Water sorption and hygroscopic changes of five core buildup composite resins / 中华口腔医学杂志

Objective@#To evaluate water sorption and hygroscopic dimensional changes of five core buildup composite resins, and to provide references for material modification on water sorption.@*Methods@#Five commercial core buildup materials (group A: Smart Dentin ReplacementTM; group B: NanoFil; group C: ParaCoreTM; group D: LuxaCore Z; group E: EmbraceCoreTM Resin Cement) were fabricated to disk-shaped specimens: (15.0±0.1) mm diameter, (2.0±0.1) mm thickness (n=10). Specimens were thoroughly irradiated with curing lights. The initial mass in air was recorded, and the initial mass in deionized water was recorded. Five specimens of each group were immersed in deionized water for 28 d. They were weighed as a function of different immersion time (1, 2, 3, 4, 5, 6, 7, 14, 28 d). The mass in air was recorded, and the displayed mass in deionized water was recorded. Archimedes' principle was applied to calculate the dimensional changes. The other five specimens of each group were stored in artificial saliva and were tested by the same methods.@*Results@#All specimens gained weight and hygroscopic changes during 28 d immersion. When stored in deionized water, the apparent mass change of group A [(10.6±0.9) μg/mm3] and the dimensional change of group A [(0.39±0.10)%] were the lowest, while the mass change of group E [(48.0±0.2) μg/mm3] and the dimensional change of group E [(3.16±0.13)%] were the highest (P<0.05). In artificial saliva, the lowest apparent mass change was found in group A [(11.8±1.0) μg/mm3] while the highest change was found in group E [(47.4±3.5) μg/mm3] (P<0.05). The lowest dimensional change was found in group C [(0.37±0.09)%] and the highest was found in group E [(3.07±0.19)%] in artificial saliva (P<0.05).@*Conclusions@#Water sorption and dimensional changes vary in immersion fluids with different osmotic pressure. Water sorption and dimensional changes of core buildup composite resins are highly correlated with test materials in both of the deionized water and artificial saliva.

Relationship between activation of IL-1β,IL-6 and downstream IDO activation with rat depression behaviors / 重庆医学

Objective To investigate the relationship between the rat depression behaviors induced by chronically unpredicted stress (CUS) with interleukin-1β (IL-1β),interleukin-6 (IL-6) protein expression and indole-2,3-dioxygenase (IDO) mRNA and protein expression.Methods Thirty male Sprague Dawley (SD)rats were divided into the control group (CG) and model group (MG).The solitary raise combined with CUS 28 d continued stimulus was used to establish the rat depression model.The open field test (OFT) and the force swimming test (FST) were used to evaluate the rat depression behaviors;qRT-PCR was used to determine the mRNA expression of IDO in hippocampus and cortex;Western blot was used to determine the protein expressions of IL-1β,IL-6 and IDO in hippocampus and cortex.Results Compared with the CG group,the OFT score in the rats of the MG group was significantly decreased(P＜0.01),the immobility time in FST was significantly extended (P＜0.00),the expression of IDO mRNA in hippocampus and cortex was significantly increased (P＜0.01) and the protein expression of IL-1β,IL-6 and IDO in hippocampus and cortex was significantly increased (P＜0.05).Conclusion The rat depression behaviors induced by CUS may be associated with the increase of intracerebral inflammatory cytokine expression and inducing IDO over-expression.

Research on relationship between abnormal regulation of histone acetylation and depression in rats / 中国药理学通报

Aim To study the role of histone acetyla-tion and its involvement in the depression-like behav-iors of rats induced by chronic unpredictable stress (CUS ). Methods Thirty male Sprague Dawley (SD ) rats were randomly divided into control group and model group.The method of solitary condition with CUS for consecutive 28 days was used to establish the rat depression model.The open-field test (OFT)and the forced swimming test (FST)were used to evaluate the depressive behaviors of rats;the real time PCR was used to detect the change of HDAC2 mRNA, and Western blot was used to determine the protein expres-sions of H3,H4,acH3 and acH4 in the prefrontal cor-tex and hippocampus of rats.Results Model group showed obvious depression-like behaviors with decrea-sing locomotive activity in OFT (P <0.01 )and in-creasing immobility time in FST (P<0.01),up-regu-lating the mRNA and protein expression of HDAC2 (P<0.0 1 ),and down-regulating the protein expression of acH3 and acH4 (P<0.01)in the prefrontal cortex and hippocampus significantly,compared with control group.Conclusion The mechanism of depressive be-haviors of rats induced by CUS may be associated with down-regulating the level of histone acetylation modifi-cation.

