Preparation of nanometer δ- and β-bismuth trioxide by vacuum vapor-phase oxidation

A stable δ- and β-bismuth trioxide was prepared at room temperature by vacuum vapor-phase oxidation. The average crystal size of products was 14.6 nm (by XRD), the d(0.5) value was in the range from 62 nm to 69 nm, and geometric standard deviation(GSD) was from 1.42 to 1.64. The results show that δ-Bi2O3 is formed when quenching rates is rapid and β-Bi2O3 is formed when it is slow. The size of grains increases with rising reaction temperature, flow rate of carrier gas, residual pressure of system and longer growing time of grains.

Giant saturation absorption of tungsten trioxide film prepared based on the seedless layer hydrothermal method

Nonlinear materials have gained wide interest as saturable absorbers and pulse compression for pulsed laser applications due to their unique optical properties.This work investigates the third-order nonlinear phenomenon of tungsten trioxide(WO_(3))thin films.The giant nonlinear absorption and nonlinear refractive index of WO_(3)thin films were characterized by Z-scan method at 800 nm.We experimentally observed the giant saturable absorption(SA)and nonlinear refractive index of WO_(3)thin films prepared by the seedless layer hydrothermal method,with SA coefficient being as high as-2.59×105cm·GW^(-1).The SA coefficient is at least one order of magnitude larger than those of the conventional semiconductors.The nonlinear refractive index n_(2)of WO_(3)film has been observed for the first time in recent studies and the corresponding coefficient can be up to 1.793 cm^(2)·GW^(-1).The large third-order nonlinear optical(NLO)response enables WO_(3)thin films to be promising candidates for optoelectronic and photonic applications in the near-infrared domain.

Hesperidin attenuates arsenic trioxide-induced cardiac toxicity in rats

Objective:To explore the cardioprotective effect of hesperidin against arsenic trioxide-induced cardiac toxicity in rats.Methods:Cardiac toxicity was induced by oral administration of 4 mg/kg arsenic trioxide for 30 days.Hematological,biochemical,electrocardiography,echocardiography,and histopathological examinations were performed.Results:Hesperidin decreased the neutrophil-to-lymphocyte ratio,calcium,creatine kinase-myoglobin binding,lactate dehydrogenase,IL-6,and lipid peroxidation,as well as increased sodium and potassium concentration and superoxide dismutase and catalase activity in arsenic trioxide-intoxicated rats.Moreover,it reduced peak systolic velocity and end-diastolic velocity while increasing heart rate.Arsenic trioxide-induced histopathological damage to cardiac tissue was prominently alleviated by hesperidin treatment.Conclusions:Hesperidin attenuates arsenic trioxide-induced cardiac toxicity in rats.Therefore,it can be further explored as a cardioprotective agent.

Plasma synthesis of various polymorphs of tungsten trioxide nanoparticles using gliding electric discharge in humid air:characterization and photocatalytic properties

A gliding electric arc(glidarc)discharge generates a low-temperature plasma at atmospheric pressure.When the discharge occurs in humid air as the feed gas,the chemistry of a glidarc plasma consists of in situ formation of HO°and NO°as the primary chemical species.Tungsten trioxide(WO_(3))nanoparticles were successfully prepared by exposure of a liquid precursor to glidarc plasma.The WO_(3)samples were calcined at three different temperatures(300℃,500℃and 800℃),resulting in different pure polymorphs:γ-WO_(3)(at 300℃),β-WO_(3)(at 500℃)andα-WO_(3)(at 800℃)according to x-ray diffraction analysis.The identification of WO_(3)compounds was also confirmed by attenuated total reflection Fourier transform infrared spectroscopy analysis.Increase in the calcination temperature of WO_(3)induced a decrease in its specific surface area according to Brunauer–Emmett–Teller nitrogen physisorption analysis.The UV-visible results showed that the absorption bands of plasma-WO_(3)samples were more intense than those of WO_(3)samples obtained by a precipitation route,a classical method used for comparison.Consequently,this parameter can improve the photocatalytic properties of WO_(3)under visible light.The photodegradation(in sunlight conditions)of gentian violet,chosen as a model pollutant,confirmed the photocatalytic properties of plasma-WO_(3)samples.This novel synthesis method has great potential to improve the efficiency of advanced tungsten trioxide-based functional material preparation,as well as in pollution-reducing and energy-saving tungsten extractive metallurgy.

