Objective To investigate the inhibitory effects and mechanism of ginsenoside Rg3 on vasculogenic mimicry of human breast cancer MCF-7 cell line. Methods The MCF-7 cells at logarithmic growth phase were obtained, and were cultured with different concentrations (0, 20, 50, 100, 150 and 300 mg/L) of ginsenoside Rg3. Cells cultured without Rg3 were served as controls. The IC50 were determined by CCK8 assay and anti-angiogenic effects were performed for testing the potential of tube-like structure (TLSs) formation. The expression levels of VEGF-A, MMP 9 and HIF-1αwere detected by Western blotting and real-time PCR. The secreted contents of VEGF-A and MMP9 were detected by enzyme linked immunosorbent assay (ELISA). Results The ginsenoside Rg3 suppressed the proliferation of MCF-7 cells in a dose-dependent manner, in which IC50 was (115.34±8.50) mg/L. The formation numbers of TLSs in MCF-7 cells were significantly inhibited by Rg3 in concentration dependent manner in 50 mg/L, 100 mg/L and 150 mg/L for (19.0 ± 1.0), (15.0 ± 1.5), and (10.0±1.7) vs. controls (22.0±1.8, F=150.805, P<0.05). The mRNA and protein expression levels of VEGF-A, MMP9 and HIF-1αprotein were inhibited by 50 mg/L,100 mg/L and 150 mg/L Rg3 vs. controls (P<0.05). Meanwhile, the contents of VEGF-A in MCF-7 cell supernatant was down-regulated by 50 mg/L,100 mg/L and 150 mg/L Rg3 vs. controls (P<0.05). The contents of MMP-9 in MCF-7 cell supernatant was down-regulated by 100 mg/L and 150 mg/L Rg3 vs. controls (P<0.05). There was no significant difference in MMP-9 expression between 50 mg/L group and control group. Conclusion The ginsenoside Rg3 is able to inhibit the vasculogenic mimicry of MCF-7 cells, which may be related with the down-
regulation of VEGF-A, MMP9 and HIF-1α.

Objective To study the relationship of peripheral vascular disease(PVD) with gender and serum uric acid in patients with type 2 diabetes.Methods Lower extremities of 82 male and 70 female patients with type 2 diabetes were screened for PVD by color Doppler uhrasonography,and the levels of serum uric acid,fasting blood glucose,glycosylated hemoglobin and serum lipid were examined.Results In male,serum uric acid(328.12?107.30) ?mol/L,age(65.00?9.66) yrs,durations of diabetes(7.38?6.17) yrs, HBA_1Cc(7.74?1.83)% were significantly higher in the diabetic patients with PVD than those in patients without PVD.And these changes were not shown in female patients.In male,the detectable rate of PVD(82.14%)in diabetics with high level uric acid was also increased than that in normal uric acid group(53.70%).Conclusion The higher level of serum uric acid in type 2 diabetics was closely related with the occurrence of peripheral vascular disease in male.So we should actively control the level of serum uric acid in male.

The clinical data of one case of laryngeal neuroendocrine carcinoma in our hospital were respectively analyzed. The patient was a 61-year-old male, and complained of progressive pain of right ear for 7-year, it was misdiagnosed as glossopharyngeal neuralgia and larynx hemangioma. This patient was achieved total laryngectomy and bilateral cervical lymph nodes dissection. As of 12 months after surgery, the patient remains under follow-up observation, and no findings indicating obvious recurrence or metastasis has been observed. This disease is a rare and highly malignant tumor that is lack of specific feature in clinical performances. Recognition at larynx is essential so that proper patient management can be initiated.
Carcinoma, Neuroendocrine ; diagnosis ; therapy ; Humans ; Laryngeal Neoplasms ; diagnosis ; therapy ; Male ; Middle Aged

