Effect of Date of Planting on Soybean Sudden Death Syndrome

The objectives of this project was to study the effect of planting date on the onset of soybean sudden death syndrome (SDS). It is believed, that avoiding planting soybeans into wet cold soil may delay or lower the severity of SDS. Planting date for soybeans is important and can have a large effect on yield potential.

Death of Dr Francisco Javier Ayala-Carcedo, Spanish INHIGEO Member, at Burgos, Spain, 28 November 2004

Death of Dr Francisco Javier Ayala-Carcedo, Spanish lNHIGEO Member, at Burgos, Spain, 28 November 2004

Implication of the oep16-1 mutation in a flu-independent, singlet oxygen-regulated cell death pathway in Arabidopsis thaliana

Singlet oxygen is a prominent form of reactive oxygen species in higher plants. It is easily formed from molecular oxygen by triplet–triplet interchange with excited porphyrin species. Evidence has been obtained from studies on the flu mutant of Arabidopsis thaliana of a genetically determined cell death pathway that involves differential changes at the transcriptome level. Here we report on a different cell death pathway that can be deduced from the analysis of oep16 mutants of A. thaliana. Pure lines of four independent OEP16-deficient mutants with different cell death properties were isolated. Two of the mutants overproduced free protochlorophyllide (Pchlide) in the dark because of defects in import of NADPH:Pchlide oxidoreductase A (pPORA) and died after illumination. The other two mutants avoided excess Pchlide accumulation. Using pulse labeling and polysome profiling studies we show that translation is a major site of cell death regulation in flu and oep16 plants. flu plants respond to photooxidative stress triggered by singlet oxygen by reprogramming their translation toward synthesis of key enzymes involved in jasmonic acid synthesis and stress proteins. In contrast, those oep16 mutants that were prone to photooxidative damage were unable to respond in this way. Together, our results show that translation is differentially affected in the flu and oep16 mutants in response to singlet oxygen.

Air Mines. Urban Space Station

Air Mines The sky over the city's port was the color of a faulty screen, only partly lit up. As the silhouette of nearby buildings became darker, but more clearly visible against the fading blur-filter of a background, the realization came about how persistent a change had been taking place. Slowly, old wooden water reservoirs and rattling HVAC systems stopped being the only inhabitants of roofs. Slightly trembling, milkish jellyfish-translucent air volumes had joined the show in multiples. A few years ago artists and architects seized upon the death of buildings as their life-saving media. Equipped with constructive atlases and instruments they started disemboweling their subjects, poking about their systems, dumping out on the street the battered ugliness of their embarrassing bits and pieces, so rightly hidden by facades and height from everyday view. But, would you believe it? Even ?old ladies?, investment bankers or small children failed to get upset. Of course, old ladies are not what they used to be. It was old ladies themselves that made it happen after years of fights with the town hall, imaginative proposals and factual arguments. An industry with little financial gains but lots of welcome externalities was not, in fact, the ground for investment bankers. But they too had to admit that having otherwise stately buildings make fine particulate pencils with their facades was not the worse that could happen. Yes, making soot pencils had been found an interesting and visible end product of the endeavor, a sort of mining the air for vintage writing tools one can actually touch. The new view from the street did not seem as solid or dignified as that of old, and they hated that the market for Fine Particulates Extraction (FPE, read efpee) had to be applied on a matrix of blocks and streets that prevented undue concentration of the best or worse solutions. It had to be an evenly distributed city policy in order for the city to apply for cleaning casino money. Once the first prototypes had been deployed in buildings siding Garden Avenue or Bulwark Street even fast movers appreciated the sidekick of flower and plant smell dripping down the Urban Space Stations (USS, read use; USSs, read uses) as air and walls cooled off for a few hours after sunset. Enough. It was all nice to remember, but it was now time to go up and start the lightweight afternoon maintenance of their USS. Coop discussions had taken place all through the planning and continued through the construction phase as to how maintenance was going to be organized. Fasters had voted for a pro, pay a small amount and let them use it for rent and produce. In the end some neighbors decided they were slow enough to take care and it was now the turn. Regret came periodically, sometimes a week before, and lasted until work actually started. But lately it had been replaced by anxiety when it needed to be passed over to the next caretaker. It did not look their shift was good enough and couldn?t wait to fix it. Today small preparations needed to be made for a class visit next day from a nearby cook school. They were frequenters. It had not been easy, but it shouldn?t have been that hard. In the end, even the easiest things are hard if they involve a city, buildings and neighbors. On the face of the data, the technicalities and the way final designs had been worked out for adaptation to the different settings, the decision of where to go was self evident, but organization issues and the ever-growing politics of taste in a city of already-gentrified-rodents almost put the project in the frozen orbit of timeless beautiful future possibilities. This is how it was. A series of designs by XClinic and OSS had made it possible to adapt to different building structures, leave in most cases the roof untouched and adapted a new technology of flexing fiberglass tubes that dissipated wind pressure in smooth bending.......

