塔里木盆地寒武系盐下超深层领域资源量巨大,震旦系是该领域风险勘探的重要层系之一,虽然早些年该层系内尚未取得较大突破,但当前深层震旦系的勘探已经初现成效,进一步突破值得期望,其中储层特征、品质和规模认识不深是制约下一步勘探的重要因素之一.研究以塔里木盆地西北缘阿克苏地区柯坪露头区为例,在对震旦系奇格布拉克组进行精细解剖的基础上,系统地开展了330个样品的铸体薄片分析和6个样品的氩离子抛光—扫描电镜分析,同时优选4个典型微生物白云岩储层样品,开展了基于工业CT的储层三维微观孔喉结构表征.结果表明:①奇格布拉克组微生物白云岩储层主要发育粒间(溶)孔、粒内(溶)孔、晶间(溶)孔、微生物格架孔、溶蚀孔洞和溶缝,其中泡沫绵层石白云岩和黏结颗粒白云岩的孔洞最发育,储层孔隙的发育与岩相具有明显的相关性;②奇格布拉克组微生物白云岩储层为具有中高孔、中低渗特征的孔隙—孔洞型储层,平均孔隙度为3.3％,最大孔隙度为19.6％,优质储层厚度约为53.7 m(孔隙度≥2.5％),储地比约为0.31,具有一定规模;③微孔隙(孔径≤10μm)在不同类型微生物白云岩中普遍发育,对提高储层的储集性能具有重要意义,初步推断其形成主要与微生物早期热解作用有关,热解形成的有机酸和CO2对碳酸盐矿物溶蚀和初始孔隙的保存起到了重要作用.研究成果为塔里木盆地寒武系盐下超深层领域勘探提供了可靠依据.

塔里木盆地柯探1井和轮探1井相继在下寒武统吾松格尔组获得高产工业油气流,突破了整体富泥的传统层系评价定位,但目前对吾松格尔组岩相古地理研究几乎为空白,制约了有利储集相带评价与预测.综合利用阿克苏地区露头资料、录井岩屑、C/O同位素曲线、测井及地震资料,分析了塔里木盆地吾松格尔组沉积期古地理格局、沉积环境及储层分布.结果表明:①吾松格尔组沉积期沉积充填序列及地层分布受塔南、乌恰及温宿三大台内古隆和边缘凹陷控制.古隆起区吾松格尔组超覆沉积,厚度薄,发育混积潮坪、弱镶边台地相;边缘凹陷地层齐全、厚度大,发育深水盆地相和局限潟湖相.②吾松格尔组沉积序列总体表现为一个完整的"海侵—海退"沉积旋回,轮南至古城地区超覆发育塔里木盆地寒武系第一套弱镶边型台地边缘,联合控制沉积期混积潮坪—局限台地的发育.③吾松格尔组发育台缘丘滩、礁后滩及潮上—潮间带薄层台内滩3类白云岩储集层,分布面积大.其中,主要发育于轮南—古城地区的台缘丘滩和礁后滩白云岩储层品质较高,预测面积达12070 km2.以储集层预测为基础,评价认为轮南—古城地区与上覆膏盐岩盖层构成新的一套有利储盖组合且轮探1井已获突破,是下一步重点探索的有利区带.

塔里木盆地寒武系盐下地层资源量巨大,上震旦统奇格布拉克组是该领域风险勘探的重要层系之一,但当前该层系勘探尚未取得重大突破,其中岩相古地理格局及储集层主控因素认识不深是制约勘探突破的重要因素之一.文中以乌什地区昆盖阔坦剖面为研究对象,通过地层精细描述和104块岩石薄片分析,并优选样品开展常微量元素、稀土元素、碳氧锶同位素、白云石有序度及U-Pb同位素年龄测试,分析了奇格布拉克组沉积环境及白云岩成因.结果表明:(1)塔里木盆地乌什地区昆盖阔坦剖面奇格布拉克组厚约141 m,主要发育叠层石、凝块石、泡沫绵层石3种微生物白云岩和鲕粒、粘结颗粒2种与微生物作用相关的颗粒岩,并根据相序组合可以划分为4个段,自下而上构成碳酸盐缓坡背景下的内缓坡潮坪—微生物丘滩沉积序列;(2)地球化学分析表明,奇格布拉克组沉积时期研究区整体处于温暖、干旱气候条件下的近岸浅水环境,海水具有较高盐度、较高水温和氧化—弱氧化特征,海平面先逐渐上升后快速下降;(3)奇格布拉克组白云岩形成于准同生—浅埋藏期,白云石化流体为具有较高盐度的海水.该研究成果不仅可以为塔里木盆地晚震旦世岩相古地理研究提供依据,还可以为储集层主控因素分析提供依据.