Objective To explore the the cellular damage of hippocampus neuron in a rat model of chronic cerebral hypoperfusion. Methods Rat model of chronic cerebral hypoperfusion was established by permanent bilateral common carotid arteries occlusion (2VO). Eight weeks after the operation,the brains were removed and examined with histological stains, electron microscope, flow cytometer and Western Blotting. Results Compared with the control group,the arrangement of hippocampus neurons in 2VO rats appeared to be more irregular, and the number of the neurons decreased partly ( CA2: ( 34.75 ± 3.40) vs (49.25 ± 9.67 ), P ＜ 0. 05; DG: ( 73.50 ± 9.26)vs ( 90.75 ± 4.35 ), P ＜ 0. 05 ). By electron microscopic study of hippocampus neurons in 2VO rats, the nuclei became smaller and the heterochromatin assembled in the border of the nuclei in some neurons, while cytoplasm swelled,especially in mitochondria and endoplasmic reticulum. The rate of apoptosis of hippocampus neurons in 2VO rats( (9. 117 ±2. 540)% ) ,detected by the flow cytometer,was higher than that of sham group( (4. 750 ±3.481 ) % ) (P ＜ 0. 05 ). The expression of pro-caspase-3 in hippocampus of 2 VO rats was not altered significantly compared with the control group(P ＞ 0. 05 ). Conclusion The cellular damage of hippocampus neuron in 2VO rats was mainly caused by apoptosis.

Vectors used to carry foreign genes play an important role in gene therapy, among which, the adeno-associated virus (AAV) has many advantages, such as nonpathogenicity, low immunogenicity, stable and long-term expression and multiple-tissue-type infection, etc. These advantages have made AAV one of the most potential vectors in gene therapy, and widely used in many clinical researches, for example, Parkinson's disease. This paper introduces the biological characteristics of AAV and the latest research progress of AAV carrying neurotrophic factor, dopamine synthesis related enzymes and glutamic acid decarboxylase gene in the gene therapy of Parkinson's disease.
Animals ; Aromatic-L-Amino-Acid Decarboxylases ; genetics ; Dependovirus ; genetics ; Gene Transfer Techniques ; Genetic Therapy ; Genetic Vectors ; Glial Cell Line-Derived Neurotrophic Factor ; genetics ; Glutamate Decarboxylase ; genetics ; Humans ; Nerve Growth Factors ; genetics ; Neurturin ; genetics ; Parkinson Disease ; therapy

China ; Humans ; Laparoscopy ; education ; Mentors ; Urology ; education

Objective To observe the effect of resveratrol on cognitive impairment in rats after chronic cerebral hypoperfusion,and to explore the underlying antioxidant mechanism of resveratrol.Methods The chronic cerebral hypoperfusion model was induced by permanent occlusion of bilateral common carotid arteries (2VO) in rats.Healthy male Wistar rats were randomly divided into 3 groups:sham-operated group,2VO group and 2VO+resveratrol group.Spatial learning and memory were assessed using the Morris water maze at 4 weeks after the occlusion.The levels of 4-Hydroxynonenal (4-HNE) and 8-Hydroxy-2′-deoxyguanosine (8-OHdG) in the cortex and hippocampal CA1 areas were detected using immunohistochemistry staining,for reflecting the lipid peroxidation and oxidative DNA damage.Results The escape latencies from the third day to the fifth day were longer in 2VO group than in sham-operated group[(42.1+5.4)s vs.(25.1±3.3)s,(36.4±4.4)s vs.(12.4±3.3) s,(30.4±4.0)s vs.(8.1±3.4)s,q=10.91、14.54 and 14.07,all P ＜0.01],while the time spent in the object square was shorter in 2VO group than in sham-operated group[(12.9+2.5)s vs.(18.9+2.2)s,q=6.47,P＜0.01].Compared with 2VO group,the escape latencies in 2VO+resveratrol group from the third day to the fifth day were shorter[(29.5+4.0)s,(25.6±4.3)s and (19.8±4.2)s,q=7.71,6.22 and 6.37,all P＜0.01],while the time spent in the object square was longer[(16.5±1.8)s,q=3.83,P＜0.05].Compared with the shamoperated group,the mean integral optical density (IOD) of 4-HNE and 8-OHdG in the cortex and hippocampus CA1 area were increased in 2VO group (265.1 + 9.0 vs.168.2 + 6.0,37.8 + 5.0 vs.24.0+4.0,q=31.89 and 7.48,both P＜0.01).And in the 2VO+resveratrol group,the mean IOD of 4-HNE and 8-OHdG in the cortex and 8-OHdG in hippocampus CA1 area were lower than in 2VO group (195.1±7.0,26.0±4.3,q=23.03 and 6.49,both P＜0.01).Conclusions Resveratrol can improve the cognitive impairment in rats after chronic cerebral hypoperfusion,which may be related to preventing oxidative damage.

