Treatment of edentulous jaws with fixed implant supported denture is a complex procedure with high technical difficulty.In the present paper,the characteristics of screw retained implant denture and key points of manufacture are introduced in details.

Background:Upon inhibition of STAT3 signaling pathway,cucurbitacin-I elicits anticancer effect in various malignancies. However,the anticancer effect and underlying mechanism of cucurbitacin-I in gastric cancer is still elusive. Aims:To explore the effect of low nanomolar cucurbitacin-I on cell proliferation,cell cycle and apoptosis in human gastric cancer cells and the underlying mechanism in vitro. Methods:Human gastric adenocarcinoma cell lines AGS and HGC-27 were treated with cucurbitacin-I at low nanomolar concentration. The anti-proliferative effect of cucurbitacin-I was detected by CCK-8 assay and colony formation assay. Flow cytometry was used to assess the cell cycle and apoptosis. Expressions of cell cycle-related proteins,as well as activation of related pathways such as caspase-3 / PARP apoptotic pathway,STAT3, GADD45α and JNK/ p38 MAPK signaling pathways were determined by Western blotting. Results:Cucurbitacin-I markedly inhibited the growth of gastric cancer cells at low nanomolar concentration by inducing G2 / M phase arrest and apoptosis via a STAT3-independent manner. Furthermore,it was revealed that the anticancer effect of cucurbitacin-I was associated with up-regulation of GADD45α,activation of JNK/ p38 MAPK signaling pathway and the subsequent apoptotic events. Conclusions:The present study provides new insights into the mechanism of anticancer effect of cucurbitacin-I, supporting cucurbitacin-I as an attractive therapeutic drug in gastric cancer.

Aim To investigate whether rosuvastatin induced reduction of atherosclerotic plaque was related to the expression of Sialyltransferase ( ST6 Gal-Ⅰ) in ApoE-/ - mice. Methods Six-weeks old ApoE-/ -mice fed with high fat were divided randomly into three groups: baseline group ( n=12 ) , control group ( n=12 ) and rosuvastatin group ( n =12 ) . Sixteen weeks later, control group was sacrificed. Serum and aortic intima were saved. Control group and rosuvastatin group were fed for seven weeks continually. Concentra-tions of serum lipids(TC, TG, LDL and HDL) were analyzed. Sections from the aortic root were examined by Hematoxylin-Eosin( HE) staining. The size of ath-erosclerotic lesion in each section was evaluated. Ex-pression of ST6 Gal-Ⅰ in aortic intima was detected by immunohistochemistry. Results Plasma TG and LDL-C, plaque areas and intimal thickness of control group were significant higher than those of baseline group ( P<0. 05 ) . Those results indicated that the AS model was successfully constructed. After seven weeks, the plaque areas and concentrations of serum lipids of rosu-vastatin group were obviously smaller than those of con-trol group(P<0. 05). The expression of ST6Gal-Ⅰin aortic root was decreased in control group compared to the baseline, and which was increased in control group compared to the rosuvastatin group. Conclusion Ro-suvastatin could inhibit the progression of atherosclero-sis, which might be related to the expression of ST6Gal-Ⅰ in aortic root.

OBJECTIVEThis study aims to detect microRNA-17(mir-17) expression on the osteogenic differentiation of advanced glycation end products (AGEs)-stimulated hunman periodontal ligament stem cells (HPDLSCs) and to analyze the influence of these cells on this process.

METHODSHPDLSCs were isolated using limited dilution technique. After osteogenic differentiation occurred, different time points of mir-17 expression in the experimental groups were detected by real time polymerase chain reaction (PCR). The mir-17 overexpression and inhibition were evaluated using cell transfection technique. Differences in gene expressions were detected by real time PCR; differences in protein expressions were analyzed by Western blot.

RESULTSThe mir-17 expression was reduced after osteogenic differentiation occurred at 3, 7, and 14 d compared with that in the control group (P < 0.05). The expression levels of bone sialoprotein (BSP), Runt-related transcription factor-2 (Runx-2)and alkaline phosphatase (ALP) in the experimental groups were lower than those in the mimic control group when mir-17 expression increased. In addition, the protein expression levels of Runx-2 in the experimental groups were lower than those in the control group. The expression levels of BSP, Runx-2 and ALP in the experimental groups were higher than those in the inhibitor control group when mir-17 expression decreased. Likewise, the protein expression levels of Runx-2 in the experimental groups were higher than those in the control group.

