Objective To study the efficacy and safety of mifepristone combined with the end of pregnancy in the treatment of uterine scar pregnancy.Methods50 cases of the experimental group in our hospital from February 2014 to December 2016 during the termination of pregnancy uterine scar pregnancy in this study in the research process, no scar uterine pregnancy were 50 as the control group in the process of research.The experimental group and the control group patients were given mifepristone treatment, oral use, patients in the drug treatment of third days should be carried out taking the drug misoprostol experiment, fasting medication, placed in the posterior fornix of vagina.Comparative analysis of the experimental group and the control group of patients with treatment effects and adverse reactions.ResultsAfter a period of treatment, the experimental group and the control group, the time of vaginal discharge and the amount of vaginal bleeding and uterine contractions were no significant difference in the time, not statistically significant.The experimental group of 50 patients, the number of effective treatment for 47 cases, the effective rate was 94%.The control group of 50 patients, the number of effective treatment for the treatment of 48 cases, the effective rate was 96%.As a result, there was no significant difference between the experimental group and the control group in the treatment efficacy, which was not statistically significant (P>0.05).The incidence of adverse reactions in the experimental group was 10%, and the incidence of adverse reactions in the control group was 8%.As a result, there was no significant difference between the experimental group and the control group in the incidence of adverse reactions, which was not statistically significant.ConclusionMifepristone combined with carboprost suppository in the treatment of uterine scar end effect is good, high treatment efficiency, reduce the incidence of adverse reaction, high safety, can reduce the patients caused by trauma to a great extent, is further applied in clinical significance.

Objective:To investigate the therapeutic effect of cardiac rehabilitation exercise on ventricular remodeling in patients with acute myocardial infarction undergoing percutaneous coronary intervention.Methods:A total of 100 patients with acute myocardial infarction undergoing percutaneous coronary intervention who received treatment in Wenzhou Central Hospital from June 2018 to June 2019 were included in this study. They were randomly divided into a rehabilitation group and a conventional treatment group ( n = 50/group). Patients in the conventional treatment group underwent conventional postoperative rehabilitation education while those in the rehabilitation group received targeted cardiac rehabilitation exercise. After surgery, all patients were followed up for 12 months. Real time three-dimensional echocardiography was used to evaluate ventricular remodeling (left ventricular ejection fraction, left ventricular end-diastolic volume , left ventricular end-systolic volume, left ventricular remodeling index) and ventricular synchrony (Tmsv-16dif, Tmsv-16sd, Tmsv16-dif%, Tmsv16-sd%) before and 3, 6 and 12 months after surgery. In addition, serum levels of ventricular remodeling indexes (fibroblast growth factor 23, PICP and PIIINP) were measured. The incidence of cardiovascular end-point events within 12 months was calculated. Results:At 3, 6 and 12 months after surgery, left ventricular ejection fraction was (51.81 ± 5.43)%, (55.88 ± 5.46)%, (55.63 ± 5.57)% in the rehabilitation group, which was significantly higher than (47.16 ± 5.38)%, (52.31 ± 5.44)%, (51.84 ± 5.59)% respectively in the conventional treatment group ( t = 4.302, 3.275, 3.396, all P < 0.05). At 3, 6 and 12 months after surgery, left ventricular end-diastolic volume was (124.65 ± 15.56) mL, (98.54 ± 14.54) mL, (99.82 ± 13.18) mL, respectively in the rehabilitation group, which was lower than (132.64 ± 16.58) mL, (112.55 ± 15.61) mL and (114.84 ± 17.35) mL, respectively in the conventional treatment group ( t = 2.485, 4.644, 4.874, all P < 0.05). At 6 and 12 months after surgery, left ventricular end-systolic volume was (52.26 ± 5.48) mL and (52.15 ± 5.32) mL respectively in the rehabilitation group, which was significantly lower than (57.92 ± 5.46) mL and (58.51 ± 5.72) mL in the conventional treatment group ( t = 5.174, 5.757, both P < 0.05). At 6 and 12 months after surgery, left ventricular remodeling index was (1.75 ± 0.42) g/mL and (1.74 ± 0.35) g/mL respectively in the rehabilitation group, which was significantly higher than (1.52 ± 0.37) g/mL and (1.50 ± 0.32) g/mL, respectively in the conventional treatment group ( t = 2.906, 3.579, both P < 0.05). At 3, 6 and 12 months after surgery, Tmsv-16dif ( t = 2.753, 4.283, 4.088, all P < 0.05), Tmsv-16sd ( t = 5.134, 4.326, 4.670, all P < 0.05), Tmsv-16dif% ( t = 7.714, 8.587, 7.800, all P < 0.05) and Tmsv16-sd% ( t = 9.004, 14.061, 10.305, all P < 0.05) respectively in the rehabilitation group, were significantly lower than those in the conventional treatment group. At 3, 6 and 12 months after surgery, fibroblast growth factor 23 ( t = 6.303, 5.053, 4.619, all P < 0.05). PICP ( t = 3.772, 2.798, 3.788, all P < 0.05) and PIIINP ( t = 3.110, 5.912, 4.294, all P < 0.05) in the rehabilitation group were significantly lower than those in the conventional treatment group. Within 12 months, the total incidence of cardiovascular end-point events in the rehabilitation group [12.00% (6/50)] was significantly lower than that in the conventional treatment [32.00% (16/50)] ( χ2 = 5.828, P < 0.05). Conclusion:Cardiac rehabilitation exercise can improve ventricular remodeling and synchrony in patients with acute myocardial infarction undergoing percutaneous coronary intervention and reduce the incidence of cardiovascular end-point events.

