Objective To design a new experimental facility to induce rat diffuse axonal injury model. Methods Rat diffuse axonal injury was induced by a new experimental facility,which was developed to let the rat head spin 90 degree at the moment to cause shearing injury.Vital sign and behavior of rat were measured simultaneously.The rats were sacrificed at 2 h,6 h,12 h,24 h,36 h,72 h and 10 d after injury,respectively,and the brain tissues were removed to prepare paraffin section.Then silver staining and HE staining were conducted to investigate changes of axonal fibers. Results There were unconsciousness,respiratory rhythm disturbance and hyporeflexia of pupil light reflex immediately after injury,and reactiveness decrease and activity retardation still existed even after resuming consciousness.At anatomical scene,subarachnoid hemorrhage or cerebroventricular haemorrhage were widespread.At an early stage,there were swelling,collapse,and axonal retraction ball formation at cortico-medulla junction,callosum,brainstem,and cerebellar white matter under microscope.But at the later stage,gitter cell proliferation and nest-like aggregation were major pathophysiological changes at focal brain tissue. Conclusion The new experimental facility is suit able to be used to induce rat diffuse axonal injury,since it is convenient,controlable,and precise.

BACKGROUND: Endothelium-dependent vasodilatation (EDD) has been assessed by intracoronary acetylcholine infusion and digital subtraction angiography. However, its applications in continuous observing on early onset, progression and outcomes of clinical interventions of the disease are limited due to the potential trauma of the method. OBJECTIVE: This study was designed to assess the changes in brachial EDD in patients with hyperlipidemia using high-resolution ultrasound and to compare the outcomes of the patients to those of the healthy individuals. DESIGN: Case-control study SETTING: This study was carried out at the Cardiology Department and the Ultrasound Department of Xinyang CentralHospital PARTICIPANTS: Sixty patients with hyperlipidemia, 37 males and 23females, with an age ranging from 36 to 75 years old, were selected at the Cardiology Department of Xinyang Central Hospital from May 2001 to March 2002. They were divided into 3 groups according to abnormalities in blood lipid, as hypercholesterolemia group (HC, 20 cases),hypertriacylglycerolemia group (HTG, 20 cases) and mixed hyperlipidemia group (HLP,20 cases). Twenty voluntary individuals with normal physical examination findings were allocated into control group, 12 males and 8 females. Informed consents were obtained from all the eligible. METHODS: The brachial artery inner diameter and the changes in blood flow of the brachial artery were assessed using high-resolution ultrasound.After the patients having a rest for more than 10 minutes, the inner diameter (D0) and the baseline blood flow of their brachial artery were measured. The blood pressure cuff was placed under the elbow with a pressure at 300 mm Hg, lasting for 4 to 5 minutes and followed with a sudden deflation. 15 s after deflation, the reactive brachial artery inner diameter (D1) and the blood flow of the brachial artery were detected. The patients took another rest for more than 15 minutes and after the artery restored to a normal condition,the patients took nitroglycerol sublingually at a dose of 400 μg. Three to four minutes later, the brachial artery inner diameter (D2) and the blood flow of the brachial artery were detected. The increasing rate of the inner diameter of brachial artery were calculated, the increasing rate of reactive brachial artery inner diameter (%)= (D1-D0)/D0×100% and the increasing rate of post-treatment brachial artery inner diameter (%)=(D2-D0)/D0 ×100%.Meanwhile, the increasing rate of reactive blood flow (%)=(reactive blood flow-baseline blood flow)/ baseline blood flow (100% and the increasing rate of post-treatment blood flow (%)=(the post-treatment blood flow-baseline blood flow)/baseline blood flow×100%. MAIN OUTCOME MEASURES:In three hyperlipidemia groups and the control group, the inner diameter of the brachial artery were measured under resting conditions, in reactive congestion status and after sublingual nitroglycerol treatment respectively using high-resolution ultrasound. RESULTS: All the 60 patients with hyperlipidemia and 20 healthy controls entered the analysis procedure. In HC group, HTG group and HLP group, the increasing rate of reactive brachial-artery inner diameter were significantly lower than that in control group [(5.7±3.2)%, (5.4±3.0)%,(3.8±2.4)%, (11.3±3.1)%,P ＜ 0.05], which was most significant in HLP group. The increasing rate of both the reactive and the post-treatment blood flow in three experimental groups and the increasing rate of the post-treatment brachial-artery inner diameter were not significant (P ＞ 0.05). CONCLUSION:EDD were impaired significantly in patients with hyperlipidemia. High-resolution ultrasound is capable of assessing EDD accurately and reliably.

ABSTARCT:Objective To investigate the effects of the transcription factor SRY-related high-mobility-group box 2 (Sox2)related to stem cells on the invasion and migration of cervical squamous carcinoma cell line SiHa and its mechanism.Methods The expression of Sox2 was detected in Sox2 stably over-expressed cell line SiHa-Sox2 and negative control SiHa-EGFP cells by RT-PCR and Western blotting,respectively.The effects of Sox2 on the invasion and migration capacities of SiHa cells were detected by wound-healing assay and transwell assay.The expression of β-catenin was detected by Western blot.Results Compared with that of SiHa-EGFP cells,the expression of Sox2 at both mRNA and protein levels was obviously upregulated in SiHa-Sox2 cells.The migration and invasion capacities of SiHa-Sox2 cells were increased significantly (P <0.01 ),and the expression of β-catenin increased dramatically compared with that of the control cells.Conclusion Sox2 promotes the invasion and migration capacities of SiHa cells by increasing the expression of β-catenin and activating Wnt signaling pathway, which contributes to the development of cervical cancer.