Effect of different conditions on the whole blood platelet aggregation indu- ced by adenosine diphosphate (ADP) was reported. The results showed that the sample preparation of whole blood aggregation was relatively simple and quick, and a little volume of blood was used. Because the platelets interact with the blood cells in physiological environment, it may reflect the function of platelets objectively. Under our experimental conditions, aspirin and prostacyclin substance could inhibit the platelet aggregation (4.34?1.10?) induced by ADP. Their inhibition rate was 49.5% and 80% respectively, and the platelet aggregation was 2.19?0.74? and 0.87?0.75? (P

AIM:To observe the changes in vascular endothelial growth factor (VEGF) expression and the cell numbers of cellular necrosis in hippocampus CA1 area after cerebral ischemia and hypothermia postconditioning (HPC). METHODS: The focal thrombotic cerebral ischemia was induced by photochemical reaction in tree shrews. 6 h after ischemia, HPC was executed by a focal homoeothermic equipment, which reduced the brain temperature and maintained at 31-32 ℃ for 1 h. VEGF expression in hippocampus CA1 area was detected by immunohistochemistry. The numbers of death cells were counted and the ultrastructure was observed under the electron microscope. RESULTS: Compared to control group, VEGF expressions increased in neuron of hippocampus CA1 area at 24 h, and decreased at 72 h in HPC group (P

AIM: The present study was designed to examine changes in monoamine oxidase (MAO) activity during cerebral ischemia and whether ginkgolide B's brain protection challenges with inhibiting monoamine oxidase. METHODS: The focal thrombotic cerebral ischemia was formed by photochemistry-induced in tree shews .MAO activities in different areas which include ischemic,core, penumbra and contralater and serum, were tested by enzyme color-compared way. The protein contents in different area above was examined by amino acid autoanalytic apparatus. RESULTS: MAO activities in ischemic core in different group were much lower than that in the sham operation group [(15.41?1.63)?10 3 U/g protein] and contralatetral areas [(15.47?1.66)?10 3 U/g protein], with its peak at seventy-two hours after occlusion, but that in penumbra [(25.37?2.01)?10 3 U/g protein] and serum [(210.04?20.67)?10 3U/L] ascended. There were significant differences in MAO activities between ischemic group and control (P

AIM: To observe the changes of VEGF expression in different subfield of brain in tree shrews during hyperglycemia and focal cerebral ischemia, in order to explore the relationship between cerebral ischemia, hyperglycemia and VEGF. METHODS: High blood glucose in tree shrews was induced by intraperitoneal injection of streptozotoctin. Focal cortical thrombotic cerebral ischemia was induced by photochemical method in tree shrews. At 4 h, 24 h and 72 h after cerebral ischemia, the histopathological changes and hippocampal neuronal density were examined. VEGF expressions in the ischemic core, penumbra and contralateral cerebral cortex were detected by immunohistochemistry technique at different times after cerebral ischemia. RESULTS: The results of histopathological study showed that there was infarction zone in the exposured cerebral cortex at 4 h after photochemical reaction, and the damage was most severe at 24 h, subsequently accompanied with the glia multiplication and rehab reaction at 72 h. The animals in hyperglycemic ischemic group suffered from greater neurological lesion than the normoglycemic stroke animals, especially at 24 h (P<0.01) and 72 h (P<0.05) after cerebral ischemia. Immunohistochemical analyses of VEGF expression revealed that it started to increase at 4 h after brain ischemia in the penumbra, reached a peak at 24 h, and weakened at 72 h. The stimulated VEGF production was also observed in hyperglycemic only group. When hyperglycemia and brain ischemia were combined, the VEGF expression was higher than that in hyperglycemic only group (P<0.05). Compared to normoglycemic ischemic group, no additivity of the effects of hyperglycemia combined with brain ischemia was observed. CONCLUSION: (1) The model of experimental hyperglycemia and cerebral ischemia is replicated successfully by applying the method combined in vivo injection of streptozotocin in the lower primate tree shrew with thrombotic focal cerebral ischemia. (2) This study shows that hyperglycemia aggravates the focal cerebral ischemia damage. (3) Cerebral ischemia and hyperglycemia both can independently up-regulate VEGF expression, but there is no additional increase in VEGF expression when hyperglycemia combined with brain ischemia is applied.

Objective To seek the effect of SGK1 on the protection and prognosis of cerebral ischemia reperfusion. Methods Animal model of rats was used to construct them into experimental group(A)and control group(B). The impact of cerebral ischemia reperfusion on the hippocampus neuron cell apoptosis was simulated by making the overexpression of SGK1 and using PI3K inhibitors LY294002 to deal with animal models. Results The overexpression of SGK1 could reduce the neuron cell apoptosis caused by cerebral ischemia reperfusion to a certain extent,reverse the expressions of Cleaved aspas 3 protein,pro-apoptotic protein Bax and inhibitor of apoptoasis protein Bcl-2 through the PI3K/Akt-mediated signaling pathway. Conclusion SGK1 can protect the tissues with ischemia-reperfusion,which may provide the biological evidence for future clinical applications.

