A critical phenomenon is an intrinsic feature of traffic dynamics, during which transition between isolated local flows and global flows occurs. However, very little attention has been given to the question of how the local flows in the roads are organized collectively into a global city flow. Here we characterize this organization process of traffic as "traffic percolation," where the giant cluster of local flows disintegrates when the second largest cluster reaches its maximum. We find in real-time data of city road traffic that global traffic is dynamically composed of clusters of local flows, which are connected by bottleneck links. This organization evolves during a day with different bottleneck links appearing in different hours, but similar in the same hours in different days. A small improvement of critical bottleneck roads is found to benefit significantly the global traffic, providing a method to improve city traffic with low cost. Our results may provide insights on the relation between traffic dynamics and percolation, which can be useful for efficient transportation, epidemic control, and emergency evacuation.emergence | percolation | traffic T raffic, as a large-scale and complex dynamical system, has attracted much attention, especially on its dynamical transition between free flow and congestion (1-3). The dynamics of traffic have been studied using many types of models (4-11), ranging from models in macroscopic scales based on the kinetic gas theory or fluid dynamics to approaches in microscopic scales with equations for each car in the network. However, there is still a gap between the microscopic behavior of individual vehicles and the emergence of macroscopic city traffic. Indeed, a fundamental question has rarely been addressed: how the local flows in roads interact and organize collectively into global flow throughout the city network. This knowledge is not only necessary to bridge the gap between local traffic and global traffic, but also essential for developing efficient traffic control strategies.There are mainly two obstacles in studying how the collective network dynamics of real traffic emerge from local flows. The first obstacle is the lack of valid methods to quantify the dynamical organization of traffic in the road network. The second is the lack of data on traffic dynamics in a network scale. To overcome the first obstacle, we develop here a quantitative framework based on percolation theory, which combines evolving traffic dynamics with network structure. In this framework, instead of the commonly used structural topology, only roads in the network with speed larger than a variable threshold are considered functionally connected. In this way, we can characterize and understand the formation process of traffic dynamics.To overcome the second obstacle of missing data on a network scale and understand the organization processes of real traffic in a network, we collected and analyzed velocities of more than 1,000 roads with 5-min segments records measured in a road network in a cen...

The Brn-3 subfamily of POU-domain transcription factor genes consists of three highly homologous members-Brn-3a, Brn-3b, and Brn-3c-that are expressed in sensory neurons and in a small number of brainstem nuclei. This paper describes the role of Brn-3c in auditory and vestibular system development. In the inner ear, the Brn-3c protein is found only in auditory and vestibular hair cells, and the Brn-3a and Brn-3b proteins are found only in subsets of spiral and vestibular ganglion neurons. Mice carrying a targeted deletion of the Brn-3c gene are deaf and have impaired balance. These defects ref lect a complete loss of auditory and vestibular hair cells during the late embryonic and early postnatal period and a secondary loss of spiral and vestibular ganglion neurons. Together with earlier work demonstrating a loss of trigeminal ganglion neurons and retinal ganglion cells in mice carrying targeted disruptions in the Brn-3a and Brn-3b genes, respectively, the Brn-3c phenotype reported here demonstrates that each of the Brn-3 genes plays distinctive roles in the somatosensory, visual, and auditory͞ vestibular systems.A number of transcription factors have been implicated in decisions related to neuronal vs. nonneuronal cell fate, regional specification in the nervous system, or determination of the terminally differentiated phenotype. For example, bHLH factors such as neuroD and the achaete-scute family control neural vs. ectodermal cell fates (1, 2), Hox genes control regional specification along the neuraxis (3), and several POU-domain genes act at late stages to control the survival and final differentiated phenotype of particular neuronal subtypes (4). The POU-domain family was intially defined by the mammalian pituitary-specific transcription factor Pit-1͞ GHF-1, the octamer binding proteins Oct-1 and Oct-2, and the Caenorhabditis elegans gene Unc-86 (5). Genetic studies in mice and humans indicate that many POU-domain genes function in the terminal stages of central nervous system development. SCIP͞Tst-1͞Oct-6 controls the differentiation of Schwann cells (6-8), Pit-1͞GHF-1 is required for the normal development of the anterior pituitary (9), Brn-4͞RHS2͞ POU3F4 is required for the normal development of the middle ear (10), and Brn-2 is required for the specification of subsets of neurons in the hypothalamus (11,12).The class IV POU-domain group is defined by the Unc-86 gene (13), the Drosophila I-POU gene (14,15), and the three vertebrate Brn-3 genes (16-20). The Unc-86 protein is found exclusively within a subset of neurons and neuroblasts, and Unc-86 loss-of-function mutations affect some of these cells by causing a daughter cell to assume the fate of its mother or by altering cell phenotypes postmitotically (21-23). In mammals, the three highly homologous class IV POU-domain genes, Brn-3a, Brn-3b, and Brn-3c (also referred to as Brn-3.0, Brn-3.2, and Brn-3.1, respectively), are expressed in distinct but overlapping patterns in the developing and adult brainstem, retina, and dorsal root and trigemina...

