Objective:To analyze the prognosis of replanted permanent teeth in children and associated factors. To determine the onset time of root resorption and related factors. Methods: Clinical data of replanted teeth treated in Department of Pediatric Dentistry, Peking University, School and Hospital of Stomatology, from January 2000 to December 2006,were collected, and the follow-up period was no less than six months. The Fisher's exact test and cox regression were used for statistical analysis. Results: The study comprised of 39 patients with 50 replanted permanent teeth. The periodontium healing rate was 18%, while root resorption rate was 82%. Replacement resorption was the most common type of root resorption (64%).The factors significantly affecting periodontium healing were stage of root development and storage of avulsed teeth.Stage of root development and the time of endodontic treatment significantly affected the onset time of root resorption(P<0.05). Conclusion: Replacement resorption is the most common type of root resorption. The factors significantly affecting periodontium healing are stage of root development and storage of avulsed teeth. Stage of root development and the time of endodontic treatment significantly affect the onset time of root resorption.

This research is to investigate and analyze the reading characteristics of students in medical college of Foshan Science and Tecnoology University during their clinical practice period,to understand the trainee's reading motive,their expectation of a reading teacher,and their demanding of serve from the college library,thus exploring the method and the countermeasures of the reading guides

The preparation method, serum stability, efficiency of cellular uptake and apoptosis induction of the cell penetrating peptide TAT and cleavable PEG co-modified liposomes loaded with paclitaxel (C-TAT-Lipo) were investigated. The best preparation procedure was performed by orthogonal test based on single factor screening method. First, the paclitaxel (PTX)-loaded liposomes were prepared by filming-rehydration method, evaluated with entrapment efficiency and polydispersity index. The morphology of C-TAT-Lipo was characterized by transmission electron microscopy. Turbidity variations were monitored in the presence of fetal bovine serum (FBS) to evaluate the serum stability of the liposomes developed here. Next, the efficiency of cellular uptake of different Rho-PE-labeled liposomes on B16F1 cells in vitro was evaluated by confocal laser scanning microscopy (CLSM) and flow cytometry. The quantitative analysis of apoptosis induced by different PTX-loaded liposomes was performed by Annexin V-FITC/PI double staining. The optimal formulation was as follows: Chol : lipid: 1 : 8 (molar ratio); drug : lipid: 1 : 40 (mass ratio); lipid concentration: 3 mmol x L(-1); temperature of hydration: 25 degrees C. The mean size and polydispersity index of C-TAT-Lipo were about (97.97 +/- 3.68) nm and 0.196 +/- 0.037, the zeta potential was (-0.89 +/- 0.45) mV, the entrapment efficiency of paclitaxel was (90.16 +/- 1.53)%. The particle sizes did not exhibit significant variations in 50% FBS over 24 h at 37 degrees C. The efficiency of cellular uptake of the C-TAT-Lipo increased 1.40 fold following the cleavage of PEG. Apoptosis analysis showed 59.3% increase of the apoptosis and necrosis profile of C-TAT-Lipo after the detachment of PEG shells, which was markedly higher than that of N-TAT-LP with or without glutathione and SL, respectively. The results indicate that the C-TAT-Lipo is successfully prepared by filming-rehydration method and shows significant antitumor activities.
Animals ; Annexin A5 ; Apoptosis ; Cell Line, Tumor ; Cell-Penetrating Peptides ; pharmacology ; Fluorescein-5-isothiocyanate ; analogs & derivatives ; Liposomes ; chemistry ; Melanoma, Experimental ; Mice ; Microscopy, Confocal ; Paclitaxel ; pharmacology ; Particle Size ; Polyethylene Glycols ; chemistry

0.05).Conclusions:There was no difference in terms of both effect and toxicity among the three regimens. All of them were effective and could be well tolerated by advanced colorectal cancer patients.

OBJECTIVETo explore the molecule mechanism of Salidroside inducing directional differentiation of mouse mesenchymal stem cells (MSCs) into neuronal cells.