Arsenic trioxide inhibites transgenic tumor necrosis factor-α promoter activity in vascular smooth muscle cells and THP-1 monocytes in vitro

Aim This study was to evaluate the effect of arsenic trioxide （As2O3） on the transgenic TNF-α promoter activity in cultured vascular smooth muscle cells （VSMCs） and THP-1 monocytes. Methods Human TNF-α promoter was constructed by reporter gene system and was transiently transfected into VSMCs and THP-1 in vitro. The promoter activity was tested by luciferase activity with or without LPS and Ang Ⅱ stimulation, before and after different dosage of As2O3 treatment. Results 1. TNF-α promoter effectively expressed in VSMCs and THP-1 compared with CMV promoter （58.3% and 80.9%, respectively）. Both LPS and Ang Ⅱ significantly up-regulated TNF-α promoter activity （P〈0.05）. 2. As2O3 significantly inhibited, both intact and LPS/Ang Ⅱ stimulated promoter activity, in a dose dependent manner （P〈0.05）, and in both cell type. Conclusion These results manifested that, the inhibition effect of As2O3 on the activity of human TNF-α promoter indicated its potential inhibition on pro-inflammatory cytokine genes expression at transcriptional level and its potential anti-inflammatory property in the cardiovascular system.

Studies on the Mechanism of Arsenic Trioxide-Induced Apoptosis in HepG_2 Human Hepatocellular Carcinoma Cells

OBJECTIVE To study the anti-tumor effect of arsenic trioxide on the HepG2 human hepatocellular carcinoma cell line, and to explore its mechanism of action. METHODS The MTT assay was used to determine the inhibitory effect of As2O3 on HepG2 cells at various As2O3 concentrations. The expression of p-JNK, caspase-3 and PARP was detected by Western blots. RESULTS As2O3 markedly inhibited the growth of the HepG2 cells and induced apoptosis. The results of Western blot analysis showed that the As2O3-induced apoptosis was accompanied by caspase-3 and PARP activation. p-JNK was detected at 10 min following As2O3 treatment, and preceded to peak at 20 min, and decreased by 30 min. The total protein content did not obviously change. The activation of JNK occurred prior to cell apoptosis. SP600125, a JNK inhibitor, suppressed the As2O3-induced activation of caspase-3 and PARP cleavage. CONCLUSION As2O3 inhibits the proliferation of human HepG2 hepatocellular carcinoma cells by inducing apoptosis in vitro. As2O3-induced apoptosis is accessed through the caspase-3 pathway. The JNK signal-transduction pathway and caspase-3 are involved upstream in the As2O3 induced HepG2 apoptotic response.

Induction of apoptosis by arsenic trioxide and hydroxycamptothecin in gastric cancer cells in vitro