AIM:To study the effects of ischemic postconditioning(PC) on regional cerebral blood flow(rCBF) and astrocyte(AS) activation in hippocampus CA1 area and to explore the possible mechanism of ischemic PC affecting glial fibrillary acidic protein(GFAP) expression during focal cerebral thrombosis.METHODS:The thrombotic focal cerebral ischemia was induced by photochemical reaction in tree shrews,and ischemic postconditioning was established by cliped ipsilateral carotid of the animal at 4 h after cerebral ischemia.The rCBF and GFAP expressions in hippocampus CA1 area were detected,respectively,by laser-Doppler(LD) fowmeter and immunohistochemistry.RESULTS:The numbers of GFAP positive cells were increased markedly and GFAP expression enhanced(P

Objective To explore the effect of Plan. Do-Check-Act on homogenization of nursing processes in ICU. Methods A total of 36 nurses were selected to implement Plan. Do-Check-Act in ICU according to evidence-based medicine. Their nursing was inspected by a senior nurse. The differences of the following items before and after Plan. Do-Check-Act were compared: nursing quality comprehensive quality control index and specialized quality control index. Results After the implementation of Plan. Do-Check-Act, comprehensive quality control index of clinical nursing quality score by (89.28 ± 2.36) points up to (97.45±1.38) points, and there was significant difference(t=-7.310, P<0.01). The specialized quality control indicators including the incidence of ventilator associated pneumonia, the incidence of catheter-related bloodstream infection, the incidence of catheter-associated urinary tract infections, the incidence of accidental extubation, the incidence of pressure sores, the incidence of glycemic out of control, the incidence of sedation out of control and retention time were 26.2%(53/202), 17.8%(36/202), 18.8%(38/202), 11.9%(24/202), 2.5%(5/202), 18.3%(37/202), 15.3%(31/202), (168.0 ± 3.3) h before the implementation and 7.1%(14/196), 3.1%(6/196), 4.1%(8/196), 0.5%(1/196), 0, 3.6%(7/196), 3.1%(6/196), (96.0±4.2) h after the implementation. There were significant differences (χ2=4.913-25.907, t=66.195, all P<0.01). Conclusions The Plan. Do-Check-Act is an effective way to improve nursing quality of ICU to make it homogeneous, reduce adverse nursing and iatrogenic complications.

A new photochemical method was employed to cause regional cerebral throm-bosis in the rats by intravenous injection of the rose bengal (1mg/100g body weight)and focal illumination (with a filtered xenon lamp, ?560nm and △?60nm) of the intackskull surface. The regional cerebral blood flow (rCBF), stroke volume (SV), cardiac out-put(CO), heart rate(HR) and the regional blood flow of heart, liver, spleen, kidney andadrenal were used as indexes. The effects of cerebral hemodynamic alterations on cardiacfunction during photochemical reaction were discussed. The results showed that rCBF, SV,CO decreased markedly as compated with the contralateral (P

AIM: To observe the changes in platelet-activating factor(PAF) receptor binding characteristics and explore the action of PAF on formation of thrombotic core and penumbra following local cerebral ischemia.METHODS: Neuron's membrane protein was abstracted, and the local cerebral ischemia model were induced by photochemistry in tree shrews. The PAF binding sites on central neuron membrane were studied by -PAF binding assay.RESULTS: There were two different affinities of PAF receptors on tree shrew's brain cell membrane, with kD 1=( 3.61 ? 0.72 ) nmol/L and kD 2=(17 04?2 41) nmol/L, corresponding respectively to maximum number of binding sites: Bmax1=(1 457 94?168 01) pmol/g protein and Bmax2=(5 017 40?742 16) pmol/g protein. The binding sites decreased in ischemic core, penumbra and contralateral regions at 4,24 and 72 h after ischemia ( P

Objective To find the effect and potential mechanism of ischemic postconditioning relief rCBF and VEGF expression during focal cerebral thrombosis.Methods The thrombotic focal cerebral ischemia was induced by photochemical reaction in tree shrews.The rCBF and VEGF expression in hippocampus CA1 area were detected,by laser-Doppler(LD) fowmeter and immunohistochemistry.Results rCBF reduces along with temporal lasting in cerebral thrombus,especially in 24 h;VEGF expression enhanced after cerebral ischemic,express of VEGF in 12 h is the most intensification(P0.05),mostly in 12 h(P