Induced growth of high quality ZnO thin films by crystallized amorphous ZnO

This paper reports the induced growth of high quality ZnO thin film by crystallized amorphous ZnO. Firstly amorphous ZnO was prepared by solid-state pyrolytic reaction, then by taking crystallized amorphous ZnO as seeds （buffer layer）, ZnO thin films have been grown in diethyene glycol solution of zinc acetate at 80 ℃. X-ray Diffraction curve indicates that the films were preferentially oriented [001] out-of-plane direction of the ZnO. Atomic force microscopy and scanning electron microscopy were used to evaluate the surface morphology of the ZnO thin film. Photoluminescence spectrum exhibits a strong ultraviolet emission while the visible emission is very weak. The results indicate that high quality ZnO thin film was obtained.

Vascular endothelial growth factor induced angiogenesis following focal cerebral ischemia/reperfusion injury in rabbits

BACKGROUND： Therapeutic angiogenesis has opened up new pathway for the treatment of ischemic cerebrovascular disease in recent years. The exploration of the effect of vascular endothelial growth factor （VEGF） on inducing angiogenesis following ischemia/reperfusion injury can provide better help for the long-term treatment of cerebrovascular disease in clinic. OBJECTIVE： To observe the effect of VEGF on inducing angiogenesis following focal cerebral ischemia /reperfusion injury in rabbits through the angiogenesis of microvessels reflected by the expression of the factors of vascular pseudohemophilia. DESIGN： A randomized controlled animal tria SETTNG： Department of Medical Imaging, Second Hospital of Hebei Medical University MATERIALS： Sixty-five healthy male New Zealand rabbits of clean degree, weighing （2.6±0.2） kg, aged 4.5-5 months, were used. The polyclonal antibody against vascular pseudohemophilia （Beijing Zhongshan Company）, recombinant VEGF165 （Peprotech Company, USA）, biotinylated second antibody and ABC compound （Wuhan Boster Company） were applied. METHODS： The experiments were carried out in the Laboratory of Neuromolecular Imaging and Neuropathy, Second Hospital of Hebei Medical University from May to August in 2005. （1） The rabbits were randomly divided into three groups： sham-operated group （n=15）, control group （n=25） and VEGF-treated group （n=-25）. In the control group and VEGF-treated group, models were established by middle cerebral artery occlusion （MCAO） induced focal cerebral ischemia/reperfusion. In the VEGF-treated group, VEGF165 （2.5 mg/L） was stereotactically injected into the surrounding regions of the infarcted sites immediately after the 2-hour ischemia/reperfusion; Saline of the same dosage was injected in the control group. But the rabbits in the sham-operated group were only drilled but not administrated. （2） The experimental indexes were observed on the 3^rd 7^th, 14^th, 28^th and 70^th days of the experiment respectively, 3 rabbits in the sham-operated group and 5 in the control group and VEGF-treated group were observed at each time point. The brain tissues in the surrounding regions of the infarcted sites were collected. The positive expressions of the factors of vascular pseudohemophilia in vascular endothelial cells were analyzed with immunohistochemical method. The microvessels in unit statistical field were counted with the imaging analytical software. MAIN OUTCOME MEASURES： The changes of microvascular density in the brain tissue and the positive expressions of the factors of vascular pseudohemophilia in the surrounding regions of the infarcted sites were observed on the 3^rd 7^th, 14^th, 28^th and 70^th days of the experiment. RESULTS： All the 65 New Zealand rabbits were involved in the analysis of results without deletion. Changes of the number of microvessels at different time points in each group： There were no obvious changes at different time points in the sham-operated group. The numbers of microvessels at 7 and 14 days were obviously more in the control group than in the sham-operated group [（6.0±1.1）, （9.0±0.9） microvessels; （3.0±1.1）, （3.0±1.1） microvessels; P〈 0.05-0.01], and those at 3, 7, 14 and 28 days were obviously more in the VEGF-treated group than in the control group [（8.3±2.0）, （13.4±1.4）, （15.5±2.3）, （6.8± 1.0） microvessels; （3.4±0.6）, （6.0±1.1）, （9.0±0.9）, （3.2±0.8） microvessels; P 〈 0.01]. （2） Positive expressions of the factors of vascular pseudohemophilia in the surrounding regions of infarcted sites： There were no obvious changes at different time points in the sham-operated group. In the control group, the changing law of the expressions was the same as that for the number of microvessels that the expression began to mildly increase at 7 days, reached the peak value at 14 days, and began to reduce at 28 days. In the VEGF-treated group, the expression was obviously increased at 3 days, also reached the peak value at 14 days, and reduced to the normal level at 70 days, but the expressions were obviously stronger than those in the control group at the same time points. CONCLUSION： Angiogenesis can be obviously induced in rabbits after the focal cerebral ischemia/reperfusion injury is treated with VEGF for 18 days.