CONCLUSIONAGEs inhibit the osteogenic differentiation of HPDLSCs by affecting mir-17 expression.

Alkaline Phosphatase ; Cell Differentiation ; Glycation End Products, Advanced ; Humans ; MicroRNAs ; Osteogenesis ; Periodontal Ligament ; Stem Cells

OBJECTIVEThe effect of advanced glycation end products (AGEs) on the osteogenic differentiation of humanperiodontal ligament stem cells(hPDLSCs) was discussed. Changes in the Wnt signaling pathway during glycation were also determined.

METHODSIn vitro tissue explanting method was primarily applied. Limiting diluted clone was cultured to obtain hPDLSCs in vitro. The subjects were divided into two groups: the healthy group (N-hPDLSCs) and the AGEs-stimulating group (A-hPDLSCs). Osteoblast mineralization was induced in the experimental groups. The following processes were performed: alizarin red staining; alkaline phosphatase (ALP) staining; real time polymerase chain reaction (real time PCR) for detecting osteogenic genes and Wnt classical pathway-related factors, DKK-1 and β-catenin; Western blot analysis. Bone protein and β-catenin were correlated in the nuclear expression.

RESULTSThe cells were osteogenically induced. ALP staining showed that the N-hPDLSCs displayed the deepest color. Alizarin red staining indicated that the A-hPDLSCs group had less calcified nodules than the N-hPDLSCs group. The real time PCR results suggested that the expression of relative osteogenic genes in A-hPDLSCs was quite low. Statistically significant differences in differentiation were found between groups (P < 0.05). The Western blot result was similar to that of real time PCR. Classical Wnt signaling pathway-related factor β-catenin was higher in A-hPDLSCs than in N-hPDLSCs. By contrast, DKK-1, which is an inhibitor in the Wnt pathway, had a significantly lower expression rate in A-hPDLSCs than in N-hPDLSCs. The Western blot result also showed that β-catenin expression in the nucleoprotein in A-hPDLSCs was notably higher than in N-hPDLSCs.

CONCLUSIONAGEs can inhibit hPDLSCs osteogenic differentiation. AGEs induce changes in the normal periodontal ligament stem cells classical Wnt pathway. Canonical Wnt pathway is reactivated because of AGEs stimulation.

Cell Differentiation ; Glycation End Products, Advanced ; Humans ; In Vitro Techniques ; Osteoblasts ; Osteogenesis ; Periodontal Ligament ; Stem Cells ; Wnt Proteins ; Wnt Signaling Pathway ; beta Catenin

OBJECTIVETo study the factors influencing short-term prognosis of tuberculous meningitis (TBM) in children.

METHODSThe clinical data of 137 hospitalized children with TBM between January 2007 and February 2011 were retrospectively reviewed. A total of 30 potential factors influencing short-term prognosis of TBM were evaluated by univariate analysis and multivariate logistic regression analysis.

RESULTSClinical staging showed that of the 137 children 21 cases (15.3%) were in the early stage, 67 cases (48.9%) in the medium stage and 49 cases (35.8%) in the late stage of TBM. The univariate analysis revealed 8 factors associated with a poor short-term prognosis: clinical stage of TBM (late), coma, positive Babinski signs, cranial nerve involvements, paralysis, seizures, obvious abnormalities in brain computed tomography (CT) or magnetic resonance imaging (MRI) and elevated protein concentrations in cerebrospinal fluid (CSF). Factors associated with a favourable short-term prognosis for TBM included glucocorticoid steroids therapy, positive reaction of PPD skin test and an increased length of stay in hospital. Multivariate logistic analysis revealed two independent risk factors for a poor short-term prognosis: clinical stage of TBM (late) (OR: 11.168, 95%CI: 3.521-35.426) and positive signs of meningeal irritation (OR: 4.275, 95%CI: 1.043-17.521). An increased length of stay in hospital was shown as a favorable factor (OR: 0.893, 95%CI: 0.825-0.968).

CONCLUSIONSLate-stage TBM and positive signs of meningeal irritation suggest a poor prognosis, while an appropriately longer length of stay in hospital may contribute to a favorable short-term prognosis for children with TBM.