信息社会的发展必然触及教育领域，移动互联网为大学课堂的网络化构建了技术平台。传统课堂的“互联网+”转型升级必要且可行，关键是确立“以人为本”的教学理念，达成优势互补，这将成为教育现代化的必然选择。

Tumor necrosis factor- α (TNF- α ) is a critical proinflammatory cytokine regulating neuroinflammation. Elevated levels of TNF- α have been associated with various neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. However, the signaling events that lead to TNF- α -initiated neurotoxicity are still unclear. Here, we report that RIP3-mediated necroptosis, a form of regulated necrosis, is activated in the mouse hippocampus after intracerebroventricular injection of TNF- α . RIP3 deficiency attenuates TNF- α -initiated loss of hippocampal neurons. Furthermore, we characterized the molecular mechanism of TNF- α -induced neurotoxicity in HT-22 hippocampal neuronal cells. HT-22 cells are sensitive to TNF- α only upon caspase blockage and subsequently undergo necrosis. The cell death is suppressed by knockdown of CYLD or RIP1 or RIP3 or MLKL, suggesting that this necrosis is necroptosis and mediated by CYLD-RIP1-RIP3-MLKL signaling pathway. TNF- α -induced necroptosis of HT-22 cells is largely independent of both ROS accumulation and calcium influx although these events have been shown to be critical for necroptosis in certain cell lines. Taken together, these data not only provide the first in vivo evidence for a role of RIP3 in TNF- α -induced toxicity of hippocampal neurons, but also demonstrate that TNF- α promotes CYLD-RIP1-RIP3-MLKL-mediated necroptosis of hippocampal neurons largely bypassing ROS accumulation and calcium influx.

党的十八大报告提出我们高等教育今后应将着力点放在提高教学质量和科技创新能力上，面对高等教育发展的新形势，如何改进大学课堂教学是当前大学教育所面临的一项紧迫任务。课堂中调动学生课堂学习的积极性和参与性是最大程度的发挥教师主导性的先决条件，教师灵活组织课堂，推进教学内容的重要手段之一即因情境选择提问。目前，有关高校课堂组织教学方式已进行了一系列的探讨，但对于教师如何在课堂提问机制运行和改革中发挥作用仍缺乏相关研究，本文以高校生理教学为例进行探讨，以提高学生对于生理学基础学科学习积极性，推进高校生理学教学改革创新。

Abstract Abstract 3141 TWIST encodes a typical basic helix-loop-helix transcription factor. Twist-2, as a member of this family was recently identified as a negative regulator of normal murine myelopoiesis (Sharabi AB. et al. PLoS Biol. 2008, 6:2786-2800), however the expression and functional role of TWIST2 in normal and leukemic human myeloid cells is poorly understood. To address this, we detected the transcript expression of TWIST2 from CD34+ cells of 19 AML patients compared with those of their normal counterparts from 6 healthy donors, and found that the expression of this transcript was 5-fold decreased in the patients. A lentiviral vector, which could only express YFP was used as control; and then the other lentiviral vector to express TWIST2 plus YFP was constructed and validated to efficiently infect various human AML cell lines including THP-1, Dami, HEL, HL60, NB4 and SHI-1. Using all these cell lines, we found that averagely the control cells could expand in the liquid culture 46-fold within 6 days, however the TWIST2 overexpressed cells could only increase 7-fold; moreover in the colony-forming cell (CFC) assays with both Dami and THP-1 cells, the TWIST2 overexpressed cells lost nearly 80% CFC capacities compared with those of control cells (n=3, P<0.05). Next we found that more TWIST2 overexpressed cells could reside in the G0/G1 phase compared with control cells (61% vs. 44%, n=2, P<0.05) and accordingly less TWIST2 overexpressed cells were present in the G2/S/M phase compared with control cells (39% vs. 56%, n=2, P<0.05). In addition, the control and TWIST2 viruses infected Dami (2×106 cells/mouse) and THP-1 cells (4×106 cells/mouse) were subcutaneously injected into nude mice without irradiation respectively, and the control cells could generated tumors (7/7 mice with Dami cells and 2/8 mice with THP-1 cells) but not the TWIST2 overexpressed cells (0/8 mice with Dami cells and 0/6 mice with THP-1 cells) within 4 weeks. To obtain molecular insights of how TWIST2 suppressed the tumourgenesis capacity of these cells, microarray analysis (Agilent 44K) were used to assess the differentially expressed transcripts between control and TWIST2 overexpressed THP-1 cells (from 3 independent experiments). Some examples of the differentially expressed genes included CCND1, RBBP9 and EPHB4, which were down-regulated in the TWIST2 overexpressed cells compared with control cells; in the other hand CDKN1A (p21Cip1), TP53INP1, DDI1 and AKTIP, which were up-regulated in the TWIST2 overexpressed cells compared with control cells. Taken together, these data demonstrated that the TWIST2 was deregulated in human AML patients, and suggested it might play a tumor suppressor role in these cells. Disclosures: No relevant conflicts of interest to declare.