The principle of treating spirit in clinical acupuncture-moxibustion in terms of three-layer thought / 中国针灸

Treating spirit,which relates to many philosophical theories and techniques,is key to the effect of acupuncture-moxibustion therapy. According tomonism and the three-layer thought of nature-earth-human,it is believed that the spirit means the ability or possibility to communicate with the nature-earth-human,and response refers to the spirit-interlinking progress between persons and the nature-earth-human. While treating spirit is seen as keeping learning and practicing the progress. The author describes treating spirit by acupuncture-moxibustion in terms of metaphysics and examples. It believes that treating spirit is inevitable as three-layer thought,which stems from traditional Chinese culture,is permeating into acupuncture-moxibustion theory. Treating spirit,a combination between medical ethics and techniques,indicates that doctors understand patients and diseases both generally and detailedly,with mental requirement for the two parts.

TNF-αmediated activation of IDO pathway involved in mechanism of depression in rats induced by CUS / 中国药理学通报

Aim To investigate the relationship be-tween the depression-like behaviors of rats induced by chronically unpredictable stress( CUS) and the protein expression of tumor necrosis factor alpha( TNF-α) , in-dole-2 , 3-dioxygenase ( IDO ) and 3-hydroxyl amino acid oxygenase( HAAO) . Methods Thirty male Spra-gue Dawley( SD) rats were randomly divided into con-trol group and model group. CUS plus solitary condi-tion were used to establish the depression model. The open field test ( OFT ) and the force swimming test ( FST ) were used to evaluate the depression-like behaviors of rats ;Western blot was used to determine the protein expressions of TNF-α, IDO and HAAO in the prefrontal cortex and hippocampus of rats. Results Model group rats showed obvious depression-like be-haviors with increasing immobile time in FST ( P <0. 01) and decreasing locomotive activity in OFT( P<0. 01 ) , and up-regulating the protein expression of TNF-α, IDO and HAAO in the prefrontal cortex and hippocampus significantly ( P <0. 05 ) , compared with control group rats. Conclusion The depression-like behaviors of rats induced by CUS may be associated with the activation of IDO-HAAO pathway mediated by TNF-α.

Effects of PPARβand NO on high glucose and insulin-induced cardio-myocyte hypertrophy / 中国病理生理杂志

AIM:To investigate the role of peroxisome proliferator-activated receptor β( PPARβ)-nitric oxide (NO) signal pathway in cardiomyocyte hypertrophy induced by high glucose (25.5 mmol/L) and insulin (0.1 μmol/L) ( HGI) .METHODS: The cardiomyocyte hypertrophy was characterized in rat primary cardiomyocytes by measuring the cell surface area, protein content, and the mRNA expression of atrial natriuretic factor (ANF).The mRNA and protein ex-pression were measured by real-time PCR and Western blotting , respectively .The activity of NO synthase ( NOS) and NO content were measured by a reagent kit through ultraviolet spectroscopy .RESULTS:HGI induced profound change of hy-pertrophic morphology , and significantly increased the cell surface area , protein content and mRNA expression of ANF (P<0.01), but decreased the expression of PPARβat mRNA and protein levels (P<0.05).At the same time, the ex-pression of inducible NOS (iNOS) was obviously elevated (P<0.01), which occurred in parallel with the rising NOS ac-tivity and NO concentration (P<0.01).GW0742 (1 μmol/L), a selective PPARβagonist, inhibited the cardiomyocyte hypertrophy induced by HGI ( P<0.01 ) , and up-regulated the expression of PPARβat both mRNA and protein levels . Meanwhile, GW0742 also inhibited the increases in iNOS expression , NOS activity, and NO content induced by HGI , which were abolished by GSK0660 (1 μmol/L), a selective PPARβantagonist (P<0.01).CONCLUSION: PPARβdown-regulation and the following iNOS-NO activation are involved in the cardiomyocyte hypertrophy induced by HGI .