AIM To study the effects of arsenic trioxide andHCPT on different degrees of differentiated gastriccancer cells（SGC-7901,MKN-45,MKN-28）withrespect to both cytotoxicity and induction ofapoptosis in vitro.METHODS The cytotoxicity of As2O3 and HCPTon gastric cancer cells was determined by MTTassay.Morphologic changes of apoptosis ofgastric cancer cells were observed by lightmicroscopy and transmission electron microscopy.Apoptosis and cell cycle changes of gastric cancercells induced by HCPT and As2O3 were investigatedby TUNEL method and flow cytometry.RESULTS As2O3 and HCPT had remarkablecytotoxic effects on different degrees ofdifferentiated gastric cancer cells.The IC50ofAs2O3 on well differentiated gastric cancer cellMKN-28,moderately differentiated gastric cancercell SGC-7901,and poorly differentiated gastriccancer cell MKN-28 were 8.91 μmol/L,10.57μmol/L,and 11.65 μmol/L,respectively.The IC50of HCPT on MKN-28,SGC-7901,and MKN-45 were9.35 mg/L,10.21 mg/L,and 12.63 mg/Lrespectively after 48 h treatment.After 12 h ofexposure to both drugs,gastric cancer cellsexhibited morphologic features of apoptosis,including cell shrinkage,nuclear condensation, and formation of apoptotic bodies.A typicalsubdiploid peak before G0/G1 phase was observedby flow cytometry.The apoptotic rates of SGC-7901,MKN-45,and MKN-28 were 13.84%,22.52%,and 9.68%,respectively after 48 hexposure to 10 μmol/L As2O3.The apoptotic ratesof SGC-7901,MKN-45,and MKN-28 were 21.88%,12.35%,and 30.26%,respectively after 48 hexposure to 10 mg/L HCPT.The apoptotic indicewere 7%-15% as assessed by TUNEL method.The effect of As2O3 on SGC-7901 showedremarkable cell cycle specificity,which inducedcell death in G1 phase,and blocked G2/M phase.HCPT also showed a remarkable cell cyclespecificity,by inducing cell death and apoptosis inG1 phase and arrest of proliferation at S phase.CONCLUSION As2O3 and HCPT exhibitsignificant cytotoxicity on gastric cancer cells byinduction of apoptosis.As2O3 and HCPT mighthave a promising prospect in the treatment ofgastric cancer,which needs to be further studied.

Recent advances in arsenic trioxide encapsulated nanoparticles as drug delivery agents to solid cancers

Since arsenic trioxide was first approved as the front line therapy for acute promyelocytic leukemia 25 years ago,its anti-cancer properties for various malignancies have been under intense investigation.However,the clinical successes of arsenic trioxide in treating hematological cancers have not been translated to solid cancers.This is due to arsenic＇s rapid clearance by the body＇s immune system before reaching the tumor site.Several attempts have henceforth been made to increase its bioavailability toward solid cancers without increasing its dosage albeit without much success.This review summarizes the past and current utilization of arsenic trioxide in the medical field with primary focus on the implementation of nanotechnology for arsenic trioxide delivery to solid cancer cells.Different approaches that have been employed to increase arsenic＇s efficacy,specificity and bioavailability to solid cancer cells were evaluated and compared.The potential of combining different approaches or tailoring delivery vehicles to target specific types of solid cancers according to individual cancer characteristics and arsenic chemistry is proposed and discussed.

Arsenic trioxide induces apoptosis of human gastrointestinal cancer cells

AIM: To investigate the changes in apoptosis in gastrointestinal cancer cells from patients with gastrointestinal cancers treated with arsenic trioxide (As2O3); and to study the possible molecular mechanisms of such changes by detecting the expression levels of p53 and Bcl-2.

Effect of arsenic trioxide on human hepatoma cell line BEL-7402 cultured in vitro

AIM To study the effect of a varyingconcentrations of arsenic trioxide on humanhepatoma cell line BEL-?402 cultured in vitro andits mechanism of action.METHODS The BEL-7402 cells were treatedwith arsenic trioxide（at the concentrations of0.5,1,2 μmol/L,respectively）for 4 successivedays.The cell growth and proliferation wereobserved by cell counting and cell-growth curve.Morphologic changes were studied withelectronmicroscopy.Flow cytometry was usedto assay celI-DNA distribution and the proteinexpression of Bcl-2 and Bax detected byimmunocytochemical method.RESULTS The cell growth was significantlyinhibited by varying concentrations of arsenictrioxide as revealed by cell counting and cell-growth curve,which was dose- and time-dependent.Arsenic trioxide treatment at 0.5,1and 2 μmol/L resulted in a sub-G1 cell peak,theapoptosis rate of the control group was 9.31%and that of 0.5 μmol/L arsenic trioxide 15.53%,no significant difference was seen between thetwo.The apoptosis rates of 1,2 μmol/L arsenictrioxide were 19.10% and 21.87% respectively,which were much higher（both P【0.05）.Decrease of G0/G1 phase cells and increase of Sphase cells were observed by flow cytometry,suggesting the inhibition effect of 0.5,1,2 μmol/L arsenic trioxide on BEL-7402 cell lay in the G0/G1 phase.Morphologic changes such asintact cell membrane,nucleic condensation,apoptotic body formation were seen undertransmission electronmicrescopy,whereas the0.5 mol/L arsenic trioxide-treated BEL-7402cells showed decrease of nucleocytoplasmicratio,round nucleus,well-differentiatedorganelles in the cytoplasm.The processes andmicrovilli on the cell surface of the experimentalgroups under scanning electron microscopy weresignificantly decreased.High expressions ofBcl-2 and Bax were detected in 1 and 2 μmol/Larsenic trioxide-treated cells,these were 46%,87.33% and 83.08%,95.83% respectively,among which that of Bax was more significant.Arsenic trioxide treatment at 0.5 μmol/Lresulted in a higher expression level of Bcl-2 andlower expression level of Bax,which were8.81% and 3.83% respectively,as comparedwith that of the control group（15.33%）（P1【0.01,P2【0.01）.CONCLUSION Arsenic trioxide not onlyinhibited proliferation but also induced apoptosisof human hepatoma cell line BEL-7402.Theinduced-apoptosis effect of 1,2 μmol/L arsenictrioxide was related to the expression level ofBcl-2 and Bax.