Objective To clarify the characterization of a chromosomal translocation involveingNUP98 at 11p15 in hybrid acute leukemia.Methods Chromosome preparation was made using directmethOd or short—term culture of bone marrow cells.Karyotypic analysis was carried out by R—bandingtechnique.Chromosame painting was performed using whole chromosome painting(WCP) for chromosomes 3 and 11.Interphase and metaphase fluorescence in situ hybridization(FISH) assays wereperformed using a BAC RP11— 120E20(AC060812) probe,which covered ahnost entire NUP98 gene at11p15.Results R—banded analysis revealed a karyoiype of 47, XX,t(3,11)(q13,p15),+21.Chromosome painting further confirmed this translocation between chromosomes 3 and 11.Both inter— phase—and metaphase—FISH demonstrated that NUP98 gene was involved in this chromosomal rearrangment.Conclusion We have identified a new chromosomal rearrangement involving NUP98 gene at 11p15.This discovery made a foundation for further research on the new partner gene of NUP98 and its function in leukemogenesis.

OBJECTIVE:To explore the clinical and experimental features of acute leukemia (AL) with trisomy 4.METHODS:A retrospective analysis on the clinical and laboratory data of 21 cases of AL with trisomy 4 was performed. Chromosomes were prepared using direct method and/or short-term (24 h) cultures of bone marrow cells. Karyotypic analysis was carried out by using R-banding technique. Thirteen cases were studied by interphase fluorescence in situ hybridization (FISH) by using a chromosome 4-specific alpha -satellite DNA probe labeled by spectrum Green to ascertain the presence of a clone with trisomy 4. Five cases with t (8; 21) revealed by karyotypic analysis were detected by dual-color FISH using t (8; 21) translocation probe to confirm the AML1/ETO rearrangement.RESULTS:All the patients with AL and trisomy 4 were with de novo AL except two cases with secondary AL. M2 was the most frequent Franch-American-British(FAB) subtype in this series (9/21 cases). The initial leukocyte count more than 10x 10(9)/L was seen in 16 cases. An enlargement of liver, spleen and/or lymph nodes in varying degrees was found in 15 cases. Among 15 cases received immunophenotypic analysis, 11 cases showed CD34 positivity and 6 cases co-expressed myeloid and lymphocyte antigens. Karyotypic analysis disclosed clonal trisomy 4 in 18 cases and one cell with +4 in 3 cases. Isolated trisomy 4 was found in 7 cases, while 14 cases had other abnormalities besides trisomy 4 among which t (8; 21) was found in 8 cases. Dual-color FISH confirmed that all 13 cases including 3 cases having one cell with +4 on karyotypic analysis had clonal trisomy 4. Dual-color FISH confirmed that all 5 cases with t (8; 21) had AML1/ETO rearrangement.CONCLUSION:AL patients with trisomy 4 have unique clinical and experimental features and a poor prognosis.

Objective To clarify the characterization of a chromosomal translocation involveing NUP98 at 11p15 in hybrid acute leukemia.Methods Chromosome preparation was made using direct method or short-term culture of bone marrow cells.Karyotypic analysis was carried out by R-banding technique.Chromosome painting was performed using whole chromosome painting(WCP) for chromosomes 3 and 11.Interphase and metaphase fluorescence in situ hybridization(FISH) assays were performed using a BAC RP11-120E20(AC060812) probe,which covered almost entire NUP98 gene at 11p15.Results R-banded analysis revealed a karyotype of 47,XX,t(3,11)(q13,p15),+21.Chromosome painting further confirmed this translocation between chromosomes 3 and 11.Both interphase-and metaphase-FISH demonstrated that NUP98 gene was involved in this chromosomal rearrangment. Conclusion We have identified a new chromosomal rearrangement involving NUP98 gene at 11p15.This discovery made a foundation for further research on the new partner gene of NUP98 and its function in leukemogenesis.