Adolescent ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Male ; Prognosis ; Retrospective Studies ; Tuberculosis, Meningeal ; complications ; diagnosis

Humans ; Subacute Sclerosing Panencephalitis

ObjectiveTo investigate the expression of nuclear factor kappa B(NF-kB)-related mRNA and protein in bone tissue of rats with chronic fluorosis.MethodsThirty-six healthy SD rats,weighting 100 - 120 g,were randomly divided into three groups (twelve in each group ).Rats of control group were fed with tap water (NaF ＜ 1 mg/L) and the experimental rats were exposed to NaF(low-dose group:5 mg/L,high-dose group:50mg/L) through drinking water.All rats were killed at the eight month and metaphysic of femoral was collected.Bone tissues were stained with hematoxylin-eosin and observed under optical microscope.Bone fluorine was detected by ashing-fluorin ion selective electrode method.Serum content of tartrate-resistant acid phosphatase 5b(TRACP 5b)was detected by enzyme-linked immunosorbent assay(ELISA).The expressions of p50,p65 and IkBα's mRNA and protein in bone tissue was detected by real-time PCR and immunohistochemistry.ResultsBone sclerosis was observed under optical microscope.The contents of bone fluorine in both the low and high doses fluoride groups [(6.32 ± 1.23),( 10.89 ± 1.56) mg/kg] were significantly higher than that of the control [(3.06 ± 1.01 ) mg/kg,all P ＜ 0.05],and of that the high fluoride group was significantly higher than that of the low fluoride group(P ＜ 0.05).Serum content of TRACP 5b of the low fluoride group[(3.45 ± 1.85)U/L] was significantly higher than that of the control[(1.26 ± 0.23)U/L,P ＜ 0.05],but that of the high fluoride group[(2.74 ± 1.85)U/L] was lower than that of the low dose group(P ＜ 0.05).The mRNA expressions of p50 and IkBα in the low fluoride group(4.41 ± 0.44,1.15 ± 0.25) were significantly higher than that of the control(1.46 ± 0.10,0.26 ± 0.07,all P ＜ 0.05),but that of the high fluoride group(0.69 ± 0.09,0.14 ± 0.03) was lower than that of the low dose group(all P ＜ 0.05).The protein expressions of p50 and IkBα in the low fluoride group(152.96 ± 7.87,156.20 ± 9.75) were significantly higher than that of the control( 125.63 ± 9.85,118.97 ± 6.94,all P ＜ 0.05),but the high fluoride groups' ( 120.56 ±9.57,114.50 ± 7.61 ) was significantly lower than that of the low dose group(all P ＜ 0.05).ConclusionFluoride can lead to altered gene expression of NF-kB pathway,and the latter may be involved in fluoride induced bone damage.

