地层超覆油藏勘探技术在陈家庄地区馆陶组的应用

通过地质综合分析,明确了陈家庄地区馆下段地层超覆油藏的油气分布规律主要受古地貌、地层超覆边界、岩性变化及储盖组合的控制,而地层和储层空间分布的定量解释是制约地层超覆油藏勘探的关键。根据该区馆下段地层超覆油藏的地质特征,应用相适应的勘探技术,对储层进行了定量分析,即应用残余厚度法、地震沿层切片等技术方法确定了古地貌特征及地层超覆线的位置;应用实际地质模型进行了正演计算,用来确定地层超覆上倾尖灭位置;在精细的测井资料校正基础上进行了测井波阻抗约束反演,用来确定储层厚度和预测孔隙度。应用上述技术方法最终完成了研究区储层厚度的定量解释、储层平面分布和储层孔隙度的预测,探明了馆陶组地层超覆油藏的规模,控制含油面积为33.2 km2,储量为4.740×107t;累积探明含油面积为20.6 km2,储量为2.807×107t,取得了显著的勘探效果和经济效益。     

Multiple roles of the DSCR1 (Adapt78 or RCAN1) gene and its protein product Calcipressin 1 (or RCAN1) in disease

The DSCR1 (Adapt78) gene¹ is transiently induced by stresses to temporarily protect cells against further potentially lethal challenges. However, chronic expression of the DSCR1 (Adapt78) gene has now been implicated in several pathological conditions including Alzheimer’s disease, Down syndrome and cardiac hypertrophy. Calcipressin 1 has been shown to function through direct binding and inhibition of the serine threonine protein phosphatase Calcineurin. Pharmacological inhibition of calcineurin, by the immunosuppressive drugs cyclosporin A and FK506, affects a wide variety of diseases. It is, therefore, likely that this endogenous calcineurin inhibitor, calcipressin 1, may also play a role in a variety of human diseases. ¹Please note that the mammalian DSCR1 gene is also called Adapt78 or RCAN1, and its protein products have been named Calcipressin1, MCIP1 and RCAN1. A proposal to adopt a single gene name of RCAN1 and a protein name RCAN1 (for Regulator of Calcineurin) has been endorsed by the HUGO Gene Nomenclature Committee, but final approval must await agreement from a majority of researchers in the field. Received 2 March 2005; received after revision 27 May 2005; accepted 19 July 2005     

Biomedicine and diseases: the Klippel-Trenaunay syndrome, vascular anomalies and vascular morphogenesis

Vascular morphogenesis is a vital process for embryonic development, normal physiologic conditions (e.g. wound healing) and pathological processes (e.g. atherosclerosis, cancer). Genetic studies of vascular anomalies have led to identification of critical genes involved in vascular morphogenesis. A susceptibility gene, VG5Q (formally named AGGF1), was cloned for Klippel-Trenaunay syndrome (KTS). AGGF1 encodes a potent angiogenic factor, and KTS-associated mutations enhance angiogenic activity of AGGF1, defining ‘increased angiogenesis’ as one molecular mechanism for the pathogenesis of KTS. Similar studies have identified other genes involved in vascular anomalies as important genes for vascular morphogenesis, including TIE2, VEGFR-3, RASA1, KRIT1, MGC4607, PDCD10, glomulin, FOXC2, NEMO, SOX18, ENG, ACVRLK1, MADH4, NDP, TIMP3, Notch3, COL3A1 and PTEN. Future studies of vascular anomaly genes will provide insights into the molecular mechanisms for vascular morphogenesis, and may lead to the development of therapeutic strategies for treating these and other angiogenesis-related diseases, including coronary artery disease and cancer.Received 24 November 2004; received after revision 21 January 2005; accepted 2 March 2005     

Ethanol inhibits insulin expression and actions in the developing brain

Ethanol-induced cerebellar hypoplasia is associated with inhibition of insulin-stimulated survival signaling. The present work explores the mechanisms of impaired insulin signaling in a rat model of fetal alcohol syndrome. Real-time quantitative RT-PCR demonstrated reduced expression of the insulin gene in cerebella of ethanol-exposed pups. Although receptor expression was unaffected, insulin and insulin-like growth factor (IGF-I) receptor tyrosine kinase (RTK) activities were reduced by ethanol exposure, and these abnormalities were associated with increased PTP1b activity. In addition, glucose transporter molecule expression and steady-state levels of ATP were reduced in ethanol-exposed cerebellar tissue. Cultured cerebellar granule neurons from ethanol-exposed pups had reduced expression of genes encoding insulin, IGF-II, and the IGF-I and IGF-II receptors, and impaired insulin- and IGF-I-stimulated glucose uptake and ATP production. The results demonstrate that ethanol inhibits insulin-mediated actions in the developing brain by reducing local insulin production and insulin RTK activation, leading to inhibition of glucose transport and ATP production.Received 30 December 2004; received after revision 1 March 2005; accepted 10 March 2005     

