Objective To investigate the short-term and long-term effect of motor imagery training on visual imagery and kinesthetic imagery of athletes.Methods Twenty athletes majoring in the sports training of Capital University of Physical Education were selected into the experimental group,while 20 counterparts majoring in the human kinetic science were selected into the control group.All subjects received motor imagery training,and were assessed their visual imagery and kinesthetic imagery at three before the training,as well as ten minutes and 48 hours after the training.Results The repetitive measurement and analysis of variance showed that the visual imagery and kinesthetic imagery scores had the main effect of time factor [FvI (2,37)=7.57,P＜0.01;FK1 (2,37)=ll.75,P＜0.01)],as the scores were the highest at ten minutes after training,the second highest at 48 hours after training and the lowest before training.The visual imaginary scores increased significantly after the training,but had no significant difference 48 hours after the training compared to that before the training.After the training the kinesthetic imagery scores increased significantly and then declined slowly,and there were significant differences in the score before and 48 hours after the training (P=0.009).The experimental group and the control group had the same change trend in the visual and kinesthetic imagery scores.The average scores of the former group were higher than the latter at the same time points but without significant differences.The visual and kinesthetic imagery scores had no main effect of group factor,and there was no interaction effect of time factor and group factor.Conclusion Motor imagery training could increase the ability of visual and kinesthetic imagery of people never participating in motor imagery training and the short-term effect was more obvious.The long term effect of motor imagery training was more significant on kinesthetic imagery than visual imagery.

The mechanism of injury on the human glomerular endothelial cells (ciGENC) induced by preeclampsia serum was investigated. Concentration of maternal serum sFlt-1 protein was detected by ELISA. Fluorescently-labeled bovine serum albumin infiltrating through lower chamber of Transwell was measured by multifunction microplate reader. Morphologic change of ciGENC was observed under inverted phase contrast microscope. The concentration of sflt-1 in preeclampsia groups was significantly increased as compared with control group (P<0.01). Permeability in preeclampsia groups was significantly increased as compared with control group (P<0.01). By contrast with severe preeclampsia group, the permeability of ciGENC monolayer in mild preeclampsia group was decreased significantly (P<0.05). Intervention of exogenous VEGF significantly decreased permeability of ciGENC in preeclampsia groups. It was concluded that sFlt-1 increased ciGENC permeability by damaging integrity of endothelial barrier function.

This study investigated the effect of epigenetic modification of maspin on extravillous trophoblastic function. The mRNA expression of maspin in placentae from normotensive and preeclamptic pregnant women was detected by RT-PCR. TEV-1 cells, a human first-trimester extravillous trophoblast cell line, were cultured and treated with CoCl(2) (300 μmol/L) to induce chemical hypoxia and with 5-aza (500 nmol/L) to induce demethylation. The mRNA expression of maspin in TEV-1 cells subjected to different treatments was determined by RT-PCR, and the proliferative and migratory abilities of TEV-1 cells were assessed by cell counting kit-8 (CCK-8) and Transwell assays. Our results showed that the maspin mRNA expression level in placentae from preeclamptic women was much higher than that from normotensive women. CoCl(2) or 5-aza could up-regulate the mRNA expression of maspin and significantly suppress the proliferation and migration of TEV-1 cells. It was concluded that the epigenetic modification in promoter region of maspin contributes to incomplete trophoblast invasion, which offers a novel approach for predicting and treating placental dysfunction.

Objective To investigate effects of histone deacetylase 1 (HDAC1) gene silencing on proliferation and apoptosis of pancreatic cancer cell line PaTu8988. Methods The PaTu8988 cells were cultured and divided into control group (untreated), negative control group (treated with 30 nmol/L negative siRNA), low HDAC1 group (treated with 15 nmol/L HDAC1 siRNA) and high HDAC1 group (treated with 30 nmol/L HDAC1 siRNA). The real-time PCR and Western blot were used to detect the efficiency of HDAC1 gene silencing on mRNA and protein levels ,respectively, at 48 hours after transfection of HDAC1 siRNA. Cell proliferation and apoptosis were evaluated using cell counting kit and flow cytometry, respectively. Results Forty-eight hours after transfection of HDAC1 siRNA, the expression of HDAC1 mRNA level in PaTu8988 cells was 46.1%±6.1% in low HDAC1 group and 32.3%±1.4% in high HDACI group, which were lower than that in control group (100.0%±3.4%) and negative control group (87.4%±28.3%,P<0.05). The expression of HDAC1 protein was higher in control and negative control groups than in low and high HDAC1 groups. Cell survival rate was 100.0%±17.1% in control group, 87.1%±5.0% in negative control group, 68.7%±4.7% in low HDAC1 group and 61.6%±2.0% in high HDAC1 group with significant difference (P<0.05). Meanwhile, the cell apoptic rate in control (4.20%±0.95%) and negative control (4.59%±1.26%) groups was lower than that in low (10.09%±1.36%) and high (11.19%±6.07%) HDACI groups (P<0.05). Conclusions HDACI siRNA can effectively and specifically inhibit the expression of HDAC1 and proliferation of PaTu8988 cells and induce cell apoptosis.