Objective To investigate the relationship between change of relevant gene of nuclear factor kappa B(NF-κB) and osteoclast apoptosis in bone injury of rats with chronic fluorosis,and to reveal the mechanism of skeletal fluorosis.Methods Thirty-six healthy SD rats,weighting 100-120 g,were randomly divided into three groups(twelve in each group).Rats of control group were fed with tap water(NaF ＜ 1 mg/L) and the experimental rats were exposed to NaF(low-dose group:5 mg/L,high-dose group:50 mg/L) through drinking water to established chronic fluorosis model.All rats were killed at the eight month and metaphysic of femoral was collected.Bone tissues were stained with hematoxylin-eosin and observed under optical microscope.Serum content of tartrateresistant acid phosphatase 5b (TRACP 5b) was detected by enzyme-linked immunosorbent assay (ELISA).Osteoclast was identified and counted by tartrate-resistant acid phosphatase staining(TRAP).The expression of p50,IκBα,Bcl-2 and Bax's mRNA and protein of bone tissue was detected by Real-time PCR and immunohistochemistry.Results Bone sclerosis was observed under optical microscope.The content of TRACP 5b in serum and the number of osteoclast in the low fluoride group[(3.45 ± 1.85)U/L,(6.75 ± 1.29)/slice]were significantly higher than that of the control[(1.26 ± 0.23)U/L,(3.92 ± 1.38)/slice,all P ＜ 0.05],but that of the high fluoride group [(2.74 ± 1.85)U/L,(3.33 ± 1.07)/slice]were lower than that of the low dose group(all P ＜ 0.05).The mRNA expressions of p50,IκBα,Bcl-2 and Bax in low fluoride group(4.41 ± 0.44,1.15 ± 0.25,2.02 ± 0.11,1.25 ± 0.22) were significantly higher than that of the control(1.46 ± 0.10,0.26 ± 0.07,1.00 ± 0.06,0.74 ± 0.09,all P ＜ 0.05),but the high fluoride groups' (0.69 ± 0.09,0.14 ± 0.03,0.95 ± 0.08,0.62 ± 0.08) were lower than that of the low dose group(all P ＜ 0.05).The protein expressions of p50 and IκBα in the low fluoride group (152.96 ± 7.87,156.20 ± 9.75) were significantly higher than that of the control(125.63 ± 9.85,118.97 ± 6.94,all P ＜ 0.05),but the high fluoride group(120.56 ± 9.57,114.50 ± 7.61) were lower than the low dose group(all P ＜ 0.05).The protein expressions of Bcl-2 and Bax(170.61 ± 6.60,160.77 ± 7.66) and the ratio of Bcl-2/Bax (1.07 ± 0.08) were higher than the control(l10.73 ± 5.27,114.64 ± 5.83,0.96 ± 0.04,all P＜ 0.05),but the high fluoride group(81.70 ± 8.00,99.93 ± 3.83,0.81 ± 0.08) were lower than that of the control and the low dose group (all P ＜ 0.05).There was a significant positive correlation between protein expression of p50,IκBα and Bcl-2/Bax (r =0.587,0.676,all P ＜ 0.05).Conclusions Chronic fluorosis can cause change of the relevant gene of NF-κB in rat bone tissues and osteoclast apoptosis.The mechanism of skeletal fluorosis might be related to the abnormal of osteclast apoptosis caused by changes of NF-κB p50 and IκBα.

Objective To observe the expression of phosphoinositide 3-kinase(PI3K) and protein kinase B1 (Akt1) in PI3K/Akt signaling pathway in rat bones with fluorosis, and to reveal the mechanisms of the skeletal fluorosis. Methods Thirty-six SD rats were randomly divided into 3 groups (control group, low-dose fluorosis group, high-dose fluorosis group) and 12 rats were in each group according to body weight. The rats were fed with different concentrations of fluoride (NaF) to establish fluorosis models. Controls were fed with tap water( < 0.5 mg/L), experimental animals in low- or high-dose groups were fed with water containing NaF 5.0,50.0 mg/L, respectively. Rats were sacrificed after 6 months of treating with fluoride and the serum was kept for testing the bone metabolic markers of none gla protein(BGP) and cathepsin K(Cath-K) by enzyme-linked immunosorbent assay(ELISA), the proteins and mRNA levels of PI3K and Akt1 in rat bones were detected by immunohistochemistry and real time PCR, respectively. Results Each group of serum BGP and Cath-k were compared, the difference was statistically significant(F = 73.45,39.36, all P < 0.05). The contents of BGP[(1.99 ± 0.62), (2.38 ± 0.16)μg/L] and Cath-K [(89.07 ± 19.66), (110.16 ± 9.81)pmol/L] in the low-and high-dose fluorosis groups were higher than those in the control group[(0.15 ± 0.03)μg/L,( 18.32 ± 2.27)pmol/L], and the high fluorosis group was obviously higher than the low fluorosis group (all P < 0.05). Each group of serum PI3K and Akt1 protein and mRNA were compared, the difference was statistically significant(F- 178.16,118.08,38.81,52.31, all P< 0.05). Compared to the control group (181.55 ± 4.24,188.46 ± 2.18,3.84 ± 1.69,4.33 ± 0.89), the protein and mRNA expressions of PI3K(171.66 ± 2.85,154.12 ± 4.15,11.31 ± 4.18,20.54 ± 6.68), Akt1(177.47 ± 3.16,156.42 ± 3.18,12.52 ± 3.13,19.43 ± 5.36) were higher in the low- and high-dose fluorosis groups (all P < 0.05), and the high fluorosis group was obviously higher than the low fluorosis group (all P < 0.05). Conclusions BGP and Cath-K contents could be used as bone metabolic indices in the endemic fluorosis disease. Fluoride can increase the expression of PI3K and Akt1 mRNA and protein in bone tissue of fluorosis rats, and PI3K/Akt1 signaling pathway may be involved in the pathogenesis of bone injury caused by fluoride.