Shoshonitic enclaves in the high Sr/Y Nyemo pluton, southern Tibet: Implications for Oligocene magma mixing and the onset of extension of the southern Lhasa terrane

Post-collisional potassic and high Sr/Y magmatism in the Lhasa terrane provides critical constraints on the timing and mechanism of subduction of Indian lithosphere and its role in the uplift of the Tibetan Plateau. Here, we report whole-rock geochemistry, mineral geochemistry, zircon U Pb ages, and in situ zircon Hf isotope ratios for the Nyemo pluton, a representative example of such magmatism. The Nyemo pluton is composed of high Sr/Y host rocks and coeval shoshonitic mafic microgranular enclaves (MMEs). Whole-rock compositions of the host rocks and MMEs form linear trends in Harker diagrams, consistent with modification of both end-members by magma mixing. Although the main high Sr/Y phase of the pluton formed by partial melting of the lower crust of the thickened Lhasa terrane, the MMEs display abnormally enriched light rare earth elements, low whole-rock ε_(Nd)(t) and low zircon ε_(Hf)(t) that suggest derivation from low degree melting of hydrous and enriched mantle. Based on the occurrence of shoshonitic magma and high La/Yb and high Sr/Y with adakitic affinity host rocks around 30 Ma, the Nyemo pluton is best explained as a record of onset of extension that resulted from convective removal of the mantle lithosphere beneath Tibet in the Oligocene

Forest carbon stocks and fluxes in physiographic zones of India

<p>Abstract</p> <p>Background</p> <p>Reducing carbon Emissions from Deforestation and Degradation (REDD+) is of central importance to combat climate change. Foremost among the challenges is quantifying nation's carbon emissions from deforestation and degradation, which requires information on forest carbon storage. Here we estimated carbon storage in India's forest biomass for the years 2003, 2005 and 2007 and the net flux caused by deforestation and degradation, between two assessment periods i.e., Assessment Period first (ASP I), 2003-2005 and Assessment Period second (ASP II), 2005-2007.</p> <p>Results</p> <p>The total estimated carbon stock in India's forest biomass varied from 3325 to 3161 Mt during the years 2003 to 2007 respectively. There was a net flux of 372 Mt of CO₂in ASP I and 288 Mt of CO₂in ASP II, with an annual emission of 186 and 114 Mt of CO₂respectively. The carbon stock in India's forest biomass decreased continuously from 2003 onwards, despite slight increase in forest cover. The rate of carbon loss from the forest biomass in ASP II has dropped by 38.27% compared to ASP I.</p> <p>Conclusion</p> <p>With the Copenhagen Accord, India along with other BASIC countries China, Brazil and South Africa is voluntarily going to cut emissions. India will voluntary reduce the emission intensity of its GDP by 20-25% by 2020 in comparison to 2005 level, activities like REDD+ can provide a relatively cost-effective way of offsetting emissions, either by increasing the removals of greenhouse gases from the atmosphere by afforestation programmes, managing forests, or by reducing emissions through deforestation and degradation.</p

Crude Oil-Degradation and Plasmid Profile of Nitrifying Bacteria Isolated from Oil-Impacted Mangrove Sediment in the Niger Delta of Nigeria

The crude oil degradability and plasmid profile of autotrophic nitrifying bacteria, Nitrosomonas and Nitrobacter species, isolated from mangrove sediment in the Niger Delta of Nigeria were studied. The effects of temperature, pH and optical density on the utilization of different carbon sources by the bacteria were also investigated. Results showed that nitrifying bacteria could utilize kerosene, diesel oil, jet fuel and engine oil as carbon sources. None utilized hexane and xylene but moderate growth was observed in benzene, phenol and toluene. However, their ability to utilized crude oil varied both in rates of utilization and in growth profiles. Mixed culture of the isolates degrades 52 % of crude oil introduced into the medium followed by Nitrosomonas sp. with 40 % degradation. The least was Nitrobacter sp. with 20 % degradation. The ability of the autotrophs to degrade crude oil was found to be plasmid-mediated through curing experiment and electrophoresis. The size of the plasmid involved was estimated to be 23 kb. The high crude oil utilization of the mixed culture implies that nitrifying bacteria isolated from contaminated ecosystem are excellent crude oil degraders and can be harnessed for bioremediation purposes

A multicentre validation of Metasin: a molecular assay for the intraoperative assessment of sentinel lymph nodes from breast cancer patients

