Objective:To establish three-dimensional(3D)finite element model of the mandible first molar,and to study the stress distribution.Methods:3D finite element model of the mandible first molar was constructed by CT image reconstruction technique.Then MIMICS software was used to separate the areas and finish 3D calculation.GEOMAGIC software was applied to modify and generate a NURBS surface in each patch.All components of the model were assembled under the ANSYS preprocessor.Specific material parame-ters were selected to simulate the various restoration and dentin status.The 3D finite element model was applied to analyze the stress distribution of the molar under 1 4 different pressure loading conditions.Results:The 3D finite element model of the mandible first molar was established,which was consistent to the situation observed in the clinical environment.The pressure loading n2,n8,n9,n1 0,n1 1 , n1 2,n1 3,n1 4 can be used to represent the bite pressure.Conclusion:It is a practical and accurate way to establish 3D finite element model by CT image reconstruction technique and reverse engineering software MIMICS and GEOMAGIC.

Objective:To establish three-dimensional(3D) finite element models of the first mandibular molar restored with three post and core systems.Methods:Three 3D finite element models of the restored first mandibular molars were constructed by using CT image reconstruction technique.Then MIMICS software was used to separate the areas and to finish 3D calculation.GEOMAGIC software was applied to modify and generate a NURBS surface in each patch.All components of the models were assembled under the ANSYS preprocessor.Specific materials parameters were selected to simulate the various restoration and dentin status.Results:The 3D finite element models of restored first mandible molars were successfully established,which were consistent to the situation observed in the clinical environment.Conclusion:It is a practical and accurate method to establish three-dimensional finite element models by CT image reconstruction technique and reverse engineering software MIMICS and GEOMAGIC.

AIM: To know the psychological conditions of various cataract patients in pre- and post-operative periods.METHODS: From June 2008 to June 2009, 278 cataract patients had been asked to complete a questionnaire anonymously of their self-evaluation of symptoms scale (SCL) before and after operation. In their pre-operative and post-operative surveys, the results were compared with the norms respectively. Patients were divided into two groups. Group A were age-related cataract patients; while Group B were cataract patients with glaucoma, trauma or metabolic disease.RESULTS: When cataract patients' masculine scores of somatization, depression, anxiety and fear factors before and after the operation rank higher than the norms, the differences had statistical significance(P＜0.05), especially the somatization factor(P＜0.01).While cataract patients with diseases such as glaucoma, trauma or diabetes got higher marks than age-related cataract patients in the aspects of anxiety, somatization, depression (P<0.05), and fear factors, the differences were of statistical significance(P<0.01).CONCLUSION: Cataract patients both in pre- and post- and operative periods have somatization behaviors and emotions of depression, anxiety and fear. Cataract patients with glaucoma, trauma or diabetes especially anxiety have more obvious symptoms than age-related cataract patients.

Objective To determine whether rabbit articular chondrocytes express growth factor genes delivered by recombined rat TGF beta 1,IGF 1 and what other influences on chondrocytes are,and to determine which gene is the best one for osteoarthritis therapy.Methods Monolayer cultures of rabbit articular chondrocytes were infected with recombinant plasmid pcDNA 3 and pAT 153 carrying genes encoding the following growth factors respectively:TGF beta 1 and IGF 1.The synthesis of TGF beta 1,IGF 1 and type Ⅱ collagen was measured by in situ hybridization,immunohistochemistry,immunofluoroscopy,flow cytometer and 3 H TdR radiolabeling.Results The expression of TGF beta1,IGF 1 and type Ⅱ collagen was high beyond control levels ( P

Objective To analyze the risk factors of early renal damage in children with Henoch Schonlein purpura(HSP).Methods The clinical data of 196 children with HSP admitted to our hospital from April 2012 to January 2016 were analyzed retrospectively.They were divided into the renal damage group and non-renal damage group within 90 d after confirmed diagnosis.The related clinical data such as serum immunoglobulin and urinary microalbumin were compared between the two groups,and the risk factors of early renal damage in children with HSP were screened.Results There were significant differences between the two groups on age,joint symptoms,recurrent purpura,persistent rash,gastrointestinal bleeding and abdominal pain(with χ2 or t of 11.345,16.223,11.275,43.211,12.592,17.771,P<0.05).The white blood cell count,platelet count,immunoglobulin A(IgA) level and urinary albumin level also showed significant differences between the two groups(t=33.750,60.442,9.451,8.458,P<0.05).The multivariate regression analysis showed that the independent risk factors for early renal damage in children with HSP included age(OR=2.703),recurrent purpura(OR=2.721),persistent skin rash(OR=1.782),gastrointestinal bleeding(OR=11.472),abdominal pain(OR=2.046),IgA level(OR=1.221) and urine microalbumin(OR=3.214).Conclusion Age,recurrent purpura,persistent skin rash,gastrointestinal bleeding,abdominal pain,IgA level and urine microalbumin are closely related to early renal damage in children with HSP.

