OBJECTIVE：To explore the possible mechanism of astragalus in improving cardiac function.METHODS：To observe the effects of astragalus,added to basic anti-heart-failure therapy,on cardiac function and TNF in 45 cases of thronic heart failure.RESULTS：In comparison with basic therapy group,the improvement of cardiac function was more obvious and the level of serum TNF-α was lower in astragalus group.CONCLUSION：Astragalus probably has the action of decreasing TNF resulting in improvement of cardiac function.

Objective　To investigate the nutrition value of w heat flour fortified with lysine，vitamin B1，vitamin B2，vitamin A. Methods　White rat cut off milk were allocated into four gro ups ( Ⅰ、Ⅱ、Ⅲ、Ⅳ)at random. Control group (Ⅰ) was raised with ordinary wheat flou r non-fortified and experiment group (Ⅱ、Ⅲ、Ⅳ) were raised with nutriment wh eat flour with different prescription. The observer watched each group of animal periodically in weight, nitrogen balance, food raised efficiency , thermal energy efficiency, protein efficiency ratio, and swimming persisting ti me under burdon, and so on. Results　After raised for 28 days amo ng each group, the targets mentioned above in experiment group was found significently higher than that of control. Conclusions 　The wheat flour possessed higher nutrition evaluation of protein which benefit s the development of white rat when fortified with lysine and some kinds of th e vitamins.

[Objective] To study the relationship between syndrome patterns of traditional Chinese medicine and bcl- 2 oncogene, p53 suppression gene mRNA expressions in precancerous lesions of gastric cancer (PIGC). [Methods] Forty PLGC cases were endoscopically and pathologically confinned, including 24 cases of moderate dysplasia of gastric mucosa, 9 cases of severe dysplasia, 7 cases of incomplete colonic intestinal metaplasia. Of the 40 cases, 10 were complicated with Qi stagnation, 12 with stomach-heat, and 18 with blood stasis, mRNA expression of bcl- 2 oncogene and p53 suppression gene were detected in situ by molecular hybridization method. [Results] The mRNA overexpression of bcl- 2 oncogene and p53 suppression gene were found in PLGC, and the expression was gradually increased with the progress of lesions. In the complicated cases, the mRNA expression of bcl- 2 oncogene and p53 suppression gene were the least in the cases with Qi stagnation and less in the cases with stomach- heat than in the cases with blood stasis. [Conclusion] Abnormal mRNA expression of bcl- 2 oncogene and p53 suppression gene were found in PLGC cases and related with different complicated cases, indicating the specificity of different syndrome patterns.

Objective To observe the 3 years or more effects on optical correction,refraction,and orthokeratology with rigid gas permeable contact lens(RGPCL) wearing in patients with keratoconus.Design Retrospective case series.Participant 73 keratoconus patients(136 eyes) fitted with RGPCL.Methods Patients wearing RGPCL for 3 years or more in Peking University Optometry & Ophthalmology Center were observed.Correct visual acuity was determined before and at 1,2 and 3 years of lens wearing,and the refractive power,corneal curvature,corneal astigmatism and corneal morphological changes were measured with auto-refractomer/keratometer and keratoconus screening analysis system of computer-assisted corneal topography at the same time.The changes of base curve and RGPCL power were also compared.All patients were divided into mild keratoconus group(Group A),moderate and severe keratoconus group (Group B).Main Outcome Measures Visual acuity,refractive power,base curve of RGPCL,corneal topography parameters.Results The patients wore RGPCL for 49.3?15.3 months(36-76 months).At the initial visit,uncorrected visual acuity(UVA) was 3.76?0.45, corrected visual acuity with spectacles(SPVA) was 4.57?0.53,and with RGPCL(RGPVA) was 4.89?0.14.RGPVA was improved significantly (F=171.994,P=0.000).RGPVA at last visit(4.95?0.11) was better than that at initial visit(t=-6.733,P=0.000),which was more significant in group B than that in group A.The rate for RGPVA more than 0.8 at the initial,1 year,2 years and 3 years of lens wearing was 85.13%,86.76%,85.60%and 84.62%respectively.At the initial visit and last visit,the myopia diopters and the corneal astigmatism were 7.13?4.01D vs.6.23?3.42D(P=0.014) and 6.23?3.24D vs.4.42?2.34D(P=0.000) respectively.The RGPCL base curve and lens power were 7.38?0.50 mm vs.7.54?0.42 mm(P=0.000),and -6.22?3.59 D vs.-5.33?3.09 D(P=0.000) respectively. The changes of power and base curve of lens in group B were more significant than that in group A.The decrease of 9 corneal topography parameters between initial visit and last visit was significant statistically(all P