METHODSThe mouse multipotent mesenchymal precursor cell line (D1) was taken as the objective. Cultured MSCs were divided into the negative control group (complete culture solution), the positive control group (containing 1 mmol/L β-mercaptoethanol), the Salidroside induced group (20 mg/L Salidroside), and the blocked group (20 ng/ ml DKK1, a special inhibitor of Wnt/β-catenin signal pathway). All cells were inoculated in a 6-well plate (1 x 10(4) cells/cm2) and grouped for 24 h. The expression of p-catenin was detected by fluorescence Immunochemistry in the negative control group, the positive control group, and the Salidroside induced group. The expression of neuron-specific enolase (NSE), beta 3 class III tubulin (β-tubulin III), nuclear receptor related factor 1 (Nurr1), glial fibrillary acidic protein (GFAP) mRNA, Wnt3a, β-catenin, low-density lipoprotein receptor-related protein6 (LRP6), Axin mRNA were detected using reverse transcrip- tion PCR (RT-PCR). The expression of β-catenin and NSE protein were analyzed by Western blot in the negative control group, the positive control group, and the Salidroside induced group. Ca2+ chelating agents (EGTA), L-type Ca2+ channel blocker (Nifedpine), and IP3Ks special inhibitor (LY294002) were used to block Ca2+ signal pathway respectively. The expression of Wnt3a, LRP-6, Axin, glycogen syn- thase kinase (GSK-3), and β-catenin mRNA were detected by RT-PCR. The β-catenin protein expression was analyzed using Western blot.

RESULTSCompared with the positive control group, β-catenin protein was strong positively expressed; the expression of Wnt3a, β-catenin, LRP6, Axin, NSE, β-tubulin III, Nurr1 mRNA, and NSE protein were obviously up-regulated in the Salidroside induced group (P < 0.01). Compared with the positive control group and the Salidroside induced group, β-catenin, NSE, Nurr1, and β-tubulin III mRNA expression decreased; β-catenin and NSE protein expression were also down-regulated in the blocked group (P < 0.01). Compared with the Salidroside induced group, the expression of Wnt3a, LRP-6, β-catenin, and Axin mRNA were down-regulated in the Ca2+ signal blocked group and the salidroside induced group (P < 0.01, P < 0.05).

CONCLUSIONSalidroside affected directional differentia- tion of MSCs into neuronal cells through Wnt/β-catenin and Ca2+ signal pathway.

Animals ; Cell Differentiation ; drug effects ; Glucosides ; pharmacology ; Glycogen Synthase Kinase 3 ; Lipoproteins, LDL ; Low Density Lipoprotein Receptor-Related Protein-6 ; Mesenchymal Stromal Cells ; physiology ; Mice ; Neurons ; Phenols ; pharmacology ; Phosphopyruvate Hydratase ; RNA, Messenger ; Signal Transduction ; Wnt Signaling Pathway ; physiology ; beta Catenin ; metabolism

BACKGROUND:Studies on high glucose exposure in human periodontal ligament cel s usual y focus on the biological behaviors, pathways and secretory factors, but whether the metabolic memory is involved is little known. OBJECTIVE:To investigate the metabolic memory of high glucose exposure in human periodontal ligament cel s. METHODS:Human periodontal ligament cel s were primarily cultured and identified. Cel s at 5-8 passages were selected and randomized into four groups. Group A (controls):DMEM containing 5.5 mmol/L glucose for 8 days;group B (5-day memory group):DMEM containing 35 mmol/L glucose for 3 days and DMEM containing 5.5 mmol/L glucose for 5 days;group C (3-day memory group):DMEM containing 35 mmol/L glucose for 5 days and DMEM containing 5.5 mmol/L glucose for 3 days;group D (8-day high glucose group):DMEM containing 35 mmol/L glucose for 8 days. The cel proliferation was detected by cel counting kit-8, the cel apoptosis was determined by flow cytometry, and the levels of total proteins and alkaline phosphatase were investigated using ELISA. RESULTS AND CONCLUSION:Compared with the control group, the cel proliferation in the other three groups was significantly reduced (P<0.05), the number of apoptotic cel s was significantly increased, while the levels of total proteins and alkaline phosphatase were significantly decreased (P<0.05). These results suggest that high glucose causes persistent changes in human periodontal ligament cel s by inhibiting cel viability, increasing the apoptosis and downregulating the levels of the total proteins and alkaline phosphatase