Aim To study the regulatory effects of PMA,a PKC activator,on Kir 2.3 channel function expressed in Xenopus oocytes and COS-7 cells,and PIP2 involvement in these regulations.Methods Kir 2.3 channel was expressed in Xenopus oocytes and COS-7 cell by RNA microinjection and DNA transfection using calcium phosphate precipitate,respectively.Two-electrode-voltage-clamp and whole-cell patch clamp were used to record the Kir 2.3 current in Xenopus oocytes and COS-7 cell.The PIP2 hydrolysis was detected by confocal microscopy.Results PMA significantly inhibited Kir 2.3 current in Xenopus oocytes.But PMA had no effect on the Kir 2.3 current expressed in COS-7 cell,in which activation of M1 receptor,however,induced a significant inhibition of Kir 2.3 current.It was reported recently that PMA could trigger the PIP2 hydrolysis in membrane of oocytes.Thus PKC inhibition of Kir 2.3 current seen in oocytes could be the result of PIP2 hydrolysis.Following the same line,the inability of PKC inhibition of Kir 2.3 current seen in COS-7 cells would suggest PKC could not induce PIP2 hydrolysis in these cells. This hypothesis was tested by monitoring the PIP2 level in COS-7 cell membrane by confocal microscopy.Dynamic changes in membrane PIP2 level were imaged using GFP fluorescence signal that had been tagged to the PLC?1PH domain known to be able to bind PIP2 specifically. There was no significant change of PIP2 level on COS-7 cell membrane after longtime treatment of PMA,whereas again,the activation of M1 receptor by ACh induced a significant change in the PIP2 level.These results were in perfect agreement with the electrophysiological results.Conclusions PMA,through activation of PKC,inhibited Kir 2.3 current expressed in Xenopus oocytes but not in COS-7 cells.Similarly PMA induced significant reduction in membrane PIP2 level in Xenopus oocytes but not in COS-7 cells. PIP2 hydrolysis plays an important role in PKC-induced inhibition of the Kir channel currents.

Abnormalities, Multiple ; diagnosis ; Adolescent ; Humans ; Male ; Spleen ; abnormalities ; Testis ; abnormalities

Aim To study the modulation of KCNQ2/3 potassium cha nn els by extracellular pH.Methods In vitro transcription was used to synthesize cRNA of KCNQ2/3 potassium channels.The cRNA was injected into Xenopus oocytes to express the KCNQ2/3 channel.The modulation of KCNQ2/3 potass ium channels by extracellular pH was studied by two electrodes voltage clamp tec hniques.Results KCNQ2/3 currents were inhibited and current-vo ltage relationship of activation were shifted to the right with decreased extrac ellular pH. pH modulation of KCNQ2/3 currents was voltage dependent,with a more pronounced effect at more negative potentials above the activation threshold (-60 mV). Extracelluar pH also decreased activation and deactivation kinetics of KCNQ2/3 currents.Conclusion KCNQ2/3 channels, known to contr ibute to neuronal excitability, were modulated by extracelluar pH. The profound effects of the extracelluar pH exerted on KCNQ2/3 channel may play an important role during physiology neuronal activity and pathological events such a s epileptic seizures, cerebral ischemia and shock etc.

Aim To visualize the dynamics of PtdIns(4,5)P 2 hyd ro lysis and resynthesis, and modulate it by pharmacological agents wortmannin, LiC l, U73122 and neomycin. Methods We used a fusion construct of g reen fluorescent protein(GFP) with the PH domain of phospholipase C ?1(PL C ?1PH)(PLC ?1PH-GFP) known to bind PtdIns(4,5)P 2 specifically , and laser-scanning confocal microscopy to trace PtdIns(4,5)P 2 translocatio n. Results Stimulation of endogenous P 2Y receptors by ATP in CHO cells induced a reversible PLC ?1PH-GFP translocation, indicating Pt dIns(4,5)P 2 hydrolysis through the receptor-mediated phospholipase C (PLC) ac tivation. Wortmannin and LiCl did not affect the translocation of PLC ?1PH -GFP from plasma membrane to cytosol but blocked the recovery after the translo cation. The transient translocation from plasma membrane was blocked by the PLC inhibitor U73122 but was not affected by another PLC inhibitor neomycin. However , in the absence of PLC ?1PH-GFP expression, neomycin inlibited the recep tor-induced PLC hydrolysis of PtdIns(4,5)P 2.Conclusion PLC ?1PH-GFP can be used as a valuable fluorescence probe to visualize the dyn amic change of PtdIns(4,5)P 2 in living cells. Wortmannin, LiCl, U73122 and neo mycin have distinct modulation effects on PtdIns(4,5)P 2 metabolism. PLC ?1 PH,when bound to PtdIns(4,5)P 2,prevents neomycin from inhibiting PLC hydro lyzing PtdIns(4,5)P 2.