PPARβ-related signal pathway involves in the effect of polydatin on high glucose-and insulin-induced cardiomyocyte hypertrophy / 中国药理学通报

Aim To investigate the effect of polydatin on cardiomyocyte hypertrophy induced by high glucose (25.5 mmol·L -1 )and insulin (0.1 μmol ·L -1 ) (HGI)and its possible influence on peroxisome prolif-erator-activated receptor-β (PPARβ)/nuclear tran-scription factor-κB (NF-κB)/nitric oxide (NO)signa-ling pathway.Methods The cardiomyocyte hypertro-phy was characterized in rat primary cardiomyocytes by measuring the cell surface area,protein content,and atrial natriuretic factor (ANF)mRNA expression.The mRNA and protein expressions were measured by qRT-PCR and Western blotting,respectively.The activity of NO synthase (NOS)and NO content were measured by reagent kit through ultraviolet spectroscopy.Results HGI significantly induced cardiomyocyte hypertrophy which increased the cell surface area,protein content and ANF mRNA expression (P <0.01 ).Meanwhile, the expressions of PPARβmRNA and protein reduced while the NF-κB p65 and iNOS expressions increased significantly which occurred in parallel with rising NOS activity and NO concentration (P <0.01 ).Polydatin (0.1,1,10 μmol·L -1 )inhibited the cardiomyocyte hypertrophy induced by HGI (P <0.01 ),and re-versed the mRNA and protein expressions of PPARβ, NF-κB p65 and iNOS,and NOS activity,as well as NO content.These effects of polydatin were abolished by GSK0660 (1 μmol·L -1 ),a selective PPARβan-tagonist (P <0.05 ).Conclusion Polydatin resists HGI-induced cardiomyocyte hypertrophy,which may be mediated by PPARβup-regulation,and then NF-κB-iNOS-NO pathway inactivation.

Effect of GW0742 on endothelial dysfunction induced by high glucose in isolated rat thoracic aorta / 中国药理学通报

Aim To investigate the effect of GW0742 on the endothelial dysfunction induced by high glucose (glucose at 55 mmol · L -1 )in isolated rat thoracic aorta and its related mechanisms.Methods The end othelium-dependent relaxation of acetylcholine was per-formed in the absence or presence of GW0742 at differ-ent concentrations under high glucose condition.The structure of aorta was observed by HE staining.Moreo-ver,the content of NO was also measured by nitrate re-duction method.The mRNA and protein expression were detected by quantitative real-time PCR and West-ern blot,respectively.Results Compared with the control group,acetylcholine-induced vasodilatation was impaired by high glucose.Meanwhile,the structures of endothelial cells and smooth muscle cells were also in-terrupted.Furthermore, the expressions of PPARβmRNA and protein reduced while the NF-κB p65 ex-pression increased significantly which occurred in par- allel with decreasing eNOS expression and NO concen-tration (P <0.01 ).GW0742 (0.01 ,0.1 ,1 μmol· L -1 )restored the relaxation of acetylcholine in a dose-dependent manner,and reversed the mRNA and pro-tein expression of PPARβ,NF-κB p65 and eNOS,as well as NO content (P <0.01 ).Conclusion GW0742 attenuates the injury of endothelial dysfunc-tion induced by high glucose,which may be,at least partly,mediated by the up-regulation of PPARβ,then the down-regulation of NF-κB,and the activation of eNOS-NO signal pathway.

COX2-PGI2/TXA2 signal pathway involved in protective mechanism of PDTC pretreatment against global cerebral ischemia reperfusion rat hippocampus injury / 中国药理学通报