Treatment of patients sustaining a complete spinal cord injury remains an unsolved clinical problem because of the lack of spontaneous regeneration of injured central axons. A 38-year-old man sustained traumatic transection of the thoracic spinal cord at upper vertebral level Th9. At 21 months after injury, the patient presented symptoms of a clinically complete spinal cord injury (American Spinal Injury Association class A-ASIA A). One of the patient's olfactory bulbs was removed and used to derive a culture containing olfactory ensheathing cells and olfactory nerve fibroblasts. Following resection of the glial scar, the cultured cells were transplanted into the spinal cord stumps above and below the injury and the 8-mm gap bridged by four strips of autologous sural nerve. The patient underwent an intense pre- and postoperative neurorehabilitation program. No adverse effects were seen at 19 months postoperatively, and unexpectedly, the removal of the olfactory bulb did not lead to persistent unilateral anosmia. The patient improved from ASIA A to ASIA C. There was improved trunk stability, partial recovery of the voluntary movements of the lower extremities, and an increase of the muscle mass in the left thigh, as well as partial recovery of superficial and deep sensation. There was also some indication of improved visceral sensation and improved vascular autoregulation in the left lower limb. The pattern of recovery suggests functional regeneration of both efferent and afferent long-distance fibers. Imaging confirmed that the grafts had bridged the left side of the spinal cord, where the majority of the nerve grafts were implanted, and neurophysiological examinations confirmed the restitution of the integrity of the corticospinal tracts and the voluntary character of recorded muscle contractions. To our knowledge, this is the first clinical indication of the beneficial effects of transplanted autologous bulbar cells.

Quakingviable (qk(v)) is a well known dysmyelination mutation. Recently, the genetic lesion of qk(v) has been defined as a deletion 5' to the qkI gene, which results in the severe reduction of the qkI-encoded QKI RNA-binding proteins in myelin-producing cells. However, no comprehensive model has been proposed regarding how the lack of QKI leads to dysmyelination. We hypothesized that QKI binds to myelin protein mRNAs, and the lack of QKI causes posttranscriptional misregulation, which in turn leads to the loss of the corresponding myelin proteins. To test this hypothesis, we developed an RNase protection assay to directly measure the mRNA isoforms encoding the myelin basic proteins (MBPs) in the brain. Our result suggested that isoform-preferential destabilization of MBP mRNAs in the cytoplasm was responsible for the reduced MBPs in the qk(v)/qk(v) brain during early myelination. In addition, we detected markedly reduced MBP mRNAs in the qk(v)/qk(v) myelin fraction with concomitant accumulation of MBP mRNAs associated with membrane-free polyribosomes. Presumably, the impaired localization of MBP mRNAs to the myelin membrane may cause insufficient incorporation of the newly synthesized MBPs into the myelin sheath. Finally, we observed interactions between QKI and MBP mRNAs, and removing MBP 3'UTR significantly reduced QKI-binding. Taken together, these observations suggest that misregulation at multiple posttranscriptional steps is responsible for the severe reduction of MBPs in qk(v) dysmyelination, presumably because of the lack of interactions between MBP mRNAs and the QKI RNA-binding proteins.

