Hypoxia in the northern Gulf of Mexico: Does the science support the Plan to Reduce, Mitigate, and Control Hypoxia?

We update and reevaluate the scientific information on the distribution, history, and causes of continental shelf hypoxia that supports the 2001 Action Plan for Reducing, Mitigating, and Controlling Hypoxia in the Northern Gulf of Mexico (Mississippi River/Gulf of Mexico Watershed Nutrient Task Force 2001), incorporating data, publications, and research results produced since the 1999 integrated assessment. The metric of mid-summer hypoxic area on the Louisiana-Texas shelf is an adequate and suitable measure for continued efforts to reduce nutrients loads from the Mississippi River and hypoxia in the northern Gulf of Mexico as outlined in the Action Plan. More frequent measurements of simple metrics (e.g., area and volume) from late spring through late summer would ensure that the metric is representative of the system in any given year and useful in a public discourse of conditions and causes. The long-term data on hypoxia, sources of nutrients, associated biological parameters, and paleoindicators continue to verify and strengthen the relationship between the nitrate-nitrogen load of the Mississippi River, the extent of hypoxia, and changes in the coastal ecosystem (eutrophication and worsening hypoxia). Multiple lines of evidence, some of them representing independent data sources, are consistent with the big picture pattern of increased eutrophication as a result of long-term nutrient increases that result in excess carbon production and accumulation and, ultimately, bottom water hypoxia. The additional findings arising since 1999 strengthen the science supporting the Action Plan that focuses on reducing nutrient loads, primarily nitrogen, through multiple actions to reduce the size of the hypoxic zone in the northern Gulf of Mexico

Half brain irradiation in a murine model of breast cancer brain metastasis: Magnetic resonance imaging and histological assessments of dose-response

Background: Brain metastasis is becoming increasingly prevalent in breast cancer due to improved extra-cranial disease control. With emerging availability of modern image-guided radiation platforms, mouse models of brain metastases and small animal magnetic resonance imaging (MRI), we examined brain metastases\u27 responses from radiotherapy in the pre-clinical setting. In this study, we employed half brain irradiation to reduce inter-subject variability in metastases dose-response evaluations. Methods: Half brain irradiation was performed on a micro-CT/RT system in a human breast cancer (MDA-MB-231-BR) brain metastasis mouse model. Radiation induced DNA double stranded breaks in tumors and normal mouse brain tissue were quantified using γ-H2AX immunohistochemistry at 30 min (acute) and 11 days (longitudinal) after half-brain treatment for doses of 8, 16 and 24 Gy. In addition, tumor responses were assessed volumetrically with in-vivo longitudinal MRI and histologically for tumor cell density and nuclear size. Results: In the acute setting, γ-H2AX staining in tumors saturated at higher doses while normal mouse brain tissue continued to increase linearly in the phosphorylation of H2AX. While γ-H2AX fluorescence intensities returned to the background level in the brain 11 days after treatment, the residual γ-H2AX phosphorylation in the radiated tumors remained elevated compared to un-irradiated contralateral tumors. With radiation, MRI-derived relative tumor growth was significantly reduced compared to the un-irradiated side. While there was no difference in MRI tumor volume growth between 16 and 24 Gy, there was a significant reduction in tumor cell density from histology with increasing dose. In the longitudinal study, nuclear size in the residual tumor cells increased significantly as the radiation dose was increased. Conclusions: Radiation damages to the DNAs in the normal brain parenchyma are resolved over time, but remain unrepaired in the treated tumors. Furthermore, there is a radiation dose response in nuclear size of surviving tumor cells. Increase in nuclear size together with unrepaired DNA damage indicated that the surviving tumor cells post radiation had continued to progress in the cell cycle with DNA replication, but failed cytokinesis. Half brain irradiation provides efficient evaluation of dose-response for cancer cell lines, a pre-requisite to perform experiments to understand radio-resistance in brain metastases

Electronic structure and the glass transition in pnictide and chalcogenide semiconductor alloys. Part I: The formation of the ppσpp\sigma-network