Background Laser assisted subepithelial keratomileusis (LASEK) is one of surgical procedures for refractive correction.Dilute alcohol that is used for the removal of epithelium during LASEK induces the apoptosis of corneal epithelial cells.Researches showed that thymosin β4 (Tβ4) can arrest apoptosis, but whether Tβ4 plays inhibitory effect on ethanol-induced damage of corneal epithelial cells is still unelucidated.Objective The aim of this study was to investigate the protective effects of Tβ4 on ethanol-induced rabbit corneal epithelial cell damage in vitro.Methods The corneal tissue of deendothelium was obtained from 10 New Zealand white rabbits.Corneal epithelial cells were cultured in vitro by using explant culture method.Cultured cells were identified by detecting the expression of keratin 12 and connexin 43 with reverse transcription PCR (RT-PCR).The cells of second generation were collected and divided into 4 groups.The cells were regularly cultured in the normal control group, and Tβ4 was added in the culture medium at the final concentration of 1 μg/ml in the Tβ4 treated group.Ethanol-induced rabbit corneal epithelial cell damage models were established by adding PBS containing 20％ alcohol in medium for 20 seconds in the model group,and Tβ4 was added in the medium of model cells at the final concentration of 1 μg/ml in the model+Tβ4 group.The survival rate of the cells was detected by MTT assay, and the apoptosis rate of the cells was examined by TUNEL method.The relative expression levels of cyclin D1 mRNA and cyclin-depensent protein kanase 4 (CDK4) mRNA in the cells were detected by real-time flurescenee quantitative PCR.The content of bcl-2 protein in the cells was detected by ELISA assay.Spectrophotometry was employed to measure the activity of caspase-3.The study complied with the Regulation for the Adminstration of Affairs Concerning Experimental Animals by State Science and Technology Commission.Results The mean cell survival rate was (52.1 ± 14.07) ％ in the model group,which was significantly reduced in comparison with 100％ of the normal control group and (77.7± 19.60) ％ of the model+Tβ4 group (P=0.001 ,P=0.035).TUNEL staining revealed more positive cells in the model group and the model+Tβ4 group,and the percentage of TUNEL positive cells was (30.0±6.7)％ in the model+Tβ4 group, showing an evident decline in comparison with (42.4±4.0)％ of the model group (P=0.01).The relative expression levels of cyclin D1 mRNA and CDK4 mRNA were 0.93±0.17 and 0.88±0.09 in the model+Tβ4 group, which were significantly higher than 0.68±0.05 and 0.54±0.07 in the model group (P=0.027,0.002).ELISA assay exhibited that bcl-2 content in the cells was considerably lower,and caspase-3 activity was significantly higher in the model group than those in the model+Tβ4 group (P =0.030,0.021).Conclusions Tβ4 plays a protective effect on rabbit corneal epithelial cells from apoptosis by lowing the caspase 3 activity and increasing bcl-2 content in ethanoldamaged rabbit corneal epithelial cells.In addition, Tβ4 promotes the regrowth of corneal epithelial cells by upregulating the expression of cyclin D1 and CDK4.

