Animals ; Cardiovascular Diseases ; etiology ; Cerebrovascular Disorders ; etiology ; Homocysteine ; metabolism ; Humans ; Methylenetetrahydrofolate Reductase (NADPH2) ; genetics ; Polymorphism, Genetic

Animals ; Benzodiazepines ; pharmacology ; Ducks ; physiology ; Growth Hormone ; blood ; Insulin-Like Growth Factor I ; metabolism ; Serum ; metabolism ; Weight Gain ; drug effects

Objective:To study the effect of electroacupuncture (EA) at the Pericardium Meridian on the heart function of volunteers with acute hypoxia, and to provide scientific evidence for the acupoints selection along the affected meridian in acupuncture-moxibustion therapy. Methods:Based on a self-control design, eighteen healthy volunteers were recruited in the study. Points from the Pericardium Meridian [Neiguan (PC 6), Ximen (PC 4), Quze (PC 3) and Tianquan (PC 2)], non-Pericardium Meridian point [Shousanli (LI 10)], non-meridian and non-acupoint points [1.0-1.5 cm lateral to Neiguan (PC 6) and Ximen (PC 4), respectively on both sides], and a blank control (only inhaling low-oxygen gas without EA stimulation) were selected to observe, once every week, 10 sessions in total, and only 1 acupoint was observed once. The volunteers inhaled low-oxygen gas mixture (10.8% O2 and 89.2% N2) for 30 min to imitate acute hypoxia. EA was conducted when the gas mixture was inhaled for 10 min and then lasted for 20 min; meanwhile, hemodynamic indexes such as cardiac output (CO), cardiac index (CI), systemic vascular resistance (SVR), systemic vascular resistance index (SVRI), left cardiac work (LCW), left cardiac work index (LCWI) and heart rate (HR) were recorded on a hemodynamic monitor. Results:EA at the acupoints of Pericardium Meridian significantly down-regulated the increased CO/CI, LCW/LCWI, and HR (P<0.05), and significantly up-regulated the decreased SVR/SVRI in hypoxia (P<0.05); EA at other meridian acupoints or at non-meridian and non-acupoint points didn't produce such effects. Conclusion: EA at the Pericardium Meridian can obviously improve the cardiac hyper-activation caused by acute hypoxia in healthy volunteers.

Objective To analyze the gene expression profiles in relation to the migration ability of adult human bone marrow-derived neural stem cells (Md-NSCs), and identify the genetic basis of the high migration potential of Md-NSCs in the central nervous system (CNS). Methods Adult human bone marrow stromal celIs(BMSCs) obtained from adult healthy volunteers were induced to differentiate into Md-NSCs in vitro, and the expressions of the genes related to cell invasiveness and metastasis were investigated by microarray analysis. Quantitative real-time PCR (RT-PCR) was used to verify the microarray results. Results The results of microarray analysis revealed significant overexpressions of the genes MMP1, MMP2, MMP17, ITGA3, RhoB, RhoC and RhoD in the Md-NSCs as compared with the expressions in fresh normal human adult bone marrow cells depleted of red blood cells. Quantitative RT-PCR verified the overexpression ofMMP2 gene by 2.84×100 folds, ITGA3 gene by 2.22×102folds, and RhoC gene by 4.92×100 folds. Conclusion The high migration potential of the Md-NSCs in the CNS is probably associated with the overexpression of the genes that promote cell invasiveness and metastasis. These overexpressed genes are also important oncogenes, and therefore the tumorigenicity of the Md-NSCs warrants further investigation.

Seven compounds were isolated from Onychium japonicum by macroporous resin, silica gel, ODS, Sephadex LH-20 column chromatography and semi-preparative HPLC. Their structures were identified by NMR, MS and other spectroscopic methods as onychone A (1), quercetin (2), quercetin-3-O-α-L-rhamnoside (3), kaempferol-7-O-β-D-glucopyranoside (4), kaempferol-3-O-α-L-rhamnopyranoside (5), (-)-prunin (6), and norathyriol (7). Compound 1 is a novel macrocyclic flavonoid, and all the others are reported from this plant for the first time. In vitro cytotoxic activities of compounds 1-7 were evaluated by MTS testing with five cancer cell lines. Compound 7 exhibited weak cytotoxicity against tumor cell lines A549, SMMC-7721, and SW480.