The role of nerve growth factor inducible protein B in the pathogenesis of levodopa-induced dyskinesias

Objective： To study the role of the expression of nerve growth factor inducible protein B gene （NGFI-B） in striatum in the pathogenesis of levodopa-induced dyskinesias （LID）. Methods： The rat model of LID was treated with SCH 23390（1 mg/kg ip,a dopamine D1 antagonist） and haloperidol （1 mg/kg ip,a dopanfme D2 antagonist） respectively. Reverse transcriptase-polymerase chain reaction （RT-PCR） was used to measure the expression of NGFI-B mRNA in stiiatam and the behavior changes were observed. Resuits： After treatment with SCH23390, abnormal involuntary movement （AIM） in LID rats was decreased （ P 〈 0.05 ） and the expression of NGFI-B mRNA in striatum did not change significantly. After treatment with haloperidol, the changes of AIM in LID rats were not significant and the expression of NGFI-B mRNA was increased significantly（ P 〈 0.01）. Conclusion： LID is associated with over-expression of NGFI-B in striatum. Abnormal activity in the direct pathway and the basal ganglia circuit could be involved in the occurrence of LID.

Maternal Lead Exposure Induces Down-regulation of Hippocampal Insulin-degrading Enzyme and Nerve Growth Factor Expression in Mouse Pups

Lead exposure is a known potential risk factor for neurodegenerative diseases such as Alzheimer’s disease （AD）. Exposure to lead during the critical phase of brain development has been linked with mental retardation and hypophrenia in later life.

Direct Observation of Growth and Self-assembly of Pt Nanoclusters in Water with the Aid of a Triblock Polymer Using in situ Liquid Cell Transmission Electron Microscopy （TEM）

Triblock copolymers are playing important roles in nanomaterial synthesis, and the nanomaterial forming mechanisms need to be studied in detail. In situ liquid cell transmission electron microscopy （TEM） is a powerful tool for real time observation of the dynamic growth behavior of nanomaterials in liquid with high resolution, and could be used for the above task. Here we report the observation of the growth and self-assembly of Pt nanoclusters with the aid of an ethylene oxide-propylene oxide-ethylene oxide triblock copolymer （PEO-PPO-PEO） F 127 using in situ liquid cell TEM, with the nanocluster growth and formation procedures being tracked. Nano objects were seen to appear, drift and rotate with time, and then form into certain shaped nanoclusters under the electron beam irradiation. Further interestingly, in the thicker liquid layer region, the nanoclusters appeared to be fluffy, with average size keeping increase with time, while in the thinner region, the clusters were thinner, and got densified with time. The difference in precursor availability due to liquid layer thickness and charging effects is attributed to such a phenomenon.

Effect of calycosin on left ventricular ejection fraction and angiogenesis in rat models with myocardial infarction

OBJECTIVE:To evaluated the effect of calycosin on left ventricular ejection fraction and angiogenesis.METHODS:Adult male Sprague-Dawley rats were randomly assigned into calycosin-treated groups(0.5,1,2,and 4 mg/kg qd),a dimethyl sulfoxide(DMSO),or a sham-operated control group.The myocardial ischaemia(Ml) model was intraperitoneally administered calycosin for 28 days.The survival rates and left ventricular ejection fractions(LVEF)were compared between groups.The expression levels of vascular endothelial growth factor(VEGF)and cluster of differentiation 31(CD31) in ischaemic myocardium were also measured and compared.RESULTS:The construction of MI model resulted in a LVEF reduction of 50% compared with the sham-control.After 28 days,the LVEF value was 10% higher when calycosin(4 mg/kg) was administered compared with the DMSO group.The expression of VEGF and CD31 showed a dose-dependent manner when calycosin was administrated.The calycosin-treated(4 mg/kg) group displayed a twofold increase in VEGF expression at both the mRNA and protein levels compared with the DMSO group.In addition,CD31 expression in the microvascular increased 1.5-fold in the 4 mg/kg calycosin-treated group.CONCLUSION:Calycosin improved left ventricular ejection fraction in the MI rat models,induced VEGF expression in the ischaemic myocardium,increased CD31 expression and promoted angiogenesis.