Objective To evaluate intra- and interatrial asynchrony and its determinants in aged patients with paroxysmal atrial fibrillation (PAF) by using tissue Doppler imaging. Methods Ninty-one patients without PAF (control group, including 40 elder patients and 51 non-elder patients) and 52 aged patients with PAF were included. As to assessment of intra- and interatrial synchronicity, the atrioventricular plane were selected on the right atrial (RA) free wall, interatrial septum (IAS), and left atrial (LA) free wall. The time differences from the onset of the P wave to the onset of the A wave at the left atrium (P-LA), the IAS (P-IAS), and the right atrium (P-RA) were measured. Intra-atrial asynchrony was defined as the differences between P-IAS and P-RA (RA asynchrony) and between P-LA and P-IAS (LA asynchrony). Interatrial asynchrony was defined as the difference between P-LA and P-RA. Stepwise regression was made to determine the influencing factors for atrial asynchrony in aged patients with PAF. Results Compared with the control group, aged patients with PAF had significant LA and interatrial asynchrony (P＜0.01). Multivariate stepwise regression demonstrated that systolic blood pressure (x2), age (x1) and left ventricular mass index (LVMI x5) entered the regression equation in aged patients with PAF (Y=-57.241+0.481 x1+0.223 x2+0.294 x5). Conclusions Aged patients with PAF have LA and interatrial asynchrony. LVH, aged and SBP are important factors leading to these asynchronies in the aged patients with PAF.

Objective To explore the effects of homocysteine (Hcy) on neural stem cell (NSC) proliferation and the mRNA expression level of Notch1 and Hes1 related Notch signaling pathway from neonatal rats in vitro. Methods NSCs from neonatal rats were cultured by serum-free culture method in vitro. Cells were divided into four groups: control group (Hcy-C), low dose Hcy (Hcy-L) group, middle dose Hcy (Hcy-M) group and high dose Hcy (Hcy-H) group. NSCs were iden- tified by immunofluorescent staining using the antibodies against Nestin, β-tubulin Ⅲ and GFAP. The proliferation ability of NSCs was detected by MTT. The mRNA expressions of Notch1 and Hes1 were detected by Real-time PCR. Results In the serum free suspension medium, neurospheres that consisted of a great number of nestin-positive cells were found. β-tu- bulin Ⅲ positive neurons and GFAP positive astrocytes were detected by immunofluorescence staining on the 6 th day of cell induction. MTT assay showed that the cell viability was significantly lower in three Hcy treatment groups than those of con- trol group (P ＜ 0.05). And the effect of concentration-dependent was observed. The results of RT-PCR showed that mRNA expression of Hes1 was significantly lower in three Hcy treatment groups than that in control group (P ＜ 0.05). The mRNA ex- pression of Notch1 was significantly lower in Hcy-H group than that of other three groups (P ＜ 0.05). The mRNA expression of Notch1 was significantly lower in Hcy-M group than that of Hcy-L group and control group (P ＜ 0.05). Conclusion Hcy could inhibit the proliferation of NSCs by down-regulating mRNA expression levels of Notch1 and Hes1 genes related to Notch signal pathway.

Objective To explore the effect of folic acid on neural stem cells(NSCs) proliferation from fetal rats in vitro.Method NSCs were isolated and cultured by microdissection,mechanical blowing and serum-free suspension culture,and identified by immunofluorescent staining using antibody against nestin.BrdU(5’bromo-2’deoxyuridine) was used to mark dividing neural stem cells.Cultured NSCs were divided into four groups:control group,low,high dose group(liquid media with added 4,40 mg/L folic acid),and deficiency group(liquid media with added 0.4 mg/L methotrexate,MTX).Monotetrazolium(MTT) and double-label immunofluorescence technique detected NSCs proliferation under the condition of folic acid.Results In the serum-free suspension medium,neurospheres that consisted of a great number of nestin-positive cells could be obtained.The proliferative ability of NSCs were observed by BrdU labeling methods.MTT assay and double-label immunofluorescence for nestin+BrdU showed that the growth tendency was increased with folate concentration in the medium.Compared with control group,NSCs growth rate of folate group was significantly increased in vitro.Conclusion The culture of NSCs isolated from fetal rats possesses the abilities of proliferation and self-regeneration.Folic acid may stimulate proliferation of NSCs efficiently.

