An asteroid breakup 160 Myr ago as the probable source of the K/T impactor

The terrestrial and lunar cratering rate is often assumed to have been nearly constant over the past 3 Gyr. Different lines of evidence, however, suggest that the impact flux from kilometre-sized bodies increased by at least a factor of two over the long-term average during the past approximately 100 Myr. Here we argue that this apparent surge was triggered by the catastrophic disruption of the parent body of the asteroid Baptistina, which we infer was a approximately 170-km-diameter body (carbonaceous-chondrite-like) that broke up 160(-20)+30Myr ago in the inner main asteroid belt. Fragments produced by the collision were slowly delivered by dynamical processes to orbits where they could strike the terrestrial planets. We find that this asteroid shower is the most likely source (>90 per cent probability) of the Chicxulub impactor that produced the Cretaceous/Tertiary (K/T) mass extinction event 65 Myr ago.     

Optimization of Time-Varying Parking Charges and Parking Supply in Networks with Multiple User Classes and Multiple Parking Facilities

The optimization of parking charges and parking supply over the time of a day is an important problem in the design of transportation networks. This paper presents a bilevel model to determine the opti-mal time-varying parking charges and parking supply in road networks with multiple user classes and different types of parking facilities. The upper level of the model aims to maximize the network net benefit in response to the parking charges and parking supply, whereas the lower level is a time-dependent network equilibrium problem with elastic demand. A descent-gradient-based solution algorithm is adapted to solve the model. The numerical results show that the implementation of time-varying parking charges and parking supply is useful to effectively cater to the time-varying demand with different parking needs. The model provides a powerful tool for strategically designing parking locations and evaluating various parking policies.     

Stream denitrification across biomes and its response to anthropogenic nitrate loading

Anthropogenic addition of bioavailable nitrogen to the biosphere is increasing and terrestrial ecosystems are becoming increasingly nitrogen-saturated, causing more bioavailable nitrogen to enter groundwater and surface waters. Large-scale nitrogen budgets show that an average of about 20-25 per cent of the nitrogen added to the biosphere is exported from rivers to the ocean or inland basins, indicating that substantial sinks for nitrogen must exist in the landscape. Streams and rivers may themselves be important sinks for bioavailable nitrogen owing to their hydrological connections with terrestrial systems, high rates of biological activity, and streambed sediment environments that favour microbial denitrification. Here we present data from nitrogen stable isotope tracer experiments across 72 streams and 8 regions representing several biomes. We show that total biotic uptake and denitrification of nitrate increase with stream nitrate concentration, but that the efficiency of biotic uptake and denitrification declines as concentration increases, reducing the proportion of in-stream nitrate that is removed from transport. Our data suggest that the total uptake of nitrate is related to ecosystem photosynthesis and that denitrification is related to ecosystem respiration. In addition, we use a stream network model to demonstrate that excess nitrate in streams elicits a disproportionate increase in the fraction of nitrate that is exported to receiving waters and reduces the relative role of small versus large streams as nitrate sinks.     

Mapping and sequencing of structural variation from eight human genomes

Genetic variation among individual humans occurs on many different scales, ranging from gross alterations in the human karyotype to single nucleotide changes. Here we explore variation on an intermediate scale--particularly insertions, deletions and inversions affecting from a few thousand to a few million base pairs. We employed a clone-based method to interrogate this intermediate structural variation in eight individuals of diverse geographic ancestry. Our analysis provides a comprehensive overview of the normal pattern of structural variation present in these genomes, refining the location of 1,695 structural variants. We find that 50% were seen in more than one individual and that nearly half lay outside regions of the genome previously described as structurally variant. We discover 525 new insertion sequences that are not present in the human reference genome and show that many of these are variable in copy number between individuals. Complete sequencing of 261 structural variants reveals considerable locus complexity and provides insights into the different mutational processes that have shaped the human genome. These data provide the first high-resolution sequence map of human structural variation--a standard for genotyping platforms and a prelude to future individual genome sequencing projects.     

Evasion of the p53 tumour surveillance network by tumour-derived MYC mutants

The c-Myc oncoprotein promotes proliferation and apoptosis, such that mutations that disable apoptotic programmes often cooperate with MYC during tumorigenesis. Here we report that two common mutant MYC alleles derived from human Burkitt's lymphoma uncouple proliferation from apoptosis and, as a result, are more effective than wild-type MYC at promoting B cell lymphomagenesis in mice. Mutant MYC proteins retain their ability to stimulate proliferation and activate p53, but are defective at promoting apoptosis due to a failure to induce the BH3-only protein Bim (a member of the B cell lymphoma 2 (Bcl2) family) and effectively inhibit Bcl2. Disruption of apoptosis through enforced expression of Bcl2, or loss of either Bim or p53 function, enables wild-type MYC to produce lymphomas as efficiently as mutant MYC. These data show how parallel apoptotic pathways act together to suppress MYC-induced transformation, and how mutant MYC proteins, by selectively disabling a p53-independent pathway, enable tumour cells to evade p53 action during lymphomagenesis.