Extracellular HIV-1 virus protein R causes a large inward current and cell death in cultured hippocampal neurons: Implications for AIDS pathology

The small HIV-1 accessory protein Vpr (virus protein R) is a multifunctional protein that is present in the serum and cerebrospinal fluid of AIDS patients. We previously showed that Vpr can form cation-selective ion channels across planar lipid bilayers, introducing the possibility that, if incorporated into the membranes of living cells, Vpr might form ion channels and consequently perturb the maintained ionic gradient. In this study, we demonstrate, by a variety of approaches, that Vpr added extracellularly to intact cells does indeed form ion channels. We use confocal laser scanning microscopy to examine the subcellular localization of fluorescently labeled Vpr. Plasmalemma depolarization and damage are examined using the anionic potential-sensitive dye bis(1,3-dibutylbarbituric acid) trimethine oxonol and propidium iodide (PI), respectively, and the effect of Vpr on whole-cell current is demonstrated directly by using the patch-clamp technique. We show that recombinant purified extracellular Vpr associates with the plasmalemma of hippocampal neurons to cause a large inward cation current and depolarization of the plasmalemma, eventually resulting in cell death. Thus, we demonstrate a physiological action of extracellular Vpr and present its mechanistic basis. These findings may have important implications for neuropathologies in AIDS patients who possess significant amounts of Vpr in the cerebrospinal fluid.

Phosphatidylcholine-specific phospholipase C regulates glutamate-induced nerve cell death

Phosphatidylcholine-specific phospholipase C (PC-PLC) is a necessary intermediate in transducing apoptotic signals for tumor necrosis factor and Fas/Apo-1 ligands in nonneuronal cells. The data presented here show that PC-PLC also is required in oxidative glutamate-induced programmed cell death of both immature cortical neurons and a hippocampal nerve cell line, HT22. In oxidative glutamate toxicity, which is distinct from excitotoxicity, glutamate interferes with cystine uptake by blocking the cystine/glutamate antiporter, indirectly causing a depletion of intracellular glutathione. A PC-PLC inhibitor blocks oxidative glutamate toxicity, and exogenous PC-PLC potentiates glutamate toxicity. The inhibition of PC-PLC uncouples the cystine uptake from glutamate inhibition, allowing the maintenance of glutathione synthesis and cell viability. These data suggest that PC-PLC modulates neuronal cell death through a mechanism that is distinct from that involved in nonneuronal apoptosis.

CXCR4 and CD4 mediate a rapid CD95-independent cell death in CD4+ T cells

AIDS is characterized by a progressive decrease of CD4+ helper T lymphocytes. Destruction of these cells may involve programmed cell death, apoptosis. It has previously been reported that apoptosis can be induced even in noninfected cells by HIV-1 gp120 and anti-gp120 antibodies. HIV-1 gp120 binds to T cells via CD4 and the chemokine coreceptor CXCR4 (fusin/LESTR). Therefore, we investigated whether CD4 and CXCR4 mediate gp120-induced apoptosis. We used human peripheral blood lymphocytes, malignant T cells, and CD4/CXCR4 transfectants, and found cell death induced by both cell surface receptors, CD4 and CXCR4. The induced cell death was rapid, independent of known caspases, and lacking oligonucleosomal DNA fragmentation. In addition, the death signals were not propagated via p56lck and Giα. However, the cells showed chromatin condensation, morphological shrinkage, membrane inversion, and reduced mitochondrial transmembrane potential indicative of apoptosis. Significantly, apoptosis was exclusively observed in CD4+ but not in CD8+ T cells, and apoptosis triggered via CXCR4 was inhibited by stromal cell-derived factor-1, the natural CXCR4 ligand. Thus, this mechanism of apoptosis might contribute to T cell depletion in AIDS and might have major implications for therapeutic intervention.

LFG: An anti-apoptotic gene that provides protection from Fas-mediated cell death

Programmed cell death regulates a number of biological phenomena, and the apoptotic signal must itself be tightly controlled to avoid inappropriate cell death. We established a genetic screen to search for molecules that inhibit the apoptotic signal from the Fas receptor. Here we report the isolation of a gene, LFG, that protects cells uniquely from Fas but not from the mechanistically related tumor necrosis factor α death signal. LFG is widely distributed, but remarkably is highly expressed in the hippocampus. LFG can bind to the Fas receptor, but does not regulate Fas expression or interfere with binding of an agonist antibody. Furthermore LFG does not inhibit binding of FADD to Fas.

Maternal death and obstetric care audits in Nigeria : a systematic review of barriers and enabling factors in the provision of emergency care

Acknowledgements We would like to thank Yutaka Osakabe for co-ordinating the retrieval of full text articles. The John D. and Catherine T. MacArthur Foundation supported this study, grant number 12-100074-000-INP

Revival of oscillation from mean-field-induced death : Theory and experiment

Submitted ACKNOWLEDGMENTS T. B. acknowledges the financial support from SERB, Department of Science and Technology (DST), India [Project Grant No.: SB/FTP/PS-005/2013]. D. G. acknowledges DST, India, for providing support through the INSPIRE fellowship. J. K. acknowledges Government of the Russian Federation (Agreement No. 14.Z50.31.0033 with Institute of Applied Physics RAS).

Neuronal death in the central nervous system demonstrates a non-fibrin substrate for plasmin

Mice deficient for plasminogen exhibit a variety of pathologies, all of which examined to date are reversed when the animals are also made fibrin(ogen) deficient. These results suggested that the predominant, and perhaps exclusive, physiological role of plasminogen is clearance of fibrin. Plasminogen-deficient mice also display resistance to excitotoxin-induced neurodegeneration, in contrast with wild-type mice, which are sensitive. Based on the genetic interaction between plasminogen and fibrinogen, we investigated whether resistance to neuronal cell death in the plasminogen-deficient mice is dependent on fibrin(ogen). Unexpectedly, mice lacking both plasminogen and fibrinogen are resistant to neurodegeneration to levels comparable to plasminogen-deficient mice. Therefore, plasmin acts on substrates other than fibrin during experimental neuronal degeneration, and may function similarly in other pathological settings in the central nervous system.