A Simple Method of Electrospun Tungsten Trioxide Nanofibers with Enhanced Visible-Light Photocatalytic Activity

The present study involves the fabrication of tungsten trioxide(WO3) nanofibers by an electrospinning technique using polyvinyl pyrrolidone(PVP)/citric acid/tungstic acid as precursor solution. It was found that the PVP concentration was one of the most crucial processing parameters determining the final properties of WO3 nanofibers. The optimum concentration of PVP was from 75 to 94 g L-1. The average diameter of the nanofibers increases with increasing the PVP concentration, whereas it is decreased after sintering and orthorhombic structure were formed at 500 °C. The photocatalytic properties of the as-synthesized nanofibers were also investigated by degrading methylene blue and twofold efficiency was obtained compared with that of commercial WO3 microparticles.

A study on arsenic trioxide inducing in vitro apoptosis of gastric cancer cell lines

INTRODUCTION Cell apoptosis,which involves the biologic regulation of the numbers and vital activity of cells,is an important metaboloc process in both normal cells and tumor cells.

Cell cycle arrest and apoptotic cell death in cultured human gastric carcinoma cells mediated by arsenic trioxide

AIM: To investigate the effect of arsenic trioxide on human gastric cancer cell line MKN45 with respect to both cytotoxicity and induction of apoptosis in vitro. METHODS: MKN45 cells were treated with arsenic trioxide (As2O3) at the concentration of 1, 5, and 10 μmol/L, respectively, for three successive days. Cell growth and proliferation were observed by cell counting and trypan blue exclusion. Cytotoxicity of As2O3 was determined by MTT assay. Morphologic changes were studied with light microscopy. Flow cytometry was used to assay cell DNA distribution and apoptotic cells were confirmed with terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and DNA electrophoresis. RESULTS: The growth of MKN45 cells was significantly inhibited by As2O3 which was confirmed by colony-forming assay. After 7 d of culture with various concentrations of As2O3, colony-forming capacity of MKN45 cells decreased with As2O3 increment in comparison with that of control group. The inhibitory rate of colony-formation was 38.5%, 99.1%, and 99.5% when the concentration of As2O3 was 1, 5, and 10 μmol/L in culture medium, respectively. The cell number of a single colony in drug treatment groups was less than that of control group. The cell-killing rate of As2O3 to MKN45 cells was both dose- and time-dependent with an IC50 of (11.05±0.25) μmol/L After incubation in 10 μmol/L As2O3 for 24 h, the cell-killing rate was 27.1%, and it was close to 50% after 48 h. The results showed that As2O3 induced time- and dose-dependent apoptosis in MKN45 cells, blocked at G2/M phase. The apoptotic peak (sub-G1 phase) appeared and cell apoptotic rate in MKN45 cells was 18.3-32.5% after treatment by 10 umol/L As2O3 for 48 h. The percentage of G2/M cell of the experimental groups was 2.0-5.0 times than that of the control group. Gel electrophoresis of DNA from cells treated with each concentration of As2O3 for 48 h revealed a 'ladder' pattern, indicating preferential DNA degradation at the internucleosomal, linker DNA sections. TUNEL also demonstrated strand breaks in DNA of MKN45 cells treated with As2O3, while control cells showed negative labeling. CONCLUSION: As2O3 can induce apoptosis of human gastric carcinoma cells MKN45, which is the basis of its effectiveness. It shows great potential in the treatment of gastric carcinoma.