Aim To investigate the effects and mecha-nism of nuclear factor-κ B inhibitor, PDTC, on global cerebral ischemia reperfusion ( GCIR ) rat hippocam-pus. Methods Forty-eight adult male Sprague-Daw-ley rats were randomly divided into one control group receiving sham operation and three experimental groups all receiving global cerebral ischemia for 20 min. In PDTC 100 mg·kg-1 group ( P100 ) and PDTC 200 mg ·kg-1 group ( P200 ) , PDTC 100 mg · kg-1 or PDTC 200 mg·kg-1 was injected ip one hour before ischemi-a respectively. Spatial learning and memory function of rats were tested using Morris water maze. HE staining was employed to observe pathological changes of hipp-ocampal neurons. Expression of COX2 was measured by Western blot, and the content of PGI2 and TXA2 in rat hippocampus was detected by enzyme-linked immu-nosorbent assay. Results A significant increase of es-cape latency was observed in GCIR group compared to the sham operation group(P<0.05). PDTC 100 mg· kg-1 and PDTC 200 mg · kg-1 significantly reduced escape latency ( P <0.05 ) and histopathological injury in CA1 region of hippocampus. PDTC 100 mg · kg-1 and PDTC 200 mg · kg-1 also reduced COX2 expres-sion, PGI2 content, TXA2 content and PGI2/TXA2 . Conclusion Pretreatment with PDTC can protect hip-pocampus from GCIR injury through inhibition of COX2 expression and PGI2/TXA2 .

Analysis of dental and craniofacial research programs supported by National Natural Science Foundation / 中华医学科研管理杂志

ObjectiveTo enhance the fund efficiency of dental research programs supported by National Natural Science Foundation (NSFC) and to reveal the achievements and progresses of the funds.MethodsThe data of programs in dental and craniofacial field supported by NSFC from 1999 to 2006 and completed between 2003 and 2009 were collected based on the final reports by the investigators.The data of personnel training,research publication,patent,awards,and academic communication at domestic and international levels were all collected and analysed. Results There were 307 grants in total,including 185 general programs,73 Young Scientists Funds,13 regional funds,3 Key Programs,1 National Science Fund for Distinguished Young Scholars and 32 others.An average of 4 postgraduate students was trained by each program.In general,the outcomes of general programs were better than those of Young Scientists Fund,and the latter was better than regional fund.There was steady increase each year in the amount of papers published in SCI journals,and about half of the investigators published SCI papers.In addition,9 patents were registered and 13 prizes were won, and the investigators participated 610 domestic and international exchanges.Conclusions The continuously increase of NSFC support in dental field has led to substantial achievement,although patent application,the quality of papers and novel ideas need to be improved.

PPAR-α involves in cardiomyocyte hypertrophy induced by high glucose and insulin / 中国病理生理杂志

AIM: To study the role of peroxisome proliferator-activated receptor-α (PPAR-α) signal transduction pathway in cardiac hypertrophy induced by high glucose and insulin (HGI). METHODS: The cultured neonatal rat cardiomyocytes were used to observe the effect of fenofibrate (FF), a selective PPAR-α agonist, on cardiomyocyte hypertrophy induced by HGI (glucose at concentration of 25.5 mmol/L and insulin at 0.1 μmol/L). The cardiomyocyte hypertrophic responses were assayed by measuring the cell surface area, protein content, and mRNA expression of atrial natriuretic factor (ANF). The expressions of mRNA and protein were assayed by real -time PCR and Western blotting. RESULTS: In cultured cardiomyocytes, HGI induced profound change of hypertrophic morphology, the significant increase in cell surface area, protein content and ANF mRNA expression compared to those in vehicle control (P<0.01), but the expressions of PPAR-α mRNA and protein decreased significantly (P<0.05). At the same time, the expression of cyclooxygenase 2 (COX-2), one of the PPAR-α downstream effectors was obviously elevated (P<0.05). However, FF (0.1, 0.3 and 1 μmol/L) inhibited the cardiomyocyte hypertrophy induced by HGI in a concentration-dependent manner (P<0.01). FF at concentration of 0.3 μmol/L increased the expressions of PPAR-α in both mRNA and protein levels (P<0.05) and inhibited the expressions of COX-2 (P<0.05), which were abolished by MK 886 (0.3 μmol/L), a selective PPAR-α antagonist (P<0.05). CONCLUSION: PPAR-α signal transduction pathway and its downstream effector COX-2 might involve in the cardiomyocyte hypertrophy induced by HGI.

Investigation and exploration of pharmacological theory teaching / 中华医学教育探索杂志

To improving the teaching quality of the pharmacology theory teaching,we adopt questionnaire to understand the students’ request of teaching method and teaching content,thus to elevate the teaching overall level by raising their ability to teach and study.