Semiconductor glasses exhibit many unique optical and electronic anomalies. We have put forth a semi-phenomenological scenario (J. Chem. Phys. 132, 044508 (2010)) in which several of these anomalies arise from deep midgap electronic states residing on high-strain regions intrinsic to the activated transport above the glass transition. Here we demonstrate at the molecular level how this scenario is realized in an important class of semiconductor glasses, namely chalcogen and pnictogen containing alloys. Both the glass itself and the intrinsic electronic midgap states emerge as a result of the formation of a network composed of $\sigma$-bonded atomic $p$-orbitals that are only weakly hybridized. Despite a large number of weak bonds, these $pp\sigma$-networks are stable with respect to competing types of bonding, while exhibiting a high degree of structural degeneracy. The stability is rationalized with the help of a hereby proposed structural model, by which $pp\sigma$-networks are symmetry-broken and distorted versions of a high symmetry structure. The latter structure exhibits exact octahedral coordination and is fully covalently-bonded. The present approach provides a microscopic route to a fully consistent description of the electronic and structural excitations in vitreous semiconductors.Comment: 22 pages, 17 figures, revised version, final version to appear in J. Chem. Phy

Draft genome sequences of gammaproteobacterial methanotrophs isolated from marine ecosystems

The genome sequences of Methylobacter marinus A45, Methylobacter sp. strain BBA5.1, and Methylomarinum vadi IT-4 were obtained. These aerobic methanotrophs are typical members of coastal and hydrothermal vent marine ecosystems

Regulation of the apoptotic genes in breast cancer cells by the transcription factor CTCF

CTCF is a highly conserved and ubiquitous transcription factor with versatile functions. We previously demonstrated that elevated protein levels of CTCF in breast cancer cells were associated with the specific anti-apoptotic function of CTCF. We used proteomics and microarray approaches to identify regulatory targets of CTCF specific for breast cancer cells. Among the CTCF identified targets were proteins involved in the control of apoptosis. A proapoptotic protein, Bax, negatively regulated by CTCF, was chosen for further investigation. Repression of the human Bax gene at the transcriptional level by CTCF in breast cancer cells was confirmed by real-time PCR. Two CTCF binding sites within the Bax promoter were identified by electrophoretic mobility shift assay and footprinting. In reporter assays, the Bax-luciferase reporter construct, containing CTCF-binding sites, was negatively regulated by CTCF. In vivo, CTCF occupied its binding sites in breast cancer cells and tissues, as confirmed by chromatin immunoprecipitation assay. Our findings suggest a possible mechanism of the specific CTCF anti-apoptotic function in breast cancer cells whereby CTCF is bound to the Bax promoter, resulting in repression of Bax and inhibition of apoptosis; depletion of CTCF leads to activation of Bax and apoptotic death. CTCF binding sites in the Bax promoter are unmethylated in all cells and tissues inspected. Therefore, specific CTCF interaction with the Bax promoter in breast cancer cells, and the functional outcome, may depend on a combination of epigenetic factors characteristic for these cells. Interestingly, CTCF appears to be a negative regulator of other proapoptotic genes (for example, Fas, Apaf-1, TP531NP1). Conversely, stimulating effects of CTCF on the anti-apoptotic genes (Bcl-2, Bag-3) have been observed. Taken together, these findings suggest that specific mechanisms have evolved in breast cancer cells to protect them from apoptosis; regulation of apoptotic genes by CTCF appears to be one of the resistance strategies

Spatial complementarity and the coexistence of species

Coexistence of apparently similar species remains an enduring paradox in ecology. Spatial structure has been predicted to enable coexistence even when population-level models predict competitive exclusion if it causes each species to limit its own population more than that of its competitor. Nevertheless, existing hypotheses conflict with regard to whether clustering favours or precludes coexistence. The spatial segregation hypothesis predicts that in clustered populations the frequency of intra-specific interactions will be increased, causing each species to be self-limiting. Alternatively, individuals of the same species might compete over greater distances, known as heteromyopia, breaking down clusters and opening space for a second species to invade. In this study we create an individual-based model in homogeneous two-dimensional space for two putative sessile species differing only in their demographic rates and the range and strength of their competitive interactions. We fully characterise the parameter space within which coexistence occurs beyond population-level predictions, thereby revealing a region of coexistence generated by a previously-unrecognised process which we term the triadic mechanism. Here coexistence occurs due to the ability of a second generation of offspring of the rarer species to escape competition from their ancestors. We diagnose the conditions under which each of three spatial coexistence mechanisms operates and their characteristic spatial signatures. Deriving insights from a novel metric — ecological pressure — we demonstrate that coexistence is not solely determined by features of the numerically-dominant species. This results in a common framework for predicting, given any pair of species and knowledge of the relevant parameters, whether they will coexist, the mechanism by which they will do so, and the resultant spatial pattern of the community. Spatial coexistence arises from complementary combinations of traits in each species rather than solely through self-limitation