Objective DNA methytransferase 1(DNMT1)is highly expressed in many cancers and lowly expressed in normal adult cells.This study was to assess effects of DNMT1 gene silencing on proliferation and apoptosis of pancreatic cancer cell line PaTu8988.Methods It is divided into four groups:Control group,Lipofectamine 2000 group,Negative control siRNA(N-siRNA)group(30 nM)and siRNA group(30nM).The expression levels of DNMT1 mRNA were detected by real-time PCR to assess the efficiency of DNMT1 gene silencing.Cell proliferation was analyzed by WST-8 assay;Cell apoptosis was evaluated by flow cytometry.Results Relative to Control group,48h after transfection of DNMT1 siRNA,The inhibitory rates of DNMT1 mRNA levels in PaTu8988 cells was(86.0±4.3)%.Cell survival rate was declined to 47.6±5.6%from Control group(100.7±3.0%),Lipofectamine 2000 group(64.5±6.8%),N-siRNA group(68.1±4.1%)(P＜0.05);Cell apoptosis rate was increased from Control group(7.51±1.12)%to siRNA group (14.94±2.89)%(P＜0.05),respectively,48h after transfection of DNMT1 siRNA.Conclusions DNMT1siRNA can efficiently and specifically knockdown the expression of DNMT1 mRNA and inhibit the proliferation of PaTu8988 cells,and induce cell apoptosis.It provides evidence for gene therapy of pancreatic cancer.

Objective To investigate the expressions of DNA methyltransferase 1 (DNMT1) in pancreatic carcinoma and its clinical significance.Methods 30 samples of pancreatic cancer tissues and paired para-cancerous tissues were collected from patients who underwent curative pancreatectomy.The levels of DNMT1 mRNA were detected by real-time RT-PCR.Expressions of DNMT1 protein were detected by streptavidin peroxidase immunohistochemistry.The relationships between expression of DNMT1 and clinicopathological findings were analyzed.Results The value of relative quantification (RQ) of DNMT1 mRNA in human pancreatic cancer tissues was 2.32 (1.17 ～ 5.17 ), which was significant higher than 0.78 (0.07 ～3.14) in para-cancerous tissues(P ＜0.05).The index of expression of DNMT1 protein in human pancreatic cancer tissues was (54.5 ±21.2)% ,which was significant higher than( 10.9 ± 15.0)% in paracancerous tissues (P ＜ 0.01 ).Patients were divided into the high DNMT1 group (n = 19) with above 54.5% of the DNMT1 positively cancer cells and the low DNMT1 group ( n = 11 ) with less than 54.5% of the DNMT1 positively cancer cells.The high expression of DNMT1 was correlated significantly with clinical staging ( x2 =6.897, P = 0.029), lymph node metastasis ( x2 = 4.739, P = 0.029) and neural invasion ( x2 = 5.44, P =0.020).On the other hand, no association between DNMT1 expression and age, gender, tumor location,tumor size, tumor differentiation, the serum CEA and CA19-9 levels could be found.Conclusions DNMT1 mRNA and protein was highly expressed in pancreatic cancer tissues.High expression of DNMT1 might be related to the aggressiveness of pancreatic cancer, lymph node metastasis and neural invasion.

