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Objective To study the changes of toll-like receptor 9 (TLR9) signaling transduction in the peri-infarct cortex of rats with middle cercbral artery occlusion (MCAO). Methods The MCAO models were established in 48 SD rats using intraluminal filament method and reperfusion was performed by removing the filament 90 min after occlusion.Sham-operated group was established as controls (n=24).At 6 h,and 3,7 and 14 d after reperfusion,National Institutes of Health of neurological deficit scale was performed; the brain tissues were dyed by TTC staining; the cerebral infarct volumes were measured,and the protein expressions of TLR9,nuclear factor-kappaB (NF-kappaB,P65),tumor necrosis factor-α (TNFα),interferon regulatory factor-7 (IRF7) and interferon-β (IFNβ) in the peri-infarct cortex and contralateral cortex were detected by Western blotting. Results Neurological scale scores and infract volumes of the MCAO rats gradually decreased at 6 h,and 3,7 and 14 d after repeffusion;with the time prolongation,the protein expression of TLR9,IRF7 and IFNβ gradually increased,while the protein expressions of NFκ B (P65) and TNFα ascended first and then descended with the highest expression level at 7 d.The differences of the same protein expressions between each 2 time points were statistically significant (P＜0.05). At the same observation time point, the protein expression in the peri-infarct cortex was significantly higher than that in the contralateral cortex (P＜0.05).The expressions of NFκB (P65) and TNF-α were significantly higher than those of IRF7and IFN-β at 6 h,and 3 and 7 d,respectively; but the results were opposite at 14 h (P＜0.05).These proteins were not detected in the sham-operated group at all time points. Conclusions TLR9 inflammatory pathways and cell protection pathways were activated in ischemic cortex, which may be involved in the process of inflammatory impairment and tissue repair after cerebral infarction.
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Objective To analyze the gene expression profiling in the periinfarct cortex in the late stage after stroke onset in renovascular hypertensive rats (RHRs) with gene chip technology.Methods RHRs were induced by the method of Goldblatt's 2k2c operation. Cerebral infarction was also induced by permanent middle cerebral artery occlusion (pMCAO) in RHRs. Sham-operated group was established as controls. Total RNA was extracted from the perinfarct cerebral cortex in injured hemisphere 7 d after pMCAO, and the RNA was performed fluorescence labeling, followed by hybridization with 5705 oligo chips. And then, scanning was performed; the data was collected and chosen for microarray analysis using oligonucleotide arrays. Resuits In total, 197 genes were expressed differentially, including 174 genes up-regulated expression and 23 genes down-regulated expression. The up-regulated genes were distributed among all 12 functional categories; the down-regulated genes were distributed only in the categories of transport, transcription regulator, signal,response to stress, metabolism and cell adhesion. Among the 12 functional categories, only 17differentially expressed genes were not previously reported to be associated with brain ischemia/infarction. Conelusion Active gene expression at late stage of cerebral infarction may imply the molecular mechanisms of injury or repair, being the targets of therapeutic intervention.
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This paper discussed the basic elements and the key technology of developing hospital equipment information system (HEIS), proposed the compatible fields' standard, and designed the system architecture and the core database structure. Following the method, we can establish robust HEIS, which can satisfy hospitals' equipment managing regulations, and accord with the work flow. The system has higher accuracy, efficiency and capability to counter risk.
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Equipos y Suministros de Hospitales , Sistemas de Información en Hospital , Diseño de SoftwareRESUMEN
Objective To investigate the therapeutic effect of human urinary kallidinogenase in patients with acute cerebral infarction and explore the mechanism by blood oxygen level dependent functional magnetic resonance imaging (BOLD-fMRI). Methods twenty-three patients with acute cerebral infarction were randomized into control group (n=11) and treatment group (n=12) to receive conventional treatment and additional human urinary kallidinogenase treatment for 12 to 14 days, respectively. BOLD-fMRI was performed, and the affected forefinger muscle strength and NIHSS score were recorded before and after the treatment. Results In the treatment group, the activated frequency and volume in the sensorimotor cortex (SMC) ipsilateral to the infarct increased significantly after the treatment (11/12 vs 4/12; 99.58±169.41 vs 105.17±197.23, P<0.05). The inerernent in the activated volume in the SMC was significantly greater in the treatment group than in the control group (94.42±51.57 vs 16.09±106.61, P<0.05). The forefinger muscle strength and NIHSS score in the treatment group improved significantly after treatment (2.67±1.44 vs 1.25±1.48; 4.92±2.94 vs 10.42±3.80, P<0.05), and the improvement in NIHSS score was significantly greater in the treatment group than in the control group (5.50±1.31 vs 3.18±2.48, P<0.05). Conclusion The therapeutic effect of human urinary kallidinogenase on acute cerebral infarction is mediated essentially by promoting the activation in the SMC in the functional area of the brain.
