Magnetic patterning of (Ga,Mn)As by hydrogen passivation

We present an original method to magnetically pattern thin layers of (Ga,Mn)As. It relies on local hydrogen passivation to significantly lower the hole density, and thereby locally suppress the carrier-mediated ferromagnetic phase. The sample surface is thus maintained continuous, and the minimal structure size is of about 200 nm. In micron-sized ferromagnetic dots fabricated by hydrogen passivation on perpendicularly magnetized layers, the switching fields can be maintained closer to the continuous film coercivity, compared to dots made by usual dry etch techniques

Hypoxia-induced long non-coding RNA Malat1 is dispensable for renal ischemia/reperfusion-injury

Renal ischemia-reperfusion (I/R) injury is a major cause of acute kidney injury (AKI). Non-coding RNAs are crucially involved in its pathophysiology. We identified hypoxia-induced long non-coding RNA Malat1 (Metastasis Associated Lung Adenocarcinoma Transcript 1) to be upregulated in renal I/R injury. We here elucidated the functional role of Malat1 in vitro and its potential contribution to kidney injury in vivo. Malat1 was upregulated in kidney biopsies and plasma of patients with AKI, in murine hypoxic kidney tissue as well as in cultured and ex vivo sorted hypoxic endothelial cells and tubular epithelial cells. Malat1 was transcriptionally activated by hypoxia-inducible factor 1-a. In vitro, Malat1 inhibition reduced proliferation and the number of endothelial cells in the S-phase of the cell cycle. In vivo, Malat1 knockout and wildtype mice showed similar degrees of outer medullary tubular epithelial injury, proliferation, capillary rarefaction, inflammation and fibrosis, survival and kidney function. Small-RNA sequencing and whole genome expression analysis revealed only minor changes between ischemic Malat1 knockout and wildtype mice. Contrary to previous studies, which suggested a prominent role of Malat1 in the induction of disease, we did not confirm an in vivo role of Malat1 concerning renal I/Rinjury

Integrative Analysis of Many Weighted Co-Expression Networks Using Tensor Computation

The rapid accumulation of biological networks poses new challenges and calls for powerful integrative analysis tools. Most existing methods capable of simultaneously analyzing a large number of networks were primarily designed for unweighted networks, and cannot easily be extended to weighted networks. However, it is known that transforming weighted into unweighted networks by dichotomizing the edges of weighted networks with a threshold generally leads to information loss. We have developed a novel, tensor-based computational framework for mining recurrent heavy subgraphs in a large set of massive weighted networks. Specifically, we formulate the recurrent heavy subgraph identification problem as a heavy 3D subtensor discovery problem with sparse constraints. We describe an effective approach to solving this problem by designing a multi-stage, convex relaxation protocol, and a non-uniform edge sampling technique. We applied our method to 130 co-expression networks, and identified 11,394 recurrent heavy subgraphs, grouped into 2,810 families. We demonstrated that the identified subgraphs represent meaningful biological modules by validating against a large set of compiled biological knowledge bases. We also showed that the likelihood for a heavy subgraph to be meaningful increases significantly with its recurrence in multiple networks, highlighting the importance of the integrative approach to biological network analysis. Moreover, our approach based on weighted graphs detects many patterns that would be overlooked using unweighted graphs. In addition, we identified a large number of modules that occur predominately under specific phenotypes. This analysis resulted in a genome-wide mapping of gene network modules onto the phenome. Finally, by comparing module activities across many datasets, we discovered high-order dynamic cooperativeness in protein complex networks and transcriptional regulatory networks

