海洋可控源电磁数据预处理方法研究

海洋可控源电磁法是探测海底油气资源和矿产资源的一种新兴的海洋地球物理勘探方法。本文提出了一套海洋可控源电磁数据预处理方法,包括时频转换和预白处理、时钟漂移补偿、随机噪音估计、叠加窗口选择、方位校正、椭圆极化分析、主轴旋转以及合并航道数据等等,并用实例详细说明了各种处理方法及其应用效果。

Involvement of ERK1/2 and p38 MAPK in up-regulation of 14-3-3 protein induced by hydrogen peroxide preconditioning in PC12 cells

Objective To investigate the protective effects of hydrogen peroxide preconditioning （HPP） on the pheochromocytoma （PC12） cells treated with 1-methyl-4-phenylpyridinium （MPP^＋） and to explore the potential mechanisms. Methods The viability and apoptosis of PC 12 cells were determinded by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay and 4′,6′-diamidino-2-phenylindole （DAPI） staining, respectively. The expressions of 14-3-3 protein and phospholylated p38 mitogen-activated protein kinase （MAPK） were determined by Western blot. Enzyme-linked immunosorbent assay （ELISA） was used to measure the activity of extracellular signal-regulated protein kinase 1/2 （ERK1/2）. Results The cell viability decreased and the number of apoptotic cells increased dramatically in MPP^＋ group compared with that in Control group. HPP induced a significant increase in cell viability and a marked decrease in population of apoptotic cells of the MPP^＋- treated PC 12 cells, accompanied with up-regulation of 14-3-3 protein and increase of ERK 1/2 and p38 MAPK activities. The 14-3-3 protein expression was positively correlated with the phosphorylation of ERK1/2. Furthermore, inhibition of the ERK1/2 with PD98059 abolished the 14-3-3 protein up-regulation in PC 12 cells induced by HPP. Conclusion HPP protects PC 12 cells against MPP＋ toxicity by up-regulating 14-3-3 protein expression through the ERK1/2 and p38 MAPK signaling pathways.

Effects of ischemic preconditioning on cyclinD1 expression during early ischemic reperfusion in rats

AIM： To observe the effect of ischemic preconditioning on cyclinD1 expression in rat liver cells during early ischemic reperfusion.METHODS： Fifty-four SD rats were randomly divided into ischemic preconditioning group （IP）, ischemia/ reperfusion group （IR） and sham operation group （SO）. The IP and IR groups were further divided into four sub-groups （n = 6）. Sham operation group （SO） served as the control group （n = 6）. A model of partial liver ischemia/reperfusion was used, in which rats were subjected to liver ischemia for 60 min prior to reperfusion. The animals in the IP group underwent ischemic preconditioning twice for 5 min each time prior to the ischemia/reperfusion challenge. Alter 0, 1, 2, and 4 h of reperfusion, serum and liver tissue in each group were collected to detect the level of serum ALT, liver histopathology and expression of cyclinD1 mRNA and protein. Flow cytometry was used to detect cell cycle as the quantity indicator of cell regeneration. RESULTS： Compared with IR group, IP group showed a significantly lower ALT level in 1h to 4h sub-groups （P 〈 0.05）. Proliferation index（PI） indicated by the S-phase and G2/M-phase ratio [（S＋G2/M）/（G0/G1＋S＋G2/M）] was significantly increased in IP group at 0 and 1 h （26.44 ± 7.60% vs 18.56 ± 6.40%,41.87 ± 7.27% vs 20.25 ± 6.70%, P 〈 0.05）. Meanwhile, cyclinD1 protein expression could be detected in IP group. But in IR group, cyclinD1 protein expression occurred 2 h alter reperfusion. The expression of cyclinD1 mRNA increased significantly in IP group at 0 and 1h （0.568 ± 0.112 vs 0.274 ± 0.069, 0.762 ± 0.164 vs 0.348 ± 0.093,P 〈 0.05）.CONCLUSION： Ischemic preconditioning can protect liver cells against ischemia/reperfusion injury, which may be related to cell proliferation and expression of cyclinD1 during early ischemic reperfusion.

Efficient and Comprehensive Utilizatio℃n of Hemicellulose in the Corn Stover

Pretreatment of the corn stover powder by dilute sulphuric acid （solid-liquid ratio 1 ： 20） at 130 for 30 min was carried out with 89.09% of the hemicellulose removed. After filtration, the xylose-rich corn stover pretreatment liquid, whose fermentable sugar was from hemicellulose hydrolysis only, consisting of 81.16% xylose and 15.27% glucose, was used to cultivate genetic recombinant Escherichia coli BL21 with human-like collagen （HLC） expression enhanced by 50.00% and 63.71% xylose consumption.