Long-term observation of the mineral trioxide aggregate extrusion into the periapical lesion:a case series

One-step apexification using mineral trioxide aggregate(MTA) has been reported as an alternative treatment modality with more benefits than the use of long-term calcium hydroxide for teeth with open apex.However,orthograde placement of MTA is a challenging procedure in terms of length control.This case series describes the sequence of events following apical extrusion of MTA into the periapical area during a one-step apexification procedure for maxillary central incisor with an infected immature apex.Detailed long-term observation revealed complete resolution of the periapical radiolucent lesion around the extruded MTA.These cases revealed that direct contact with MTA had no negative effects on healing of the periapical tissues.However,intentional MTA overfilling into the periapical lesion is not to be recommended.

Effect of diboron trioxide on the crushing strength and smelting mechanism of high-chromium vanadium–titanium magnetite pellets

The effect of diboron trioxide(B_2O_3) on the crushing strength and smelting mechanism of high-chromium vanadium–titanium magnetite pellets was investigated in this work. The main characterization methods were X-ray fluorescence, inductively coupled plasma–atomic emission spectroscopy, mercury injection porosimetry, X-ray diffraction, metallographic microscopy, and scanning electron microscopy–energy-dispersive X-ray spectroscopy. The results showed that the crushing strength increased greatly with increasing B_2O_3 content and that the increase in crushing strength was strongly correlated with a decrease in porosity, the formation of liquid phases, and the growth and recrystallization consolidation of hematite crystalline grains. The smelting properties were measured under simulated blast furnace conditions; the results showed that the smelting properties within a certain B_2O_3 content range were improved and optimized except in the softening stage. The valuable element B was easily transformed to the slag, and this phenomenon became increasingly evident with increasing B_2O_3 content. The formation of Ti(C,N) was mostly avoided, and the slag and melted iron were separated well during smelting with the addition of B_2O_3. The size increase of the melted iron was consistent with the gradual optimization of the dripping characteristics with increasing B_2O_3 content.

Anti-hepatoma effect of arsenic trioxide on experimental liver cancer induced by 2-acetamidofluorene in rats

AIM： To study the anti-hepatoma efficiency of arsenic trioxide （As2O3） in the treatment of experimental rat hepatocellular carcinoma （HCC） induced by 2-acetamidofluorene （2-FAA） and to elucidate the possible mechanisms. METHODS： SD rats （2 mo old） had been fed with 2-FAA for 8 wk to induce HCC, and then they were treated with As2O3 or matrine. On d 29, the rats were killed and the liver was weighed and liver tumors were counted. The histological changes of liver tissue were observed under microscope, and the cellular dynamic parameters were studied by flow cytometry. Immunohistochemistry （two-step method） was used to observe the expression of vascular endothelial growth factor （VEGF） and micro-vessel density （MVD） on consecutive sections. The pathological parameters were also analyzed, the levels of serum aspartate aminotransferase （AST）, alanine aminotransferase （ALT）, total bilirubin （TBi）, and direct bilirubin （DBi）. RESULTS： The number of liver tumors decreased significantly in groups treated with As2O3, especially in medium-dose （1 mg/kg） group （t = 2.80, P〈0.01）. As2O3 caused HCC cell death via apoptosis; necrosis was seen and apoptosis was common when the dose was 1 mg/kg. Proliferation index decreased sharply in medium-dose （1 mg/kg） group （7.87±4.11 vs24.46±6.49, t= 2087, P〈0.01）, but not in 0.2 mg/kg group. However, S-phase fraction decreased dramatically in both groups, it reached the bottom level only when the dose was i mg/kg compared with control （0.40±0.13 vs3.01±0.51, t= 2.97, P〈0.01）, and it was obviously accompanied with accumulation of cells in G0/G1 （G0/G1 restriction）. The expressions of VEGF and MVD in medium-dose （1 mg/kg） group were significantly lower than normal saline group （0.63±0.74 vs2.44±0.88, P〈0.05; 15.75±3.99 vs47.44±13.41, t= 2.80, P〈0.01）. Compared with normal saline group, mediumand low-dose groups As203 and matrine lowered the levels of ALT in serum （61.46±9.46, 63.75±20.40, 61.18±13.00 vs 108.98±29.86, t= 2.14, P〈0.05）, but had no effect onthe level of serum AST, TBi, and DBi. CONCLUSION： As203 had inhibitory effect on growth of experimental HCC in rats induced by 2-FAA, but had no obvious effect on normal hepatic cells. The mechanisms may involve decrease of cell division, accumulation of cells in G0/G1 phase, apoptosis of tumor cells, and inhibitory effect on angiogenesis through blocking VEGF.