Objective To investigate the changes in mitoehondrial membrane potential of the rat neurons after acute brain contusion and laceration injuries. Methods Seventy Sprague-Dawley (SD)rats were randomized into the sham injury group(n=10)and brain injury group.The brain injury group was divided into 6 subgroups(n=10)for observation at 1,6,and 24 h and 2,3,and 7 days after acutebrain contusion and laceration injury,which was induced by impact of the brain with a flee-falling object.In the brain slices labeled with fluorescent JC-l staining,the changes in the mitoehondrial membrane potential of the neurons were observed under confocal laser scanning microscopy at the indicated time points.The neuronal apoptosis Was detected using Hoehesd3342 staining and TUNEL assay,and the number of apoptotic neurons was determined under optical microscope.The ultrastructural alterations of the neurons were observed with transmission electron microscopy. Results Compared with that of the sham injury group,the mitoehondrial membrane potential of the neurons decreased significantly 1 h alterthe brain injury(P<0.01),reachingthe lowestlevel at 24 h,and maintained the low level aRerwards.Apoptotie neurons were identified in the brain slices with Hochest33342 staining.One hour after the brain injury,TUNEL assay revealed a small number of positive neurons,which increased significantly at 6 h(P<0.01)and reached the highest level at 48 h.The alteration pattern of the number of the positive neurons showed a 24-h delay in compariSOIl witll that of the mitochondrial membrane potential aRer the brain trauma.Under electronmicroscope.the mitocbondria of the neurons exhibited only slight swelling at l h. and obvious morphological changes of the mitochondria occurred 6 h after the brain trauma,accompanied by chromatin fragmentation,presence of marginal nuclei and broadened nuclear membrane;nuclear condensation and chromatolysis were observed in the neurons 24 h after the brain trauma.Conclusion In rats with acute brain contusion and laceration injuries,the mitochondrial membrane potential of the neurons decreases early(<1h)after the brain injury,which induces apoptosis of the neurons.

Objective To observe the effect of acidic fibroblastic growth factor (aFGF) on traumatic brain edema. Methods Recombinant human aFGF (10mg/ml) was continuously injected into the intraventricle for 12 h before brain traumatic injury in rats, and the brain water content was determined and the histological and ultrastructural changes in the brain tissue observed. Results Brain edema and neuronal damage were reduced remarkably by the administration of aFGF. Conclusion aFGF can obviously alleviate brain edema and neuronal damage.

Objective To observe the effect of acidic fibroblastic growth factor (aFGF) on traumatic brain edema. Methods Recombinant human aFGF (10mg/ml) was continuously injected into the intraventricle for 12 h before brain traumatic injury in rats, and the brain water content was determined and the histological and ultrastructural changes in the brain tissue observed. Results Brain edema and neuronal damage were reduced remarkably by the administration of aFGF. Conclusion aFGF can obviously alleviate brain edema and neuronal damage.

Aim To investigate the effect of TaorenHonghua drug pair on intervertebral disc degeneration (IVDD) in rats.Methods Fifty healthy Wistar rats were randomly divided into control group,model group,sham group,meloxicam group and Taoren-Honghua drug pair group,with 10 rats in each group.We established dynamic and static forces imbalance of cervical disc degeneration model or sham surgery in rats.12 weeks later,rats were intragastrically administered with meloxicam,Taoren-Honghua drug pair or saline for 30 days.C4/5 and C6/7 discs were harvested from rats.ABOG staining was used for observation of intervertebral disc morphology,real time PCR for mRNA expressions of type Ⅱ collagen (Col Ⅱ) and type Ⅹ collagen (Col Ⅹ),and immunohistochemical staining for Col Ⅱ and Col Ⅹ.Results Compared with model group,Col Ⅱ expression increased,while Col X expression decreased in chondrocyte of intervertebral disc in Taoren-Honghua-treated group(P ＜ 0.01).Conclusion Taoren-Honghua drug pair could delay the degeneration of cartilage endplate in rat intervertebral disc.

Objective In order to study the localization of NMDA receptor protein on the neuron membrane, a new immunocytochemistry method to visualize and quantify 3D earmark the membrane protein in nanometer scale has been achieved by atomic force microscope (AFM) with labeled colloid gold particle. Methods First step, the distribution of the anti-NMDAR1 IgG-SPA-gold complexes molecule on the surface of mica had been scanned by AFM and the characteristic 3D conformation was analyzed by particle software. Then the 3D conformation was contrasted with the IgG-SPA-gold complexes molecules combined with the neuron membrane surface and that were compared with the results of light microscope, laser confocal microscope and scanning electron microscope. Results The 3D conformation of IgG-SPA-gold scanned through mica surface shows the average diameter of globe particles is 49 nm. The neuron membrane NMDA receptor protein combined with IgG-SPA-gold immunocomplexes are globe or cosh shapes . Its average diameter is 53 nm. The long axis section is a typical two apexes structure. Conclusion AFM could determine the situation and 3D conformation of NMDAR protein on neuron membrane surface in nanometer scale. NMDAR single molecule could combine with one or two colloidal gold particles. Colloidal gold particle scanned by AFM in situ is a new detecting method of immunocytochemistry.