ObjectiveTo assess the effects of DNA methyhransferase 1 ( DNMT1 ) gene silencing on DNMTs activity and methylated CpG sites of hMLH-1 in pancreatic cancer cell line PaTu8988.Methods DNMT1 siRNA and negative control siRNA was constructed by Ambion Company of United States.Then they were transfected into pancreatic cancer cell line PaTu8988 at the concentrations of 15,30 nmol/L,and the cells without transfection was used as the control group.Real-time PCR and Western blotting were applied to detect the DNMT1 mRNA and protein expression,and DNMTs activity was detected by using DNMTs activity assay kit.Change of methylation of CpG island of hMLH-1 was detected by bisulfite sequencing PCR (BSP).The expression of hMLH-1 mRNA was detected by Real-time PCR.ResultsAt 48 h after transfection,Realtime RT-PCR analysis showed that the levels of DNMT1 mRNA in DNMT1 siRNA group ( 15 nmol/L) and DNMT 1 siRNA group (30 nmol/L) were 0.573 ± 0.026 and 0.143 ± 0.044,which were significantly lower than those in control group 1.020 ±0.217 and negative siRNA 15 nmol/L group 0.900 ±0.475,and negative siRNA 30 nmol/L group 0.938 ± 0.327 (P ＜0.05 ).Western blotting analysis showed that the level of DNMT1 protein of DNMT1 siRNA group was also lower than those of negative siRNA and control groups.DNMT activity in DNMT1 siRNA15,30 nmol/L groups was 0.364 ± 0.124and 0.250 ± 0.072,which were significantly lower than those in control group 0.931 ± 0.065and negative siRNA group 0.665 ± 0.055 and 0.472 ± 0.040.DNMT activity was positively correlated with DNMT1 mRNA expression ( r =0.69,P ＜ 0.01 ).DNMT1 RNA interference decreased 8 methylated CpG sites of hMLH-1 to 1 site.Concluslons DNMT1siRNA can specifically inhibit the expression of DNMT1 gene of PaTu8988 and DNMT activity,and can decrease methylated CpG sites of hMLH-1 gene.

Dyskeratosis congenita (DC) is a rare disease and a genetic heterogeneity of bone marrow failure, characterized by muco-cutaneous triad of mucosal leukoplakia, abnormal skin pigmentation, nails dystrophy and often involving multiple organs or systems. The inheritance patterns of DC include X-linked recessive, autosomal dominant and recessive patterns. However, the inheritance patterns in 30%-40% of DC patients remained unknown. Dyskeratosis congenita is difficult to diagnose because of its genetic and clinical heterogeneity. This article will review and discuss the state-of-the-art progresses in genetics, clinical manifestation, diagnosis, differential diagnosis, treatment and prognosis of DC.

In recent years,various methods for detecting exogenous and endogenous hypochlorite have been studied,considering its essential role as a biomolecule.However,the existing technologies still pose obstacles such as their invasiveness,high costs,and complicated operation.In the current study,we developed a glow-type chemiluminescent probe,hypochlorite chemiluminescence probe(HCCL)-1,based on the scaffold of Schaap's 1,2-dioxetane luminophores.To better explore the physiological and pathological functions of hypochlorite,we modified the luminophore scaffold of HCCL-1 to develop several probes,including HCCL-2,HCCL-3,and HCCL-4,which amplify the response signal of hypo-chlorite.By comparing the luminescent intensities of the four probes using the IVIS? system,we determined that HCCL-2 with a limit of detection of 0.166 μM has enhanced sensitivity and selectivity for tracking hypochlorite both in vitro and in vivo.

This study investigated the effect of epigenetic modification of maspin on extravillous trophoblastic function. The mRNA expression of maspin in placentae from normotensive and preeclamptic pregnant women was detected by RT-PCR. TEV-1 cells, a human first-trimester extravillous trophoblast cell line, were cultured and treated with CoCl(2) (300 μmol/L) to induce chemical hypoxia and with 5-aza (500 nmol/L) to induce demethylation. The mRNA expression of maspin in TEV-1 cells subjected to different treatments was determined by RT-PCR, and the proliferative and migratory abilities of TEV-1 cells were assessed by cell counting kit-8 (CCK-8) and Transwell assays. Our results showed that the maspin mRNA expression level in placentae from preeclamptic women was much higher than that from normotensive women. CoCl(2) or 5-aza could up-regulate the mRNA expression of maspin and significantly suppress the proliferation and migration of TEV-1 cells. It was concluded that the epigenetic modification in promoter region of maspin contributes to incomplete trophoblast invasion, which offers a novel approach for predicting and treating placental dysfunction.
Adult ; Chorionic Villi ; physiology ; Epigenesis, Genetic ; genetics ; Female ; Humans ; Pregnancy ; Serpins ; genetics ; Trophoblasts ; physiology