Inhibitory effect of arsenic trioxide on angiogenesis and expression of vascular endothelial growth factor in gastric cancer

AIM: To investigate the inhibitory effect of As2O3 on angiogenesis of tumor and expression of vascular endothelial growth factor (VEGF) in tumor cells in vivo and in vitro. METHODS: The solid tumor model was formed in nude mice with the gastric cancer cell line SGC-7901. The animals were randomly divided into three groups. As2O3 was injected into the arsenic-treated groups (2.5 mg/kg and 5 mg/kg) and the same volume of saline solution was injected into the control group. Microvessel density (MVD) and expression of VEGF were detected with immunofluorescence laser confocal technology. Further expression of VEGF protein and VEGF mRNA was measured with Western bloting and fluorescence quantitative RT- PCR in SGC-7901 cells treated with As2O3. RESULTS: In nude mice, after treatment with 5 mg/kg and 2.5 mg/kg As2O3 respectively, about 50% and 30% tumor growth inhibition were observed correspondingly (P < 0.05, P < 0.05). Decrease in MVD appeared in As2O3-treated tumors compared with control group (P < 0.001, P < 0.001). MVD in tumors was significantly lower in 5 mg/kg group than in 2.5 mg/kg group (P < 0.01). The fluorescence intensity levels of VEGF in tumor cells were significantly lowered in the arsenic-treated groups (P < 0.01, P < 0.01). The fluorescence intensity level of VEGF in 5 mg/kg group was lower than that in 2.5 mg/ kg group (P < 0.01). In vitro, the expression of VEGF protein decreased in dose- and time-dependent manner after the treatment with As2O3, but in VEGF mRNA no significant difference was found between the control group and the treated groups. CONCLUSION: As2O3 can inhibit solid tumor growth by inhibiting the formation of new blood vessels. One of the mechanisms is that As2O3 can inhibit VEGF protein expression.

Effect of arsenic trioxide on vascular endothelial cell proliferation and expression of vascular endothelial growth factor receptors Flt-1 and KDR in gastric cancer in nude mice

AIM： To investigate the effect of arsenic trioxide （As2O3） on expression of vascular endothelial growth factor receptor-1 （VEGFR-1, Flt-1） and VEGFR-2 （KDR） in human gastric tumor cells and proliferation of vascular endothelial cells.METHODS： The solid tumor model was formed in nude mice with the gastric cancer cell line SGC-7901. The animals were treated with As2O3. Microvessel density （MVD） and expression of Flt-1 and KDR were detected by immunofluorescence laser confocal microscopy. SGC-7901 cells were treated respectively by exogenous recombinant human VEGF165 or VEGF165 ＋ As2O3. Cell viability was measured by MTT assay. Cell viability of ECV304 cells was measured by MTT assay, and cell cycle and apoptosis were analyzed using flow cytometry.RESULTS： The tumor growth inhibition was 30.33% and 50.85%, respectively, in mice treated with As2O3 2.5 and 5 mg/kg. MVD was significantly lower in arsenic-treated mice than in the control group. The fluorescence intensity levels of Flt-1 and KDR were significantly less in the arsenic-treated mice than in the control group. VEGF165 may accelerate growth of SGC7901 cells, but As2O3 may disturb the stimulating effect of VEGF165. ECV304 cell growth was suppressed by 76.51%, 71.09% and 61.49% after 48 h treatment with As2O3 at 0.5, 2.5 and 5 μmol/L, respectively. Early apoptosis in the As2O3- treated mice was 2.88-5.1 times higher than that in the controls, and late apoptosis was 1.17-1.67 times higher than that in the controls.CONCLUSION： Our results showed that As2O3 delays tumor growth, inhibits MVD, down-regulates Flt-1 and KDR expression, and disturbs the stimulating effect of VEGF165 on the growth of SGC7901 cells. These results suggest that As2O3 might delay growth of gastric tumors through inhibiting the paracrine and autocrine pathways of VEGF/VEGFRs.

