Scale and scope of maritime cargoes through the Arctic Passages

This paper investigates the sources of goods being shipped through the Arctic passages, and trade generated in the Arctic, including oil and gas exploitation. Furthermore, it assesses the present situation for maritime cargo shipped from the Far East to Northwestern Europe and North America. Two main types of cargo are predicted to pass through the Arctic passages in the future. First, about 10 million t of liquefied natural gas will be delivered from Russia and the Nordic Arctic to the Far East by 2030. Second, there will be two-way trade flow of containerized cargo from the Far East to Europe and the United States through the Northeast, Central and Northwest Passages. This will relieve pressure on present routes from the Far East to Northwestern Europe and North America. If Arctic navigation is technically possible in all seasons and shipping costs fall to those of ordinary ships, then assuming an equal share of shipping volume with the traditional canal routes, the maximum container freight passing through the Arctic passages by 2030 will be approximately 17.43 million TEUs (Twenty-foot Equivalent Units) per year, which is 85% of the volume transported on traditional canal routes in 2011. We conclude that there will be large-scale gas transportation through the Northeast Passage in the near future, and transit shipping across the Arctic will focus more on container transportation. The differences in shipping costs between Arctic routes and traditional canal routes are also compared

Role of phosphatase of regenerating liver 1 (PRL1) in spermatogenesis

The PRL phosphatases are oncogenic when overexpressed but their in vivo biological function is less well understood. Previous gene deletion study revealed a role for PRL2 in spermatogenesis. We report here the first knockout mice lacking PRL1, the most related homolog of PRL2. We found that loss of PRL1 does not affect spermatogenesis and reproductive ability of male mice, likely due to functional compensation by the relatively higher expression of PRL2 in the testes. However, PRL1-/-/PRL2+/- male mice show testicular atrophy phenotype similar to PRL2-/- mice. More strikingly, deletion of one PRL1 allele in PRL2-/- male mice causes complete infertility. Mechanistically, the total level of PRL1 and PRL2 is negatively correlated with the PTEN protein level in the testis and PRL1+/-/PRL2-/- mice have the highest level of PTEN, leading to attenuated Akt activation and increased germ cell apoptosis, effectively halting spermatozoa production. These results provide the first evidence that in addition to PRL2, PRL1 is also required for spermatogenesis by downregulating PTEN and promoting Akt signaling. The ability of the PRLs to suppress PTEN expression underscores the biochemical basis for their oncogenic potential