patients were instructed to use toothpaste containing fluoride, a fluoride mouthwash was not prescribed. The treatment period was 9-26 months (mean 18 months).②Patients were rechecked at intervals of 4 weeks postoperatively. Each bonded tooth was checked for loose or missing brackets, and failures were recorded. A color transparency of anterior teeth area was taken using a standardized photographic technique. The enamel surface conditions were classified at a magnification of ×10. The condition of enamel surface recorded was made according to the scoring system by Geiger before treatment and at debonding.MAIN OUTCOME MEASURES: ①The number and site of bonding failures.②Enamel surface conditions at before treatment and debonding.RESULTS: Forty patients were all involved in the result analysis. Eliminating 4 teeth occurring bond failure and 4 teeth of opposite side at anterior teeth, a total of 232 teeth were evaluated.①The number and sit of bonding failures: There was no significant difference between the failure rates of RMGI adhesive and composite resin cement (P > 0.05). Significantly more premolar brackets failed than incisor brackets.②Decalcification of enamel surface: At debonding after treatment, the incidence rates of white spots in the surfaces bonded with the RMGI were significantly lower than that in the composite resin (25.9%, 38.8%, P < 0.05).CONCLUSION:The use of RMGI for brackets bonding results in a significant reduction in the incidence of white spot at debonding. Reducing etching time may obtain a similar survival rate with the routine etching time.

This stued examined the effects of nutritional support in 56 patients suffer from COPD. The influence of nutritional support on lung function and arteny blood gases after infusion of an amino acid solution (7% Fan Ming) were observed. The results suggested theft PaO2, FEV1. FVC levels were increased significantry compared to the control group. PaOz decreased significantly in Fan Ming infusion group compared 100 control group.

The development of the cochlear aqueduct and its aging change were investiga-ted in 234 temporal bones,ranging from 12-week-old embryo to adult by the lightmicroscope.The width of inner and outer opening,width and length of thecochlear aqueduct were parallel with the advance of fetal age.The length of thecochlear aqueduct at one year old was about the length of adult cochlear aqueduct.The diameter of the cochlear aqueduct at the child was wider than that of theadult.On the basis of morphology of the cochlear aqueduct and its characteristicof age,the developmental rule of the cochlear aqueduct,its function and clinicalsignificance were discussed.

Objective To probe the new mechanism of simvastatin on high-fat diet-induced kidney dam-age. Methods Female SD rats were subjected to a standard control diet(SCD)or high-fat diet(HFD)for 20 weeks,then the HFD group was randomly divided into HFD group and HFD group with simvastatin treatment (HFD+ST,10mg·kg-1·d-1 )for another 8 weeks. The expression of adiponectin,adiponectin receptors R1 and R2, Adenosine 5′-monophosphate(AMP)-activated protein kinase(AMPK),peroxisome proliferator-activated receptorα(PPARα),glucose regulated protein 78(GRP78)and GADD153(CHOP)in kidney were assessed respective-ly. Results Body weight and serum lipid levels in HFD group significantly increased ,expression of adiponectin and its receptors significantly down-regulated. Phosphorylation of AMPKα and PPARα expression decreased,and expression of GRP78 and CHOP up-regulated significantly. Above indexes in simvastatin treatment groups improved significantly. Conclusion Simvastatin can improve high-fat induced kidney damages ,probably by increasing expression of adiponectin and its receptors ,decreasing endoplasmic reticulum stress.

Objective: To detect the gene expression of Ku70, Ku80, ERCC4, lig4 and DNA-PKcs in non-homologous end joining pathway in human pdmary glioma tissues and normal brain tissues and to explore the underlying mechanism. Methods: The expression levels of Ku70, Ku80, ERCC4, lig4 and DNA-PKcsin in 36 glioma samples and 12 normal brain tissue samples were measured by SYBR Green real-time quantitative PCR. Methylation of DNA-PKcs was detected by methylation-specific PCR (MSP). Results: There was no significant difference in Ku70, Ku80, ERCC4 and lig4 expression between human primary glioma and normal brain tissues (P<0.05), while DNA-PKcs was significantly up-regulated (P= 0.002). The expression of DNA-PKcs was significantly higher in grade Ⅲ and Ⅳ glioma than that in grade Ⅱ glioma and normal brain tissues (P<0.05). Moreover, glioma tissues showed weaker methylation than normal brain tissues. Conclusion: The up-regulation of DNA-PKcs may be associated with pathogenesis of glioma. Demethylation of DNA-PKcs promoter is an important reason for its up-regulated expression in glioma.

