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Ecosystem function (particularly CO2 fluxes and the subsequent atmospheric transport), synoptic‐scale weather (e.g., midlatitude cyclones), and interactions between ecosystems and the atmosphere can be investigated using a weather‐biosphere‐online‐coupled model. The Vegetation Photosynthesis and Respiration Model (VPRM) was coupled with the Weather Research and Forecasting (WRF) model in 2008 to simulate “weather‐aware” biospheric CO2 fluxes and subsequent transport and dispersion. The ability of the coupled WRF‐VPRM modeling system to simulate the CO2 structures within midlatitude cyclones, however, has not been evaluated due to the lack of data within these weather systems. In this study, VPRM parameters previously calibrated off‐line using eddy covariance tower data over North America are implemented into WRF‐VPRM. The updated WRF‐VPRM is then used to simulate spatiotemporal variations of CO2 over the contiguous United States at a horizontal grid spacing of 12 km for 2016 using an optimized downscaling configuration. The downscaled fields are evaluated using remotely sensed data from the Orbiting Carbon Observatory‐2, Total Carbon Column Observing Network, and in situ aircraft measurements from Atmospheric Carbon and Transport‐America missions. Evaluations show that WRF‐VPRM captures the monthly variation of column‐averaged CO2 concentrations (XCO2) and episodic variations associated with frontal passages. The downscaling also successfully captures the horizontal CO2 gradients across fronts and vertical CO2 contrast between the boundary layer and the free troposphere. WRF‐VPRM modeling results indicate that from May to September, biogenic fluxes dominate variability in XCO2 over most of the contiguous United States, except over a few metropolitan areas such as Los Angeles.

BackgroundThe presence of loss-of-heterozygosity (LOH) mutations in cancer cell genomes is commonly encountered. Moreover, the occurrences of LOHs in tumor suppressor genes play important roles in oncogenesis. However, because the causative mechanisms underlying LOH mutations in cancer cells yet remain to be elucidated, enquiry into the nature of these mechanisms based on a comprehensive examination of the characteristics of LOHs in multiple types of cancers has become a necessity.MethodsWe performed next-generation sequencing on inter-Alu sequences of five different types of solid tumors and acute myeloid leukemias, employing the AluScan platform which entailed amplification of such sequences using multiple PCR primers based on the consensus sequences of Alu elements; as well as the whole genome sequences of a lung-to-liver metastatic cancer and a primary liver cancer. Paired-end sequencing reads were aligned to the reference human genome to identify major and minor alleles so that the partition of LOH products between homozygous-major vs. homozygous-minor alleles could be determined at single-base resolution. Strict filtering conditions were employed to avoid false positives. Measurements of LOH occurrences in copy number variation (CNV)-neutral regions were obtained through removal of CNV-associated LOHs.ResultsWe found: (a) average occurrence of copy-neutral LOHs amounting to 6.9 % of heterologous loci in the various cancers; (b) the mainly interstitial nature of the LOHs; and (c) preference for formation of homozygous-major over homozygous-minor, and transitional over transversional, LOHs.ConclusionsThe characteristics of the cancer LOHs, observed in both AluScan and whole genome sequencings, point to the formation of LOHs through repair of double-strand breaks by interhomolog recombination, or gene conversion, as the consequence of a defective DNA-damage response, leading to a unified mechanism for generating the mutations required for oncogenesis as well as the progression of cancer cells.Electronic supplementary materialThe online version of this article (doi:10.1186/s12920-015-0104-2) contains supplementary material, which is available to authorized users.

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