Objective To observe the expression of neural nicotinic acetylcholine receptor subunit α3 (α3nAChR) and extracellular regulated protein kinases (ERK1/2),c-Jun N-terminal kinase (JNK),p38 kinases of mitogen-activated protein kinase (MAPK) pathway in human neuroblastoma cell line SH-SY5Y overexposed to fluoride,and try to investigate the molecular mechanism of cell damage caused by overexposure of fluoride.Methods The SH-SY5Y cell with low expression of α3nAChR suppressed by silence interference RNA served as α3nAChR silence group;the normal SH-SY5Y cell served as control group,and the effect of silencing of αt3nAChR gene in SHSY5Y was detected by Western blotting and real-time PCR;SH-SY5Y cell was treated with different concentrations of fluoride (0.000,0.005,0.050,0.500,1.000,2.500,5.000 mmol/L),the safe concentration of fluoride in SHSY5Y cell was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay;the SH-SY5Y cell of control group and α3nAChR silence group were treated with 4.000 mmol/L fluoride for 0,4,8,12,24,36,48 h according to the results of MTT assay;the expression of ERK1/2,JNK,p38 kinases of MAPK pathway in SH-SY5Y at protein levels was measured by Western blotting.Results The expression of α3nAChR mRNA (0.04 ± 0.03) and protein (12.0 ± 2.5) in α3nAChR silence group was decreased significantly compared with those of control group (1.00 ± 0.11,100.0 ± 11.3,t =24.58,28.80,all P ＜ 0.05).The viability of SH-SY5Y cell treated with 5.000 mmol/L fluoride (0.53 ± 0.15) was decreased significantly compared with that of SH-SY5Y cell treated with 0.000 mmol/L fluoride (1.05 ± 0.05,P ＜ 0.05).The increased expression of phospho-ERK1/2 was found in α3nAChR silence group and control group incubated with fluoride with time prolonged,and the expression of phospho-ERK1/2 increased significantly at time points 24,36 and 48 h (188.33 ± 7.33,200.00 ± 10.01,213.33 ± 11.55;125.33 ± 5.69,136.00 ± 4.52,155.33 ± 6.51) compared to 0 h in the same groups (100.00 ± 0.00,100.00 ± 0.00,all P ＜ 0.05),and the expression of phospho-ERK1/2 was higher significantly in α3nAChR silence group than those of control group (t =9.26,7.63,5.72,all P ＜ 0.05);no change of expression of total-ERK1/2 in the two groups was found with the passage of time.The gradually increased expression of phospho-JNK was found in α3nAChR silence group and control group,among which,the expression of phospho-JNK in o3nAChR silence group at time points 12,24,36 and 48 h (154.00 ± 6.25,149.00 ± 5.57,156.00 ± 6.08,141.67 ± 2.52) and in control group at 8,12,24,36,48 h (133.33 ± 10.69,173.00 ± 4.00,175.00 ± 11.79,200.67 ± 11.93,200.33 ± 18.58) was compared to those at 0 h in the same groups (100.00 ± 0.00,100.00 ± 0.00),and the difference was significant (all P ＜ 0.05);the higher expression of phospho-JNK was found in α3nAChR silence group other than control group at 8,12,24,36,48 h (t =-4.28,-5.02,-2.89,-8.33,-6.18,all P ＜ 0.05);no change of expression of total-JNK was found in the two groups (P ＞ 0.05).The increased expression of phospho-p38 was detected in control group at time points 24,36 and 48 h (120.33 ± 4.51,122.00 ± 7.55,119.67 ± 7.57) compared to 0 h in the same groups (100.00 ± 0.00,all P ＜ 0.05),and the expression of phospho-p38 was significantly higher than that in α3nAChR silence group at the same time points (93.33 ± 9.61,94.00 ± 5.01,98.33 ± 5.69,t =-4.01,-6.73,-5.59,all P ＜ 0.05);no change of expression of total-p38 was found in the two types of SH-SY5Y cells treated with fluoride (P ＞ 0.05).Conclusion When SH-SY5Y cells are exposed to fluoride;activation of ERK1/2 may be not depend on α3nAChR;α3nAChR may have protected the cell from apoptotic injury caused by activation of JNK pathway,and the activation of p38 may be depend on nAChRα3.

