Trade and Management: Exclusive Economic Zones and the Changing Japanese Surimi Market

The United States' increasing competitive advantage in international seafood trade in Alaska walleye pollock. Theragra chalcogramma, has contributed to higher prices for surimi-based goods and structural changes in seafood production and trade in Japan. The objectives of this analytical investigation include: 1) Evaluation of the role reversal of Japan and the United States in international seafood trade and 2) quantification of the impact of rising prices of frozen surimi on household consumption of surimi-based foods in Japan. This study documents Japan's regression from "seafood self-sufficiency" to increasing dependence on imported products and raw materials. In particular, Japan's growing dependence on American fishermen and seafood producers is described. Surimi production by the United States, and its emerging dominance over Japanese sources of supply, are especially significant. Results of the analysis suggest that Japanese consumer demand for surimi-based food stuffs correlates directly with "competitive" food prices, e.g., pork, chicken, and beef, and inversely with personal income. Also revealed is how rising household income and relative price shifts among competing animal protein sources in the Japanese diet have contributed to declining household consumption of surimi-based foods, specifically, and a shift away from seafoods in favor of beef, in general. The linkages between, for example. Japanese domestic seafood production and consumption, international trade in marine products, and resource management decisions in the U.S. EEZ present a picture of a changing global marketplace. Increasingly, actions in one arena will have perhaps profound implications in the others

Parent-perceived isolation and barriers to psychosocial support: A qualitative study to investigate how peer support might help parents of burn-injured children

Introduction: Burn injuries can be traumatic and distressing for the affected child and family, with a prolonged period of recovery. This research explores parents’ experiences of support following their child’s injury and their thoughts on peer support specifically.Methods: Thirteen semi-structured interviews were conducted with parents/caregivers, a mean of three years after their child’s injury, either face-to-face or remotely. Responses were analysed using thematic analysis.Results: Analysis produced four themes and 11 sub-themes. These described parents’ experiences of loss, change, isolation and access to psychosocial support. This paper focuses on themes of isolation and parents’ access to psychosocial support.Discussion: Findings indicate that parents access psychosocial support following their child’s injury and often find it helpful; however, there is a prevailing sense of isolation. Parents often seek information online and find that this is lacking. Many parents reported that peer support would be valuable to them, particularly the sharing of experiential knowledge.Conclusion: An online resource may be beneficial for parents, but further research is needed to confirm the exploratory data gained to date, ensuring that any resource developed would meet the identified needs of parents

Tissue of origin determines cancer-associated CpG island promoter hypermethylation patterns

ABSTRACT: BACKGROUND: Aberrant CpG island promoter DNA hypermethylation is frequently observed in cancer and is believed to contribute to tumor progression by silencing the expression of tumor suppressor genes. Previously, we observed that promoter hypermethylation in breast cancer reflects cell lineage rather than tumor progression and occurs at genes that are already repressed in a lineage-specific manner. To investigate the generality of our observation we analyzed the methylation profiles of 1,154 cancers from 7 different tissue types. RESULTS: We find that 1,009 genes are prone to hypermethylation in these 7 types of cancer. Nearly half of these genes varied in their susceptibility to hypermethylation between different cancer types. We show that the expression status of hypermethylation prone genes in the originator tissue determines their propensity to become hypermethylated in cancer; specifically, genes that are normally repressed in a tissue are prone to hypermethylation in cancers derived from that tissue. We also show that the promoter regions of hypermethylation-prone genes are depleted of repetitive elements and that DNA sequence around the same promoters is evolutionarily conserved. We propose that these two characteristics reflect tissue-specific gene promoter architecture regulating the expression of these hypermethylation prone genes in normal tissues. CONCLUSIONS: As aberrantly hypermethylated genes are already repressed in pre-cancerous tissue, we suggest that their hypermethylation does not directly contribute to cancer development via silencing. Instead aberrant hypermethylation reflects developmental history and the perturbation of epigenetic mechanisms maintaining these repressed promoters in a hypomethylated state in normal cells.Publisher PDFPeer reviewe

The mating-specific Gα interacts with a kinesin-14 and regulates pheromone-induced nuclear migration in budding yeast

As a budding yeast cell elongates toward its mating partner, cytoplasmic microtubules connect the nucleus to the cell cortex at the growth tip. The Kar3 kinesin-like motor protein is then thought to stimulate plus-end depolymerization of these microtubules, thus drawing the nucleus closer to the site where cell fusion and karyogamy will occur. Here, we show that pheromone stimulates a microtubule-independent interaction between Kar3 and the mating-specific Gα protein Gpa1 and that Gpa1 affects both microtubule orientation and cortical contact. The membrane localization of Gpa1 was found to polarize early in the mating response, at about the same time that the microtubules begin to attach to the incipient growth site. In the absence of Gpa1, microtubules lose contact with the cortex upon shrinking and Kar3 is improperly localized, suggesting that Gpa1 is a cortical anchor for Kar3. We infer that Gpa1 serves as a positional determinant for Kar3-bound microtubule plus ends during mating. © 2009 by The American Society for Cell Biology

Effective intra-S checkpoint responses to UVC in primary human melanocytes and melanoma cell lines

