Superconductivity induced by Ni doping in BaFe2_2As2_2

A series of 122 phase BaFe$_{2-x}$Ni$_x$As$_2$ ($x$ = 0, 0.055, 0.096, 0.18, 0.23) single crystals were grown by self flux method and a dome-like Ni doping dependence of superconducting transition temperature is discovered. The transition temperature $T_c^{on}$ reaches a maximum of 20.5 K at $x$ = 0.096, and it drops to below 4 K as $x$ $\geq$ 0.23. The negative thermopower in the normal state indicates that electron-like charge carrier indeed dominates in this system. This Ni-doped system provides another example of superconductivity induced by electron doping in the 122 phase.Comment: 7 pages, 5 figures, revised version, added EDX result, accepted for special issue of NJ

Superconductivity induced by cobalt doping in iron-based oxyarsenides

Chemical doping has recently become a very important strategy to induce superconductivity especially in complex compounds. Distinguished examples include Ba-doped La$_2$CuO$_4$ (the first high temperature superconductor), K-doped BaBiO$_3$, K-doped C$_{60}$ and Na$_{x}$CoO$_{2}\cdot y$H$_{2}$O. The most recent example is F-doped LaFeAsO, which leads to a new class of high temperature superconductors. One notes that all the above dopants are non-magnetic, because magnetic atoms generally break superconducting Cooper pairs. In addition, the doping site was out of the (super)conducting structural unit (layer or framework). Here we report that superconductivity was realized by doping magnetic element cobalt into the (super)conducting-active Fe$_2$As$_2$ layers in LaFe$_{1-x}$Co$_{x}$AsO. At surprisingly small Co-doping level of $x$=0.025, the antiferromagnetic spin-density-wave transition in the parent compound is completely suppressed, and superconductivity with $T_c\sim$ 10 K emerges. With increasing Co content, $T_c$ shows a maximum of 13 K at $x\sim 0.075$, and then drops to below 2 K at $x$=0.15. This result suggests essential differences between previous cuprate superconductor and the present iron-based arsenide one.Comment: 4 pages, 4 figure

Superconductivity in Co-doped SmFeAsO

Here we report the synthesis and basic characterization of SmFe1-xCoxAsO (x=0.10, 0.15). The parent compound SmFeAsO itself is not superconducting but shows an antiferromagnetic order near 150 K, which must be suppressed by doping before superconductivity emerges. With Co-doping in the FeAs planes, antiferromagnetic order is destroyed and superconductivity occurs at 15 K. Similar to LaFe1-xCoxAsO, the SmFe1-xCoxAsO system appears to tolerate considerable disorder in the FeAs planes. This result is important, which indicates difference between cuprare superconductors and the iron-based arsenide ones.Comment: 11 pages, 3 figure

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

International audienceIn 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field