Aims: Treatment strategies for breast cancer continue to evolve. No uniformity exists in the UK for the management of node‐positive breast cancer patients. Most centres continue to use conventional histopathology of sampled sentinel lymph nodes (SLNs), which requires delayed axillary clearance in up to 25% of patients. Some use touch imprint cytology or frozen section for intraoperative testing, although both have inherent sensitivity issues. An intraoperative molecular diagnostic approach helps to overcome some of these limitations. The aim of this study was to assess the clinical effectiveness of Metasin, a molecular method for the intraoperative evaluation of SLNs. Methods and results: RNA from 3296 lymph nodes from 1836 patients undergoing SLN assessment was analysed with Metasin. Alternate slices of tissue were examined in parallel by histology. Cases deemed to be discordant were analysed by protein gel electrophoresis. There was concordance between Metasin and histology in 94.1% of cases, with a sensitivity of 92% [95% confidence interval (CI) 88–94%] and a specificity of 97% (95% CI 95–97%). Positive and negative predictive values were 88% and 98%, respectively. Over half of the discordant cases (4.4%) were ascribed to tissue allocation bias (TAB). Conclusions: Clinical validation of the Metasin assay suggests that it is sufficiently sensitive and specific to make it fit for purpose in the intraoperative setting

Broad targeting of resistance to apoptosis in cancer

Apoptosis or programmed cell death is natural way of removing aged cells from the body. Most of the anti-cancer therapies trigger apoptosis induction and related cell death networks to eliminate malignant cells. However, in cancer, de-regulated apoptotic signaling, particularly the activation of an anti-apoptotic systems, allows cancer cells to escape this program leading to uncontrolled proliferation resulting in tumor survival, therapeutic resistance and recurrence of cancer. This resistance is a complicated phenomenon that emanates from the interactions of various molecules and signaling pathways. In this comprehensive review we discuss the various factors contributing to apoptosis resistance in cancers. The key resistance targets that are discussed include (1) Bcl-2 and Mcl-1 proteins; (2) autophagy processes; (3) necrosis and necroptosis; (4) heat shock protein signaling; (5) the proteasome pathway; (6) epigenetic mechanisms; and (7) aberrant nuclear export signaling. The shortcomings of current therapeutic modalities are highlighted and a broad spectrum strategy using approaches including (a) gossypol; (b) epigallocatechin-3-gallate; (c) UMI-77 (d) triptolide and (e) selinexor that can be used to overcome cell death resistance is presented. This review provides a roadmap for the design of successful anti-cancer strategies that overcome resistance to apoptosis for better therapeutic outcome in patients with cancer

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Genome-Scale Metabolic Modeling Elucidates the Role of Proliferative Adaptation in Causing the Warburg Effect

The Warburg effect - a classical hallmark of cancer metabolism - is a counter-intuitive phenomenon in which rapidly proliferating cancer cells resort to inefficient ATP production via glycolysis leading to lactate secretion, instead of relying primarily on more efficient energy production through mitochondrial oxidative phosphorylation, as most normal cells do. The causes for the Warburg effect have remained a subject of considerable controversy since its discovery over 80 years ago, with several competing hypotheses. Here, utilizing a genome-scale human metabolic network model accounting for stoichiometric and enzyme solvent capacity considerations, we show that the Warburg effect is a direct consequence of the metabolic adaptation of cancer cells to increase biomass production rate. The analysis is shown to accurately capture a three phase metabolic behavior that is observed experimentally during oncogenic progression, as well as a prominent characteristic of cancer cells involving their preference for glutamine uptake over other amino acids

Serum Metabolomics Reveals Higher Levels of Polyunsaturated Fatty Acids in Lepromatous Leprosy: Potential Markers for Susceptibility and Pathogenesis

Leprosy is an infectious disease caused by the obligate intracellular bacterium Mycobacterium leprae. M. leprae infects the skin and nerves, leading to disfigurement and nerve damage, with the severity of the disease varying widely. We believe there are multiple factors (genetic, bacterial, nutritional and environmental), which may explain the differences in clinical manifestations of the disease. We studied the metabolites in the serum of infected patients to search for specific molecules that may contribute to variations in the severity of disease seen in leprosy. We found that there were variations in levels of certain lipids in the patients with different bacterial loads. In particular, we found that three polyunsaturated fatty acids (PUFAs) involved in the inhibition of inflammation were more abundant in the serum of patients with higher bacterial loads. However, we do not know whether these PUFAs originated from the host or the bacteria. The variations in the metabolite profile that we observed provide a foundation for future research into the explanations of how leprosy causes disease