The objective of this study was to assess potential functional attenuation or inactivation of the intra-S checkpoint during melanoma development. Proliferating cultures of skin melanocytes, fibroblasts and melanoma cell lines were exposed to increasing fluences of UVC and intra-S checkpoint responses were quantified. Melanocytes displayed stereotypic intra-S checkpoint responses to UVC qualitatively and quantitatively equivalent to those previously demonstrated in skin fibroblasts. In comparison to fibroblasts, primary melanocytes displayed reduced UVC-induced inhibition of DNA strand growth and enhanced degradation of p21Waf1 after UVC, suggestive of enhanced bypass of UVC-induced DNA photoproducts. All nine melanoma cell lines examined, including those with activating mutations in BRAF or and NRAS oncogenes, also displayed proficiency in activation of the intra-S checkpoint in response to UVC irradiation. The results indicate that bypass of oncogene-induced senescence during melanoma development was not associated with inactivation of the intra-S checkpoint response to UVC-induced DNA replication stress

Variable outcome and methylation status according to CEBPA mutant type in double-mutated acute myeloid leukemia patients and the possible implications for treatment

Although CEBPA double-mutated (CEBPA^{DM}) acute myeloid leukemia is considered to be a favorable-risk disease, relapse remains a major cause of treatment failure. Most CEBPA^{DM} patients have a classic biallelic mutant combination with an N-terminal mutation leading to production of p30 protein plus a C-terminal loss-of-function in-frame indel mutation (CEBPA^{Classic-DM}), but approximately one-third of cases have one or more non-classic mutations, with diverse combinations reported, and there is little information on the consequences of such mutants. We evaluated outcome in a cohort of 104 CEBPA^{DM} patients, 79 CEBPA^{Classic-DM} and 25 with non-classic mutants, and found that the latter may have poorer survival (5-year overall survival 64% vs. 46%; P=0.05), particularly post relapse (41% vs. 0%; P=0.02). However, for this analysis, all non-classic cases were grouped together, irrespective of mutant combination. As CEBPA^{DM} cases have been reported to be hypermethylated, we used methylation profiling to assess whether this could segregate the different mutants. We developed a CEBPA^{Classic-DM} methylation signature from a preliminary cohort of 10 CEBPA^{DM} (including 8 CEBPA^{Classic-DM}) and 30 CEBPA wild-type (CEBPA^{WT}) samples, and independently validated the signature in 17 CEBPA^{Classic-DM} cases. Assessment of the signature in 16 CEBPA^{DM} cases with different non-classic mutant combinations showed that only 31% had a methylation profile equivalent to CEBPA^{Classic-DM} whereas for 69% the profile was either intermediate between CEBPA^{Classic-DM} and CEBPA^{WT} or equivalent to CEBPA^{WT}. These results suggest that CEBPA^{DM} cases with non-classic mutants may be functionally different from those with CEBPA^{Classic-DM} mutants, and should not automatically be included in the same prognostic group. (AML12 is registered under ISRCTN17833622 and AML15 under ISRCTN17161961)

Elevated FOXG1 and SOX2 in glioblastoma enforces neural stem cell identity through transcriptional control of cell cycle and epigenetic regulators

Glioblastoma multiforme (GBM) is an aggressive brain tumor driven by cells with hallmarks of neural stem (NS) cells. GBM stem cells frequently express high levels of the transcription factors FOXG1 and SOX2. Here we show that increased expression of these factors restricts astrocyte differentiation and can trigger dedifferentiation to a proliferative NS cell state. Transcriptional targets include cell cycle and epigenetic regulators (e.g., Foxo3, Plk1, Mycn, Dnmt1, Dnmt3b, and Tet3). Foxo3 is a critical repressed downstream effector that is controlled via a conserved FOXG1/SOX2-bound cis-regulatory element. Foxo3 loss, combined with exposure to the DNA methylation inhibitor 5-azacytidine, enforces astrocyte dedifferentiation. DNA methylation profiling in differentiating astrocytes identifies changes at multiple polycomb targets, including the promoter of Foxo3 In patient-derived GBM stem cells, CRISPR/Cas9 deletion of FOXG1 does not impact proliferation in vitro; however, upon transplantation in vivo, FOXG1-null cells display increased astrocyte differentiation and up-regulate FOXO3. In contrast, SOX2 ablation attenuates proliferation, and mutant cells cannot be expanded in vitro. Thus, FOXG1 and SOX2 operate in complementary but distinct roles to fuel unconstrained self-renewal in GBM stem cells via transcriptional control of core cell cycle and epigenetic regulators.H.B. was supported by a Wellcome Trust Clinician Research Training Fellowship. E.J. was supported by the Biotechnology and Biological Sciences Research Council. M.A.M.-T. is supported by an EMBO training fellowship. K.F. is supported by a studentship from Cancer Research UK (A19680). R.B. is supported by a studentship from the Science Without Borders Program (CAPES, Brazil). D.S. is a Cancer Research UK Career Development Fellow (reference C47648/A20837), and work in his laboratory is also supported by a Medical Research Council University grant to the MRC Human Genetics Unit. S.M.P. is a Cancer Research UK Senior Research Fellow (A17368)