Objective To clarify the characterization of a chromosomal translocation involveing NUP98 at 11p15 in hybrid acute leukemia.Methods Chromosome preparation was made using direct method or short-term culture of bone marrow cells.Karyotypic analysis was carried out by R-banding technique.Chromosome painting was performed using whole chromosome painting(WCP) for chromosomes 3 and 11.Interphase and metaphase fluorescence in situ hybridization(FISH) assays were performed using a BAC RP11-120E20(AC060812) probe,which covered almost entire NUP98 gene at 11p15.Results R-banded analysis revealed a karyotype of 47,XX,t(3,11)(q13,p15),+21.Chromosome painting further confirmed this translocation between chromosomes 3 and 11.Both interphase-and metaphase-FISH demonstrated that NUP98 gene was involved in this chromosomal rearrangment. Conclusion We have identified a new chromosomal rearrangement involving NUP98 gene at 11p15.This discovery made a foundation for further research on the new partner gene of NUP98 and its function in leukemogenesis.

NUP98是相对分子质量为98×103的核孔素蛋白,主要参与核内、外RNA和蛋白质的转运.野生型NUP98本身无致癌能力,但与多个伙伴基因形成融合基因后可导致恶性血液病的发生.本文对恶性血液病中累及NUP98的染色体异常的分子学研究进展作一综述.

The NUP98 gene has been reported to be fused with at least 17 partner genes in leukemia with 11p15 translocation. An adult patient with de novo acute myeloid/T lymphocytic leukemia harboring t(3;11)(q29q13;p15) has been investigated to characterize the genes involved in that translocation. Through molecular cytogenetic analysis, we identified a fusion transcript between NUP98 gene and a novel partner gene named as NUP98 related gene (NRG) at 3q29. Further molecular analysis showed that exon 13 of NUP98 was fused in-frame to exon 10 of NRG. Moreover, the segment from 3q13 to 3q29 translocated at 11p15 had been inverted and accompanied by the deletion of the distal portion of breakpoint at chromosome 3q29. Interestingly, the NUP98-NRG protein showed nuclear and cytoplasmic distribution, a pattern different from that of wild type NUP98 or NRG. When assayed in a GAL 4 reporter system, the fusion gene showed an aberrant trans-regulatory activity. Transfection in HL-60 cells demonstrated that NUP98-NRG could promote cell proliferation, survival and arrest differentiation. Therefore, NUP98-NRG may exert transforming effects by interfering with the cellular mechanism of transcriptional regulation. Our data provide thus new evidence that NUP98-related molecular abnormality is a recurrent genetic event in leukemogenesis.

OBJECTIVE:To investigate the laboratory and clinical features of 7 cases of acute lymphoblastic leukemia (ALL) with dic(7;9) (pll;pll).METHODS:Cytogenetic examination of bone marrow cells was performed by direct method or short-term culture method. R banding technique was used for karyotype analysis. bcr/abl fusion gene was detected by interphase FISH using dual-color bcr/abl probe in 6 cases. FISH using chromosome 7-specific alpha-satellite DNA probe and chromosome 9-specific alpha-satellite DNA probe and chromosome painting using whole chromosome 7 and 9 paints probes were performed respectively.RESULTS:Seven (0.88%) of 800 ALL patients were found to have dic(7;9) abnormality. Among them, dic(7;9) was the sole abnormality in 2 cases, t(9;22), other additional aberrations besides dic(7;9) in 4 cases and dic (7;9) with other abnormalities but no t(9;22) in one case. Hyperleukocytosis (> 100 x 10(9)/L) was found in 4 cases with dic(7;9) and t(9;22), and patients without t(9;22) had WBC < 100 x 10(9)/L. Enlargement of liver, spleen and/or lymph nodes were found in 6 cases. Immunophenotyping showed that 5/6 cases of dic (7;9) ALL were of B lineage. Dual-color FISH detected bcr/abl rearrangement in 3/6 cases and confirmed that the centromere of the derivative chromosome was originated from both chromosomes 7 and 9. A reciprocal translocation between chromosomes 7 and 9 was proved by chromosome painting.CONCLUSION:dic(7;9) was a rare, but recurrent chromosome abnormality in ALL and had some clinical and laboratory features.