Objective To evaluate the effect of propofol on the endoplasmic reticulum stress-mediated apoptosis during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Eighty adult male Sprague-Dawley rats,weighing 240-280 g,were randomly divided into 4 groups (n =20 each):shame operation group (group S) ; focal cerebral I/R group (group FCIR); propofol pretreatment group (group P); intralipid pretreatment group (group Ⅰ).Focal cerebral I/R was induced by 4 h middle cerebral artery occlusion followed by reperfusion.Propofol was infused at a rate of 12 mg· kg-1 · h-1 starting from 30 min before ischemia until 15 min of ischemia in group P,while intralipid was given instead of propofol in group I.Neurological deficit scores (NDSs) were measured at 6 h of reperfusion in 10 rats chosen from each group and the rats were then sacrificed.Their left brains were removed for determination of brain water content.The left 10 rats were sacrificed and their brains were immediately removed for determination of the expression of C/EBP homologous protein (CHOP),Bcl-2,and activated caspase-3 in the left hippocampi by Western blot.Results Compared with group S,NDSs and brain water content were significantly increased,the expression of CHOP and activated caspase-3 was up-regulated,and the expression of Bcl-2 was down-regulated in group FCIR,NDSs was increased in group P (P ＜ 0.05).Compared with group FCIR,NDSs and brain water content were significantly decreased,the expression of CHOP and activated caspase-3 was down-regulated,and the expression of Bcl-2 was up-regulated in group P,and no significant change was found in each parameter in group Ⅰ (P ＞ 0.05).Conclusion Propofol can reduce focal cerebral I/R injury through inhibition of the endoplasmic reticulum stress-mediated apoptosis in rats.

AIM:MicroRNAs ( miRNAs) were recognized to play significant roles in cardiac hypertrophy .But, it remains unknown whether cyclin/Rb pathway is modulated by miRNAs during cardiac hypertrophy .This study investigates the potential roles of microRNA-1 (miR-1) and microRNA-16 (miR-16) in modulating cyclin/Rb pathway during cardiomyocyte hypertrophy .METHODS:An animal model of hypertrophy was established in a rat with abdominal aortic constriction (AAC).In addition, a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocyte .RESULTS:miR-1 and-16 expression were markedly de-creased in hypertrophic myocardium and hypertrophic cardiomyocytes in rats .Overexpression of miR-1 and -16 suppressed rat cardiac hypertrophy and hypertrophic phenotype of cultured cardiomyocytes .Expression of cyclins D1, D2 and E1, CDK6 and phosphorylated pRb was increased in hypertrophic myocardium and hypertrophic cardiomyocytes , but could be reversed by enforced expression of miR-1 and -16.CDK6 was validated to be modulated post-transcriptionally by miR-1, and cyclins D1, D2 and E1 were further validated to be modulated post-transcriptionally by miR-16.CONCLUSION: Attenuations of miR-1 and -16 provoke cardiomyocyte hypertrophy via derepressing the cyclins D1, D2, E1 and CDK6, and activating cyclin/Rb pathway.

AIM:To investigate the effect of miR-214 on cardiomyocyte hypertrophy and the expression of the potential target genes . METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular car-diomyocytes (NMVCs).Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Wes-tern blotting, respectively.RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-in-duced hypertrophic cardiomyocytes .Dual luciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly in-creased in the hypertrophic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hy-pertrophy-related genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .

AIM:To determine circular RNA (circRNA) profiles in the diabetic mouse myocardium , and to investigate the effect of circRNA_000203 on fibrotic phenotypes in cardiac fibroblasts .METHODS:Masson trichrome stai-ning was performed on the myocardium of the diabetic db /db mice and the non diabetic db/m control mice .circRNA ex-pression profile in the diabetic myocardium was detected by circRNAs microarray .The expression of circRNA_000203 was determined by real time fluorescence quantitative PCR ( RT-qPCR ) .Recombinant circRNA_000203 adenovirus was pre-pared for enforced the expression of circRNA_000203 in mouse cardiac fibroblasts.The expression of Col1a2, Col3a1andα-SMA was determined in circRNA_000203-modified cardiac fibroblasts , respectively .RESULTS:Masson trichrome stai-ning showed that fibrosis was increased in the diabetic mouse myocardium .The results of circRNA array detection revealed that circRNAs were dysregulated in the diabetic myocardium .circRNA_000203 was up-regulated in the diabetic myocardi-um.Significant over-expression of circRNA_000203 was achieved in the cardiac fibroblasts after infection with the recombi-nant circRNA_000203 adenovirus.The mRNA and protein expression of Col1a2, Col3a1 and α-SMA was significantly in-creased in the cardiac fibroblasts with over-expression of circRNA_000203.CONCLUSION:circRNA_000203 is up-regu-lated in the diabetic mouse myocardium .It has pro-fibrotic effect on the cardiac fibroblasts .