Objective To explore the role of homocysteine(Hcy)on angiogenesis at peri infarct region after focal cere-bral ischemia in rats, to elucidate inhibitory factors of angiogenesis, and to establish a clinic foundation for clinical brain functional recovery. Methods Spragur-Dawley (SD) male rats (n=36) were randomly divided into three groups with 12 rats in each group including Sham Operation (SO) group, Middle cerebral artery occlusion (MCAO) group and MCAO+Hcy group. The rats in Sham and MCAO groups were intra-peritoneally injected with 5 mL/(kg·d) saline and rats in MCAO+Hcy group were injected with 2%5 mL/(kg·d) Hey solution from the same route. MCAO was introduced by intraluminal filament meth-od after 7 d Hcy intervention. Rat brains were harvested on the 7th day after MCAO. BrdU(50 mg/kg, as a marker of cell pro-liferation)was intraperitoneally injected three days before the rats were killed. High performance liquid chromatography (HPLC)was used to measure serum Hcy concentration in rats. Brain infarction size was observed by TTC staining. Immuno-fluorescence staining was used to detect the number of BrdU+/laminin+cells at the thalamus of infarction side. Results Se-rum Hcy concentration significantly higher in MCAO+Hcy group than in SO and MCAO groups(P<0.05). Brain damage increased and the number of BrdU+/laminin+cells decreased in MCAO+Hcy group compared with those of MCAO group (P<0.05). Conclusion Increased Hcy concentration in rats lead to more severe damage of cerebral infarction as well as to inhibit the angiogenesis at surrounding ischemia area.

Objective To investigate the effects of folic acid on apoptosis of neural cells after focal cerebral ischemia injury in rats and the mechanisms.Method Thirty two adult male Sprague-Dawley(SD) rats were randomly divided into sham operation group(SO),middle cerebral artery occlusion group(MCAO),MCAO+ low dose folic acid group(MCAO+FA-L) and MCAO+ high dose folic acid group(MCAO+FA-H).The model of middle cerebral artery occlusion(MCAO) was set up by using intraluminal filament method.The rats were sacrificed at D7 day after cerebral ischemia.The apoptotic rate of neural cells was examined by TUNEL test,and the expression of pERK1/2 protein was detected by Western blotting method,The MDA content and serum SOD and GSH-Px activities in rats were measured before and 28d after folic acid treatment and 7th day after ischemia.Results Compared with ischemia group,the apoptotic rate of neural cells and MDA content in both folic acid supplemented groups were decreased significantly(P

BACKGROUND: Previous studies have verified that under normal culture of neural stem cells (NSCs), folic acid can accelerate proliferation of NSCs by phosphorylation of mitogen activated protein kinase path activation ERK1/2. OBJECTIVE: To investigate the effect of folic acid on NSC extracellular signal regulatory protein kinase pERK1/2 under hypoxic condition. METHODS: NSCs from Neonatal rats were cultured in vitro by serum-free culture method, and incubated in a flask at 1×10~8/L. Except normal control group, self-made hypoxia equipment was used in the hypoxia model, folic acid deficiency and folic acid supplemented groups at day 3. At 37 ℃, hypoxia culture was conducted in the thermostat for 6 hours. The contents of folic acid were 4 mg/L, 4 mg/L, 0.65 mg/L, 8 mg/L in the four groups. Cells following 6 days were collected to count the density using trypan blue. RT-PCR was utilized to detect pERK1/2 mRNA expression. Western blot assay was employed to determine pERK1/2 protein expression. RESULTS AND CONCLUSION: Compared with the normal control group, the proliferation of NSCs and the expression of ERK1/2mRNA and pERK1/2 protein were decreased significantly in the hypoxia model group. Compared with the hypoxia model group, the proliferation of NSCs and the expression of ERK1/2mRNA and pERK1/2 protein were increased in the folic acid supplemented group, whereas decreased in the folic acid deficiency group. There were significant differences among groups (P < 0.001). Above-described results verified that folic acid supplementation can activate ERK1/2 phosphorylatin and accelerate proliferation of NSCs under hypoxia condition.

Objective To study the effects of folate(Fol) on proliferation,apoptosis and the antioxidative capacity of the NSCs under hypoxia in vitro.Method The NSCs taken from infant rats brain were cultured by serum-free medium in vitro and divided into four group which were normal control group(NC),hypoxia group(Hyp),Hpy+Fol-D(folate deficient)group and Hpy+Fol group.Except NC group,the other groups were cultured in hypoxia condition for 6 h.The proliferation of NSCs after hypoxia damage was detected by MTT test.The NSCs were collected after being cultured 6 d and then the activity of SOD and GSH-PX was examined.The expression of activated caspase-3 was detected by Western blot.Results Compared with NC group,the proliferation of NSCs and the activity of SOD and GSH-PX decreased significantly after hypoxia,while the expression of activated caspase-3 increased0 The proliferation of NSCs and the activity of SOD and GSH-PX in Hyp group were significantly higher than Hyp+Fol-D group but much lower than Hpy+Fol group(P