Pparγ2 Is a Key Driver of Longevity in the Mouse

Aging involves a progressive physiological remodeling that is controlled by both genetic and environmental factors. Many of these factors impact also on white adipose tissue (WAT), which has been shown to be a determinant of lifespan. Interrogating a transcriptional network for predicted causal regulatory interactions in a collection of mouse WAT from F2 crosses with a seed set of 60 known longevity genes, we identified a novel transcriptional subnetwork of 742 genes which represent thus-far-unknown longevity genes. Within this subnetwork, one gene was Pparg (Nr1c3), an adipose-enriched nuclear receptor previously not associated with longevity. In silico, both the PPAR signaling pathway and the transcriptional signature of Pparγ agonist rosiglitazone overlapped with the longevity subnetwork, while in vivo, lowered expression of Pparg reduced lifespan in both the lipodystrophic Pparg1/2-hypomorphic and the Pparg2-deficient mice. These results establish Pparγ2 as one of the determinants of longevity and suggest that lifespan may be rather determined by a purposeful genetic program than a random process

Polariton-polariton interaction constants in microcavities

International audienc

The coral proto free ocean carbon enrichment system (CP-FOCE): Engineering and development

Ocean acidification is driven by increasing atmospheric CO and represents a key threat to the Great Barrier Reef (GBR) and other coral reefs globally. Previous investigations have depended on studies in aquaria that are compromised by reduced ecological complexity and buffering capacity, and problems associated with containment. These aquaria studies also include artifacts such as artificial flow, light, temperature, and water quality conditions. In order to avoid these issues a new technology was needed for in situ science. This need was the driver behind development of the Free Ocean Carbon Enrichment (FOCE) approach. FOCE is similar in approach to the Free Air Carbon Enrichment (FACE) experiments pursued on land for almost two decades. FOCE as a systems concept was developed at the Monterey Bay Aquarium Research Institute (MBARI) to perform controlled in situ studies on the effects of increased carbon dioxide on ocean environments. FOCE systems inject carbon dioxide enriched water into the desired control volume to lower the environmental pH to a specified value. The challenge of maintaining reef conditions while manipulating the carbonate chemistry further advanced the FOCE concept. A shallow water reef version of FOCE was needed to perform this research at the University of Queensland. Working with MBARI the University of Queensland developed the Coral Proto - Free Ocean Carbon Dioxide Enrichment (CP - FOCE) system. Although the CP-FOCE does not differ conceptually from the original FOCE it is different in a couple of respects. First, it requires that a region of the coral flat be semi-enclosed in the chamber section of CP-FOCE. This allows the required amount of CO to be optimised. Second, by closing the enclosure off fully for a short time, the oxygen levels and carbonate chemistry can be accurately measured to determine net production/respiration as well as the calcification/dissolution rates of the organisms living within the chamber. In this paper we present the engineering details of the CP-FOCE system design. This paper details the unique engineering design and challenges of the CP-FOCE system The paper briefly outlines the chemical and biological requirements that provided the technical specifications for CP-FOCE to successfully study the impacts of the changing water chemistry on the physiology of calcareous reef organisms including corals and calcareous algae. We have also a brief outline of the methods used to perform measurements of calcification and dissolution rates. Additionally, we include discussion on production and respiration rates in CP-FOCE systems when maintained at ambient and two different increased pCO scenarios. We present technical results of this first deployment and address future plans for modifications and deployments of CP-FOCE. Forthcoming peer reviewed papers will describe the biological, chemical, and geochemical responses

Living coral tissue slows skeletal dissolution related to ocean acidification

Climate change is causing major changes to marine ecosystems globally, with ocean acidification of particular concern for coral reefs. Using a 200 d in situ carbon dioxide enrichment study on Heron Island, Australia, we simulated future ocean acidification conditions, and found reduced pH led to a drastic decline in net calcification of living corals to no net growth, and accelerated disintegration of dead corals. Net calcification declined more severely than in previous studies due to exposure to the natural community of bioeroding organisms in this in situ study and to a longer experimental duration. Our data suggest that reef flat corals reach net dissolution at an aragonite saturation state (ΩAR) of 2.3 (95% confidence interval: 1.8-2.8) with 100% living coral cover and at ΩAR > 3.5 with 30% living coral cover. This model suggests that areas of the reef with relatively low coral mortality, where living coral cover is high, are likely to be resistant to carbon dioxide-induced reef dissolution