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| 1 | Patterns and Dynamics of Rifting on Passive Continental Margin from Shelf to Slope of the Northern South China Sea:Evidence from 3D Analogue Modeling显示文摘Affected by thermal perturbation due to mantle uprising, the rheological structure of the lithosphere could be modified, which could lead to different rifting patterns from shelf to slope in a pas-sive continental margin. From the observed deformation style on the northern South China Sea and analogue modeling experiments, we find that the rift zone located on the shelf is characterized by half grabens or simple grabens controlled mainly by long faults with large vertical offset, supposed to be formed with normal lithosphere extension. On the slope, where the lithosphere is very hot due to mantle upwelling and heating, composite grabens composed of symmetric grabens developed. The boundary and inner faults are all short with small vertical offset. Between the zones with very hot and normal lithosphere, composite half grabens composed of half grabens or asymmetric grabens formed, whose boundary faults are long with large vertical offset, while the inner faults are relatively short. Along with the thickness decrease of the brittle upper crust due to high temperature, the deformation becomesmore sensitive to the shape of a pre-existing weakness zone and shows orientation variation along strike. When there was a bend in the pre-existing weakness zone, and the basal plate was pulled by a clockwise rotating stress, the strongest deformation always occurs along the middle segment and at the transition area from the middle to the eastern segments, which con-tributes to a hotter lithosphere in the middle segment, where the Baiyun (白云) sag formed. | 孙珍 周蒂 吴世敏 钟志洪 Myra Keep 姜建群 樊浩 | 2009 | Journal of China University of Geosciences2009，20，1： | 14 |
| 2 | Brain iron overload following intracranial haemorrhage显示文摘Intracranial haemorrhages,including intracerebral haemorrhage(ICH),intraventricular haemorrhage(IVH)and subarachnoid haemorrhage(SAH),are leading causes of morbidity and mortality worldwide.In addition,haemorrhage contributes to tissue damage in traumatic brain injury(TBI).To date,efforts to treat the long-term consequences of cerebral haemorrhage have been unsatisfactory.Incident rates and mortality have not showed significant improvement in recent years.In terms of secondary damage following haemorrhage,it is becoming increasingly apparent that blood components are of integral importance,with haemoglobin-derived iron playing a major role.However,the damage caused by iron is complex and varied,and therefore,increased investigation into the mechanisms by which iron causes brain injury is required.As ICH,IVH,SAH and TBI are related,this review will discuss the role of iron in each,so that similarities in injury pathologies can be more easily identified.It summarises important components of normal brain iron homeostasis and analyses the existing evidence on iron-related brain injury mechanisms.It further discusses treatment options of particular promise. | Thomas Garton Richard F Keep Ya Hua Guohua Xi | 2016 | Stroke & Vascular Neurology2016，1，4： | 11 |
| 3 | Mechanisms of brain injury after intracerebral haemorrhage显示文摘 | Guohua Xi Richard F Keep Julian T Hoff | 2006 | Lancet Neurology2006，，1： | 4 |
| 4 | Role of lipocalin 2 in intraventricular haemoglobin-induced brain injury显示文摘Objective:Our recent studies have shown that blood components,including haemoglobin and iron,contribute to hydrocephalus development and brain injury after intraventricular haemorrhage(IVH).The current study investigated the role of lipocalin 2(LCN2),a protein involved in iron handling,in the ventricular dilation and neuroinflammation caused by brain injury in a mouse model of IVH.Design:Female wild-type(WT)C57BL/6 mice and LCN2-deficient(LCN2^(−/−))mice had an intraventricular injection of haemoglobin,and control mice received an equivalent amount of saline.MRI was performed presurgery and postsurgery to measure ventricular volume