NO pathway involves in the anti-hypertrophic effects of fenofibrate induced by high glucose and insulin / 中国药理学通报

Aim To investigate the role of fenofibrate (FF),a selective PPAR-? agonist,in cardiac hypertrophy induced by high glucose and insulin (HGI) and its mechanisms related to nitric oxided (NO) signal transduction pathway. Methods The cultured neonatal rat cardiomyocytes were used to observe the effects of FF on cardiomyocyte hypertrophy induced by HGI (glucose at 25.5 mmol?L-1 and insulin at 0.1 ?mol?L-1),and the cardiomyocyte hypertrophic responses were assayed by measuring the cell surface area,protein content,and atrial natriuretic factor (ANF) mRNA expression. The expressions of mRNA and protein were assayed by Real-time PCR and Western blot,as well as NOS activity and NO concentration in cultured media were determined by using the spectrophotometry and nitrate reluction method.Results In cultured cardiomyocytes,FF (at 0.1,0.3 and 1 ?mol?L-1) could inhibit the cardiomyocyte hypertrophy induced by HGI in a concentration-dependent manner (P

Role of calcineurin signal transduction pathway in the inhibition of cardiac hypertrophy by L-arginine in vivo and in vitro / 中国药理学通报

Aim To study the role of calcineurin signal transduction pathway in the anti-hypertrophic effect of L-arginine in vivo and in vitro.Methods The hypertrophic effects was assayed by calculating the right ventricular hypertrophy index(RVHI=right ventricle weight/left ventricle and septum weight),and atrial natriuretic peptide(ANP)mRNA expression in rat right ventricle hypertrophy model induced by monocrotaline(MCT) or by measuring the cell diameter,protein content,and ANP mRNA expression in hypertrophic cardiomyocyte induced by prostaglandin F2?(PGF2?).For mechanism studies,the intracellular free calcium concentration([Ca2+]i) in cultured cardiomyocytes was measured by using Fura 2/AM as a fluorescent indicator.ANP and CaN mRNA expressions,and expressions of CaN and its downstream effectors,NFAT3 and GATA4 proteins were assayed by RT-PCR and Western blot,respectively,in vivo and in vitro.Results In MCT-hypertrophic model,prevention-and treatment-administration of L-arginine,a nitric oxide(NO) precursor,200 mg?kg-1?d-1,could obviously inhibit the elevated RVHI and ANP mRNA expression;similar to that found in vivo.Addition of L-arginine 1 mmol?L-1 could markedly inhibit the increased cell diameter,protein content and the expression of ANP mRNA in the hypertrophic cardiomyocyte induced by PGF2? 100 nmol?L-1,and it could also decrease the elevated [Ca2+]i in vitro;notably,the above dose or concentration of L-arginine could blunt the elevated expressions of calcineurin mRNA and the calcineurin-,NFAT3-,GATA4-proteins induced by MCT or by PGF2?.These effects of L-arginine were blocked by NG-nitro-L-arginine-methyl ester,a NO synthase inhibitor,in vivo and in vitro.Conclusion These results suggest that calcineurin signal transduction pathway may play an important role in the NO-induced inhibition of cardiac hypertrophy.The anti-hypertrophic effects of L-arginine may involve the decrease of [Ca2+]i,and then inhibit the activated calcineurin pathway,through the release of NO.