ObjectiveTo observe the effects of enriched environment on depressive-like behaviors induced by chronic stress in rats.MethodsAdult rats were randomly divided into stress group and the control group,then after 21 days of stress,rats were raised in an enrich environment (EE) or standard environment (SE)for 28 days.Open field test,forced swimming test and sucrose preference test were used to detect depressive-like behavior in rats.Results ( 1 ) Open field test showed that grid crossing,standing and rearing in stress ( no gap)rats were significantly reduced ( 13.88 ±4.38 vs 45.00 ± 10.19,9.13 ±2.54 vs 16.38 ±4.11 and 4.78 ± 1.39vs 10.51 ± 2.52 ; n =8 ; P＜ 0.01 respectively) ; but grid crossing and standing in stress + EE rats were significantly increased than stress + SE rats (41.61 ± 10.53 vs 26.25 ± 6.18 and 16.79 ± 3.49 vs 11.25 ± 3.12 ; n =8 ; P＜0.01 and P＜0.05 respectively).(2) Sucrose preference tests showed that sucrose consumption and sucrose preference％ in stress ( no gap) rats were significantly decreased than those in the control group ( 5.22 ± 0.94 vs 10.61 ±2.59 and (49.11 ±6.77)％ vs(63.38 ±8.36)％ ; n=8; P＜0.01 respectively).(3) Forced swimming test showed that immobility time was increased in stress ( no gap) rats ( ( 19.5 ± 5.43 ) s vs ( 12.75 ± 3.9 ) s; n =8 ; P ＜ 0.05 ) and was restored by EE compared to SE rats ( ( 10.25 ± 3.57) s vs ( 17.75 ± 5.45 ) s; n =8 ; P ＜ 0.05).ConclusionChronic stress can reduce depressive-like behaviors,and EE can restore depressive-like behaviors induced by chronic stress.

Objective This study was to investigate the association of certain single nucleotide polymorphisms (SNPs) of the ER with genetic susceptibility to ISS .Methods Genomic DNA was extracted from peripheral blood of children with ISS (n=355) and of normal growth and development individuals as controls from Jiangxi province (n=345) .The association between the ER gene polymorphisms with the height-related clinical traits was analysed .Results The allele T of rs6557177 is significantly lower in the ISS group than in the control group(P=0 .021 ,OR=0 .624) .The clinical indexes of two kinds of different genotypes were analyzed and compared ,there was no statistical difference(P>0 .05) .Conclusion The allele T of rs6557177 of ER gene is a protection factor of ISS .C gene and T gene grouping clinical parameters (hight ,weight ,IGF-1 ,IGFBP3 ,E2 and BMI) were analyzed and found no statistically significant difference .

Objective To explore the effect of lysophosphatidic acid(LPA)on blood-brain barrier(BBB) permeability and its possible mechanism.Methods LPA or LPA+suramin(L+S)were stereotaxically injected into the right eaudate nucleus in SD rats in vivo.Evans blue(EB)was used to quantitatively measure the permeability of BBB at different time points.The expression of matrix metalloproteinase-9 was detected by immunohistochemistry technique.The pathological ultrastruetural changes of BBB were assessed by transmission electron microscopy.Results The BBB permeability began to increase after LPA administered into ipsilateral eaudate nucleus,and reached the peak at 24h.Then the permeability of BBB gradually lowered after 48h.In comparison with the same time points of control group,there were quite significant differences(P＜0.01).After L+S was injected,the change of BBB permeability had differences in comparison with those of LPA group in the same time points,(P＜0.05).MMP-9 positive cells were mainly vascular endothelial cells.The numbers of MMP-9 positive blood vessels grew at 6h in LPA group,and the expression of it reached maximum at 24h,then the number of it decreased at 48h,showing significant statistical differences in comparison with the L+S group(P＜0.01),It was observed microscopically that ultrastrueture of BBB of the LPA group was changed sharply,such as basement membrane roughed and fragmented,astroeyte end-feet swolled markedly and perivaseular space enlarged obviously.But there were no remarkable changes in BBB in L+S group.Conclusion LPA can induce increase of BBB permeability and its possible mechanism is the strong expression of MMP-9 protein produeted by endothelial cells through the mediation of LPA receptor,leading to degradation of basement membrane.