Objectives:To determine the content of aminoacids in gastric cancer tissue and study the relationship between alterations of amino acids and cancer stages.　Methods:19 free amino acids of cancer tissue and paracancerous normal mucose were determined in 41 cases of gastric cancer.　Results:Most free amino acids were significantly increased in gastric cancer tissue as compared with those of paracancerous normal gastric tissue.The contents of proline,valine,methionine,isoleucine,leucine in advanced gastric cancer were significantly higher than those in early cases.　Conclusions:Gastric tumor tissue contains high amount of most free amino acids particularly in cases with advanced cancer..

Objective To assess the effect of low-dose cytarabine and aclarubicin in combination with gran-ulocyte colony-stimulating factor (G-CSF) protocol (CAG) in patients with acute myeloid leukemia (AML),and to understand the potential factors affecting the outcome of CAG induction therapy, therefore to find the optimum pa-tients for CAG therapy. Methods Twenty-one AML patients were enrolled in the current study. All patients were treated with CAG regimen including cytarabine (10 mg/m~2, subcutaneously, every 12 h, days 1 - 14), lacinomycin (5～7 mg/m~2,intravenously,every day, days 1 -8) ,and G-CSF (200 μg/m~2,subcutaneously, every day,12 h be-fore Ara-C was given) priming. Results The overall complete remission (CR) rate of the 21 AML patients was 66.7% (14/21). The CR rates was 87.5% (7/8) in patients older than 60 yrs,60.0% (9/15) in the refractory or relapsed patients,83.3% (5/6) in the MDS transformed AML patients. The CR rates for patients with hyperprolif-erative BM and median to poor proliferative BM were 33.3% and 91.7% ,respectively(P =0.009). The median o-verall survival (OS) time of the 21 AML patients was 450 days. Two-year survival rate estimated by Kaplan-Meier Method was 30.6%. The overall median disease free survival (DFS) was 165 days. The median OS time for those refractory or relapsed was 435 days. The median OS time for those with poor cytogenetic state or standard or good cytogenetic state was 140 days and 620 days, respectively (P = 0.001). The median OS time for patients with hyperproliferative BM and median to poor proliferative BM was 321 days and 620 days, respectively (P = 0.05). The median recovery time of granulocytes above 1.0×10~9/L was 8 days. The median duration of fever was 3.5 days. The rate of infections exceeding WHO grade Ⅱ was 42.9%. No early death occurred. Conclusions The CAG induction therapy may have a higher CR rate in patients with refractory or relapsed AML, elderly AML and secondary AML from MDS transformation, and extend the median overall survival time in refractory or relapsed patients. CAG therapy can not improve the outcome of patients whose BM was in high grade proliferation state or whose cytogenetic state was poor. CAG therapy can shorten the duration of agranulocytosis and decrease the inci-dence of serious infection. Therefore, CAG therapy is worth recommending to patients who can not endure the rou-tine intensive chemotherapy.

