阿尔金断裂带构造活动的40Ar/39Ar年龄证据

通过对阿尔金山阿克塞和当金山地区出露的元古代、早古生代变质岩样品中云母、角闪石和钾长石单矿物的40Ar/39Ar同位素测年研究, 获得了4组年龄数据, 其中远离阿尔金中部剪切带的样品给出461～445.2和414.9～342.8 Ma的坪年龄, 这两组年龄分别代表了被阿尔金断裂错移的岩块在晚奥陶世～早志留世和泥盆纪发生构造热事件的记录, 应同南北祁连洋槽的闭合相关.在北部构造带中受变形作用改造的花岗片麻岩样品给出178.4～137.5 Ma的坪年龄, 可以解释为阿尔金断裂带在中晚侏罗世～早白垩世发生构造活动的年龄记录, 这一构造热事件与拉萨地块向北拼贴碰撞有关.在阿尔金中部剪切带中的样品给出了36.4和26.3 Ma的两个坪年龄, 说明阿尔金中部剪切带在始新世末发生明显的走滑活动, 并且伴有强烈的绿片岩相变质作用, 这一事件在青藏高原北部的大部分地区都有所表现, 与印度-欧亚板块碰撞后的陆内俯冲有关.该研究表明阿尔金断裂带在印度-欧亚板块汇聚的大陆构造背景下具有多次脉冲式活动的特征.     

The role of thrombospondin-1 in apoptosis

The thrombospondins are a family of extracellular proteins that participate in cell-to-cell and cell-to-matrix communication. They regulate cellular phenotype during tissue genesis and repair. Five family members, each representing a separate gene product, probably exist in most vertebrate species. Like most extracellular proteins, the thrombospondins are composed of several structural domains that are responsible for the numerous biological functions that have been described for this protein family. Considerable progress has been made towards understanding the function of thrombospondins. The role of thrombospondin in the process of apoptosis or programmed cell death has recently come into focus. In this review we will concentrate on the role of thrombospondin-1 in the broad field of apoptotis research. Received 5 December 2001; received after revision 28 March 2002; accepted 28 March 2002     

Travel at low energetic cost by swimming and wave-riding bottlenose dolphins.

Over the past 50 years there has been much speculation about the energetic cost of swimming and wave-riding by dolphins. When aligned properly in front of the bow of moving ships in the stern wake of small boats, on wind waves, and even in the wake of larger cetaceans, the animals appear to move effortlessly through the water without the benefit of propulsive strokes by the flukes. Theoretically, body streamlining as well as other anatomical and behavioural adaptations contribute to low transport costs in these animals. The economy of movement permitted by wave-riding has been perceived as an energetic advantage for the swimming dolphin, but has been hard to prove in the absence of physiological data for exercising cetaceans. Here we determine the aerobic and anaerobic costs of swimming and wave-riding in bottlenose dolphins and find that the minimum cost of transport for swimming dolphins is 1.29 +/- 0.05 J kg-1 m-1 at a cruising speed of 2.1 m s-1. Aerobic costs are nearly twice as high for swimming seals and sea lions, and 8-12 times higher for human swimmers. Wave-riding by dolphins provides additional benefits in terms of speed. The results indicate that behavioural, physiological and morphological factors make swimming an economical form of high-speed travel for dolphins.     

~(40)Ar/~(39)Ar age evidence for Altyn fault tectonic activities in western China

As the northern boundary of the Tibetan Plateau theAltyn fault is a huge NEE strike-slip fault belt in the inner Asian continent. Its formation and evolution are closelyrelated to the uplift of the whole plateau and the mass es-cape to the east. In recent years the Altyn fault has be-come a hot point of geological study in the Tibetan Pla-teau. The formation age of the Altyn fault was argued for a long time. Some researchers emphasized that the Altyn fault had commenced since early Paleo…     

The biology of cell locomotion within three-dimensional extracellular matrix

Cell migration in three-dimensional (3-D) extracellular matrix (ECM) is not a uniform event but rather comprises a modular spectrum of interdependent biophysical and biochemical cell functions. Haptokinetic cell migration across two-dimensional (2-D) surfaces consists of at least three processes: (i) the protrusion of the leading edge for adhesive cell-substratum interactions is followed by (ii) contraction of the cell body and (iii) detachment of the trailing edge. In cells of flattened morphology migrating slowly across 2-D substrate, contact-dependent clustering of adhesion receptors including integrins results in focal contact and stress fiber formation. While haptokinetic migration is predominantly a function of adhesion and deadhesion events lacking spatial barriers towards the advancing cell body, the biophysics of the tissues require a set of cellular strategies to overcome matrix resistance. Matrix barriers force the cells to adapt their morphology and change shape and/or enzymatically degrade ECM components, either by contact-dependent proteolysis or by protease secretion. In 3-D ECM, in contrast to 2-D substrate, the cell shape is mostly bipolar and the cytoskeletal organization is less stringent, frequently lacking discrete focal contacts and stress fibers. Morphologically large spindle-shaped cells (i.e., fibroblasts, endothelial cells, and many tumor cells) of high integrin expression and strong cytoskeletal contractility utilize integrin-dependent migration strategies that are coupled to the capacity to reorganize ECM. In contrast, a more dynamic ameboid migration type employed by smaller cells expressing low levels of integrins (i.e., T lymphocytes, dendritic cells, some tumor cells) is characterized by largely integrin-independent interaction strategies and flexible morphological adaptation to preformed fiber strands, without structurally changing matrix architecture. In tumor invasion and angiogenesis, migration mechanisms further comprise the migration of entire cell clusters or strands maintaining stringent cell-cell adhesion and communication while migrating. Lastly, cellular interactions, enzyme and cytokine secretion, and tissue remodeling provided by reactive stroma cells (i.e. fibroblasts and macrophages) contribute to cell migration. In conclusion, depending on the cellular composition and tissue context of migration, diverse cellular and molecular migration strategies can be developed by different cell types.     

FAN1 mutations cause karyomegalic interstitial nephritis, linking chronic kidney failure to defective DNA damage repair

Chronic kidney disease (CKD) represents a major health burden. Its central feature of renal fibrosis is not well understood. By exome sequencing, we identified mutations in FAN1 as a cause of karyomegalic interstitial nephritis (KIN), a disorder that serves as a model for renal fibrosis. Renal histology in KIN is indistinguishable from that of nephronophthisis, except for the presence of karyomegaly. The FAN1 protein has nuclease activity and acts in DNA interstrand cross-link (ICL) repair within the Fanconi anemia DNA damage response (DDR) pathway. We show that cells from individuals with FAN1 mutations have sensitivity to the ICL-inducing agent mitomycin C but do not exhibit chromosome breakage or cell cycle arrest after diepoxybutane treatment, unlike cells from individuals with Fanconi anemia. We complemented ICL sensitivity with wild-type FAN1 but not with cDNA having mutations found in individuals with KIN. Depletion of fan1 in zebrafish caused increased DDR, apoptosis and kidney cysts. Our findings implicate susceptibility to environmental genotoxins and inadequate DNA repair as novel mechanisms contributing to renal fibrosis and CKD.