The dimension of a system is one of the most fundamental quantities to characterize its structure and basic physical properties. Diffusion 1 and vibrational excitations 2 , for example, as well as the universal features of a system near a critical point depend crucially on its dimension 3,4 . However, in the theory of complex networks the concept of dimension has been rarely discussed. Here we study models for spatially embedded networks and show how their dimension can be determined. Our results indicate that networks characterized by a broad distribution of link lengths have a dimension higher than that of the embedding space. We illustrate our findings using the global airline network and the Internet and argue that although these networks are embedded in two-dimensional space they should be regarded as systems with dimension close to 3 and 4.5, respectively. We show that the network dimension is a key concept to understand not only network topology, but also dynamical processes on networks, such as diffusion and critical phenomena including percolation.Networks consist of entities (nodes) and their connections (links) 5 . Usually, networks are embedded either in two-or in threedimensional space. For example, airline and Internet networks, as well as friendship networks where the nodes are the residences of friends, are embedded in the two-dimensional surface of the earth, whereas the neuronal network in the brain is embedded in a complex three-dimensional structure. If in a d-dimensional lattice, the links connect only neighbouring nodes (in space), then the dimension of the network is trivially identical to the dimension of the embedding space. In most cases, however, links are not short ranged, their length distribution is broad, connecting also distant nodes. The question we pose here is: Is there a finite dimension that characterizes such a spatially embedded network and how can we determine it? The knowledge of the dimension 6,7 is not only important for a structural characterization of the network, but is also crucial for understanding the function of the network, as the dimension governs the dynamical processes in the network.In network theory, the dimension of a network has been rarely considered. Research 8-13 has focused on two types of networks where the links between the nodes are either short range, connecting only nearby nodes (like a lattice), or long range, connecting any two nodes with the same probability. In the short range case, the dimension d of the network is identical to the dimension of the embedding space, whereas in the long range case the embedding space is irrelevant and the network can be regarded as having an infinite dimension. As a consequence, the mean distance between two nodes scales with the number of nodes N as N 1/d in the short range case, and as log N (ref. 14) or log log N (ref. Many real networks, however, do not fall into these categories, and the lengths of their links are characterized by a broad power law distribution. For example, in a mobile phone communicati...

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Increased intraocular pressure (IOP) damages the retinal ganglion cell axons as they pass through the optic nerve head (ONH). The massive connective tissue structure of the human lamina cribrosa is generally assumed to be the pressure transducer responsible for the damage. The rat, however, with no lamina cribrosa, suffers the same glaucomatous response to raised IOP. Here, we show that the astrocytes of the rat ONH are "fortified" by extraordinarily dense cytoskeletal filaments that would make them ideal transducers of distorting mechanical forces. The ONH astrocytes are arranged as a fan-like radial array, firmly attached ventrally to the sheath of the ONH by thick basal processes, but dividing dorsally into progressively more slender processes with only delicate attachments to the sheath. At 1 week after raising the IOP by an injection of magnetic microspheres into the anterior eye chamber, the fine dorsal processes of the ONH astrocytes are torn away from the surrounding sheath. There is no indication of distortion or compression of the axons. Subsequently, despite return of the IOP toward normal levels, the damage to the ONH progresses ventrally through the astrocytic cell bodies, resulting in complete loss of the fortified astrocytes and of the majority of the axons by around 4 weeks. We propose that the dorsal attachments of the astrocytes are the site of initial damage in glaucoma, and that the damage to the axons is not mechanical, but is a consequence oflocalized loss of metabolic support from the astrocytes (Tsacopoulos and Magistretti (1996) J Neurosci 16:877-885).

Three-dimensional specimens of the volant fossil bird Gansus yumenensis from the Early Cretaceous Xiagou Formation of northwestern China demonstrate that this taxon possesses advanced anatomical features previously known only in Late Cretaceous and Cenozoic ornithuran birds. Phylogenetic analysis recovers Gansus within the Ornithurae, making it the oldest known member of the clade. The Xiagou Formation preserves the oldest known ornithuromorph-dominated avian assemblage. The anatomy of Gansus, like that of other non-neornithean (nonmodern) ornithuran birds, indicates specialization for an amphibious life-style, supporting the hypothesis that modern birds originated in aquatic or littoral niches.