Objective: To investigate the therapeutic effects of allogeneic hematopoietic stem cell transplantation (allo-HSCT) with FLAG sequential busulfan/cyclophosphamide(Bu/Cy) conditioning regimen for refractory/relapsed acute myeloid leukemia. Methods: From February 2012 to June 2017, 21 patients with refractory/relapsed acute myeloid leukemia underwent allo-HSCT with FLAG sequential Bu/Cy conditioning regimen. Transplantation-related complications and clinical outcome were retrospectively analyzed. Results: After conditioning, no hepatic veno-occlusive disease (VOD) and grade Ⅲ hemorrhagic cystitis occurred. 76.2% (16/21) patients had fever with 4 septicemia. One patient died of septic shock before engraftment. Twenty patients achieved neutrophil engraftment with a median time of 13 days (range, 10 to 21 days). Seventeen patients achieved platelet engraftment with a median time of 18 days (range, 9 to 25 days). The cumulative incidence of acute graft-versus-host disease (aGVHD) was 39.5%, and 3 patients developed grade Ⅲ-Ⅳ aGVHD. Of 19 patients who survived more than 100 days after transplantation, 4 had local chronic graft-versus-host disease (cGVHD). Of 21 patients, the median survival time was 15 months (range, 0.5 to 67 months) post-transplantation. Transplantation-related mortality rate was 28.7%. Leukemia relapse occurred in 4 patients with a median time of 4 months (range, 3 to 8 months) after transplantation. The cumulative relapse rate at 1 year was 21.4%. The 1-year and 3-year overall survival (OS) rates were 60.7% and 54.9% respectively. Log-rank analysis revealed that bone marrow blasts ≥ 20% or extramedullary leukemia before transplantation, poor platelet engraftment and grade Ⅲ-Ⅳ aGVHD were significantly related to shortened OS (P<0.05). Conclusions Allo-HSCT with FLAG sequential Bu/Cy conditioning regimen in patients with refractory/relapsed myeloid leukemia has acceptable transplantation-related risk and relapse rate. The 1-year and 3-year OS rates are comparable with those in remission patients.

Background: The mitogen-activated extracellular signal-regulated kinase 1/2 (MEK1/2) inhibitor trametinib has shown promising therapeutic effects on melanoma, but its efficacy on colorectal cancer (CRC) is limited. Synthetic lethality arises with a combination of two or more separate gene mutations that causes cell death, whereas individual mutations keep cells alive. This study aimed to identify the genes responsible for resistance to trametinib in CRC cells, using a synthetic lethal short hairpin RNA (shRNA) screening approach. Methods: We infected HT29 cells with a pooled lentiviral shRNA library and applied next-generation sequencing to identify shRNAs with reduced abundance after 8-day treatment of 20 nmol/L trametinib. HCT116 and HT29 cells were used in validation studies. Stable ring finger protein 183 (RNF183)-overexpressing cell lines were generated by pcDNA4-myc/his-RNF183 transfection. Stable RNF183-knockdown cell lines were generated by infection of lentivi-ruses that express RNF183 shRNA, and small interference RNA (siRNA) was used to knock down RNF183 transiently. Quantitative real-time PCR was used to determine the mRNA expression. Western blotting, immunohistochemical analysis, and enzyme-linked immunosorbent assay (ELISA) were used to evaluate the protein abundance. MTT assay, colony formation assay, and subcutaneous xenograft tumor growth model were used to evaluate cell proliferation. Results: In the primary screening, we found that the abundance of RNF183 shRNA was markedly reduced after treatment with trametinib. Trametinib induced the expression of RNF183, which conferred resistance to drug-induced cell growth repression and apoptotic and non-apoptotic cell deaths. Moreover, interleukin-8 (IL-8) was a downstream gene of RNF183 and was required for the function of RNF183 in facilitating cell growth. Additionally, elevated RNF183 expression partly reduced the inhibitory effect of trametinib on IL-8 expression. Finally, xenograft tumor model showed the synergism of RNF183 knockdown and trametinib in repressing the growth of CRC cells in vivo. Conclusion: The RNF183-IL-8 axis is responsible for the resistance of CRC cells to the MEK1/2 inhibitor trametinib and may serve as a candidate target for combined therapy for CRC.

Objective To describe the demographic and clinical characteristics of patients with the diagnosis of multiple myeloma(MM)and to analyse the outcome of difierent regimens for the treatment of MM.Methods The study reviewed 332 MM cases diagnosed within the period from January 1,2002 to December 31,2002.These patients were tracked via their records to a total period of three years.Results First-line treatment:Totally 332 patients were included,among them 325(97.9%)patients received chemotherapy and 7(2.1%)patients received stem cell transplantation(SCT);Second-line treatment:197 patients were included,among them 190(96.5%)patients received chemotherapy and 7(3.6%)patients received SCT;Third-line treatment:92 patients were included,among them 88(95.7%)patients received chemotherapy and 4(4.4%)patients received SCT.Major adverse effects were follows:severe infection 19.3%,severe anaemia 19.3%,phlebothrombosis 1.2%,thrombocytopenia 16.9%,fever associated with neutropenia 18.1%.Conclusions Some curative effects can be achieved by using traditional treatment plans to treat patients suffering from MM,but new methods are expected to improve the prognosis.