Objective To explore the effectiveness of the home-community-hospital network management (HCHNM) on the prevention and treatment of stroke.Methods From June to December 2011,HCHNM was implenented in Qingdao of Shandong Province to prevent and treat stroke patients.According to community residents healthcare records,A total of 80 stroke patients were randomly selected from Badahu and Fushanhou communities (study group) and another 80 patients from Zhongshan Road and Liaoning Road communities (control group).A household questionnaire survey was then conducted among these participants.Chi-square test and t test were used for data analysis.Results The overall effective rate of the study group was 86.25％ (69/80),which was significantly higher than that of the control group (67.5％) (x2=221.807,P＜0.05).The study group also showed largely improved quality of life (total score:t=4.593;physical fitness,family activities,movement,mood,self-care ability,social activities,upper limb function and work ability scores:t values were 7.775,2.244,5.329,3.832,5.463,2.979,5.924 and 3.555,respectively; all P＜0.05),although language,character,thinking and vision abilities had no statistically significant difference from the control group (t values were 0.561,1.466,0.831 and 1.000,respectively; all P＞0.05).The scores of daily activities and life satisfaction of the study group were higher than those of the control group,while per capita medical cost was much lower (t values were 12.998,20.760 and-29.777,respectively; all P＜0.05).Conclusions As an effective,safe and economy therapy model,HCHNM could improve rehabilitation,self-care ability,quality of life,and life satisfaction of community stroke patients.In addition,it greatly mitigates medical burden.

Background Peroxisome proliferator-activated receptor gamma (PPARγ) is one of nuclear transcription factors.It plays potential anti-inflammation,anti-fibrogenesis,anti-angiogenesis and neuroprotection roles in human.So the study of its physiological and pathological function in human and animals is still a focus.To understand the distribution of PPARγ in ocular tissues is important for the target treatment of eye diseases.Objective Current study was to investigate the expression of PPARγ in different parts of eye in rodent.Methods Cornea,lens,ciliary,retina and optical nerve were isolated from 6 SPF C57BL/6J mice and 1 SD rat.Western blot assay was used to detect the expressions of PPARγprotein in cornea,lens and retina.Immunohistochemistry was used to locate the distribution of PPARγ protein in cornea,lens,ciliary,retina and optical nerve.Also,the co-expression of PPARγ with glutamine synthetase (GS) (a Müller cell specific marker) and glial fibrillary acidic protein (GFAP)(an astrocyte specific marker) in retina and optic nerve was detected by immunofluorescent double staining.Results Western blot assay showed that PPARγ was expressed in the cornea,lens and retina of the mice.Immunohistochemistry revealed that PPARγ mainly located at corneal epithelium with the strongest staining in the basal cells,but only weak staining was seen in corneal endothelial cells and stroma cells.PPARγ was strongly expressed in epithelial cells and shallow cortex layer of mouse lens.In mouse retina,PPARγ was extensively and richly expressed in retinal ganglion cell layer,inner and outer plexiform layers and inner nuclear layer.In addition,PPARγ was also expressed in the non-pigmented epithelial cells in ciliary body.The co-locations of PPARγexpression with GS in retinal tissue and PPARγ expression with GFAP in optical nerve tissue were found in the mice.Conclusions PPARγis proved to distribute extensively in different ocular tissues.These results offer basis for the target treatment of relevant eye diseases.

In order to explore the effects of Panax notoginoside (PNS) on the expression of transforming growth factor β1 (TGF-β1) and Smad-7 in renal tissues of diabetes, a rat model of diabetic nephropathy was set up by intravenous injection of streptozotocin (STZ). Wistar rats were randomly divided into normal group, diabetic control group, group treated by PNS at low-dosage (PL), group treated by PNS at high-dosage (PH) and group treated by catopril (C), respectively. Fasting blood glucose (FBG), renal index, endogenous creatinine clearance rate (C(Cr)) and urinary albumin (UAlb) in 24 h were examined after 6 weeks. Meanwhile, the expressions of TGF-β1 and Smad7 in renal tissues were immunohistochemically dectected. At the end of the sixth week, FBG, renal index, C(cr), UAlb were all elevated significantly in control group (P<0.01). The expression of TGF-β1 protein was increased while Smad7 protein decreased in renal tissue (P<0.01). However, the treatment with PNS reversed the aforementioned changes in renal tissues of diabetic rats. These results indicate that PNS possess a protective effect on the kidney of diabetic rats and it might protect kidney by inhibiting the expression of TGF-β1 protein and enhancing the expression of Smad7 protein.