Application of autologous peripheral blood stem cell transplantation in children with malignant tumor

Objective To investigate if low dose total body irradiation (TBI, 6.0- 9.0 Gy) combined with intensified chemotherapy followed by autologous peripheral blood stem cell transplantation results in better survival in children with refractory leukemia or solid tumors.Methods Twenty-one children with malignant tumors were included in this study. There were 14 males and 7 females aged 3.5- 12 years. Underlying disease included high-risk acute lymphoblastic leukemia (ALL, CR1 in 3 children and CR2 in 5 children), acute myeloblastic leukemia (AML, 9 children), nonHodgkin' s lymphoma stage Ⅳ (2 children), and neuroblastoma stage Ⅳ (2 children). The peripheral hematopoietic stem cells were collected six to eleven months after complete response, mobilized with high dose chemotherapy alone or combined with GM-CSF or G-CSF. The conditioning regimen consisted of chemotherapy with two to three combinations of the following drugs: cyclophosphamide,arabinosylcytosine, McNU, etopside, and Idarubicin on the basis of TBI (6.0-9.0Gy). A mean of (1.8 ± 0.5) × 108/kg autologous mononuclear cells were transplanted. The patients were followed up after transplantation.Results Severe bone marrow suppression occurred in all patients around day + 7. Peripheral white blood cell count decreased to 0 in all patients at day + 4.8 ± 2.9, and platelet count decreased to less than 20× 109/L at day + 9.0 ± 2.6. Successful engraftment was achieved in 21 patients, but four died of infection at day + 17, + 20, + 31 and + 67, respectively. Recovery of white blood cell (WBC) to 10 × 109/L, absolute neutrophil count to 0.5 × 109/L, platelet count to 20 × 109/L occurred on 21 ± 12,26± 13, and 27 ± 10 days, respectively. During the follow up period, three patients relapsed at + 5months, + 1.5 years, and + 2 years 10 months, respectively. One patient died of intracranial hemorrhage at +8 months. Thirteen patients had event-free survival for 2 - 12 years, with a mean of 6.7±3.4 years.Conclusion Our preliminary data suggest that myeloablative therapy with low dose TBI (6.0 - 9.0 Gy)combined with intensified chemotherapy followed by autologous paripheral blood stem cell transplantation might be associated with favorable results in children with refractory leukemia or solid tumors.

Duplicate preconditioning with sevoflurane in vitro improves neuroprotection in rat brain via activating the extracellular signal-regulated protein kinase

Objective Sevoflurane preconditioning has been demonstrated to reduce cerebral ischemia–reperfusion（IR） injury,but the underlying mechanisms have not been fully elucidated.Besides,different protocols would usually lead to different results.The objective of this study was to determine whether dual exposure to sevoflurane improves the effect of anesthetic preconditioning against oxygen and glucose deprivation（OGD）injury in vitro.Methods Rat hippocampal slices under normoxic conditions（95%O2/5%CO2）were pre-exposed to sevoflurane 1,2 and 3 minimum alveolar concentration （MAC）for 30 min,once or twice,with 15-min washout after each exposure.The slices were then subjected to 13-min OGD treatment（95%N2/5%CO2,glucose-free）,followed by 30-min reoxygenation.The population spikes（PSs）were recorded in the CA1 region of rat hippocampus.The percentage of PS amplitude at the end of 30-min reoxygenation to that before OGD treatment was calculated,since it could indicate the recovery degree of neuronal function.In addition,to assess the role of mitogen-activated protein kinases（MAPKs）in preconditioning,U0126,an inhibitor of extracellular signal–regulated protein kinase（MEK-ERK1/2,ERK1/2 MAPK）,and SB203580,an inhibitor of p38 MAPK,were separately added 10 min before sevoflurane exposure.Results Preconditioning once with sevoflurane 1,2,and 3 MAC increased the percentage of PS amplitude at the end of 30-min reoxygenation to that before OGD treatment,from（15.13±3.79）%（control）to（31.88±5.36）%, （44.00±5.01）%,and（49.50±6.25）%,respectively,and twice preconditioning with sevoflurane 1,2,and 3 MAC increased the percentage to（38.53±4.36）%,（50.74±7.05）%and（55.86±6.23）%,respectively.The effect of duplicate preconditioning with sevoflurane 3 MAC was blocked by U0126[（16.23±4.62）%].Conclusion Sevoflurane preconditioning can induce neuroprotection against OGD injury in vitro,and preconditioning twice enhances this effect.Besides,the activation of extracellular signal–regulated protein kinase（MEK-ERK1/2,ERK1/2 MAPK）may be involved in this process.