Effects of nimodipine and fructose-1,6-diphosphate on cerebral damage in carbon monoxide poisoning mice / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To study the dose- and time-dependent protective effects and the synergistic effects of nimodipine (NMDP) and fructose-1,6-diphosphate (FDP) against cerebral damage induced by acute carbon monoxide (CO) poisoning in mice.</p><p><b>METHODS</b>Male mice were exposed to CO 170 mL/kg, i.p. After CO intraperitonealy exposure, mortality of mice, change in memory function estimated by passive avoidance test, the pathomorphologic observation of brain tissue slices, as well as changes of activities of monoamine oxidase (MAO)-B and Ca(2+)-Mg(2+)-ATPase in cerebral tissue were studied. In dose-dependent protective effect study, NMDP (10.6, 5.3, 2.7 mg/kg) and FDP (2.6, 1.3, 0.67 g/kg) was injected ip, respectively 15 min after CO exposure. To study the time-effect relationship of drugs, NMDP (5.3 mg/kg) and FDP (1.3 g/kg) were administered ip respectively 15 minutes, 45 minutes and 120 minutes after CO exposure. The combination of NMDP (2.7 mg/kg) and FDP (0.67 g/kg) was administered ip15 minutes, 45 min and 120 minutes after CO exposure to study the synergism of the two drugs.</p><p><b>RESULTS</b>Either NMDP (10.6, 5.3 mg/kg) or FDP (2.6, 1.3 g/kg) administered ip within 15 minutes after CO exposure significantly decreased the impairment of memory function and mortality rate induced by CO, inhibited the decrease of Ca(2+)-Mg(2+)-ATPase activity, blunted the rising of MAO-B activity and prevented the delayed hippocampal neuronal death in poisoning mice. To our surprise, the combined use of NMDP (2.7 mg/kg) and FDP (0.67 g/kg) within 15 minutes after CO exposure had similar effects to that in NMDP (10.6, 5.3 mg/kg) and FDP (2.6, 1.3 g/kg).</p><p><b>CONCLUSIONS</b>These results suggest that the impairment of CO on brain can be attenuated if NMDP or FDP are administered sufficiently and quickly as soon as possible after CO exposure and there exists a synergism of FDP and NMDP against CO poisoning damage.</p>

PPAR-? involves in cardiomyocyte hypertrophy induced by high glucose and insulin / 中国病理生理杂志

AIM:To study the role of peroxisome proliferator-activated receptor-? (PPAR-?) signal transduction pathway in cardiac hypertrophy induced by high glucose and insulin (HGI). METHODS:The cultured neonatal rat cardiomyocytes were used to observe the effect of fenofibrate (FF),a selective PPAR-? agonist,on cardiomyocyte hypertrophy induced by HGI (glucose at concentration of 25.5 mmol/L and insulin at 0.1 ?mol/L). The cardiomyocyte hypertrophic responses were assayed by measuring the cell surface area,protein content,and mRNA expression of atrial natriuretic factor (ANF). The expressions of mRNA and protein were assayed by real -time PCR and Western blotting. RESULTS:In cultured cardiomyocytes,HGI induced profound change of hypertrophic morphology,the significant increase in cell surface area,protein content and ANF mRNA expression compared to those in vehicle control (P

Calcineurin signal transduction pathway involves in cardiomyocyte hypertrophy induced by prostaglandin F_(2?) / 中国病理生理杂志

AIM:To study the role of prostaglandin F2?(PGF2?) in cardiac hypertrophy and its relation with calcineurin(CaN) signal transduction pathway in vitro.METHODS:The cultured neonatal rat cardiomyocyte was used to observe the hypertrophic effect of PGF2?,and the hypertrophic response was assayed by measuring the cell diameter,protein content and atrial natriuretic factor(ANF) mRNA expression.For mechanism studies,the intracellular free calcium concentration([Ca2+]i) in cultured cardiomyocytes was measured by using Fura-2/AM as a fluorescent indicator.ANF and CaN mRNA expressions,and the expressions of CaN and its downstream effectors,NFAT3 and GATA4 proteins were assayed by RT-PCR and Western blotting,respectively.RESULTS:In cultured cardiomyocytes,PGF2? induced profound hypertrophic morphology change and the significant increase in cell diameter,and protein content in a concentration-dependent manner compared with those in vehicle control(P

Effect of polydatin on endothelial function in aorta vascular strips of healthy rabbits treated with ADMA / 中草药

ObjectTo study the effect of polydatin (PD) and asymmetric dimethylarginine (ADMA) on the endothelial function in aorta vascular strips of healthy rabbits and the interaction between PD and ADMA. MethodsDose-response curves of phenylephrine (PE) on the aortic strips with or without ADMA and/or PD. E max and Kd from PE were obtained and compared. ResultsNormal aortic strips could not respond to ADMA. Pretreatment with either PD or ADMA had no effect on the contractive response of aortic strips to PE. But PD could significantly weaken the contractive response of aortic strips pretreated with ADMA caused by PE in a dose-dependent manner, increase Kd and decrease E max of PE. ConclusionEither ADMA or PD alone does not influence the normal aortic strip contractive functions, the PE affinity to ?-receptor, and E max. But PD could noncompetitively antagonize the contractive reaction of aortic strips to PE in the presence of ADMA.