血清中生物高分子活性中心离子分布与高血压病患者血液流变学参数之间的关系

计算高血压患者血清中生物高分子活性中心离子（Ti、V、Cr、Mn、Mo、Zn，Fe、Co、Ni、Cu等过渡金属元素）的分布，发现高血压患者可以分成阴平阳升、阴降阳升、阴平阳降、阴阳两降四型。进一步研究发现这四型患者血清中生物高分子活性中心离子的分布参数与中医高血压各证型（肝阳上亢、阴虚阳亢、肝肾阴虚、阴阳两虚）的血液流变学参数（η低切、η高切、Lb、Hct、ηp）之间有很明显的相关性。所以作者认为生物高分子活性中心离子的分布参数可以作为高血压中医辨证分型的微观定量依据之一。     

骨髓增生异常综合征的细胞凋亡分子机制(综述)

骨髓增生异常综合征的基本病理特征是骨髓的无效造血。骨髓造血细胞的凋亡增加是导致无效造血的主要原因之一。目前认为 ,骨髓基质细胞分泌的细胞因子如肿瘤坏死因子 (TNF -α)、转化生长因子 β(TGF - β) ,Fas受体 /配体的高表达 ,凋亡调节基因的异常 ,如促凋亡基因 (Bax、Bad)与抗凋亡基因 (Bcl- 2、Bcl-X)的比值增高 ,及半胱氨酸 /天冬氨酸特异的蛋白酶 (caspases)的过度激活等 ,与病人的骨髓造血细胞凋亡增加有关。     

Human Genome and Diseases:¶Cellular and molecular aspects of Zellweger syndrome and other peroxisome biogenesis disorders

Peroxisomes are single-membrane-bound organelles present in virtually all eukaryotic cells. They are involved in numerous metabolic processes, both catabolic and anabolic, including β-oxidation of very long chain fatty acids, metabolism of hydrogen peroxide, plasmalogen biosynthesis and bile acid synthesis. In several genetic diseases, there is either isolated deficiency of a specific peroxisomal protein (single-protein deficiencies) or a defect in the formation of the organelle with loss of multiple peroxisomal functions (peroxisome biogenesis disorders). X-linked adrenoleukodystrophy is an example of the former, and the Zellweger spectrum of the latter. Peroxisome biogenesis disorders are inherited in an autosomal recessive manner and result from mutations in any of at least 12 PEX genes that encode peroxins. This article reviews the peroxisomal system, the clinical, biochemical and molecular aspects of peroxisomal disorders, and discusses recent scientific advances in the understanding of peroxisome biogenesis. Received 16 October 2001; received after revision 2 January 2002; accepted 3 January 2002     

Chronic gestational exposure to ethanol impairs insulin-stimulated survival and mitochondrial function in cerebellar neurons

Chronic gestational exposure to ethanol has profound adverse effects on brain development. In this regard, studies using in vitro models of ethanol exposure demonstrated impaired insulin signaling mechanisms associated with increased apoptosis and reduced mitochondrial function in neuronal cells. To determine the relevance of these findings to fetal alcohol syndrome, we examined mechanisms of insulin-stimulated neuronal survival and mitochondrial function using a rat model of chronic gestational exposure to ethanol. In ethanol-exposed pups, the cerebellar hemispheres were hypoplastic and exhibited increased apoptosis. Isolated cerebellar neurons were cultured to selectively evaluate insulin responsiveness. Gestational exposure to ethanol inhibited insulin-stimulated neuronal viability, mitochondrial function, Calcein AM retention (membrane integrity), and GAPDH expression, and increased dihydrorosamine fluorescence (oxidative stress) and pro-apoptosis gene expression (p53, Fas-receptor, and Fas-ligand). In addition, neuronal cultures generated from ethanol-exposed pups had reduced levels of insulin-stimulated Akt, GSK-3β, and BAD phosphorylation, and increased levels of non-phosphorylated (activated) GSK-3β and BAD protein expression. The aggregate results suggest that insulin-stimulated central nervous system neuronal survival mechanisms are significantly impaired by chronic gestational exposure to ethanol, and that the abnormalities in insulin signaling mechanisms persist in the early postnatal period, which is critical for brain development. Received 21 January 2002; received after revision 28 February 2002; accepted 25 March 2002     

SD大鼠心气虚证动物模型的建立与评价

目的　探讨心气虚证动物模型的建立方法。方法　SD大鼠 4 0只采用基础进食量 2 4d ,每日按自身体重的5 %强迫负重游泳至力竭 ,大剂量灌服心得安 2 4mg 10 0g等综合方法建立心气虚证动物模型 ,其中 2 0只作为人参药物反证组。并设立正常对照组 4 0只 ,以进一步证明所建立模型是心气虚证动物模型。结果　与正常对照组比较 ,模型组大鼠心脏收缩功能和舒张功能均有所下降 ,反映虚证的SOD含量减少 ,MDA含量增加。而所有定量指标均发生了符合心气虚证的变化。结论　采用基础进食量、强迫负重游泳及大剂量灌服心得安的综合方法建立心气虚证动物模型是可行的