Multispecies Sustainability

The sustainability concept in its current form suffers from reductionism. The common interpretation of ‘meeting the needs of the present without compromising the ability of future generations to meet their own needs’ fails to explicitly recognize their interdependence with needs of current and future non-human generations. Here, we argue that the focus of sustainability on human well-being – a purely utilitarian view of nature as a resource for humanity – limits its conceptual and analytical power, as well as real-world sustainability transformation efforts. We propose a broadened concept of ‘multispecies sustainability’ by acknowledging interdependent needs of multiple species’ current and future generations. We develop the concept in three steps: (1) discussing normative aspects, fundamental principles underlying the con- cept, and potential visual models, (2) showcasing radically diverging futures emerging from a scenario thought experiment based on the axes sustainable-unsustainable and multispecies-anthropocentric, and (3) exploring how multispecies sustainability can be applied to research and policy-making through two case studies (a multispecies stakeholder framework and the Healthy Urban Microbiome Initiative)

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

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Nurses' perceptions of aids and obstacles to the provision of optimal end of life care in ICU

Contains fulltext : 172380.pdf (publisher's version ) (Open Access

Comparative Analysis of Stk11/Lkb1 versus Pten Deficiency in Lung Adenocarcinoma Induced by CRISPR/Cas9

This study focused on STK11, PTEN, KRAS, and TP53, which are often found to be mutated in lung cancer. We compared Stk11 and Pten implication in lung cancer in combination with loss of Trp53 and gain of function of Kras in a CRISPR/Cas9 mouse model. Mice with loss of Stk11, Trp53, and KrasG12D mutation (SKT) reached human endpoint at around four months post-initiation. In comparison, mice with loss of Pten, Trp53, and KrasG12D mutation (PKT) survived six months or longer post-initiation. Pathological examination revealed an increase in proliferation in SKT deficient lung epithelia compared to PKT. This difference was independent of Pten loss, indicating that loss of Pten is dispensable for cell proliferation in lung adenocarcinoma. Furthermore, tumors with loss of Stk11, Trp53, and KrasG12D mutation had a significantly higher progression rate, monitored by PET/MRI scanning, compared to mice with loss of Pten, Trp53, and KrasG12D mutation, revealing that mutations in Stk11 are essential for adenocarcinoma progression. Overall, by using the CRISPR/Cas9 mouse model of lung adenocarcinoma, we showed that mutations in Stk11 are a key driver, whereas loss of Pten is dispensable for adenocarcinoma progression

Transposon copy number in the RMCE-in HEK, HeLa, and murine ES cell clones.

<p><b>(A)</b> Southern blot of selected genomic DNA from <i>KpnI</i> digested HEK, (<b>B)</b> HeLa and <i>PstI</i> digested (<b>C)</b> mES clones. A 700bp dCTP³² labeled RFP probe (red rectangle <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0161471#pone.0161471.g001" target="_blank">Fig 1A</a>) identified transposition of the gene cassette at bands > 2900bp as illustrated in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0161471#pone.0161471.g001" target="_blank">Fig 1A</a>. Clone numbers are depicted above each lane.</p