Role of Low Dosage Arsenic Trioxide on Pulmonary Dendritic Cells in Asthmatic Mice

Objective: To investigate the distribution and recruitment of pulm onary dendritic cells (DCs) and the influence of low dosage arsenic trioxide (As 2O 3) on them in the airway of asthmatic mice. Methods: Thirty BALB/c mice were randomly divided into 3 groups: the control group, the asthmat ic group and the As 2O 3 treated group. The mice asthmatic model was induced v ia sensitizing with peritoneal injection of ovalbumin (OVA) for two times and th en provocated with aerosol inhalation of OVA for a week. The treated group was p eritoneally injected with 0.2 ml solution of As 2O 3 (4mg/kg) 0.5h after each provocation. The immunohistochemistry and computerised image analysis were appli ed to detect quantitatively the DCs in the lung and airway of mice. Resul ts: All intraepithelial nonlymphoid dendritic cells 145 (NLDC 145) throughout the respiratory tree in the mice of the control group formed a netwo rk with the density of DCs varying from (575±54) cells/mm 2 epithelial surface in the large airway, to (68±12) cells/mm 2 epithelial surface in the small ai rway. The distribution of airway NLDC 145 + in the asthmatic group was simil ar to that in the control group, but its density was significantly upregulated ( P <0.01). The distribution of airway NLDC 145 in the treated group was sim ilar to that in the asthmatic group, only its density was significantly downregu lated ( P <0.01). Conclusion: There is an integral network of N LDC 145 + throughout the respiratory tree. To downregulate the density but n ot change the distribution of pulmonary DCs could be an important therapeutic me chanism of low dosage As 2O 3 in treating asthma.

Effect of acid etching on marginal adaptation of mineral trioxide aggregate to apical dentin:microcomputed tomography and scanning electron microscopy analysis

The present investigation assessed the effect of acid etching on marginal adaptation of white- and gray-colored mineral trioxide aggregate （MTA） to apical dentin using microcomputed tomography （micro-CT） and scanning electron microscopy （SEM）. Sixty-four extracted single-rooted human maxillary teeth were used. Following root-end resection and apical preparation, the teeth were equally divided into four groups according to the following root end filling materials： （i） white-colored MTA （WMTA）, （ii） etched WMTA （EWMTA）, （iii） gray-colored MTA （GMTA） and （iv） etched GMTA （EGMTA）. After 48 h, the interface between root-end filling materials and the dentinal walls was assessed using micro-CT and SEM. Data were statistically analyzed using the KruskaI-Wallis and Dunn tests. Micro-CT analysis revealed gap volumes between the apical cavity dentin walls and EGMTA, GMTA, EWMTA and WMTA of （0.007 1±0.004） mm3, （0.053±0.002） mm3, （0.003 6±0.001） mm3 and （0.005 9±0.002） mm3 respectively. SEM analysis revealed gap sizes for EGMTA, WMTA, EWMTA and GMTA to be （492.3±13.8） μm, （594.5±17.12）μm, （543.1±15.33） μm and （910.7±26.2）μm respectively. A significant difference in gap size between root end preparations filled with GMTA and EGMTA was found （P〈O.05）. No significance difference in gap size between WMTA and EWMTA were found in either SEM or micro-CT analysis. In conclusion, pre-etching of apical dentin can provide a better seal for GMTA but not for WMTA.