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Objective To explore the relationship between the long-term presence of hypoxic tissue and astrocyte activation after cerebral infarction in rats. Methods Middle cerebral artery occlusion was performed in rats to induce permanent brain ischemia (PI group) or transient isehemia for 1.5 h followed by reperfusion (1.5 h IR group). Double immunofluorescence staining with EF5 and gliai fibrillary acidic protein (GFAP) antibodies was used to observe the hypoxic tissue and status of astrocyte activation, respectively. On days 1, 3, 7 and 14 after the operation, GFAP fluorescence intensity and the presence of hypoxic tissue in the ischemic cortex were observed. Results The hypoxic tissues were present from day 3 to day 14 after the operation in 1.5 h IR group, but disappeared after day 3 in PI group. GFAP fluorescence intensity in the hypoxic tissue was significantly higher than that in the surrounding tissues at all the observation time points (P<0.05). GFAP fluorescence intensity increased progressive in both groups with the lapse of time (P<0.05), reaching the peak level on day 7 followed then by gradual declination. On each of the time points for observation, GFAP fluorescence intensity in 1.5 h IR group was significantly higher than that in PI group (P<0.05). Conclusion Astrocyte activation is especially obvious in the hypoxic brain tissues after cerebral infarction, which is closely associated with the long-term existence of hypoxic tissues.
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Objective To investigate the effects ofkallikrein gene transfer on microvascularproliferation around the cerebral infarct and on the recovery of regional cerebral blood flow (rCBF)following ischemia/reperfusion injury in rats. Methods The rats with cerebral ischemia/reperfusioninjury induced by middle cerebral artery occlusion (MCAO) were randomly assigned into blank controlgroup, saline group, and pAdCMV-HTK treatment group and received corresponding injections into thetissues around the infarct area. Each group was divided into 3 subgroups (n=10) for observation at 12, 24and 72 h after the treatment. The neurological deficits of the rats before and after the treatment wereevaluated using neurological severity scores (NSS), and the expressions of exogenous human tissuekallikrein (HTK) and vascular endothelial growth factor (VEGF) in the brain tissues were detectedimmunohistochemically. TIC staining was performed to measure the changes in the infarct size.14C-iodoantipyrine tracing technique was used to define the rCBF in the rats. Results Compared tothe blank control group, the cerebral infarct size was significantly reduced in pAdCMV-HTK group 24 hafter the treatment, and was further reduced at 72 h (P<0.05). At 24 h after the treatment, the NSS inpAdCMV-HTK group was significantly lower than that in the blank euntrol and saline groups (P<0.05),and was further reduced at 72 h (P<0.01). After MCAO, the VEGF-positive cells were found mostly inthe cortex and the white matter around the infarct area. The expression of VEGF in pAdCMV-HTK groupwas markedly higher than that in the other two groups at 12, 24, and 72 h after the treatment (P<0.05). Inall the 3 groups, the rCBF around the infarct was slightly decreased as compared to that in thecontralateral hemisphere, pAdCMV-HTK slightly increased the rCBF 12 h after the injection (P>0.05),and significant increase in the rCBF occurred 24 h and 72 h after the injection (P<0.05). ConclusionKallikrein gene transfer following cerebral ischemia/reperfusion injury promotes vascular proliferationaround the infarct and increases the rCBF to reduce the infarct volume and attenuate neurological deficitsin rats.