and the brains were used for either immunohistochemistry or western blot.Results:Ventricular dilation was observed in WT mice at 24 h after haemoglobin(25 mg/mL,20µL)injection(12.5±2.4 vs 8.6±1.5 mm^(3) in the control,p<0.01).Western blotting showed that LCN2 was significantly upregulated in the periventricular area(p<0.01).LCN2 was mainly expressed in astrocytes,whereas the LCN2 receptor was detected in astrocytes,microglia/macrophages and neurons.Haemoglobin-induced ventricle dilation and glia activation were less in LCN2^(−/−)mice(p<0.01).Injection of high-dose haemoglobin(50 mg/mL)resulted in lower mortality in LCN2^(−/−)mice(27%vs 86%in WT;p<0.05).Conclusions:Intraventricular haemoglobin caused LCN2 upregulation and ventricular dilation.Haemoglobin resulted in lower mortality and less ventricular dilation in LCN2^(−/−)mice.These results suggest that LCN2 has a role in haemoglobin-induced brain injury and may be a therapeutic target for IVH. | Hajime Shishido Yasunori Toyota Ya Hua Richard F Keep Guohua Xi | 2016 | Stroke & Vascular Neurology2016，1，2： | 3 |
| 5 | Behavioral Tests After Intracerebral Hemorrhage in the Rat显示文摘 | Ya Hua Timothy Schallert Richard F. Keep Jimin Wu Julian T. Hoff Guohua Xi | 2002 | Stroke: Journal of the American Heart Association2002，，10： | 3 |
| 6 | The Deleterious or Beneficial Effects of Different Agents in Intracerebral Hemorrhage: Think Big, Think Small, or Is Hematoma Size Important?显示文摘 | Richard F. Keep Guohua Xi Ya Hua Julian T. Hoff | 2005 | Stroke2005，，7： | 3 |
| 7 | 中枢给予5-羟色胺2C受体拮抗剂对DOCA高血压大鼠血压的作用显示文摘目的 :本实验是为了证实中枢神经系统的 5 -HT2C受体是否参与了血压的调节和高血压的发病。方法 :使用SD造模DOCA高血压大鼠 ,通过植入右侧脑室的不锈钢导管 ,用微型渗透泵以恒定速率慢性脑室输注选择性 5 -HT2C受体拮抗剂RS1 0 2 2 2 1 ,观察拮抗中枢神经 5 -HT2C受体后对DOCA高血压大鼠血压的影响。另一个实验使用SD大鼠 ,慢性脑室输注选择性 5 -HT2C受体促进剂MK2 1 2 ,以及MK2 1 2和RS1 0 2 2 2 1同时输注 ,以进一步证实 5 -HT2C受体对大鼠血压的作用。结果 :脑室输注RS1 0 2 2 2 1能减低DOCA大鼠血压的发展 ,MK2 1 2能使SD大鼠发展为高血压 ,而同时使用RS1 0 2 2 2 1的SD大鼠血压则保持正常。结论 :中枢神经系统 5 | 司晓晨 Parvine Shakui Richrd F Keep | 2003 | 中国病理生理杂志2003，19，1： | 2 |
| 8 | Systemic complement depletion diminishes perihematomal brain edema in rats显示文摘 | Xi G Hua Y Keep R F | 2001 | Stroke2001，32，1： | 2 |
| 9 | Erythrocytes and delayed brain edema formation following intracerebral hemorrhage in rats显示文摘 | Xi G Keep RF Hoff yr | 1998 | J Neurosurg1998，89，6： | 1 |
| 10 | Mechanisms of brain injury after intracerebral hemorrhage显示文摘 | Xi G Keep RF Hoff JT | 2006 | Lancet Neurol2006，5，： | 1 |
| 11 | Erythrocytes and delayed brian edema formation following intracerebral hemorrhage in rats显示文摘 | Xi G Keep KF HOOT | 1998 | J Neumsu1998，89，60： | 1 |
| 12 | Complement activation in the brain after experimental intracerebral hemorrhage显示文摘 | Hua Y Xi G Keep RF | 2000 | J Neurosurg2000，92，6： | 1 |
| 13 | Characterization of an improved double hemorrhage rat model for the study of delayed cerebral vasospasm显示文摘 | Lee JY Huang DL Keep R | 2008 | J Neurosci Methods2008，2，： | 1 |
| 14 | Er ythrocy tes and delayed brainedema formation following intracerebral hemorrhage in rats显示文摘 | Xi G Keep RF Hoft JT | 1998 | J Neurosurg1998，89，5： | 1 |
| 15 | Purification of bacterially expressed single chain Fv antibodies for clinical applications using metal chelate chromatography显示文摘 | Casey J L Keep P A Chester K A etal | 1995 | J Immun Method1995，179，： | 1 |
| 16 | Behavioral tests after intracerebral hemorrhage in the rat显示文摘 | Hua Y Schallert T Keep RF | 2002 | Stroke2002，33，10： | 1 |
| 17 | Attenuation of thrombin-induced brain edema by cerebral thrombin preconditioning 显示文摘 | Xi G Keep RF | 1999 | Stroke1999，30，6： | 1 |
| 18 | Complement activation in the brain after esperimental intracerebral hemorrhage 显示文摘 | HUA Y XI G KEEP R F | 2000 | Neurosurg2000，92，： | 1 |
| 19 | trocmental intracerebral hemorrhage 显示文摘 | Xi G Wagner KR keep FR | 1998 | Stroke1998，29，： | 1 |
| 20 | Hemoglobin and iron handling in brain after subarachnoid hemorrhage and the effect of deferoxa- mine on early brain injury显示文摘 | LEE J Y KEEP R F HE Y | 2010 | J Cereb Blood Flow Metab2010，30，11： | 1 |
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