目的分析具有dic(7;9)的急性淋巴细胞白血病(ALL)的临床和实验室特点.方法采用骨髓细胞直接法或短期培养法制备染色体,用R显带技术进行核型分析;采用bcr/abl双色探针和问期荧光原位杂交(FISH)技术对其中6例ALL患者进行bcr/abl重排检测;分别应用绿色荧光标记的7号和红色荧光标记的9号着丝粒探针,以及由生物素及地高辛分别标记的7号和9号全染色体涂抹探针,对6例ALL患者进行FISH和染色体涂抹分析.结果dic(7;9)ALL占同期ALL的0.88%;7例患者中2例为单纯dic(7;9),4例同时伴有t(9;22)和其他染色体异常(初诊白细胞计数＞100×109/L),1例伴有其他染色体异常而无t(9;22)(初诊白细胞计数＜100×109/L);6例患者有不同程度的肝、脾和淋巴结肿大;进行免疫表型分析的6例患者中5例为B系ALL;双色FISH检则结果示6例患者中3例为bcr/abl重排阳性,且6例患者衍生染色体着丝粒均为7号和9号着丝粒融合而成,染色体涂抹分析也证实7号和9号染色体之间发生了易位.结论dic(7;9)是ALL中一种较少见的再现性异常,并有独特的临床和实验室特点.

Objective To determine the role of peripheral α 2 receptors in carotid sinus baroreflex (CBR) resetting induced by intracerebroventricular (i.c.v.) injection of histamine (HA).Methods The left and right carotid sinus regions were isolated from the systemic circulation in 31 male Sprague-Dawley rats anesthetized with pentobarbital sodium. The intracarotid sinus pressure (ISP) was altered in a stepwise manner in vivo. ISP-mean arterial pressure (MAP) relationship curve and its characteristic parameters were constructed by fitting to the logistic function with five parameters. We observed the changes in CBR performance induced by i.c.v. HA and the effects of pretreatment with α 2 receptor selective antagonist, yohimbine (YOH), into the peripheral vein on the responses of CBR to HA.Results I.c.v. HA (60μmol·L -1 in 5μL) significantly shifted the ISP-MAP relationship curve upwards and obviously decreased the value of the reflex parameters such as MAP changing range and maximum gain (P0.05), but increased the threshold pressure (P0.05). The peripheral pretreatment of YOH (2.5μmol·L -1, in 15 μL·100 g -1 weight) could obviously intensify the above-mentioned changes of CBR induced by HA. Only peripheral intravenous injection with the same dose of YOH did not change CBR performance significantly (P0.05).Conclusion HA cerebroventricular administration could result in the rapid resetting of CBR, the decrease of reflex sensitivity and the responses of CBR to HA might be diminished by peripheral α 2 receptor activity.

The work is to observe whether human blood samples irradiated in vitro to 10cGy by X-rays could be an incentive to normal blood samples and blood cells injured by high dose radiation (1000cGy). The irradiated blood samples were cultured with blood samples collected from the same person, which were irradiated to 1000cGy or without irradiation. The cpm of H-TdR incorporation in different groups was measured after 72-hour culturing. 3 Experiment results suggested that the blood irradiated to 10cGy could stimulate the blood cells irradiated to 1000kGy to proliferate. There is something in the plasma resulting in the stimulating effect.

Objective To observe the changes of plasma ACTH level in rats induced by cold stress after i.c.v 6- OHDA Methods The animals we used in this study are adult, male Wistar rats.divided into 5 groups(n=6):control,cold stresa,i.c.v 6-OHDA,i.c.v 6-OHDA+cold stress,i .c.v saline+cold stress.Plasma ACTH was measured by radioimmunoassay.Re sults Plasma ACTH level was increased significantly by cold stress, and this changes could be blocked after 6-OHDA i.c.v.administration.Co nclusion Cold stress may activate HPA axis via catecholaminergic system .

目的观察奥克丁(SOD)对佐剂性关节炎大鼠的足爪肿胀度、全身病变的影响。方法大鼠踝关节皮内注射佐剂造成佐剂性关节炎大鼠模型，分原发性病变预防给药和继发性病变预防、治疗给药3种方案。结果不论原发性病变还是继发性病变，SOD均能剂量依赖地抑制佐剂性关节炎大鼠足爪肿胀度；在继发性病变方面，SOD还能减轻继发的全身病变情况。结论 SOD对于佐剂性关节炎大鼠具有预防性和治疗性抗炎作用。